Predictors and outcomes of treatment in hip hemiarthroplasty dislocation

Introduction

Dislocation following hip hemiarthroplasty (HHA), its incidence, predictors, treatment outcomes and mortality were investigated in a single centre series.

Methods

The prospectively collected data on neck of femur fracture admissions compiled over 11 years were reviewed. Place of residence, place of fall, past medical history, intraoperative factors (grade of surgeon, delay in surgery, type of implant and operative time), postoperative complications and mortality were compared between patients who suffered a dislocation and those who did not. In the dislocation group, the mean number of dislocations, reduction method, type and fate of implant, and mortality were investigated.

Results

Prospective data on 8,631 admissions were collected; 41% of these were managed with a HHA. The dislocation rate was 0.76%. A delay in surgery of >24 hours was associated with a fourfold increase in the dislocation risk. The majority (81%) of dislocations occurred in the first six weeks and closed manipulation was the definitive treatment in only 23% of the cases. The mortality rate was not increased following HHA dislocation.

Conclusions

The delay in surgery was the most important predictor of HHA dislocation. Closed reduction was associated with a high failure rate. While an initial attempt at closed reduction for a first dislocation is recommended, for redislocators, we recommend early exploration/revision as an alternative to repeat manipulations.     

The clonal proliferation in vitro of enriched populations of human promyelocytes and myelocytes

The proliferative capacity of normal human promyelocytes and myelocytes was demonstrated and characterized on the basis of clonal proliferation in agar. An enriched population of normal human promyelocytes and myelocytes was obtained from bone marrow using the monoclonal antibody WEM G11 and the fluorescence-activated cell sorter (FACS). In cultures stimulated by placental-conditioned medium, these cells generated peak total clone numbers between days 3 and 5 of culture. Clones disappeared rapidly thereafter. These clones were mainly of subcolony size at day 7, although some colonies were generated by this population. The clones were primarily neutrophilic in type. These cells had a plating efficiency of up to 50%, and clonal proliferation was dependent on stimulation by colony-stimulating factor (CSF).     

In vitro activation of the contact (Hageman factor) system of plasma by heparin and chondroitin sulfate E

A large number of negatively charged macromolecules, including DNA, glycosaminoglycans, and proteoglycans, were tested as possible activators of the contact (Hageman factor) system in vitro. Activation was assessed by conversion of prekallikrein to kallikrein, as determined by amidolytic assay and by cleavage of 125I-Hageman factor into 52,000- and 28,000-dalton fragments. Of particular interest to these studies, heparin proteoglycan and glycosaminoglycan from rat peritoneal mast cells, and squid chondroitin sulfate E, which is representative of the glycosaminoglycan from cultured mouse bone marrow derived mast cells, induced the reciprocal activation between Hageman factor and prekallikrein. In addition, naturally occurring heparin glycosaminoglycans from pig mucosa, bovine lung, and rat mast cells also induced activation. In contrast, native connective tissue matrix glycosaminoglycans and proteoglycans from several sources were inactive, although when one such chondroitin sulfate was further sulfated in vitro, it gained activity. When the negative charge of the activating agents was blocked by the addition of hexadimethrine bromide, the cleavage of 125I-Hageman factor in the presence of prekallikrein was prevented. The active negatively charged macromolecules induced cleavage of 125I-high molecular weight kininogen in normal plasma but not in Hageman factor-deficient or prekallikrein- deficient plasmas. Reconstitution of prekallikrein-deficient plasma with purified prekallikrein restored the kininogen cleavage upon addition of the active proteoglycans. These results suggest that both heparin from connective tissue mast cells and highly sulfated chondroitin sulfate E from cultured mouse bone marrow derived mast cells (which are considered synonomous with mucosal mast cells) could activate the contact system of plasma subsequent to an activation secretion response.     

Retroviral transduction of human progenitor cells: use of granulocyte colony-stimulating factor plus stem cell factor to mobilize progenitor cells in vivo and stimulation by Flt3/Flk-2 ligand in vitro

The clinical application of gene transfer is hindered by the availability of the multipotential stem cells and the difficulty in obtaining efficient retroviral transduction. To assess potential means by which gene transfer into human hemopoietic stem cells might be enhanced, the retroviral transduction efficiency of human bone marrow cells (BM) or peripheral blood progenitor cells (PBPC) was compared at multiple time points after in vivo administration of granulocyte colony- stimulating factor (G-CSF). This was further compared with the transduction efficiency of cells mobilized with G-CSF plus stem cell factor (SCF) in a cohort of patients randomized to receive either one or two growth factors and with normal BM function. Using the LNL6 retrovirus, retroviral transduction efficiencies of up to 19% were observed for both PBPC and BM (n = 26 patients). There was at least a 100-fold increase in PBPC with G-CSF alone and a further 30-fold increase in the total number of progenitor cells available for retroviral transduction using the combination of SCF plus G-CSF. However, pretreatment of patients with G-CSF with or without SCF did not enhance the retroviral infectability of growth factor-mobilized progenitor cells. The effect of the growth factor, Flk-2/Flt3 ligand (FL), was also examined with respect to retroviral transduction efficiency of human progenitor cells. FL plus IL-3 in vitro increased the retroviral transduction efficiency up to eightfold compared with results observed using other combinations of cytokines tested (P < .001). These findings have clinical implications both for increasing the number of target cells for in vivo gene-marking/gene-therapy studies and improving the efficiency of gene transfer.     

