Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The original 1969 definition of SIDS as "unexpected by history" and "unexplained after thorough postmortem examination" is under review in the light of two decades of experience. Suggested modifications include restricting the age to less than 1 year, stipulating that the necropsy includes appropriate histology and laboratory tests, and requiring a review of the clinical history and examination of the death scene. The use of a protocol is recommended both by professional and parent groups. Although the diagnosis of SIDS is to some extent one of exclusion, there are several typical findings which are of value in diagnosis and suggest new avenues for research. External examination is important to exclude trauma and signs of suffocation. A recent study has confirmed that petechiae on the face are rare in SIDS and if found raise the question of deliberate or accidental suffocation. Frothy fluid escaping from the nose and mouth is seen in about half of infants who die from SIDS. Postmortem hypostatic staining as an indicator of position has assumed increased importance since prone sleeping has been shown to be a major risk factor for SIDS. Evidence of sweat in clothing suggests overwrapping. Internal examination shows subserosal petechial haemorrhages in the thymus in most cases. These may be related to age and are commoner in babies dying of SIDS than in controls. Relative sparing of the cervical extension of the thymus is strong evidence for negative intrathoracic pressure, perhaps due to upper or lower airway obstruction. Other typical findings are liquid heart blood, prominent lymph nodes, and an empty bladder (which frustrates some biochemical tests in about half of cases). The lungs are usually well inflated, arguing against surfactant deficiency as a significant cause of SIDS. Microscopic evidence of pulmonary oedema and congestion is found in infant deaths for many reasons and is not discriminatory for SIDS. Minor inflammation and infection of the respiratory tract is common in SIDS and may be important by contributing to overheating, apnoea, or sensitisation to bacterial toxins. Mild fatty change in the liver is very common in infant deaths. Panlobular microvesicular fatty change is rare and may require special stains for its recognition. It indicates the necessity of searching for inherited biochemical disorders. Although these are rare in true SIDS, they are an important cause of unexpected death in infancy. Of Naeye's "tissue markers of hypoxia'', extramedullary haemopoiesis in the liver and brainstem gliosis have been confirmed. Persistence of fetal haemoglobin and raised hypoxanthine values in vitreous humour are further pointers to periods of premortem hypoxia. Painstaking neuropathology has shown delayed myelination and maturation of dendritic spines. Changes in the brain may explain the link between antenatal factors such as smoking and SIDS. A second cot death in a family requires expert examination. Minor injuries or unexplained apnoeic spells may be important retrospective clues to non-accidental injury. Investigations mus exclude inherited disorders before the death is ascribed to SIDS. Parents demand that the pathologist takes care of their baby before, during, and after the necropsy, carries out the procedure to a high standard, checks reconstruction of the body, facilitates access, and is responsible for communicating the results of the examination. The "SIDS postmortem" presents both a practical and an intellectual challenge.
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PMID:Pathological findings in SIDS. 147 51

Prolonged exposure of C57B16 mice to pure O2 at 1 ATA induced pulmonary edema associated with involution of lymphoid system and depressed immunity. The consequences of these toxic events were evaluated by 1) mortality rate, 2) determination of pulmonary water, 3) thymic and splenic cellularity, and 4) humoral (primary antibodies) and cellular (mitogenic) immune responses. Pretreatment of mice with 125 mg kg-1 of diethyldithiocarbamate (DDC) several days before exposure to O2 resulted in 1) an increase in animal survival (92-100% vs. 59% O2 controls), 2) a reduction in pulmonary edema, 3) partial stabilization of thymus and spleen lymphocyte populations, and 4) restoration of the humoral response (specific antibodies appeared earlier than in O2 control animals) and improvement of the mitogenic proliferative response of the spleen cells after hyperoxia. None of these effects were observed when DDC treatment coincided with the beginning of exposure. Our results indicated that DDC protects mice from both pulmonary and lymphoid hyperoxic injury, but only in a partial manner. It is suggested that the mechanism of this antioxidative property is indirect.
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PMID:Diethyldithiocarbamate provides partial protection against pulmonary and lymphoid oxygen toxicity. 300 45

