Intermittent subclavian artery occlusion following clavicular fracture

Although fractures of the clavicle are common, complications are rare. A 41 year old painter developed two uncommon complications of clavicular fracture, mechanical intermittent subclavian artery occlusion and subclavian vein thrombosis. Both conditions were clearly identified on the clinical symptoms and signs and confirmed with dynamic angiography and computerised tomography. Operative intervention led to complete resolution of symptoms.     

坐式排球运动与腰背肌筋膜炎的关系及其损伤预防

目的:对坐式排球运动员进行腰背肌筋膜炎损伤检查与积极治疗,并制定有效措施预防腰背肌筋膜炎损伤的发生,以提高其成绩水平。方法:实验于2006-03/07于鲁东大学体育学院完成。①选取2006年参加山东省残疾人运动会的烟台队坐式排球运动员22名,男12名,女10名,平均年龄(27±2)岁。②对22名坐式排球运动员进行腰背肌筋膜炎损伤状况检查,病历需要详细注明受伤原因、腰背部肌肉筋膜的痛点及运动障碍、确定损伤性质是急性还是慢性、确定损伤位置、抗阻力实验是否为阳性。③检查完毕后,对存在腰背肌筋膜炎损伤的运动员采用日本温热式低周波治疗器 外敷中药治疗。温热式低周波治疗器主要选择拍打、推压、按摩、左右变换按揉,每次治疗时间为15min,温度控制在38～43℃,将(-)导子放在痛点部位,( )导子放在阿是穴、肾俞、命门、腰眼等相应的治疗穴位上。中药以散寒活血祛瘀止痛为主,将川乌头、天南星、生半夏、乳香、没药、独活、马钱子、红花等混合研成粉状,加入体积分数为0.75的乙醇搅拌成糊状,用沙布制成直径约15cm饼状态物,敷于患处,6～12d为1个疗程。④治疗结束后,对所有队员1年的训练过程制定预防腰背肌筋膜炎的有效措施,即训练中加强腰背部肌肉力量和伸展性;通过温热式低周波治疗器 推拿按摩促进腰背部肌肉筋膜的放松及疲劳恢复;训练中采用肌肉牵伸性练习,注意避免牵拉过度;建立急性运动损伤档案,尽量减少急性损伤转变为慢性损伤的可能性。结果:①腰背肌筋膜炎的患病率:烟台队22名坐式排球运动员中,10名存在腰背肌筋膜炎损伤,患病率45.5%,损伤部位集中在腰背部和颈部。②腰背肌筋膜炎损伤治疗结果:采用日本温热式低周波治疗器 外敷中药治疗一两个疗程后效果良好,10名腰背肌筋膜炎损伤运动员中9名痊愈,治愈率90%。③采取预防措施后运动员腰背肌筋膜炎的发生情况:训练中采取预防措施,1年后22名坐式排球运动员腰背肌筋膜炎损伤得到明显控制,腰背肌筋膜炎患病率为29.3%,与治疗预防前比较下降16.2%,效果显著。结论:坐式排球运动损伤部位集中在腰背部和颈部,腰背肌筋膜炎是常发病。针对发病原因及时治疗并给予有效预防措施,可明显降低腰背肌筋膜炎损伤发生率,对其运动训练能力和比赛成绩的提高均具有积极意义。     

Use of fecal occult blood testing in hospitalized patients: Results of an audit

BACKGROUND:

The fecal occult blood test (FOBT), widely used as a colorectal cancer screening tool, continues to be used in hospitalized patients. However, the utility of this test for hospitalized patients is unclear.

OBJECTIVE:

To assess FOBT use in a large urban regional health authority.

METHODS:

Reports of all FOBTs performed between April 1, 2011 and March 30, 2012 from two academic and four community hospitals in Winnipeg (Manitoba) were extracted. Of 650 hospitalizations with a positive FOBT result and 1254 with a negative FOBT result, random samples of 230 and 97 charts, respectively, were reviewed. Information including demographics, admission diagnos(es), indication(s) for ordering the FOBT and clinical management was extracted.

