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OverviewWhat is retinal detachment?
Retinal detachment, or a detached retina, is a serious eye condition that affects your vision and can lead to blindness if not treated. It happens to a layer of tissue called the retina that lines the back of the eye. It involves the retina pulling away from tissues supporting it. Symptoms include flashes of light, floaters or seeing a shadow in your vision. Floaters are dark spots and squiggles in your vision.
You may experience warning signs like these before the retina detaches, as in the case of retinal tears. Retinal detachment often happens spontaneously, or suddenly. The risk factors include age, nearsightedness, history of eye surgeries or trauma, and family history of retinal detachments.
Call your eye care provider or go to the emergency room right away if you think you have a detached retina.
The retina senses light and sends signals to the brain so we can see. When the retina detaches, it cant do its job. Your vision might become blurry. And you might lose vision permanently if the detachment isnt repaired. Getting prompt treatment can save your eyesight.
Your risk for retinal detachment increases as you age. Youre also at higher risk if you have or had:
Having certain eye conditions also raises your risk for retinal detachment:
If youre at high risk for retinal detachment, talk to your healthcare provider. Your provider can help you set an eye exam and suggest other steps to protect your eye health.
Retinal detachment is rare for people who have none of the risk factors listed here.
The three causes of retinal detachment are:
Some people dont notice any symptoms of retinal detachment, while others do. It depends on severity if a larger part of the retina detaches, youre more likely to experience symptoms.
Symptoms of retinal detachment can happen suddenly and include:
Retinal detachment is usually painless. But its a serious problem that can threaten your vision. Contact a healthcare provider if you notice any symptoms.
You need an eye exam to diagnose retinal detachment. Your eye care provider will use a dilated eye exam to check your retina. Theyll put eye drops in your eyes. The drops dilate, or widen, the pupil. After a few minutes, your provider can get a close look at the retina.
Your provider may recommend other tests after the dilated eye exam. These tests are noninvasive and wont hurt. They help your provider see your retina clearly and in more detail:
Your eye care provider will discuss treatment options with you. You may need a combination of treatments for the best results.
Treatments include:
Laser (thermal) therapy or cryopexy (freezing). Sometimes, your provider will diagnose a retinal tear before the retina starts pulling away. Your provider uses a medical laser or a freezing tool to seal the tear. These devices create a scar that holds the retina in place.
Pneumatic retinopexy. Your provider may recommend this approach if the detachment isnt as extensive. During pneumatic retinopexy:
After surgery, your provider will recommend that you keep your head still for a few days to promote healing. You also may be told not to lie on your back.
Scleral buckle. During this procedure:
Vitrectomy. During a vitrectomy, your provider:
If your provider uses an oil bubble, youll have it removed a few months later. Gas and air bubbles get reabsorbed.
If you have a gas bubble, you may have to avoid activities at certain altitudes. The altitude change can increase the size of the gas bubble and the pressure in your eye. You'll have to avoid flying and traveling to high altitudes. Your provider will tell you when you can start these activities again.
You cant prevent retinal detachment, but you can take steps to lower your risk:
People who have an average risk of eye disease should get eye exams once a year. If youre at higher risk for eye disease, you may need checkups more frequently. Talk to your provider to figure out your best exam schedule.
Your outlook depends on factors like how your vision was before the retinal detachment, how extensive your detachment was and if there are any other complicating factors. Your provider will talk to you about what type of vision improvement you can expect.
In general, surgery for retinal detachment is very successful the repair works about nine out of 10 times. Sometimes, people need more than one procedure to return the retina to its place.
Its possible to get a detached retina more than once. You may need a second surgery if this happens. Talk to your provider about preventive steps you can take to protect your vision. If you notice symptoms returning, call your provider right away.
After retinal detachment surgery, you may have some discomfort. It can last for a few weeks. Your provider will discuss pain medicine and other forms of relief. Youll also need to take it easy for a few weeks. Talk with your provider about when you can exercise, drive and get back to your regular activities.
Other things you can expect after surgery:
If you have retinal detachment (or face a higher risk), ask your provider:
A note from Cleveland Clinic
Retinal detachment is a painless but serious condition. If you notice detached retina symptoms, such as sudden eye floaters, flashes of light or darkening of your vision, get care right away. Call your eye care provider or go to the emergency room. Preventive care is always the best, so protect your eyes and vision health by having regular eye exams.
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Retinal Detachment: Symptoms, Causes & Prevention - Cleveland Clinic
Toxic effects of breathing oxygen at high concentrations
Medical condition
Oxygen toxicity is a condition resulting from the harmful effects of breathing molecular oxygen (O2) at increased partial pressures. Severe cases can result in cell damage and death, with effects most often seen in the central nervous system, lungs, and eyes. Historically, the central nervous system condition was called the Paul Bert effect, and the pulmonary condition the Lorrain Smith effect, after the researchers who pioneered the discoveries and descriptions in the late 19th century. Oxygen toxicity is a concern for underwater divers, those on high concentrations of supplemental oxygen (particularly premature babies), and those undergoing hyperbaric oxygen therapy.
The result of breathing increased partial pressures of oxygen is hyperoxia, an excess of oxygen in body tissues. The body is affected in different ways depending on the type of exposure. Central nervous system toxicity is caused by short exposure to high partial pressures of oxygen at greater than atmospheric pressure. Pulmonary and ocular toxicity result from longer exposure to increased oxygen levels at normal pressure. Symptoms may include disorientation, breathing problems, and vision changes such as myopia. Prolonged exposure to above-normal oxygen partial pressures, or shorter exposures to very high partial pressures, can cause oxidative damage to cell membranes, collapse of the alveoli in the lungs, retinal detachment, and seizures. Oxygen toxicity is managed by reducing the exposure to increased oxygen levels. Studies show that, in the long term, a robust recovery from most types of oxygen toxicity is possible.
Protocols for avoidance of the effects of hyperoxia exist in fields where oxygen is breathed at higher-than-normal partial pressures, including underwater diving using compressed breathing gases, hyperbaric medicine, neonatal care and human spaceflight. These protocols have resulted in the increasing rarity of seizures due to oxygen toxicity, with pulmonary and ocular damage being mainly confined to the problems of managing premature infants.
In recent years, oxygen has become available for recreational use in oxygen bars. The US Food and Drug Administration has warned those who have conditions such as heart or lung disease not to use oxygen bars. Scuba divers use breathing gases containing up to 100% oxygen, and should have specific training in using such gases.
The effects of oxygen toxicity may be classified by the organs affected, producing three principal forms:[3][4]
Central nervous system oxygen toxicity can cause seizures, brief periods of rigidity followed by convulsions and unconsciousness, and is of concern to divers who encounter greater than atmospheric pressures. Pulmonary oxygen toxicity results in damage to the lungs, causing pain and difficulty in breathing. Oxidative damage to the eye may lead to myopia or partial detachment of the retina. Pulmonary and ocular damage are most likely to occur when supplemental oxygen is administered as part of a treatment, particularly to newborn infants, but are also a concern during hyperbaric oxygen therapy.
