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1.
Kurt Hannes Wollinsky Margret Oethinger Michaela Bü chele Patrick Kluger Wolfhart Puhl Hans-Hinrich Mehrkens 《Acta orthopaedica》1997,68(3):225-230
40 patients undergoing primary hip arthroplasty, given autologous processed blood transfusion, were randomized to receive no antibiotic prophylaxis (group A, n 20) or cefuroxime (1.5 g single injection; group B, n 20). Bacterial contamination at various steps in the autotransfusion procedure was assessed in liquid and solid culture media. the operation field and the wound drainage blood were never contaminated in either of the groups but some of the suction tips were. Parts of the Vacufix® blood collection bags of group A contained bacteria, but none in group B. Processed red blood cell concentrates in both groups showed bacterial growth. Greater blood loss did not increase the contamination rate in general. Isolated bacteria included the species Staphylococcus epidermidis, coagulase-negative staphylococci and Propionibacteria in both groups, but with different cell counts. in addition, Corynebacterium bovis et minutissimum and Moraxella were identified in group A.
In conclusion, autologous blood transfusion was a safe procedure. If contamination occurred, the bacterial count was low, and the bacteria of low pathogenicity. Antibiotic prophylaxis with cefuroxime reduced this contamination of suction tips and collection bags and limited the transfer of autologous blood products. 相似文献
In conclusion, autologous blood transfusion was a safe procedure. If contamination occurred, the bacterial count was low, and the bacteria of low pathogenicity. Antibiotic prophylaxis with cefuroxime reduced this contamination of suction tips and collection bags and limited the transfer of autologous blood products. 相似文献
2.
Effects of vitamin D and calcium supplementation on falls: a randomized controlled trial. 总被引:21,自引:0,他引:21
Heike A Bischoff Hannes B St?helin Walter Dick Regula Akos Margrith Knecht Christian Salis Matthias Nebiker Robert Theiler Michael Pfeifer Bettina Begerow Robert A Lew Martin Conzelmann 《Journal of bone and mineral research》2003,18(2):343-351
Specific receptors for vitamin D have been identified in human muscle tissue. Cross-sectional studies show that elderly persons with higher vitamin D serum levels have increased muscle strength and a lower number of falls. We hypothesized that vitamin D and calcium supplementation would improve musculoskeletal function and decrease falls. In a double-blind randomized controlled trial, we studied 122 elderly women (mean age, 85.3 years; range, 63-99 years) in long-stay geriatric care. Participants received 1200 mg calcium plus 800 IU cholecalciferol (Cal+D-group; n = 62) or 1200 mg calcium (Cal-group; n = 60) per day over a 12-week treatment period. The number of falls per person (0, 1, 2-5, 6-7, >7 falls) was compared between the treatment groups. In an intention to treat analysis, a Poisson regression model was used to compare falls after controlling for age, number of falls in a 6-week pretreatment period, and baseline 25-hydroxyvitamin D and 1,25-dihydroxyvitamin D serum concentrations. Among fallers in the treatment period, crude excessive fall rate (treatment - pretreatment falls) was compared between treatment groups. Change in musculoskeletal function (summed score of knee flexor and extensor strength, grip strength, and the timed up&go test) was measured as a secondary outcome. Among subjects in the Cal+D-group, there were significant increases in median serum 25-hydroxyvitamin D (+71%) and 1,25-dihydroxyvitamin D (+8%). Before treatment, mean observed number of falls per person per week was 0.059 in the Cal+D-group and 0.056 in the Cal-group. In the 12-week treatment period, mean number of falls per person per week was 0.034 in the Cal+D-group and 0.076 in the Cal-group. After adjustment, Cal+D-treatment accounted for a 49% reduction of falls (95% CI, 14-71%; p < 0.01) based on the fall categories stated above. Among fallers of the treatment period, the crude average number of excessive falls was significantly higher in the Cal-group (p = 0.045). Musculoskeletal function improved significantly in the Cal+D-group (p = 0.0094). A single intervention with vitamin D plus calcium over a 3-month period reduced the risk of falling by 49% compared with calcium alone. Over this short-term intervention, recurrent fallers seem to benefit most by the treatment. The impact of vitamin D on falls might be explained by the observed improvement in musculoskeletal function. 相似文献
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5.
