感染HCMV的腮腺导管上皮细胞CK和EMA丢失

目的 研究人类巨细胞病毒(HCMV)感染对腮腺导管上皮细胞表型产生的影响。方法 用免疫组化方法检测腮腺巨细胞包涵体病石蜡包埋组织中巨细胞病毒以及早期抗原、CK、EMA等的表达．结果 腮腺导管上皮细胞感染人巨细胞病毒后，作为上皮性标志物的CK和EMA表达呈阴性。结论 人巨细胞病毒感染腮腺导管上皮细胞使其CK和EMA丢失。单层上皮角蛋白网具有维持上皮细胞机械力学完整性的功能。     

人巨细胞病毒感染对腮腺导管上皮细胞角蛋白K8和K18表达的影响

目的 研究人巨细胞病毒(HCMV)感染对腮腺导管上皮细胞角蛋白K8和K18表达的影响.方法 用免疫组化方法研究腮腺巨细胞包涵体病(PCID)石蜡包埋组织中巨细胞病毒立即早期抗原和角蛋白K8、K18的表达.结果 PCID腮腺组织导管上皮出现包涵体巨细胞;包涵体巨细胞HCMV抗原DDG9/CCH2阳性;包涵体巨细胞角蛋白K8表达呈阴性,而K18表达呈强阳性.结论 HCMV感染腮腺导管上皮细胞诱发角蛋白K8降解,K18表达上调是一种反应性改变;单层上皮角蛋白网具有维持上皮细胞机械力学完整性的功能.     

结扎家兔胸导管诱发肝组织结构和功能的变化

目的 探讨胸导管结扎对肝组织结构和功能的影响.方法 选用10月龄家兔30只,随机分为两组(模型组20只和对照组10只).模型组家兔在膈脚处结扎胸导管,对照组家兔只是暴露胸导管,未结扎.对模型组和对照组的动物,取部分肝组织HE染色进行光镜观察,取部分肝组织制作电镜切片并观察;术前和术后6个月的实验动物,穿刺股静脉取血以检测肝功能.结果 肝功能结果显示,模型组家兔的总胆红素、直接胆红素和间接胆红素升高,总蛋白降低,清蛋白降低,球蛋白升高,谷草转氨酶(AST)和谷丙转氨酶(ALT)升高,和对照组相比其差异有统计学意义(P＜0.05).HE光镜观察模型组肝细胞内有大的脂滴,肝实质呈灶性、带状甚至整个肝小叶坏死.超薄组织切片透射电镜观察模型组,肝细胞内可见大小不等的脂滴,有的脂滴挤压细胞核,使之变形,肝细胞之间可见大量的胶原纤维.结论 胸导管结扎会导致肝脏形态结构和功能的变化.     

HCMV对涎腺导管上皮细胞组织蛋白酶D表达的影响

目的研究HCMV对涎腺导管上皮细胞组织蛋白酶D表达的影响。方法用免疫组化方法研究腮腺巨细胞包涵体病(PCID)石蜡包埋组织中组织蛋白酶D的表达;用Westernblot法研究HCMV感染对体外培养的涎腺导管上皮细胞组织蛋白酶D表达的影响;用半定量RT-PCR法研究HCMV对体外培养的涎腺导管上皮细胞组织蛋白酶D转录水平的影响。结果 PCID组织包涵体巨细胞组织蛋白酶D表达呈阳性。HCMV感染体外培养的涎腺导管上皮细胞0～96h,组织蛋白酶D前体和有活性的重链组织蛋白酶D缓慢上调但一直保持在正常水平以下;有活性的单链组织蛋白酶D很快上调,而且在96h达到正常水平的1.91倍;导管上皮细胞组织蛋白酶D的mRNA水平和蛋白水平呈反向平行关系。结论 HCMV可诱导涎腺导管上皮细胞活性单链形式组织蛋白酶D的表达上调。     

不同药物诱导小鼠胸腺萎缩模型的对比研究

目的:对比研究地塞米松、氢化可的松、聚肌胞苷酸以及苯甲酸雌二醇分别诱导的小鼠胸腺萎缩模型.方法:将55只雌性ICR小鼠分为5组,除对照组外分别给予地塞米松磷酸钠、氢化可的松、聚肌胞苷酸与苯甲酸雌二醇建立模型.观察其胸腺指数、脾脏指数、血细胞变化、血浆中MDA与GST水平、胸腺病理学检测、胸腺细胞凋亡以及相关蛋白的表达情...     