Oxidative damage may occur in any cell in the body but the effects on the three most susceptible organs will be the primary concern. It may also be implicated in damage to red blood cells (haemolysis),[5][6] the liver,[7] heart,[8] endocrine glands (adrenal glands, gonads, and thyroid),[9][10][11] or kidneys,[12] and general damage to cells.[13]
In unusual circumstances, effects on other tissues may be observed: it is suspected that during spaceflight, high oxygen concentrations may contribute to bone damage.[14] Hyperoxia can also indirectly cause carbon dioxide narcosis in patients with lung ailments such as chronic obstructive pulmonary disease or with central respiratory depression.[14] Hyperventilation of atmospheric air at atmospheric pressures does not cause oxygen toxicity, because sea-level air has a partial pressure of oxygen of 0.21bar (21kPa) whereas toxicity does not occur below 0.3bar (30kPa).
Central nervous system oxygen toxicity manifests as symptoms such as visual changes (especially tunnel vision), ringing in the ears (tinnitus), nausea, twitching (especially of the face), behavioural changes (irritability, anxiety, confusion), and dizziness. This may be followed by a tonicclonic seizure consisting of two phases: intense muscle contraction occurs for several seconds (tonic phase); followed by rapid spasms of alternate muscle relaxation and contraction producing convulsive jerking (clonic phase). The seizure ends with a period of unconsciousness (the postictal state). The onset of seizure depends upon the partial pressure of oxygen in the breathing gas and exposure duration. However, exposure time before onset is unpredictable, as tests have shown a wide variation, both amongst individuals, and in the same individual from day to day.[19] In addition, many external factors, such as underwater immersion, exposure to cold, and exercise will decrease the time to onset of central nervous system symptoms. Decrease of tolerance is closely linked to retention of carbon dioxide.[21][22] Other factors, such as darkness and caffeine, increase tolerance in test animals, but these effects have not been proven in humans.[23][24]
Pulmonary toxicity symptoms result from an inflammation that starts in the airways leading to the lungs and then spreads into the lungs (tracheobronchial tree). The symptoms appear in the upper chest region (substernal and carinal regions).[26][27] This begins as a mild tickle on inhalation and progresses to frequent coughing. If breathing increased partial pressures of oxygen continues, patients experience a mild burning on inhalation along with uncontrollable coughing and occasional shortness of breath (dyspnea). Physical findings related to pulmonary toxicity have included bubbling sounds heard through a stethoscope (bubbling rales), fever, and increased blood flow to the lining of the nose (hyperaemia of the nasal mucosa).[27] X-rays of the lungs show little change in the short term, but extended exposure leads to increasing diffuse shadowing throughout both lungs. Pulmonary function measurements are reduced, as noted by a reduction in the amount of air that the lungs can hold (vital capacity) and changes in expiratory function and lung elasticity.[27] Tests in animals have indicated a variation in tolerance similar to that found in central nervous system toxicity, as well as significant variations between species. When the exposure to oxygen above 0.5bar (50kPa) is intermittent, it permits the lungs to recover and delays the onset of toxicity.[29]
In premature babies, signs of damage to the eye (retinopathy of prematurity, or ROP) are observed via an ophthalmoscope as a demarcation between the vascularised and non-vascularised regions of an infant's retina. The degree of this demarcation is used to designate four stages: (I) the demarcation is a line; (II) the demarcation becomes a ridge; (III) growth of new blood vessels occurs around the ridge; (IV) the retina begins to detach from the inner wall of the eye (choroid).[30]
Oxygen toxicity is caused by exposure to oxygen at partial pressures greater than those to which the body is normally exposed. This occurs in three principal settings: underwater diving, hyperbaric oxygen therapy, and the provision of supplemental oxygen, particularly to premature infants. In each case, the risk factors are markedly different.
Exposures, from minutes to a few hours, to partial pressures of oxygen above 1.6 bars (160kPa)about eight times normal atmospheric partial pressureare usually associated with central nervous system oxygen toxicity and are most likely to occur among patients undergoing hyperbaric oxygen therapy and divers. Since sea level atmospheric pressure is about 1bar (100kPa), central nervous system toxicity can only occur under hyperbaric conditions, where ambient pressure is above normal.[31][32] Divers breathing air at depths beyond 60m (200ft) face an increasing risk of an oxygen toxicity "hit" (seizure). Divers breathing a gas mixture enriched with oxygen, such as nitrox, can similarly have a seizure at shallower depths, should they descend below the maximum operating depth allowed for the mixture.
The lungs and the remainder of the respiratory tract are exposed to the highest concentration of oxygen in the human body and are therefore the first organs to show toxicity. Pulmonary toxicity occurs only with exposure to partial pressures of oxygen greater than 0.5bar (50kPa), corresponding to an oxygen fraction of 50% at normal atmospheric pressure. The earliest signs of pulmonary toxicity begin with evidence of tracheobronchitis, or inflammation of the upper airways, after an asymptomatic period between 4 and 22 hours at greater than 95% oxygen,[34] with some studies suggesting symptoms usually begin after approximately 14 hours at this level of oxygen.[35]
At partial pressures of oxygen of 2 to 3bar (200 to 300kPa)100% oxygen at 2 to 3 times atmospheric pressurethese symptoms may begin as early as 3 hours after exposure to oxygen.[34] Experiments on rats breathing oxygen at pressures between 1 and 3 bars (100 and 300kPa) suggest that pulmonary manifestations of oxygen toxicity may not be the same for normobaric conditions as they are for hyperbaric conditions.[36] Evidence of decline in lung function as measured by pulmonary function testing can occur as quickly as 24 hours of continuous exposure to 100% oxygen,[35] with evidence of diffuse alveolar damage and the onset of acute respiratory distress syndrome usually occurring after 48 hours on 100% oxygen.[34] Breathing 100% oxygen also eventually leads to collapse of the alveoli (atelectasis), whileat the same partial pressure of oxygenthe presence of significant partial pressures of inert gases, typically nitrogen, will prevent this effect.[37]
Preterm newborns are known to be at higher risk for bronchopulmonary dysplasia with extended exposure to high concentrations of oxygen.[38] Other groups at higher risk for oxygen toxicity are patients on mechanical ventilation with exposure to levels of oxygen greater than 50%, and patients exposed to chemicals that increase risk for oxygen toxicity such the chemotherapeutic agent bleomycin.[35] Therefore, current guidelines for patients on mechanical ventilation in intensive care recommends keeping oxygen concentration less than 60%.[34] Likewise, divers who undergo treatment of decompression sickness are at increased risk of oxygen toxicity as treatment entails exposure to long periods of oxygen breathing under hyperbaric conditions, in addition to any oxygen exposure during the dive.[31]
Prolonged exposure to high inspired fractions of oxygen causes damage to the retina.[39][40][41] Damage to the developing eye of infants exposed to high oxygen fraction at normal pressure has a different mechanism and effect from the eye damage experienced by adult divers under hyperbaric conditions.[42][43] Hyperoxia may be a contributing factor for the disorder called retrolental fibroplasia or retinopathy of prematurity (ROP) in infants.[42][44] In preterm infants, the retina is often not fully vascularised. Retinopathy of prematurity occurs when the development of the retinal vasculature is arrested and then proceeds abnormally. Associated with the growth of these new vessels is fibrous tissue (scar tissue) that may contract to cause retinal detachment. Supplemental oxygen exposure, while a risk factor, is not the main risk factor for development of this disease. Restricting supplemental oxygen use does not necessarily reduce the rate of retinopathy of prematurity, and may raise the risk of hypoxia-related systemic complications.[42]
