MEX3A promotes proliferation and migration of colorectal cancer cells via PI3K/Akt signaling pathway / 解剖学报

Objective To investigate the expression of MEX3A in colorectal cancer (CRC), and to explore the effect and mechanism of MEX3A on the proliferation and migration of colorectal cancer cells. Methods Totally 327 cases of data(41 normal tissues and 286 tumor tissues) were obtained from TCGA database, and 104 cases of clinical samples (77 cases tissues and 27 paracancerous tissues) were collected for immunohistochemistry, then analysed the differences in MEX3A expression between CRC tissues and normal tissues. Western blotting and immunofluorescence staining were used to evaluate the differential expression of MEX3A in CRC cell lines. CL187 cells were selected as the follow-up research vector. Small interfering RNA of MEX3A(siMEX3A) was transfected into CL187 cells to inhibit the expression of MEX3A. The proliferation and migration of CL187 cells were measured by MTT, colony formation assay and Transwell assay. The expression of PI3K, p-PI3K, Akt and p-Akt were detected by Western blotting. Results TCGA database, immunohistochemistry and Western blotting analysis showed that MEX3A was highly expressed in colorectal cancer. The result of immunofluorescence staining showed that MEX3A was concentrated in the cytoplasm and the nucleus. In MTT, colony formation assay and Transwell assay, the proliferation and migration ability of CL187 cells in siMEX3A group decreased significantly than those in control group (P<0.05). Western blotting result showed that the expression of p-PI3K and p-Akt in siMEX3A group down-regulated significantly (P<0.05), and the inhibition of proliferation and migration ability of CL187 cells induced by siMEX3A group could be reversed by 740 Y-P via activating the PI3K/Akt signaling pathway. Conclusion MEX3A is highly expressed in colorectal cancer and promotes the proliferation and migration of CRC cells via PI3K/Akt signaling pathway.

Impact of varicocele on semen quality and inhibin B concentration in serum and seminal plasma / 中华男科学杂志

<p><b>OBJECTIVE</b>To investigate the influence of varicocele (VC) on semen parameters and the concentration of inhibin B in the serum and seminal plasma of VC men.</p><p><b>METHODS</b>We collected semen and peripheral blood samples from 95 infertile VC patients and 55 normal fertile men. We performed semen routine examination by computer-assisted semen analysis and sperm morphology examination by modified Papanicolaou staining, and measured the levels of inhibin B in the peripheral blood and seminal plasma of the subjects by ELISA.</p><p><b>RESULTS</b>Compared with the normal fertile controls, the infertile men with grade-I, -II and -III VC showed significantly lower percentages of morphologically normal sperm ([7.5 +/- 5.2]% vs [6.3 +/- 6.5]%, [2.6 +/- 3.0]% and [1.0 +/- 0.7]%, P < 0.05) and progressively motile sperm ([43.9 +/- 22.7]% vs [33.3 +/- 20.8]%, [28.9 +/- 19.8]% and [13.5 +/- 8.4]%, P < 0.05). The majority of the morphologically abnormal sperm were of the type of head deformity. The concentrations of inhibin B in the peripheral blood and seminal plasma were evidently lower in the infertile men with grade-I VC ([160.9 +/- 48.9] pg/ml and [208.3 +/- 28.1] pg/ml), grade-II VC ([150.6 +/- 44.7] pg/ml and [201.5 +/- 83.5] pg/ml), and grade-III VC ([132.6 +/- 41.5] pg/ml and [150.2 +/- 51.6] pg/ml) in comparison with those of the fertile control group ([201.0 +/- 38.1] pg/ml and [225.3 +/- 82.5] pg/ml).</p><p><b>CONCLUSION</b>Varicocele reduces sperm motility, increases sperm abnormality, decreases the concentration of inhibin B in the serum and seminal plasma, and consequently damages male fertility.</p>