聚肌胞苷酸及地塞米松诱导的胸腺萎缩及胸腺RLR 信号通路表达的比较研究

目的:比较聚肌胞苷酸Poly(I:C)、地塞米松(DEX)对小鼠胸腺的影响和RLR 通路的改变,为研究病毒感染导致胸腺受损的机制,选择合适的动物模型提供实验依据。方法:将24 只8 周龄C57BL/6 小鼠随机分组,分别给予Poly(I :C)、DEX 及生理盐水。观察胸腺指数、胸腺组织学变化、外周血中T 细胞受体重排删除环(TRECs)的含量以及初始型CD4+ T细胞的比例,并检测胸腺组织RLR/ MAVS/ IFN-α/ β通路的表达情况。结果:Poly(I;C)和DEX 都可以导致胸腺萎缩和组织结构破坏,DEX 组更严重且皮质区细胞减少更为明显。两组的TRECs 均下降。Poly(I :C)组的初始型CD4+ T 细胞有增加趋势;而DEX 组的CD4+ T 细胞初始/ 记忆亚群比例改变不明显。DEX 组RIG-Ⅰ、MDA5、LGP2 和IFN-α/ β表达上调明显;而Poly(I:C)组虽略有上调、但无统计学意义。结论:两种造模方法均可诱导胸腺功能受损。DEX 诱导的胸腺损伤更严重且伴有RLR---Ⅰ型IFN 通路的大幅上调;而在Poly(I:C)组该通路仅轻微上调。     

胸导管结扎对大鼠脂质代谢和胰组织结构的影响

目的:探讨胸导管结扎对脂质代谢的影响,揭示淋巴回流障碍诱发胰组织的显微和超微结构变化.方法:SD大鼠随机分为假手术对照组和结扎胸导管模型组.术后6个月取静脉血标本进行血脂检测;部分胰组织标本,H-E和刚果红染色光镜观察;部分胰组织进行透射电镜观察.结果:(1)模型组大鼠游离脂肪酸和甘油三酯浓度明显下降,胆固醇浓度无显著变化.(2)光镜观察显示模型组大鼠的胰腺小叶间隙增宽,脂肪堆积和淋巴管扩张.(3)透射电镜观察显示模型组大鼠的胰岛细胞间隙增宽,细胞间隙及细胞内可见大量脂滴样物质、红细胞和胶原原纤维样结构.结论:胸导管结扎可引起胰腺结构变化和影响胰腺的内、外分泌功能.     

组织工程皮肤预防腮腺切除术后并发症的荟萃分析

目的 采用荟萃分析的方法评价组织工程皮肤(TES)预防腮腺切除术后并发症的有效性和安全性.方法 系统检索相关中英文数据库,包括CENTRAL(the Cochrane Central Register of Controlled Trials)、PubMed、EMBASE、中国期刊全文数据库(CNKI)、中国生物医学文献数据库(CBM)、中文科技期刊全文数据库(VIP)、万方数字化期刊全文数据库(Wanfang)等,筛选出符合要求的25个随机对照试验,评价方法学质量并提取数据,对味觉出汗综合征(GSS)等腮腺切除术后并发症进行荟萃分析.结果 荟萃分析结果显示,与术后直接缝合相比,应用TES可以使GSS客观发生率降低84％[ RR=0.16,95％CI(0.13 ～ 0.21),P＜0.01]、GSS主观发生率降低86％ [RR=0.14,95％C/(0.10 ～ 0.19),P＜0.01];可以有效降低涎漏的发生[RR=0.23,95％CI(0.10 ～ 0.53),P＜0.01],有效改善面部凹陷畸形[RR=0.42,95％CI(0.18～0.95),P=0.04];有降低暂时性面神经麻痹发生率和增加血清积液发生率的趋势,但差异无统计学意义(均P＞0.05).结论 现有证据表明,使用TES可以有效预防腮腺切除术后GSS、面部凹陷畸形及涎漏的发生.     

