Throwing induces substantial torsional adaptation within the midshaft humerus of male baseball players

Athletes participating in unilateral dominant sports are useful models for investigating skeletal responses to mechanical loading as they provide controlled evidence in the absence of completing a randomized controlled trial. Throwing athletes may be an additional model for this purpose as they overload their dominant upper extremity enabling the contralateral side to act as an internal control and load the bones of the upper extremity purely via the generation of internal (i.e. muscular) forces without superposition of externally applied loads (i.e. impact with an external object). The aim of this study was to investigate upper extremity bone adaptation in throwing athletes and explore factors that predict this adaptation. Two cohorts were recruited—male baseball players (throwers; n = 15) and matched controls (controls; n = 15). Each subject was assessed for shoulder range and strength, and upper extremity bone mass, structure and estimated strength. Throwers had substantially greater skeletal differences between their dominant and nondominant upper extremities than controls, indicating that throwing induces greater adaptation than induced by habitual loading of the dominant upper extremity. Bone adaptation in throwers was localized to the humerus, with the midshaft humerus in the dominant upper extremity of throwers having enhanced bone mass, structure and estimated strength. The largest effect was for estimated strength of the midshaft humerus which had 30% greater polar moment of inertia (I_P) in throwers and suggests adaptation to resist torsional loads. The skeletal effect of throwing at the midshaft humerus was influenced by playing position with pitchers and catchers displaying greater dominant-to-nondominant differences than fielders, and was predicted by years throwing and dominant-to-nondominant difference in upper arm lean cross-sectional area. The latter two variables explained 67% of the variance in dominant-to-nondominant differences in I_P. Collectively, these data indicate that throwing induces substantial adaptation within the midshaft humerus. Adaptation was primarily in the direction of torsion which is consistent with biomechanical and injury data suggesting throwing introduces high magnitude torsional forces. As the magnitude of adaptation in throwers was equivalent to that observed in athletes participating in other unilateral dominant sports, throwers represent an alternative model for investigating the skeletal effects of mechanical loading.     

前列腺增生症证型与体内性激素水平的临床研究

目的:研究前列腺增生症中医证型与体内性激素水平的相关性.方法:选择500例患者,中医辨证分为血瘀下焦、膀胱湿热、肾阴亏虚、肾阳不足、肺热气闭,均在就诊次日上午抽空腹血4 mL,进行血清性激素测定.结果:T值以血瘀下焦、肾阴亏虚证较高,肾阳不足证明显偏低,两者比较差别有显著性(P＜0.01);膀胱湿热证和肺热气闭证居中,与血瘀下焦、肾阴亏虚证比较差别也具有显著性(P＜0.05).E2值以肾阳不足证明显偏高,血瘀下焦和膀胱湿热证次之,肾阴亏虚和肺热气闭证较低.各组间比较差别具有显著性(P＜0.01).结论:前列腺增生症各证型与血清性激素水平变化有一定规律可循,同时也为证型客观化、微观化提供了相应证据.     

个体成长模型在纵向研究中的应用--以大学新生交往主动性为例

目的介绍个体成长模型方法对大学新生适应能力中交往主动性的3次测查数据采用普通回归模型和个体成长模型进行分析。结果个体成长模型的拟合度比普通回归模型的拟合度要好,个体成长模型可在个体水平上分析个体随时间产生的变化。结论个体成长模型具有许多优点,熟悉这种重要的分析方法对纵向数据研究者是非常有益处的。     

谷氨酰胺和生长激素对短肠综合征患者肠道代偿作用

目的探讨谷氨酰胺和生长激素对短肠综合征(SBS)患者的肠道代偿作用。方法26例短肠综合征患者残余小肠长度为0～100(中位数42.5)cm,手术后接受肠外营养(PN)支持3-52个月,联合应用生长激素(GH)(0.10±0.06)mg·kg-1·d-1和谷氨酰胺(GLN)(0.30±0.17)g·kg-1·d-1进行肠道促代偿治疗。结果26例接受GH加GLN治疗的SBS患者,其中9例(34.6%)治疗后近期内完全摆脱PN;8例(30.8%)经治疗后明显减少了PN用量,从每周需要PN(6.0±1.0)d下降至(4.2±1.0)d,每周PN需要量从(13.6±5.2)L降至(8.2±3.3)L;9例(34.6%)在治疗后仍依赖PN维持。结论经过合适的营养支持和肠道促代偿治疗,大多数短肠综合征患者残留肠道能充分代偿,完全摆脱PN或减少PN用量,长期健康生存。     

Thyrotrophin-Releasing Hormone Raises Cytosolic Free Calcium Concentration in Human Adenomatous Somatotrophs and Corticotrophs; Comparison with in vivo Responsiveness to Thyrotrophin-Releasing Hormone in Patients with Acromegaly or Cushing's Disease

