NK/T cell lymphoma involving mediastinum: report of a case and review of literature.

Extranodal natural killer (NK)/T-cell lymphoma is a very aggressive malignant neoplasia with a poor prognosis. Herein we reported a case of NK/T cell lymphoma involving mediastinum. It was a 28-year-old Chinese male patient. The tumor cells were medium-sized, had irregularly folded nuclei, and inconspicuous or small nucleoli with coagulative necrosis. The tumor cells were positive for CD3ε, TIA-1, but negative for CD56. In situ hybridization revealed that tumor cells also expressed Epstein-Barr virus encoded RNA. To our knowledge, this is the first case of NK/T cell lymphoma involving mediastinum.

Epidermal growth factor-like domain-containing protein 7 (EGFL7) enhances EGF receptor-AKT signaling, epithelial-mesenchymal transition, and metastasis of gastric cancer cells.

Epidermal growth factor-like domain-containing protein 7 (EGFL7) is upregulated in human epithelial tumors and so is a potential biomarker for malignancy. Indeed, previous studies have shown that high EGFL7 expression promotes infiltration and metastasis of gastric carcinoma. The epithelial-mesenchymal transition (EMT) initiates the metastatic cascade and endows cancer cells with invasive and migratory capacity; however, it is not known if EGFL7 promotes metastasis by triggering EMT. We found that EGFL7 was overexpressed in multiple human gastric cancer (GC) cell lines and that overexpression promoted cell invasion and migration as revealed by scratch wound and transwell migration assays. Conversely, shRNA-mediated EGFL7 knockdown reduced invasion and migration. Furthermore, EGFL7-overexpressing cells grew into larger tumors and were more likely to metastasize to the liver compared to underexpressing CG cells following subcutaneous injection in mice. EGFL7 overexpression protected GC cell lines against anoikis, providing a plausible mechanism for this enhanced metastatic capacity. In excised human gastric tumors, expression of EGFL7 was positively correlated with expression levels of the mesenchymal marker vimentin and the EMT-associated transcription repressor Snail, and negatively correlated with expression of the epithelial cell marker E-cadherin. In GC cell lines, EGFL7 knockdown reversed morphological signs of EMT and decreased both vimentin and Snail expression. In addition, EGFL7 overexpression promoted EGF receptor (EGFR) and protein kinase B (AKT) phospho-activation, effects markedly suppressed by the EGFR tyrosine kinase inhibitor AG1478. Moreover, AG1478 also reduced the elevated invasive and migratory capacity of GC cell lines overexpressing EGFL7. Collectively, these results strongly suggest that EGFL7 promotes metastasis by activating EMT through an EGFR-AKT-Snail signaling pathway. Disruption of EGFL7-EGFR-AKT-Snail signaling may a promising therapeutic strategy for gastric cancer.

Expression of C-X-C chemokine receptor types 1/2 in patients with gastric carcinoma: Clinicopathological correlations and significance.

C-X-C chemokine receptor types 1/2 (CXCR1/2) may play multiple roles in the development and progression of a number of types of tumor. The abnormal expression of CXCR1/2 in various types of malignant tumors has been reported, but less is known with regard to gastric carcinoma. The present study was preliminarily conducted to elucidate the correlation between clinicopathological factors and the immunohistochemical expression of CXCR1/2 in patients with gastric carcinoma. The expression of CXCR1/2 in 69 specimens of sporadic gastric carcinoma and their corresponding non-neoplastic mucosa obtained by gastrectomy was assayed by immunohistochemistry (IHC) using a polyclonal anti-CXCR1/2 antibody. ERK1/2 and AKT phosphorylation and the expression of indicators of proliferation, growth and apoptosis (Bcl-2 and Bax, Cyclin D1, EGFR and Ki-67), angiogenesis (VEGF and CD34), invasion and metastasis (MMP-9, MMP-2, TIMP-2 and E-cadherin) were also detected by IHC. A total of 68 (98.6%) of the 69 patients with gastric carcinoma were found to have positive CXCR1/2 expression, which appeared to be significantly higher in gastric carcinoma compared with corresponding non-neoplastic mucosa tissues. The expression of CXCR1/2 in gastric carcinoma was significantly associated with invasion, metastasis and TNM staging (P<0.001). Correlation analysis between CXCR1/2 and pAKT (P=0.032), pERK (P<0.001), Cyclin D1 (P=0.049), EGFR (P=0.013), Bcl-2 (P=0.003), microvessel density (P=0.001), MMP-9 (P=0.013) and MMP-2 (P=0.027) expression using the Spearman test showed significant correlation in gastric carcinoma. Univariate and multivariate logistic regression analysis showed that, compared with negative or weak expression, overexpression of CXCR1/2 protein was a significant risk factor for TNM stage (P<0.001). These results preliminarily suggest that CXCR1/2 may be a useful maker for progression of the tumors and a promising target for gastric carcinoma therapy.

