Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0036690 (sepsis)
 59,461 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The study was conducted from November 1995 to May 1996 at the one general hospital in Seoul. The total subjects of this study were 412 patients who have the experience of fall accident, among them 31 was who have fallen during hospitalization and 381 was who visited emergency room and out patient clinic. The purposes of this study were to determine the characteristics, risk factors and results of fall accident and to suggest the nursing strategies for prevention of fall. Data were collected by reviewing the medical records and interviewing with the fallers and their family members. For data analysis spss/pc+ program was utilized for descriptive statistics, adjusted standardized X2-test. The results of this study were as follows: 1) Total subjects were 412 fallers, of which 245 (59.5%) were men and 167 (40.5%) were women. Age were 0-14 years 79 (19.2%), 15-44 years 125 (30.4%), 45-64 years 104 (25.2%), over 65 years 104 (25.2%). 2) There was significant association between age and the sexes (X2 = 39.17, P = 0.00). 3) There was significant association between age and history of falls (X2 = 44.41, P = .00). And history of falls in the elderly was significantly associated with falls. 4) There was significant association with age and medical diagnosis (X2 = 140.66, P = .00), chief medical diagnosis were hypertension (34), diabetes mellitus (22), arthritis (11), stroke (8), fracture (7), pulmonary tuberculosis (6), dementia (5) and cataract (5). 5) There was significant association between age and intrinsic factors: cognitive impairment, mobility impairment, insomnia, emotional problems, urinary difficulty, visual impairments, hearing impairments, use of drugs (sedatives, antihypertensive drugs, diuretics, antidepressants) (P < 0.05). But there was no significant association between age and dizziness (X2 = 2.87, P = .41). 6) 15.3% of total fallers were drunken state when they were fallen. 7) Environmental factors of fall accident were unusual posture (50.9%), slips (35.2%), trips (9.5%) and collision (4.4%). 8) Most of falls occurred during the day time, peak frequencies of falls occurred from 1 pm to 6 pm and 7 am to 12 am. 9) The places of fall accident were roads (22.6%), house-stairs (16.7%), rooms, floors, kitchen (11.2%), the roof-top, veranda, windows (10.9%), hospital (7.5%), ice or snowy ways (5.8%), bathroom (4.9%), playground, park (4.9%), subway-stairs (4.4%) and public-bathrooms (2.2%). 10) Activities at the time of fall accident were walking (37.6%), turning around or reaching for something (20.9%), going up or down stairs (19.2%), exercise, working (17.4%), up or down from a bed (2.7%), using wheelchair or walking aids, standing up or down from a chair (2.2%) and standing still (2.2%). 11) Anatomical locations of injuries by falls were head, face, neck (31.3%), lower extremities (29.9%), upper extremities (20.6%), spine, thorax, abdomen or pelvic contents (11.4%) and unspecified (2.9%). 12) Types of injures were fracture (47.6%), bruises (13.8%), laceration (13.3%), sprains (9.0%), headache (6.6%), abrasions (2.9%), intracranial hemorhage (2.4%) and burns (0.5%). 13) 41.5% of the fallers were hospitalized and average of hospitalization was 22.3 days. 14) The six fallers (1.46%) died from fall injuries. The two fallers died from intracranial hemorhage and the four fallers died of secondary infection; pneumonia (2), sepsis (1) and cellulitis (1). It is suggested that 1) Further study is needed with larger sample size to identify the fall risk factors. 2) After the fall accident, comprehensive nursing care and regular physical exercise should be emphasized for the elderly person. 3) Safety education and safety facilities of the public place and home is necessary for fall prevention.
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PMID:[A study on fall accident]. 1043 5

Families with 3 different syndromes characterized by autosomal dominant inheritance of low platelet count and giant platelets were studied. Fechtner syndrome is an autosomal-dominant variant of Alport syndrome manifested by nephritis, sensorineural hearing loss, and cataract formation in addition to macrothrombocytopenia and polymorphonuclear inclusion bodies. Sebastian platelet syndrome is an autosomal-dominant macrothrombocytopenia combined with neutrophil inclusions that differ from those found in May-Hegglin syndrome or Chediak-Higashi syndrome or the Dohle bodies described in patients with sepsis. These inclusions are, however, similar to those described in Fechtner syndrome. Other features of Alport syndrome, though, including deafness, cataracts, and nephritis, are absent in Sebastian platelet syndrome. Epstein syndrome is characterized by macrothrombocytopenia without neutrophil inclusions, in addition to the classical Alport manifestations-deafness, cataracts, and nephritis-and it is also inherited in an autosomal-dominant mode. We mapped the disease-causing gene to the long arm of chromosome 22 in an Italian family with Fechtner syndrome, 2 German families with the Sebastian platelet syndrome, and an American family with the Epstein syndrome. Four markers on chromosome 22q yielded an LOD score greater than 2.76. A maximal 2-point LOD score of 3.41 was obtained with the marker D22S683 at a recombination fraction of 0.00. Recombination analysis placed the disease-causing gene in a 3.37-Mb interval between the markers D22S284 and D22S693. The disease-causing gene interval in these 3 syndromes is similar to the interval described recently in an Israeli family with a slightly different Fechtner syndrome than the one described here. Recombination analysis of these 3 syndromes refines the interval containing the disease-causing gene from 5.5 Mb to 3.37 Mb. The clinical likeness and the similar interval containing the disease-causing gene suggest that the 3 different syndromes may arise from a similar genetic defect.
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PMID:Autosomal-dominant giant platelet syndromes: a hint of the same genetic defect as in Fechtner syndrome owing to a similar genetic linkage to chromosome 22q11-13. 1107 40