M3受体激动剂诱导大鼠腮腺细胞内AQP5和脂质筏的核转位

<正>水通道蛋白5(aquaporin,AQP5)存在于唾液腺腺泡细胞内,对调节水分转运速率和维持唾液分泌具有重要作用,AQP5功能失调会导致如增龄性口干、头面部放疗口干症、SS综合征和糖尿病口腔干燥等相关疾病的发生[1]。研究表明,M3毒蕈碱乙酰胆碱受体(M3 muscarinic acetylcholine receptor,M3-m AChR)激动剂西维美林(cevimeline)可以诱导     

敲减TLR4表达减少LPS诱导的胰腺腺泡AR42J细胞分泌炎症因子

目的:研究Toll样受体4(TLR4)对脂多糖(LPS)诱导的胰腺腺泡AR42J细胞分泌炎症因子的影响。方法:用LPS处理大鼠胰腺腺泡AR42J细胞,real-time PCR和Western blot测定细胞中TLR4表达的变化。将携带TLR4 siRNA的慢病毒感染AR42J细胞,给予LPS处理,real-time PCR和Western blot检测干扰效率,MTT法检测细胞活力,二硝基苯肼法测定乳酸脱氢酶(LDH)的漏出率,ELISA法检测细胞分泌白细胞介素1β(IL-1β)和肿瘤坏死因子α(TNF-α)的水平,硫代巴比妥酸法测定上清中丙二醛(MDA)的含量,用黄嘌呤氧化法测定上清中超氧化物歧化酶(SOD)活力,比色法检测谷胱甘肽过氧化物酶(GSH-Px)和过氧化氢酶(CAT)的活性。结果:LPS处理后的AR42J细胞中TLR4的mRNA和蛋白水平明显升高(P0.01)。携带TLR4 siRNA的慢病毒可以明显下调LPS刺激下AR42J细胞中TLR4的mRNA和蛋白水平(P0.01)。LPS处理后的AR42J细胞活力降低,LDH漏出率升高,细胞分泌的IL-1β和TNF-α增多,培养上清中MDA含量升高,SOD、GSH-Px和CAT活性降低(P0.01)。敲减TLR4表达可以提高LPS刺激下AR42J细胞的活力,降低细胞的LDH漏出率及分泌IL-1β和TNF-α的水平,减少细胞培养液中MDA的含量,提高SOD、GSH-Px和CAT的水平(P0.01)。结论:LPS诱导胰腺腺泡AR42J细胞TLR4表达,敲减其表达可以减少LPS诱导的AR42J细胞分泌IL-1β、TNF-α等炎症因子,减轻氧化损伤。     

Polyamine metabolism in rat parotid gland after duct ligation

Parotid ducts were ligated unilaterally in rats for periods from 6 h to 5 months. A slight increase in gland weight was observed during the first 24 h; thereafter, the weight gradually fell, being less than 50% of controls at 5 months. The activity of the putrescine-forming enzyme, ornithine decarboxylase (ODC), increased with peak values by 3 days and 3 weeks. However, the putrescine content had already reached its highest value by 24 h. A notably marked reduction of spermidine and spermine contents was observed by 1 day after ligation and throughout the whole time of observation. The results suggest that an inverse polyamine metabolism occurred, that is, spermine converts to spermidine which in turn converts to putrescine.     

