A correlative study of the restorative effects of endogenous and exogenous hormones on the Leydig cells, the testis and the epididymis of the regressed hedgehog Effects of hormones on hedgehog Leydig cells

The study of the effects of morphogenesis at puberty on the Leydig cells in the testis of the young hedgehog and of the subsequent changes due to the seasonal varisations, has been done. Furthermore, the restorative changes induced by the exogenous hormones in the Leydig cells and the related sex organs of the regressed hedgehogs have also been studied. It was observed that the Leydig cells from the undifferentiated mesenchyme cell-like nature in the young hedgehog, develop into an adult form possessing large number of lipids, a well-developed Golgi apparatus, complex mitochondria and extensive smooth endoplasmic reticulum. The depletion of the lipids and other regression associated changes are found in the interstitial Leydig cells but not in those situated under tunica albuginea and the latter probably function as lipid storing cells during regression. Pituitary extract, either alone or in combination, but not testosterone, could restore completely the structure of the regressed Leydig cells. Similarly, the restoration of the complete process of spermatogenesis and the structure and function of the epididymis in the regressed hedgehog was found to be dependent upon the synergistic action of both testosterone and the gonadotrophic hormones.     

二乙酰二脱水卫矛醇对小鼠白血病L1210细胞增殖的影响

目的　研究二乙酰二脱水卫矛醇 (1 ,2 :5 ,6 dianhydro 3 ,4 diacetylgalactitol,DADAG)的抗脑白血病作用及机制。方法　用小鼠脑内移植瘤模型、MTT法、DNA掺入法、流式细胞仪和Westernblot法 ,观察DADAG对小鼠脑内移植瘤和体外白血病L1 2 1 0 细胞的作用 ,并探讨作用机制。结果　DADAG对DBA/ 2小鼠脑内移植白血病L1 2 1 0 有明显的抑制作用 ;对体外白血病L1 2 1 0 细胞同样有很强的抗增殖作用 ,其IC50 值为 2 4 6mg·L- 1 。DADAG不可逆地抑制L1 2 1 0 细胞内DNA的生物合成。DADAG 2 4mg·L- 1 处理L1 2 1 0 细胞 6h后 ,细胞发生G2 /M周期阻滞 ,2 4h后达最高峰。细胞周期素B1 蛋白水平在DADAG处理 2 4h后开始下降 ,而磷酸化的细胞周期依赖性激酶CDK1在DADAG处理 6h后开始上调 ,并呈时间依赖性。结论　DADAG的抗脑白血病作用与其抑制白血病细胞的增殖密切相关     

Clinical experience with the use of rhG‐CSF in secondary autoimmune neutropenia

This paper outlines the impact of granulocyte‐colony stimulating factor (G‐CSF) used as a single modality therapy in 17 patients with secondary autoimmune neutropenia (S‐AIN) who had been treated a multiple number of times previously. Fifteen of these patients had demonstrable antineutrophil antibodies and two had cellular S‐AIN with haemopoietic inhibitory T‐cells present in the marrow. Prior to treatment, all had had problems with infection. All patients responded within 7 days of commencement of treatment. Provided G‐CSF neutrophil counts were maintained above 1 × 10⁹/l, no further infections occurred. This was achievable by using G‐CSF administered as infrequently as once every 8 days. Eight of the 17 patients remained on G‐CSF, although five switched to the glycosylated form because of side‐effects. None have developed osteoporosis despite 47.29 patient years of total experience with G‐CSF. In conclusion both glycosylated and nonglycosylated G‐CSF can be used effectively in treating AIN on a long‐term basis.     

rhGM—CSF对小鼠口腔粘膜损伤的防治作用

目的：观察rhGM-CSF对TMX致实验性小鼠口腔粘膜损伤的疗效。方法：按随机分组原则将501只昆明种小白鼠分成8组，分别在相应时间给予不同药物（MTX，CF或rhGM-CSF）的处理因素，于第1－10天光镜下观察小鼠口腔粘膜的病理改变和积分情况。结果：IDMTX致口腔粘膜损伤病变率（45％－63％）和积分率（19．4％－56％）较其它组高，且死亡率很低（小于5％）；IDMTX＋GM0（或GM2）组的口腔粘膜损伤病变率（30．53％和30．99％）和积分率（19．47％和17．25％）比IDMTX组（55．56％和36．31％）明显减少，且溃疡严重程度较轻，二者相差显著（P＜0．01）。结论：IDMTX致小鼠口腔粘膜损伤模型可以用于粘膜损伤的研究；rhGM-CSF可以减少MTX致小鼠口腔粘膜损伤，并促进粘膜损伤恢复。     

