Traditionally the cultivation mechanisms of pathological postgraduates can not fully adapt to the demand of research and society in China,to some extent,which impedes the development of pathology.Combining our practical conditions with overseas experiences,we try to make the beneficial thinking and adjustment on the existing cultivation mechanisms.

In order to study the effect of nitric oxide (NO) on the expression of hypoxia-inducible factor-1 alpha (HIF-1alpha) mRNA in hypoxic pulmonary hypertension (HPH) rats, 30 healthy male Wistar rats were randomly divided into normoxic control group, chronic hypoxic group and hypoxia plus L-arginine (L-Arg) group. The animal model of HPH was developed. The mean pulmonary arterial pressure (mPAP) was measured by inserting a microcatheter into the pulmonary artery. The HIF-1alpha mRNA expression levels were detected by in situ hybridization (ISH) and semiquantitative RT-PCR. It was found that after 14 days hypoxia, the mPAP in normoxic control group (17.6 +/- 2.7 mmHg, 1 mmHg=0.133 kPa) was significantly lower than that in chronic hypoxic group (35.8 +/- 6.1 mmHg, t=0.2918, P<0.05) and mPAP in chronic hypoxic group was higher than that in hypoxia plus L-arginine group (24.4 +/- 3.8 mmHg, t=0.2563, P<0.05). ISH showed that the expression of HIF-1alpha mRNA in the intraacinar pulmonary arteriolae (IAPA) in normoxic control group (0.1076 +/- 0.0205) was markedly weaker than that in chronic hypoxic group (0.3317 +/- 0.0683, t=3.125, P<0.05) and that in chronic hypoxic group was stronger than that in hypoxia plus L-arginine group (0.1928 +/- 0.0381, t=2.844, P<0.05). RT-PCR showed that the content of HIF-1alpha mRNA in chronic hypoxic group (2.5395 +/- 0.6449) was 2.16 times and 1.75 times higher than that in normoxic control group (1.1781 +/- 0.3628) and hypoxia plus L-arginine group (1.4511 +/- 0.3981), respectively. It is concluded that NO can reduce the mPAP by the inhibition of the expression of HIF-1alpha mRNA, which may be one of the mechanisms through which NO affects the pathogenesis of HPH.
Anoxia/metabolism ; Arginine/pharmacology ; Hypertension, Pulmonary/*metabolism ; Hypoxia-Inducible Factor 1, alpha Subunit ; Nitric Oxide/*pharmacology ; RNA, Messenger/biosynthesis ; RNA, Messenger/genetics ; Random Allocation ; Rats, Wistar ; Reverse Transcriptase Polymerase Chain Reaction ; Transcription Factors/*biosynthesis ; Transcription Factors/genetics

Neurocytoma, a rare brain tumor, is characterized by a mass located mainly in cerebral ventricles. It is prone to be misdiagnosed as oligodendroglioma or ependymoma due to their similar histopathological features in clinical practice. This study aimed to examine the clinicopathological features and differential diagnosis of central and extraventricular neurocytoma. The clinical and histopathological data of 17 patients (male: female=7:10; age: 4-41 years; mean age: 27.4 years) with central or extraventricular neurocytoma were retrospectively analyzed. These patients showed typical radiological, histopathological and immunohistochemical features of neurocytoma. The tumor tissue was found to be composed of small uniform cells with round nuclei and clear cytoplasm resembling that of oligodendroglioma and ependymoma. Immunohistochemistry revealed the tumor tissues were positive for neuronal markers such as synaptophysin (SYN) and neuronal nuclear antigen (NeuN). It was concluded histopathological features of neurocytoma overlaps with some tumors in the central neural system. Immunopositivity for SYN and NeuN can help differentially diagnose neurocytoma.

AIM:To observe the changes of nuclear factor-?B (NF-?B) activity and inducible nitric oxide synthase (iNOS) expression in hypoxic pulmonary hypertension(HPH). METHODS:The rat model of HPH was used. The NF-?B activity and iNOS expression in lung tissue were determined by immunohistochemistry(IHC), in situ hybridization (ISH), RT-PCR and Western blot.RESULTS:ISH showed that iNOS mRNA expression in intraacinar pulmonary arteriole (IAPA) in H28 d group(hypoxic treatment for 28 days) was stronger than that in normal group, H5d group and H14 d group. RT-PCR showed that the iNOS mRNA in H28 group was 2.1 times, 1.9 times and 1.8 times higher than that in normal group, H5d group and H14 d group, respectively. The nucleic anti-NF-?B stain was observed in H28 d group, which was significantly stronger, but the I-?B amount was 2.8 times, 2.7 times and 2.5 times lower than that in normal group, H5d group and H14 d group, respectively. CONCLUSION: The activity of NF-?B was correlated with the hypoxic pulmonary vessel structural remodeling and iNOS expression.