Cell death and cell proliferation during atrophy of the rat parotid gland induced by duct obstruction

Rat parotid gland atrophy after unilateral duct ligation was studied by light and electron microscopy. Death of secretory acinar cells, which took the form of apoptosis, resulted in their complete disappearance within 5 days. The remnants of the dying cells were mostly phagocytosed and degraded by macrophages within the glandular epithelium; a few were taken up by adjoining epithelial cells. The acinar cell deletion was accompanied by increased mitosis of striated and intercalated duct epithelial cells. However, over many weeks, there was enhanced apoptosis of duct cells, which eventually led to marked shortening of intercalated ducts. Apoptosis of capillary endothelial cells was observed and may account for the reduction in the capillary bed known to accompany gland atrophy. The end-stage lesion comprised small numbers of ducts in a condensed stroma. Compensatory hyperplasia, involving proliferation of duct and acinar cells, was demonstrated in the contralateral glands.     

Sarcomatoid salivary duct carcinoma of the parotid gland

Salivary duct carcinoma (SDC) is a high-grade neoplasm known to histologically resemble high-grade ductal carcinoma in situ of the breast. We describe 3 cases of sarcomatoid salivary duct carcinoma, a heretofore unreported variant of SDC. Each case was a composite of SDC and sarcomatoid carcinoma and histologically similar to reported cases arising in the breast. The clinicopathologic features, including immunohistochemistry, of 3 cases were investigated. In the 3 men, ages 56, 68, and 70 years, the resected parotid tumors measured 1.5, 3.5, and 1.5 cm, respectively. Only the 3.5-cm tumor extended beyond the parotid gland into soft tissue. This patient died at 3 years with pulmonary metastases. The other patients were free of disease at 6 and 12 months. Histologically, each case was a composite of usual-type SDC and sarcomatoid carcinoma. SDC showed typical cribriform architecture, whereas anaplastic, spindled cells constituted the sarcomatoid areas. Immunohistochemically, epithelial elements stained as follows: cytokeratin (AE1/AE3 & CAM 5.2) positive in 3 of 3 cases, EMA positive in 3 of 3 cases, vimentin negative in 3 of 3 cases, desmin negative in 3 of 3 cases, c-erbB-2 positive in 1 of 2 cases. Sarcomatoid elements stained as follows: AE1/AE3 negative in 3 of 3 cases, CAM 5.2 rare positive cell in 1 of 3 cases, EMA focally positive in 3 of 3 cases, vimentin positive in 3 of 3 cases, desmin negative in 3 of 3 cases, c-erbB-2 negative in 2 of 2 cases. Electron microscopy, performed in one case, showed scattered junctional complexes congruent with epithelial differentiation. Immunohistochemical results, EMA and CAM 5.2 positivity, and ultrastructural findings supported our belief that these unique biphasic tumors represented SDC with sarcomatoid carcinoma. We conclude an element of sarcomatoid carcinoma rarely may arise in association with SDC, and it is erroneous to diagnose such tumors as "carcinosarcoma."     

Salivary duct carcinoma in situ of the parotid gland

Aims: To describe three cases of purely in situ salivary duct carcinoma, so as better to define the entity. Methods and results: Three primary tumours of the parotid gland are presented, in each case composed of cysts and ducts and lined by high nuclear grade epithelial cells. All parts of each tumour were surrounded by a myoepithelial cell rim and there was no evidence of invasion. The tumour cells expressed immunohistochemical markers seen in invasive salivary duct carcinoma of usual (high‐grade) type. In two cases the androgen receptor (AR) reaction was strong, but there was no immunohistochemical expression of HER2 protein or gene amplification by in situ hybridization. In the remaining case, fewer nuclei stained for AR, but both HER2 protein and gene amplification were demonstrated. Conclusions: Salivary duct carcinoma in situ is morphologically similar to breast ductal carcinoma in situ and, although our cases are few, salivary duct carcinoma in situ can possibly be subdivided into luminal and non‐luminal cell types, as can analogous mammary neoplasms. The present study cannot determine whether low‐grade cribriform cystadenocarcinoma, architecturally similar but immunohistochemically different, is part of the spectrum of salivary duct carcinoma in situ, or whether it represents a separate entity.     