A Suspicious Breast Lesion Detected by Dynamic Contrast-Enhanced MRI and Pathologically Confirmed as Capillary Hemangioma: a Case Report and Literature Review

Breast capillary hemangioma is a type of benign vascular tumor which is rarely seen. Little is known about its presentation on dynamic contrast-enhanced magnetic resonance imaging (DCE-MRI). Here, we describe a case of suspicious breast lesion detected by DCE-MRI and pathologically confirmed as capillary hemangioma. Our case indicates that a small mass with a superficial location, clear boundary, and homogeneous enhancement on DCE-MRI indicates the possible diagnosis of hemangioma, whereby even the lesion presents a washout type curve.

Effects of heparanase inhibition by RNA interference on proliferation, invasiveness and apoptosis of lung cancer cells / 中华病理学杂志

<p><b>OBJECTIVE</b>To investigate the effects of heparanase expression inhibition on the proliferation, invasiveness and apoptosis of human lung adenocarcinoma cell line A549 cells.</p><p><b>METHODS</b>Recombinant eukaryotic expression plasmid pshRNA-Hpa targeting human heparanase gene was constructed. A549 cells were cultured in DMEM and transfected with pshRNA-Hpa. The expression of heparanase mRNA and protein were examined by RT-PCR and Western blot. The proliferation, invasiveness and apoptotic rates of A549 cells were determined by MTT method, matrigel invasion assays and flow cytometry respectively.</p><p><b>RESULTS</b>The expression levels of heparanase mRNA and protein were down-regulated in A549 transfected with pshRNA-Hpa. The number of cells penetrating matrigel and the proliferation ability of A549 cells transfected with pshRNA-Hpa were reduced significantly compared to the control cells. The apoptotic rate of A549 cells transfected with pshRNA-Hpa was 12.53% +/- 0.34%, being significantly higher than that of the control cells (both P < 0.01). Western-blot showed that inhibition of heparanase expression led to reduced Akt phosphorylation.</p><p><b>CONCLUSIONS</b>The recombinant plasmid pshRNA-Hpa effectively inhibited the expression of heparanase, thus suppressing the proliferation and invasion and inducing apoptosis of A549 cells. The effects may be due to the down-regulation of Akt phosphorylation level.</p>

Nasal and pharyngeal non-Hodgkin lymphomas and their relationship with Epstein-Barr virus: a report of 158 cases / 中华病理学杂志

<p><b>OBJECTIVE</b>To study the clinical features, immunophenotypes and the significance of Epstein-Barr virus infection in primary nasal and pharyngeal non-Hodgkin's lymphomas in Shenyang.</p><p><b>METHODS</b>One hundred and fifty eight cases of primary nasal and pharyngeal non-Hodgkin's lymphomas were included in this study. The samples were stained with haematoxylin and eosin for histological examination. Immunohistochemistry studies were performed using monoclonal antibodies, including CD3 for T-lymphocytes, CD20 for B-lymphocytes, and CD56 and CD57 for NK cells. All cases were reclassified according to the new WHO classification of lymphomas (2001). In situ hybridization detection of EBV-encoded small nuclear RNA (EBER-1) was performed in 99 cases.</p><p><b>RESULTS</b>Overall, 101 (63.9%) of the 158 NHL were extranodal NK/T cell lymphomas (nasal type), 23 (14.6%) were nonspecific peripheral T cell lymphomas and the remaining 34 cases (21.5%) were B cell lymphomas. The primary sites of involvement were the nasal cavity (53.2%, 84/158), the tonsil (24.7%, 39/158) and the pharynx (22.1%, 35/158). Among 99 cases studied by EBER-1 in situ hybridization, a positive detection was seen in 70/71 cases (98.6%) of extranodal NK/T cell lymphoma (nasal type), 8/12 cases (66.7%) of T cell lymphoma, and 7/16 cases (43.8%) of B cell lymphoma.</p><p><b>CONCLUSIONS</b>Among primary nasal and pharyngeal NK lymphomas, extranodal NK/T cell lymphoma (nasal type) is the most common type and is strongly associated with EBV infection. The pathological diagnosis of nasal and pharyngeal lymphomas should take considerations of the anatomic sites and immunophenotypical features.</p>