Biologic properties in vitro of a recombinant human granulocyte- macrophage colony-stimulating factor

Recombinant human granulocyte-macrophage colony-stimulating factor (rH GM-CSF) was purified to homogeneity from medium conditioned by COS cells transfected with a cloned human GM-CSF cDNA and shown to be an effective proliferative stimulus in human marrow cultures for GM and eosinophil colony formation. The specific activity of purified rH GM- CSF in human marrow cultures was calculated to be at least 4 X 10(7) U/mg protein. Clone transfer experiments showed that this proliferation was due to direct stimulation of responding clonogenic cells. Acting alone, rH GM-CSF did not stimulate erythroid colony formation, but in combination with erythropoietin, increased erythroid and multipotential colony formation in cultures of peripheral blood cells. rH GM-CSF had no proliferative effects on adult or fetal murine hematopoietic cells, did not induce differentiation in murine myelomonocytic WEHI-3B cells, and was unable to stimulate the survival or proliferation of murine hematopoietic cell lines dependent on murine multi-CSF (IL 3). rH GM- CSF stimulated antibody-dependent cytolysis of tumor cells by both mature human neutrophils and eosinophils and increased eosinophil autofluorescence and phagocytosis by neutrophils. From a comparison of these effects with those of semipurified preparations of human CSF alpha and -beta, it was concluded that rH GM-CSF exhibited all the biologic activities previously noted for CSF alpha.     

Isolation and characterization of growth factor(s) from a human B-cell lymphoma

We demonstrate that human neoplastic B cells (Br cells) contain a cytoplasmic protein of molecular mass 60 Kd that exhibits B-cell growth factor (BCGF) activity on growth factor-dependent long-term human B cells as well as on autochthonous tumor cells. This 60-Kd protein is recognized by antibodies against a similar intracellular 60-Kd protein derived from normal human lymphocytes. These results demonstrate that the two proteins share epitope homology. Microculture bioassays indicate that neoplastic and normal 60-Kd proteins are capable of driving neoplastic B cells through S-phase. Western immunoblot analysis indicates that neoplastic B cells secrete 60- as well as 14-Kd protein. Immunoaffinity-purified proteins secreted by Br cells exhibit BCGF activity in anti-IgM or dextran sulfate-preactivated human B cells. In addition, a double-antibody immunofluorescence staining technique was used to demonstrate that Br cells express cell surface receptors for BCGF molecule(s). These studies provide support for the autocrine growth model for neoplastic human B cells and suggest that the autocrine growth factor derived from such tumor cells is similar if not identical to normal BCGF molecules.     

角膜移植260例病因分析并与国外数据比较

目的:总结进行角膜移植手术患者的病因学资料,并与国外相应统计资料比较。方法:收集2001-12/2005-12在南昌大学医学院第一附属医院眼科接受角膜移植手术的260例患者(260眼)的临床资料做以统计,内容包括性别、年龄,与角膜移植相关的临床诊断、手术方法等,患者均知情同意。患者的病种统计以出院时第一诊断为基准。260例患者中行单纯板层角膜移植125例,单纯穿透性角膜移植63例,联合羊膜覆盖33例,联合角膜缘干细胞移植术20例,联合结膜瓣遮盖术19例。术后半年进行视力评估,视力<3.7为盲。结果:260例角膜移植患者全部进入结果分析,无脱落。①260例患者中男162例,女98例,年龄(24±19)岁。角膜移植的病因按病例数由多至少排列,首位为角膜炎后角膜白斑,计86例(占3.08%),尤以病毒性角膜炎为主;外伤后角膜疤痕病变居第2位,计78例(占30%),随后为角膜溃疡并穿孔、蚕食性角膜溃疡、圆锥角膜、角膜皮样瘤、角膜营养不良、角膜失代偿、角膜葡萄肿以及角膜原位癌。角膜炎后角膜白斑病毒性角膜炎后最为多见,而国外类似的统计表明大泡性角膜病变占据首位。②术后半年260例角膜移植患者的脱盲率达94%。结论:与发达国家角膜移植最常见病因为大泡性角膜病变不同,角膜炎后角膜白斑、外伤后角膜疤痕、角膜溃疡并穿孔依次是国内角膜移植最常见的原因。