Hyperoxic myopia has occurred in closed circuit oxygen rebreather divers with prolonged exposures.[43][45][46] It also occurs frequently in those undergoing repeated hyperbaric oxygen therapy.[40][47] This is due to an increase in the refractive power of the lens, since axial length and keratometry readings do not reveal a corneal or length basis for a myopic shift.[47][48] It is usually reversible with time.[40][47]
A possible side effect of hyperbaric oxygen therapy is the initial or further development of cataracts, which are a increase in opacity of the lens of the eye which reduces visual acuity, and can eventually result in blindness. This is a rare event, associated with lifetime exposure to raised oxygen concentration, and may be under-reported as it develops very slowly. The cause is not fully understood, but evidence suggests that raised oxygen levels may cause accelerated deterioration of the vitreous humour due to degradation of lens crystallins by cross-linking, forming aggregates capable of scattering light. This may be an end-state development of the more commonly observed myopic shift associated with hyperbaric treatment.[49]
The biochemical basis for the toxicity of oxygen is the partial reduction of oxygen by one or two electrons to form reactive oxygen species, which are natural by-products of the normal metabolism of oxygen and have important roles in cell signalling.[51] One species produced by the body, the superoxide anion (O2),[52] is possibly involved in iron acquisition.[53] Higher than normal concentrations of oxygen lead to increased levels of reactive oxygen species.[54] Oxygen is necessary for cell metabolism, and the blood supplies it to all parts of the body. When oxygen is breathed at high partial pressures, a hyperoxic condition will rapidly spread, with the most vascularised tissues being most vulnerable. During times of environmental stress, levels of reactive oxygen species can increase dramatically, which can damage cell structures and produce oxidative stress.[19][55]
While all the reaction mechanisms of these species within the body are not yet fully understood,[56] one of the most reactive products of oxidative stress is the hydroxyl radical (OH), which can initiate a damaging chain reaction of lipid peroxidation in the unsaturated lipids within cell membranes.[57] High concentrations of oxygen also increase the formation of other free radicals, such as nitric oxide, peroxynitrite, and trioxidane, which harm DNA and other biomolecules.[19][58] Although the body has many antioxidant systems such as glutathione that guard against oxidative stress, these systems are eventually overwhelmed at very high concentrations of free oxygen, and the rate of cell damage exceeds the capacity of the systems that prevent or repair it.[59][60][61] Cell damage and cell death then result.[62]
Diagnosis of central nervous system oxygen toxicity in divers prior to seizure is difficult as the symptoms of visual disturbance, ear problems, dizziness, confusion and nausea can be due to many factors common to the underwater environment such as narcosis, congestion and coldness. However, these symptoms may be helpful in diagnosing the first stages of oxygen toxicity in patients undergoing hyperbaric oxygen therapy. In either case, unless there is a prior history of epilepsy or tests indicate hypoglycaemia, a seizure occurring in the setting of breathing oxygen at partial pressures greater than 1.4bar (140kPa) suggests a diagnosis of oxygen toxicity.[63]
Diagnosis of bronchopulmonary dysplasia in newborn infants with breathing difficulties is difficult in the first few weeks. However, if the infant's breathing does not improve during this time, blood tests and x-rays may be used to confirm bronchopulmonary dysplasia. In addition, an echocardiogram can help to eliminate other possible causes such as congenital heart defects or pulmonary arterial hypertension.[64]
The diagnosis of retinopathy of prematurity in infants is typically suggested by the clinical setting. Prematurity, low birth weight, and a history of oxygen exposure are the principal indicators, while no hereditary factors have been shown to yield a pattern.
The prevention of oxygen toxicity depends entirely on the setting. Both underwater and in space, proper precautions can eliminate the most pernicious effects. Premature infants commonly require supplemental oxygen to treat complications of preterm birth. In this case prevention of bronchopulmonary dysplasia and retinopathy of prematurity must be carried out without compromising a supply of oxygen adequate to preserve the infant's life.
Oxygen toxicity is a catastrophic hazard in scuba diving, because a seizure results in high risk of death by drowning.[66] The seizure may occur suddenly and with no warning symptoms. The effects are sudden convulsions and unconsciousness, during which victims can lose their regulator and drown.[67] One of the advantages of a full-face diving mask is prevention of regulator loss in the event of a seizure. Mouthpiece retaining straps are a relatively inexpensive alternative with a similar but less effective function.[66] As there is an increased risk of central nervous system oxygen toxicity on deep dives, long dives and dives where oxygen-rich breathing gases are used, divers are taught to calculate a maximum operating depth for oxygen-rich breathing gases, and cylinders containing such mixtures should be clearly marked with that depth.[22]
The risk of seizure appears to be a function of dose a cumulative combination of partial pressure and duration. The threshold for oxygen partial pressure below which seizures never occur has not been established, and may depend on many variables, some of them personal. the risk to a specific person can vary considerably depending on individual sensitivity, level of exercise, and carbon dioxide retention, which is influenced by work of breathing.[66]
In some diver training courses for these types of diving, divers are taught to plan and monitor what is called the 'oxygen clock' of their dives. This is a notional alarm clock, which ticks more quickly at increased oxygen pressure and is set to activate at the maximum single exposure limit recommended in the National Oceanic and Atmospheric Administration Diving Manual.[22] For the following partial pressures of oxygen the limits are: 45 minutes at 1.6bar (160kPa), 120 minutes at 1.5bar (150kPa), 150 minutes at 1.4bar (140kPa), 180 minutes at 1.3bar (130kPa) and 210 minutes at 1.2bar (120kPa), but it is impossible to predict with any reliability whether or when toxicity symptoms will occur.[70][71] Many nitrox-capable dive computers calculate an oxygen loading and can track it across multiple dives. The aim is to avoid activating the alarm by reducing the partial pressure of oxygen in the breathing gas or by reducing the time spent breathing gas of greater oxygen partial pressure. As the partial pressure of oxygen increases with the fraction of oxygen in the breathing gas and the depth of the dive, the diver obtains more time on the oxygen clock by diving at a shallower depth, by breathing a less oxygen-rich gas, or by shortening the duration of exposure to oxygen-rich gases.[73] This function is provided by some technical diving decompression computers and rebreather control and monitoring hardware.[74][75]
Diving below 56m (184ft) on air would expose a diver to increasing danger of oxygen toxicity as the partial pressure of oxygen exceeds 1.4bar (140kPa), so a gas mixture must be used which contains less than 21% oxygen (a hypoxic mixture). Increasing the proportion of nitrogen is not viable, since it would produce a strongly narcotic mixture. However, helium is not narcotic, and a usable mixture may be blended either by completely replacing nitrogen with helium (the resulting mix is called heliox), or by replacing part of the nitrogen with helium, producing a trimix.