Classical galactosaemia (Mendelian Inheritance in Man, no 230400) is an autosomal recessive disorder of galactose metabolism caused by a deficiency of the enzyme galactose-1-phosphate uridyltransferase (GALT). The GALT enzyme is responsible for the conversion of galactose-1-phosphate with UDP glucose to glucose-1-phosphate and UDP galactose. The gene encoding for GALT is located on chromosome 9p13. Patients present with hepatomegaly, liver failure, food intolerance, hypoglycaemia, muscle hypotonia, sepsis and cataract. Treatment involving the total restriction of lactose-containing foods is life-saving but many patients develop late complications such as problems of mental development, disorders of motor function, disorders of speech and hypergonadotrophic hypogonadism.
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PMID:[From gene to disease; galactosemia and galactose-1-phosphate uridyltransferase deficiency]. 1475 29

We present a patient with bilateral endophthalmitis as the presenting sign of meningococcal septicemia. Systematic examination and vitreous tap conclusively identified the microbe, and appropriate treatment was administered, with good recovery of vision.
J Cataract Refract Surg 2005 Feb
PMID:Meningococcal septicemia presenting as bilateral endophthalmitis. 1576 69

Enterovirus uveitis (EU) is a new infant eye disease that was first detected and identified in Russia in 1980-1981. Three subtypes of human echoviruses (EV19K, EV11A, and EV11/B) caused 5 nosocomial outbreaks of EU in different Siberian cities and towns in 1980-1989, by affecting more than 750 children mainly below one year of age. Sporadic and focal EU cases (more than 200) were also retrospectively diagnosed in other regions of Russia and in different countries of the former Soviet Union. There were following clinical manifestations: common symptoms of the infection; acute uveitis (rapid focal iridic destruction, pupillary deformities, formation of membranes in the anterior chamber of the eye); and in 15-30% of cases severe complications, cataract, glaucoma, vision impairments. Uveitis strains EV19 and EV11 caused significant uveitis in primates after inoculation into the anterior chamber of the eye, as well as sepsis-like fatal disease with liver necrosis after venous infection. The uveitis strains are phylogenetically and pathogenetically close for primates to strains EV19 and EV11 isolated from young children with sepsis-like disease. The contents of this review have been published in the Reviews in Medical Virology, 2004, vol. 14, p. 241-254.
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PMID:[Acute enterovirus uveitis in infants]. 1607 33

Classical galactosaemia (McKusick 230400) is an: autosomal recessive disorder of galactose metabolism, caused by a deficiency of the enzyme galactose-1-phosphate uridyltransferase (GALT; EC 2.7.712). Most patients present in the neonatal period, after ingestion of galactose, with jaundice, hepatosplenomegaly, hepatocellular insufficiency, food intolerance, hypoglycaemia, renal tubular dysfunction, muscle hypotonia, sepsis and cataract. The gold standard for diagnosis of classical galactosaemia is measurement of GALT activity in erythrocytes. Gas-chromatographic determination of urinary sugars and sugar alcohols demonstrates elevated concentrations of galactose and galactitol. The only therapy for patients with classical galactosaemia is a galactose-restricted diet, and initially all galactose must be removed from the diet as soon as the diagnosis is suspected. After the neonatal period, a lactose-free diet is advised in most countries, without restriction of galactose-containing fruit and vegetables. In spite of the strict diet, long-term complications such as retarded mental development, verbal dyspraxia, motor abnormalities and hypergonadotrophic hypogonadism are frequently seen in patients with classical galactosaemia. It has been suggested that these complications may result from endogenous galactose synthesis or from abnormal galactosylation. Novel therapeutic strategies, aiming at the prevention of galactose 1-phosphate production, should be developed. In the meantime, the follow-up protocol for patients with GALT deficiency should focus on early detection, evaluation and, if possible, early intervention in problems of motor, speech and cognitive development.
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PMID:Classical galactosaemia revisited. 1683 75

