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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute fatal pulmonary embolism is one cause of sudden death which should be guarded against. It is the most often missed diagnosis in sudden death cases within the hospital. Clinical pictures of 10 patients with acute fatal pulmonary embolism proved by autopsy were examined to elucidate the problems of diagnosis, and to look for an effective treatment, and a method of prevention. Common risk factors were old age and immobility due to stroke or postoperative state. Common past histories were hypertension, diabetes mellitus, obesity, atrial fibrillation and hyperlipidemia. Electrocardiogram and echocardiogram showed that in these patients there was definite evidence of acute right ventricular overload. High doses of intravenous urokinase should be given whenever acute cardiovascular collapse develops in such high risk patients. Emergent pulmonary angiogram and pulmonary embolectomy could be life-saving in patients with acute massive pulmonary embolism. Prevention is, however, the best treatment. In addition to anticoagulation medication, frequent change of body position and early mobilization are important precautions to prevent fatal pulmonary embolism developing in such patients.
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PMID:[Acute fatal pulmonary embolism: its prevention, diagnosis and treatment]. 236 72

Pulmonary embolism following postoperative deep venous thrombosis is a very serious complication with a high mortality rate. Though this disorder has been thought to be rare in Japanese, its occurrence seems to be increasing recently because of changes in eating habits, increase of average age and the frequent practice of venous catheterization. Two cases of the pulmonary embolism following deep venous thrombosis after surgery are reported, and possible causes of the deep venous thrombosis are discussed. Case 1: A 48 year-old obese female was operated on for a posterior fossa dural arteriovenous malformation. On the 4th postoperative day, she developed a pain and swelling in the left leg and low back pain. On the 18th postoperative day, she fell into a state of shock following the sudden onset of a severe back pain and respiratory distress. After diagnosis of the pulmonary embolism, she was immediately treated with urokinase, warfarin and aspirin. Her obesity was considered to be one of the risk factors of the postoperative deep venous thrombosis. Case 2: A 62 year-old female with a ruptured cerebral aneurysm could not get out of bed because of postoperative mental disturbance. A central venous pressure catheter was inserted into the right femoral vein for two weeks postoperatively. One month after surgery, she complained of swelling and a dull pain in the right leg without cardiorespiratory symptoms. Lung perfusion scintigraphy showed asymptomatic pulmonary embolism. She was treated immediately. Both long bed rest and femoral venous catheterization were considered as risk factors possibly leading to deep venous thrombosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Postoperative pulmonary embolism in neurosurgical practice: report of two cases]. 321 Dec 80

Fibrinolysis is essential for maintaining the fluency of blood flow. Attenuated fibrinolytic activity has been frequently detected in coronary artery disease, peripheral vascular diseases, diabetes, hyperlipidaemia and obesity. The biologically active product of fibrinolytic system is plasmin. Generation of plasmin is regulated by plasminogen activators (PA) and their inhibitors (PAI). Vascular endothelial and smooth muscle cells synthesize tissue-type and urokinase-type PA (tPA and uPA) and their major physiological inhibitor, PAI-1. The production of fibrinolytic regulators is modulated by a number of biological factors related to thrombosis and atherosclerosis, including coagulation factors, hormones, growth factors, inflammatory mediators and lipoproteins. Several anticoagulants, including heparin, hirudin and hirulog-1, affect the production of fibrinolytic regulators in vascular cells. Studies in knockout mice demonstrated that mice deficient in PA or plasminogen are susceptible to thrombosis during inflammation or injury. Overexpression of uPA or deficiency of PAI-1 promotes neointima and aneurysm formation, which is probably due to active remodelling of extracellular matrix in vascular wall caused by excess plasmin. Long-term effect of treatment with thrombolytic agents or in atheroscleronic cardiovascular diseases remains to be defined. Future studies on determination of the role of PA and PAI in vascular remodelling may help understand the mechanism for neointima formation and orient the prevention of restenosis following vascular procedures.
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PMID:Vascular cell-derived fibrinolytic regulators and atherothrombotic vascular disorders (Review). 985 42