Upregulation of C-X-C chemokine receptor type 1 expression is associated with late-stage gastric adenocarcinoma.

Chemokine receptors play multiple roles in the development and progression of various tumor types. The aim of this study was to examine C-X-C chemokine receptor type 1 (CXCR1) protein expression in gastric adenocarcinoma and to investigate the clinical implications of CXCR1 upregulation. Expression of CXCR1 protein in 83 specimens of sporadic gastric adenocarcinoma and their corresponding non-neoplastic mucosa obtained by gastrectomy was assayed using immunohistochemistry. The intensity of immunostaining in tumor tissue was considered strong when tumor tissue staining was more intense than in the corresponding non-neoplastic mucosa; the intensity was null when staining was weaker in the tumor than in the corresponding non-neoplastic mucosa; and the intensity was weak when staining was similar in both tissues. Microvascular density in tumor tissue and its corresponding non-neoplastic mucosa was measured using monoclonal antibody against CD34. A strong correlation was observed between elevated CXCR1 protein expression and tumor stage (P<0.05). T stage, N stage and overall stage positively correlated with CXCR1 protein expression. Microvascular density was higher in tumors with strong CXCR1 protein expression, but the correlation with CXCR1 was not linear (P=0.07). Multiple logistic regression analyses showed that, compared to no or weak expression, overexpression of CXCR1 protein was a significant risk factor for high N stage (N2, N3). These results indicate that CXCR1 may be considered as a new and promising target for gastric adenocarcinoma therapy.

An investigation and pathological analysis of two fatal cases of cadmium poisoning.

Pollution associated with population growth, and with industrial and urban development has led to a serious decline in the water quality of Chinese rivers. Cadmium (Cd) is recognized as one of the most toxic metals and is strongly accumulated by organisms. Humans are exposed to cadmium originating from the environment and from industrial pollution. In spite of thousands of published studies on Cd, there is little information on its pathological features seen in human autopsy. The gross and pathological findings of forensic autopsies of two case of cadmium poisoning are presented and related to an epidemiological investigation. In both cases, multiple organ damage was observed, involving brain, lung, liver, kidney, red blood cells, and platelets, which is consistent with reports in the literature. In particular, in both cases, transmission electron microscopy revealed a large number of dense lysosomal and phagocytic particles in the cytoplasm near the nucleus, indicating the need for a genotoxic study of cadmium. Our observations provide new clues for the future recognition and prevention of Cd poisoning.

Activator protein-1 involvement in proliferation inhibition by gene silencing of Twist in gastric cancer cells.

AIMS: To study the role of the Twist gene in growth of gastric cancer cell line MKN45 and the possible mechanisms involved. METHODS: Human gastric carcinoma MKN45 cells were stably transfected with Twist antisense plasmid using the lipofectamine transfection technique. Expression of Twist in Twist antisense plasmid transfected cells (TwistAS), non-transfected cells (NT) and non-specific Twist antisense plasmid transfected cells (CON) were examined by Western blotting. Cell growth ability in vitro was evaluated by MTT and clone formation assays. Xenograft cancer models were established by nude mouse transfer method. Activator protein-1 (AP-1) DNA binding activity was measured by electrophoretic mobility shift assay (EMSA). The expression of c-Jun and c-Fos were examined by Western blotting. The mRNA level of cyclin D1 was detected by RT-PCR. RESULTS: TwistAS inhibited cell growth and proliferation. In vitro, the cloning efficiency of TwistAS cells (8.0  ±  0.6%) was significantly lower compared to that in NT (26.5  ±  1.1%) and CON (22.7  ±  1.2%). In vivo, the average tumour weight was lighter in the TwistAS group (425.3  ±  20.8  mg) compared with the CON group (1217.0  ±â€Š 50.2  mg) and the NT group (1120.6  ±â€Š 75  mg). TwistAS inhibited AP-1 activity in MKN45 cells (15.3  ±  3.2% versus 50.2  ±â€Š 3.6% and 52.4  ±  3.8%). TwistAS inhibited the expression of c-Fos in MKN45 cells (20.4  ±  3.8% versus 72.5  ±  3.6% and 75.3  ±â€Š 4.0%) but not c-Jun (p < 0.05). cyclin D1 mRNA level was significantly lower in TwistAS cells (40.5  ±  3.8%) than that in CON (132  ±â€Š 5.4%) and NT cells (130  ±  5.2%). CONCLUSIONS: This study demonstrated that down-regulation of the Twist gene suppressed the proliferation of MKN45 gastric cancer cells by negatively regulating the AP-1 activity resulting in the cyclin D1 mRNA level decreasing.

