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841.
Molecular analysis of Polish patients with factor VII deficiency 总被引:4,自引:1,他引:4
We analyzed the mutations in patients from 10 Polish kindreds with a bleeding diathesis due to factor VII deficiency. Patients from eight families had plasma levels of factor VII coagulant activity (VII:C) and factor VII antigen (VII:Ag) that were less than 4% of normal. The coding sequence of the factor VII gene was amplified from genomic DNA by polymerase chain reaction (PCR). Sequencing demonstrated a C to T transition at position 10798 resulting in Ala294Val, a G to A transition at 10976 resulting in Arg353Gln, and a single bp deletion at 11125 to 11128 causing a frameshift mutation in the triplet encoding amino acid 404. Homozygosity for the three sequence alterations was confirmed with the restriction enzymes AvaII and MspI and allele specific PCR, respectively. A homozygous patient from a ninth family with levels of VII:C and VII:Ag of 4% and 17%, respectively, had Ala294Val and the frameshift mutation, but not Arg353Gln. Investigation of a homozygous patient from a tenth kindred with VII:C and VII:Ag of 11% and 47%, respectively, demonstrated Ala294Val and Arg353Gln, but not the frameshift mutation. Based on the above data, we conclude that the frameshift mutation in the codon for amino acid 404 is associated with marked reductions in VII:C, Arg353Gln can decrease plasma levels of factor VII in the presence of other mutations in the factor VII gene, and Ala294Val results in a dysfunctional factor VII molecule. 相似文献
842.
Glucocorticoids and lymphocytes. III. Effects of glucocorticoid administration on lymphocyte glucocorticoid receptors 总被引:2,自引:0,他引:2
To determine the effects of glucocorticoid administration on the number of measured lymphocyte glucocorticoid receptor sites and the duration of such effects, seven normal volunteers were studied. Glucocorticoid receptor levels of the lymphocytes circulating in the blood of each volunteer were determined. Glucocorticoid was then administered in a regimen of a total of four doses of dexamethasone 4 mg p.o. every 6 hr. Determinations of the number of receptors were performed at 6 hr and at various subsequent times after the end of dexamethasone administration. When compared to baseline receptor numbers, six volunteers showed a decrease in receptor number after glucocorticoid administration (median maximum decrease 2,046 sites/cell). The fall in receptor number occurred rapidly, reaching a nadir within 30 hr from the end of glucocorticoid administration. The return of receptor number to baseline was more gradual, requiring from 3 to as long as 17 days in one subject. Our results suggest that in order to accurately interpret glucocorticoid receptor numbers in human lymphoid cells, glucocorticoid should not have been administered for 3 wk prior to determinations of receptor levels. 相似文献
843.
Value of monoclonal anti-CD22 (p135) antibodies for the detection of normal and neoplastic B lymphoid cells 总被引:1,自引:0,他引:1
Mason DY; Stein H; Gerdes J; Pulford KA; Ralfkiaer E; Falini B; Erber WN; Micklem K; Gatter KC 《Blood》1987,69(3):836-840
Two monoclonal antibodies (To15 and 4KB128) specific for the B cell- associated CD22 antigen (135,000 mol wt) are described. On immunoenzymatic analysis of cryostat tissue sections, these antibodies strongly label both mantle zone and germinal center B lymphoid cells in secondary lymphoid follicles (and also scattered extrafollicular lymphoid cells) but are unreactive with other cell types (with the exception of weak reactivity with some epithelioid histiocytes). These reactions differ from those of monoclonal antibodies B1 and B2 (anti- CD20 and CD21) but are similar to those of the pan-B antibody B4 (anti- CD19). One of the anti-CD22 antibodies (To15) has been tested extensively by immunoenzymatic labeling on greater than 350 neoplastic lymphoid and hematological samples. The CD22 antigen was found in tissue sections in most B cell-derived neoplasms, the major exceptions being myeloma (all cases negative) and a small proportion of high-grade lymphoma (6% of cases negative). In cell smears, the antigen could be found on neoplastic cells in most B cell lymphoproliferative disorders, including common acute lymphoblastic leukemia (ALL) (90% positive) and B cell chronic lymphocytic leukemia (CLL) (89% positive). We conclude that anti-CD22 antibodies are of value for identification of human B cell lymphoproliferative disorders (especially when used in conjunction with anti-CD19 antibodies). Previous reports that the CD22 antigen is absent from many B cell neoplasms are probably due to its being expressed within the cytoplasm of immature B cells rather than on their surface. 相似文献
844.