The effect of thyrotrophin-releasing hormone (TRH) on intracellular free Ca²⁺ concentration, [Ca²⁺)i, was investigated with the fluorescent dye fura-2 in cell suspensions obtained from 13 human growth hormone-secreting adenomas and 6 adrenocorticotrophin-secreting adenomas. Preoperatively, 9 out of 13 acromegalic patients showed a positive growth hormone response to TRH administration while none of the 6 patients with Cushing's disease had a plasma adrenocorticotrophin increase after TRH injection. In all the growth hormone-secreting adenomas the addition of TRH (100 nM) caused a significant rise in [Ca²⁺]i (from a resting level of 133±40 (±SD) to a value of 284±119 nM at 100 nM TRH, n = 42; P<0.001). The transient induced by TRH was found to have a dual origin, one due to Ca²⁺ mobilization from intracellular stores which was maintained in presence of EGTA (3mM) and verapamil (10 μM) and a plateau phase due to Ca²⁺ influx from the extracellular media. Somatostatin (0.1 μM) lowered both resting [Ca²⁺]i and TRH-induced transients. The effect of gonadotrophin-releasing hormone on [Ca²⁺]i was evaluated on cell suspensions obtained from 6 growth hormone-secreting adenomas. Gonadotrophin-releasing hormone (100 nM) caused a marked rise in [Ca²⁺]i (from 179±25 to 283±15nM) on the cell suspension obtained from the only in vivo responsive adenoma while it was ineffective in the remaining 5. Although TRH was ineffective in modifying plasma adrenocorticotrophin levels in all patients with Cushing's disease, in 5 out of 6 tumors the addition of 100 nM TRH caused a significant rise in [Ca²⁺]i (from 102.5 ± 36 to 163±66 nM, n = 22; P < 0.005). However, the effect of TRH on [Ca²⁺]i was significantly lower than that caused by arginine vasopressin, a physiological stimulator of adrenocorticotrophin release ([Ca²⁺]i values; 145±78 nM at 100 nM TRH versus 300±140 at 10 nM arginine vasopressin, n = 15; P<0.05). Moreover, the effect of arginine vasopressin on [Ca²⁺]i was detectable at concentrations as low as 0.1 nM while TRH was effective at concentrations higher than 1 nM. By contrast, gonadotrophin-releasing hormone was ineffective in increasing [Ca²]i in all the adrenocorticotrophin-secreting adenomas studied. Collectively, these data indicate that sensitivity to TRH is present in almost all the growth hormone- and adrenocorticotrophin-secreting adenomas independently of the responsiveness of the individual patients to the peptide.     

Regulation of Basal and Nursing-Induced Secretion of Growth Hormone in the Neonatal Rat: The Involvement of Serotonergic, Muscarinic Cholinergic, Alpha2-Adrenergic, Somatostatin and Growth Hormone-Releasing Hormone Systems

Various neural factors are involved in the suckling-induced increase in serum growth hormone (GH) levels in neonatal rats, and, in the present study the serotonergic, cholinergic, somatostatin and GH-releasing hormone (GHRH) systems were investigated. The serotonin (5-HT) precursor 5-hydroxy-L-tryptophan (5-HTP) and the 5-HT receptor agonist quipazine maleate stimulated serum GH levels in 2-day-old rat pups separated from their mothers for 6 h. The increase in serum GH during suckling was further elevated by 5-HTP. The 5-HT antagonist cyproheptadine decreased serum GH levels in separated 2-day-old pups, and although it reduced the amplitude of the suckling-induced increase in serum GH concentration, it did not alter the increase in serum GH on a percentage basis. The effect of the cholinergic muscarinic antagonist atropine sulfate (ATR) was similar to that of cyproheptadine. Moreover, in separated pups, ATR prevented the increase in serum GH induced by 5-HTP. In contrast with 2-day-old pups, ATR completely eliminated the suckling-induced release of GH in 10-day-old rats. However, ATR failed to prevent GH release induced by the α₂-adrenergic agonist clonidine HCI in 10-day-old male pups. While thyrotropin-releasing hormone increased serum GH levels, rat GHRH failed to alter serum GH levels either in separated or in suckled 2-day-old rat pups. Immunoneutralization for rat GHRH eliminated the increase in serum GH induced by clonidine HCI in 10-day-old pups, but (on a percentage basis) failed to prevent the GH-increasing effect of suckling in 2-day-old pups. While somatostatin failed to significantly decrease serum GH in separated 2-day-old pups, it effectively decreased serum GH levels in 2-day-old pups which were suckled. Cysteamine, which depletes hypothalamic somatostatin, increased serum GH in separated 2-day-old pups, and further increased the suckling-induced levels of serum GH. Cysteamine partially prevented the GH-decreasing effect of ATR. The present findings suggest that 1) the serotonergic and cholinergic systems are involved in the regulation of GH secretion as early as day 2 postpartum; 2) the serotonergic and cholinergic systems modulate the basal, and do not modulate the suckling-induced levels of serum GH; 3) the serotonergic system may exert its stimulatory influence on GH secretion only in the presence of a functional muscarinic cholinergic system; 4) the cholinergic system, at least in part, stimulates GH secretion via a cysteamine-sensitive system (probably by inhibiting somatostatin); 5) the cholinergic system is not functionally coupled with the α₂-adrenergic system, which stimulates GH secretion via rat GHRH; 6) since in 10-day-old pups clonidine HCI was effective only in males, while suckling was effective in both sexes, the α₂-adrenergic system is not involved in the suckling-induced increase of serum GH; and finally 7) neither somatostatin nor rat GHRH seem to be involved in the suckling-induced changes in serum GH. The findings are consistent with the hypothesis that the high circulating GH levels in the neonatal rat are due to alternative GH-releasing factors, perhaps thyrotropin-releasing hormone or γ-aminobutyric acid. The neurohumoral mediator of the suckling-induced GH release in neonatal rats remains to be identified.     