Down-regulated miRNA-214 induces a cell cycle G1 arrest in gastric cancer cells by up-regulating the PTEN protein.

To detect the expression of miRNA-214 in human gastric cancer cell lines of BGC823, MKN45 and SGC7901, and to identify the effect of miRNA-214 on cell cycle and apoptosis of these cells. Expression of miRNA-214 in human normal gastric mucosal cell line GES-1 and human gastric cancer cell lines was detected by real-time reverse-transcription polymerase chain reaction. Antisense-miRNA-214 oligonucleotides were transfected transiently into gastric cancer cell lines to down-regulate the expression of miRNA-214. The cell cycle and apoptosis were studied by flow cytometry assay. PTEN, one of the target genes of miRNA-214 was detected by using of immunocytochemistry and Western blotting. MiRNA-214 was overexpressed in gastric cancer cell lines of BGC823, MKN45 and SGC7901 compared with normal gastric mucosal cell line GES-1. Antisense-miRNA-214 oligonucleotides significantly down-regulated the expression of miRNA-214, and increased the portion of G1-phase and decreased the portion of S-phase in BGC823 and MKN45 cells. The immunocytochemistry test and Western blotting analysis showed that the down-regulation of miRNA-214 could significantly up-regulate the expression of PTEN in BGC823 and MKN45 cells. MiRNA-214 is overexpressed in human gastric cancer cell lines of BGC823, MKN45 and SGC7901. The down-regulation of miRNA-214 could induce a G1 cell cycle arrest in them, the up-regulation of PTEN maybe one of the mechanism.

TRX is up-regulated by fibroblast growth factor-2 in lung carcinoma.

We have previously shown that exogenous fibroblast growth factor-2 (FGF-2) inhibits apoptosis of the small-cell lung cancer (SCLC) cell line NCI-H446, but the underlying mechanism remains unknown. In this study, the protein profiles of FGF-2-treated and untreated NCI-H446 cells were determined by 2-D gel electrophoresis combined with matrix-assisted laser desorption/ionization time-of-flight mass spectrometry and bioinformatics. Differential expression analysis of the protein profiles after FGF-2 treatment identified a total of 24 protein spots, of which nine were up-regulated and 15 were down-regulated. Four proteins were identified by MALDI-TOF-MS: thioredoxin (TRX), visfatin, ubiquitin carboxyl-terminal hydrolase L1 (UCHL1) and Cu/Zn superoxide dismutase (CuZn-SOD). Western blotting revealed that TRX was up-regulated in NCI-H446 and A549 cells treated with FGF-2. Furthermore, immunohistochemical staining confirmed that both FGF-2 and TRX were overexpressed in lung cancer tissues and could be correlated with both lymph node metastasis and clinical stage. These data indicate that TRX may be involved in the FGF-2 signaling pathway.

[Forensic analysis of 74 tumor related medical malpractice cases].

OBJECTIVE: To analyze the causes of medical malpractice in patients with tumor, to determine the medical responsibility, and to recommend the related preventions. METHODS: Seventy four medical malpractice cases, which were involved in tumor and collected from 2000 to 2009 in medicolegal expertise center of west China, were analyzed retrospectively. RESULTS: The medical malpractice cases in the patients with tumor showed an increasing tendency in recent years. The main causes are missed diagnosis, misdiagnosis, improper chemotherapy and neglect of complications. The causes of medical malpractice were different in the different levels of medical services. The occurrence of medical malpractice in surgery and OB-GYN showed more frequent than the others. CONCLUSION: Forensic pathology autopsy is important to resolve medical malpractice of tumor patients by finding out the cause of death and clarifying the medical responsibility. The occurrence of medical malpractice could be reduced by the clinical doctors through improving serve consciousness, obtaining the patients' trust, improving the medical treatment, following related laws and rules, fulfiling duty of medical careness.

The effects of hepatitis C virus non-structural protein 3 on cell growth mediated by extracellular signal-related kinase cascades in human hepatocytes in vitro.