Pulmonary oxygen toxicity is an entirely avoidable event while diving. The limited duration and naturally intermittent nature of most diving makes this a relatively rare (and even then, reversible) complication for divers. Established guidelines enable divers to calculate when they are at risk of pulmonary toxicity.[78][79][80] In saturation diving it can be avoided by limiting the oxygen content of gas in living areas to below 0.4 bar.
The presence of a fever or a history of seizure is a relative contraindication to hyperbaric oxygen treatment.[81] The schedules used for treatment of decompression illness allow for periods of breathing air rather than 100% oxygen (oxygen breaks) to reduce the chance of seizure or lung damage. The U.S. Navy uses treatment tables based on periods alternating between 100% oxygen and air. For example, USN table 6 requires 75minutes (three periods of 20minutes oxygen/5minutes air) at an ambient pressure of 2.8 standard atmospheres (280kPa), equivalent to a depth of 18 metres (60ft). This is followed by a slow reduction in pressure to 1.9atm (190kPa) over 30minutes on oxygen. The patient then remains at that pressure for a further 150minutes, consisting of two periods of 15minutes air/60minutes oxygen, before the pressure is reduced to atmospheric over 30minutes on oxygen.
Vitamin E and selenium were proposed and later rejected as a potential method of protection against pulmonary oxygen toxicity.[83][84][85] There is however some experimental evidence in rats that vitamin E and selenium aid in preventing in vivo lipid peroxidation and free radical damage, and therefore prevent retinal changes following repetitive hyperbaric oxygen exposures.[86]
Bronchopulmonary dysplasia is reversible in the early stages by use of break periods on lower pressures of oxygen, but it may eventually result in irreversible lung injury if allowed to progress to severe damage. One or two days of exposure without oxygen breaks are needed to cause such damage.[14]
Retinopathy of prematurity is largely preventable by screening. Current guidelines require that all babies of less than 32weeks gestational age or having a birth weight less than 1.5kg (3.3lb) should be screened for retinopathy of prematurity at least every two weeks.[87] The National Cooperative Study in 1954 showed a causal link between supplemental oxygen and retinopathy of prematurity, but subsequent curtailment of supplemental oxygen caused an increase in infant mortality. To balance the risks of hypoxia and retinopathy of prematurity, modern protocols now require monitoring of blood oxygen levels in premature infants receiving oxygen.[88]
In low-pressure environments oxygen toxicity may be avoided since the toxicity is caused by high partial pressure of oxygen, not merely by high oxygen fraction. This is illustrated by modern pure oxygen use in spacesuits, which must operate at low pressure (also historically, very high percentage oxygen and lower than normal atmospheric pressure was used in early spacecraft, for example, the Gemini and Apollo spacecraft).[89] In such applications as extra-vehicular activity, high-fraction oxygen is non-toxic, even at breathing mixture fractions approaching 100%, because the oxygen partial pressure is not allowed to chronically exceed 0.3bar (4.4psi).[89]
During hyperbaric oxygen therapy, the patient will usually breathe 100% oxygen from a mask while inside a hyperbaric chamber pressurised with air to about 2.8bar (280kPa). Seizures during the therapy are managed by removing the mask from the patient, thereby dropping the partial pressure of oxygen inspired below 0.6bar (60kPa).
A seizure underwater requires that the diver be brought to the surface as soon as practicable. Although for many years the recommendation has been not to raise the diver during the seizure itself, owing to the danger of arterial gas embolism (AGE), there is some evidence that the glottis does not fully obstruct the airway.[91] This has led to the current recommendation by the Diving Committee of the Undersea and Hyperbaric Medical Society that a diver should be raised during the seizure's clonic (convulsive) phase if the regulator is not in the diver's mouthas the danger of drowning is then greater than that of AGEbut the ascent should be delayed until the end of the clonic phase otherwise.[67] Rescuers ensure that their own safety is not compromised during the convulsive phase. They then ensure that where the victim's air supply is established it is maintained, and carry out a controlled buoyant lift. Lifting an unconscious body is taught by most recreational diver training agencies as an advanced skill, and for professional divers it is a basic skill, as it is one of the primary functions of the standby diver. Upon reaching the surface, emergency services are always contacted as there is a possibility of further complications requiring medical attention.[92] The U.S. Navy has procedures for completing the decompression stops where a recompression chamber is not immediately available.
The occurrence of symptoms of bronchopulmonary dysplasia or acute respiratory distress syndrome is treated by lowering the fraction of oxygen administered, along with a reduction in the periods of exposure and an increase in the break periods where normal air is supplied. Where supplemental oxygen is required for treatment of another disease (particularly in infants), a ventilator may be needed to ensure that the lung tissue remains inflated. Reductions in pressure and exposure will be made progressively, and medications such as bronchodilators and pulmonary surfactants may be used.[94]
Divers manage the risk of pulmonary damage by limiting exposure to levels shown to be generally acceptable by experimental evidence, using a system of accumulated oxygen toxicity units which are based on exposure time at specified partial pressures. In the event of emergency treatment for decompression illness, it may be necessary to exceed normal exposure limits to manage more critical symptoms.[95]
Retinopathy of prematurity may regress spontaneously, but should the disease progress beyond a threshold (defined as five contiguous or eight cumulative hours of stage 3 retinopathy of prematurity), both cryosurgery and laser surgery have been shown to reduce the risk of blindness as an outcome. Where the disease has progressed further, techniques such as scleral buckling and vitrectomy surgery may assist in re-attaching the retina.
Repeated exposure to potentially toxic oxygen concentrations in breathing gas is fairly common in hyperbaric activity, particularly in hyperbaric medicine, saturation diving, underwater habitats, and repetitive decompression diving. Research at the National Oceanic and Atmospheric Administration (NOAA) by R.W. Hamilton and others determined acceptable levels of exposure for single and repeated exposures. A distinction is made between acceptable exposure for acute and chronic toxicity, but these are really the extremes of a possible continuous range of exposures. A further distinction can be made between routine exposure and exposure required for emergency treatment, where a higher risk of oxygen toxicity may be justified to achieve a reduction of a more critical injury, particularly when in a relatively safe controlled and monitored environment.
