StemCell Therapy

Fathers Day is celebrated on different days in various places around the world, but most of them honor their dads on the third Sunday in June. Somehow it is always so difficult to come up with an idea of what could be the best present to show our love to our dads as they rarely need anything, and actually, nothing seems good enough to express our gratitude.

But what it takes is just a little bit of creativity. This woman on TikTok decided that she could recreate some of her dads photos from his youth and make a cute video for him, showing how similar they actually look.

More info: TikTok

Image credits: lakynthrifts

TikToker lakynbowman, also known as Lakyn Bowman, is a 26-year-old woman from West Tennessee who has a business of transforming her thrift finds into home decor to promote sustainability.

She is also quite busy creating content on social media, especially on TikTok, where she shares her thrift finds for her home, her business and also shows what outfits can be composed of second-hand clothing.

Image credits: lakynthrifts

Image credits: lakynthrifts

Bored Panda has already talked about one of her videos that went viral with 8.8 million views a few months ago. In that video, Lakyn decided to recreate her grandmothers photos from when she was young as a gift for her birthday.

She wanted to surprise her grandma and did her hair and makeup exactly like in the pictures. The granddaughter also found some clothes that looked very similar and posed in the same way as her grandma did. If you would like to read more, you can follow this link.

Image credits: lakynbowman

This time we are looking at her latest photo recreation video that she dedicated to her dad in honor of Fathers Day. She again found similar-looking clothes and manipulated her hair to look like she had a short bob like her dad when he was a kid. She nailed the poses and the comparison shots are proof that these two people are definitely family.

Lakyn herself confessed in the text overlay in the video that she was a bit freaked out looking at her dads old photos and seeing how much the two of them look alike, and its fascinating to observe with the naked eye how genes work.

Image credits: lakynbowman

Image credits: lakynbowman

While seeing photos side by side is very satisfying, the best part about this gift was the dads reaction. Lakyn posted a video of her dad watching the montage for the first time and it made the dad quite emotional as he couldnt stop smiling.

The man recognized his jersey and his coat, praising his daughter for doing such a good job. Actually, he was so impressed that he wanted to see the video a couple of more times.

You can hear Lakyn asking her dad which of the recreations he liked the most and his answer was I like all of them! But he was especially happy about the one in which she was wearing a red jacket because it was the actual jacket he wore in that photo.

The dad also revealed a little bit of more context to the photo in which he was wearing a blue shirt. Apparently, he was a cheerleader for a while because he wasnt allowed to play more than 2 basketball games on a weekend, so he asked if he could participate in the game as a cheerleader.

Image credits: lakynbowman

Image credits: lakynbowman

The dad said that he remembered all of the photos and you could see the nostalgia in his eyes reminiscing about the times he did sports. He also said that he really misses his dark hair, as now it has silver strands in it.

He noticed that Lakyn even has his eyebags and they both agreed that Lakyn is definitely her fathers kid. Lakyn confessed that she was really excited to do this because couldnt grasp how her face could be so similar to her dads.

Image credits: lakynbowman

Image credits: lakynbowman

Before surprising her dad with the video, Lakyn did one for her mom on Mothers Day as well. Lakyn isnt so sure that she has any physical similarities with her mom, but she has heard from some people that they do. With the power of makeup, clothes, poses and filters, it would be hard to think that the two women are strangers.

Moms reaction was as wholesome as the dads. She loved the result and told Lakyn that the swing picture in the park was actually taken by her, even though she didnt remember that because she was so little.

Image credits: lakynbowman

Its quite impressive how children can grow up looking so similar to their parents and even though its easily explained by science, its mesmerizing nonetheless.

Have you ever looked at your parents pictures from their youth and were surprised to discover you now look like them? Do you see the similarities between Lakyn and her dad in these pictures? Let us know in the comments!

See the article here:
Genetics Really Said Copy And Paste: People Are Amazed At How Similar This Woman Looks To Her Dad In These 5 Recreation Photos - Bored Panda

Varicose veins are a very common manifestation of chronic venous disease, affecting over 30% of the population in Western countries. In America, chronic venous disease affects over 11 million men and 22 million women aged 4080 years old. Left untreated it can escalate to multiple health complications including leg ulcers and ultimately amputations. A new international study by Oxford researchers published on 2 June 2022 in Nature Communications establishes for the first time, a critical genetic risk score to predict the likelihood of patients suffering with varicose veins to require surgery, as well as pointing the way towards potential new therapies.

In a vasttwo-stage genome-wide association study of varicose veins in 401,656 individuals from UK Biobank, and replication in 408,969 individuals from 23andMe, Oxford researchers identified 49 genetic variants that increase the risk of varicose veins. They highlighted pathways including problems with the connective tissues of the body, and the immune system as key players in varicose vein pathology.

This study was an interdisciplinary collaborative effort across the Medical Sciences Division at the University of Oxford. Researchers from theNuffield Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, theNuffield Department of Surgical Sciencesand theNuffield Department of Women's & Reproductive Healthworked withan Americancommercial, direct to consumer genotyping company called23andMeto explore which people were moresusceptible to developingVaricose veins.

Lead authorProfessor Dominic Furnisscommented: 'The inclusion of surgeons in the research team was vital as they enabled the identification of patients whose disease was more severe, and they had therefore had surgery. This lead to the discovery of49 genetic variants at 46 areas into the genome thatpredisposes to Varicose veins. This breakthroughgreatly improves our team's knowledge of the biology of Varicose veins, and it will be the foundation of further research into the biology and potentially new treatment'.

Co-authorProfessor Krina Zondervansaid: 'This large study brings together a great deal of new evidence of the genetics underlying varicose veins, a condition that is highly prevalent in women and in pregnancy. It opens up exciting new avenues for the development of new future treatments.'

Reference:Ahmed WUR, Kleeman S, Ng M, et al. Genome-wide association analysis and replication in 810,625 individuals with varicose veins. Nat Commun. 2022;13(1):3065. doi: 10.1038/s41467-022-30765-y

This article has been republished from the following materials. Note: material may have been edited for length and content. For further information, please contact the cited source.

Continued here:
49 Genetic Variants That Increase the Risk of Varicose Veins Identified - Technology Networks

Different structures were detected between the Brazilian and US genetic bases

Principal component analysis (PCA) revealed that most Brazilian cultivars (red circle) were grouped with a subgroup of US cultivars (green circle). Most of them belonged to MG VI, VII, VIII and IX (Fig.1A). Based on the Evanno criterion (Fig.1B), the structure results based on four groups (K=4) showed a high K value (312.35), but the upper-most level of the structure was in two groups (K=2; K=1885.43).

Population structure analysis between Brazilian and US germplasms. (A) Principal component analysis of Brazilian and US soybean cultivars based on SNPs markers; (B) Delta K as a function of the number of groups (K); (C) assignment coefficients of individual cultivars (bar plots) considering K=2; and (D) considering K=4.

Considering K=2 (Fig.1C), the Brazilian cultivars jointly presented an assignment to the Q1 group (green) equal to 86.7% which was much higher than that observed for the US cultivars (43.9%). Considering K=4 (Fig.1D), the Brazilian cultivars jointly presented an assignment to the Q2 group (red) of only 4.7% while the US cultivars jointly presented an assignment to the Q2 group of 27.4%. The Q1 group (green) has a lower assignment in Brazilian cultivars than US accessions (11.1%, and 30.1%, respectively). These results demonstrate that the set of Brazilian cultivars has a narrower genetic base compared to US cultivars.

When we compared the cultivars between maturity groups, we observed a clear differentiation between early and late groups. The highest genetic distances (0.4158) observed were between MG 000 and MG VIII-IX cultivars (Supplementary Table S1).

To examine the influence of maturity groups on population structure, we analyzed the average assignment coefficients (K=4) of Brazilian and US cultivars for each maturity group (Supplementary Figure S1). Brazilian cultivars from maturity group V presented Q1, Q2, Q3, and Q4 equal to 30.4%, 1.9%, 32.1, and 32.0%, respectively; US cultivars from this same maturity group (V) presented means of Q1, Q2, Q3, and Q4 equal to 9.2%, 8.2%, 65.1%, and 17.6%, respectively. This result indicates that, although belonging to the same maturity group, the Brazilian group V cultivars present considerably different allelic frequencies than the US cultivar group V cultivars, especially for Q3 and Q4. US cultivars belonging to earlier maturity groups (00, 0, I, and II) had significantly higher mean assignment coefficient to Q2 group (red) compared to other later maturity groups (V=8.2%, VI=8.1%, VIII=5.0%, and IX=13.6%). In the case of Brazilian cultivars, the average assignment coefficients for Q2 were much lower (V=1.9%, VI=4.2%, VII=5.6%, VIII=4.9% and IX=4.9%). These results demonstrate an important allelic pool that distinguishes early to late genetic materials present in Q2.

In general, the Brazilian germplasm showed few differences between maturity groups (Supplementary Table S1 and Fig.2A). This was also observed when we generated a population structure analysis exclusively with these cultivars (Fig.2C). In contrast, the US germplasm showed a high variation of genetic distance when we analyzed their maturity groups (Supplementary Table S1) with a clear clustering of cultivars (Fig.2B), which is more obvious when we observed their exclusive population structure analysis (Fig.2D). The results show that early cultivars tend to be genetically distant from late cultivars in the US. The maturity groups from the southern-breeding program of the US (V, VI, VII, VIII, and IX) tend to be less genetically divergent versus northern groups (00, 0, I, II, III, and IV). This agrees with previous studies indicating distinct Northern and Southern genetic pools in the US6. There is a low divergence among US soybean cultivars from maturity groups higher than V (Fig.2B). In contrast, cultivars from MG 00 and 0 were more genetically distant from cultivars of MG III and IV while maturity groups I-II were an intermediate group. The population structure analysis showed a high influence of Q2 in cultivars with MG 00-II. For cultivars in MG III and IV, we observed an increase of Q1. Finally, there is a high influence of Q3 in cultivars with maturity groups higher than V, which agrees with the genetic distance data.

Population structure analysis of Brazilian and US cultivars according to their maturity groups. Principal component analysis (PCA) within Brazilian (A) and US (B) germplasms for each maturity groups; population structure of the Brazilian (C) and the US (D) genetic basis arranged according to their maturity groups.

The results demonstrate that both genetic bases had few increases in genetic distance among modern genetic materials (releases after 2000) when compared to cultivars from the 1950s to 1970s (Supplementary Table S2). According to the IBS genetic distance mean, the Brazilian genetic base was more diverse over the decades compared to US germplasm especially when we compared cultivars released before the 1970s and released after the 2000s (Supplementary Table S2).

Average assignment coefficients (Q1, Q2, Q3, and Q4) from genetic structure results were calculated for both germplasm pools. All accessions were sorted according to their origin and decade of release (Fig.3). We observed high genomic modifications over the decades in the Brazilian germplasm. Modern genetic materials (20002010) had Q1, Q2, Q3, and Q4 values of 36.8%, 2.3%, 31.7%, and 26.0%, respectively, while old accessions (1950-1960s) had means of Q1, Q2, Q3, and Q4 equal to 1.6%, 6.6%, 7.0%, and 84.7%, respectively. A high decrease was observed for Q4 starting in the 1990s whereas Q1 and Q3 highly increased during the same period. For the US genetic base, we observed an increase of Q3 and a decrease of Q2 over time. Old cultivars (19501970) had Q1, Q2, Q3, and Q4 values of 36.0%, 33.7%, 12.3%, and 18.1%, respectively, while modern cultivars (20002010) had Q1, Q2, Q3, and Q4 of 24.3%, 17.5%, 40.3%, and 17.8%, respectively.

Mean assignment coefficients of the Brazilian and US cultivars belonging to the different decades of release (1950 to 2010) to STRUCTURE groups (Q1, Q2, Q3, and Q4) considering K=4.

