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Query: UMLS:C0032285 (pneumonia)
 54,520 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Patterns of mortality among members of the Seneca Nation of Indians between January 1, 1955, and December 31, 1984, were investigated. The study cohort consisted of all members of the Seneca Nation residing in New York State who were listed in the tribal rolls as of January 1, 1955 (n = 3,262). Deaths among cohort members were identified through a computer match against New York State vital records files. Sex-specific standardized mortality ratios (SMRs) were calculated on the basis of mortality patterns exhibited by the general population of New York State, exclusive of New York City. Seneca Nation males demonstrated an excess of deaths from all causes (SMR = 124), while all-cause mortality among Seneca Nation females did not differ from that expected (SMR = 106). Both males and females exhibited excess mortality from infectious diseases, diabetes mellitus, cirrhosis of the liver, and accidents and injuries. Excess mortality was also noted among males for deaths due to atherosclerosis and hernia/intestinal obstruction and among females for deaths due to pneumonia, chronic nephritis, and homicide. Both sexes exhibited a deficit of deaths due to malignant neoplasms and circulatory diseases. Findings from this study will be useful to those responsible for the planning and implementation of health care programs among the Seneca Nation of Indians and other Native American groups.
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PMID:Mortality in a northeastern Native American cohort, 1955-1984. 292 27

To determine the relative importance of multiple interrelated factors that have been considered to contribute to pulmonary infarction, the authors performed a discriminant analysis on consecutively autopsied patients with pulmonary embolism. From the clinic records of 45 individuals, the authors tabulated the underlying illness, history of valvular or ischemic heart disease, right and left ventricular failure, sepsis, shock, malignancy, premortem functional status, and the clinician's suspicion of pulmonary embolism. At postmortem examination, the authors measured and recorded the extent of emphysema, pneumonia, neoplasia, pulmonary vascular atherosclerosis; thickness and dilatation of both cardiac ventricles; the presence of valvular heart disease; the number, diameter, and amount of occlusion of the pulmonary arteries that contained thromboemboli; the extension of the clot, the size of the infarct; the Reid-Index; and the thickness of pulmonary and bronchial arterial wall. The major determinants of infarction were as follows: poor premortem functional status, the number of lobes having emboli, left ventricular failure, and the presence of lung cancer. The authors then tested the equation generated from these patients on 21 additional patients. The discriminant function correctly classified 81% of first group and predicted the occurrence of infarction in new patients with 70% accuracy. The size of the infarct was most correlated with the use of vasodilators and the embolic burden.
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PMID:Factors associated with pulmonary infarction. A discriminant analysis study. 401 73

The authors have explored the suitability of the Mongolian gerbil as a model in aging research and reviewed data on major factors in gerbil morbidity and mortality. The gerbil is a semi-desert rodent, introduced relatively recently into biomedical research. It is moderately prolific, has a maximum survival of about 208 weeks and is easily maintained. Maternal neglect, fighting and epidemic diseases (Tyzzer's disease, salmonellosis, pneumonia) are potential causes of mortality in gerbil colonies. Obese or breeding gerbils may exhibit hyperadrenocorticism, diabetes, non-lipoid arteriosclerosis and secondary lesions in several organs. There is a high prevalence of spontaneous neoplasms in aged gerbils, especially tumors of the adrenal cortex, ovary and skin. The gerbil is a useful model of experimentally-induced stroke, but has proven unsuitable for studies of cholesterol-induced atherosclerosis. The normal and pathological anatomy of periodontal disease in the gerbil is similar in many respects to that of man.
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PMID:The Mongolian gerbil in aging research. 739 11

