The Journal of laboratory and clinical medicine最新文献_第7页

The effect of interferon alpha 2b on the expression of cytoskeletal proteins in an in vitro model of wound contraction. 干扰素α 2b对体外创面收缩模型细胞骨架蛋白表达的影响。

The Journal of laboratory and clinical medicine Pub Date : 1995-11-01

B Nedelec, Y J Shen, A Ghahary, P G Scott, E E Tredget

{"title":"The effect of interferon alpha 2b on the expression of cytoskeletal proteins in an in vitro model of wound contraction.","authors":"B Nedelec, Y J Shen, A Ghahary, P G Scott, E E Tredget","doi":"","DOIUrl":"","url":null,"abstract":"Wound contraction is an essential component of wound healing. However, the development of scar contractures in tissues and organs disrupts normal organ integrity and produces functional deformities. Although interferons alpha and gamma inhibit extracellular matrix protein production by fibroblasts, their effects on cytoskeletal protein mediated-wound contraction are as yet unclear. The fibroblast-populated collagen lattice is an in vitro assay that simulates wound contraction. When matched pairs of human hypertrophic scar and normal dermal fibroblast cultures established from patients recovering from a thermal injury were used, interferon-alpha 2b exposure before lattice formation was found to significantly inhibit contraction in a treatment time-dependent manner (p < 0.05). Fibroblasts generated contractile forces that were triphasic and serum sensitive (p < 0.01). Comparison of hypertrophic scar and normal dermal fibroblasts revealed no significant differences in ability to induce lattice contraction. Northern blot analysis of mRNAs for the intracellular contractile proteins revealed that interferon-alpha 2b significantly down-regulated mRNA levels of the actin isoforms beta and gamma (50% to 60%) but had no significant effect on alpha-tubulin, vimentin, and alpha-actinin. Fibroblast-populated collagen lattices were stained with rhodamine-labeled phalloidin to reveal filamentous actin proteins. Marked morphologic alterations of the stress fibers were associated with reductions in lattice contraction after interferon-alpha 2b treatment. Thus interferon-alpha 2b's inhibition of wound contraction in vitro is associated with reductions in mRNA for beta and gamma actin and distinct morphologic alterations in fibroblast stress fiber morphology.","PeriodicalId":23085,"journal":{"name":"The Journal of laboratory and clinical medicine","volume":"126 5","pages":"474-84"},"PeriodicalIF":0.0,"publicationDate":"1995-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18601588","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Antibodies to neutrophil cytoplasmic antigens induce monocyte chemoattractant protein-1 secretion from human monocytes. 中性粒细胞细胞质抗原抗体诱导单核细胞分泌趋化蛋白-1。

The Journal of laboratory and clinical medicine Pub Date : 1995-11-01

B L Casselman, K S Kilgore, B F Miller, J S Warren

{"title":"Antibodies to neutrophil cytoplasmic antigens induce monocyte chemoattractant protein-1 secretion from human monocytes.","authors":"B L Casselman, K S Kilgore, B F Miller, J S Warren","doi":"","DOIUrl":"","url":null,"abstract":"Antibodies to neutrophil cytoplasmic antigens (ANCA) have been found in the serum samples of patients with a number of vasculitides (e.g., Wegener's granulomatosis, small vessel vasculitis, and idiopathic necrotizing and cresentic glomerulonephritis). Although detection of ANCA in serum samples has proven to be useful diagnostically and in selected activity of disease monitoring situations, the pathogenetic role of ANCA in vasculitis remains ill-defined. We sought to determine whether purified ANCA promotes the secretion of monocyte chemoattractant protein-1 (MCP-1) from isolated human peripheral blood monocytes. P (perinuclear)- and C (cytoplasmic)- ANCA were purified from the serum samples of patients with either Wegener's granulomatosis, small vessel vasculitis, or idiopathic necrotizing and cresentic glomerulonephritis. Human peripheral blood monocytes from healthy subjects were incubated with either C-ANCA immunoglobulin G (IgG), P-ANCA IgG, or nonspecific IgG, and the conditioned media were analyzed for MCP-1 activity. A monocyte chemotaxis assay was utilized to functionally quantify secreted chemotactic activity. Secretion of monocyte chemotactic activity was found to be antibody concentration-dependent and time-dependent, with maximal chemotaxis measured in media collected 24 hours after the addition of either C- or P-ANCA IgG. A specific antibody directed against human MCP-1 largely inhibited monocyte chemotaxis, indicating that MCP-1 is the predominant monocyte chemotactic mediator present in the conditioned medium. An MCP-1 enzyme-linked immunosorbent assay further supported the conclusion that P- and C-ANCA IgG can trigger MCP-1 secretion by monocytes. These data indicate that incubation of monocytes with ANCA promotes the dose-dependent release of the chemotactic beta-chemokine MCP-1.(ABSTRACT TRUNCATED AT 250 WORDS)","PeriodicalId":23085,"journal":{"name":"The Journal of laboratory and clinical medicine","volume":"126 5","pages":"495-502"},"PeriodicalIF":0.0,"publicationDate":"1995-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18599662","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Compensation for the interracial variance in the cutaneous synthesis of vitamin D. 对不同种族间皮肤合成维生素D差异的补偿。