Correlation between MMP-2 activation and MT1-MMP mRNA expression in thymic epithelial tumors / 中华病理学杂志

<p><b>OBJECTIVE</b>To study the relationship between activation of pro-MMP-2 and expression of matrix metalloproteinases (MMP)-2, MT1-MMP and tissue inhibitor of metalloproteinases (TIMP)-2 mRNA in thymoma and thymic carcinoma; and to study the molecular mechanism of invasion and metastasis of thymic epithelial tumors.</p><p><b>METHODS</b>Fresh tissue specimens of thymoma, thymic carcinoma and normal thymus were included. The mRNA expression of MMP-2, MT1-MMP and TIMP-2 were analyzed by real-time reverse transcription polymerase chain reaction. The pro-MMP-2 activation ratio and its localization were determined by gelatin zymography and film in-situ gelatin-Zymography, respectively. Correlation of mRNA expression of MMP-2, MT1-MMP and TIMP-2 was investigated in tumors with different histological subtypes and clinical stages.</p><p><b>RESULTS</b>There were no significant differences in the expressions of MMP-2, MT1-MMP and TIMP-2 mRNA between I and II stage or III and IV stage thymomas (P > 0.05). However, significant differences of the expressions were observed between three tumor groups: I-II stage, III-IV stage and thymic carcinomas (P < 0.005), and between three histological subtypes: AB-B1 (lymphocyte-rich and mixed types), B2-B3 (cortical and predominantly polygonal cells types) and thymic carcinomas (P < 0.05). Expression levels of MT1-MMP and TIMP-2 mRNA were correlated with pro-MMP-2 activation ratio (Spearman rank correlation: r = 0.7235, r = 0.7647, P < 0.005). The expression of MMP-9 did not show significant differences between thymomas and thymic carcinomas.</p><p><b>CONCLUSIONS</b>MMP-2, MT1-MMP and TIMP-2 mRNA expression levels are correlated with the histologic subtypes and clinical stages of thymoma. The mRNA expressions of MT1-MMP and TIMP-2 are correlated with the activation ratio of pro-MMP-2. It is speculated that upregulation of MT1-MMP gene expression may induce an activation of pro-MMP-2 through TIMP-2.</p>

Study of androgen receptor and phosphoglycerate kinase gene polymorphism in major cellular components of the so-called pulmonary sclerosing hemangioma / 中华病理学杂志

<p><b>OBJECTIVE</b>To study the clonality of polygonal cells and surface cuboidal cells in the so-called pulmonary sclerosing hemangioma (PSH).</p><p><b>METHODS</b>17 female surgically resected PSH were found. The polygonal cells and surface cuboidal cells of the 17 PSH cases were microdissected from routine hematoxylin and eosin-stained sections. Genomic DNA was extracted, pretreated through incubation with methylation-sensitive restrictive endonuclease HhaI or HpaII, and amplified by nested polymerase chain reaction for X chromosome-linked androgen receptor (AR) and phosphoglycerate kinase (PGK) genes. The length polymorphism of AR gene was demonstrated by denaturing polyacrylamide gel electrophoresis and silver staining. The PGK gene products were treated with Bst XI and resolved on agarose gel.</p><p><b>RESULTS</b>Amongst the 17 female cases of PSH, 15 samples were successfully amplified for AR and PGK genes. The rates of polymorphism were 53% (8/15) and 27% (4/15) for AR and PGK genes respectively. Polygonal cells and surface cuboidal cells of 10 cases which were suitable for clonality study, showed the same loss of alleles (clonality ratio = 0) or unbalanced methylation pattern (clonality ratio < 0.25).</p><p><b>CONCLUSIONS</b>The polygonal cells and surface cuboidal cells in PSH demonstrate patterns of monoclonal proliferation, indicating that both represent true neoplastic cells.</p>

