Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020672 (hypothermia)
 17,327 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sarin (O-isopropylmethylphosphonofluoridate) is a highly toxic nerve agent produced for chemical warfare. Sarin is an extremely potent acetylcholinesterase (AchE) inhibitor with high specificity and affinity for the enzyme. Death by sarin is due to anoxia resulting from airway obstruction, weakness of the muscles of respiration, convulsions and respiratory failure. The main clinical symptoms of acute toxicity of sarin are seizures, tremors and hypothermia. Exposure to sarin during incidents in Japan in 1994, 1995 and 1998, and possible exposure to low levels of sarin during the Gulf War, resulted in the deaths and injury of many people in Japan and caused possible long-term health effects on Gulf War veterans. Symptoms related to sarin poisoning in Japan still exist 1-3 years after the incident and include fatigue, asthenia, shoulder stiffness and blurred vision. Sarin produced seizures in rats and pigs. Recent studies showed that long-term exposure to low levels of sarin caused neurophysiological and behavioral alterations. Toxicity from sarin significantly increased following concurrent exposure to other chemicals such as pyridostigmine bromide. Further research to examine effects of sarin on the cellular and the molecular levels, gene transcription, endocrine system as well as its long-term impact is needed.
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PMID:Sarin: health effects, metabolism, and methods of analysis. 1238 97

A 73-year-old woman with a history of hypertension and hyperlipidemia presented with a sharp pain ranging from the right shoulder to the upper limb. She had suffered a sharp pain at rest accompanied by general fatigue and nausea for about ten months prior to admission. Her white blood cell count was 12,800/microl, and her serum C-reactive protein was 17.5 mg/dl. A chest computed tomography scan revealed an aneurysmal change of the origin of the brachiocephalic artery. Pseudoaneurysm due to infection and aortic dissection was considered as a preoperative diagnosis. A total arch replacement was performed under cardiopulmonary bypass, deep hypothermia, and selective cerebral perfusion. Postoperatively, a bacteriologic culture of the contents of the aneurysm revealed Staphylococcus aureus. Perioperative administration of antibiotics was effective and the postoperative course was uneventful.
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PMID:Mycotic pseudoaneurysm of the brachiocephalic artery. 1507 52

Life in the concentration camps of the Third Reich was like living on another planet. The prisoners, stripped of all rights, experienced constant humiliation, uncertain survival and endless terror. Living conditions were harsh, characterized by crowding, poor sanitation and personal hygiene, lack of proper clothing and heating. The days began early with long marches and slave labor. Sleep was short and interrupted, and fatigue was constant and severe. Above all hoovered the dark cloud of ever-present famine. The prisoners were given about a fourth of the daily calorie requirements, and the food lacked vital components such as vitamins and other essential ingredients. The psychological stress was extreme, yet morbidity and mortality were mainly due to infections, injuries and hunger. Lice, scabies and other skin diseases were common. Typhus fever was ever-present, both endemic and epidemic, with a fatal outcome. Many suffered from tuberculosis, typhoid, dysentery, pneumonia and other infections diseases. Injuries were common, caused by beating, punitive whiplashing and other forms of physical abuse, gunshot wounds and dog-bites. Skull injuries with brain contusions and hemorrhages were prevalent, as well as fractured limbs, ribs and pelvic bones. Blunt injuries to chest and abdomen often had fatal outcomes due to the perforation of viscera and peritonitis or as a result of massive hemorrhage from ruptured blood vessels. The harsh winters were marked by frozen gangrenous limbs and hypothermia. Yet, the most ominous condition was the "hunger disease" with its multiple clinical expressions which, in their extreme form, led to the emaciated "musleman" and eventual death.
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PMID:[Morbidity in the concentration camps of the Third Reich]. 1511 84

