目的:探讨异体脱钙骨基质复合BMP修复节段性骨缺损的能力。方法:64只新西兰大白兔采用桡骨15mm节段性骨缺损模型,随机分为4组,A组植入异体脱钙骨基质(Demineralized Bone Matrix,DBM)与牛骨形态发生蛋白(Bovine Bone Morphogentic Protein,bBMP)复合材料,B组植入异体DBIM,C组植入异体骨粒,D组为空白对照组。术后4、8、12、16w,进行放射学检查、病理组织学检查和计算机图像分析新生骨面积。结果:异体DBM与bBMP复合材料组骨生成、新骨面积和骨连接情况明显优于异体DBM组、异体骨粒组和空白对照组。结论:异体DBM复合BMP材料通过骨诱导和骨传导两种方式修复骨缺损,是一种较为理想、具有高效成骨活性的植骨材料。 相似文献
The toxic benthic dinoflagellate Ostreopsis lenticularis hosts a variety of symbiont bacterial flora. Laboratory cultured Ostreopsis clones require the presence of symbiotic Pseudomonas/Alteromonas bacterial strains for growth and toxicity development. Three culturable bacterial strains associated with Ostreopsis were identified as Pseudomonas/Alteromonas strain 1, Pseudomonas/Alteromonas strain 2 and Acinetobacter. Denaturing gradient gel electrophoresis (DGGE) analyses of extracted Ostreopsis associated bacterial DNAs indicated that there were three culturable and four non-culturable associated bacterial strains. The results presented here are the first report of the presence of unculturable bacterial symbionts in a toxic benthic dinoflagellate. Ostreopsis lost toxicity when exposed to elevated temperatures in the field and laboratory culture and subsequently recovered toxicity at reduced temperatures. Ostreopsis associated culturable Pseudomonas/Alteromonas bacterial strains were significantly reduced in dinoflagellate cultures exposed to elevated temperatures. The decreased toxicity of O. lenticularis exposed to elevated temperatures and their subsequent recovery of toxicity in periods of reduced thermal stress may have resulted from the effects of elevated temperature on the spectrum of culturable and unculturable bacterial species interacting with their Ostreopsis host. 相似文献
Involvement of free-radical oxidations in the aging process has been a topic of interest since Harman's original contribution.
Because of the close association between aging and Alzheimer disease (AD) and the qualitative similarity in the neuropathology
of both conditions, it has been proposed by many investigators that oxidative stress may be important in AD. If such modality
of injury was indeed involved, one should expect to find markers of oxidation and heat shock (since free radicals are key
mediators of heat-shock induction) in brains of patients with AD. In fact, several studies documented abnormal expression
of antioxidant enzymes and heat-shock proteins (HSP) along with other markers of oxidation in AD brains. We showed that abnormally
expressed antioxidant enzymes are topographically associated with senile plaques and neurofibrillary tangles, and that the
activity of these enzymes is (contrary to what one would expect) markedly reduced. These findings have recently been confirmed
by other investigators. Despite a large amount of evidence that suggests an association between oxidative stress and the pathogenesis
of AD, it is not yet known whether oxidative stress is a cause or consequence of the disorder. Future research efforts regarding
the oxidative stress hypothesis of AD should include attempts, at generating AD pathology by oxidative means in laboratory
animals, determining the role and integrity of the heat-shock response in AD, as well as that of various antioxidant systems,
growth factors, and hormones with antioxidant and neuroprotective properties. 相似文献
Abstract: Blast cells derived from peripheral blood of patients with acute myelogenous leukaemia (AML) were cultured in vitro and interleukin 1 receptor antagonist (IL1RA) concentrations determined in culture supernatants. AML blasts derived from patients classified as AML-M4 and AML-M5 subtype showed an increased release of IL1RA. IL1α and IL1β caused a similar increase in AML blast release of IL1RA, and addition of anti-ILl antibodies decreased IL1RA release. IL1RA release from AML blasts was also increased by stem cell factor, tumour necrosis factor α (TNFα), granulocyte-macrophage colony-stimulating factor and macrophage colony-stimulating factor, whereas interleukin 3, interleukin 6, leukaemia inhibitory factor and granulocyte colony- stimulating factor did not significantly alter IL1RA release. When investigating IL1RA serum levels, serum concentrations were decreased in acute leukaemia patients with chemotherapy-induced cytopenia compared with healthy controls. Serum levels of both IL1RA as well as IL1β and soluble TNFα receptors increased when the leucopenic patients developed complicating bacterial infections. 相似文献
In this in-vivo study, dialysate and serum endotoxin was evaluated before and after haemodialysis with small-pore (PS400) and large-pore (PS600) polysulphone dialysers, and before and after haemodiafiltration with the PS600 filter. The source of the endotoxin was the presence in dialysate of Pseudomonads at a concentration of 10(3)-10(4) CFU/ml. Endotoxin was measured by a modified chromogenic limulus amoebocyte lysate (LAL) assay. In spite of dialysate endotoxin concentrations greater than 100 pg/ml, no changes in pre- versus posttreatment LAL reactivity were observed in PS400 dialysis and PS600 haemodiafiltration. In contrast, PS600 haemodialysis was related to an increase in serum LAL reactivity from 1.3 +/- 1.5 to 3.8 +/- 2.0 pg/ml (n = 15, P less than 0.01), and five patients (33.3%) showed a post-dialysis value in excess of 5 pg/ml. Our data are consistent with the absence of in-vivo endotoxin transfer during haemodialysis with small-pore dialyser membranes, and during haemodiafiltration with membranes with larger pores. An increase in LAL reactivity during haemodialysis with membranes with larger pores is, however, present, presumably due to the occurrence of backdiffusion/filtration with that specific strategy. 相似文献