Expression of connexin 43 in lung cancer and its correlation with E-cadherin / 中华病理学杂志

<p><b>OBJECTIVE</b>To investigate the expression of connexin 43 and E-cadherin in lung cancer and to study the interaction between the two molecules.</p><p><b>METHODS</b>The expression and correlation of connexin 43 and E-cadherin were evaluated by immunohistochemistry (S-P method) in 85 samples of primary squamous cell carcinoma and adenocarcinoma of the lung. In addition, connexin 43 expression vector was transfected into the lung giant cell carcinoma cell line LH(7) followed by analyses of connexin 43 and E-cadherin expressions, the growth rates and cell cycle profiles of the transfected cells.</p><p><b>RESULTS</b>Comparing with the adjacent non-neoplastic lung tissue, expression of connexin 43 and E-cadherin was decreased in a correlative fashion in both squamous cell carcinomas and adenocarcinomas. Their expression reversely correlated to the degree of tumor cell differentiation, P-TNM stage, and status of lymph note metastasis. The expression of connexin 43 and E-cadherin increased significantly after transfection of connexin 43 expression vector into the LH(7) cells (P < 0.05). Both expressions were limited in the cytoplasm before or after the transfection. The proliferation rate of LH(7) cells was significantly decreased by connexin43 expression (P < 0.05), along with an increase of cell population at G(1) phase and a decrease of percentage of cells in S and G(2) phases (P < 0.05).</p><p><b>CONCLUSIONS</b>Squamous cell carcinoma and adenocarcinoma of lung have a low level of connexin 43 and E-cadherin expression, which are correlated with the clinicopathologic features of the tumors. Transfection expression of connexin 43 gene induces an E-cadherin overexpression and an inhibition of LH(7) cell proliferation indicating the significant role of onnexin 43 in the regulation of cell proliferation.</p>

Significance of caveolin-1 expression in primary lung cancer / 中华病理学杂志

<p><b>OBJECTIVE</b>To study the expression of caveolin-1 in primary lung cancer and its relationship with microvessel density and clinicopathologic parameters.</p><p><b>METHODS</b>Immunohistochemical study for caveolin-1 and CD34 was performed on paraffin sections of 154 cases of primary lung cancer and adjacent non-neoplastic lung parenchymal tissue, as well as 36 cases with nodal metastasis. Microvessel density was analyzed by CD34 immunostaining. Western blot assay was also employed in tumor and non-neoplastic lung tissues of the 50 cases (25 cases of pulmonary squamous cell carcinoma and 25 cases of pulmonary adenocarcinoma) with fresh specimens available.</p><p><b>RESULTS</b>Immunohistochemical study showed that non-neoplastic bronchial and alveolar epithelium was positive for caveolin-1 (membranous and cytoplasmic). The expression rate of caveolin-1 in lung cancer was 59.1%, which was significantly lower than that in normal lung tissues (P < 0.01). Western blot assay confirmed that the expression of caveolin-1 in pulmonary squamous cell carcinoma and adenocarcinoma was lower than in surrounding non-neoplastic lung tissues (P < 0.01). Caveolin-1 expression in pulmonary small cell carcinoma (7.1%) was significantly lower than that in non-small cell carcinoma (64.3%) (P < 0.01). Within the group of non-small cell carcinoma, the expression of caveolin-1 was much higher in patients with lymph node metastasis (P = 0.005). The expression was also higher in stage III and IV than in stage I and II disease (P = 0.042).</p><p><b>CONCLUSIONS</b>The expression of caveolin-1 is lower in lung cancer tissues than that in non-small cell carcinoma, it is also significantly correlated with tumor stage and lymph node metastasis. Caveolin-1 may play some role in the progression of pulmonary non-small cell carcinoma.</p>