Competitors in triathlons experience a range of environmental conditions and physiological demands in excess of that found in individual sport events of comparable duration. Consequently, there is a broad range of possible medical problems and complications that must be taken into account when preparing for such races. For most competitors, an Olympic-distance triathlon typically takes between 2-4 hours to complete. This race begins with a swimming segment of 1500 m. Given the wide variety of race venues found around the world, these swims occur in an assortment of water temperatures (from warm to cold) and conditions (from ocean surf to lake calm). Swimmers often exit the water in a state of moderate dehydration and hypothermia and then immediately start the 40 km cycling leg. Many do so in their swimming attire. A wide variety of road surfaces, technically challenging topography, variable environmental conditions and dramatically changing velocities can be encountered on the cycle course. The race concludes with a 10 km running leg. Since it is the final leg, it is often completed in higher ambient temperatures than those encountered at the start, with the athlete possibly running in a significant state of dehydration and fatigue. Other medical problems commonly encountered in triathlon include: muscle cramping, heat illness, postural hypotension, excessive exposure to ultraviolet radiation, musculoskeletal injuries and trauma, gastrointestinal problems as well as post-race bacterial infection, immunosuppression, sympathetic nervous system and psychological exhaustion, and haemolysis. The rate of occurrence of such events and the severity of their potentially negative outcomes is a function of the methods used by both the race organisers and the competitors to prevent or respond to the conditions imposed by the race. Triathletes also commonly compete in both shorter 'sprint distance' events (in the range of a 0.75 km swim, 20 km cycle and 5 km run) and longer events including both one-half and full Ironman distances (2.5 and 3.8 km swim, 80 and 180 km cycle, 20 and 42 km run, respectively), as well as ultra-distance events that exceed the Ironman distance. In the longer events, the previously mentioned medical considerations are further magnified and additional considerations such as hyponatraemia can also occur. Reducing risk associated with these concerns is accomplished by: taking into account weather and water temperature/conditions data prior to event scheduling; effective swim, cycle and run course organisation and management; environmental monitoring prior to and during the event; the implementation of a water safety plan; provision of appropriate fluid replacement throughout the course; implementation of helmet use and non-drafting regulations in the cycling leg; and competitor knowledge regarding fluid replacement, biomechanical technique, physical preparation, safe equipment and course familiarity. Despite these concerns, triathlon participation appears to relatively safe for persons of all ages, assuming that high-risk adults undertake health screening.
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PMID:Medical considerations in triathlon competition: recommendations for triathlon organisers, competitors and coaches. 1570 78

Hill walking is a popular recreational activity in the developed world, yet it has the potential to impose severe stress simultaneously upon several regulatory systems. Information regarding the physiological strain imposed by prolonged walking outdoors in adverse climatic conditions was reported almost four decades ago and recent research has extended some of this work. These data indicate that once the walker fatigues and starts to slow or stops walking altogether, the rate of heat production falls dramatically. This decrease alone predisposes to the development of hypothermia. These processes, in adverse weather conditions and/or during periods when the level of exertion is low (with low heat production), will be accelerated. Since the majority of walkers pursue this activity in groups, the less fit walkers may be more susceptible to fatigue when exercising at a higher relative intensity compared with their fitter counterparts. The best physiological offset for hypothermia is to maintain heat production by means of exercise, and so fatigue becomes a critical predisposing factor; it is as important to facilitate heat loss, especially during periods of high exertion, as it is to maintain heat production and preserve insulation. This can be partly achieved by clothing adjustments and consideration of the intensity of exercise. Failure to provide adequate energy intake during hill walking activities has been associated with decreased performance (particularly with respect to balance) and impaired thermoregulation. Such impairments may increase susceptibly to both fatigue and injury whilst pursuing this form of activity outdoors. The prolonged low to moderate intensity of activity experienced during a typical hill walk elicits marked changes in the metabolic and hormonal milieu. Available data suggest that during hill walking, even during periods of acute negative energy balance, blood glucose concentrations are maintained. The maintenance of blood glucose concentrations seems to reflect the presence of an alternative fuel source, a hormonally induced increase in fat mobilisation. Such enhancement of fat mobilisation should make it easier to maintain blood glucose by decreasing carbohydrate oxidation and promoting gluconeogenesis, thus sparing glucose utilisation by active muscle. During strenuous hill walking, older age walkers may be particularly prone to dehydration and decreased physical and mental performance, when compared with their younger counterparts. In summary, high rates of energy expenditure and hypohydration are likely to be closely linked to the activity. Periods of adverse weather, low energy intake, lowered fitness or increased age, can all increase the participants' susceptibility to injury, fatigue and hypothermia in the mountainous environment.
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PMID:Physiological and metabolic aspects of very prolonged exercise with particular reference to hill walking. 1602 74