The Repex (repetitive exposure) method, developed in 1988, allows oxygen toxicity dosage to be calculated using a single dose value equivalent to 1 minute at atmospheric pressure called an Oxygen Tolerance Unit (OTU), is used to avoid toxic effects over several days of operational exposure. Some dive computers will automatically track the dosage bases on depth and selected gas mixture. The limits allow a greater exposure when the person has not been exposed recently, and daily allowable dose decreases with an increase in consecutive days with exposure.[95] These values may not be fully supported by current data.[97]
A more recent proposal uses a simple power equation, Toxicity Index (TI) = t2 PO2c, where t is time and c is the power term. This was derived from the chemical reactions producing reactive oxygen or nitrogen species, and has been shown to give good predictions for CNS toxicity with c = 6.8 and for pulmonary toxicity for c = 4.57.[97]
For pulmonary toxicity, time is in hours, and PO2 in atmospheres absolute, TI should be limited to 250.
For CNS toxicity, time is in minutes, PO2 in atmospheres absolute, and a TI of 26,108 indicates a 1% risk.
Although the convulsions caused by central nervous system oxygen toxicity may lead to incidental injury to the victim, it remained uncertain for many years whether damage to the nervous system following the seizure could occur and several studies searched for evidence of such damage. An overview of these studies by Bitterman in 2004 concluded that following removal of breathing gas containing high fractions of oxygen, no long-term neurological damage from the seizure remains.[19][98]
The majority of infants who have survived following an incidence of bronchopulmonary dysplasia will eventually recover near-normal lung function, since lungs continue to grow during the first 57 years and the damage caused by bronchopulmonary dysplasia is to some extent reversible (even in adults). However, they are likely to be more susceptible to respiratory infections for the rest of their lives and the severity of later infections is often greater than that in their peers.[99][100]
Retinopathy of prematurity (ROP) in infants frequently regresses without intervention and eyesight may be normal in later years. Where the disease has progressed to the stages requiring surgery, the outcomes are generally good for the treatment of stage 3 ROP, but are much worse for the later stages. Although surgery is usually successful in restoring the anatomy of the eye, damage to the nervous system by the progression of the disease leads to comparatively poorer results in restoring vision. The presence of other complicating diseases also reduces the likelihood of a favourable outcome.
The incidence of central nervous system toxicity among divers has decreased since the Second World War, as protocols have developed to limit exposure and partial pressure of oxygen inspired. In 1947, Donald recommended limiting the depth allowed for breathing pure oxygen to 7.6m (25ft), which equates to an oxygen partial pressure of 1.8bar (180kPa). Over time this limit has been reduced, until today a limit of 1.4bar (140kPa) during a recreational dive and 1.6bar (160kPa) during shallow decompression stops is generally recommended. Oxygen toxicity has now become a rare occurrence other than when caused by equipment malfunction and human error. Historically, the U.S. Navy has refined its Navy Diving Manual Tables to reduce oxygen toxicity incidents. Between 1995 and 1999, reports showed 405 surface-supported dives using the heliumoxygen tables; of these, oxygen toxicity symptoms were observed on 6 dives (1.5%). As a result, the U.S. Navy in 2000 modified the schedules and conducted field tests of 150 dives, none of which produced symptoms of oxygen toxicity. Revised tables were published in 2001.[105]
The variability in tolerance and other variable factors such as workload have resulted in the U.S. Navy abandoning screening for oxygen tolerance. Of the 6,250 oxygen-tolerance tests performed between 1976 and 1997, only 6 episodes of oxygen toxicity were observed (0.1%).[106][107]
Central nervous system oxygen toxicity among patients undergoing hyperbaric oxygen therapy is rare, and is influenced by a number of a factors: individual sensitivity and treatment protocol; and probably therapy indication and equipment used. A study by Welslau in 1996 reported 16 incidents out of a population of 107,264 patients (0.015%), while Hampson and Atik in 2003 found a rate of 0.03%.[108][109] Yildiz, Ay and Qyrdedi, in a summary of 36,500 patient treatments between 1996 and 2003, reported only 3 oxygen toxicity incidents, giving a rate of 0.008%.[108] A later review of over 80,000 patient treatments revealed an even lower rate: 0.0024%. The reduction in incidence may be partly due to use of a mask (rather than a hood) to deliver oxygen.[110]
Bronchopulmonary dysplasia is among the most common complications of prematurely born infants and its incidence has grown as the survival of extremely premature infants has increased. Nevertheless, the severity has decreased as better management of supplemental oxygen has resulted in the disease now being related mainly to factors other than hyperoxia.[38]
In 1997 a summary of studies of neonatal intensive care units in industrialised countries showed that up to 60% of low birth weight babies developed retinopathy of prematurity, which rose to 72% in extremely low birth weight babies, defined as less than 1kg (2.2lb) at birth. However, severe outcomes are much less frequent: for very low birth weight babiesthose less than 1.5kg (3.3lb) at birththe incidence of blindness was found to be no more than 8%.[102]
Central nervous system toxicity was first described by Paul Bert in 1878.[111][112] He showed that oxygen was toxic to insects, arachnids, myriapods, molluscs, earthworms, fungi, germinating seeds, birds, and other animals. Central nervous system toxicity may be referred to as the "Paul Bert effect".[14]
Pulmonary oxygen toxicity was first described by J. Lorrain Smith in 1899 when he noted central nervous system toxicity and discovered in experiments in mice and birds that 0.43bar (43kPa) had no effect but 0.75bar (75kPa) of oxygen was a pulmonary irritant.[29] Pulmonary toxicity may be referred to as the "Lorrain Smith effect".[14] The first recorded human exposure was undertaken in 1910 by Bornstein when two men breathed oxygen at 2.8bar (280kPa) for 30minutes, while he went on to 48minutes with no symptoms. In 1912, Bornstein developed cramps in his hands and legs while breathing oxygen at 2.8bar (280kPa) for 51minutes.[3] Smith then went on to show that intermittent exposure to a breathing gas with less oxygen permitted the lungs to recover and delayed the onset of pulmonary toxicity.[29]
Albert R. Behnke et al. in 1935 were the first to observe visual field contraction (tunnel vision) on dives between 1.0bar (100kPa) and 4.1bar (410kPa).[113][114] During World War II, Donald and Yarbrough et al. performed over 2,000 experiments on oxygen toxicity to support the initial use of closed circuit oxygen rebreathers.[39] Naval divers in the early years of oxygen rebreather diving developed a mythology about a monster called "Oxygen Pete", who lurked in the bottom of the Admiralty Experimental Diving Unit "wet pot" (a water-filled hyperbaric chamber) to catch unwary divers. They called having an oxygen toxicity attack "getting a Pete".[116][117]
In the decade following World War II, Lambertsen et al. made further discoveries on the effects of breathing oxygen under pressure and methods of prevention.[118][119] Their work on intermittent exposures for extension of oxygen tolerance and on a model for prediction of pulmonary oxygen toxicity based on pulmonary function are key documents in the development of standard operating procedures when breathing increased pressures of oxygen. Lambertsen's work showing the effect of carbon dioxide in decreasing time to onset of central nervous system symptoms has influenced work from current exposure guidelines to future breathing apparatus design.[21][22]