RESULTS:

Thirty-four percent (650 of 1904) of hospitalizations with an FOBT had a positive FOBT result. Family medicine physicians ordered approximately one-half of the reviewed FOBTs. The most common indication for ordering an FOBT was anemia. Of those with a positive FOBT, 66% did not undergo further gastrointestinal investigations. Of those with a positive FOBT and overt gastrointestinal bleeding and/or melena who underwent endoscopy, 60% had their endoscopy performed before the FOBT result being reported while 38% underwent their endoscopy ≥3 days after the stool sample was collected. There were minimal differences in clinical practices between academic and community hospitals.

CONCLUSIONS:

The present study suggests that FOBT results in hospitalized patients may have little beneficial impact on clinical management. Hospital laboratories may be better served in directing resources to other tests.     

High-molecular-weight kininogen is exclusively membrane bound on endothelial cells to influence activation of vascular endothelium

An important biologic function of high-molecular-weight kininogen (HK) is to deliver bradykinin (BK) to its cellular receptors. Internalization and degradation of HK may provide a mechanism by which endothelial cells modulate the production of BK and control its activities. Therefore, we investigated the binding and subsequent distribution of biotinylated-HK (biotin-HK) associated with human umbilical vein endothelial cells (HUVEC). HUVEC bound 3 to 4 times more HK and with greater avidity at 1 to 3 hours at 37 degrees C than at 4 degrees C (Bmax = 1.0 +/- 0.02 x 10(7) molecules/cell, kd = 7 +/- 3 nmol/L v Bmax = 2.6 +/- 0.2 x 10(6) molecules/cell, kd = 46 +/- 8 nmol/L). However, there was no evidence that the difference was caused by internalization of HK at the higher temperature. First, the same amount of biotin-HK was associated with nonpermeabilized and permeabilized HUVEC using buffers containing 20 to 50 mumol/L zinc ion in the absence or presence of 2 mmol/L calcium ion. Second, binding of biotin-HK to HUVEC was approximately 92% reversible at 1 hour when the cells were maintained at both 37 degrees C and 4 degrees C. Third, neither chloroquine nor primaquine altered the amount of biotin-HK bound to HUVEC. Fourth, biotin-HK bound to HUVEC was almost completely removed by pronase. Fifth, the nonpermeable dye, crystal violet, almost completely quenched the fluorescence signal emitted by HUVEC-associated fluorescein isothiocyanate (FITC) HK. Finally, the localization of HUVEC-bound FITC-HK was restricted to the membrane as shown by laser scanning confocal microscopy. The expression of HK binding sites had an absolute requirement for metabolic energy, but was not dependent on new protein synthesis. Membrane-bound HK contributed to the anticoagulant nature of endothelial cells by blocking human alpha-thrombin binding and its resultant induction of prostacyclin formation. These studies indicate that HK is not internalized by HUVEC, but remains primarily on cell surfaces to be accessible for BK liberation and to modulate the binding and actions of alpha-thrombin.     

Hematopoietic growth factors for graft failure after bone marrow transplantation: a randomized trial of granulocyte-macrophage colony- stimulating factor (GM-CSF) versus sequential GM-CSF plus granulocyte- CSF