Metabolic depression, an adaptive biological process for energy preservation, is responsible for torpor, hibernation and estivation. We propose that a form of metabolic depression, and not mitochondrial dysfunction, is the process underlying the observed hypometabolism, state-dependent neurobiological changes and vegetative symptoms of major depression in humans. The process of metabolic depression is reactivated via differential gene expression in response to perceived adverse stimuli in predisposed persons. Behavior inhibition by temperament, anxiety disorders, genetic vulnerabilities, and early traumatic experiences predispose persons to depression. The proposed theory is supported by similarities in the presentation and neurobiology of hibernation in bears and major depression and explains the yet unexplained neurobiological changes of depression. Although, gene expression is suppressed in other hibernators by deep hypothermia, bears were chosen because they hibernate with mild hypothermia. Pre-hibernation in bears and major depression with atypical features are both characterized by fat storage through overeating, oversleeping, and decreased mobility. Hibernation in bears and major depression with melancholic features are characterized by withdrawal from the environment, lack of energy, loss of weight from not eating and burning stored fat, changes in sleep pattern, and the following similar neurobiological findings: reversible subclinical hypothyroidism; increased concentration of serum cortisol; acute phase protein response; low respiratory quotient; oxidative stress response; decreased neurotransmitter levels; and changes in cyclic-adenosine monophosphate-binding activity. Signaling systems associated with protein phosphorylation, transcription factors, and gene expression are responsible for the metabolic depression process during pre-hibernation and hibernation. Antidepressants and mood stabilizers interfere with the hibernation process and produce their therapeutic effects by normalizing the fluctuation of activities in the different signaling systems, which are down-regulated during hibernation and depression and up-regulated during exodus from hibernation and the hypomanic or manic phase of mood disorders. The ways individuals cognitively perceive, understand, communicate, and react to the vegetative symptoms of depression, from downregulation in energy production, and in the absence of known medical causes, produce the other characteristics of depression including guilt, helplessness, hopelessness, suicidal phenomena, agitation, panic attacks, psychotic symptoms, and sudden switch to hypomanic or manic episodes. The presence of one or more of these characteristics depends on the person's neuropsychological function, its social status between the others, and the other's response to the person. Neurobiological changes associated with metabolic depression during entrance, maintenance, and exodus from hibernation in bears is suggested as a natural animal model of human depression and mood disorders.
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PMID:Metabolic depression in hibernation and major depression: an explanatory theory and an animal model of depression. 1606 29

Human patients with renal disease frequently develop disturbed sleep and severe fatigue. To develop a model for studying factors that contribute to these symptoms, we characterized the sleep patterns of various strains of mice after acute challenge with the fungal organism Candida albicans. After intravenous administration to mice, C. albicans typically colonizes the kidney, producing acute pyelonephritis. Various strains of inbred mice demonstrate marked variation in the temperature and sleep responses that develop after challenge, with individual strains generally showing increased or reduced somnolence in association with fever or hypothermia, respectively. C. albicans-infected mice may be a useful model for identifying the genes and mechanisms that link sleep, temperature, fatigue, and the immune response.
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PMID:Sleep and temperature responses of inbred mice with Candida albicans-induced pyelonephritis. 1694 52

