Morphology of bacterial flora in root canals associated with apical abscesses

Background Apical abscess is an inflammatory process in the peri-radicular tissues caused by biofilms in the necrotic root canal systems. Therefore, a comprehensive analysis of the bacterial colonization is required for a better understanding of the pathogenesis. This study aimed to investigate the patterns of bacterial infection of root canals of teeth with apical abscesses and to determine whether histological and microbiological findings correlated with clinical conditions. Methods Eighteen samples from 18 teeth with apical pathological lesions were analyzed. Nine patients with acute apical abscesses experienced severe pain, and nine patients were asymptomatic with a sinus tract. After extraction, each affected root was divided into two halves. One half was processed for histobacteriologic analysis and examined using light microscopy, and the other half was analyzed using scanning electron microscopy （SEM） to determine the patterns of microbial colonization of the root canals. Results The appearance of each sample subjected to SEM was consistent with the histobacteriologic findings despite the presence or absence of clinical symptoms. Intraradicular biofilms comprising cocci, rods, and/or filaments of amorphous materials were observed in the apical third of the main root canals in all samples. The bacterial biofilms covering the main root canal walls also penetrated the dentinal tubules to varying depths. The morphologies of biofilms varied, and a unique pattern of intraradicular infection was not identified. Conclusion Intraradicular infections formed complex and variable multispecies biofilms and their presence did not correlate with clinical symptoms.     

Point Mutation in the Parkin Gene on Patients with Parkinson''''s Disease

Summary;To investigate the distribution of possible novel mutations from parkin gene in variant sub-set of patients with Parkinson’s disease(PD)in China and explore whether parkin gene plays an im-portant role in the pathogenesis of PD,70 patients were divided into early-onset group and late-onsetgroup; 70 healthy subjects were included as controls.Genomic DNA from 70 normal controls andfrom those of PD patients were extracted from peripheral blood leukocytes by using standard proce-dures.Mutations of parkin gene(exon 1—12)in all the subjects were screened by PCR-single strandconformation polymorphism(SSCP),and further sequencing was performed in tue samples with ab-normal SSCP results,in order to confirm the mutation and its location.A new missense mutationGly284Arg in a patient and 3 abnormal bands in SSCP electrophoresis from samples of another 3 pa-tients were found.All the DNA variants were sourced from the samples of the patients with early-on-set PD.It was concluded that Parkin point mutation a     

Experimental study on dynamic regulation of acetylcholine in striatum of rat parkinson disease model and behavior observation

In order to explore the role of acetylcholine in the pathogenesis of Parkinson’s disease (PD),the changes in the concentration of acetylcholine (Ach) in the striatum,the apoptosis of substantia nigra cells,the ultrastructure and the changes of Nissl cells in rats during the morbidity of PD,and the corresponding behaviors in rats with PD were observed.Rat PD model was established by using the modified Thomas method.Eighty-one rats were randomly divided into normal control,sham operation and PD groups and their behavior features were observed at post-operative day (POD) 7,14 and 21 as three subgroups (n=9 each).The concentration of Ach in the striatum was determined by using high-performance liquid chromatography.The apoptosis of substantia nigra cells was assayed by using TUNEL method.The ultrastructural changes in the substantia nigra were observed under the electron microscopy,and the survival of neurons in the substantia nigra area was examined by using Nissl staining.In PD group at POD 7 to 21,the damage in the substantia nigra area was gradually aggravated,the concentration of Ach,apoptosis rate and turns of rotation were gradually increased,and the number of Nissl cells was gradually reduced over the time as compared with the normal control and sham operation groups (all P<0.05).It was concluded that there exist dynamic changes in Ach concentration,ethology and apoptosis of the substantia nigra cells during the morbidity of PD,suggesting the contribution of apoptosis to the morbidity of PD,and critical role of Ach in the pathogenesis of PD.     

Lipoprotein glomerulopathy: clinical features and pathological characteristics in Chinese

Background Lipoprotein glomerulopathy (LPG), once recognized as a rare glomerular disease, has been reported around the world in recent years. In this study, we reported 8 patients of LPG and aimed to explore the clinical features and pathological characteristics of LPG under light microscope, immunofluorescence staining, and electron microscope.Methods Clinical manifestations were recorded on the day of renal biopsy. Biochemical patterns of lipids and lipoproteins were detected by routine examination. Plasma concentrations of apo B and apo E were determined by radial immunodiffusion assays. Biopsy specimens were then processed for lightmicroscopy, immunohistochemical staining for immunoglobulins and complement components, and electron microscopy. Glomerular deposition of apo A, B, and E were detected using monoclonal antibodies on cryostatic sections.Results All of the eight patients presented with edema, microscopic hematuria, severe proteinuria,anemia, and enlarged kidney size. Biochemical profiles revealed high levels of triglycerides, apo B,and apo E. We noted increments of glomerular size and lipoprotein thrombi occupying capillary lumina in the glomeruli of all patients. Immunofluorescence staining showed that the thrombi were strongly positive for apo A, B, and E. Granules and various sizes of vacuoles were observed in the thrombi under electron microscope.Conclusion Compared with previous reports on LPG in other countries, unique clinical and pathological features were found in this group of Chinese LPG patients.     