Southard J Kernozek TW Ragan R Willson J 《International journal of sports medicine》2012,33(5):381-385
Noncontact mechanisms, such as landing from a jump, account for over 70% of all anterior cruciate ligament injuries. Increased knee and hip flexion during landing has been suggested to decrease anterior cruciate ligament tension; however, current literature utilizing knee modeling approaches has not investigated this. Our purpose was to compare estimated anterior cruciate ligament tension in females between a typical and flexed knee and hip drop landing performance. A sagittal plane knee model based on kinematic, kinetic, electromyography, and cadaveric data was used to estimate forces on the anterior cruciate ligament during a typical and flexed drop landing for 23 females. Model estimated peak anterior cruciate ligament tension decreased by 10% during the flexed landing performance (p=0.008). This was accounted for by an increase in hamstring shear force by 6% of body weight and a reduction in patellar tendon shear force and femur-tibia shear force by 3% of body weight each. Results suggest that simple verbal cues for increased knee and hip flexion during landing may be effective in reducing anterior cruciate ligament tension and potential risk of injury during landing. 相似文献
845.
Ragan R Kernozek TW Bidar M Matheson JW 《Archives of physical medicine and rehabilitation》2002,83(6):872-875
OBJECTIVE: To investigate the effect of cushion thickness on subcutaneous pressures during seating by using a finite element modeling approach. DESIGN: Seat-interface pressure measurements were used in a computational model. SETTING: Biomechanics laboratory. PARTICIPANT: A single healthy man (weight, 70 kg). INTERVENTIONS: Subject sat upright either with or without cushions of various heights. Seat-interface pressures measured by using a sensor mat interfaced to a personal computer sampling at 15 Hz. MAIN OUTCOME MEASURES: Peak seat-interface pressure; finite-element software was used to model the buttock, ischial tuberosity, and seat cushion. Subcutaneous stresses were calculated from the model. RESULTS: The region of highest subcutaneous stress in the soft tissue was concentrated within 1 or 2 cm of the ischial tuberosity, with the maximum compressive stress inferior to the bottom surface of the ischial tuberosity. The maximum subcutaneous stress, maximum seat-interface pressure, and maximum subcutaneous shear stress each changed with cushion thickness. Subcutaneous pressures decreased with thicker cushions, but almost all of the reduction was obtained with an 8-cm cushion. The amount of subcutaneous shear stress increased slightly for thicker cushions. The maximum subcutaneous stress was greater than the maximum interface pressure but not by a constant factor. Instead, the former was consistently larger by 0.7 to 0.8 N/cm(2). CONCLUSIONS: Cushion use reduced the maximum subcutaneous stress inferior to the ischial tuberosity. However, increasing the cushion thickness beyond 8 cm was ineffective in further reducing subcutaneous stress. It was also found that seat-interface pressures were a good indicator of the subcutaneous stress reduction in seating. 相似文献
846.
T cell growth factor receptors. Quantitation, specificity, and biological relevance 总被引:101,自引:44,他引:101 下载免费PDF全文
To examine directly the hypothesis that T cell growth factor (TCGF) interacts with target cells in a fashion similar to polypeptide hormones, the binding of radiolabeled TCGF to various cell populations was investigated. The results indicate that TCGF interacts with activated T cells via a receptor through which it initiates the T cell proliferative response. Internally radiolabeled TCGF, prepared from a human T leukemia cell line and purified by gel filtration and isoelectric focusing, retained biological activity and was uniform with respect to size and charge. Binding of radiolabeled TCGF to TCGF-dependent cytolytic T cells occurred rapidly (within 15 rain at 37 degrees C) and was both saturable and largely reversible. In addition, at 37 degrees C, a receptor- and lysosome-dependent degradation of TCGF occurred. Radiolabeled TCGF binding was specific for activated, TCGF-responsive T cells. Whereas unstimulated lymphocytes of human or murine origin and lipopolysaccharide-activated B cell blasts expressed few if any detectable binding sites, lectin- or alloantigen-activated cells had easily detectable binding sites. Moreover, compared with lectin- or alloantigen-activated T cells, long-term TCGF-dependent cytolytic and helper T cell lines and TCGF-dependent neo-plastic T cell lines bound TCGF with a similar affinity (dissociation constant of 5-25 pM) and expressed a similar number of receptor sites per cell (5,000-15,000). In contrast, a number of TCGF-independent cell lines of T cell, B cell, or myeloid origin did not bind detectable quantities of radiolabeled TCGF. Binding of radiolabeled TCGF to TCGF-responsive cells was specific, in that among several growth factors and polypeptide hormones tested, only TCGF competed for binding. Finally, the relative magnitude of T cell proliferation induced by a given concentration of TCGF closely paralleled the fraction of occupied receptor sites. As the extent of T cell clonal expansion depends on TCGF and on the TCGF receptor, the dissection of the molecular events surrounding the interaction of TCGF and its receptor that these studies permit, should provide new insight into the hormonelike regulation of the immune response by this lymphokine. 相似文献
847.