Deletion of Brca2 exon 27 causes hypersensitivity to DNA crosslinks,chromosomal instability,and reduced life span in mice 总被引:1,自引:0,他引:1
Donoho G Brenneman MA Cui TX Donoviel D Vogel H Goodwin EH Chen DJ Hasty P 《Genes, chromosomes & cancer》2003,36(4):317-331
The Brca2 tumor-suppressor gene contributes to genomic stability, at least in part by a role in homologous recombinational repair. BRCA2 protein is presumed to function in homologous recombination through interactions with RAD51. Both exons 11 and 27 of Brca2 code for domains that interact with RAD51; exon 11 encodes eight BRC motifs, whereas exon 27 encodes a single, distinct interaction domain. Deletion of all RAD51-interacting domains causes embryonic lethality in mice. A less severe phenotype is seen with BRAC2 truncations that preserve some, but not all, of the BRC motifs. These mice can survive beyond weaning, but are runted and infertile, and die very young from cancer. Cells from such mice show hypersensitivity to some genotoxic agents and chromosomal instability. Here, we have analyzed mice and cells with a deletion of only the RAD51-interacting region encoded by exon 27. Mice homozygous for this mutation (called brca2(lex1)) have a shorter life span than that of control littermates, possibly because of early onsets of cancer and sepsis. No other phenotype was observed in these animals; therefore, the brca2(lex1) mutation is less severe than truncations that delete some BRC motifs. However, at the cellular level, the brca2(lex1) mutation causes reduced viability, hypersensitivity to the DNA interstrand crosslinking agent mitomycin C, and gross chromosomal instability, much like more severe truncations. Thus, the extreme carboxy-terminal region encoded by exon 27 is important for BRCA2 function, probably because it is required for a fully functional interaction between BRCA2 and RAD51. 相似文献
6.
Laforin preferentially binds the neurotoxic starch-like polyglucosans, which form in its absence in progressive myoclonus epilepsy 总被引:4,自引:0,他引:4
Chan EM Ackerley CA Lohi H Ianzano L Cortez MA Shannon P Scherer SW Minassian BA 《Human molecular genetics》2004,13(11):1117-1129
Lafora disease (LD) is a fatal and the most common form of adolescent-onset progressive epilepsy. Fulminant endoplasmic reticulum (ER)-associated depositions of starch-like long-stranded, poorly branched glycogen molecules [known as polyglucosans, which accumulate to form Lafora bodies (LBs)] are seen in neuronal perikarya and dendrites, liver, skeletal muscle and heart. The disease is caused by loss of function of the laforin dual-specificity phosphatase or the malin E3 ubiquitin ligase. Towards understanding the pathogenesis of polyglucosans in LD, we generated a transgenic mouse overexpressing inactivated laforin to trap normal laforin's unknown substrate. The trap was successful and LBs formed in liver, muscle, neuronal perikarya and dendrites. Using immunogold electron microscopy, we show that laforin is found in close proximity to the ER surrounding the polyglucosan accumulations. In neurons, it compartmentalizes to perikaryon and dendrites and not to axons. Importantly, it binds polyglucosans, establishing for the first time a direct association between the disease-defining storage product and disease protein. It preferentially binds polyglucosans over glycogen in vivo and starch over glycogen in vitro, suggesting that laforin's role begins after the appearance of polyglucosans and that the laforin pathway is involved in monitoring for and then preventing the formation of polyglucosans. In addition, we show that the laforin interacting protein, EPM2AIP1, also localizes on the polyglucosan masses, and we confirm laforin's intense binding to LBs in human LD biopsy material. 相似文献
7.
R.G. Webster V.S. Hinshaw W.J. Bean K.L. Van Wyke J.R. Geraci D.J. St. Aubin G. Petursson 《Virology》1981,113(2):712-724
An influenza A virus antigenically similar to A/FPV/Dutch/27 (Hav1Neq1) [H7N7] was isolated from harbor seals (Phoca vitulina) that had died of acute hemorrhagic pneumonia on Cape Cod Peninsula, beginning in the winter of 1979–1980. High titers of virus were obtained from the lungs and lower titers from the brains of the seals. Although antigenic analyses and characterization of the RNAs show that all of the genes and gene products are closely related to different avian influenza viruses, biologically the virus behaves more like a mammalian strain. The seal virus replicated and produced pneumonia in experimentally infected harbor seals, but the clinical course and pathology were less severe than in the natural infection; the virus also replicated in ferrets, cats, and pigs but produced no disease. In avian species, the seal influenza virus replicated poorly, produced no disease signs, and was not shed in the feces. Although the seal influenza virus can cause conjunctivitis in humans who have known contamination of the eyes from infected animals, serological studies detected no evidence of seroconversion among persons working with infected seals or with the virus. Preliminary studies detected antibodies to this virus in harbor seals on the New England coast but not in harbor seals, gray seals, or fur seals from other areas, suggesting that this virus may be a new introduction to this species. An Hav1Neq1 [H7N7] virus was also isolated from feral ducks in Iceland in 1980, but the two viruses could be distinguished by analysis of their RNAs and host range. The A/Seal/Mass/1/80 influenza virus provides the first evidence suggesting that a strain deriving all of its genes from one or more avian influenza viruses can be associated with severe disease in a mammalian population in nature. Whether this breach of species specificity represents a unique event in influenza evolution remains to be determined, but raises the possibility that human or animal influenza viruses may be derived directly from avian strains. 相似文献
8.