Clinicopathologic and ultrastructural observation of primary pulmonary cryptococcosis:a study of 37 cases

Objective To investigate the pathologic diagnosis and ultrastructure features of primary pulmonary cryptococcosis (PC). MethodsRetrospective analysis was made on 37 cases of PC with histochemical stain and light microscopy observations. Transmission electron microscopy was performed on 19 cases. ResultsThree of 37 cases were confirmed by fine needle aspiration biopsy while the other 34 patients by open-chest exploratory operation.Pathologic findings: cryptococcosis neoformans (CN) were detected in all cases,2 with gelatinous lesions and 35 non-casating granuloma. The revealing rate of CN with the mucicarmine stain(MC),periodic acid-Schiff stain(PAS), alcian blue (AB) and Grocott methenamine-silver (GMS) was 85.2% (23/27), 97.3% (36/37), 64.9% (24/37) and 96.3% (26/27), respectively. All CNs detected by transmission electron microscopy had capsules and most of them possessed simple structure with undeveloped cellular organelles and cell cataplasia. Some CNs had cellular nucleus, nucleoli, mitochondria and vacuoles. The detective rate of CNs by transmission electron microscope was 89.5 % (17/19). ConclusionAbsent of specific clinical manifestations and radiographic features, fine needle aspiration biopsy and open biopsy remain the chief approaches in the diagnosis of PC. It could be further helpful by using light microscopy and transmission electron microscopy to make definitive diagnosis and differential diagnosis as well as MS, GMC and PAS histochemical staining.     

TRANSFORMING GROWTH FACTOR-β AND FIBROBLAST GROWTH FACTOR INDUCE LENS EPITHELIAL EXPLANT METAPLASIA： IMPLICATIONS FOR THE FORMATION OF SUBCAPSULAR OPACIFICATION

Objective. This study was to investigate the effects of transforming growth factor-β(TGFβ) and fibroblast growth factor (FGF) in the subcapsular opaeification formation of the lens. Methods. Lens epithelial explants from 10-day-old rats were cultured with TGFβ1 or TGFβ2 in the presence of FGF for 5 days, then were examined by light and electron microscopy, and by immunolocalization of α-smooth muscle(α-sm) actin and type Ⅰ collagen. Resets. In TGFβ/FGF-treated explants,extensive proliferation oeeured, with formation of spindle and star-shaped cells. These cells showed ultrastructure and biochemical features of fibroblast or myofibroblast.Prominent Golgi apparatus and rough endoplaie reticulum were observed in scene cells, Intracellular microfilaments with cytoplasmic dense bodies and membrane associated dense bodies, features of smooth muscle cells, were also observed. Some cells showed reactivity to α-sin actin antibody. TGFβ/FGF-treated explants were strongly stained with type I collagen antibody. Conclusion. In the presence of FGF, TGFβ1 and TGFβ2 induced lens epithelial cell(LEC)proliferation and transformation into fibroblast or myofibroblast like ceils, with producing of abundant collagen matrix in the explants. The changes are similar to the metaplasia that oeeurrs in subeapsular opacification of the lens. The findings suggest that TGFβ and FGF plays a role in the pathogenesis of subcapsular opacification of the lens.     

MORPHOLOGY OF ERYTHROCYTES IN URINE:SIGNIFICANCE AND MECHANISM OF POLYMORPHISM FORMATION

Urine specimens from patients with a variety of urinary tract diseases and from healthy subjects were examined by phase-contrast microscopy. Urinary erythrocytes showed polymorphism in 68/69 patients with glomerulone-phritis while in 53/55 patients with nonglomerular lesions of the urinary tract, haematuria was characterised by isomorphism The morphologic patterns of urinary erythrocytes in 17 uremic patients varied with the underlying lesions. In 45 healthy individuals, urinary erythrocytes were also polymorphic although counts were less than 8000 cells/ml. After taking a treadmill exercise test, the urinary erythrocyte counts in 31 normal subjects increased significantly without any change in cell morphology. Administration of frusemide to patients with glomerular bleeding altered urinary erythrocyte morphology from polymorphism to isomorphism with increased numbers of uniform cells appearing in the urine.Possible mechanisms of erythrocyte polymorphism were investigated in vivo and in vitro The results indicated that polymorphism resulted from exposure to sequential changes in osmolality during passage of erythrocytes through the renal tubules. Scanning electron microscopy of erythrocytes confirmed the lindings seen on light microscopy     