Effects of HCMV on phenotypes of parotid duct epithelial cells and its mechanisms / 中华实验和临床病毒学杂志

<p><b>OBJECTIVE</b>To investigate the effects of HCMV infection on phenotypes of parotid duct epithelial cells and relative mechanisms.</p><p><b>METHODS</b>The expressions of immediate early antigen of HCMV, pan cytokeratin and cathepsin D etc. were detected by immunohistochemical staining in tissues of parotid cytomegalic inclusion disease.</p><p><b>RESULTS</b>Cytokeratin which acts as an epithelial marker became negative while staining of Cathepsin D was intensified in parotid duct epithelial cells after infected by HCMV.</p><p><b>CONCLUSION</b>It demonstrated that cytokeratin was lost through over-expression of Cathepsin D in parotid duct epithelial cells infected by HCMV.</p>

Clinical significance of heparanase and basic fibroblast growth factor expression in human non-small cell lung cancer / 中华病理学杂志

<p><b>OBJECTIVE</b>To assess protein and mRNA expression levels of heparanase and basic fibroblast growth factor (bFGF) genes in human non-small cell lung cancer (NSCLC) and their roles in tumor invasion, metastasis and prognosis.</p><p><b>METHODS</b>A total of 115 paraffin-embedded and 45 fresh-frozen tissue specimens of NSCLC were studied by immunohistochemistry, Western Blot and in situ hybridization to evaluate the protein and mRNA expression status of heparanase and bFGF genes. The data was analyzed by SPSS statistical software.</p><p><b>RESULTS</b>Both human heparanase and bFGF were highly expressed in NSCLC cells, in contrast to none or a low expression in normal lung tissue. Expression of heparanase also showed a significantly higher than that in the normal tissue by Western blot (P = 0.041). Immunohistochemistry showed that heparanase expression was both cytoplasmic and membranous. The agreement between heparanase and bFGF was significant. A significant correlation was found between the expression of either protein and TNM stage, vascular invasion, lymphatic metastasis and microvascular density (MVD). Co-expression of the two proteins demonstrated an even higher correlation with the tumor stage and MVD. In addition, expression of bFGF correlated with tumor cell differentiation. Data of a multivariate analysis indicated that tumor cell differentiation, vascular invasion, lymphatic metastasis and expression of bFGF were identified as significant prognostic parameters.</p><p><b>CONCLUSIONS</b>Both heparanase and bFGF may play important roles in tumor angiogenesis, metastasis, and prognosis of NSCLC.</p>

Expression of p120ctn and its significance in non-small cell lung cancer / 中华病理学杂志

<p><b>OBJECTIVE</b>To investigate the expression of p120(ctn) in non-small cell lung cancer (NSCLC) and its correlation with the clinical and pathologic parameters.</p><p><b>METHODS</b>Immunohistochemistry (S-P method) was used to detect the expression of p120(ctn) in 143 NSCLC cases. The variation of protein expression was further analyzed in 36 cases by Western blot. The correlation with clinical and pathologic parameters was studied.</p><p><b>RESULTS</b>Immunohistochemically, normal bronchial cells showed membranous expression for p120(ctn), while NSCLC was characterized by cytoplasmic or diminished membranous staining. The rate of abnormal p120(ctn) expression was 79.7% (114/143). There was a significant correlation between abnormal expression of p120(ctn) and tumor differentiation, clinical stage, lymph node metastasis and poor prognosis (< 0.05), but not histologic typing. Western blot showed that the total amount of p120(ctn) in normal bronchial cells was significantly higher than that in NSCLC. The p120(ctn) isoform 1 (120,000) and isoform 3 (100,000) were expressed in normal lung tissue, while there was a reduced expression or absence of isoform 1 in NSCLC.</p><p><b>CONCLUSION</b>The expression of p120(ctn) is abnormal in NSCLC; p120(ctn) may serve as a useful prognostic marker for NSCLC.</p>