The Journal of laboratory and clinical medicine Pub Date : 1995-11-01

L Y Matsuoka, J Wortsman, T C Chen, M F Holick

{"title":"Compensation for the interracial variance in the cutaneous synthesis of vitamin D.","authors":"L Y Matsuoka, J Wortsman, T C Chen, M F Holick","doi":"","DOIUrl":"","url":null,"abstract":"We investigated the homeostatic compensation for the lower cutaneous synthesis of vitamin D in heavily melanized persons. Vitamin D2 (50,000 IU) was administered in a single oral dose to 24 young adults, 12 blacks and 12 whites, matched for age, gender, and socioeconomic status. We also included a group of eight healthy elderly white adults as representatives of a population with a nonracial mechanism for decreased cutaneous vitamin D synthesis. Plasma determinants were performed under basal conditions and at 6, 10, and 24 hours after vitamin D intake. Basal 25-hydroxyvitamin D (25-OH-D) levels were significantly lower in blacks (12.5 +/- 2.2 ng/ml (mean +/- SEM)) and in elderly whites (19.2 +/- 1.9 ng/ml), compared with young whites (30.2 +/- 3.0 ng/ml (p < 0.0001)); levels of basal 1,25-dihydroxyvitamin D (1,25(OH)2 -D) did not differ between groups. The vitamin D blood curve was similar between groups after the oral vitamin D2 load. Increases in 25-OH-D were 91.7 +/- 15.9% in blacks, 18.8 +/- 5.2% in young whites, and 28.6 +/- 6.9 in elderly whites; 1,25(OH)2-D levels increased slightly and did not differ between groups, although in blacks the change over time was significant (p < 0.05). As a whole, the study populations exhibited a strong relation between basal and peak 25-OH-D (r = -0.80; p < 0.001). Levels of intact parathyroid hormone and serum calcium of blacks and young whites did not differ within or between groups throughout the test.(ABSTRACT TRUNCATED AT 250 WORDS)","PeriodicalId":23085,"journal":{"name":"The Journal of laboratory and clinical medicine","volume":"126 5","pages":"452-7"},"PeriodicalIF":0.0,"publicationDate":"1995-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18601585","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Surfactant protein-D modulates interaction of Pneumocystis carinii with alveolar macrophages. 表面活性剂蛋白d调节卡氏肺囊虫与肺泡巨噬细胞的相互作用。

The Journal of laboratory and clinical medicine Pub Date : 1995-11-01

A H Limper, E C Crouch, D M O'Riordan, D Chang, Z Vuk-Pavlovic, J E Standing, K Y Kwon, A Adlakha

引用次数: 0

Iron metabolism and oxidative stress during acute and chronic phases of experimental inflammation: effect of iron-dextran and deferoxamine. 实验性炎症急性和慢性阶段的铁代谢和氧化应激:铁葡聚糖和去铁胺的作用。

The Journal of laboratory and clinical medicine Pub Date : 1995-11-01

J Muntané, P Puig-Parellada, M T Mitjavila

{"title":"Iron metabolism and oxidative stress during acute and chronic phases of experimental inflammation: effect of iron-dextran and deferoxamine.","authors":"J Muntané, P Puig-Parellada, M T Mitjavila","doi":"","DOIUrl":"","url":null,"abstract":"Iron overload induces a rise in lipid peroxidation, but there are no data on the effects of iron administered in vivo on the production of free radicals by inflammatory cells. Further, there is lack of agreement about the benefits of deferoxamine (Dfx) in the treatment of anemia and oxidative stress during inflammation and chronic diseases. In this study, iron-dextran (Fe-dextran) or Dfx was administered subcutaneously during the acute and chronic phases of carrageenan-induced granuloma. Several parameters related to iron metabolism, inflammatory cell activity, and lipid peroxidation were measured in liver, plasma, and the inflammatory exudate. Treatment with Fe-dextran increased iron content in plasma and in stores, increased production of superoxide anion (O2-) by inflammatory cells and lipid peroxidation, and also altered the inflammatory process. Dfx mobilized iron from stores without modifying essential parameters related to anemia or to the level of lipid peroxidation induced by inflammation. We conclude that treatment with Fe-dextran had a beneficial effect on recovery from the anemia of inflammation. Nevertheless, the high levels of loosely-bound iron found after Fe-dextran treatment in plasma and in exudate contribute to the increase in oxidative stress. Dfx treatment had no effect on anemia or on lipid peroxidation.","PeriodicalId":23085,"journal":{"name":"The Journal of laboratory and clinical medicine","volume":"126 5","pages":"435-43"},"PeriodicalIF":0.0,"publicationDate":"1995-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18601583","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Osteoporosis and hypercalciuria secondary to excessive salt ingestion. 骨质疏松症和高钙尿症继发于盐摄入过多。