Microsurgical treatment of Nelson’s syndrome

Objective To discuss the etiology, diagnostic criteria and treatment of Nelson’s syndrome.Methods Twenty-three patients with Nelson’s syndrome who were treated in our department over the last 19 years were analyzed retrospectively.Removal of adenoma by the transsphenoidal approach was done in 21 patients and by transfrontal craniotomy in 2.The follow-up period ranged from six months to nine years.Results The incidence of Nelson’s syndrome was 7.7% in a series of 300 patients with Cushing’s disease treated by microsurgery in the same period.Hyperpigmentation was relieved and adrenocorticotropic hormone (ACTH) levels decreased in all patients after tumor excision.Eight patients with visual disturbance improved after surgery.The curative and remission rates were 56.5% and 26.1%, respectively.Conclusions Transsphenoidal microsurgical removal of pituitary ACTH adenoma is the first choice in the prevention and treatment of Nelson’s syndrome.Regular follow-up examinations should be performed over a long time.     

A Retrospective and Comparative Study of Familial and Non-familial Bullous Lichen Planus

In order to compare the clinical characteristics of familial and non-familial bullous lichen planus (BLP), the archival data of 36 BLP patients with positive family history and 21 BLP patients with negative family history diagnosed according to the clinical features and histopathology were collected in our department from 1956 to 2003. The clinical features were analyzed and compared. There were significant differences between familial and non-familial BLP in age of onset, duration of disease and extension of eruption (P<0.01). It was concluded that familial BLP appeared to differ from the non-familial form in its earlier age of onset, longer duration of the disease, more extensive eruption and more tendency to involve nails. Hereditary factors may play a role in the pathogenesis of familial BLP.     

Clinical and histopathologic features of biofilm-associated chronic rhinosinusitis with nasal polyps in Chinese patients

Background  Biofilms have given new insights to the understanding of pathogenesis of chronic rhinosinusitis (CRS). However, the link between biofilms formation and local inflammatory response remains poorly defined in CRS with nasal polys. The aim of this study was to determine the potential association of the presence of biofilms in the nasal mucosal tissues with clinical features in Chinese patients, which had CRS with nasal polyps (CRSwNP).

Methods  A total of 19 patients with CRSwNP and 12 patients with non-CRS were subjected to endoscopic surgery and their nasal mucosal tissue specimens were examined histologically and by scanning electron microscopy (SEM). Their demographic and clinical features were recorded.

Results  Thirteen (68.4%) out of the 19 specimens from patients with CRSwNP, but none from control patients, were positive for biofilms that displayed typical characteristics of bacterial and fugal structures. The presence of biofilms in the nasal mucosal tissues was associated with significantly greater values of purulent nasal discharge and preoperative Lund-Kennedy scores, higher levels of serum total IgE and percentages of subjects with endoscopic surgery (ESS) history in patients with CRSwNP, and more severe inflammation in the nasal mucosal tissues of patients with CRSwNP.

Conclusion  Our study demonstrated the presence of biofilms in the nasal mucosal tissues of many patients, contributing to the understanding of the pathogenic process of CRSwNP in Chinese patients.

     

多系统萎缩的研究进展

多系统萎缩是一种迟发性神经系统变性疾病,以自主神经功能障碍、帕金森病及小脑性共济失调为特征性表现。现已证实,神经胶质细胞内包涵体是此病的特征性病理学标志物,主要成分是一种高度磷酸化的α-突触核蛋白。此蛋白在包涵体内的异常聚集,使患者少突胶质细胞的功能出现异常、髓鞘破裂,最终导致神经元变性。现就近几年多系统萎缩在临床表现、发病机制和修订后的诊断标准等方面进行综述,以期为该病的早期诊断和治疗提供帮助。     

侵袭性血管黏液瘤的免疫组化特征与鉴别诊断

目的探讨侵袭性血管黏液瘤的免疫组化特征和鉴别诊断。方法对发生在外阴部侵袭性血管黏液瘤4例进行组织学和免疫组化检测,以2例血管肌纤维母细胞瘤为对照。结果大阴唇3例4～6cm直径、小阴唇1例1cm直径;平均年龄36岁。复发1例。瘤细胞Vim、SMA、MSA、Des、CD34均呈阳性,ER、PR阳性细胞数>50%,Ki-67阳性指数<1%,CK和S100蛋白均阴性。结论病理形态和免疫组化明确诊断侵袭性血管黏液瘤,与血管肌纤维母细胞瘤明显重叠,两者可能属同一谱系的两种肿瘤。可能属女性生殖道下部的原始间叶细胞衍化。     