Skin deposits in hereditary cystatin C amyloidosis 总被引:3,自引:0,他引:3
Eiríkur Benedikz Hannes Blöndal Gunnar Gudmundsson 《Virchows Archiv : an international journal of pathology》1990,417(4):325-331
Summary Clinically normal skin from 47 individuals aged 9–70 years was investigated. Cystatin C amyloid deposits were found in various locations of the skin by light and/or electron microscopy, in all 12 patients with a clinical history of hereditary cystatin C amyloidosis (HCCA). Six asymptomatic individuals, who had the Alu 1 restriction fragment length polymorphism (RFLP) marker reported to cosegregate with the disease, also had cystatin C amyloid deposits in the skin. Three asymptomatic individuals (age 17–46) belonging to the HCCA families were without amyloid in the skin but had Alu 1 RFLP marker. Skin from 12 individuals who served as controls and skin from 14 close relatives of the patients was negative for amyloid. Punch biopsy of the skin is a simple procedure which is of value for the diagnosis of HCCA, even before the appearance of clinical symptoms. This method might also be of use in following progression of the disease. 相似文献
9.
alpha(v)beta(3) Integrin in central nervous system tumors 总被引:1,自引:0,他引:1
Lim M Guccione S Haddix T Sims L Cheshier S Chu P Vogel H Harsh G 《Human pathology》2005,36(6):665-669
alpha(v)beta(3) Is an integrin specifically expressed in endothelial cells of newly forming blood vessels. Integrin-mediated angiogenesis is hypothesized to play a central role in the development and the progression of central nervous system neoplasms. Accordingly, it is considered a potential target for antiangiogenic therapy. In the current study, we compare the expression of alpha(v)beta(3) in ependymomas, oligodendrogliomas, pilocytic astrocytomas, medulloblastomas, and vestibular schwannomas (acoustic neuromas). Samples of 5 tumors of each of the 5 tumor types were harvested surgically and frozen. After the pathological diagnosis was confirmed, immunohistochemistry was performed using an anti- alpha(v)beta(3) monoclonal antibody (LM609). The expression of alpha(v)beta(3) was assessed using a 4-tiered (0-3) grading scheme reflecting the percentage of positively staining vessels. All vestibular schwannomas demonstrated strong (grade 3) alpha(v)beta(3) expression. The expression was uniformly prominent in Antoni B regions of the tumors. Of 5 ependymomas, 4 demonstrated uniformly strong alpha(v)beta(3). Oligodendrogliomas, medulloblastomas, and pilocytic astrocytomas demonstrated more variable alpha(v)beta(3). alpha(v)beta(3) may contribute significantly to angiogenesis in vestibular schwannomas and ependymomas. Despite the high vascular density of oligodendrogliomas, pilocytic astrocytomas, and medulloblastomas, these tumors had variable moderate alpha(v)beta(3) expression. This discrepancy suggests temporal and/or regional variability in the angiogenesis in these types of tumor. This study provides the first demonstration of alpha(v)beta(3) expression in vestibular schwannomas, medulloblastomas, and pilocytic astrocytomas. 相似文献
10.
Józef Dulak Agnieszka Loboda Agnieszka Jazwa Anna Zagorska Jacob D?rler Hannes Alber Wolfgang Dichtl Franz Weidinger Matthias Frick Alicja Jozkowicz 《Endothelium》2005,12(5-6):233-241
The pleiotropic effects of statins, inhibitors of 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase, have been recently extended to the modulation of angiogenesis. Here, to get more insight into the statins action, the authors have investigated the effect of atorvastatin on the expression of several angiogenic and inflammatory genes in human umbilical endothelial cells (HUVECs). Atorvastatin was proangiogenic at the dose of 10 nM, and antiangiogenic at the concentrations of 1 to 10 micro M. Moreover, these higher concentrations inhibited also the proliferation of HUVECs induced by vascular endothelial growth factor (VEGF). Lower doses of atorvastatin did not influence endothelial cell proliferation. Importantly, atorvastatin at the micromolar concentrations diminished the production of interleukin (IL)-8, a proinflammatory and proangiogenic chemokine, and inhibited the synthesis of urokinase plasminogen activator (uPA), a potent proinflammatory mediator. However, it decreased also the expression of plasminogen activator inhibitor-1 (PAI-1) and thrombospondin-1 (TSP-1), the inhibitors of angiogenesis. Atorvastatin stimulated the expression of angiopoietin (Ang)-2 and moderately enhanced the expression of endothelial nitric oxide synthase (eNOS), whereas heme oxygenase-1 (HO-1) was not significantly affected. In conclusion, the present findings points to other angiogenesis-related effects of atorvastatin, which may be of relevance to the beneficial influence of statins in cardiovascular system. 相似文献