The Journal of laboratory and clinical medicine Pub Date : 1995-11-01

M A Palmieri, J A Pitcock

引用次数: 0

Effects of insulin-like growth factor I on phosphate transport in cultured proximal tubule cells. 胰岛素样生长因子I对培养近端小管细胞中磷酸盐转运的影响。

The Journal of laboratory and clinical medicine Pub Date : 1995-11-01

R Hirschberg, H Ding, C Wanner

{"title":"Effects of insulin-like growth factor I on phosphate transport in cultured proximal tubule cells.","authors":"R Hirschberg, H Ding, C Wanner","doi":"","DOIUrl":"","url":null,"abstract":"In vivo, proximal tubule cells are exposed to insulin-like growth factor I (IGF-I) that is present in serum or in proximal tubule fluid. For example, in the nephrotic syndrome, proximal tubule fluid contains IGF-I at biologically meaningful concentrations in association with IGF-binding protein-2 (IGFBP-2). IGF-I has also been shown to decrease the urinary excretion of phosphate (Pi) in normal subjects. We hypothesized that IGF-I can raise tubule cell Pi absorption directly through an apical as well as a basolateral tubule receptor mechanism, specifically, through IGF-I (type I) receptors as compared to IGF-II (type II) or insulin receptors. Studies were performed in cultured proximal tubule cells that express high-affinity IGF-I receptors. Stimulation of cells selectively at the apical or basolateral membrane with IGF-I (10(-9) to 10(-7) mol/L) increases Pi absorption by up to 80%, but a significant counterdirectional Pi flux in the apical-to-basolateral direction does not occur. The effect of IGF-I on Pi transport appears to be specific inasmuch as the transport of alanine is not affected by the peptide. IGFBP-2 does not inhibit this effect of IGF-I, but the IGF-I-induced increase in Pi transport is inhibited by a neutralizing anti-IGF-I receptor monoclonal antibody. Exposure of the cells to IGF-II (10(-7) mol/L) but not to insulin selectively at the apical membrane tends to increase Pi transport, and this IGF-II effect is also blocked by the anti-IGF-I receptor antibody.(ABSTRACT TRUNCATED AT 250 WORDS)","PeriodicalId":23085,"journal":{"name":"The Journal of laboratory and clinical medicine","volume":"126 5","pages":"428-34"},"PeriodicalIF":0.0,"publicationDate":"1995-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18601582","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Role of dopamine in the exaggerated phosphaturic response to parathyroid hormone in the remnant kidney. 多巴胺在残肾对甲状旁腺激素过度磷酸化反应中的作用。

The Journal of laboratory and clinical medicine Pub Date : 1995-11-01

J Isaac, T J Berndt, F G Knox

{"title":"Role of dopamine in the exaggerated phosphaturic response to parathyroid hormone in the remnant kidney.","authors":"J Isaac, T J Berndt, F G Knox","doi":"","DOIUrl":"","url":null,"abstract":"The remnant kidney (RK) exhibits an exaggerated phosphaturic response to parathyroid hormone (PTH) infusion. Increased urinary dopamine synthesis per nephron has been demonstrated in the remnant kidney, and dopamine infusion is phosphaturic. Therefore, the role of dopamine in the exaggerated phosphaturic response to PTH infusion in the RK was evaluated. To obtain the RK model, Sprague-Dawley rats were anesthetized and subjected to right nephrectomy as well as surgical ablation of the left renal poles. Sham surgery was performed in the other groups of rats. Four weeks later, acute experiments were performed in these animals. Two hours after thyroparathyroidectomy, a control clearance was taken. Subsequently, PTH (33 U/kg bolus, 1 U/kg/min) was infused for 60 minutes, followed by a 30-minute experimental clearance. In the rats with an RK, the increase in the fractional excretion of phosphate (FEPi) in response to PTH infusion was (delta 38.5% +/- 4.2%, n = 12). In an additional group of rats with an RK, the specific DA-1 receptor antagonist (SCH 23390, 25 micrograms/kg/min) was infused for 30 minutes, a control clearance was taken, and then PTH was infused. Infusion of SCH 23390 significantly blunted the phosphaturic response to PTH (FEPi, delta 24.0% +/- 7.7%, n = 7). In contrast, the phosphaturic response to PTH was similar in the rats that underwent sham surgery in the presence (delta FEPi, 25.4% +/- 1.6%, n = 5) and absence of infusion of SCH 23390 (delta FEPi 24.7 +/- 3.1%, n = 6).(ABSTRACT TRUNCATED AT 250 WORDS)","PeriodicalId":23085,"journal":{"name":"The Journal of laboratory and clinical medicine","volume":"126 5","pages":"470-3"},"PeriodicalIF":0.0,"publicationDate":"1995-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18601587","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Endothelial cell injury induced by plasmin in vitro. 纤溶酶体外诱导内皮细胞损伤。