Hepatitis C virus (HCV) infection has become a severe health problem worldwide. The viral proteins are believed to be among the most important factors that contribute to HCV mediated pathogenesis. Accumulated evidence demonstrating that HCV non-structural protein 3 (NS3) possesses oncogenic potential, and is involved in the regulation of cell proliferation has been documented. In this study, we emphasized the effect of HCV NS3 protein on cell proliferation in the immortally normal hepatocyte QSG7701 cells. The cell line transfected with plasmid expressing NS3 protein showed enhanced cell growth, extracellular signal-related kinase (ERK) activation, DNA binding activities of transcription factors of activator protein 1 (AP-1) and NF-kappaB, and cyclin D1 overexpression, but without activation of Jun amino-terminal kinase or p38. Pre-treatment of NS3 protein expressing cells with ERK inhibitor, PD98059, blocked the activation of AP-1 and NF-kappaB, and inhibited cyclin D1 expression and cell proliferation. The results suggest that NS3-mediated cell growth occurs through activation of ERK/AP-1 and NF-kappaB/cyclin D1 cascades.

A case of mesothelial/monocytic incidental cardiac excrescence and literature review.

Mesothelial/monocytic incidental cardiac excrescence (MICE) is a rare entity which is an amalgam of mesothelial cells, histiocytes, and fibrin, often found occasionally during cardiac valve replacement. We report a case in a 25-year-old Chinese female with serous mitral stenosis and patent foramen ovale. Routine and immunohistochemical stains and ultrastructure examination revealed the vegetation was predominantly composed of histocytes with scattered mesothelial cells. In fact nodular histiocytic/mesothelial hyperplasia (NHMH) is a similar lesion to MICE. MICE and NHMH could be unified, and NHMH may be a better choice.

Reduced stratifin expression can serve as an independent prognostic factor for poor survival in patients with esophageal squamous cell carcinoma.

UNLABELLED: Stratifin plays an important role in cancer biology by interfering with intracellular signalling pathways and cell-cycle checkpoints. Decreased expression of stratifin gene has been reported to be a poor prognostic indicator in a variety of human malignant tumors. AIM: To clarify the role and prognostic significance of stratifin in esophageal squamous cell carcinoma (ESCC). METHODS: The alteration of stratifin messenger RNA (mRNA) and protein was analyzed by reverse-transcription and quantitative real-time polymerase chain reaction (QRT-PCR) and Western blotting in 20 paired ESCC and nonneoplastic esophageal mucosa tissues, respectively. Then, immunohistochemistry (IHC) was used to evaluate expression of stratifin in tissues of 148 ESCC patients (including the former 20 pairs of tissues) and correlate it with clinicopathological parameters and prognosis of ESCC patients. RESULTS: The stratifin level of mRNA and protein was markedly downregulated in ESCC tissue compared with in corresponding nonneoplastic esophageal epithelium (P<0.05). Similarly, the positive rate of stratifin protein expression was lower in the esophageal cancer than in paired nonneoplastic esophageal epithelium as detected by IHC (P=0.007). Statistically, the downregulation of stratifin expression was correlated with tumor infiltration depth (P=0.003), lymph node metastasis (P=0.008), distant metastasis (P=0.013), and lymphovascular invasion (P=0.007) of ESCC. Furthermore, the reduced stratifin expression was associated with shorter 5-year survival rate of ESCC patients after curative surgery (P<0.0001). On the basis of univariate and multivariate Cox regression analysis, we found that reduced stratifin expression, T4 stage, lymph node metastasis, and distant metastasis were independent risk factors for worse prognosis in ESCC patients. CONCLUSION: The present report indicates that stratifin could be a useful indicator for prognosis of this disease, as well as a potential target for more effective therapy.

Increased expression of prohibitin and its relationship with poor prognosis in esophageal squamous cell carcinoma.

Prohibitin, a potential tumor suppressor, has been shown to be an anti- proliferative protein, a regulator of cell-cycle progression and in apoptosis. Recently, it was found to be over-expressed in breast cancer and gastric cancer, and it has been suggested as a biomarker in those diseases. To clarify the role and the prognostic significance of prohibitin expression in esophageal squamous cell carcinoma (ESCC), we analyzed the expression in ESCC and their corresponding nonneoplastic epithelia tissues by immunohistochemistry(IHC), Western blotting and real-time quantitative reverse transcription polymerase chain reaction(QRT-PCR).The relationship between prohibitin expression and clinicopathological variables was examined by statistical analysis. The findings suggested the up-regulation of prohibitin play an important role in the carcinogenesis of ESCC. The over-expression of prihibitin was significantly correlated with the depth of tumor, lymph node metastasis, distant metastasis, lymphatic invasion and vascular invasion of ESCC. These results suggested that prohibitin(+), lymph node metastasis and distant metastasis could be the independent risk factors for worse prognosis in ESCC patients.

[Effect of ß-catenin gene silencing by shRNA on biologic characteristics of human esophageal carcinoma cells].