嗅神经上皮瘤的临床病理分析

分析嗅神经上皮瘤（嗅神经母细胞瘤）的临床、病理特点,探讨免疫组化技术和电镜在嗅神经上皮瘤诊断中的应用价值。方法对１９例嗅神经上皮瘤进行了临床分析,光镜复查,免疫组化检测,４例做了透射电镜观察。结果嗅神经上皮瘤主要发生于中青年,起病缓慢,首发症状以单侧鼻塞和鼻出血为多见,病理形态为小圆细胞和短梭形细胞呈巢状及弥散分布,菊形团结构少见或缺如;免疫组化检测ＮＳＥ、Ｓｙｎ阳性,ＣＫ、Ｓ－１００等部分阳性,ＧＦＡＰ阴性;电镜超微结构２例在胞质内找到神经分泌颗粒,３例在胞质内发现中间丝、微丝和基膜,１例有细胞连接和神经突起。结论嗅神经上皮瘤这个名称较嗅神经母细胞瘤更确切,诊断除常规病理外,尚需借助于免疫组化检测,分化差的病例只能通过电镜或其他先进的手段来解决。     

RBCD患者角膜上皮细胞的凋亡

目的观察Reis Bücklers角膜营养不良（RBCD）中角膜上皮细胞的凋亡现象,探讨凋亡在RBCD发病机制中可能的作用。方法2家系中4例RBCD患者(经基因检测均明确为TGFB I基因R124L突变),取其板层或穿透性角膜移植术后的病变角膜,HE及特殊染色后行光学显微镜观察;超薄切片后行透射电子显微镜观察超微结构;采用脱氧核糖核苷酸末端转移酶介导的缺口末端标记法（TUNEL）检测病变角膜中凋亡细胞的表达。以4例正常角膜组织标本为对照。结果RBCD患者角膜上皮细胞微绒毛减少或消失,基底细胞间有小块高电子密度物质,基底细胞出现凋亡现象,前弹力层及前部基质中可见大量棒状高电子密度沉淀物。TUNEL染色发现角膜上皮基底细胞层凋亡细胞,凋亡细胞阳性率为（15.02±3.09）%,显著高于正常对照角膜（P＜0.01）。结论RBCD患者存在角膜上皮基底细胞凋亡,可能是造成角膜前弹力层异常沉淀及其临床症状的原因之一。     

15例腹腔炎性肌纤维母细胞瘤的临床病理分析

目的报道和总结腹腔炎性肌纤维母细胞瘤的临床特点,以提高医生对该病的诊疗水平。方法收集15例患者的临床资料,分析和总结其主要的临床病理特点。结果本组病例包括男性8例,女性7例,发病年龄为4～63岁。发生部位包括肝脏(5例)、膀胱(3例)、肠系膜(2例)、胃(1例)、脾(1例)、直肠(1例)、肾上腺(1例)、腹膜腔(1例)。多部位受累者2例。临床症状包括发热、乏力、纳差、肿块局部疼痛等。常伴有贫血,纤维蛋白原增高。病理学检查可见胶原性基质中呈束状排列的梭形细胞伴淋巴细胞、浆细胞等炎性细胞浸润。免疫组化显示梭形细胞表达波形蛋白Vim(15/15)、平滑肌肌动蛋白SMA(15/15)和肌特异性蛋白MSA(15/15),部分表达ALK(6/15)、Calponin(6/15)、Desmin(5/15)、CK(4/15)。13例行肿瘤完整切除,1例行肿瘤部分切除,1例仅行活检。随访11～65个月,13例术后无瘤生存。结论腹腔炎性肌纤维母细胞瘤是一种罕见的间叶源性肿瘤。累及部位不同导致临床表现多种多样。诊断主要依靠病理学检查和免疫组化检测。手术完整切除是大多数患者的有效治疗方法。     