Expression of T cell factor-4 in non-small-cell lung cancer / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>T cell factor-4 (TCF-4) plays an important role in development and carcinogenesis. Recently, the role of TCF-4 has been described in colon cancer and other cancers. However, whether TCF-4 plays a similar role in lung cancer is unknown. To answer this question, we studied the expression of TCF-4 protein and mRNA in non-small-cell lung cancer (NSCLC) and the relation of TCF-4 expression pattern to histological type and cell differentiation.</p><p><b>METHODS</b>Tissue samples from sixty cases of pathologically diagnosed NSCLC and eight normal tissue samples were obtained between September 2001 and March 2003. Immunohistochemistry was used to investigate the distribution of TCF-4 protein. The staining patterns of the tumors were divided into 4 categories: nuclear staining alone or nuclear staining greater than cytoplasmic staining; cytoplasmic staining or cytoplasmic staining greater than nuclear staining; equal nuclear and cytoplasmic staining; no nuclear staining or cytoplasmic staining. The integrated optical density (OD) values of all sections were analyzed by UIC MetaMorph image analysis software. The expression of TCF-4 mRNA was detected by one-step reverse transcription-polymerase chain reaction (RT-PCR). The integrated density values of the PCR products were analyzed semi-quantitatively.</p><p><b>RESULTS</b>Immunohistochemistry showed that there was no expression of TCF-4 in normal tissue. However, TCF-4 was expressed in 86.7% (52/60) of NSCLC samples, mainly in the nuclei of tumor cells. Furthermore, there was a significant difference in TCF-4 localization patterns between squamous cell carcinomas and adenocarcinomas (P < 0.05). The integrated OD values of TCF-4 expression was significantly higher in tumors with moderate-poor cell differentiation than in well differentiated tumors (51.63 +/- 6.67 vs 46.13 +/- 12.31, P < 0.01). There was no TCF-4 mRNA expression in normal tissue. However, 63.9% (23/36) of carcinoma samples expressed TCF-4 mRNA. TCF-4 mRNA expression was significantly higher in tumors with moderate-poor cell differentiation than in well differentiated tumors (P < 0.05). There were no significant differences in mRNA expression in comparison with histological type.</p><p><b>CONCLUSIONS</b>The sub-cellular distribution of TCF-4 may correlate with NSCLC histological type. High expression of TCF-4 mRNA and protein may be associated with the degree of cell differentiation in NSCLC.</p>

Expressions of Axin and beta-catenin in non-small cell lung cancer / 中华病理学杂志

<p><b>OBJECTIVE</b>To investigate the protein expression of Axin and beta-catenin, the exon 3 mutation status of beta-catenin and their clinicopathological correlations in non-small cell lung cancer (NSCLC).</p><p><b>METHODS</b>A total of 100 NSCLC samples and their corresponding normal lung tissues were obtained from the patients undergoing surgery in the First Affiliated Hospital of China Medical University between 2001 and 2003. Protein expressions of Axin and beta-catenin were detected by immunohistochemistry. DNA sequence alterations of exon 3 of beta-catenin were investigated by polymerase chain reaction (PCR) and direct sequencing.</p><p><b>RESULTS</b>A reduced membranous expression rate of beta-catenin was observed in 80.0% of the cases (80/100) along with a nuclear expression rate of 26.0% (26/100). There was a significant difference in beta-catenin expression between well and poorly differentiated NSCLCs. Well to moderately differentiated NSCLCs showed a reduced expression rate of 70.0% (35/50), in contrast to 90.0% (45/ 50) in poorly differentiated tumors (P = 0.012). Reduced beta-catenin expression rate was 87.3% (48/55) in cases with lymph node metastasis, in contrast to 71.1% (32/45) in cases without lymph node metastasis (P = 0.044). The positive expression rate of Axin was 48.0% (48/100). Well to moderately differentiated NSCLCs demonstrated a 60.0% positive expression rate of Axin (30/50), much higher than poorly differentiated tumors [36.0% (18/50), P = 0.016]. The positive expression rate of Axin in beta-catenin nuclear expressed NSCLCs was 15.4% (4/26), much lower than cases without beta-catenin nuclear expression [59.5% (44/74), P < 0.001]. Axin nuclear expression was found in two cases in this study, suggesting that it may function as a nuclear-cytoplasmic shuttling protein. PCR and direct sequencing failed to reveal any exon 3 mutation of beta-catenin gene.</p><p><b>CONCLUSIONS</b>The reduced membranous expression of beta-catenin is associated with poorly differentiated and lymph node positive NSCLCs. The expression of Axin is inversely correlated with the degree of tumor differentiation and nuclear expression of beta-catenin. The exon 3 mutations do not contribute to the abnormal protein expression of beta-catenin in NSCLCs.</p>