Modification during the 1990s became more evident upon analysis of the PCA and genetic structure results of the Brazilian genetic base considering the decades of release (Fig.4A and C). We observed an increase in the influence of the Q2 in modern genetic materials (20002010) when we compared the results to old genetic materials (19501970). In contrast, the US genetic base showed few variations over time according to the average of genetic distance (Supplementary Table S2), PCA, and the exclusive population structure analysis (Fig.4B and D). These results suggest a large influence of new alleles in the Brazilian germplasm after the 1990s.

Population structure of Brazilian and US cultivars according to their decade of release. Principal component analysis (PCA) within Brazilian (A) and US (B) germplasm for each decade; population structure of the Brazilian (C) and the US (D) genetic bases arranged according to their decade of release.

Seventy-two SNPs with FST0.4 between Brazilian and US cultivars were identified (Supplementary Table S3). These SNPs are located on chromosomes 1, 4, 6, 7, 9, 10, 12, 16, 18, and 19 (Supplementary Figure S2). Twenty-six 100-Kbp genomic regions with a high degree of diversification between Brazilian and US genetic bases were also found (Table 1). The results for Tajimas D showed that these regions had balancing events that maintained the diversity of their bases. Two regions on chromosome 6 (47.3 47.4 Mbp and 47.347.4 Mbp) and another on chromosome 16 (31.1031.20 Mbp) had few variations in Brazilian accessions (Supplementary Table S4). In contrast, the allele distribution for most of the SNPs present in these genomic regions in US germplasm was higher compared to Brazilian germplasm. An opposite scenario was observed for the other three regions located on chromosomes 7 (6.30 6.40 Mbp), 16 (30.70 30.80), and 19 (3.00 3.10) (Supplementary Table S4). The allele variance was higher in the Brazilian genetic base than US germplasm for these three intervals.

Six SNPs located close to maturity loci E1 (Chr06: 20,207,077 to 20,207,940bp)14, E2 (Chr10: 45,294,735 to 45,316,121bp)15, and FT2a (Chr16: 31,109,999 to 31,114,963)16 had a large influence on the differentiation of the Brazilian and US genetic bases (Fig.5). For the SNPs ss715607350 (Chr10: 44,224,500), ss715607351 (Chr10: 44,231,253), and ss715624321 (Chr16: 30,708,368), we found that the alternative allele was barely present in US germplasm whereas the Brazilian genetic base had an equal distribution between reference and alternative alleles. When we examined the SNPs ss715624371 (Chr16: 31,134,540) and ss715624379 (Chr16: 31,181,902), the frequency of the alternative allele remains low in the US germplasm. However, the alternative alleles of these two SNPs were present in more than 78% of the Brazilian accessions in contrast to the previous three SNPs. Finally, the alternative allele for SNPs ss715593836 (Chr06: 20,019,602) and ss715593843 (Chr06: 20,353,073) were extremely rare in Brazilian germplasm with only 2% of the accessions carrying them. In contrast, the US germplasm had an equal distribution of reference and alternative alleles in their accessions. However, all accessions with the alternative alleles belonged to MGs lower than VI with less than five cultivars in MG V.

The allele frequency distribution for SNPs close to loci (A) E1 (chromosome 6), (B) E2 (chromosome 10), and (C) FT2a (chromosome 16) in Brazilian and US germplasms.

Ten SNPs were identified related to the genes modifier mutations present in Brazilian and US germplasm; these were distributed on chromosomes 4, 6, 10, 12, 16, and 19 (Supplementary Table S5). These SNPs had differing allele frequencies and could distinguish both genetic bases. Six modifications had a clear influence on the maturity of the accessions whereas two of these had a large influence in some decades of breeding (Supplementary Figure S3). The SNP ss715593833 had a similar haplotype as two SNPs described as close to the E1 loci (ss715593836 and ss715593843) due to the linkage disequilibrium (LD) among them. At the end of this chromosome, we also observed another three relevant SNPs in LD: ss715594746, ss715594787, and ss715594990. In the US germplasm, we observed a decrease in the alternative allele in accessions with MG values lower than IV. We detected other relevant modifications on chromosome 12 for SNPs ss715613204 and ss715613207. Both SNPs had a minor allele frequency higher than 0.35 in Brazilian germplasm with an increase in the alternative allele in cultivars with MGs higher than VII. In contrast, alternative alleles for both SNPs were extremely rare in the US germplasm except for accessions with MG higher than VII.

There were 312 genomic regions that differentiate northern (00 IV MG) and southern (V IX MG) cultivar groups (Supplementary Table S6), which included the Dt1 locus. We compared the SNPs observed in the genomic region close to the Dt1 gene (Chr19: 45.2045.30 Mbp) with the growth habit phenotype data available for 284 lines at the USDA website (www.ars-grin.gov). The phenotypic data suggests that these SNPs are associated with growth habit. Moreover, our diversity analysis demonstrated a putative selective sweep for the Dt1 gene in the northern germplasm, which has the dominant loci fixed for Dt1; the southern lines tend to be more diverse compared to the northern US cultivars (Supplementary Table S7). In contrast, other genomic regions have lower nucleotide diversity in southern accessions compared to the northern accessions. An important disease resistance gene cluster was observed on chromosome 13 bearing four loci: Rsv1, Rpv1, Rpg1, and Rps317,18,19,20. In this interval, we observed two genomic regions (29.70 29.80 Mbp and 31.90 32.00 Mbp) under putative selective sweeps in the southern germplasm (Supplementary Table S8).

Besides these regions, 1,401 SNPs with FST values higher than 0.40 between northern and southern US cultivars were also identified (Supplementary Table S9). In addition, there were 23 SNPs with FST values higher than 0.70 spread on chromosomes 1, 3, 6, and 19. Seven of them were located close to another important soybean locus: E1 (involved in soybean maturity control) (Supplementary Table S10). These SNPs clearly differentiate northern and southern US cultivars with the reference allele fixed in northern genetic materials, and the alternative alleles in southern accessions. Gene modification in US germplasm was also detected in our study. One hundred twenty-six SNPs were identified in FST analysis modifying 125 genes (Supplementary Table S11).

Finally, we detected 1,557 SNPs with FST values higher than 0.40 between super-early cultivars (00 0 MG) and early cultivars (III IV MG) (Supplementary Table S12). Seventeen SNPs had FST values higher than 0.70 spread on chromosomes 4, 7, 8, and 10. The SNPs identified on chromosome 10 were close to the E2 locus. We also detected 168 SNPs associated with modifications in 164 genes (Supplementary Table S13).

We observed two SNPs with large differences in allelic frequencies in the Brazilian germplasm (Supplementary Figure S4). On chromosome 4, SNP ss715588874 (50,545,890bp) had a decrease of the allele A in cultivars released after 2000 with only nine of the 45 Brazilian cultivars with this allele. A similar situation was observed on chromosome 19 for ss715633722 (3,180,152bp) with half of the modern accessions having the presence of allele C. Both SNPs had similar distribution according to their decades in the US genetic base with a large influence of reference alleles.

There were 126 genomic regions spread on almost all soybean chromosomes in Brazilian cultivars. The only exception was chromosome 20 (Supplementary Table S14). Our analysis between cultivars released before and after 1996 identified 30 putative regions under breeding sweep events. Thirteen regions had a decrease in diversity in modern genetic cultivars according to Tajimas D and results. Two genomic regions observed were close to important disease resistance loci: one on chromosome 13 (30.30 30.40 Mbp) close to the resistance gene cluster (with Rsv1, Rpv1, Rpg1, and Rps3)17,18,19,20 and another on chromosome 14 (1.70 1.80 Mbp) with a southern stem canker resistance loci21,22. In contrast, thirty-one genomic regions had an increase in diversity in modern cultivars, which suggested putative introgression events in these accessions. Two genomic regions were observed, on chromosome 2 (40.90 40.10 Mbp) and 9 (40.3040.40 Mbp). Thesewere previously reported to have an association with ureide content and iron nutrient content, respectively23,24.

Besides these regions, there were also 409 SNPs with FST values higher than 0.40, distributed across all soybean chromosomes. There were 73 SNPs with FST values higher than 0.70 (Supplementary Table S15). Some of these SNPs were also reported to be associated with important soybean traits such as plant height, seed mass, water use efficiency, nutrient content, and ureide content23,24,25,26,27.

We also identified gene modifications with a high impact on the Brazilian genetic base when we compared cultivars according to their decade of release. Of the 409 SNPs identified in FST analysis, we observed 40 SNPs causing modifications in 39 soybean genes (Supplementary Table S16). Three SNPs with FST values higher than 0.70 were associated with non-synonymous modifications: ss715588896 (Glyma.04G239600 a snoaL-like polyketide cyclase), ss715607653 (Glyma.10g051900 a gene with a methyltransferase domain), and ss715632020 (Glyma.18G256700 a PQQ enzyme repeat).

Follow this link:
Genetic relationships and genome selection signatures between soybean cultivars from Brazil and United States after decades of breeding | Scientific...

PAID CONTENT | Earlham's Judy Marshall went to her primary care physician for help with losing weight...he told her that "genetics" would not allow that to happen. Judy changed doctors looking for an answer...their answer was a bunch of pills. Judy decided to visit with Dr. Vince Hassel to see if the ChiroThin system would be the solution to her weight loss and health goals. The answer is a BIG YES! She lost 20-25 pounds on the program and is now even more focused on her own well-being and is ecstatic with the results! If you follow his advice and stick to the program, Dr. Hassel's plan WILL WORK where other's fail, period. LEARN MORE at http://www.weightlossindesmoines.com or call/text 515-423-8396

Go here to read the rest:
Earlham woman loses weight with ChiroThin after her own doctor told her "genetics" wouldn't allow that to happen | Paid Content - Local 5 -...

Fernside dairy farmer Julie Bradshaw is passionate about the ability of genetics to create the most efficient herd of cows. Photo / Supplied

A five-year irrigation study has helped Julie Bradshaw make science-based decisions on her Fernside dairy farm.

Bradshaw also uses genetics to improve her herd, as part of her goal to reduce her farm's environmental footprint.

Bradshaw took part in the National Institute of Water and Atmospheric Research (NIWA) co-innovation study from 2016 to 2021.

The study provided landowners with real-time data and forecasts to make science-based irrigation decisions.

This data included measured rainfall, soil moisture, soil temperature, drainage and estimated evaporation, as well as two, six and 15-day rainfall and weather forecasts.

The practical study gave each farmer a fantastic insight into their own land and irrigation practices, while also providing a broader picture of what was happening in the catchment, Bradshaw said.

Having access to precise data also helped Bradshaw and her neighbouring farmers to apply exactly the right amount of irrigation and fertiliser at the right time which aided in mitigating environmental impacts.

"It was amazing. We had so much data and information that we had never had before," she said.

"[This] has helped us make decisions about irrigation and fertiliser use ... backed up by facts and scientific data."

Having these records also made it easier for Farm Environment Plans and audits, Bradshaw said.

"We can show that we have been using our water resource correctly."

All farmers involved in the study were able to see each other's data and this high level of transparency helped the group understand what was happening in various parts of the catchment, Bradshaw said.

"We have always been very open - it's just information and data about water. Getting to know more about other farms is helpful because we are learning from each other along the way."

Although the study had ended, Bradshaw still logged in to the group's website most days to enable her to make accurate decisions about water allocation for the Cust Main Drain Water User's Group.

The group was established 25 years ago to manage water allocation during the irrigation season when water takes were restricted.

"It has been such a bonus to be able to see where everyone is sitting in terms of the moisture on their paddocks, as this helps me to allocate the water more accurately to where it is needed.

"Not only do you see today's moisture levels but you also get a future reading, so you can see where things are heading."