Delay in hematologic recovery after bone marrow transplantation (BMT) can extend and amplify the risks of infection and hemorrhage, compromise patients' survival, and increase the duration and cost of hospitalization. Because current studies suggest that granulocyte- macrophage (GM) colony-stimulating factor (CSF) may potentiate the sensitivity of hematopoietic progenitor cells to G-CSF, we performed a prospective, randomized trial comparing GM-CSF (250 micrograms/m2/d x 14 days) versus sequential GM-CSF x 7 days followed by G-CSF (5 micrograms/kg/d x 7 days) as treatment for primary or secondary graft failure after BMT. Eligibility criteria included failure to achieve a white blood cell (WBC) count > or = 100/microL by day +21 or > or = 300/microL by day +28, no absolute neutrophil count (ANC) > or = 200/microL by day +28, or secondary sustained neutropenia after initial engraftment. Forty-seven patients were enrolled: 23 received GM-CSF (10 unrelated, 8 related allogeneic, and 5 autologous), and 24 received GM- CSF followed by G-CSF (12 unrelated, 7 related allogeneic, and 5 autologous). For patients receiving GM-CSF alone, neutrophil recovery (ANC > or = 500/microL) occurred between 2 and 61 days (median, 8 days) after therapy, while those receiving GM-CSF+G-CSF recovered at a similar rate of 1 to 36 days (median, 6 days; P = .39). Recovery to red blood cell (RBC) transfusion independence was slow, occurring 6 to 250 days (median, 35 days) after enrollment with no significant difference between the two treatment groups (GM-CSF: median, 30 days; GM-CSF+G- CSF; median, 42 days; P = .24). Similarly, platelet transfusion independence was delayed until 4 to 249 days (median, 32 days) after enrollment, with no difference between the two treatment groups (GM- CSF: median, 28 days; GM-CSF+G-CSF: median, 42 days; P = .38). Recovery times were not different between patients with unrelated donors and those with related donors or autologous transplant recipients. Survival at 100 days after enrollment was superior after treatment with GM-CSF alone. Only 1 of 23 patients treated with GM-CSF died versus 7 of 24 treated with GM-CSF+G-CSF who died 16 to 84 days (median, 38 days) after enrollment, yielding Kaplan-Meier 100-day survival estimates of 96% +/- 8% for GM-CSF versus 71% +/- 18% for GM-CSF+G-CSF (P = .026). These data suggest that sequential growth factor therapy with GM-CSF followed by G-CSF offers no advantage over GM-CSF alone in accelerating trilineage hematopoiesis or preventing lethal complications in patients with poor graft function after BMT.(ABSTRACT TRUNCATED AT 400 WORDS)     

Early human thymocyte proliferation is regulated by an externally controlled autocrine transforming growth factor-beta 1 mechanism

Early thymocytes undergo extensive proliferation after their entry into the thymus, but cellular interactions and cytokines regulating this intrathymic step remain to be determined. We analyzed the effects of various T-cell growth factors and cellular interactions on in vitro proliferation of early CD2+CD3/TCR-CD4-CD8- (triple negative [TN]) human thymocytes. Freshly isolated TN cells were then assayed for their growth capacity after incubation with CD2I+III-monoclonal antibody (MoAb), recombinant human interleukin-2 (IL-2), IL-7, and/or IL-4. These cells displayed significant proliferative responses with IL-4, IL- 7, or CD2-MoAb+IL-2. The addition of recombinant transforming growth factor beta (TGF beta) or autologous irradiated CD3+CD8+CD4- cells to TN cell cultures dramatically decreased their growth responses to IL-2 and IL-7, whereas IL-4-induced proliferation was less sensitive to growth inhibition. We thus asked whether the CD8+ cell-derived inhibitory effect was due to TGF beta. The addition of neutralizing anti-TGF beta MoAb completely abolished CD8+ cell-derived inhibition of TN cell growth. Analysis of CD8+ cell-derived supernatants indicated that these cells had low TGF beta 1 production capacity, whereas TN cells secrete significantly high levels of TGF beta 1. Cell fixation studies showed that TN cells were the source of the TGF beta. TGF beta 1 released from TN cells was in the latent form that became the active inhibitory form through interaction of TN cells with CD8+ cells. Together, these data suggest a role for TGF beta 1 as an externally controlled, autocrine inhibitory factor for human early thymocytes, with a regulatory role in thymic T-cell output.