AIM: To investigate the expression of phosphatidylinositol 3-kinase (PI-3K) during the proliferation of the hypoxic pulmonary arterial smooth muscle cells(PASMC). METHODS: The cultured PASMC was divided into two groups: serum-free medium (SFM) group and 48 hours hypoxia (H48h) group. Immunohistochmistry(IHC) and Flowcytometer(FCM) were used to detect the cultured PASMC. RESULTS: The positive expression of PI-3K p110 existed in both cultured PASMC groups. The staining intensity in H48h group (0 1891?0 0301) was significantly stronger than that in SFM group (0 1025?0 0164, P

Purpose To investigate the clinicopathological features, histogenesis, morphological characteristics, immunophenotypes and differential diagnosis of primary extragonadal yolk sac tumor ( eYST) . Methods Clinicopathological data, morphological charac-teristics and immunophenotypes results of 40 cases of eYST were retrospectively studied and the relevant literatures were reviewed. Re-sults All 40 patients, which included 24 male and 16 female, aged from 6 months to 42 years with a 12 years average age and 17 (42.5%) cases were over 12 years old. Mediastinum, sacrococcygeal, retroperitoneal, pineal gland and vagina were involved in 16 (40.0%), 12(30.0%), 5(12.5%), 4(10.0%) and 3(7.5%), respectively. All 40 cases included 32(80.0%) cases pure YSTs, while other 8(20.0%) cases contained other one or two types of germ cell tumor (GCT) components. Conclusions Primary eYST is rare, mediastinum and sacrococcygeal are the most common anatomic sites for eYST, and these mediastinal tumor patients are overwhelmingly confined to adult males, whose average age are significantly older than that in sacrococcygeal, retroperitoneal, pineal gland and vaginal tumor patients (P<0.05), while other sites eYST are restricted to prepubertal children. Adult eYST contain other types of GCT components in some cases, and children's counterparts are always pure YST. Extragonadal eYST manifestate pleomorphic histological features, which combine with immunohistochemical markers is definite value for diagnosis, differential diagnosis.

This study examined the effect of astilbin on the proliferation of rat aortic smooth muscle cells (RASMCs) induced by angiotensin II (AngII) and explored the possible mechanisms. Cell proliferation model of RASMCs was induced by treatmente with AngII. Cells were randomly divided to 8 groups. Normally cultured VSMCs serves as blank control group; in AngII model group, cells were treated with AngII at 10(-7) mol/L; in three astilbin groups, cells were treated with 10, 15, 30 mg/L of astilbin; in three AngII+astilbin groups, cells were treated with AngII (at 10(-7) mol/L) and astilbin at 10, 15, 30 mg/L. Cell proliferation ability was detected by MTT method and the cell cycles and proliferation index were flow cytometrically determined. The expression of c-myc mRNA was assessed by using reverse transcription polymerase chain reaction (RT-PCR), and the expression of NF-κB in RASMCs was immunocytochemically observed. Our results showed that MTT metabolism in RASMCs in the basic and AngII stimulated situation was inhibited by astilbin, and the cells numbers of G(0)/G(1) phase were increased and that of G(2)/S phase were decreased markedly. Not only highly expression of c-myc gene stimulated by AngII could be inhibited by Astilbin significantly, but also the expression of NF-κB protein can be down regulated by Astilbin. We are led to conclude that astilbin astilbin can inhibit the AngII-mediated proliferation of RASMCs by blocking the transition of RASMCs from G(0)/G(1) phase to S phase and by down-regulating the expression of NF-κB, c-myc gene.

0.05). The production of TNF-? in LPS group was higher than that in control group (61 ng/L vs 156 ng/L, q=5.12, P

Objective: To investigate the clinicopathological features, morphological characteristics, immunophenotypes of littoral cell angioma (LCA) in spleen, and to provide new evidence for making diagnosis and avoiding misdiagnosis.Methods: Clinicopathological data, histological characteristics of 13 cases of LCA were retrospectively studied and immunohistochemical staining was imposed on the paraffi-nembedded specimens, and 5 cases of cavernous hemangioma, 4 cases of normal littoral cells of spleens were used as control groups, simultaneously.Results: All the 13 LCA patients included 7 males and 6 females, aged from 39 to 70 years with an average of 54.2 years and a median age of 55 years.Among these tumor patients, 6 cases were accompanied by malignances, benign tumors or inflammation states at abdominal cavities, and 7 cases were accidentally discovered by physical examinations.Grossly, spleens contained solitary or multiple gray red nodules ,which ranged from 0.5 to 6.2 cm in diameter.Histologically, tumors were composed by anastomosing vascular spaces which were lining by plump, rounded to cuboidal littoral cells that extended into vascular lumens.Usually, papillary frameworks that were covered by these cells were also seen extending into the lumens in some areas.Other types of histiocytoid cells were identified in lumens and the sizes were larger than the littoral cells.Both types of cells absented cytologic atypia.Immunohistochemical study demonstrated that the littoral cells in all cases were positive for vascular endothelial and histiocyte markers, such as CD21, CD31, CD68, polyclone FⅧRAg and ERG, while these cells were negative for CD8, CD34, and WT-1.These findings manifested that immunophenotype of littoral cell in LCA distinctive from that in controls.Conclusion: LCA is a benign lesion, which frequently occurs in the elderly.Its etiology remains confusion, however, immune dysregulation may associate with it because of the concomitance with other tumor or inflammation in some cases.The littoral cells in LCA show a hybrid endothelial-histiocytic phenotype on immunohistochemistry, therefore these cells may have features that intermediate between those of endotheliocytes and histiocytes.Emphasizing the histological findings and immunophenotypes is significant for diagnosis and differential diagnosis.

With the development of imaging technology,the detection rate of gallbladder benign lesions has increased year by year.And part of the diseases may evolve into gallbladder cancer through a series of pathophysiologic processes.There are some misunderstandings in the understanding of gallbladder benign lesions for surgeons,so it is difficult for the clinical decision-making.The relationship between gallbladder benign lesions and gallbladder cancer should be correctly understood.Surgeons can neither exaggerate the risk of gallbladder cancer nor miss optimal timing of operation.The key point of the diagnosis and treatment of gallbladder benign lesions should be based on making full use of imaging data and strictly grasp pre-and intraoperative indications,and it is important to identify the malignant transformation of gallbladder benign lesions as soon as possible and carry out standardized treatment.