Last year Bradshaw and her husband Peter received the Sire Proving Scheme Farmers of the Year Award from the Livestock Improvement Corporation (LIC).

The couple had worked with LIC for 15 years and the award recognised their record-keeping and commitment to having their entire herd DNA-tested.

"We have a KiwiCross herd which is a cross between Holstein-Friesian and Jersey cows," she said.

"I am really passionate about the ability of genetics to improve your overall herd quality. Having 99 per cent of the ancestry of the cows recorded is an immense help when doing the breeding."

Bradshaw believed improving the overall quality of the herd meant, that if she needed to reduce her stock levels in the future, she knew exactly which animals had the best genetics to meet future farming limits.

She was committed to using science to reduce her impact on local waterways.

"Genetics and DNA testing are so helpful when you think about the possibility of reducing herd numbers in the future.

"We must think ahead and use science to help us make the best decisions both for our business operation and for the environment."

Bradshaw was also participating in a six-month farming project, which examined how the next generation of farmers used innovation to improve their practices.

Waimakariri Landcare Trust (WLT) and Waimakariri Irrigation Limited (WIL) have partnered with the Ministry for Primary Industries (MPI) for this project, with support from MPI's Sustainable Food and Fibre Futures fund, along with Environment Canterbury, Ballance, and DairyNZ.

Bradshaw aimed to learn more about genetics through the course of the MPI innovation project.

"We have three cows that LIC would like a bull calf out of, so that will be an interesting process to follow.

She was also keen to use the MPI innovation project to improve the quality of the grass throughout the farm.

"With the colder and wetter spring we had last year, followed by a cloudy and cooler summer, our grass didn't contain enough sugar and energy for the cows. We want to work on that throughout this project."

Go here to see the original:
Science and genetics used to boost Fernside farm - New Zealand Herald

Frans Jordaan and Dr Ben Greyling, researchers at the Agricultural Research Council, write about the importance of choosing bulls based on breeding and performance indices, rather than their visual appearance.

The days of buying bulls based purely on their functional appearance are over. While functional efficiency is important, it is also crucial that the buyer does his or her homework regarding the genetic potential and merit of the bulls prior to the auction so as to be able to make an informed decision on the day of the auction.

Auction catalogues are, however, not always easy to interpret and can be challenging for commercial and stud breeders during the auction amidst a lot of activity going on and no time to waste between the lots on auction.

If breeders are knowledgeable regarding the interpretation of best linear unbiased prediction (BLUP) values, which depict an animals genetic potential, it can be a huge advantage in helping them meet their breeding objectives much quicker.

It needs to be asked whether breeders really understand these figures and the use of breeding values as a selection tool for choosing the best bull for their herds.

It will always be risky to buy a registered bull without breeding values, especially since a bull can have such a huge genetic impact on a cowherd. In addition to this, genetic improvement is a slow process and can only be achieved over generations.

This implies that the wrong choice of bull can be so detrimental to your herd that it can be costly to recover from the damage caused and will be a setback to achieving your breeding goals.

Always keep in mind that genetic change is easy to bring about, but to accomplish it in a positive direction (improvement in weaning weights and breeding values, for example) is much more difficult to achieve. If a stud breeder succeeds in achieving genetic improvement, it will also be of benefit to commercial beef producers by enabling them to increase profitability in their enterprises.

Often, experienced breeders will say that they are quite familiar with certain breeding lines and bulls in the breed, and that they can recognise the qualities they want in a bull.

However, variation within a breed is also a reality; frame type, for instance, can differ within a breed, and bulls at a younger age that are still in a developing phase can make visual selection quite challenging. Also keep in mind that the visual appearance of an animal is not just the result of breeding, but a combination of breeding (genetics), management and feeding.

It is also important to note that good genetics can be hidden with poor feeding, and bad genetics with good feeding. Although functional efficiency will also always be important, the wrong choice of bull can have a negative effect that may only be discovered after one generation or, in some cases, even later in the production cycle of a calf crop.

A phenotypic wean index of above 100 is really no guarantee of good genetic material. It only implies that the animal gave an above-average performance within his own contemporary group. The genetic quality of the group will determine the level of genetics.

Important factors to consider related to genetic principlesThe following are factors to considering when choosing a bull for your operation:

Blup valuesIt is important to keep in mind that breeding values across breeds are not comparable, which means that a breeding value of +5 for the weaning weight of a Bonsmara bull is not comparable with that of a Simmentaler bull with the same breeding value of +5.

The breed average of the specific breed should rather be a benchmark of whether or not the bull is better or worse than the average animal in that breed for a specific trait, such as wean direct. It is important for commercial farmers to be aware of this so they do not make this mistake regarding different breeds.

Breeding valuesThere is good news for commercial beef producers who are familiar with indices. Breeding value indices also appear on some of the breeds auction catalogues and can be interpreted as normal indices, such as phenotypic wean indices.

A breeding value index of 100 means the animal is average for a specific trait within the whole breed and not just within his contemporary group. The same principle applies for an animal with a breeding value index above 100, which will be genetically better than the average animal in the breed for a specific trait.

Obviously, the commercial breeder will focus more on growth traits because this is of more economic value to him/her, but the stud breeder can also ensure that other traits of importance are captured in young potential breeding animals, which will ultimately be to the benefit of the commercial breeder. Reproduction, the most important trait when it comes to genetic selection, should already be captured in the young bulls genetic ability and be to the benefit of the bull buyer.

If the buyer interprets breeding values correctly, the following selection decisions are possible:

Balanced breeding valuesA bull should breed smaller calves at birth, but not too small! A calf that is too small at birth will also end up as a small, undesirable calf at wean because of the high correlation between birth-, wean- and year-old weights. The ideal bull for replacement heifers will be above breed average for wean direct and maternal traits.

Beef breeders are primarily meat producers, and post-wean growth will always be important, especially to feedlots. It is therefore important for a breeding bull to be at least on breed average for growth traits such as weight at weaning, one year and 18 months.

But be cautious to select for extreme breeding values for post-wean weights. Weight at 18 months is also an indication of mature weight, and if selection on growth is the only priority, the result will be bigger cows with higher maintenance requirements. If a poor or extensive environment cannot support these bigger-framed animals, it will have a negative influence on calving percentage.

The feed-conversion-ratio breeding value is also important for feedlots, and a smaller value or below breed average value is more desirable, as in the case of the phenotypic feed conversion ratio value.

The less feed needed to increase live body weight by 1kg, the more efficient the animal is in a feedlot environment. Feed conversion ratio is a combination of two traits, namely growth rate and feed intake, and is an indication of how efficiently the animal can transform feed into meat.

To improve reproduction or the fertility of your herd, always keep the reproduction statistics of the bulls dam in mind. In addition to this, the scrotal circumference breeding value of the bull has to be on or above breed average.

Email Frans Jordaan at [emailprotected], or Dr Ben Greyling at [emailprotected].

See the original post here:
Genetics-based guidelines to buying a bull at an auction - Farmer's Weekly SA

Recent reports of poliovirus detected in samples from a sewage treatment works in London have rightly generated significant concern among public health agencies and medical staff. The poliovirus detected is what is called vaccine-derived poliovirus this is not wild poliovirus.

There are currently two poliovirus vaccines: the oral poliovirus vaccine (OPV) and the inactivated poliovirus vaccine (IPV). Vaccine-derived poliovirus is linked to the use of the OPV as this vaccine uses weakened poliovirus to produce an immune response.

The weakened poliovirus can still infect people and be shed by the vaccinated person. This can result in the weakened virus spreading from person to person. And in rare cases, this weakened poliovirus can change to a more dangerous strain of the virus that can cause disease.

In areas with high levels of vaccination, the community is protected and the spread of the more dangerous virus is stopped. But in areas with lower vaccination rates, unvaccinated people may be exposed to poliovirus that has originated as a weakened vaccine strain but is now a more dangerous version. This virus is referred to as a vaccine-derived poliovirus.

As the global vaccine initiatives have resulted in the near eradication of poliovirus, the number of cases of vaccine-derived poliovirus has overtaken the number of infections with wildtype poliovirus. In 2021, there were 697 new cases of vaccine derive poliovirus compared with just six cases of wildtype poliovirus, globally.

Vaccination with IPV does not immunise people with an infectious virus. Instead, it uses poliovirus that has been chemically inactivated. This means the virus is unable to infect people, removing the risk of vaccine-derived poliovirus. This vaccine is considered very safe. For this reason, many countries have moved away from using OPV and adopted IPV.

The UK switched from using OPV to IPV in 2004. However, OPV remains an incredibly effective vaccine that has been instrumental in bringing about the near eradication of poliovirus and remains widely used throughout the world.

While there is no risk of vaccine-derived poliovirus infection when using the IPV, the making of IPV does lead to a potential biohazard risk. To make IPV, large volumes of infectious poliovirus must be produced and then inactivated. This large-scale production of poliovirus has inherent risks and any breach of biocontainment in a population with low vaccine coverage can have serious consequences as poliovirus could be reintroduced.

Vaccination strategies with either OPV or IPV, therefore, involve a certain level of risk. In either case, the risk is astonishingly low. However, for some time scientists have been seeking to develop new and safer methods for poliovirus vaccination. One potential candidate for a new poliovirus vaccine is the use of virus-like particles (VLPs).

VLPs are assembled from the proteins that make up the outer shell of the virus, called a capsid. This allows the immune system to react to this empty shell and triggers a protective immune memory response, so the next time the immune system is exposed to a viral capsid (such as in the case of a viral infection), it can generate an effective response that rapidly controls and eliminates the virus.

Because VLPs contain no genetic material from the virus, they are safe to manufacture and use without the risk of spreading the actual disease. This method has already been used very effectively to produce the human papillomavirus vaccine.

A further advantage of using VLP vaccines for a disease such as poliovirus is the potential to produce VLPs in production systems such as yeast. At the University of Leeds, we have shown that yeast can be made to produce poliovirus VLPs and then grown in large quantities.

The production system for these VLPs uses a similar infrastructure to other yeast-based manufacturing, such as the brewing of beer. This means that large quantities of VLPs can be produced quickly and safely in a very cost-effective way.

Go here to see the original:
Polio: we're developing a safer vaccine that uses no genetic material from the virus - The Conversation

Researchers have found that people whose genes put them at increased risk of dementia can reduce their chances of getting the condition by up to 43% if they follow seven habits for healthy living.

It was already thought that a healthy lifestyle could cut the risk of dementia, but until now it has been less clear if this applied to people with genetic variants that make them more likely to develop the condition.

The World Health Organization (WHO) says dementia is the seventh leading cause of death among all diseases worldwide and is responsible for millions of older people enduring disability and dependency. With the proportion of older people increasing in almost every country, the WHO expects dementia cases to rise to 139 million by 2050.

A study from the American Academy of Neurology investigated whether people with a higher genetic risk could reduce their chances of getting the condition. Researchers followed almost 12,000 people for 30 years and scored them on how closely they followed the American Heart Associations Lifes Simple 7 a list of lifestyle habits linked to good cardiovascular health.

Adopting a healthy lifestyle can help reduce dementia risk, even for people genetically predisposed to develop the condition.

Image: American Heart Association

1. Manage your blood pressure. Keeping your blood pressure within a healthy range reduces the strain on your heart, arteries and kidneys.

2. Control cholesterol. High cholesterol contributes to plaque which can clog arteries and lead to heart disease and stroke.

3. Reduce blood sugar. High levels of blood sugar can damage your heart, kidneys, eyes and nerves.

4. Get active. Theres strong evidence daily physical activity increases the length and quality of your life.

5. Eat better. A healthy diet is one of the best ways to prevent cardiovascular disease.

6. Lose weight. Shedding a few pounds can reduce the burden on your heart, lungs, blood vessels and skeleton.

7. Stop smoking. Smokers have a higher risk of developing a range of serious illnesses including heart disease.

Participants in the dementia study were asked to score themselves on a scale of 0 to 14 depending on how closely they followed all seven healthy habits. Researchers also calculated their genetic risk, based on whether they had variants linked to a higher or lower chance of getting Alzheimers disease, which is a major cause of dementia.