Retinopathy of prematurity was not observed before World War II, but with the availability of supplemental oxygen in the decade following, it rapidly became one of the principal causes of infant blindness in developed countries. By 1960 the use of oxygen had become identified as a risk factor and its administration restricted. The resulting fall in retinopathy of prematurity was accompanied by a rise in infant mortality and hypoxia-related complications. Since then, more sophisticated monitoring and diagnosis have established protocols for oxygen use which aim to balance between hypoxic conditions and problems of retinopathy of prematurity.[102]
Bronchopulmonary dysplasia was first described by Northway in 1967, who outlined the conditions that would lead to the diagnosis.[122] This was later expanded by Bancalari and in 1988 by Shennan, who suggested the need for supplemental oxygen at 36weeks could predict long-term outcomes.[123] Nevertheless, Palta et al. in 1998 concluded that radiographic evidence was the most accurate predictor of long-term effects.[124]
Bitterman et al. in 1986 and 1995 showed that darkness and caffeine would delay the onset of changes to brain electrical activity in rats.[23][24] In the years since, research on central nervous system toxicity has centred on methods of prevention and safe extension of tolerance.[125] Sensitivity to central nervous system oxygen toxicity has been shown to be affected by factors such as circadian rhythm, drugs, age, and gender.[126][127][128][129] In 1988, Hamilton et al. wrote procedures for the National Oceanic and Atmospheric Administration to establish oxygen exposure limits for habitat operations.[78][79][80] Even today, models for the prediction of pulmonary oxygen toxicity do not explain all the results of exposure to high partial pressures of oxygen.[130]
Recreational scuba divers commonly breathe nitrox containing up to 40% oxygen, while technical divers use pure oxygen or nitrox containing up to 80% oxygen to accelerate decompression. Divers who breathe oxygen fractions greater than of air (21%) need to be educated on the dangers of oxygen toxicity and how to manage the risk. To buy nitrox, a diver may be required to show evidence of relevant qualification.[131]
Since the late 1990s the recreational use of oxygen has been promoted by oxygen bars, where customers breathe oxygen through a nasal cannula. Claims have been made that this reduces stress, increases energy, and lessens the effects of hangovers and headaches, despite the lack of any scientific evidence to support them.[132] There are also devices on sale that offer "oxygen massage" and "oxygen detoxification" with claims of removing body toxins and reducing body fat.[133] The American Lung Association has stated "there is no evidence that oxygen at the low flow levels used in bars can be dangerous to a normal person's health", but the U.S. Center for Drug Evaluation and Research cautions that people with heart or lung disease need their supplementary oxygen carefully regulated and should not use oxygen bars.[132]
Victorian society had a fascination for the rapidly expanding field of science. In "Dr. Ox's Experiment", a short story written by Jules Verne in 1872, the eponymous doctor uses electrolysis of water to separate oxygen and hydrogen. He then pumps the pure oxygen throughout the town of Quiquendone, causing the normally tranquil inhabitants and their animals to become aggressive and plants to grow rapidly. An explosion of the hydrogen and oxygen in Dr Ox's factory brings his experiment to an end. Verne summarised his story by explaining that the effects of oxygen described in the tale were his own invention (they are not in any way supported by empirical evidence).[134] There is also a brief episode of oxygen intoxication in his "From the Earth to the Moon".[135]
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Eye condition
Medical condition
A posterior vitreous detachment (PVD) is a condition of the eye in which the vitreous membrane separates from the retina.[1]It refers to the separation of the posterior hyaloid membrane from the retina anywhere posterior to the vitreous base (a 34mm wide attachment to the ora serrata).
The condition is common for older adults; over 75% of those over the age of 65 develop it. Although less common among people in their 40s or 50s, the condition is not rare for those individuals. Some research has found that the condition is more common among women.[2][3]
When this occurs there is a characteristic pattern of symptoms:
As a posterior vitreous detachment proceeds, adherent vitreous membrane may pull on the retina. While there are no pain fibers in the retina, vitreous traction may stimulate the retina, with resultant flashes that can look like a perfect circle.[citation needed]
If a retinal vessel is torn, the leakage of blood into the vitreous cavity is often perceived as a "shower" of floaters. Retinal vessels may tear in association with a retinal tear, or occasionally without the retina being torn.[citation needed]
A Weiss ring can sometimes be seen with ophthalmoscopy as very strong indicator that vitreous detachment has occurred. This ring can remain free-floating for years after detachment.[citation needed]
The risk of retinal detachment is the greatest in the first 6 weeks following a vitreous detachment, but can occur over 3 months after the event.
The risk of retinal tears and detachment associated with vitreous detachment is higher in patients with myopic retinal degeneration, lattice degeneration, and a familial or personal history of previous retinal tears/detachment.
The vitreous (Latin for "glassy") humor is a gel which fills the eye behind the lens. Between it and the retina is the vitreous membrane. With age the vitreous humor changes, shrinking and developing pockets of liquefaction, similar to the way a gelatin dessert shrinks and detaches from the edge of a pan. At some stage the vitreous membrane may peel away from the retina. This is usually a sudden event, but it may also occur slowly over months.
Age and refractive error play a role in determining the onset of PVD in a healthy person. PVD is rare in emmetropic people under the age of 40 years, and increases with age to 86% in the 90s. Several studies have found a broad range of incidence of PVD, from 20% of autopsy cases to 57% in a more elderly population of patients (average age was 83.4 years).[4][citation needed]
People with myopia (nearsightedness) greater than 6 diopters are at higher risk of PVD at all ages.Posterior vitreous detachment does not directly threaten vision. Even so, it is of increasing interest because the interaction between the vitreous body and the retina might play a decisive role in the development of major pathologic vitreoretinal conditions, such as epiretinal membrane.[citation needed]
PVD may also occur in cases of cataract surgery, within weeks or months of the surgery.[5]
The vitreous membrane is more firmly attached to the retina anteriorly, at a structure called the vitreous base. The membrane does not normally detach from the vitreous base, although it can be detached with extreme trauma. However, the vitreous base may have an irregular posterior edge. When the edge is irregular, the forces of the vitreous membrane peeling off the retina can become concentrated at small posterior extensions of the vitreous base. Similarly, in some people with retinal lesions such as lattice retinal degeneration or chorio-retinal scars, the vitreous membrane may be abnormally adherent to the retina. If enough traction occurs the retina may tear at these points. If there are only small point tears, these can allow glial cells to enter the vitreous humor and proliferate to create a thin epiretinal membrane that distorts vision. In more severe cases, vitreous fluid may seep under the tear, separating the retina from the back of the eye, creating a retinal detachment. Trauma can be any form from a blunt force trauma to the face such as a boxer's punch or even in some cases has been known to be from extremely vigorous coughing or blowing of the nose.