Pneumocystis carinii (P.c.) pneumonia was induced in 40 rats by a prolonged corticosteroid treatment (group 1); 40 healthy rats of equal weight constituted the control group (group 2); 9 rats received the same corticosteroid treatment as group 1, together with trimethoprim-sulfamethoxazole (TMP-SFZ) in order to prevent P.c. multiplication (group 3). We could distinguish the respiratory effects induced by corticosteroids from those caused by P.c. pneumonia (group 3 vs group 1). For six weeks the blood leukocyte count, the weight of the spleen and the thymus and the pulmonary status were monitored. Blood gases and acid-base status were measured in conscious rats. There was no pulmonary oedema. The infected P.c. rats had a low PaCO2 and a slight disturbance of blood oxygenation, exemplified by A-aDO2 of 30 mmHg, compared with 17.5 mmHg in control rats and 17 mmHg in TMP-SFZ treated rats. P.c. infected rats had a lymphocyte depletion induced by corticosteroids. They did not exhibit respiratory distress. P.c. pneumonia alone in rats did not cause frank hypoxemia.
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PMID:Respiratory and pulmonary alterations in experimental Pneumocystis carinii pneumonia in rats. 391 91

Dibutylhexamethylenediamine (DBHMD), a polymer intermediate, is strongly alkaline and is corrosive to eyes and skin. Its inhalation toxicity was defined in rats in both acute and subchronic studies. A 4-hr LC50 of 0.22 mg/litre was obtained for DBHMD of either 80.6 or 98.25% purity. Clinical signs of irritation were apparent during and immediately following exposure and no delayed deaths occurred. The mortality dose-response line was relatively steep. Reduction of exposure times to 5 min produced an LC50 of 51 mg/litre, with similar clinical signs and a steep dose-response line. These data suggest that the product of concentration and time (Ct) is constant for exposure times ranging from 5 min to 4 hr. Repeated (ten) exposures to 0.0125 mg/litre caused no signs of adverse response in rats. A concentration of 0.0234 mg/litre caused some mortality, mucous-membrane irritation, changes in haematological parameters (including erythrocyte counts, haemoglobin, concentration and total and differential leucocyte counts) and an increased acidity and decreased volume of urine. Death at this exposure level was attributed to cardiac failure secondary to pulmonary oedema and congestion, with evidence of hepatic congestion, diffuse cardiac myocytolysis and oedema, and thymic atrophy and congestion. Changes in the heart and thymus were seen in one of two rats killed after the tenth exposure. Clinical and pathological changes observed after the ten exposures were absent after a 14-day recovery period. DBHMD is highly toxic following acute inhalation and produces a steep dose-response following either single or multiple exposures.
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PMID:Inhalation toxicity of dibutylhexamethylenediamine in rats. 653 32

IL-18 is a new type of inflammatory cytokine similar to but distinct from IL-12 and IL-1beta. One intriguing property of IL-18 is synergism with IL-12 in many respects. In this study we examined the in vivo synergistic effects of IL-18/IL-12 in mice and found lethal toxicity accompanying an elevated IFN-gamma level in the serum. Since treatment with IL-18 alone did not have any apparent toxicity, and treatment with IL-12 alone showed only limited toxicity in our system, the synergy between the two cytokines was all the more remarkable. The major symptoms of the toxicity were weight loss, diarrhea, hemorrhagic colitis, splenomegaly, fatty liver, and atrophic thymus, most of which are similarly found in endotoxin-induced septic shock. However, in contrast to septic shock, TNF-alpha was not induced. The involvement of IFN-gamma in the toxicity was further studied in detail. Treatment of athymic nude mice with anti-asialo-GM1 did not reduce the toxicity, whereas anti-IFN-gamma treatment of wild-type mice alleviated it. When IFN-gamma-deficient mice were treated with IL-18/IL-12, the majority of them showed mortality and toxicity with severe pulmonary edema. These results indicate that IL-18/IL-12 treatment induces severe adverse effects through not only IFN-gamma-dependent mechanisms but also IFN-gamma-independent processes.
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PMID:IFN-gamma-dependent and -independent mechanisms in adverse effects caused by concomitant administration of IL-18 and IL-12. 1070 27