Alzheimers Diesease, a result of rapid ageing that causes dementia, is a growing concern. Dementia, the seventh leading cause of death worldwide, cost the world $1.25 trillion in 2018, and affected about 50 million people in 2019. Without major breakthroughs, the number of people affected will triple by 2050, to 152 million.

To catalyse the fight against Alzheimer's, the World Economic Forum is partnering with the Global CEO Initiative (CEOi) to form a coalition of public and private stakeholders including pharmaceutical manufacturers, biotech companies, governments, international organizations, foundations and research agencies.

The initiative aims to advance pre-clinical research to advance the understanding of the disease, attract more capital by lowering the risks to investment in biomarkers, develop standing clinical trial platforms, and advance healthcare system readiness in the fields of detection, diagnosis, infrastructure and access.

The participants had an average age of 54 when the research started. Around 9,000 had European ancestry and 3,000 African ancestry.

By the end of the study 1,603 people with European ancestry and 631 people with African ancestry had developed dementia. Those with the highest scores for following a healthy lifestyle were much less likely to have dementia, including participants who had genetic variants linked to Alzheimers.

Study author Adrienne Tin, from the University of Mississippi Medical Centre in Jackson, says: The good news is that even for people who are at the highest genetic risk, living this same healthier lifestyle [is likely to] lower risk of dementia.

Alzheimers is among the 10 leading causes of death in the US.

Image: Statista/Alzheimers Association

In those with European ancestry, participants with the highest scores for living healthily were up to 43% less likely to get dementia than those scoring lower. For those with African ancestry, following the healthy habits was linked to a 17% lower risk of developing the condition. But the studys authors say the smaller numbers of people with African heritage taking part means the findings are less certain for this group, so more research is needed.

Dr Rosa Sancho, from Alzheimers Research UK, told The Times: Dementia risk depends on many factors. Some, like our age and genetic make-up, we cannot change, while others like diet and exercise, we can. This study supports the idea that what is good for the heart is also good for the brain.

If adopting these seven healthy habits can reduce the number of people who get dementia, it wont just be individuals who benefit. The World Health Organization says dementia has high global social and economic costs too. Informal carers - including family and friends - spend an average of five hours a day caring for sufferers, and the global financial bill is expected to be more than $2.8 trillion by 2030.

There are many organizations around the world working to help accelerate advances in prevention and treatment of the condition. Davos Alzheimers Collaborative is led by the World Economic Forum and The Global CEO Initiative on Alzheimers Disease and is investing $700 million over six years into drug development and healthcare diagnostics.

Speaking at a meeting of the DAC Learning Laboratory in May 2022, its co-chair, George Vradenburg, highlighted the importance of remembering that Alzheimers can affect anyone, regardless of their economic, racial or geographic status.

We are explicitly global in character. We want to make sure from the very beginning of this effort that we involve low- and middle-income countries and that we pay attention to all societies, all resource settings and all racial and ethnic legacies as we move forward on the path to cure Alzheimers.

Written by

Simon Read, Senior Writer, Formative Content

The views expressed in this article are those of the author alone and not the World Economic Forum.

See the article here:
7 lifestyle habits which can halve your risk of dementia - World Economic Forum

Quenton Tompkins family tree is deeply rooted in rural McCormick County, South Carolina.

His grandfather was a sharecropper in McCormick. His mother, who turns 88 this month, grew up as the youngest of 24 children. Branches of aunts, uncles, and cousins now stretch from Florida to Chicago.

And although 48-year-old Tompkins has heard plenty of stories, his family holds its secrets, too.

He didnt know until he was an adult that his grandfather died of leukemia. And hes still unsure if his fathers bout with prostate cancer runs in the family. Tompkins mother and her siblings have dealt with a range of health issues, including diabetes, heart attacks, and strokes, but he still doesnt know what killed his grandmother more than 70 years ago.

Those are questions I go through personally, said Tompkins, a lobbyist for the Medical University of South Carolina. Theres another side to knowing where you come from.

Twenty-two years ago, President Bill Clinton announced the completion of a draft version of the Human Genome Project, a breakthrough he described as the language in which God created life. He predicted that scientists, armed with genetic discoveries, would find cures for Alzheimers disease, cancer, Parkinsons disease, and diabetes in the coming years.

Clintons prediction, of course, hasnt yet come to pass. But researchers in Charleston are hopeful that a large genetics research project underway across South Carolina may help scientists address some of the states persistent health disparities, which disproportionately impact its Black residents and regularly rank among the nations worst.

The university health system intends to enroll 100,000 of South Carolinas 5 million residents in genetic testing over the next four years in hopes of better understanding how DNA influences health. Researchers also want to recruit participants who reflect the diversity of the states population.

Its an ambitious goal. With nearly 27% of South Carolina residents identifying as Black or African American, the MUSC genetics research project, called In Our DNA SC, would if successful accomplish something most other genetics research projects have failed to do. Historically, diverse participation in this type of research has been very low.

Theres a trust factor. Its plain and simple, said Tompkins, who is developing an outreach program for the project.

He referenced Henrietta Lacks, a Black woman in Baltimore whose cells were used without her or her familys knowledge for research purposes by doctors at Johns Hopkins University in the 1950s, and the Tuskegee syphilis study, conducted over nearly 40 years starting in the 1930s. Researchers deceived hundreds of Black men enrolled in the study, telling them they were being treated for syphilis when, in fact, they were left untreated, even after penicillin became widely available.

Those are still fresh in many peoples minds, Tompkins said. Weve come a long way from those stories it doesnt dismiss what happened but there are a lot more controls and oversight in place to ward those things off from happening again.

But its not only history feeding this distrust. Bias and racism evident in medicine today contribute to the problem.

Diversity in genetics research is so low that approximately 90% of participants in projects launched since the first sequencing of the human genome have been individuals of European descent or those who identify as white, said Dr. Shoa Clarke, a pediatric cardiologist and geneticist at Stanford University.

These numbers affect real-life health care. Clarke and others published research last year showing that a DNA-based tool used to assess a patients risk of developing high cholesterol works reliably well only when administered to those of Northern European descent. Thats because the tool was developed using information from genetic bio-banks largely made up of DNA from white people. And aside from a large DNA bank compiled by the Department of Veterans Affairs, this is generally the norm.

Human beings, regardless of race, are more than 99% genetically identical, but small variations and mutations passed down through generations can influence health outcomes in huge ways, Clarke explained.

Genetics is not the cause of health disparities, he said. But as we move toward using genetics in clinical settings, its very possible they could create new disparities.

In South Carolina, health disparities between Black and white patients are already acute, said Marvella Ford, a researcher at MUSCs Hollings Cancer Center in Charleston.

South Carolina compared to the rest of the country were usually in the bottom tier, Ford said. The prostate cancer mortality rate in South Carolina, for example, is 2 times higher for Black men than white men, she said.

When you look at most other chronic conditions, she said, you see the same thing.

She called the genetics project at MUSC a great opportunity to open the doors. Even so, the topic of recruiting Black research participants for genetics studies is complex.

Theres debate on how we should be doing this work, said Shawneequa Callier, an attorney and an associate professor of bioethics at George Washington University. Theres just so much diversity in Africa. Its the cradle of humanity.

Men and women transported to Charleston and other American port cities during the transatlantic slave trade came from a wide region of Africa mostly from West Central Africa, but in large numbers from regions farther north, too. Once in America, they were often separated and forced hundreds of miles apart. This explains why someone whose ancestors lived on one of South Carolinas barrier islands may have inherited different genetic variants than someone from a multigenerational Black family inland in McCormick County, just north of Augusta, Georgia.

Thats also why categorizing genetics research participants simply as Black or African American, without more context, may not yield particularly useful research insights, Callier said.

If you dont study the data and study it well, thats a real dereliction of ethical duty, Callier said.

Those who choose to participate in the MUSC project stand to benefit from it directly, its organizers said. After submitting a saliva sample, each participant will receive a report indicating if they have one or more of three genetic conditions that may put them at a higher risk for heart disease and certain cancers such as one of the BRCA mutations linked to breast cancer. If they test positive for one of these conditions, they will be connected at no cost to a genetics counselor, who can assist with information and treatment options related to a patients inherited risks. Participants will also learn where their ancestors likely lived.

The de-identified DNA data will then be used by researchers at MUSC, as well as those at Helix, a private California-based genomics company, which will process the saliva samples and extract the genetic information from each participants sample. Researchers at MUSC and Helix have indicated they hope to use the results to better figure out how DNA affects population health. Heather Woolwine, an MUSC spokesperson, said the project will cost $15 million, some of which will be paid to Helix. Hospital revenue will fund the research, she said.

Tompkins expects to receive a lot of questions about how it all will work. But hes used to questions. He said he encountered much of the same hesitancy when he helped set up MUSC covid testing and vaccine sites across the state. Many people regardless of race worried microchips or tracking technology had been embedded into the covid vaccines, he said.

Tompkins found that the key to persuading residents in rural parts of the state to consider the covid vaccine was to seek out invitations from trusted, local leaders, then set up events with them. South Carolinas covid vaccination rate remains lower than the national average, but Tompkins said some skeptics have been more receptive to MUSCs message because the hospital system has focused on building relationships with organizers outside Charleston. He hopes to use those relationships to spread word about the new genetics research project.

You have to build those relationships and find community champions that can help you open doors and gather people, he said. Then, its about letting them choose.

By Lauren SausserKaiser Health News is a nonprofit news service covering health issues. It is an editorially independent program of the Kaiser Family Foundation, which is not affiliated with Kaiser Permanente.

Read the original here:
Addressing the 'Trust Factor': South Carolina Researchers Tackle Health Disparities Using Genetics - Physician's Weekly

It has been more than two years since the start of the global COVID-19 pandemic. Throughout that time, for some people, the infections became more frequent and hit closer to home. Their friends contracted coronavirus, and sometimes their children, grandparents and most of their co-workers too. It seemed to be only a matter of time before they would contract the virus as well but their luck never ran out it seems as if some people have never been knowingly infected with COVID-19 in over two years even after the wave of infections caused by the highly transmissible omicron variant.

If you ask them the reason, you'll hear all sorts of suppositions. For example, regular long trips on the underground will build up your resistance by repeatedly exposing you to small viral loads.

"This hypothesis falls in the realm of speculation," says Dr. Ulf Dittmer, director of the Institute of Virology at Essen University Hospital in Germany.

Some people not previously infected attribute it to scrupulously following COVID-19 precautions. Others thank their lucky stars for not contracting the virus from a contact person who later tested positive or while they partied at a club. Still, others wonder if they had an asymptomatic infection that wasn't detected, for instance before testing was widely available. Or maybe they did have symptoms but tested negative because the sample was collected improperly or the timing was inopportune.

Scientific attempts at an explanation go deeper, but there's no single definitive answer as to why some people still haven't caught COVID-19. A combination of factors could be the reason.

"A number of hypotheses appear plausible," says Dr. Leif Erik Sander, director of the Department of Infectious Diseases and Respiratory Medicine at Charit University Hospital in Berlin.

First of all, it's important to bear in mind that a significant number of COVID-19 infections go largely or completely unnoticed. In a systematic review and meta-analysis published late last year in the Journal of the American Medical Association (JAMA) Network Open, the authors noted that about 40% of people with a confirmed COVID-19 diagnosis were asymptomatic at the time of the test. The finding was based on 95 international studies involving nearly 30 million people.

The frequency of testing obviously plays a role in detecting infections. If you're not tested regularly, there's a greater chance you won't become aware of a mild or asymptomatic infection.

