瑞芬太尼复合丙泊酚麻醉在经眶上锁孔入路切除鞍区巨大肿瘤中的应用

目的:探讨瑞芬太尼复合丙泊酚静脉麻醉在经眶上锁孔入路切除鞍区巨大肿瘤中的应用。方法:42例鞍区巨大肿瘤均行经眶上锁孔入路切除手术,随机分为2组,A组行瑞芬太尼复合丙泊酚持续泵注维持麻醉;B组行芬太尼复合丙泊酚持续泵注维持麻醉。分别记录2组平均动脉压、心率、呼气末二氧化碳分压、苏醒参数(睁眼时间、自主呼吸恢复时间、拔管时间)及术后并发症情况。结果:2组患者的麻醉过程平稳,均能顺利完成手术,麻醉效果满意。无1例术后出现麻醉相关并发症。但A组在插管后和拔管后血压、心率的变化小于B组(P<0.05);各项苏醒参数也优于B组(P<0.05)。结论:与芬太尼比较,瑞芬太尼复合丙泊酚静脉麻醉,诱导时间更短,麻醉维持期血流动力学更稳定,清醒快而完全,更适于经眶上锁孔入路鞍区巨大肿瘤切除手术。     

PTTG 在垂体腺瘤各亚型中的表达与分析

目的:研究PTTG与垂体瘤的各亚型的相关性.方法:用免疫组化方法检测92例垂体肿瘤病人PTTG.其中29例GH,20例PRL,10例ACTH,11例FSH/LH,9例TSH和13例无功能腺瘤.结果:PTTG在细胞质内显著表达,各亚型中GH型是表达最高,PRL腺瘤表达最低,各亚型的阳性表达率与PRL亚型阳性表达率对比均有统计学意义.结论:重体腺瘤不同垂体亚型中PTTG的表达阳性率及表达强度不同,PTTG检测,可为早期诊断垂体腺瘤( GH、PRL、ACTH、FSH/LH、TSH)亚型和无功能型提供参考.     

单鼻孔-蝶窦入路显微切除垂体腺瘤

目的探讨单鼻孔-蝶窦入路显微切除垂体腺瘤的临床意义。方法回顾性分析鼻-蝶窦显微入路切除垂体腺瘤50例的治疗效果。结果肿瘤全切除35例,次全切除11例,大部分切除4例。术后脑脊液漏5例,尿崩症12例,术后临床症状均有不同程度改善,无死亡病例。结论鼻-蝶窦入路显微切除垂体腺瘤具有创伤小、风险低、术后并发症少、费用低等特点,是目前垂体腺瘤切除术的首选治疗方法。     

垂体大腺瘤1.5T MR扩散加权成像的参数优化

目的探讨在1.5T MR上应用头线圈进行垂体大腺瘤扩散加权成像（DWI）的可行性,并优化序列参数,探索理想的层厚和b值。方法随机选取15名健康志愿者及15例垂体大腺瘤患者,测定b值分别为300、800、1200s/mm2时的信号强度、背景噪声及垂体瘤的表观扩散系数（ADC）值。比较不同b值时正常垂体的信号强度、质量指数及信噪比的差异;同一b值时垂体大腺瘤平均ADC值的差异。结果 （1）正常垂体DWI图像各b值时的信号强度随b值增加而显著降低（P〈0.01）,而噪声则与b值无关（P〉0.05）;（2）b=800s/mm2时,垂体大腺瘤的平均ADC值为（1.032±0.059）×10^-3mm^2/s,正常垂体平均ADC值为（4.025±0.382）×10^-3mm^2/s,两者差异有统计学意义（P〈0.05）;（3）b=800s/mm^2时,层厚3、4mm对垂体瘤显示评分明显高于2mm（P〈0.05）,层厚4mm时图像伪影比3mm和2mm明显（P〈0.05）。结论 1.5T MR行垂体大腺瘤DWI是可行的。以层厚3mmb值为800s/mm2的图像质量为佳。     

重组人类肝细胞生长因子对胶质瘤C6细胞垂体瘤转化基因的影响

目的探讨重组人类肝细胞生长因子（rhHGF）对胶质瘤细胞垂体瘤转化基因（PTTG）的影响。方法体外培养胶质瘤C6细胞,给予不同浓度的rhHGF（0、10、20、30μG/L）,半定量逆转录聚合酶链式反应（RT-PCR）检测PTTGmRNA表达,Western blot检测P1TG蛋白表达。结果不同浓度rhHGF作用后C6细胞PTFGmRNA表达与蛋白水平均增高,且随着浓度的增加,其升高越明显,各组间差异有统计学意义（P〈0．01）。结论rhHGF可上调PTTG的表达,且呈剂量依赖性。     