Glucocorticoids (GCs) are the mainstay of asthma therapy; however, major side effects limit their therapeutic use. GCs influence the expression of genes either by transactivation or transrepression. The antiinflammatory effects of steroids are thought to be due to transrepression and the side effects, transactivation. Recently, a compound, RU 24858, has been identified that demonstrated dissociation between transactivation and transrepression in vitro. RU 24858 exerts strong AP-1 inhibition (transrepression), but little or no transactivation. We investigated whether this improved in vitro profile results in the maintenance of antiinflammatory activity (evaluated in the Sephadex model of lung edema) with reduced systemic toxicity (evaluated by loss in body weight, thymus involution, and bone turnover) compared with standard GCs. RU 24858 exhibits comparable antiinflammatory activity to the standard steroid, budesonide. However, the systemic changes observed indicate that transactivation events do occur with this GC with similar potency to the standard steroids. In addition, the GCs profiled showed no differentiation on quantitative osteopenia of the femur. These results suggest that in vitro separation of transrepression from transactivation activity does not translate to an increased therapeutic ratio for GCs in vivo or that adverse effects are a consequence of transrepression.
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PMID:Therapeutic benefit of a dissociated glucocorticoid and the relevance of in vitro separation of transrepression from transactivation activity. 1116 Feb 46

The investigation committee of Japanese Society of Legal Medicine has investigated 459 forensic autopsy cases of battered children from 1990-1999. The age range was 0-4 years of 381 cases (83%). Of them, the age less than 1 year was high as 161 cases (35.1%). The cause of death including head injury was 161 cases (35.1%), suffocation caused by nasal blockages 37 cases (8.1%), strangulation 32 cases (7.0%), and drowning 30 cases (6.5%) was revealed. In case of assailant, own mother was 226 cases (49.2%), own father was 73 cases (15.9%) and stepfather 46 cases (10.0%) were reported. The intention of cruelty was that the body was positively assaulted (84.3%) and duration was less than 2 months in 136 cases (67%). The nature of cruelty was that beating by other hands (16.8%) in 77 cases and pushed away and threw (1.7%) in 8 cases and those complex (7.8%) in 36 cases. The motive of cruelty when he assailant was own mother (209 cases) was as fellow: 1. Mentally abnormal (15.3%), 2. Irresponsibility (14.4%), 3. Victim cries (5.7%). When the assailant was own father (63%), the motive of cruelty was as 1. Victim cries (12.7%), 2. Lack of love (7.9%), 3. Reassisted attitude (6.3%). Reported death in high temperature was in 29 cases (6.3%) and strangulation was in 27 cases (5.9%). The homicide was 13% and neither care nor protection (neglect) was 2.7%. The physical conditions of battered children were emaciated and stunted growth in 128 cases (31.2%). The past history of medical consultation to the medical hospital was 32 cases (17.8%). Among the injuries, external findings consist of abrasions and bruises were 147 cases (32%) and internal findings were 70 cases (16.7%) mainly numerous gastro-intestinal tract injuries than liver and lungs. In addition, lung edema (16.8%) in 68 cases, thymus atrophy (12.6%) in 51 cases and amalgamation (4.5%) in 18 cases were reported. The injury around the anus and genitalia were 13 cases (3.2%). The bone fracture was not observed in 368 cases (80.2%) out of 459. Among the intracranial injuries, subdural haemastoma or amalgamation were 31.6% (145 cases) out of 459.
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PMID:[Forensic autopsy cases of battered children in Japan (1990-1999)]. 1241 34

Currently available murine staphylococcal enterotoxin B (SEB) shock models require pretreatment with various agents to increase mouse sensitivity to SEB. This study was performed to show that C3H/HeJ mice are highly susceptible to intranasal SEB inoculation, which caused toxic shock without using pretreatment agents. For this purpose, mice were injected intranasally with different doses of SEB and observed for up to 1 month. The median lethal dose of SEB was determined using the probit procedure. Tissue samples were taken at different time points for histopathological examination. The LD(50) was found at 1.6 microg/g (95% fiducial limit (f.l.) 0.7 to 2.2), the LD(80) at 2.7 microg/g (95% f.l. 1.9 to 4.0) and the LD(90) at 3.6 microg/g (95% f.l. 2.7 to 6.4). Histopathologic examination revealed pulmonary edema and bronchopneumonia. Mucosal-associated lymphoid tissue first became activated, followed by increasing lymphocyte apoptosis and depletion. In the liver there were intralobular and portal inflammatory foci with increasing lymphocyte apoptosis and degenerative necrosis. The splenic white pulp was characterized by early activation and subsequent depletion of lymphoid follicle germinal centers. The thymus initially was activated, followed by increasing apoptosis and migration of lymphoid cells from the cortex to the medulla. The pathological features detected in the mice were similar to those of rhesus monkeys treated with SEB aerosol challenge.
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PMID:Murine lethal toxic shock caused by intranasal administration of staphylococcal enterotoxin B. 1285 Nov 2

