Squamous cell carcinoma arising in a diabetic foot ulcer

Diabetic complications such as poor circulation and nerve damage can result in loss of sensation and slower wound healing in the lower extremities. The possibility of malignancy arising in association with chronic osteomyelitis in the diabetic foot should also be considered.     

Cost-effectiveness of Clinical Pathway in Coronary Artery Bypass Surgery

Few studies have been devoted to the exploration of the effect of clinical pathways on coronary artery diseases treated with coronary artery bypass (CAB) surgery. This study was aimed to investigate the cost and effectiveness of the clinical pathway on CAB surgery in a medical center. With a retrospective dataset in 2003–2007, 212 CAB surgery patients were included. Data of the costs and postoperative complication occurrence and length of stays were the focus and patient demographics, surgical risk indicator EuroSCORE, surgical conditions were collected. It revealed that there was differentiation across specified cost items in beating heart CAB surgery patients, but not for heart arrest CAB surgery patients with and without clinical pathways enrolled. In addition, there was no difference in postoperative complication occurrence in CAB surgery patients enrolled into clinical pathways. However, robotic beating heart CAB surgery patients enrolled clinical pathways were shown to have less postoperative ordinary ward stay than those not enrolled clinical pathways. CAB surgery patients’ age and surgical risks were related to their postoperative lengths of stay to some extent.     

中药独活活性成分香豆素及其甙的化学研究

独活为伞形科重齿毛当归(Angelica pubescens Maxim.F.biserrataShan et Yuan)的根及根茎,为常用中药,有祛风通络,活血舒筋,宜通百脉的作用。治腰膝酸痛,手脚挛痛。本研究证明独活有抑制血小板聚集抗血栓形成的作用,可能为独活善行血分,活血舒筋,宜通百脉的作用机制之一。我们将湖北资丘产独活以CH_2Cl_2,C_2H_5OH及H_2O提取,各提取部位分别按Born     

Suppression of lymphocyte activation and functions by a leukemia cell-derived inhibitor.

An inhibitor isolated from the serum-free culture medium of human myeloid leukemic HL-60 cells was able to suppress mitogen- and alloantigen-stimulated proliferative responses of normal lymphocytes in a dose-dependent manner. In vitro production, concentration, and purification by column chromatography and electrophoresis revealed that the inhibitor was produced constitutively, required RNA synthesis, and had a molecular weight in the range of 40,000-60,000. The inhibitor was also produced in vitro by myeloid leukemia cells isolated from patients with acute myelogenous leukemia. In a similar manner, the inhibitory material suppressed proliferative responses of allogeneic and autologous lymphocytes. Suppression was accompanied by drastically reduced production of interleukin 2 and lymphokines, which regulate differentiation of myeloid leukemia cells, and suppression was reversed by addition of exogenous interleukin 2. The inhibitor did not suppress clonogenic proliferation of normal granulocytes and macrophages suggesting that inhibition of production or interference with interleukin 2 activity as a possible mechanism. These interactions between leukemia cells and lymphocytes have shed new light on the immunosuppression and growth advantage of leukemia cells. Inhibitory activity of HL-60 cells was diminished after they were induced to differentiate, indicating that differentiation induced by lymphokines may be an effective means of controlling leukemia.     

Interleukin-1 (22-K factor) induces release of granulocyte-macrophage colony-stimulating activity from human mononuclear phagocytes

An electrophoretically pure preparation of natural human interleukin-1 (IL-1) was shown to stimulate in vitro colony formation in human bone marrow cultures. Day 4 myeloid cluster-forming cells (CFC), as well as early (day 7) and late (day 10) granulocyte-macrophage colony-forming units (CFU-GM) were stimulated in a dose-dependent fashion. At optimal concentrations of IL-1, the number of day 4 CFC reached 72%, the number of day 7 CFU-GM reached 32%, and the number of day 10 CFU-GM reached 80% of the respective numbers of colonies obtained by addition of crude leukocyte-conditioned medium (LCM). The IL-1-induced stimulatory effect on CFU-GM growth could be completely neutralized by a rabbit anti-IL-1 antiserum. Colony growth was abrogated by depleting the marrow cell suspensions of phagocytic cells prior to IL-1 addition. Conversely, the effect could be reintroduced by addition of marrow-derived adherent cells to bone marrow cell suspensions that had been depleted of both phagocytic and E rosetting T cells. Furthermore, media conditioned by bone marrow-derived adherent cells or by peripheral blood mononuclear phagocytes in the presence but not in the absence of IL-1, stimulated in vitro colony growth of phagocyte-depleted bone marrow cell suspensions. These results indicate that IL-1 induces release of granulocyte-macrophage colony-stimulating activity (GM-CSA) from human mononuclear phagocytes.     

Glucose 6-phosphate dehydrogenase mutations causing enzyme deficiency in a model of the tertiary structure of the human enzyme

Human glucose 6-phosphate dehydrogenase (G6PD) has a particularly large number of variants resulting from point mutations; some 60 mutations have been sequenced to date. Many variants, some polymorphic, are associated with enzyme deficiency. Certain variants have severe clinical manifestations; for such variants, the mutant enzyme almost always displays a reduced thermal stability. A homology model of human G6PD has been built, based on the three-dimensional structure of the enzyme from Leuconostoc mesenteroides. The model has suggested structural reasons for the diminished enzyme stability and hence for deficiency. It has shown that a cluster of mutations in exon 10, resulting in severe clinical symptoms, occurs at or near the dimer interface of the enzyme, that the eight-residue deletion in the variant Nara is at a surface loop, and that the two mutations in the A- variant are close together in the three-dimensional structure.     

Mortality hazard functions as related to neutropenia at different times after marrow transplantation

We characterized the relationship between severe neutropenia and risk of death in 2,276 patients after marrow transplantation to define objective and clinically relevant criteria that could be used to judge the timing and potential value of interventions designed to improve survival in patients with delayed initial engraftment. Proportional hazard models were used to estimate the relative risk of death before day 100 among patients alive on any given day with an absolute neutrophil count (ANC) less than 100/microL compared with those alive on the same day with an ANC > or = 100/microL. Between day 10 and 14, the risk ratio remained close to 1.0, indicating that the risk of death before day 100 for patients with an ANC less than 100/microL was similar to that for patients with an ANC > or = 100/microL. Between day 15, when 38% of patients had an ANC less than 100/microL, and day 26, when 3.8% of patients had an ANC less than 100/microL, the risk ratio showed an overall upward trend, indicating that patients with an ANC less than 100/microL had a higher risk of death before day 100 than those with an ANC > or = 100/microL. Thereafter, the risk ratio fluctuated between 2.01 and 5.78, indicating consistently higher risks of mortality in patients with severe neutropenia. However, allogeneic and autologous transplant recipients each had distinctive risk ratio patterns. These results could be helpful in deciding the appropriate timing for treatment given to improve graft function after marrow transplantation.