17β‐estradiol regulation of the mRNA expression of t‐type calcium channel subunits: Role of estrogen receptor α and estrogen receptor β

Low‐voltage‐activated (T‐type) calcium channels are responsible for burst firing and transmitter release in neurons and are important for exocytosis and hormone secretion in pituitary cells. T‐type channels contain an α1 subunit, of which there are three subtypes, Cav3.1, ‐3.2, and ‐3.3, and each subtype has distinct kinetic characteristics. Although 17β‐estradiol (E2) modulates T‐type calcium channel expression and function, little is known about the molecular mechanisms involved. We used real‐time PCR quantification of RNA extracted from hypothalamic nuclei and pituitary in vehicle and E2‐treated C57BL/6 mice to elucidate E2‐mediated regulation of Cav3.1, ‐3.2, and ‐3.3 subunits. The three subunits were expressed in both the hypothalamus and the pituitary. E2 treatment increased the mRNA expression of Cav3.1 and ‐3.2, but not Cav3.3, in the medial preoptic area and the arcuate nucleus. In the pituitary, Cav3.1 was increased with E2 treatment, and Cav3.2 and ‐3.3 were decreased. To examine whether the classical estrogen receptors (ERs) were involved in the regulation, we used ERα‐ and ERβ‐deficient C57BL/6 mice and explored the effects of E2 on T‐type channel subtypes. Indeed, we found that the E2‐induced increase in Cav3.1 in the hypothalamus was dependent on ERα, whereas the E2 effect on Cav3.2 was dependent on both ERα and ERβ. However, the E2‐induced effects in the pituitary were dependent on only the expression of ERα. The robust E2 regulation of T‐type calcium channels could be an important mechanism by which E2 increases the excitability of hypothalamic neurons and modulates pituitary secretion. J. Comp. Neurol. 512:347–358, 2009. © 2008 Wiley‐Liss, Inc.     

Expression of neurotensin and its receptors in pituitary adenomas

The neurotensin (NT) produced in the hypothalamus and in pituitary gonadotrophs and thyrotrophs participates in neuroendocrine regulation. Recently, the involvement of this peptide in normal and neoplastic cell proliferation has been postulated. In the present study, we evaluated the expression of NT and its receptors (NTR1, 2 and 3) in a series of 50 pituitary adenomas [11 growth hormone (GH)-, eight prolactin (PRL)-, four adrenocorticotrophic hormone (ACTH)- and 27 nonfunctioning adenomas]. NT mRNA expression was significantly higher in functioning compared to nonfunctioning adenomas and with normal pituitary. Nonfunctioning pituitary adenomas showed lower expression of NT mRNA than normal pituitary. In the immunohistochemical study of functioning adenomas, NT was colocalised with GH, PRL and ACTH secreting cells. In nonfunctioning adenomas, the NT immunoreactivity intensity was variable among the samples. NTR3 mRNA expression was observed in all examined samples and was higher in the adenomas, both functioning and nonfunctioning, compared to normal pituitary. By contrast, NTR1 and NTR2 mRNA were not detected in either pituitary adenomas or normal tissue. The higher expression of NTR3, as well as the expression of NT by tumoural corticotrophs, lactotrophs and somatotrophs, which are cells types that do not express this peptide in the normal pituitary, suggests that NT autocrine and/or paracrine stimulation mediated by NTR3 may be a mechanism associated with the tumourigenesis of functioning adenomas.     