Posterior Vitreous Detachment is diagnosed via dilated eye examination. For some patients the vitreous gel is extremely clear and so it can be hard to see the PVD. In these cases, additional imaging such as Optical Coherence Tomography (OCT) or ocular ultrasound are used.[6]
Therapy is not required or indicated in posterior vitreous detachment, unless there are associated retinal tears, which need to be repaired.[7] In absence of retinal tears, the usual progress is that the vitreous humor will continue to age and liquefy and floaters will usually become less and less noticeable, and eventually most symptoms will completely disappear.[7] Prompt examination of patients experiencing vitreous humor floaters combined with expeditious treatment of any retinal tears has been suggested as the most effective means of preventing certain types of retinal detachments.[8]
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Induced pluripotent stem cells (iPSCs) provide a powerful starting material to model human disease in relevant cell types. iPSCs may be generated from patients of any genetic background and possess the capacity to differentiate into almost any desired terminal cell type.
Although additional investigation is needed, researchers are beginning to focus on the potential utility of iPSCs as a tool for drug development, modeling of disease, and transplantation medicine.
Using ATCCs complete feeder- and xeno-free culture systems, researchers can generate standardized, quality controlled, and highly characterized human iPSCs lines. ATCCs iPSCs are derived by episomal, retroviral, or Sendai viral reprogramming. After gaining pluripotent status, the iPSCs may then be induced to differentiate into many cell types. These cells are valuable materials in the study of differentiation, tissue repair, disease pathogenesis, and drug discovery and development.
ATCC is a licensee of iPS Academia Japans induced pluripotent stem (iPS) cell patent portfolio and is able to bring complete cell culturing solutions for iPSCs to the research community.
ATCC iPSCs are tested for pluripotency, karyotype, growth potential, and sample purity. These authenticated materials are backed by meticulous quality control procedures, making them ideal as reference standards for physiologically relevant in vitro research.
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Human Induced Pluripotent Stem Cells | ATCC
Meet our Cybercrime Expert
Our Cybercrime Expert at EUPOL COPPS can easily be described as a smile in uniform. Esther Sense, an experienced Police Officer from Germany, holding the rank of Chief Police Investigator, joined EUPOL COPPS earlier this year and aside from her years of experience in her fields of expertise, has brought to the Mission a sunny demeanor that is a pleasure to witness daily. Esther is always ready with a kind word and a pleasant greeting, which of course, made our interview with her all the more pleasant.Tell us a little about yourself (nationality, professional background and experience and expertise)I hail from Hannover, Germany. I joined the German Police Force in 2001 and spent the first years of duty in the riot police and carrying out patrol service. In 2008 I was seconded to one of the first, newly founded Cybercrime Units in Germany, where I was part of the team building the unit from scratch.From 2013 to 2016 I worked in an IT-Development Department as a software developer for police related software.Since 2013 I have been seconded to the IT-Forensic Department. First as a regular Officer for IT-Forensics and since 2020, following a three year course at the federal CID and at university, I became a certified expert for IT-Forensic with specialisation in Linux and Car Forensics.Explain your portfolio here at EUPOL COPPSI am seconded by Germany as a Cybercrime Expert within the Police Advisory Section, and my direct counterpart is the Cybercrime Department of the Palestinian Civil Police. My portfolio seeks to support the PCP in their cybercrime endeavours, taking into account the many challenges they face, such as lack of updated equipment. I also support them on a more holistic level, including raising awareness of cybercrime within the population, a topic which is not only increasing in importance, but is one which is of direct interest to the community as a whole.What do you enjoy most about forming part of EUPOL COPPS, and about working in the Region?Working with our counterparts, as well as all Mission Members, and building friendships with such a diverse set of colleagues. Operating in a sensitive theatre such as ours, I feel very fortunate to witness different cultures in my daily life, and to call this historically special place in the world home. It is a very special experience, and one which I appreciate daily.What are the challenges you face, and how, in your view, may they be overcome?As with any other branch of the PCP, a number of political issues contribute towards the challenges faced in executing the PCPs mandate on a daily basis. The Cybercrime Department is relatively new within the PCP, founded in 2013. In keeping with their mandate, the department works on a high technical level, which is hardly understandable for non-technical persons. Since digital evidence becomes more and more important for criminal investigations, I am of the view that this department needs to increase their capacities, specially in the forensic lab, to ensure a proper and acceptable way of collecting evidence and to prevent illegal investigation methods. This has to be done not only by expanding the working environment to contend the rising numbers of cases in the Palestinian Territories, but also through constant training in investigation of digital evidence and data privacy to face the challenges that come with this very fast evolving and internationally linked field of police work.Esther, thank you so much for sharing your thoughts with the PPIO Team. Your portfolio is indeed fascinating. Despite the challenges, keep up your positive approach and we are always on hand to continue to support your highly commendable efforts!
The Community Policing Team within the Police Advisory Section here at EUPOL COPPS is composed of two very experienced colleagues, hailing from Italy and Canada respectively. Pietro Tripodi, Sostituto Commissario della Polizia di Stato holds the post of Community Policing Senior Advisor, and joined EUPOL COPPS in November 2021; whilst Sergeant Brian Lowe, Halton Regional Police Service is our Community Policing Advisor and joined the Mission in October 2021.Whilst Pietro and Brian have had very diverse careers, the evident silver thread is their years of experience (over 70 years between them) in their respective Police forces, which in turn has enabled them to not only form an excellent team, but to establish a strong and fruitful working relationship with our local counterparts, as they successfully execute their mandate within the Mission.The Community Policing Team sat down with the PPIO Team and shared their experience within EUPOL COPPS.Tell us a little about yourself (nationality, professional background and experience and expertise)Pietro: Im a Police Officer serving in the Italian State Police for the last 36 years. During my careerI have held various roles, such as armed response patrol crew and supervisor, as part of United Nation Police in Kosovo and as part of the European External Action Service as a duty officer within the Situation Room and at the Military Staff Watch Keeping Capability.Brian: I am seconded by the Royal Canadian Mounted Police to this Mission. I hold a Bachelor of Arts in Criminology, and have 35 years of policing experience and have been involved in community patrol, investigations, SWAT, Explosive Disposal, Ground Search and Rescue and Marine Patrol.My skill set includes planning, training, and operations of the various functions I have worked within.Explain your portfolio here at EUPOL COPPSPietro: Within the Mission I hold the post of Senior Police Advisor for the Community Oriented Police. In a nutshell the duties and responsibilities revolve around advising our counterparts within the Palestinian Civilian Police the best way to close the gap between the Police and society as a whole. Not an easy task given our area of operation and its challenges, but we are fortunate to enjoy an excellent working relationship with our counterparts, both centrally and throughout the districts, which in turn enables us to execute our mandate strategically and in partnership with the PCP.Brian: I am a Community Policing Advisor, and my role is to provide my PCP counterparts with strategic advice on Community Policing operations and training. As Pietro has mentioned, our working relationship with our local counterparts is a very fruitful one, and this thanks to our joint efforts in establishing a solid ground for our partnership, which goes from strength to strength.What do you enjoy most about forming part of EUPOL COPPS, and about working in the Region?Pietro: Forming part of EUPOLCOPPS is a truly rewarding experience: The Mission is formed of colleagues from all around EU as well as from Contributing Countries. That creates a very unique melting pot in term of fields of expertise and personal experience. Within the EUPOLCOPPS Police Advisory Section I have the pleasure to lead a Community Policing team in which Brian, my Canadian colleague and friend, and I ensure that our duties and responsibilities meet the requirements of our direct counterparts, and that we are able to positively contribute to the Community Policing portfolio within the PCP. The clear perception of everyday efforts by all Mission members in order to make a difference in working with our respective counterparts is what makes me proud to work in the Region.Brian: aside from our operational activities coming to fruition, what I value is the unique opportunity to meet and work with so many colleagues and local citizens from a wide variety of operational, national and cultural backgrounds.What are the challenges you face, and how, in your view, may they be overcome?Pietro: It is evident that EUPOLCOPPS operates in quite a delicate and unique right in the middle of the longest standing conflict in history. That places on our shoulders the added responsibility to understand the present situation and to do our utmost to collaborate closely with our local and international counterparts, drawing from our personal experience and expertise, thus exchanging best practices and solid policing values, the ultimate goal being the building of a modern Police Force enjoying the full trust of the society.Brian: Changing mindset in regard to adapting more community policing approaches versus the traditional reactive catching bad guys approach. While old school reaction to calls from the public still forms a significant percentage of police work, getting ahead of issues in response to community input and tackling problems in a collaborate multi-stakeholder approach is an effective tool when added to the police tool kit.Pietro and Brian, thank you! The PPIO Team is very pleased to support your endeavours. Given that your portfolio is very closely linked to ours in terms of public perception and trust in the local Authorities, we look forward to our continued partnership on our projects. Keep up the good work and the excellent teamwork!