Hyponatremia is often associated with arginine vasopressin (AVP) dysregulation that is regulated by the hypothalamo-neurohypophyseal tract in response to changes in plasma osmolality, commonly in patients with the syndrome of inappropriate antidiuretic hormone secretion (SIADH). Potentially lethal complications of hyponatremia most frequently involve the central nervous system and include anorexia, fatigue, lethargy, delirium, seizures, hypothermia and coma, and require prompt treatment. Chronic hyponatremia also complicates patient care and is associated with increased morbidity and mortality, particularly among patients with congestive heart failure. Conventional treatments for hyponatremia (e.g. fluid restriction, diuretic treatment, and sodium replacement) may not be effective in all patients and can lead to significant adverse events. Preclinical and clinical trial results have shown that AVP receptor antagonism is a promising approach to the treatment of hyponatremia that directly addresses the effects of increased AVP and consequent decreased aquaresis, the electrolyte-sparing excretion of free water. Agents that antagonize V(2) receptors promote aquaresis and can lead to increased serum sodium. Dual-receptor antagonism, in which both V(2) and V(1A) receptors are blocked, may provide additional benefits in patients with hyponatremia.
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PMID:Hyponatremia, arginine vasopressin dysregulation, and vasopressin receptor antagonism. 1717 May 24

A 60-year-old woman presented to her primary care physician with fatigue and anemia. Laboratory evaluation revealed a hemoglobin level of 9.8 g/dL and an erythrocyte sedimentation rate (ESR) of 64 mm/hour. She subsequently developed nocturnal episodes of diaphoresis, confusion, and hypothermia. Capillary glucose measurements during the spells revealed hypoglycemia. During two supervised fasts, the patient's plasma glucose levels fell to 35 mg/dL and 32 mg/dL, respectively. Plasma insulin and C-peptide levels were appropriately suppressed, but a low concentration of beta-hydroxy-butyrate and normal increase of plasma glucose concentration after a glucagon injection suggested the presence of an insulin-like substance. Computed tomographic (CT) scan of the abdomen and subsequent positron emission tomographic (PET) scan revealed extensive lymphadenopathy. Biopsy of periaortic lymph nodes revealed Hodgkin's disease of the mixed cellularity type. Following chemotherapy, a complete remission ensued, the spells abated, and hypoglycemia was not induced by a 23-hour fast. We believe that the patient's Hodgkin's disease was producing an insulin-like substance. The observations of others suggest that this substance may be an autoantibody to the insulin receptor.
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PMID:Recurrent hypoglycemia and hypothermia in a patient with Hodgkin's disease. 1719 56

According to the 2006 Canadian Red Cross Drowning Report, 2007 persons died of cold-water immersion in Canada between 1991 and 2000. These statistics indicate that prevention of cold-water immersion fatalities is a significant public health issue for Canadians. What should a person do after accidental immersion in cold water? For a long time, aquatic safety organizations and government agencies stated that swimming should not be attempted, even when a personal flotation device (PFD) is worn. The objective of the present paper is to present the recent scientific evidence making swimming a viable option for self-rescue during accidental cold-water immersion. Early studies in the 1960s and 1970s led to a general conclusion that "people are better off if they float still in lifejackets or hang on to wreckage and do not swim about to try to keep warm". Recent evidence from the literature shows that the initial factors identified as being responsible for swimming failure can be either easily overcome or are not likely the primary contributors to swimming failure. Studies over the last decade reported that swimming failure might primarily be related not to general hypothermia, but rather to muscle fatigue of the arms as a consequence of arm cooling. This is based on the general observation that swimming failure developed earlier than did systemic hypothermia, and can be related to low temperature of the arm muscles following swimming in cold water. All of the above studies conducted in water between 10 and 14 degrees C indicate that people can swim in cold water for a distance ranging between about 800 and 1500 m before being incapacitated by the cold. The average swimming duration for the studies was about 47 min before incapacitation, regardless of the swimming ability of the subjects. Recent evidence shows that people have a very accurate idea about how long it will take them to achieve a given swimming goal despite a 3-fold overestimation of the absolute distance to swim. The subjects were quite astute at deciding their swimming strategy early in the immersion with 86% success, but after about 30 min of swimming or passive cooling, their decision-making ability became impaired. It would therefore seem wise to make one's accidental immersion survival plan early during the immersion, directly after cessation of the cold shock responses. Additional recommendations for self-rescue are provided based on recent scientific evidence.
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PMID:Self-rescue swimming in cold water: the latest advice. 1762 98


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