R Silvis ; WH Steup ; A Brand ; KA Zwinderman ; CB Lamers ; G Griffioen ; HG Gooszen 《Transfusion》1994,34(3):242-247
BACKGROUND: Perioperative blood transfusion (BT) appeared to have adverse effects on survival after surgery for malignant tumors while pretransplantation BT suppressed allograft rejection. Interest grew in the effect of BT on postoperative recurrence of Crohn's disease. STUDY DESIGN AND METHODS: To determine the effect of perioperative BT on the recurrence of Crohn's disease after primary surgery, the medical histories of 148 patients with Crohn's disease, 62 males and 86 females (49 nonparous and 37 parous), were reviewed. Eighty-seven patients received perioperative BT. RESULTS: Overall, perioperative BT showed no effect on recurrence. Patients with Crohn's disease limited to the ileum had a better prognosis with regard to recurrence than did patients with Crohn's disease located in the colon or located in both ileum and colon, but the difference was not significant. Perioperative transfusion seemed to protect against recurrent disease after colon resection, which might be explained by the fact that colon resections, which often necessitate perioperative BT, generally result in a shorter bowel segment at risk for recurrent disease. Overall, parous women showed a worse prognosis than nonparous females and men (p = 0.022). Transfusions had a beneficial effect in parous women (p = 0.068) and, after correction for type of operation, this beneficial effect was significant (p = 0.026). After perioperative BT, parous women had a similar prognosis with respect to recurrent Crohn's disease as nonparous females and men. CONCLUSION: Perioperative BT has a beneficial effect on the postoperative recurrence of Crohn's disease in parous women. 相似文献
848.
对291例颈动脉内膜剥脱术后患者进行随访研究,1例术后即期死亡;22例(6.3%)在术后发生脑中风,17例为中度中风,5例为严重中风,即期中风的病因包括:14例手术部位颈动脉血栓形成(14/22,64%),4例术中或术后即期脑栓塞,2例阻断颈动脉所致脑缺血,1例脑出血,1例原因不明。此外讨论了术后中风的危险因素和处理方法。 相似文献
849.
In vitro generation of tumor-specific cytotoxic lymphocytes. Secondary allogeneic mixed tumor lymphocyte culture of normal murine spleen cells 下载免费PDF全文
In vivo or in vitro immunity to murine leukemia virus (MuLV)-induced leukemia cells which do not effectively produce virus, has been difficult to demonstrate. Because immunizations with allogeneic murine leukemia cells have been used to confer syngeneic tumor immunity to virus- producing cells, we attempted to generate lymphocytes, cytotoxic to syngeneic nonproducer leukemia cells, by stimulating normal murine spleen cells with allogeneic nonproducer leukemia cells in mixed tumor lymphocyte culture (MTLC) reactions in vitro. Secondary allogeneic MTLC of normal C57BL/6 or DBA/2 spleen cells effectively produced syngeneic tumor-specific cytotoxic lymphocytes. Target cells lysed in lymphocyte- mediated cytolysis (LMC) assays, included both Friend and Rauscher virus- induced syngeneic murine leukemia cells and chemically-induced hematopoietic tumor cells. Syngeneic tumor cells were lysed regardless of whether they produced infectious MuLV or expressed viral antigens gp-71, p-30, or p-12 at the cell surface. Syngeneic normal cells (thymus, lymph node, or Concanavalin A-stimulated spleen cells) used as targets in LMC assays were uneffected by lymphocytes harvested from secondary allogeneic MTLC. Several other in vitro culture treatments including secondary syngeneic MTLC and repetitive mixed lymphocyte culture stimulations were incapable of generating tumor-specific cytotoxic lymphocytes. Based upon these results, we propose that secondary MTLC stimulation of normal spleen cells with allogeneic nonproducer leukemia cells selects for the proliferation of two subpopulations of antigen-specific cytotoxic lymphocytes. The population capable of effecting syngeneic tumor cell lysis is directed against tumor-associated cell surface antigens which may be distinct from viral structural proteins or glycoproteins. The growth of these tumor-specific cytotoxic lymphocytes may be enhanced by a soluble allogeneic effect factor produced by the proliferation of the second subpopulation of lymphocytes generated in repetitive allogeneic MTLC, namely those lymphocytes with specificities directed against differing histocompatibility antigens. 相似文献
850.