Effects of glycine and methylprednisolone on hemorrhagic shock in rats / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>Methylprednisolone (MP), a synthetic glucocorticosteroid, has been broadly studied in experiments on endotoxin-induced shock and septic shock. This study was designed to ascertain whether glycine and MP can protect against organ injury and death caused by hemorrhagic shock, and to elucidate the underlying mechanisms of these protective effects in rats.</p><p><b>METHOD</b>To establish a shock model, Wistar rats were bled to maintain mean arterial pressure at 30-50 mmHg for 1 hour and subsequently resuscitated with the shed blood and normal saline. Just prior to resuscitation, the rats were randomly assigned to four groups: sham group (operation performed without inducing shock), shock group, shock + glycine group (glycine injected at the beginning of resuscitation) and shock + MP group (MP injected at the beginning of resuscitation).</p><p><b>RESULTS</b>(1) Seventy-two hours after resuscitation, the survival rate of rats from the shock group had decreased to 20%, while the survival rates of rats from the shock + glycine and shock + MP groups were 77.8% and 80%, respectively. The difference was significant (P <0.05). (2) Eighteen hours after resuscitation, pathological alterations in the organs of the rats were apparent. In rats from the shock group, edema, interstitial leukocyte infiltration, and cellular degeneration occurred in the liver, lungs, kidneys, and heart. Glycine and MP reduced these pathological changes significantly. (3) Eighteen hours after resuscitation, the levels of creatine phosphokinase, transaminases, and creatine were elevated significantly in rats from the shock group, indicating injury to the heart, liver, and kidneys, while these levels were elevated only slightly in the shock + glycine and shock + MP groups. The differences were significant (P <0.01). (4) There were significant increases in intracellular calcium and production of tumor necrosis factor (TNF-alpha) by isolated Kupffer cells stimulated by endotoxin after hemorrhagic shock. These changes were completely prevented by glycine and MP (P <0.01).</p><p><b>CONCLUSION</b>Glycine and MP reduce organ injury and mortality caused by hemorrhagic shock by preventing increase of intracellular calcium levels in Kupffer cell, suppressing Kupffer cell activation, decreasing the production of TNF-alpha by Kupffer cells, and blocking systemic inflammatory responses.</p>

Human cytomegalovirus inhibits proliferation of duct epithelial cells of human salivary gland / 中华口腔医学杂志

<p><b>OBJECTIVE</b>To investigate the effects of human cytomegalovirus (HCMV) on the proliferation of duct epithelial cells of human salivary gland (HSG).</p><p><b>METHODS</b>The expression of proliferating cell nuclear antigen (PCNA) and p53 were studied in 11 cases of parotid cytomegalic inclusive disease (PCID) using immunohistochemical staining method. The effects of human cytomegalovirus (HCMV) on the proliferation of HSG were investigated by MTT method in vitro. The expression of PCNA in HSG infected by HCMV was examined using immunocytochemical staining and Western blotting.</p><p><b>RESULTS</b>PCNA was expressed weakly in most of megalic inclusion cells which were positive for HCMV, while all the megalic inclusion cells were p53 negative in all 11 cases of PCID. HCMV inhibited proliferation of HSG in vitro in a time dependent and dose dependent manner. Down-regulation of PCNA was shown in infected cells.</p><p><b>CONCLUSION</b>HCMV inhibits proliferation of HSG and down-regulation of PCNA may be an expression of the inhibition.</p>