And your genes can play a role too in whether or not you get COVID-19.

"There are people who, owing to genetic characteristics, can't easily be infected with malaria or HIV (the virus that causes AIDS), for instance. In certain gradations this will also be true of Sars-CoV-2," says Sander, adding that the genetic factors aren't completely understood, however.

As virologist Dittmer explains, human leukocyte antigens (HLA) molecules, which are encoded by a complex of genes, play an important part in the body's immune response to pathogens such as Sars-CoV-2. He adds that a person's blood group, too, not only influences disease severity but perhaps also susceptibility to infection with the virus.

The protection provided by vaccinations is probably often underestimated. Although levels of antibodies in your blood able to bind to and neutralize invading coronaviruses decline some time after injection with a vaccine, "protection nevertheless remains significant for months," Sander says. "That, too, reduces infections."

Immune responses to COVID-19 vaccines vary from person to person. "If the response is especially good, vaccination in combination with a previous infection with one of the four endemic common cold coronaviruses can also play a role," he suggests.

According to Dittmer, a particular subclass of antibodies has been found to provide especially good protection from a novel coronavirus infection. "Measuring them is complicated though, so for the time being no one will know whether they've got these antibodies or not," he says.

The fact that children who get COVID-19 tend to have either no or only mild symptoms is down to their generally having an innate immune response that's stronger than the immune response of adults, according to Sander. It's often "preactivated," so to say.

Another phenomenon worth mentioning is that for a few days after getting an infection, people are typically less susceptible to infection with another pathogen. "This is due in part to interferons, which are defensive proteins in mucous membranes that also reduce susceptibility to Sars-CoV-2 in the event of contact with it in that time window," Sander says.

He also notes that some people's immune system may rid their body of the virus very quickly: "In a Swedish study, researchers detected specific T-cells (a type of white blood cell that's part of the immune system) in people who didn't test positive after contact with infected household members a sign their immune system had indeed engaged Sars-CoV-2 even though an infection or antibodies against the virus weren't always detectable."

So what are we to conclude? If you think you've somehow managed to skirt a COVID-19 infection, you may already have one behind you. Or you may have benefited from certain temporary circumstances, as-yet-unexplained genetic factors and/or dumb luck.

"Just because you haven't had COVID-19 yet doesn't mean you're permanently safe," Sander warns. "A new coronavirus variant, or a different set of circumstances, can totally change that."

The Daily Sabah Newsletter

Keep up to date with whats happening in Turkey, its region and the world.

SIGN ME UP

You can unsubscribe at any time. By signing up you are agreeing to our Terms of Use and Privacy Policy. This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.

Read the rest here:
Dumb luck, genetics? Why have some people never caught COVID-19? | Daily Sabah - Daily Sabah

Marine biologists at Scripps Institution of Oceanography at UC San Diego have created a line of sea urchins whose genetic makeup is fully mapped and can be edited to study human disease genes. The creation of these new research model organisms will accelerate the pace of marine biomedical research.

Sea urchins, like fruit flies or lab rats, have been an organism used in research for more than a century. Even before this breakthrough, sea urchins led to the discovery of a protein family known as cyclins that guides division of cells. That knowledge went on to become the basis of current cancer treatments and earned cyclins discoverers a Nobel Prize.

Now Scripps marine biologist Amro Hamdoun and colleagues have taken this research to a new level by developing lines of sea urchins that can be used as genetic models using the gene editing technology known as CRISPR. The modified sea urchins are derived from the fast-growing species, Lytechinus pictus, also known as the painted sea urchin.

The team describes its results June 6 in the journal Development.

Hamdoun said the new sea urchins could serve as a new workhorse organism in marine biomedical research, capable of being cultivated to adulthood in four to six months at room temperature. Presently many species of sea urchins are used around the world to study the developmental origins of diseases, and the effects of pollutants on human and marine health. But few can be grown in the lab and genetically modified like other lab animals. Having this new genetically enabled urchin could dramatically enhance the efficiency, reproducibility, and utility of those studies.

Sea urchins have long been a favorite model organism for marine biologists, but they have been bottlenecked by not having stable genetics, Hamdoun said. This work breaks that final barrier. This genetically enabled urchin will be an important resource for the large community of researchers who use urchins in their labs.

The research was an unexpected silver lining from the COVID pandemic which impacted operations in research labs around the country for more than two years. In the case of Hamdouns lab, team members developed a sense of mission that motivated them to continue with the work.

It gave us something positive to focus on, Hamdoun said. The team spent two years intently focused on solving the barriers to making a genetically enabled sea urchin. Once we figured out how to make the precise modifications we wanted, we next had to figure out how to efficiently culture the urchins and select the modified animals. It is a real testament to the groups dedication that they accomplished this despite the adverse circumstances. I like to think that while many people were home growing cool things like houseplants or sourdough starters, we were also growing something interesting, but it was a biomedical research animal.

Besides Hamdoun, co-authors of the study included Himanshu Vyas, Jose Espinoza, Catherine Schrankel, Kasey Mitchell, Katherine Nesbit, Elliot Jackson, Nathan Chang, Yoon Lee, and Deirdre Lyons of Scripps Oceanography as well as researchers from University of North Carolina Charlotte and Wilmington campuses.

The National Institutes of Health Program on Oceans and Human Health and the National Science Foundation funded the research.

Read more:
Genetics Breakthrough in Sea Urchins to Aid in Biomedical Research - Scripps Institution of Oceanography

June 8, 2022 | The pioneering OneK1K study in Australia has identified an immune fingerprint of seven autoimmune disorders using single-cell RNA sequencing (scRNA-seq). The general framework, which combines the scRNA-seq data with genotype data to classify individual cells, can be applied to many different diseases, including other autoimmune disorders, cardiovascular diseases, neuroinflammatory conditions, and cancer where the immune system is thought to play a role, according to Joseph Powell, director of cellular science at the Garvan Institute of Medical Research.

Selection of the original seven diseasesmultiple sclerosis, rheumatoid arthritis, lupus, type 1 diabetes, spondylitis, inflammatory bowel disease, and Crohns diseasewere based on their prevalence in the world of autoimmune diseases and high genetic component, he says. The study relied on scRNA-seq data from 1.27 million peripheral blood mononuclear cells collected from 982 healthy donors, many of whom carry the genetic loci found in people who have these diseases.

Take Crohns disease, which has molecular markers found on roughly 190 positions in the genome, Powell cites as an example. On average, patients collectively have roughly 90 risk alleles at those loci, but individually about 60. It is the difference between having 60 and 90 that takes you over the threshold and leads to occurrences of disease.

This phenomenon holds true for most every disease afflicting humans, which is why a big population group is ideal for gaining mechanistic insights on disease-associated genes, he continues. At the cellular level, genome regulation changes brought on by those genes are the same even if there is no clinical manifestation of disease.

Using a Mendelian randomization approach, Powell and his colleagues uncovered the causal route by which 305 loci contribute to autoimmune disease through changes in gene expression in specific cell types and subsetsand that these genetic mechanisms are the same for healthy individuals as in autoimmune disease cohorts. Results published recently in Science (DOI: 10.1126/science.abf30).

Single-cell RNA sequencing was used to look at genetic variants affecting gene expression in 14 different immune cell types, says Powell. It is the largest study to date linking disease-causing genes to specific types of immune cells.

Researchers developed a classification method based on the transcriptomic signature found in individual cells and aligned it back to what is currently understood about more common immune cell types at the top of the hierarchy (e.g., T cells, CD4, CD8, nave to memory B cells). Although 68 immune cells have been classified, they focused on those they were sure to find enough copies of across the OneK1K cohort to confidently link the genetic differences between people to the signatures in the cells.

Tissue-To-Tissue Variability

Powell says he has been interested in genetic control of gene expression, and its contribution to disease, for more than a decade now. For many years, this involved bulk RNA analysis that produces an average signal.

An important clue emerged when researchers began seeing how vastly different the genetics worked in one tissue versus another, he says. Only a few years ago, the Genotype-Tissue Expression Program (GTEx) of the National Institutes of Health examined RNA sequencing samples from 49 tissues of postmortem donors to characterize genetic associations for gene expression and found regulatory associations for almost all genes. Cell type composition was identified as a key factor in understanding gene regulatory mechanisms.

That study showed instances where genetic effects were seen in one tissue and not another, or generated completely different effects, Powell notes. It was published in 2020 when scRNA-sequencing was just emerging as a staple technologyand Powell had just started his computational genomics laboratory at the Garvan Institute.

We were stuck with this interesting question: If we see these differences between tissues, and know the tissues are comprised of really distinct cell types with really specific functional roles, and the transcriptomic cell signatures are different, can we try to create a system to undo the genetics we saw in tissue inside a cell? That led Powell and his colleagues to scale up their scRNA-sequencing efforts.

At the time, the vast amount of generated transcript data generated from 1,000 individuals would have made scRNA-sequence data entirely cost-prohibitive to generate. But Powell helped pioneer a biometric technique to pool cells from multiple samples, as well as a method to analyze the transcripts of individual cells that solved the challenge of determining what portion of them would provide the most useful information in defining a cell type.

Up until then, a few other groups had published studies using samples from perhaps 50 or 100 individuals suggesting signatures of disease, but they were all under-powered, says Powell. They could show genetic differences between cells, but they were all too under-powered to link them to disease, or to resolve why there were differences between cells.

Statistically speaking, disease fingerprints that capture the genetic heterogeneity of patients will never be fully defined, says Powell. But the OneK1K study has probably moved the needle from the 10th percentile to the 50th percentile on the saturation curve.

Powell is now aiming for the 95th percentile with a TenK10K study that will be seeking to enroll 10,000 individuals and generate single cell data on about 50 million cells. The multi-year initiative will involve partnerships with multiple hospitals across Australia, and both a healthy population group and patients newly diagnosed with autoimmune disorders, cardiovascular disease, and cancer.

Autoimmune diseases affect about one in 12 Australians, he notes. They are incurable and require lifelong treatments to minimize the damage. Patients often try many different treatments before finding one that works for them.

The genetic mechanisms are actually really generic, he says. You can learn a lot by linking what we see in [OneK1K study] data to what already know just about genetic positions in disease. Now, were taking those genetic positions from genome-wide association studies and will show mechanisms of action and specifically the cell types they are acting in.

Pure fundamental science is a major driver for the work, says Powell, knowledge creation for human disease... and making all the data publicly available. Since the Science paper published in April, he has been fielding multiple data requests daily.

The more translational outcome is the possibility that the catalogue of genetic mechanisms will be useful in predicting which treatments will work best for individual patients, Powell says. To test that hypothesis, Powells lab is in the process of conducting a series of retrospective and prospective signal-seeking studies using currently marketed drugsstarting with immunotherapy treatment of cancer.

If successful, patients will one day be able to get a very cheap test costing literally tens of dollars [in Australia anyway] to guide the clinical decision-making of their treating physician, Powell says. We think that across a population we will be able to move the efficacy of a drug from, say, 30%which is pretty common for immunotherapy and a lot of inhibitory drugs in autoimmune diseaseto 50% or 60%. Even a 10-percentile gain for a single drug would be remarkable in terms of patient impact, he adds.

Along the way, the molecular mechanisms of disease are being unearthed at the cellular RNA level and that data could be shared with pharmaceutical companies to inform their early-stage drug development work, including which targets to take forward to phase 1 clinical trials, says Powell. Already, four pharma companies and one biotech have approached him about just such partnering opportunity, which would additionally aid them in the selection of patient groups for treatment trials.

Scientific strides have been a team effort by many committed individuals, he says, crediting the 16 co-authors on the latest study hailing from Sydney, Hobart, Melbourne, Brisbane, and San Francisco. They consider themselves part of the larger, decade-long movement toward open science, marked by transparency, open communication, and access to the data and computer code used to reach conclusions.