Human cytomegalovirus (HCMV) can establish lifelong persistence after primary infection with reactivation occurring as a result of immunosuppression. There is much evidence that molecular interactions between the immune system and the HCMV are responsible for immune escape. HCMV in many cells especially in mononuclear blood cells during latency are frequently the source of transmission and spreading and results in a variety of disorders. In this review some data about acute infection in immunocompetent host (mononucleosis, hepatitis), about intrauterine HCMV infection, about infection and endogenous reinfection in bone marrow and solid organ transplant recipients (pneumonitis) and about HCMV disease in AIDS patients (encephalitis, neuropathy, retinitis, colitis) are investigated. Moreover, HCMV associated vasculitis is described in patients with myocarditis, rheumatoid arthritis or polyradiculopathy. HCMV could play an important role in atherosclerosis. Several types of human malignancy have been linked to HCMV and it has been shown that HCMV ie genes upregulate expression of cellular oncogenes. The diagnosis of HCMV infection is carried out by viremia in cell culture using immediate early antigen staining, by antigenaemia which appears to be an early quantitative and predictive tool, by HCMV DNA detection using hybridization and PCR, and by IgM and IgG antibody evaluation. Two antiviral drugs are used for treatment: ganciclovir and phosphonoformic acid; few resistant clinical isolates have been reported. Specific gammaglobulin activity is discussed. HCMV vaccine is not available.
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PMID:[Current status of human cytomegalovirus disease]. 759 23

The effects of alacepril, an angiotensin converting enzyme inhibitor, on atherogenesis were examined in rabbits fed a hypercholesterol diet. The process of atherogenesis was evaluated in vitro by high-resolution transesophageal ultrasonography (TEE phi 4 mm, 7.5 MHz), by direct histological examination and by serum lipid examination. Of the 38 subjects, 18 were designated as the control hypercholesterol group (CH) and 20 received oral alacepril at 90 mg/day (ACE) for 13-22 weeks. Three rabbits in each group died due to pneumonia. TEE enabled a clear diagnosis as either normal, early stage or late stage of atherosclerosis. The intimal-medial thickness was significantly less in the ACE group than in the CH group, but only over the middle portion of the aorta. The ACE group had a smaller area of atheromatous plaque than the CH group (atheromatous index: 37 +/- 20* and 60 +/- 30% respectively, *p < 0.02). Serum cholesterol and triglycerides were similar in the CH group (1590 +/- 653, 258 +/- 224) and the ACE group (1574 +/- 824, 303 +/- 360 respectively). In conclusion, alacepril reduced both the area of atheromatous atheroma plaque and wall hypertrophy independent of serum lipids in cholesterol-fed rabbits. In vitro miniature TEE is a dependable method for evaluating atherosclerosis in rabbits with hypercholesterolemia.
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PMID:The ACE inhibitor alacepril suppresses atherogenesis independent of serum lipids in cholesterol-fed rabbits--critical analysis with new ultrasound technique. 780 84

Graft replacement of the aortic arch aneurysms and concomitant coronary artery bypass grafting (CABG) were performed in the consecutive seven patients for the past five years between 1987 and January 1992, including three (43%) emergency operations. The etiology of aneurysms was atherosclerosis in 4, and aortic dissection in 3. There were one early death (14%) due to MRSA pneumonia, and one late death due to rupture of the abdominal aortic aneurysm 8 months postoperatively. Respiratory failure was frequently complicated immediately after the surgery. Vein grafts were anastomosed to coronary artery during the initial core cooling, and sequential cardioplegia was given through the bypass grafts. Selective cerebral perfusion was carried-out during the reconstruction of the transverse aortic arch and arch vessels in all cases. To achieve sufficient myocardial protection, and to get good postoperative hemodynamics and long-term survivors, it was important to perform the simultaneous CABG at the time of the repair for the aortic arch aneurysm in cases complicated with coronary artery disease.
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PMID:[Surgical treatment of aortic arch aneurysm associated with coronary artery disease]. 831 14

An 81-year-old female patient with an 8-year history of Parkinson's disease was hospitalized because of aspiration pneumonia. The clinical course of her pneumonia was prolonged because of dysphagia with a short period of remission, and she required a long period of bed rest. She received supportive nutrition via a nasogastric tube and many peroral medications that consisted of 3 anti-Parkinsonian drugs and 5 anti-bacterial or anti-tussive agents. Six months after admission, she vomited fresh blood through the nasogastric tube, then went into hypovolemic shock. Hemodynamic stability was temporarily achieved by blood transfusion. Gastroduodenal endoscopic examination could not reveal the exact bleeding site because of massive blood clots. Five days later, the patient died of a massive hematemesis. Autopsy revealed 2 chronic longitudinal ulcers, each 1.7 x 0.4 cm in size, in the upper portion of the esophagus. One of them had developed a fistula to the aorta. Neither esophageal carcinoma nor a foreign body was detected around the fistula. Atherosclerosis of the aorta was mild and the perforation channel was covered with the esophageal epithelium. The fistula was assumed to be a product of local esophageal injury due to drug retention.
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PMID:[Autopsy results of an elderly case of Parkinson's disease and aorto-esophageal fistula who died of a massive hematemesis during prolonged bed rest]. 833 33