The effect of glycine on survival after hemorrhagic shock in the rats / 中华外科杂志

<p><b>OBJECTIVE</b>To investigate the effect of glycine on survival after hemorrhagic shock in the rats and elucidate the underlying mechanisms.</p><p><b>METHODS</b>Wistar rats were bled to establish the shock model and subsequently resuscitated with shed blood and normal saline. Just prior to resuscitation, the rats were divided into three groups: sham group, shock group and shock + glycine group.</p><p><b>RESULTS</b>(1) 72 h after resuscitation, the survival rate of shock group decreased to 20%, while the survival rate of shock + glycine group was 77.8%, the difference was significant (P < 0.05). (2) 18 h after resuscitation, pathologic alterations of organs showed, pulmonary edema, leukocyte infiltration in interstitial tissue and cellular degeneration in shock group. Glycine reduced these pathological alterations significantly. (3) 18 h after resuscitation, creatine phosphokinase, transaminases and creatinine were elevated significantly in shock group, while these were elevated slightly in shock + glycine group, the differences were significant (P < 0.01). (4) Increases in intracellular calcium and production of TNF-alpha by isolated Kupffer cells stimulated by endotoxin were elevated significantly by hemorrhagic shock, which were totally prevented by glycine (P < 0.01).</p><p><b>CONCLUSION</b>Glycine reduces organ injury and mortality caused by hemorrhagic shock by preventing increase of intracellular calcium and production of TNF-alpha of Kupffer cells and blocking systemic inflammation responses.</p>

Expression of vascular endothelial growth factor (VEGF) C and VEGF receptor 3 in non-small cell lung cancer / 中华病理学杂志

<p><b>OBJECTIVE</b>To study the relationship between angiogenesis and lymphangiogenesis with the expression of vascular endothelial growth factor C (VEGF-C) and VEGFR-3 in human non-small cell lung cancer (NSCLC).</p><p><b>METHODS</b>Samples of 76 NSCLC cases with the neighboring noncancerous tissue were studied using anti- VEGF-C, VEGFR-3 and CD34 antibodies. Assessment of lymphatic vessel density and microvessel density (MVD) were performed.</p><p><b>RESULTS</b>VEGF-C expression in NSCLC was associating with the differentiation of tumor cells (P = 0.009). Expression of VEGF-C and VEGFR-3 was significantly associated with lymph node metastasis (P = 0.008 and P = 0.013 respectively) and lymphatic invasion (P = 0.027 and P = 0.020 respectively). A significant positive correlation was found between VEGF-C in cancer cells and VEGFR-3 in lymphatic endothelial cells (P = 0.009). The number of lymphatic vessels (P = 0.006) and microvascular (P = 0.046) in VEGF-C positive tumors was significantly larger than in VEGF-C-negative tumors. Lymphatic vessel density was closely related to lymph node metastasis (P = 0.010), lymphatic invasion (P = 0.019) and clinical stages (P = 0.015). MVD was closely related to blood metastasis (P < 0.001) and clinical stages (P < 0.001). Patients with positive VEGF-C expression had a worse prognosis than those with a negative VEGF-C expression (P < 0.001).</p><p><b>CONCLUSIONS</b>VEGF-C/VEGF-D in NSCLCs, are related to lymphangiogenesis and angiogenesis, as well as to the occurrence and the development of lung cancers. VEGF-C promotes intratumoral lymphangiogenesis via VEGFR-3, resulting facilitated invasion of cancer cells into the lymphatic vessels. VEGF-C expression can be a useful predictor of poor prognosis in NSCLC.</p>