恶性小细胞肿瘤的免疫组化分析

目的 探讨不同组织来源的恶性小细胞肿瘤特殊染色、免疫组织化学染色特征，以提高恶性小细胞肿瘤诊断的准确性。方法 应用免疫组织化学方法检测26例恶性小细胞肿瘤，观察其对检测标记的反应。结果 26例中小细胞癌占6例，HE特点为核染色质密集，染色很深，核仁不明显，多伴坏死；免疫组织化学染色表明CK、EMA具有明显特异性。结外非何杰金氏淋巴瘤6例，LCA均为阳性，1例CK部分阳性，其余标记均为有性。滑膜肉瘤4例，Vim、EMA阳性，部分瘤细胞（小多边形细胞）CK阳性。血管外皮瘤3例，部分瘤细胞SMA阳性。横纹肌肉瘤2例，MG、MSA阳性。Ewing肉瘤2例，Vim、CD99（Mic2)阳性。小细胞骨肉瘤－Ewing瘤样型1例，Vim阳性。神经母细胞瘤1例，NSE、CHG－A阳性。恶性间皮瘤1例，CEA阳性。结论 免疫组织化学标记对大部分小细胞恶性肿瘤有较明显的特异性，尤其对小细胞癌与间叶源性小细胞肿瘤间的鉴别。但间叶源性和／或起源未定的小细胞肿瘤间仅凭免疫组织化学反应尚难以准确诊断，还需仔细寻找HE形态特点，结合组织化学、电镜检查，必须时做遗传学和基因学诊断。     

神经元凋亡与颞叶癫痫患者海马硬化的关系

目的:探讨神经元凋亡与颞叶癫痫患者海马硬化的关系。方法:取24例颞叶癫痫患者手术切除标本,用光镜、电镜及原位末端标记(TUNEL)方法检测神经细胞凋亡;应用免疫组化方法检测细胞凋亡相关基因表达产物bcl-2、bax及P53蛋白的表达。结果:对照组患者光镜、电镜检查及TUNEL染色均未发现凋亡的神经细胞;癫痫组患者光镜检查及TUNEL染色未发现凋亡的神经细胞,但在电镜检查的8例标本中,3例有少量早期凋亡征象的神经元。免疫组化染色结果表明,对照组患者脑组织内bcl-2蛋白无表达,癫痫组患者脑内bcl-2蛋白表达明显增强(P<0.01);bax蛋白在癫痫组与对照组中均微弱表达,两者差异无统计学意义(P>0.05);P53蛋白在对照组中无表达,在癫痫组中表达明显增强(P<0.05)。结论:神经元凋亡部分参与了癫痫患者海马硬化的形成。bcl-2、P53蛋白在这一过程中可能发挥了作用。     

实验性汞中毒小脑变性的病理观察

目的: 探讨氯化甲基汞(MMC)中毒大鼠小脑变性的病理改变及机制.方法:本研究在大鼠服用MMC 4 mg/(kg·d)所致的亚急性汞中毒模型上,分别在服用MMC后第11、15、18和21天断头,采用组织和免疫病理技术动态观察小脑的病理演变,并采用TUNEL染色观察细胞凋亡改变,同时在电镜下观察了超微结构改变.结果:在服用MMC第18天,TUNEL染色显示小脑颗粒细胞有散在的凋亡细胞,主要位于脑回深部近白质区的颗粒层.第21天,凋亡细胞明显增加,颗粒细胞减少.MRF-1染色可见大量的小胶质细胞反应,GFAP示胶质细胞增生明显,而Purkinje细胞则保留完整.服用MMC第18天的超微结构观察表明,细胞核皱缩,体积缩小,形态不规则,电子密度增高,可见密集深染的染色质,部分细胞核破碎,呈现为均一深染的泪珠状染色质,符合凋亡改变.结论:本研究结果表明汞中毒的小脑变性的病理机制为细胞凋亡,其病理变化符合人类汞中毒表现.     

星形细胞瘤及其瘤细胞凋亡的研究:透射电镜与原位细胞凋亡检测

目的 :探讨星形细胞瘤瘤细胞及其凋亡的超微结构变化 ,为阐述肿瘤内在的生物学行为寻找形态学依据 ,分析瘤细胞凋亡与肿瘤恶性转化的关系。方法 :收集本院神经外科手术标本 ,应用透射电镜及原位细胞凋亡试剂盒对星形细胞瘤进行观察和检测。结果 :电镜下发现瘤细胞胞浆内胶质丝与发育不良 /幼稚的细胞器并存 ;瘤细胞核核内假性包涵体 ;瘤细胞间缺乏细胞连接。原位细胞凋亡检测显示 ,星形细胞瘤中低分级组瘤细胞凋亡的细胞密度明显高于高分级组 (P <0 .0 1)。结论 :瘤细胞凋亡的细胞密度随着肿瘤级数的增高而降低 ,提示星形细胞瘤瘤细胞的增殖和凋亡失衡 ,即瘤细胞无限制性增生和 /或瘤细胞不能进入凋亡。这可能是星形细胞瘤发生发展的重要因素。