An increased plasma plasminogen activator inhibitor-1 (PAI-1) level is a risk factor for myocardial infarction, particularly when associated with visceral obesity. Although the link between PAI-1 and obesity is well documented, little is known about the physiological relevance of PAI-1 production by adipose tissue. Therefore, we have compared adipose tissue development and insulin resistance plasma parameters in PAI-1-deficient mice (PAI-1(-/-)) and wild-type littermates (PAI-1(+/+)) in a model of nutritionally induced obesity. After 17 weeks of consuming a high-fat diet (HFD), PAI-1(+/+) mice showed marked obesity, with a 52% increase in body weight compared with mice that were kept on a standard fat diet (P<0.0001). This weight gain was accompanied by adipocyte hypertrophy and an increase in the number of stroma cells in the gonadal fat pad, expressed as stroma cells/adipocytes (0.67+/-0.05 versus 0.43+/-0. 02; P<0.001). In plasma, the HFD induced a marked increase in PAI-1 antigen (5.1+/-0.56 versus 2+/-0.22 ng/mL; P<0.001), fasting insulinemia (1.1+/-0.21 versus 0.21+/-0.04 ng/mL; P<0.001), and glycemia (7.4+/-0.5 versus 5+/-0.3 mmol/L; P<0.001), whereas plasma triglyceride levels were not affected. When we compared PAI-1(-/-) and PAI-1(+/+) mice on the HFD, PAI-1(-/-) mice gained weight faster than did PAI-1(+/+) mice, with a significant difference in body weight between 3 and 8 weeks of the diet (32+/-1.7 versus 26+/-1.6 g at 6 weeks; P<0.05). After 17 weeks of the HFD, its effect on weight gain and the number and size of adipocytes was similar in PAI-1(+/+) and PAI-1(-/-) mice. By contrast, the increase in the number of stroma cells presented by PAI-1(+/+) mice was not observed in PAI-1(-/-) mice. In obese PAI-1(-/-) mice, tissue-type PA activity and antigen levels in the gonadal fat pad were significantly higher than in obese PAI-1(+/+) mice (230+/-50 versus 47+/-20 arbitrary units/g, P<0.01; 40+/-13 versus 17+/-13 ng/g, P<0.05, respectively), whereas urokinase-type PA activity and antigen levels were similar in both groups. In plasma, nonobese PAI-1(-/-) mice displayed 62% higher insulin levels (P<0.05) than did PAI-1(+/+) mice. Obese PAI-1(-/-) mice displayed 68% higher triglyceride levels (P<0.01) and 21% lower glucose levels (P<0.05) than did PAI-1(+/+) mice. These data support an effect of PAI-1 on weight gain and adipose tissue cellularity in the induction of obesity in mice. Moreover, PAI-1 influences glucidolipidic metabolism. The elevated expression of PAI-1 observed in human obesity could be involved in mechanisms that control adipose tissue development.
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PMID:Influence of PAI-1 on adipose tissue growth and metabolic parameters in a murine model of diet-induced obesity. 1262 47

Adipose tissue expresses a variety of genes including tumor necrosis factor alpha and type-1 plasminogen activator inhibitor (PAI-1); and these factors, produced by adipocytes, may be associated with the risk of coronary events in obesity. In this study, we characterized the production of fibrinolytic factors including tissue-type plasminogen activator (tPA), urokinase-type PA (uPA), and PAI-1 in the differentiation of preadipocytes, and examined the hormonal regulation of these fibrinolytic factors in mature adipocytes. Mouse 3T3-L1 preadipocytes were employed as a model of adipocytes. Adipocyte differentiation was induced by insulin, dexamethasone, and 3-isobutyl-1-methyl xanthine (IBMX). alpha-Glycerophosphate dehydrogenase (GPDH) activity and glucose transporter 4 (GLUT4) mRNA, indices for adipocyte maturation, were induced on Day 4, and gradually increased. GPDH activity reached its maximum level on Day 14. The level of tPA, a major PA in preadipocytes, dramatically decreased with differentiation. On the other hand, that of uPA reciprocally increased. PAI-1 production was also dramatically induced concomitant with differentiation. In mature adipocytes, uPA production was dominant (25 microg/ml/24 h vs. 0.8 microg/ml/24 h for tPA). Total PA activity in the mature adipocytes was reduced by insulin or dexamethasone, but not by glucagon. Insulin, IBMX, and dexamethasone significantly decreased both uPA and tPA production, and increased PAI-1 production. Glucagon had no effect on the production of these fibrinolytic factors. Our results reveal that uPA is one of the markers for the differentiation of 3T3-L1 cells and that insulin, IBMX, and dexamethasone are potent regulators of the fibrinolytic activity in differentiated 3T3-L1 cells, reciprocally affecting PA and PAI-1 levels in them.
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PMID:Reciprocal regulation of tissue-type and urokinase-type plasminogen activators in the differentiation of murine preadipocyte line 3T3-L1 and the hormonal regulation of fibrinolytic factors in the mature adipocytes. 1157 6