See the original post:
Genetic Control Of Autoimmune Disease Mapped To Cellular Level - Bio-IT World

COLUMBIA, Md., June 07, 2022 (GLOBE NEWSWIRE) -- Neon Bloom, Inc. (OTC: NBCO): Bazelet Health Systems, a wholly owned subsidiary of Neon Bloom, is proud to announce the endowment of a program known as cERI (cannabis Education & Research Initiative). The program encompasses the donation by Bazelet of federally legal cannabis genetics (genetically producing 0% THC) to DEA registered research entities, such as the National Center for the Development of Natural Products at the University of Mississippi and the broader qualified scientific community wishing to conduct, disseminate and support rigorous scientific research on the clinical effects of cannabis. The companys genetics are patented, compliant with the Controlled Substances Act (CSA) and are now available to all to conduct research with our genetics.

Global scientific research of the Cannabis Sativa L. plant has been illegal because of the Controlled Substance Act (CSA). The CSA has created a decades-long pent-up demand for the scientific research of the cannabis plant by qualified research entities. In 2016, the DEAannouncedthat it was amending its longstanding policies to allow additional parties to grow cannabis for clinical research purposes. Since that time, it amended its regulations in 2020 (which became effective in January 2021) to facilitate the cultivation of marihuana for research purposes and other licit purposes to enhance compliance with the Controlled Substances Act, including registering cultivators consistent with treaty obligations but has not legalized cannabis research. In fact, to date, the DEA has only acknowledged providing a MOA (Memorandum of Agreement) to just a handful of applicants to work together to facilitate the production, storage, packaging, and distribution of marijuana. (www.dea.gov). Meanwhile, human health and the global scientific community standby helpless, until now. Our genetic library of non-GMO, patented Cannabis Sativa L. plants offers access to cannabinoids such as Cannabigerol (CBG) with no existing THC or CBD, said Dr. Francisco Ward, NBPAS-PM&R/PM, Chief Medical Officer for Bazelet which makes us a prime candidate for research endeavors.

Having been involved with the DEA regarding its amendment to facilitate the cultivation of marihuana for research purposes and other licit purposes to enhance compliance with the Controlled Substances Act, I recognize and appreciate the DEAs unique implementation challenges. I am certain our patented cannabis plants and robust plant science program can immediately deliver value to their program, their researchers, and manufacturers. For decades worldwide, cannabis plants have been almost exclusively bred to yield higher and higher concentrations of Tetrahydrocannabinol (THC) which has fueled a multi-billion recreational and high THC medical marijuana industry. This breeding habit has caused the abandonment, if you will, of hundreds of compounds in the cannabis plant to the detriment of human health, scientific study, and federal law. We have developed an unprecedented plant genetic platform for the DEA that begins with registered, US plant patent approved, Cannabis Sativa L. plants as its foundation. Our unique genetic program will allow DEA registered research entities to unlock untold scientific and human health outcomes by accessing a full array of cannabinoids and compounds found in the Cannabis Sativa L. plant, such as Cannabigerol (CBG). Our program allows the DEA from here forward, the development of world-class cannabis genetics that began with registered, US patented cannabis genetics, says Michael Elzufon, CEO of the Bazelet Health Systems.

Through our cannabis Education & Research Initiative (cERI), we are opening our genetic library to DEA registered research entities, encouraging their rigorous scientific and medical research projects with federally legal cannabis products. With the DEA slow in issuing bulk manufacturer registrations, research projects remain on hold and our patented, federally compliant cannabis genetics are an immediate solution, said Dr. Ward. He added, I look forward to collaborating with colleagues, scientists, DEA bulk manufacturer applicants and patients everywhere, to study, innovate and access the potential of this plant in the areas of neurodegenerative diseases, auto-immune diseases, vascular diseases, psychiatric diseases such as addiction, delusional states, and PTSD.

About Neon Bloom: Neon Bloom, Inc. (OTC: NBCO), doing business as Bazelet Health Systems, Inc. ("Bazelet"), holds the exclusive license to grow in the United States a patented zero-THC, high CBG Cannabis sativa L plant which received United States Patent No. PP32,725 on January 5, 2021. The patented plant, which was named PAN2020, is remarkably high in Cannabigerol (CBG) with undetectable levels (zero percent) of both Cannabidiol (CBD) and Tetrahydrocannabinol (THC). Consistent with the company's mantra to create zero-THC products (the company's Cannabis-ZERO platform), Bazelet is actively developing non-GMO cannabis Sativa plants that produce zero-THC while being rich in CBG and other valuable cannabinoids. Bazelet is a wholly owned subsidiary of the public company that manufactures and markets PECSA, a patent-pending, proprietary full extract of the PAN2020 plant with other added proprietary ingredients. PECSA stands for Plant-based EndoCannabinoid System Activator. The EndoCannabinoid System is the premier regulatory center of the body affecting mental abilities, emotions, pain, inflammation, ne and metabolic functions with receptors found primarily in the brain and immune cells. The company's primary focus is to sell and market PECSA as a non-GMO, plant-based ingredient for the global food, drug, cosmetic, and tobacco industries. To meet the anticipated worldwide demand for PECSA, Bazelet has established a vertically integrated supply chain providing operational control from patented cannabis plants to proprietary patented plant processing to GMP-produced finished products, all with traceability from seed to sale. Bazelet grows patented plants in North America, Europe, South America, and the Middle East coming online in 2023. Processing and distribution facilities are located in the U.S. and Europe.

Disclaimer:This Press Release is for informational purposes, contains forward-looking statements based on current expectations, forecasts, and assumptions with information available to us as of the date hereof, and involves risks and uncertainties. This Press Release does not constitute an offer to sell or a solicitation of offers to buy any securities of any entity. Actual results may differ materially from those implied in forward-looking statements. Forward-looking statements include statements regarding our expectations, beliefs, intentions, or strategies regarding the future and can be identified by forward-looking words such as "anticipate," "believe," "could," "estimate," "expect," "intend," "may," "should," "would" or similar words. We assume no obligation to update the information included in this Press Release, whether from new information, future events, or otherwise.

CONTACT: Dr. Mat BlantonEMAIL: media@bazelethealth.comWEBSITE: http://www.bazelethealth.com

Go here to read the rest:
Bazelet to Supply Its Federally Legal Cannabis Genetics to DEA Approved Research Entities for Rigorous Scientific Research on the Clinical Effects of...

Alameda County Superior Court Judge Jo-Lynne Q. Lee set a hearing on nationally recognized plaintiffs firm Maune Raichle French Hartley & Mudd. LLCs motion for protective order in a pending asbestos case in which the defendants experts wanted to perform genetic testing. The case is John Lohmann and Suzanne Lohmann v. Aaon, Inc., et al. Alameda County Superior Court Case No. RG21098862. In this case, the plaintiffs filed their action in May 2021 in Alameda County against several defendants alleging that Mr. Lohmann contracted mesothelioma occupationally during his career as a refrigeration equipment mechanic beginning in the early 1970s largely in California.

After appearing in the action, the defendants retained pathology experts who wanted to use Mr. Lohmanns medical data for non-litigation purposes without Mr. Lohmanns permission, because the experts believed that the information would advance science. To conduct this testing, counsel for designated defense counsel moved for discovery of Mr. Lohmanns original cytology/pathology slides and paraffin blocks and subpoenaed his health care providers. The court ordered production of those original materials. According to the plaintiffs counsel, production of Mr. Lohmanns pathology and genetic material during litigation does not thereby permit outside, personal research and analysis. Multiple defendants disagreed, however, and contend that evidence produced during litigation enters the public domain and is thereafter not protected by discovery law.

As a result, on January 7, 2022 the plaintiffs filed for a protective order under California Code of Civil Procedure 2025.420, arguing that they never discussed with defense counsel the terms by which Mr. Lohmanns pathology material was to be used. The plaintiffs asked Alameda County Superior Court to block defendants from compiling medical data for the benefit of a third partys medical database or research project. Defendants, in their written opposition and during oral argument, contend that there is no authority barring medical research on data derived during litigation. Defendants also contend that the plaintiffs are incorrectly relying on Californias discovery statutes, which only govern how the evidence is obtained, not how it can be used. Defendants also argue that research evidence derived from litigation is relevant not only for diagnosis, treatment, and cause, but also helps determine the plaintiffs damages. For example, the defendants cite to scientific research showing that patients with the BAP-1 mesothelioma marker respond better to treatment and tend to have longer life expectancies than those patients without this marker. Defendants wish to present this evidence to the jury as they decide Mr. Lohmanns claim for future medical costs and damages for shortened life expectancy.

Up until last year, defendants and the plaintiffs in Alameda County operated under an informal discovery agreement regarding a plaintiffs pathology materials. However, with more and more defense experts looking to see if a plaintiff, like Mr. Lohmann, had the BAP-1 mesothelioma marker, the Maune firm revoked this informal agreement citing privacy and concerns over genetic testing of their clients materials. Their concerns were largely centered on the actions of longtime defense pathology expert, Dr. Victor Roggli, who published an article in 2020 describing an individual previously represented by the Maune firm.[1] According to the Maune firm, Dr. Rogglis use of their clients medical data in his non-litigation research was improper. In regard to the testing for BAP-1 in particular, the plaintiffs in Lohmann are attempting to block it arguing that it has questionable value in a mesothelioma case. The plaintiffs imply in their motion that the defendants are hoping to use published research linking BAP-1 mutations and certain asbestos exposures in litigation.

It is now up to Alameda County Superior Court to decide whether these defendants and the Dr. Rogglis of the world can, legally under the Discovery Act, use a plaintiffs medical data for their own non-litigation purposes without first obtaining the plaintiffs permission. The Court has requested additional briefing from the parties on this subject before it will make this determination. Defendants are urging the Court to retain an independent expert to examine this issue.

For the Lohmann case, the hearing on the plaintiffs protective order did not go forward after the Defendants stipulated that none of their experts intended to use any of Mr. Lohmanns medical information outside of litigation.

So, for now at least, this issue has been tabled until the next case. But, if and when Alameda County does make a ruling on this issue, its decision will have a significant impact on genetic defenses for mesothelioma cases in California and, likely, elsewhere in the nation as well. The courts eventual opinion will decide whether asbestos defendants can use a plaintiffs medical data in third-party research that could potentially help gather information useful to defendants defenses to damages claims in future asbestos cases.

[1] Mujahed T, Tazelaar HD, Sukov WR, Halling KC, Davila JI, Glass C, Pavlisko EN, Strickland KC, Roggli V, Haque M, Mneimneh W, Carter E, Galateau-Salle F, Glidden D, Garcia-Kennedy R, Larsen BT. Malignant Peritoneal Mesothelioma Arising in Young Adults With Long-standing Indwelling Intra-abdominal Shunt Catheters. Am J Surg Pathol. 2021 Feb 1;45(2):255-262. doi: 10.1097/PAS.0000000000001574. PMID: 32826527.

Original post:
Alameda County Awaits Key Decision Regarding The Use of Genetic Testing in Asbestos Cases - JD Supra

The lack of diversity in genomic research could mean Africans are missing out on potential life-changing care for chronic health disorders, according to a new study published inNature Medicine.

Genetic risk scores are a tool used to estimate an individuals risk of developing a disease, based on genetic factors. Researchers are able to find out someones genetic risk score by examining a populations genetic data and linking genetic factors to various health outcomes to indicate how likely they are to experience certain conditions.

These genetic risk scores are thought to revolutionise medicine by making it possible for people to receive treatments in line with their genetic make up, as well as for early identification and prevention of diseases. However, due to the small numbers of genetic studies involving African people, there is not currently enough information to create accurate genetic risk scores to predict their vulnerability to illnesses such as heart diseases.