兔精原干细胞培养及生物学特征的初步研究

目的:建立精原干细胞的培养方法并对培养细胞的生物学特征进行研究.方法:用饲养层和无饲养层两种方法培养幼家兔精原干细胞,在倒置相差显微镜下观察培养细胞的生长和形态变化,并对细胞的糖原、脂质及c-kit受体的细胞化学和免疫细胞化学染色结果进行分析.结果:成功的分离并培养幼家兔精原干细胞.在培养细胞中精原干细胞为主体细胞,并可见少量间质细胞.根据精原干细胞体积大小和形态特点,可分为大、小两种类型.PAS染色,精原干细胞胞质呈阳性反应;免疫细胞化学染色显示,体积较小的精原干细胞c-kit受体呈强阳性反应,体积较大的大精原干细胞呈弱阳性反应;间质细胞PAS染色和c-kit受体染色呈阴性反应,而脂质染色呈强阳性反应.精原干细胞培养无论有无饲养层,均能呈集落状生长,但有饲养层的培养,细胞的生长明显优于无饲养层培养.结论:青春期前的睾丸生精小管是精原干细胞最集中、数量最多,且容易获取分离的部位;精原干细胞的成功培养为今后重建完整的生精细胞系的治疗性移植和对这类定向干细胞的发育及分化潜能的研究提供了细胞模型.     

神经干细胞静脉移植治疗脊髓损伤的实验研究

[目的]观察神经干细胞静脉移植对损伤大鼠脊髓功能的治疗作用。[方法]取孕14—16dSD胎鼠的脑室下区组织，体外培养后鉴定细胞。制作脊髓全切模型，伤后1周将Brdu标记好的神经干细胞通过尾静脉注射移植到大鼠体内，移植后及8周行皮层体感诱发电位（CSEP）检测和BBB功能评分，并留损伤脊髓处作病理切片及免疫组化染色。[结果]（1）移植后8周BBB评分损伤组、移植组都有所恢复，但都未达到正常水平，移植组恢复较好；（2）模型制作后，CSEP波均消失，细胞移植后8周移植组的波形有不同程度的恢复，但潜伏期延长；（3）移植组大鼠脊髓损伤处存在大量Brdu染色阳性细胞，表明移植的细胞在体内可到达损伤脊髓处并能存活；脊髓损伤部位NF-200及GFAP染色阳性的细胞表明移植的细胞可以分化为具有神经元和胶质细胞特性的细胞。[结论]静脉移植的神经干细胞能到达损伤区代替受损的神经元及神经胶质细胞，使损伤的脊髓功能得到一定程度的恢复。     

Changes in immune regulation in response to examination stress in atopic and healthy individuals

BACKGROUND: Stress can aggravate the allergic inflammation, but determinants of disturbed immune regulation are largely unknown. OBJECTIVE: To determine systemic immunological, local inflammatory and functional airway responses to stress in healthy and atopic individuals. METHODS: Forty-one undergraduate students, 22 with allergy of whom 16 had asthma, and 19 healthy controls, were studied in a low-stress period and in association with a large exam. Subjects completed questionnaires on stress and health behaviours, underwent lung function tests, bronchial methacholine challenge, measurements of exhaled nitric oxide and urine cortisol. Blood cells were phenotyped, and cytokines from mononuclear blood cells were analysed. RESULTS: Perceived stress and anxiety increased in both groups during the exam period while cortisol increased only in the atopy group. Cytokine production decreased broadly in response to stress in both groups, which was paralleled by an increase in the proportion of regulatory T cells (CD4(+)CD45RO(+)CD25(bright)). Interestingly, atopic individuals, but not controls, reacted with a decreased T-helper type 1/T-helper type 2 (Th1/Th2) ratio and a decrease in natural killer (NK) cell numbers in response to stress. In control subjects only, exhaled nitric oxide decreased and forced expiratory volume in one second increased during stress. CONCLUSION: Atopic and non-atopic subjects shared some immune changes in response to stress, such as a dramatic decline in cytokines and an increase in the number of regulatory T cells in peripheral blood. However, other stress-induced immune changes were unique to atopic individuals, such as a skewed Th1/Th2 ratio and reduced NK cell numbers, indicating that some pathogenic mechanisms in atopics may be more strongly affected by stress than others.     