Ghrelin induces growth hormone secretion via a nitric oxide/cGMP signalling pathway

The presence of ghrelin and its receptor, growth hormone (GH) secretagogue receptor, in the hypothalamus and pituitary, and its ability to stimulate GH release in vivo and in vitro, strongly support a significant role for this peptide in the control of somatotroph function. We previously demonstrated that ghrelin elicits GH secretion directly in somatotrophs by activating two major signalling cascades, which involve inositol phosphate and cAMP. In as much as nitric oxide (NO) and its mediator cGMP have been recently shown to contribute substantially to the response of somatotrophs to key regulatory hormones, including GH-releasing hormone, somatostatin and leptin, we investigated the possible role of this signalling pathway in ghrelin-induced GH release in vitro. Accordingly, cultures of pituitary cells from prepuberal female pigs were challenged with ghrelin (10(-8) m, 30 min) in the absence or presence of activators or blockers of key steps of the NO synthase (NOS)/NO/guanylate cyclase (GC)/cGMP route and GH secretion was measured. Two distinct activators of the NO route, S-nitroso-N-acetylpenicillamine (SNAP) (5 x 10(-4) m) and L-arginine methyl ester hydrochloride (L-AME) (10(-3) m), comparably stimulated GH secretion when applied alone. The presence of L-AME enhanced ghrelin-stimulated GH secretion, whereas SNAP did not alter its effect. Conversely, two different NOS/NO pathway inhibitors, N(w)-nitro-L-arginine methyl ester hydrochloride (10(-5) m) or haemoglobin (20 microg/ml), similarly blocked ghrelin-induced (but not basal) GH release, thus indicating that NO contributes critically to ghrelin action in somatotrophs. Moreover, incubation with a permeable cGMP analogue, 8-Br-cGMP (10(-8) m) stimulated GH secretion, but did not modify the stimulatory action of ghrelin, suggesting that cGMP could mediate the action of NO. Indeed, inhibition of GC by 10 microm LY-53,583 did not alter basal GH secretion but abolished the GH-releasing action of ghrelin. Taken together, our results provide novel evidence indicating that ghrelin requires activation of the NOS/NO route, and its subsequent GC/cGMP signal transduction pathway, as necessary steps to induce GH secretion from somatotrophs.     

Olfactory sensory neuron-specific and sexually dimorphic expression of protocadherin 20

Olfactory sensory axons navigate from the nasal cavity to the olfactory bulb and sort from among 1,000 different odorant receptor-expressing types to converge upon the same two or three glomeruli. To achieve this task during development, it is likely that multiple classes of regulatory molecules, including cell adhesion molecules, are involved. Cell adhesion molecules have been shown to be important in controlling axon guidance, fasciculation, and synapse formation. To gain further understanding of the involvement of adhesion molecules in olfactory circuitry development, we examined the dynamic and cell type specific expression of a novel protocadherin, PCDH20, in the olfactory system. PCDH20 is specifically expressed in newly differentiated olfactory sensory neurons and their axons during development. PCDH20 expression is down-regulated in the adult olfactory system, except in a small olfactory sensory neuron population. These small, discrete numbers of PCDH20-positive glomeruli in the adult olfactory bulb are consistently clustered in the ventral-caudal region in both male and female mice. However, adult males have higher numbers of PCDH20-positive glomeruli with a broader distribution, whereas adult females have fewer PCDH20-positive glomeruli with a more restricted distribution. The gender difference in PCDH20 expression may reflect olfactory receptor expression differences for gender-specific social discrimination.     

Corticotropin-releasing factor test in melancholic patients in depressed state versus recovery: a comparative study

PURPOSE: Basal adrenocorticotropin hormone (ACTH) and cortisol levels and their response to corticotropin-releasing factor (CRF) test were studied in melancholic depressive patients in depressed state and recovery, and compared with healthy controls. METHODS: Fifty-four outpatients diagnosed with unipolar depressive disorder with melancholic features according to DSM-IV and 23 healthy controls were included in the study. The Structured Clinical Interview for DSM-IV (SCID-IV) was used for diagnosis. Twenty-nine patients were in recovery, while 25 were in depressed state at the moment of the administration of the CRF test. FINDINGS: No differences were found between the recovered and depressed groups with respect to CRF test. Lower ACTH and higher cortisol levels with significant differences were shown in the neuroendocrine variables at 15, 30, and 60 min, and in peak response and increase, in the ACTH and cortisol response curves to CRF challenge between the groups of melancholic patients, both recovered and depressed, compared with the healthy control subjects. Moreover, recovered and depressed melancholic patients had a higher whole cortisol area under the curve with significant differences than the healthy control subjects. CONCLUSIONS: The crossover clinical status at the moment of the CRF test doesn't differentiate changes in the HPA axis in melancholic patients, while we did find significant differences in the group of healthy controls in comparison with the groups of melancholic patients both in depressive state and recovery. This supports the hypothesis that hypothalamic pituitary adrenal (HPA) axis shows alterations that remain in depressive patients even after recovery.