The study, led by researchers from theMRC/UVRI and the London School of Hygiene & Tropical Medicine (LSHTM) Uganda Research Unit in collaboration with those from the University of Witwatersrand in South Africa, used genetic data from 1.4 million people of diverse ancestry across sub-Saharan Africa to examine how the use of diverse and representative data can impact our ability to predict disease risk.

The team found that when genetic data from the African American population was included in genomic studies, the genetic risk score estimates were five times more accurate for people with African ancestry, compared to when data from European ancestry was used.

African Americans only comprise 1.1% of global genomic studies. These findings emphasise the importance of including Africans genetic information in genomic studies in order to gain more accurate information about genetic risk factors for disease, and better control the growing trend of chronic health disorders in Africa.

Segun Fatumo, Associate Professor of Genetic Epidemiology & Bioinformaticsat theMRC/UVRI and LSHTM Uganda Research Unit said: "Currently, genomic studies include primarily individuals with European ancestry. This means genetic risk scores in predicting risk of disease, while applicable to the European population, is not accurate or reliable for those of African ancestry. It is crucial that we address this lack of diversity in genomic data. More genomic research is required to produce genetic risk scores that are relevant and representative of the genetic diversity in African populations due to age, lifestyle, environment, and other genetic factors."

Researchers used data from Uganda and South Africa to gather genetic information using genetic risk scores to identify people within continental African populations with high and low fat levels. Their findings identified a number of inherent features in African populations, including that the genetic risk scores were more accurate for people living in urban settings in South Africa than for those in Uganda, due to differences in age, lifestyles, environments and genetics.

Additionally, by including well-known risk factors, such as age, gender, body mass index (BMI) and type 2 diabetes in the estimation of genetic risk scores, the classification of people with either high or low risks improved by 42%.

This was in contrast to conventional risk factors reported in European-based studies such as age, gender, and body mass index as significant contributors to identifying people with high and low fat levels. These findings also demonstrate that a standard genetic risk score cannot be applied across different ethnicities and nations in Africa due to genetic variability and other factors which affect risk such as age, lifestyle and environment.

The team also divided the population into three categories to indicate whether they have a low, medium or high risk of developing a disease. This could help clinicians and genetic specialists to evaluate an individuals risk of disease, especially those at high risk of developing chronic diseases.

Early diagnosis and treatment is one of the best ways to reduce the chances of developing chronic diseases such as heart and blood vessel disorders. The lack of diversity in genetic studies, and those that include African people in particular, has slowed progress in calculating individuals susceptibility to illnesses, which in turn slows their path to diagnosis and treatment.

Although genetic risk scores are not extensively used by health professionals at the moment, the researchers believe these findings provide hope for enhancing clinical care in Africa. Knowing how likely an individual is to get a disease could help them take preventative steps to diagnose it earlier, when it is easier to treat, or even cure. According to the researchers, this is crucial for detecting those who are at risk of having high levels of body fat in the future.

Dr. Tinashe Chikowore, from the University of the Witwatersrand and an author of this study, said: "Advocating for greater diversity in genetic studies will guarantee that Africa is not left out of future precision medicine initiatives, which are crucial in identifying people who are more or less susceptible to contract chronic infections."

Reference:KamizaAB, Toure SM, Vujkovic M, et al. Transferability of genetic risk scores in African populations. Nat Med. 2022. doi: 10.1038/s41591-022-01835-x

This article has been republished from the following materials. Note: material may have been edited for length and content. For further information, please contact the cited source.

See the original post:
Diversity in Genetic Research Is Key to Enhancing Treatment of Chronic Diseases in Africa - Technology Networks

Colorado State University researchers are partnering with the American Hereford Association to support cattle producers and the beef industry in finding sustainable solutions to environmental and economic challenges.

The new research aims to enhance understanding of genetic differences in seedstock relative to enteric methane production and nitrogen excretion while identifying selection tools that can help reduce beef's carbon and environmental footprint.

"We're excited to begin this cooperative research agreement with Colorado State University,"says Jack Ward, executive vice president of the American Hereford Association, one of the largest beef breed associations in the United States. "It leverages decades of research and data collected by AHA members aimed at characterizing genetics associated with production efficiency, which plays a key role in environmental and economic sustainability."

Environmental and economic challengesDirect emissions from the animal agriculture sector account for 3.8% of U.S. greenhouse gas emissions, according to the Environmental Protection Agency. Enteric methane accounts for approximately 27% of methane emissions in the U.S.

Methane emission, as a genetic trait in cattle, appears to be moderately heritable with genetic correlations to economically relevant production traits, such as measures of growth, dry matter intake and various estimates of feed efficiency.

Worldwide attention is also focusing more intently on nitrogen a byproduct of rumen fermentation. Previous research suggests genetics play a significant role in nitrogen excretion by cattle, and when selected for, an individual animal's environmental footprint can be reduced.

"We know genetic improvement of our industry is driven by gains made in the seedstock sector. One only needs to look at changes in carcass meat yield and quality over the last two decades to realize the potential for improvements in seedstock genetics to transform the entire beef industry,"says Animal Sciences Professor Mark Enns, a beef cattle geneticist and key member of the research team.

Sustainable solutions"Often, we hear criticism leveled at the beef industry regarding greenhouse gas emissions and the impact of cattle on the environment, but with little context,"Enns says. "Cattle also sequester carbon and contribute to environmental health. This project will contribute to the beef cattle industry's goal of demonstrating carbon neutrality by 2040."

Given the Hereford breed's inherent genetic advantages associated with production efficiency, Ward says documenting the relationship between traits associated with efficiency and greenhouse gas emissions is logical next step for the breed and the industry.

"Beef industry stakeholders including the National Cattlemen's Beef Association have committed to improving the environmental impact of U.S. cattle production. This project aims to develop a selection tool for the American Hereford Association and the broader cattle industry that helps producers identify genetics that will have reduced greenhouse gas emissions without sacrificing animal productivity,"says Kim Stackhouse-Lawson, director of CSU AgNext, a pioneering research collaborative developing sustainable solutions for animal agriculture.

By leveraging existing animal performance data and monitoring animal emissions, Stackhouse-Lawson explains the goal is to identify genetic traits that influence environmental emissions from individual animals and then develop selection indices that can be used to reduce the environmental impact of cattle, while maintaining, and ideally improving economic returns to producers.

"This project will also position the American Hereford Association as a sustainability leader in the beef industry through the development of genetic selection tools that can identify and inform breeders of genetics that meet climate goals without sacrificing quality, performanceand efficiency," says Stackhouse-Lawson.

Further, Enns notes the project has potential to pave new paths of revenue for cattle producers. These could include such things as verified sustainable production claims, in addition to commonly discussed carbon credits.

Supporting the beef industryThe U.S. beef cattle industry has a long history of demonstrating extraordinary gains in efficiency over time, using genetics, technology and management to produce more beef with fewer cows and less land.

"This research will help us identify ways to magnify the gains the industry has already achieved," Ward says.

"CSU is involved in this project because we are passionate about beef production and the beef industry, and the societal benefits it brings from the upcycling of human-inedible plant materials and byproducts into high-quality protein,"Enns says. "From a genetic improvement standpoint, CSU has a long history of new trait development and delivery of selection tools to the industry. As such, we feel we have much to contribute in this realm, striving to produce cattle that meet consumer demands, yet have a smaller environmental footprint."

Source: Colorado State University, whichis solely responsible for the information provided, and wholly owns the information. Informa Business Media and all its subsidiaries are not responsiblefor any of the contentcontained in this information asset.

Follow this link:
CSU partners with American Hereford Association on genetics research - Beef Magazine

A new study adds to our understanding of polar bears and brown bears' linked evolutionary histories.

Scientists have known this for a while, but the current study used a larger dataset to eke out additional detail, including DNA from an old polar bear tooth.

(Photo : HENNING BAGGER/Ritzau Scanpix/AFP via Getty Images)

The fact that these creatures were separated into different species did not prevent them from mating, as per ScienceDaily.

This has been known for some time, but the current study uses a larger dataset, including DNA from an old polar bear tooth, to elucidate the details.

The result that emerged is riddled with difficulties akin to those that have plagued human progress.

According to Charlotte Lindqvist, Ph.D., a specialist in bear genetics and associate professor of biological sciences at the University at Buffalo College of Arts and Sciences, the establishment and maintenance of species may be a chaotic process.

What's going on with polar bears and brown bears is a good analogy for what we're learning about human evolution: species separation may be imperfect.

They're witnessing multidimensional genomic mixing as diverse groups of archaic humans married with descendants of contemporary humans as more old genomes from historical population groups, particularly Neanderthals and Denisovans, have been discovered.

Another system in which this occurs is between polar bears and brown bears.

They discovered evidence of polar bear-brown bear interbreeding that preceded the study of an ancient polar bear, Lindqvist said.

Furthermore, the findings revealed a complex, entangled evolutionary history between brown and polar bears, with gene flow mostly from brown bears to polar bears.

According to the lead author, scientists previously believed that modern humans and Neanderthals evolved from a shared ancestor, and then divided into different species.

Then, she explained, researchers discovered Neanderthal DNA in current Eurasian individuals, showing that modern human groups got an influx of Neanderthal genes at some point during their common evolutionary history.

Lindqvist added that it was only afterward that scientists realized that this genetic intermingling had also enriched Neanderthal populations with current human DNA.

Interbreeding, she noted, may be complicated and not always a one-way track.

Also Read:Consequences of Climate Change: Polar Bear Population Shrinking Due to Arctic Sea Ice Melt

(Photo : JEAN CHRISTOPHE VERHAEGEN/AFP via Getty Images)

The polar bear has long been assumed to have arisen lately from its lower-latitude sister species, the brown bear, based on fossil and mitochondrial DNA data, as per the study "Polar and brown bear genomes reveal ancient admixture and demographic footprints of past climate change," that was published in the journal Proceedings of the National Academy of Sciences of the United States (PNAS).

Full mitochondrial generation sequencing, for example, has suggested a 150-kya split in these species' maternal lineages and affirmed a notably special connection between the polar bear and a hereditarily secluded population of brown bears from Alaska's Alexander Archipelago's Admiralty, Baranof, and Chichagof Islands.

A new, higher comprehensive genome for a polar bear that lived 115,000 to 130,000 years ago in Norway's Svalbard island was also created by the scientists.

The ancient polar bear's DNA was recovered from a tooth belonging to a subfossil jawbone presently kept at the University of Oslo's Natural History Museum.

Researchers predicted that polar bears and brown bears split into separate species around 1.3 to 1.6 million years ago, revising previous estimates by some of the same experts.

The age of the divide has been and continues to be a source of discussion among scientists, with historical interbreeding and a lack of fossil evidence for old polar bears among the variables that make the dating difficult to pin down, according to Lindqvist.

Related article:'Highly-Predatory' Brown Bear Killed 28 Newborn Reindeers After Waking From Hibernation

2022 NatureWorldNews.com All rights reserved. Do not reproduce without permission.

Continue reading here:
Unraveling the Tangled History of Polar Bears to Brown Bears Using Genetic Sequencing - Nature World News

Conceiving a child is like playing the lottery. Given any two parents, there are 70 trillion possible genetic combinations that any one of their children could inherit.

This genetic diversity can make siblings really different from one another, for instance, in terms of their education, income, and lifespan.

Any attempt to study or address inequality in society must consider the impact of genetic inequality.

PAIGE HARDEN: Conceiving a child is like a giant Powerball. If we think about any two parents, there are 70 trillion possible genetic combinations that any one of their children could inherit. So siblings are really different from one another, in their education, in their income, even lifespan. And genetics is part of the reason why. But to study things like genetics in relation to education or intelligence or personality, has long been a really controversial area of research. For many people, the idea of genetic differences between us is hard to reconcile with what they think of as equality.But if we care about inequality that is tied to accidents of people's birth, the kind of stroke of luck over which they have no control, then we should care about genetic inequality, because it is one of the major sources of inequality in this country.