伽玛刀治疗垂体腺瘤126例的临床分析

目的 评价伽玛刀治疗垂体腺瘤的疗效和并发症.方法 对2000年8月至2005年12月间伽玛刀治疗垂体腺瘤并有完整临床资料.病人年龄15～76岁,肿瘤最大径<10mm 68例、10～20mm 56例、>20mm 2例,伽玛刀治疗剂处方量为15～30Gy、50%～65%等剂量曲线.结果 随访1～6年,肿瘤消失75例,肿瘤缩小28例,肿瘤无变化15例,肿瘤继续增大8例.肿瘤生长控制率93.6%(118/126);激素水平恢复正常率63%(49/78),垂体功能低下发生率为15%,因肿瘤复发或激素水平未恢复再行肿瘤切除术5例.结论 伽玛刀治疗垂体腺瘤,能控制垂体腺瘤肿瘤生长,可恢复垂体内分泌功能异常改变.     

Safety, tolerability and pharmacokinetic study of recombinant human parathyroid hormone in healthy male Chinese subjects

AIM： To determine the safety, tolerability and pharmacokinetic parameters of a new drug recombinant human parathyroid hormone [ rhPTH （1-84）] in healthy male Chinese subjects. METHODS： domly divided Thirty-six healthy male volunteers were rangroups received into 3 groups. The volunteers in these single subcutaneous injection of rhPTH （ 1-84） in a dosage of 1, 2 and 4 μg/kg respectively. Blood samples were obtained before and after administration within 24 hours. The rhPTH concentrations in sennn were determined by enzyme linked immunosorbent assay （ELISA）. The pharmacokinetic parameters determined with use of standard noncompartmental analysis were the maximum serum concentration （ Cmax ）, the time to attain that concentration （ tmax ）, and the area under the serum concentration-time curve up to 24 hours（ AUC0-24 ） and up to infinity （AUC0-∞）. Dose proportionality of pharmacokinetic parameters （AUC, Cmax of every volunteer of each dosage and A UC was computed from log transformed data） and was examined by mean of analysis of variance （ANOVA） using SPSS software package. In the study, subjects＇ symptoms, objective signs, and vital signs, including blood pressure, heart rate, respiratory rate and body temperature, were checked and 12-lead electrocardiography was recorded before and after drug administration within 24 hours. Routine laboratory tests, including hematology, blood biochemistry, serum electrolyte, and urinalysis, were performed before and after drug administration within at 24 hours.[第一段]     

口腔鳞状细胞癌颈淋巴转移范围和临床病理因素间的相关性研究

目的探讨口腔鳞状细胞癌颈淋巴转移范围和临床病理因素间的关系。方法对26例已存在颈淋巴转移的原发口腔癌患者，进行颈淋巴转移范围和患者的临床病理资料的统计分析，寻找影响转移范围的主要因素。结果单因素分析发现，肿瘤生长方式和分化程度与转移范围相关。多因素分析显示，肿瘤生长方式(浸润型)和肿瘤转移范围相关。结论对颈淋巴已有转移的口腔癌患者，若原发灶为浸润性生长，肿瘤倾向于更大范围的转移。对已有颈淋巴转移的口腔癌患者，颈淋巴清扫术范围的制定，主要考虑肿瘤生长方式，适当考虑肿瘤发病部位、厚度、大小和细胞的分化程度，可以不考虑患者年龄和性别。