Our objective was to investigate the initial levels of circulating proinflammatory cytokines, such as interleukin 1β (IL-1β), interleukin 6 (IL-6), and tumour necrosis factor alpha (TNF-α), of certain acute-phase proteins, such as C-reactive protein (CRP), fibrinogen (FBN) and albumin, and of the glycoprotein fibronectin at presentation and their daily variation during the clinical course of community-acquired pneumonia (CAP) in relation to clinical and laboratory indices of infection. Thirty otherwise healthy hospitalized patients aged 48 ± 3 years (mean ± SEM) and with bacteriologically confirmed CAP were studied prospectively. IL-1β and IL-6 were found to be 15-fold higher on admission (122 ± 9 pg mL?1 and 60 ± 4 pg mL?1 respectively), whereas TNF-α was three-fold higher (102 ± 5 pg mL?1) than those of controls, all of them showing a decline towards normal. Initial CRP levels were increased 90-fold (416 ± 1 mg L?1), whereas fibronectin levels were reduced (242 ± 9 mg dL?1). The presence of parapneumonic effusion was associated with a higher TNF-α serum level (127 ± 7 vs. 86 ± 4 pg mL?1, P = 0.0002), a more rapid daily decline in TNF-α (–7.2 ± 0.7 vs. ?3.8 ± 0.5 pg mL?1 day?1, P = 0.0005), a slower rate of decline in CRP (?42.8 ± 3.0 vs. ?54.6 ± 3.0 mg L?1 day?1, P = 0.02) and a slower rate of increase in FBN (5.9 ± 1.0 vs. 11.7 ± 1.0 mg dL?1 day?1), P = 0.001]. Furthermore, daily progression of serum levels of cytokines and acute-phase proteins correlated strongly with pyrexia, erythrocyte sedimentation rate (ESR), neutrophil count, alveolar–arterial oxygen difference and radiographic resolution, clinically manifested by improvement in the patients' condition. 相似文献
Background: Reduction in salivary secretion is the hallmark of Sjögren's syndrome (SS). Calmodulin (CaM) and calmodulin binding proteins (CaMBPs) play a key role in the secretory process of saliva. Recent studies have suggested that SS‐B, an autoantibody associated with SS, is a CaMBP. This finding suggests that CaMBP may contribute to the loss of saliva in SS. To better understand the role(s) of these proteins in SS, the purpose of this study was to compare salivary CaMBPs in Sjögren's patients and controls. Methods: Saliva samples were collected from 20 patients and 20 age‐, race‐, and gender‐matched controls. CaM overlay was used to identify CaMBPs in saliva of patients and controls. Results: Higher number of salivary CaMBPs was observed among patients than controls. Conclusions: The increased number of salivary CaMBPs in SS may suggest a potential role for these proteins in the pathogenesis of the disease. 相似文献
Background. The therapy for native mitral valve endocarditis is in evolution. Antibiotics have significantly improved survival rates, but patients with complications of endocarditis may require surgical treatment.
Methods. Between January 1985 and December 1995, 146 patients underwent surgical therapy (repair or replacement) for native mitral valve endocarditis. All patients had documented bacterial endocarditis. Univariate and multivariate analyses were performed to determine predictors of hospital death, long-term event-free survival, and probability of repair. Patients were evaluated in three groups: all patients, patients with acute endocarditis, and patients with chronic endocarditis.
Results. There were ten hospital deaths (6.8%). Patients undergoing repair had a lower hospital mortality rate (p = 0.008) then those having replacement. Event-free survival was improved after mitral valve repair in the overall group (p = 0.02) and in the group with healed (chronic) endocarditis (p = 0.05). Although the acute endocarditis group demonstrated an improved event-free survival rate after mitral valve repair versus replacement (74% versus 20% at 6 years), this did not reach statistical significance.
Conclusions. We conclude that mitral valve repair is preferable to mitral valve replacement when possible, in patients with complications of endocarditis, as repair results in a lower hospital mortality and an improved long-term survival. 相似文献
An alteration in cell/matrix interactions is one of the suggested mechanisms leading to cyst formation in polycystic kidney
diseases. Most of these interactions are mediated by β1-integrins, a subfamily of integrin receptors, formed by the association
of the β1-chain with different α-subunits. To date, no study on α-integrin subunit distribution during the early stages of
cyst development has been reported. Using immunofluorescence, we analyzed the distribution of α-integrin subunits (α1, α2,
α3, α5, and α6) and basement membrane proteins in kidneys of fetuses with autosomal dominant (ADPKD) or autosomal recessive
polycystic kidney disease (ARPKD). The distribution was compared with that observed in normal fetal and post-natal kidneys,
and in fetal cystic dysplasia and Meckel syndrome. Marked increase in α1-integrin staining was observed in normal and cystic
collecting duct cells of both polycystic diseases (PKD), compared with normal and cystic controls. The distribution of integrin
subunits α2, α3, and α6 was irregular in cyst epithelial cells of PKD and cystic controls. The increased expression of the
α1-subunit specifically observed in PKD collecting duct cells may be an early consequence of the genetic defect in ARPKD.
In ADPKD it parallels the reported expression of polycystin, the protein product of PKD1. The irregular expression of α2,
α3, and α6 integrin subunits observed in all types of cysts suggests that cell/matrix interactions are altered early and may
participate in the development of cysts, perhaps by contributing to the deregulation of cell survival in cystic diseases.
Received May 28, 1996; received in revised form October 2, 1996; accepted October 25, 1996 相似文献