B cells as a target of immune modulation

B cells have recently been identified as an integral component of the immune system; they play a part in autoimmunity through antigen presentation, antibody secretion, and complement activation. Animal models of multiple sclerosis (MS) suggest that myelin destruction is partly mediated through B cell activation (and plasmablasts). MS patients with evidence of B cell involvement, as compared to those without, tend to have a worse prognosis. Finally, the significant decrease in new gadolinium-enhancing lesions, new T2 lesions, and relapses in MS patients treated with rituximab (a monoclonal antibody against CD20 on B cells) leads us to the conclusion that B cells play an important role in MS and that immune modulation of these cells may ameliorate the disease. This article will explore the role of B cells in MS and the rationale for the development of B cell–targeted therapeutics. MS is an immune-mediated disease that affects over 2 million people worldwide and is the number one cause of disability in young patients. Most therapeutic targets have focused on T cells; however, recently, the focus has shifted to the role of B cells in the pathogenesis of MS and the potential of B cells as a therapeutic target.     

Involvement of ADAM10 in axonal outgrowth and myelination of the peripheral nerve

The disintegrin and metalloproteinase 10 (ADAM10) is a membrane‐anchored metalloproteinase with both proteolytic and disintegrin characteristics. Here, we investigate the expression, regulation, and functional role of ADAM10 in axonal outgrowth and myelination of the peripheral nerve. Expression pattern analysis of 11 ADAM family members in co‐cultures of rat dorsal root ganglia (DRG) neurons and Schwann cells (SCs) demonstrated the most pronounced mRNA expression for ADAM10. In further studies, ADAM10 was found to be consistently upregulated in DRG‐SC co‐cultures before the induction of myelination. Neurons as well as SCs widely expressed ADAM10 at the protein level. In neurons, the expression of ADAM10 was exclusively limited to the axons before the induction of myelination. Inhibition of ADAM10 activity by the hydroxamate‐based inhibitors GI254023X and GW280264X resulted in a significant decrease in the mean axonal length. These data suggest that ADAM10 represents a prerequisite for myelination, although its activity is not required during the process of myelination itself as demonstrated by expression analysis of myelin protein zero (P0) and Sudan black staining. Hence, during the process of myelin formation, ADAM10 is highly upregulated and appears to be critically involved in axonal outgrowth that is a requirement for myelination in the peripheral nerve. © 2009 Wiley‐Liss, Inc.     

增生性瘢痕中血管内皮细胞生物学功能的研究

目的 探讨增生性瘢痕中血管内皮细胞的生物学功能及其与瘢痕形成的关系。方法 取人增生性瘢痕组织和正常皮肤组织，进行组织学观察。分离和纯化2种标本中的血管内皮细胞，应用酶联免疫吸附测定法分别检测单个血管内皮细胞中转化生长因子β1，（TGF-β1）、成纤维细胞生长因子2（FGF2）、血小板源性生长因子（PDGF）、内皮素1（ET-1）和血管内皮生长因子（VEGF）的水平。结果光学显微镜下可见正常皮肤微血管数目较少；增生性瘢痕微血管数目增多，血管狭长扭曲甚至闭塞。透射电镜可见增生性瘢痕中毛细血管管腔狭窄，有内皮细胞脱落。增生性瘢痕中血管内皮细胞分泌TGF-β1、PDGF、ET-1、VEGF、FGF2的水平分别为（60±8）、（30±4）、（0．12±0．03）、（52±5）、（18．1±1．2）μg／个细胞，明显低于正常皮肤（P〈0．05）。结论 增生性瘢痕中血管内皮细胞生物学功能减退，可能与瘢痕中胶原的大量产生和缺氧有关。