To investigate the potential role of tissue-type plasminogen activator (t-PA) or urokinase-type plasminogen activator (u-PA) in development of adipose tissue, we have used a nutritionally induced obesity model in t-PA (t-PA-/-) and u-PA (u-PA-/-) deficient mice. Five week old male wild-type (WT), t-PA-/- or u-PA-/- mice (n = 9 to 16) were fed a high fat diet (HFD, 42% fat). After 16 weeks of HFD, the body weight of t-PA-/- mice was significantly higher than that of WT mice (48 +/- 1.1 g vs. 39 +/- 2.2 g, p = 0.004). The total weight of the isolated subcutaneous (sc) fat deposit was higher in t-PA-/- than in WT mice (2.4 +/- 0.22 g vs. 1.2 +/- 0.29 g, p = 0.002). accompanied with higher adipocyte diameters (80 +/- 1.7 microm vs. 61 +/- 4.7 microm, p < 0.01). These differences were not observed in the intra-abdominal fat deposit. The number of stroma cells in both adipose tissue territories was increased in t-PA-/- as compared to WT mice (2.0 +/- 0.13 vs. 1.5 +/- 0.10, p = 0.2 and 3.0 +/- 0.17 vs 1.6 +/- 0.17, p = 0.0001, stroma cells/adipocytes in sc and intra-abdominal tissue, respectively), partly as a result of an increased number of endothelial cells (192 +/- 9 vs. 154 +/-18, p = 0.06 and 108 +/- 13 vs. 69 +/- 8, p = 0.04 CD31 stained/adipocyte area). In contrast the weight gain and adipose tissue development in u-PA-/- mice was not different from that in WT mice. These data suggest that t-PA but not u-PA plays a role in adipose tissue development.
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PMID:Influence of t-pA and u-PA on adipose tissue development in a murine model of diet-induced obesity. 1185 92

Several matrix metalloproteinases (MMPs), including the stromelysins MMP-3 and MMP-11, are expressed in adipose tissue. To investigate a potential role of MMP-11 (stromelysin-3) in adipose tissue development, five-week-old male wild-type mice (MMP-11+/+) or mice with deficiency of MMP-11 (MMP-11-/-) were fed a high fat diet (HFD, 42% fat) for 15 weeks. Haematologic parameters, including white and red blood cells, platelets, haemoglobin and haematocrit, and metabolic parameters including glucose, triglycerides and total cholesterol were not different for both genotypes. At the time of sacrifice, the body weight of the MMP-11-/- mice was higher than that of the MMP-11+/+ mice (36+/-1.4 g versus 29+/-0.9 g, p = 0.0002). The weight of the isolated subcutaneous (SC) and gonadal (GON) fat deposits was also higher in MMP-11-/- mice (620+/-150 mg versus 280+/-28 mg for SC fat, and 970+/-180 mg versus 430+/-62 mg, p < 0.05, for GON fat). Adipocytes in MMP-11-/- adipose tissue were hypertrophic as compared to MMP-11+/+ adipocytes (volume of 57+/-12 x 10(3) microm3 versus 31+/-2.4 x 10(3) microm3 for SC fat, and 100+/-18 x 10(3) microm3 versus 57+/-7.6 x 10(3) microm3 for GON fat; both p < 0.06). In nutritionally induced obesity models in mice a potential role of the fibrinolytic system was suggested in adipocyte hypertrophy. The hypertrophy observed in this model is, however, not related to changes in fibrinolytic parameters, as suggested by our finding that levels of t-PA, u-PA and PAI-1 antigen as well as t-PA and u-PA activity were not different in SC or GON adipose tissue extracts of both genotypes. As the main biological function of MMP-11 remains unknown, it is not clear whether the adipocyte hypertrophy in MMP-11-/- adipose tissue is directly related to the deficiency or to other pathways affected by MMP-11.
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PMID:Adipocyte hypertrophy in stromelysin-3 deficient mice with nutritionally induced obesity. 1191 87