The Journal of laboratory and clinical medicine Pub Date : 1995-10-01

K Okajima, H Abe, B R Binder

{"title":"Endothelial cell injury induced by plasmin in vitro.","authors":"K Okajima, H Abe, B R Binder","doi":"","DOIUrl":"","url":null,"abstract":"We investigated the effect of plasmin on the integrity and function of endothelial cells to elucidate the mechanism by which bleeding or rethrombosis may be induced in thrombolytic therapy. When incubated with cultured human umbilical vein endothelial cells (HUVECs), plasmin increased the endothelial permeability to serum albumin 10 minutes after the incubation. Plasmin damaged the cell membranes 30 minutes after the incubation, detached the cells from the matrix 3 hours after the incubation, and finally induced cell lysis. Such damaging effects on HUVECs were not observed with plasminogen or plasmin pretreated with aprotinin and alpha 2-plasmin inhibitor, suggesting that the catalytic function of plasmin plays an important role in inducing this damage. Sulfur 35-labeled glycosaminoglycans (35S-GAGs) of HUVECs were decreased 1 hour after the incubation of plasmin with HUVECs, and the thrombomodulin (TM) activity of HUVECs measured by protein C activation capacity was decreased 6 hours after the incubation. Neither 35S-GAGs nor the TM activity of HUVECs was decreased after the incubation of plasmin pretreated with aprotinin and alpha 2-plasmin inhibitor. These findings suggest that the nonthrombogenic properties of endothelial cells can be damaged by the proteolytic action of plasmin. Our findings, taken together, suggest that plasmin damages the endothelial barrier function, endothelial cell integrity, and nonthrombogenic properties. These damaging effects of plasmin on endothelial cells may be related to the pathophysiology of bleeding or rethrombosis observed in patients undergoing high-dose thrombolytic therapy for thrombosis.","PeriodicalId":23085,"journal":{"name":"The Journal of laboratory and clinical medicine","volume":"126 4","pages":"377-84"},"PeriodicalIF":0.0,"publicationDate":"1995-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18568083","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Estradiol inhibits mesangial cell-mediated oxidation of low-density lipoprotein. 雌二醇抑制系膜细胞介导的低密度脂蛋白氧化。

The Journal of laboratory and clinical medicine Pub Date : 1995-10-01

J Neugarten, C Ghossein, S Silbiger

{"title":"Estradiol inhibits mesangial cell-mediated oxidation of low-density lipoprotein.","authors":"J Neugarten, C Ghossein, S Silbiger","doi":"","DOIUrl":"","url":null,"abstract":"It has been suggested that hyperlipidemia may contribute to the progression of renal disease via the deleterious effects of oxidized low-density lipoprotein (LDL) on the glomerular mesangium. Because estrogens possess potent antioxidant activity, we sought to determine whether sex hormones influence the oxidation of LDL by mesangial cells. Rat mesangial cells were incubated with LDL (200 micrograms/ml), and the extent of lipid oxidation was assessed by the generation of thiobarbituric acid reactive substances (TBARS), by increased electrophoretic mobility, and by enhanced uptake of mesangial cell-modified LDL by macrophages. A progressive rise in TBARS and an increase in electrophoretic mobility was observed on incubation of LDL with mesangial cells. Coincubation with estradiol (10 mumol/L) reduced TBARS generation by 46% at 36 hours (p < 0.01) and reversed the increase in relative electrophoretic mobility (1.25 +/- 0.07 vs 1.01 +/- 0.03, p < 0.05). LDL that had been oxidized by mesangial cells in the presence of estradiol (10 mumol/L) showed reduced uptake by macrophages when compared with LDL that had been oxidized by mesangial cells in the absence of estradiol (14 +/- 2 pmol/10(6) cells per hour vs 22 +/- 3 pmol/10(6) cells per hour, p < 0.05). In contrast, neither testosterone nor estrone had any effect on these parameters. We conclude that estradiol, by virtue of its antioxidant properties, inhibits mesangial cell-mediated oxidation of LDL and reduces the uptake of mesangial cell-modified LDL by macrophages.","PeriodicalId":23085,"journal":{"name":"The Journal of laboratory and clinical medicine","volume":"126 4","pages":"385-91"},"PeriodicalIF":0.0,"publicationDate":"1995-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"18568084","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0