My name is Paige Harden. I'm a professor of psychology at the University of Texas at Austin. And I recently wrote a book called "The Genetic Lottery: Why DNA Matters for Social Equality."

I think what a lot of people don't realize is that all humans are over 99% genetically the same, regardless of their racial group. Even those differences don't fall along racial lines. So most of our DNA we have in common. That remaining less than 1%, however, is really scientifically interesting, because many of the psychological, behavioral, physical differences between us are related to that tiny fraction of our genome that differs between us. How can we figure out which genetic variants are associated with some of the psychological differences that we care about? Your risk for schizophrenia, your risk for depression, how far you go in school. I think a big part of the power of genetics is as a tool to help us understand the environment.

What are the social environments, the school contexts, the parenting environments that can turn on or turn off genetic risk? So if I'm at genetic risk for doing poorly in school, is there something about the school environment that can buffer me against that risk, such that I still go on to do well in my math class, such that I still go on to do well in college? So we're interested in bringing together the biological differences but also an understanding of the environment to see how they combine to shape children's lives.

This work, connecting genetics to things like education, continues to be controversial because people fear 'eugenics.' And that's the idea that genetic differences underlie some natural hierarchy of value, and that genetic information should be used to sort of slot people into their place or station in life. White supremacist groups will be eager consumers of genetic research in order to justify their narratives around biological hierarchy. But if scientists that have egalitarian values avoid the topic, then the only people who are consuming it and talking about what it means are these ideological extremes.

The predominant response to the eugenic perspective has been what I call 'Genome-blindness.' And that's really the idea that we should avoid talking about biological or genetic differences between people. The fear is that if something's genetic, it's natural and there's nothing we can do about it. So let's not talk about genetics lest people give up on the idea of changing social policy. And that doesn't bear out under the science. Things can be influenced by genetics, but still responsive to the environment. A great example is if you wear eyeglasses.

That's something that is genetically-caused, that we fix not by CRISPRing your genome or selecting your embryo, but by giving you an environmental intervention that you wear on your face. So, I think we can think of the antidote to eugenics not being genome-blindness, but being 'anti-eugenics.' There's a really great example of anti-eugenic policy in the United States, and that's the Americans with Disabilities Act.

If you go into an ADA compliant building, there has to be an elevator there. What's being equalized is not their functioning, so someone might still not be able to walk, they might still be in a wheelchair. What's being equalized is their ability to participate with dignity in a public space. In order to accomplish that, you actually have to recognize differences between people. What if we took that anti-eugenic disability justice perspective when we're crafting policies?

I am an egalitarian.I think of social inequality as a moral and political problem to be fixed. But at the same time, I think that biological differences between us are real and make a difference for our lives. I'm out here saying, 'Science doesn't neatly fit into ideology.' What we need to do is think about what our values are, what does the science say, and then take both of those things seriously when we're crafting policies.

Originally posted here:
Your genes affect your education. Here's why that's controversial. - Big Think

ATTR-CM (transthyretin amyloid cardiomyopathy) is a rare heart condition that can lead to heart failure. However, with an early and accurate diagnosis, ATTR-CM is often treatable.

One big question that patients have is what caused this disease? As with many serious health issues, sometimes its hard to pinpoint exactly, but usually this disease is caused by your type of lifestyle/diet, genetics, or a mix of both.

Whether you have been diagnosed early or very late in the game with this condition, changing your lifestyle habits is crucial to extending how long you can live with this type of heart disease, especially when your heart becomes too weak to effectively pump blood throughout the body.

Because ATTR-CM is often misdiagnosed or diagnosed long after symptoms first appear, it has been difficult to establish a reliable life expectancy for the condition if it is diagnosed and treated early in the disease progression.

ATTR cardiomyopathy is, unfortunately, an under-diagnosed condition, says New York cardiologist Aeshita Dwivedi, MD, who adds that greater awareness of ATTR-CM is leading to more diagnoses, which is also resulting in people starting treatment earlier in the disease process.

Some of what you will need to know can be learned by participating in a cardiac rehabilitation program. If you have been diagnosed with ATTR-CM ask your doctor about prescribing you rehab to learn about diet, exercise, medication adherence and other aspects of living with a heart condition.

Related: How Lifestyle Changes Can Help With Managing Heart Failure

Dr. Dwivedi explains that when confronted with the signs of ATTR-CM, like those of heart failure, its essential that you begin working closely with your cardiologist and follow the doctors advice about medication, checkups, lifestyle, and give thoughtful consideration to discussions of procedures, such as having a pacemaker or pump implanted.

Getting Diagnosed with ATTR-CM

Number one would be to see your doctor regularly, Dr. Dwivedi says. It is important to seek medical care for this condition, because we have good options and can change lives. Second would be talk to your doctor if any of your symptoms change. You would rather know sooner rather than later, before things get worse and when you may need hospitalization.

Related: What is the Heart Condition, ATTR-CM? What are the Symptoms?

She also recommends shifting to a heart-healthy diet that includes limited sodium intake and fats. This diet will help you achieve and maintain a healthy weight. Exercise is also important, though your capacity for physical activity will be limited. Be sure to discuss your exercise limits and concerns with your doctor or a cardiac rehab specialist.

Getting your steps in for the day and doing moderate activities very important, Dr. Dwivedi says. If exercise is new to you and you are unsure where to start, reach out to your doctor for a supervised exercise program for you to get comfortable being active.

In general, people with a family history of heart disease or other conditions should be extra vigilant for symptoms of ATTR-CM, which include those associated with heart failure, including:

There are two types of ATTR-CM:

Males are at higher risk than females for both types of ATTR-CM. And while hereditary ATTR-CM may present with symptoms at a young age, older adults are generally at higher risk for both types.

Bottom line, regardless of how you got to this point, what matters is that your condition has been accurately assessed, and you are in the care of a doctor who can try to help you achieve the best case scenario situation while living with ATTR-CM.

Contributing by SurvivorNet staff.

Learn more about SurvivorNet's rigorous medical review process.

ATTR-CM (transthyretin amyloid cardiomyopathy) is a rare heart condition that can lead to heart failure. However, with an early and accurate diagnosis, ATTR-CM is often treatable.

One big question that patients have is what caused this disease? As with many serious health issues, sometimes its hard to pinpoint exactly, but usually this disease is caused by your type of lifestyle/diet, genetics, or a mix of both.

Because ATTR-CM is often misdiagnosed or diagnosed long after symptoms first appear, it has been difficult to establish a reliable life expectancy for the condition if it is diagnosed and treated early in the disease progression.

ATTR cardiomyopathy is, unfortunately, an under-diagnosed condition, says New York cardiologist Aeshita Dwivedi, MD, who adds that greater awareness of ATTR-CM is leading to more diagnoses, which is also resulting in people starting treatment earlier in the disease process.

Some of what you will need to know can be learned by participating in a cardiac rehabilitation program. If you have been diagnosed with ATTR-CM ask your doctor about prescribing you rehab to learn about diet, exercise, medication adherence and other aspects of living with a heart condition.

Related: How Lifestyle Changes Can Help With Managing Heart Failure

Dr. Dwivedi explains that when confronted with the signs of ATTR-CM, like those of heart failure, its essential that you begin working closely with your cardiologist and follow the doctors advice about medication, checkups, lifestyle, and give thoughtful consideration to discussions of procedures, such as having a pacemaker or pump implanted.

Getting Diagnosed with ATTR-CM

Number one would be to see your doctor regularly, Dr. Dwivedi says. It is important to seek medical care for this condition, because we have good options and can change lives. Second would be talk to your doctor if any of your symptoms change. You would rather know sooner rather than later, before things get worse and when you may need hospitalization.

Related: What is the Heart Condition, ATTR-CM? What are the Symptoms?

She also recommends shifting to a heart-healthy diet that includes limited sodium intake and fats. This diet will help you achieve and maintain a healthy weight. Exercise is also important, though your capacity for physical activity will be limited. Be sure to discuss your exercise limits and concerns with your doctor or a cardiac rehab specialist.

Getting your steps in for the day and doing moderate activities very important, Dr. Dwivedi says. If exercise is new to you and you are unsure where to start, reach out to your doctor for a supervised exercise program for you to get comfortable being active.

In general, people with a family history of heart disease or other conditions should be extra vigilant for symptoms of ATTR-CM, which include those associated with heart failure, including:

There are two types of ATTR-CM:

Males are at higher risk than females for both types of ATTR-CM. And while hereditary ATTR-CM may present with symptoms at a young age, older adults are generally at higher risk for both types.

Bottom line, regardless of how you got to this point, what matters is that your condition has been accurately assessed, and you are in the care of a doctor who can try to help you achieve the best case scenario situation while living with ATTR-CM.

Contributing by SurvivorNet staff.

Learn more about SurvivorNet's rigorous medical review process.

See the rest here:
Did My Lifestyle or Genetics Cause ATTR-CM? Learning More About This Heart Condition That Often Goes Misdiagnosed - SurvivorNet

Scientists from the United Kingdom have analyzed the full genetic blueprints of more than 18,000 cancer samples, finding new patterns of mutations that could help doctors provide better, more personalized treatment

By LAURA UNGAR AP Science Writer

April 21, 2022, 6:02 PM

3 min read

Scientists have analyzed the full genetic blueprints of more than 18,000 cancer samples, finding new patterns of mutations that could help doctors provide better, more personalized treatment.

Their study, published Thursday in the journal Science, isnt the first to do such comprehensive whole genome analyses of cancer samples. But no one has ever done so many.

This is the largest cohort in the world. It is extraordinary, said Serena Nik-Zainal of the University of Cambridge, who was part of the team.

Just over 12,200 surgical specimens came from patients recruited from the U.K. National Health Service as part of a project to study whole genomes from people with common cancers and rare diseases. The rest came from existing cancer data sets.

Researchers were able to analyze such a large number because of the same improvements in genetic sequencing technology that recently allowed scientists to finally finish decoding the entire human genome more capable, accurate machines.

We can really begin to tease out the underpinnings of the erosive sort of forces that go to sort of generate cancer," said Andrew Futreal, a genomic medicine expert at MD Anderson Cancer Center in Houston who was not involved in the study.

Cancer is a disease of the genome, or full set of instructions for running cells, that occurs when changes in a persons DNA cause cells to grow and divide uncontrollably. In 2020, there were about 19 million new cancer cases worldwide.

For the study, researchers looked at 19 different types breast, colorectal, prostate, brain and others and identified 58 new clues to the causes of cancer called mutational signatures" that contribute to the development of the disease. They also confirmed 51 of more than 70 previously reported mutation patterns, Nik-Zainal said.

Some arise because of problems within a persons cells; others are sparked by environmental exposures such as ultraviolet radiation, tobacco smoke or chemicals.

Knowing more of them helps us to understand each persons cancer more precisely, which can help guide treatment, Nik-Zainal said.

Genetic sequencing is already being woven into cancer care as part of the growing trend of personalized medicine, or care based on a patients genes and specific disease. Now doctors will have much more information to draw from when they look at individual cancers.

To help doctors use this information, researchers developed a computer algorithm that will allow them to find common mutation patterns and seek out rare ones. Based on a particular pattern, Nik-Zainal said a doctor may suggest a certain course of action, such as getting immunotherapy.

Futreal said the data can also show doctors what tends to happen over time when a patient develops a cancer with a certain mutation pattern helping them intervene earlier and hopefully stop the developing disease in its tracks.

The Associated Press Health and Science Department receives support from the Howard Hughes Medical Institutes Department of Science Education. The AP is solely responsible for all content.

Read the original post:
Study mines cancer genetics to help with targeted treatment - ABC News