A nutritionally induced obesity model was used to investigate the modulation of fibrinolytic and gelatinolytic activity during the development of adipose tissue. Five week old male mice were fed a standard fat diet (SFD, 13% kcal as fat) or a high fat diet (HFD, 42% kcal as fat) for up to 15 weeks. The HFD resulted in body weights of 31 +/- 0.9 g, 38 +/- 2.0 g and 47 +/- 1.9 g at 5, 10 and 15 weeks, respectively; corresponding values for mice on the SFD were 26 +/- 0.6 g, 31 +/- 0.9 g and 31 +/- 1.2 g (all p < 0.001). The weight of the isolated subcutaneous (s.c.) or gonadal (GON) fat after 15 weeks of HFD was 1,870 +/- 180 mg or 1,470 +/- 160 mg, as compared to 250 +/- 58 mg or 350 +/- 71 mg for the SFD (p < 0.001). The HFD induced marked time-dependent hyperglycemia and elevated levels of triglycerides and total cholesterol. The HFD diet also induced a marked hypertrophy of the adipocytes as compared to the SFD, e.g. diameter of 83 +/- 3.0 microns versus 52 +/- 4.2 microns for GON adipocytes at 15 weeks (p < 0.005). Plasma plasminogen activator inhibitor-1 (PAI-1) levels were higher in mice on the HFD as compared to the SFD; they were comparable in extracts of s.c. or GON adipose tissue, whereas at different time points tissue-type (t-PA) and urokinase-type (u-PA) plasminogen activator activity was somewhat lower in the adipose tissues of mice on HFD. Gelatinolytic activity (mainly MMP-2) was detected in s.c. but not in GON adipose tissue of mice on SFD, and decreased on the HFD. In situ zymography on cryosections did not reveal different fibrinolytic activities in s.c. or GON adipose tissues of the HFD as compared to the SFD groups, whereas significantly lower gelatinolytic and higher caseinolytic activities were detected in s.c. and GON tissues of mice on the HFD (p < or = 0.05). The fibrillar collagen content was lower in adipose tissue of mice on HFD. Thus, in this model time-dependent development of adipose tissue appears to be associated with modulation of proteolytic activity.
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PMID:Modulation of fibrinolytic and gelatinolytic activity during adipose tissue development in a mouse model of nutritionally induced obesity. 1219 10

Plasminogen activator inhibitor-1 (PAI-1) is the main physiological inhibitor of tissue-type (t-PA) and urokinase-type (u-PA) plasminogen activator. Recent studies in murine models have yielded apparently conflicting data on a potential role of PAI-1 in adipose tissue development and obesity. To reinvestigate this issue, we have rederived PAI-1 deficient (PAI-1(-/-)) and wild-type (WT) mice and generated true littermates in a 81.25% C57Bl/6: 18.75% 129 SV genetic background. Male 5-week-old PAI-1(-/-) and WT mice were kept on a high fat diet (20.1 kJ/g) for 15 weeks. Body weight gain was comparable for both genotypes, and at the time of sacrifice total body weights (39+/-1.1 versus 41 +/- 1.2 g) as well as the weights of subcutaneous (SC, 1,520 +/- 110 versus 1,480 +/- 110 mg) adipose tissue were not significantly different. In contrast, the gonadal (GON, 1,900 +/- 43 versus 1,510 +/- 86 mg, p < 0.005) tissue mass was larger in PAI-1(-/-) mice. Plasma levels of insulin, leptin, glucose, triglycerides, total, HDL and LDL cholesterol were comparable for both genotypes. Immunohistochemical analysis of SC and GON adipose tissues did not reveal differences in adipocyte size or number between both genotypes, whereas blood vessel density was also comparable for GON fat but lower in SC fat of WT mice. Thus, this study in littermate mice on high fat diet did not reveal an effect of PAI-1 deficiency on body weight, and a differential effect on SC and GON adipose tissue.
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PMID:Effect of plasminogen activator inhibitor-1 deficiency on nutritionally-induced obesity in mice. 1588 93

Optimal safety for a donor is an essential condition for living-related liver transplantation (LRLT). Severe pulmonary embolism may be a rare complication for the donors, but it is potentially fatal. Various risk factors and prophylactic methods for thromboembolic complications have been described. We report here a case of severe pulmonary embolism in a living-related liver transplantation donor who underwent right liver lobectomy, although the patient had no apparent risk factor for thromboembolism except for slight obesity (body mass index = 27). In addition, the donor received prophylactic use of graduated compression stockings and intermittent pneumatic compression by use of a special device from the start of anesthesia until the patient was able to ambulate. Fortunately, the patient was successfully treated with urokinase and heparin infusion followed by warfarin administration.
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PMID:A case of suspected severe pulmonary embolism in a living-related liver transplantation donor. 1589 92


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