We report a case of unexplained bilateral corneal endothelial decompensation after a coma. A 71-year-old man with no medical history presented with bilateral endothelial decompensation that required penetrating keratoplasty of the left eye combined with cataract surgery. This coma was caused by septicemia originally due to staphylococcus infection following catheter placement in preparation for a CT scan. Visual acuity of the left eye was 20/400 and 20/100 in the right eye when the patient awoke from the coma. After examination, we noted only stromal thickening and Descemet membrane folds causing corneal edema predominating OS. The rest of the exam was normal. Six months after surgery, visual acuity improved to 20/25. The most probable physiopathological mechanism of this decompensation is an iatrogenic complication from drugs administered during the patient's stay in intensive care (oxacillin), but we cannot rule out direct aggression of a bacterium or its toxin or the decompensation of a preexisting pathology.
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PMID:[Bilateral corneal endothelial decompensation after postsepticemia coma]. 1688 31

The functional versatility and diversity of melatonin has exceeded everyone's expectations. The evidence is substantial that melatonin has multiple receptor-mediated and receptor-independent actions. Considering the unexpectedly widespread distribution of cellular membrane receptors as well as the existence of nuclear binding sites/receptors and the fact that some of melatonin's actions are receptor-independent means that melatonin likely functions in every cell with which it comes in contact. This is highlighted by the fact that there are no morpho-physiological barriers to melatonin, e.g., the blood-brain barrier. In addition to its widespread actions, melatonin synthesis occurs in widely diverse tissues with its production not being relegated to the pineal gland. This should not be unexpected given that it is present throughout the animal kingdom including species that lack a pineal gland, e.g., insects, and in single cell organisms. In this review, only a few of melatonin's effects that involve the interaction of the indoleamine with receptors are described. These functions include the control of seasonal reproduction, modulation of sleep processes and influences on bone growth and osteoporosis. Among the actions of melatonin that are likely receptor independent and that are reviewed herein include its ability to neutralize free radicals which leads to a reduction in cataract formation, reducing oxidative stress due to exposure to hyperbaric hyperoxia, ameliorating hyperthyroidism and abating the toxicity of sepsis and septic shock. These actions alone speak to the diversity of beneficial effects of melatonin; however, the review is no way near exhaustive in terms of what melatonin is capable of doing. Because of its ubiquitous benefits, the pharmaceutical industry is developing melatonin analogues which interact with melatonin receptors. Clearly, the intent of the drugs is to take advantage of some of melatonin's numerous beneficial effects.
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PMID:Medical implications of melatonin: receptor-mediated and receptor-independent actions. 1821 86

Since the introduction of HMG-CoA reductase inhibitors (statins) for lowering lipids, a large amount of data has been published demonstrating their potential benefits in conditions as varied as cancer, osteoporosis, and Alzheimer's dementia. We reviewed the published literature on MEDLINE from articles between 1950 and 2008 on the non-atheroprotective effects of statins and noted consistent benefits of statin use in improving outcomes of ventricular arrhythmias, sudden cardiac death, cardiac transplant rejection, chronic obstructive pulmonary disease, and sepsis. However, for these conditions, the level of evidence was inadequate to recommend statin use. The evidence for improving outcomes in atrial fibrillation, mortality in heart failure, contrast-induced nephropathy, cataract, age-related macular degeneration, sub-arachnoid hemorrhage, osteoporosis, dementia, and cancer incidence was conflicting and inconclusive. Furthermore, we found that most of the literature consists of small observational studies and their conclusions are often not corroborated by results from larger or randomized studies. Pending large, well designed, randomized trials, we conclude that there is no definite evidence for the use of statins in any condition besides hyperlipidemia and atherosclerosis.
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PMID:Non-atheroprotective effects of statins: a systematic review. 1992 34

Galactosemia is a treatable metabolic disorder caused by the deficiency of enzyme galactose-1-phosphate uridyl transferase (GALT) and inherited as an autosomal recessive trait. A case of neonate manifesting with recurrent Escherichia coli sepsis is presented here which turned out to be a classic galactosemia. No other common presenting features were observed in this infant except cataract on slit lamp examination. To the best of our knowledge, there is no case of galactosemia reported in literature which presented with recurrent neonatal sepsis without hepatomegaly, hyperbilirubinemia, bleeding disorder, vomiting, diarrhea, failure to thrive, hypoglycemia, coagulopathy, hemolysis or renal tubular acidosis.
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PMID:Galactosemia presenting as recurrent sepsis. 2132 Oct 7


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