Fifty-one pigs were fed a low-cholesterol basal diet, to which either 10% (by weight) of lard fat (group INORM, n = 7), 2% cholesterol plus 8% lard fat (group II, n = 33), or 2% cholesterol plus 4% lard fat plus 4% fish oil (group IIIPREV, n = 11) was added. In all pigs, the left anterior descending coronary artery and the abdominal aorta were denuded at 1 month. In the first 24 hours thereafter, three animals in group II and two in group IIIPREV died suddenly. After 3 months, 0.5% bile acids was added to the diet in groups II and IIIPREV. After 8 months the degree of atherosclerosis was evaluated in groups INORM and IIIPREV and in 14 animals from group II (IIIND). At 4 months, one animal from Group II died of pneumonia. For the next 4 months (postinduction period), the remaining 15 animals from group II received the basal diet, to which either 10% lard fat (group IILF, n = 6) or 5% lard fat plus 5% fish oil (group IIFO, n = 9) was added. The hypercholesterolemic diet increased plasma cholesterol from 2 to 9-12 mM after 8 months. Fish oil had no major effects on plasma lipids during both induction and postinduction. Superoxide production by granulocytes in response to the membrane receptor-dependent N-formyl-methionyl-leucyl-phenylalanine (fMLP) gave a higher response in group IIIND than in group INORM. In group IIIPREV, the response to phorbol myristate acetate (PMA) and fMLP was lowered, while in groups IIFO and IILF the responses to PMA and fMLP were not affected. The response to serum-treated zymosan was similar in all groups. Abrasion caused increases in free cholesterol (40%) and phospholipids (46%) in the abdominal aortas of group INORM animals. Hypercholesterolemia increased both free and esterified cholesterol in the entire aorta. Fish oil prevented accumulation of free cholesterol in the nonabraded ascending aorta during induction and further accumulation of free cholesterol and phospholipids in the abdominal aorta during postinduction. In the nonabraded ascending aorta, triglycerides were significantly (almost five times) lower in group IIFO than in group IILF. During both induction and postinduction, a large incorporation of n-3 polyunsaturated fatty acids (up to 20%) occurred in plasma and aortic cholesterol esters and phospholipids of groups IIFO and IIIPREV.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Development and regression of atherosclerosis in pigs. Effects of n-3 fatty acids, their incorporation into plasma and aortic plaque lipids, and granulocyte function. 838 31

A rabbit model was established for Chlamydia pneumoniae infection that may be helpful to understand the pathogenesis of disease in humans. Twelve, pathogen-free, 1-month-old New Zealand White rabbits were inoculated with 1.0 x 10(7) to 5.0 x 10(7) CFU of purified C. pneumoniae (ATCC strain VR 1310) via the nasopharynx (1 rabbit died immediately postinoculation, and 11 were available for study). Five controls were inoculated with the carrier buffer. Ten of the 11 study rabbits demonstrated serological evidence of acute infection (immunoglobulin G antibodies, 1:8 to > 1:16), with the weakest response at 7 days and the strongest response at 28 days, whereas none of the controls showed any seroconversion. Study animals were sacrificed in batches of three, on days 7, 14, 21, and 28, but controls were sacrificed on days 7 and 28. Two-thirds of the animals demonstrated evidence of bronchiolitis and pneumonia on days 7 and 14 and resolution by day 21. Two study rabbits demonstrated, on histology, early and intermediate lesions of atherosclerosis: one animal (day 7) showed the accumulation of foamy macrophages (fatty streak) in the arch of the aorta, and the other animal (day 14) showed spindle cell proliferation of smooth muscle cells (intermediate lesion). Focal periaortitis was seen in the same animal (day 7). C. pneumoniae elementary bodies were demonstrated by immunocytochemical stain in the lungs (n = 2), liver (n = 3), spleen (n = 5), and aorta (n = 2), one of which corresponded to the intermediate lesion. C. pneumoniae was cultured from the lungs (n = 2), liver (n = 2), spleen (n = 2), and aortic arch (n = 1). All histopathological, immunocytochemical, and cultural studies were negative in the controls. Hence, the rabbit provides a useful animal model for the study of C. pneumoniae infection and its complications, particularly atherosclerosis.
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PMID:Rabbit model for Chlamydia pneumoniae infection. 896 79