Fumonisin B1 (FB1) is a mycotoxin produced by the fungus Fusarium verticillioides (formerly Fusarium moniliforme) and is found in diverse crops such as corn, wheat, and barley. Many diseases linked to FB1, such as porcine pulmonary edema, rat hepatic cancer, and equine leukoencephalomalacia, indicate a compromised immune system. The purpose of this study was to determine whether FB1 altered immunological responses in various cell populations of Single Comb White Leghorn chicks. Cells collected for this study were obtained from those immunological organs with well-defined responses (i.e., spleen, thymus, and blood). Cell populations were exposed to 5 to 50 microg/mL FB1 in vitro for 24 to 72 h, and viability and mitogenic response were evaluated. The effects of FB1 on the mitogenic response were evaluated in cell populations from the spleen and blood stimulated with the mitogens, lipopolysaccharide, concanavalin A, and pokeweed mitogen and in thymocytes stimulated with concanavalin A. The 3-(4,5-dimethylthazol-2-yl)-diphenyl-2H-tetrazolium bromide (MTT) reduction assay was used to assess viability and mitogenic response. Fumonisin B1 decreased spleen cell viability and mitogenic response, albeit the degree of decrease varied with mitogen and time of exposure. Fumonisin B1 increased number of viable thymic cells at 50 microg/mL but had no effect on the mitogenic response of thymocytes. Fumonisin B1 had no effect on blood lymphocyte viability or mitogenic response.
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PMID:The effects of fumonisin B1 on viability and mitogenic response of avian immune cells. 1677 70

In a study of trends and magnitudes of lymphocytes proliferation, destruction or apoptosis eleven 3-month-old healthy calves were experimentally infected with the protozoan parasite Theileria parva, which is reported to cause lymphocyte proliferation. Four control calves were not infected. Infected and non-infected calves were sacrificed on days 9, 12, 16, 19, 23, 24 and 25 to examine lymphoid tissue changes and lymphocyte proliferation, apoptosis or necrosis in the thymus, spleen and lymph nodes. All infected calves developed severe East Coast fever, with enlargement of lymph nodes, dyspnoea, high fever and pulmonary oedema. Lymphocyte proliferation was not observed in lymph nodes, thymus and spleen; instead there were massive deaths of lymphocytes and other cells. The terminal severe disease caused massive lymphoid parenchyma coagulation terminating with caseation, organs and cells being undeterminable histologically. Tissues surrounding the lymph nodes were oedematous. Lymph node and thymus parenchyma were caseated and cortices and medulla indistinguishable because of severe lymphocyte and accessory cell deaths. The lymph node fibrous reticular stroma was necrotic and caseated. Lymphoid follicles in lymph nodes degenerated and lacked germinal centres. Lymph nodes, spleen and thymus were grossly enlarged, hardened, potato or cheese like, but microscopically very hypocellular and in the terminal disease acellular because of massive lymphocytes destruction. In the thymus there was extensive thymocyte and epithelioid cell necrosis and loss of distinction between cortex and medulla. The spleen white and red pulps were indistinguishable because of extensive lymphoid cell necrosis. The white pulp degenerated more than the red pulp. The massive lymphocyte deaths in the lymph nodes, thymus and spleen, without lymphocyte proliferation in this T. parva infection in calves leads to a conclusion that this parasite is lympho-destructive and lympho-degenerative in vivo rather than lympho-proliferative.
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PMID:Theileria parva infection in calves causes massive lymphocyte death in the thymus, spleen and lymph nodes without initial proliferation. 1696 42


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