Acinar degranulation in the rat parotid gland induced by neuropeptides

Vasoactive intestinal peptide (VIP, 4 microg kg(-1) min(-1)), substance P (3 microg kg(-1) min(-1)) and neurokinin A (2.5 microg kg(-1) min(-1)) were infused intravenously for 30 min in anaesthetized rats and the effects of these peptides on the parotid gland were examined. VIP reduced the numerical density of parotid acinar secretory granules, storing proteins, by 29 % and the glandular amylase activity by 33 %. Substance P reduced the number of secretory granules by 18 % but the amylase activity was unchanged. These results make VIP and substance P likely contributors to the parasympathetic non-adrenergic, non-cholinergic (NANC)-evoked parotid acinar degranulation. Neurokinin A, on the other hand, caused no reduction in granular number but reduced the glandular amylase activity by 19 %, indicating vesicular protein secretion.     

Aggressive invasive micropapillary salivary duct carcinoma of the parotid gland

The presence of invasive micropapillary component has been reported to be associated with salivary duct carcinoma and poor outcomes. Herein is described a rare case of invasive micropapillary salivary duct carcinoma of the parotid gland in a 60-year-old man. The micropapillary component was approximately 70% of the area of the tumor. Squamous differentiation was focally seen adjacent to the micropapillary component. On immunohistochemistry the ordinary salivary duct carcinoma component was positive for gross cystic disease fluid protein-15 (GCDFP-15), androgen receptor (AR), and HER2/neu, whereas both micropapillary and squamous components were negative for GCDFP-15 and AR. Immunohistochemical staining for D2-40 highlighted the lymph vessel invasion of tumor cells. This patient developed metastases in the lymph nodes of the neck, and also in the liver, lung, and brain. The lymph nodes and liver metastases had both ordinary salivary duct carcinoma and micropapillary components. The patient died of tumor 11 months after the initial surgical operation. The results support that the presence of micropapillary component is associated with more aggressive behavior of salivary duct carcinoma. It is also important for pathologists to recognize that GCDFP-15 and AR expression can be reduced in micropapillary carcinoma in the differential diagnosis of metastatic tumor.     

Crystalloids in salivary duct cysts of the human parotid gland

Summary Crystalloids found in salivary duct cysts of the human parotid gland were examined by scanning electron microscopical observations with electron probe X-ray microanalysis. The cystic spaces were filled with numerous crystalloids which had a variety of forms with slight eosinophilic and glassy appearance. Scanning electron microscopically, crystalloids were hexagonal and rhombohedral in shape, and cutting the surface showed a polycyclic structure or regular parallel lamination. By electron probe X-ray microanalysis, sulphur was the only detected element. The present study suggests that crystalloids resulted from deposition from supersaturated saliva containing sulphur containing compounds into the cystic lumen or into epithelial cytoplasm.     

Postnatal development of the duct system in the mouse parotid gland

The morphology of the parotid gland in adult mice is mouse strain-specific. C57BL/6 and C3H/He strains of mouse are representatives of two types of the morphology identified previously. The postnatal development of such morphologic differences was investigated by sialography of excised glands of these strains of mouse. It was observed that the mouse strain-dependent morphological characteristics were already present at birth, except for the branching pattern of the peripheral duct system, which became differentiated at 3 weeks of age. These results indicate that the C3H/He mouse-specific branching pattern of the peripheral ducts reflects the profile of matured secretory units and ducts, and that the C57BL/6 mouse-specific pattern resembles that of an immature C3H/He mouse.     

Salivary duct carcinoma of the parotid gland: the cytohistological features

A 62-year-old man presented with rapidly growing tumour in the right parotid region with associated pain and facial nerve palsy. Based on the fine needle aspiration cytology report of high-grade mucoepidermoid carcinoma, parotidectomy was performed which showed features of salivary duct carcinoma. The smears were reviewed to identify the potential pitfalls in the cytological diagnosis of salivary duct carcinoma.