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The EU Mission for the Support of Palestinian Police and Rule of Law
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Bone Therapeutics provides Third Quarter 2022 Business Update
Reiterates Quality and Composition of Mereo’s Significantly Refreshed Board, which has the Right Skills and Experience to Guide Mereo’s Strategy and Maximize Shareholder Value
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Mereo BioPharma Files Shareholder Circular for Upcoming General Meeting
Presentation highlights a greater than 60% reduction in acute exacerbations and need for antibiotics for chronic sinusitis patients who used XHANCE in landmark ReOpen phase 3 clinical trial program
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Optinose Announces Late Breaking Abstract Podium Presentation at IDWeek 2022
BEDMINSTER, N.J., Oct. 21, 2022 (GLOBE NEWSWIRE) -- Matinas BioPharma (NYSE AMER: MTNB), a clinical-stage biopharmaceutical company focused on improving the intracellular delivery of nucleic acids and small molecules with its lipid nanocrystal (LNC) platform technology, announced today that Jerome D. Jabbour, Chief Executive Officer of Matinas BioPharma, will present at the ThinkEquity Investment Conference on Wednesday, October 26, 2022, at 10:30 a.m. ET, and host investor meetings. The conference is being held at the Mandarin Oriental Hotel in New York City.
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Matinas BioPharma to Present at the ThinkEquity Annual Global Investment Conference
Two-week survival in Cohort 4 (all-oral regimen) was 95% in 40 patients receiving MAT2203
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Matinas BioPharma Announces Positive Interim Data from the Phase 2 EnACT Trial of MAT2203 for the Treatment of Cryptococcal Meningitis, Exceeding...
DURHAM, N.C., Oct. 21, 2022 (GLOBE NEWSWIRE) -- NightHawk Biosciences (NYSE American: NHWK), a fully integrated biopharmaceutical company focused on developing first-in-class therapies to modulate the immune system, today announced that its Scorpion subsidiary plans to host the grand opening of its San Antonio facility today, October 21.
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Nighthawk Biosciences’ Scorpion Subsidiary Announces Grand Opening of its San Antonio Facility
NEW YORK, Oct. 21, 2022 (GLOBE NEWSWIRE) -- Eyenovia, Inc. (NASDAQ: EYEN), a pre-commercial ophthalmic technology company developing the Optejet® delivery system for use both in combination with its own drug-device therapeutic programs as well as out-licensing for additional indications, today announced the company will present at the 2022 American Academy of Optometry’s Annual Meeting, which is taking place from October 26-29, 2022, at the at the San Diego Convention Center. Presentation details are below:
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Eyenovia to Present at the American Academy of Optometry’s Annual Meeting
WESTLAKE VILLAGE, Calif., Oct. 21, 2022 (GLOBE NEWSWIRE) -- Arcutis Biotherapeutics, Inc. (Nasdaq: ARQT), an early-stage commercial company focused on developing meaningful innovations in immuno-dermatology, today announced results of a nationwide survey of adults with seborrheic dermatitis and the healthcare providers who treat them that highlights the long path to diagnosis and the general lack of awareness and education about the disease. The results were presented as a poster at the 2022 Fall Clinical Dermatology Conference in Las Vegas, Nevada. The online survey was conducted by The Harris Poll on behalf of Arcutis and included 300 U.S. adults (18+ years of age) who had been diagnosed with seborrheic dermatitis by a healthcare provider, of which 84% reported their current condition to be moderate or severe, and 601 licensed U.S. healthcare providers specializing in dermatology, including dermatologists, nurse practitioners (NPs), and physician assistants (PAs).
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Nationwide Seborrheic Dermatitis Survey Shows Burdensome and Lengthy Path to Diagnosis
WALTHAM, Mass., Oct. 21, 2022 (GLOBE NEWSWIRE) -- CinCor Pharma, Inc. (NASDAQ: CINC) today announced the publication of Phase 1 clinical data for baxdrostat, a highly selective, once daily, oral small molecule inhibitor of aldosterone synthase, in the journal Hypertension Research.
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CinCor Pharma Announces Publication of Phase 1 Multiple Ascending Dose Study Data in Hypertension Research
Research shows PAD (Polyaphron Dispersion) Technology™ leads to more efficient delivery of Calcipotriene (CAL) and Betamethasone Dipropionate (BDP) than CAL/BDP topical suspension Research shows PAD (Polyaphron Dispersion) Technology™ leads to more efficient delivery of Calcipotriene (CAL) and Betamethasone Dipropionate (BDP) than CAL/BDP topical suspension
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EPI Health, a Novan Company, and MC2 Therapeutics Present New Data In Multiple Posters Highlighting WYNZORA’s® Unique PAD Technology™ at the 42nd...
Data collected shows importance of treatment formulation characteristics and speed of improvement in psoriasis symptoms to patient treatment adherence Data collected shows importance of treatment formulation characteristics and speed of improvement in psoriasis symptoms to patient treatment adherence