We report a 91-year-old man who had a stroke and died of renal failure. He had been treated for hypertension since 20 years before the onset of the present illness. In addition, he was operated on a gastric cancer 17 years previously. Otherwise he was doing well until May 29, 1991 (when he was 87-year-old) when he had sudden onset of dysarthria and right facial weakness. He was admitted to our hospital. On admission, general physical examination was unremarkable, and neurologic examination revealed a mentally sound man with slight dysarthria, right facial weakness, orolingual dyskinesia, and dysequilibrium in which he showed difficulty in tandem gait; however, no cerebellar ataxia was noted. A cranial CT scan revealed leukoaraiosis with multiple low density areas in the cerebral white matter. His BUN was 37 mg/dl and Cr 2.2 mg/dl. His neurologic symptoms cleared within the next few weeks and he was discharged with ticlopidine 100 mg q.d.. He had been doing well after the discharge except for gradual worsening of his renal function; his BUN was 65 mg/dl and Cr 3.27 mg/dl in April of 1994. On March 10, 1995, he fell down and hit his back; he became unable to walk because of pain, and he was admitted again on March 16, 1995. On admission, his blood pressure was 170/80 mmHg. There was an 1 + pitting pretibial edema; otherwise general physical examination was unremarkable. Neurologic examination revealed an alert and oriented man, however, Hasegawa's dementia scale was 23/30. Higher cerebral functions as well as cranial nerves were intact. He showed some unsteadiness of gait, however, no motor weakness or ataxia was noted. Deep tendon reflexes were diminished, but Chaddock sign was positive bilaterally. Vibration was diminished in the feet, however, pain and touch sensations were intact. Laboratory examination revealed a compression fracture of the twelfth thoracic vertebra. Blood count and chemistries were as follows; Hb 7.6 g/dl, Hct 23.3%, TP 6.0 g/dl, Alb 3.6 g/dl, BUN 87 mg/dl, Cr 4.53 mg/dl, T-Chol 174 mg/dl, HDL-Chol 49 mg/dl, Glu 156 mg/dl, Na 142 mEq/L, K 5.4 mEq/L, Cl 115 mEq/L. A urine specimen contained 1 + protein and 1 + glucose, and the sediments contained hyaline casts. A cranial CT scan was essentially same as that taken four years ago. His hospital course was complicated with pneumonia, congestive heart failure, and progressive renal failure. He was treated with intravenous fluid, chemotherapy, and other supportive measures, however, he expired from respiratory failure on April 30, 1995. He was discussed in a neurologic CPC, and the chief discussant arrived at the conclusion that the patient had Binswanger's disease in the brain, benign nephrosclerosis from arteriolosclerosis due to hypertension, congestive heart failure, and pneumonia. Opinions were divided regarding the question as to whether or not this patient had Binswanger's disease. Although his cranial CT scan revealed leukoaraiosis, his dementia and gait disturbance was only mild until his fall on March, 1995. Clinical features did not conform to those of Binswanger's disease. Postmortem examination of the right hemisphere revealed wide spread atherosclerosis and arteriolosclerosis. The kidney showed benign nephrosclerosis due to arteriolosclerosis. Sclerotic changes were also seen in the coronary arteries and the left middle cerebral artery with 70% stenosis. Myelin stain showed diffuse myelin pallor of the cerebral white matters with scattered small infarcts. Arterioles in the white matter showed arteriolosclerosis. Small infarcts were also seen in the putamen and in the thalamus. This patient appeared to have had circulatory disturbance of the white matter which is the basic abnormality causing Binswanger's disease. However, white matter changes in this patient were not quite severe enough to make a pathologic diagnosis of Binswanger's disease.
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PMID:[A 91-year-old man with a stroke, hypertension, and renal failure]. 899 Apr 84


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