OBJECTIVE: To study the effects of short hairpin RNA (shRNA) mediated gene silencing of ß-catenin on the biological characteristics of esophageal carcinoma cells, and to provide theoretical and experimental evidence for the gene therapy of esophageal carcinoma through target inhibition of ß-catenin gene. METHODS: Single strand DNA was synthesized according to the hairpin RNA sequence, and then subcloned into eukaryotic expression vector pGenesil-3 to construct a shRNA-expression pDNAs driven by human U6 promoter of ß-catenin (pGen-3-CTNNB1). One additional construct of random siRNA (pGen-3-con) without homologous to any human genes was constructed in a similar fashion as control.Positive clones were identified and verified by restriction cleavage and DNA sequencing analyses. pGen-3-CTNNB1 and pGen-3-con were then transfected into esophageal carcinoma cell line Eca-109 with liposome, respectively. Positive colonies were selected with G418. Expression of ß-catenin protein and mRNA in the transfected and nontransfected Eca-109 cells were examined by Western blotting, immunofluorescence and RT-PCR, respectively. Xenograft tumor model was used to compare the tumorigenesis of three different cells.Expressions of ß-catenin in all tumor tissues were examined by immunohistochemistry staining. The invasive abilities of three different cells were examined with transwell invasion filter and Matrigel. RESULTS: ß-catenin expression levels were found markedly decreased in Eca-109 cells transfected with pGen-3-CTNNB1. In vivo, transfection with ß-catenin shRNA greatly impeded the tumor growth, pGen-3-con (1.18 ± 0.13) g, Eca-109 (1.38 ± 0.21) g, pGen-3-CTNNB1 (0.42 ± 0.09) g, P < 0.05. Immunohistochemistry staining showed a significantly decreased expression of ß-catenin in ß-catenin shRNA transfected cells than in random shRNA transfected and nontransfected cells (P < 0.05). The infiltration abilities of esophageal carcinoma cells were significantly suppressed, pGen-3-con (81 ± 5)/HPF, Eca-109 (77 ± 6)/HPF, pGen-3-CTNNB1 (41 ± 4)/HPF, P < 0.01; along with significantly decreased migration abilities, pGen-3-con (73 ± 5)/HPF, Eca-109 (69 ± 5)/HPF, pGen-3-CTNNB1 (38 ± 4)/HPF (P < 0.05). CONCLUSIONS: There are abnormal expression of ß-catenin and activation of Wnt signaling pathway in human esophageal carcinoma cell line Eca-109. RNA interference targeting ß-catenin gene suppresses the growth of xenograft tumorigenesis in nude mouse and the invasiveness and metastatic capability of esophageal carcinoma cells.

[Comparison of mtDNA extraction from different parts of sarcosaphagous insects].

OBJECTIVE: To explore mitochondrial DNA (mtDNA) extraction effects of different parts from sarcosaphagous insects using improved cetyltriethylammnonium bromide (CTAB) method. METHODS: Thirteen Lucilia sericata (Meigen) and 13 Nicrophorus fossor (Erichson) were collected from the corpses of rabbits placed on the outdoor lawn in Huhehot district. Four parts (head, chest muscle, legs and wings) of insect were collected, and the mtDNA of all samples were extracted using CTAB method. The purity and concentration were tested using protein and nucleic acid spectrophotometry. The integrity of the extracted mtDNA and PCR products were checked by agarose gel electrophoresis. The PCR products were sequenced and the obtained sequences were imputed into GenBank for comparison. RESULTS: mtDNA were successfully extracted from 10 head samples, 6 legs samples, 4 wing samples and 13 chest muscle samples of the Lucilia sericata (Meigen). Also, mtDNA were successfully extracted from 5 head samples, 8 legs samples, 3 wing samples and 13 chest muscle samples of the Nicrophorus fossor (Erichson). CONCLUSION: mtDNA can be obtained from chest muscle and other parts of sarcosaphagous insects using the improved CTAB method.

Knockdown of fascin1 expression suppresses the proliferation and metastasis of gastric cancer cells.

AIMS: Our current investigation attempts to study the role of the fascin1 gene in growth and metastasis of gastric cancer cell line MKN45. METHODS: Small interfering RNA (siRNA) was used to inhibit fascin1 expression in the human gastric cancer cell line MKN45. Expression of fascin1 in fascin1 siRNA transfected cells (sifascin1), non-transfected cells (NT) and non-specific fascin1 siRNA cells (CON) were examined by Western blotting and reverse transcription polymerase chain reaction (RT-PCR). Cell growth ability in vitro was evaluated by MTT and clone formation assays. Cell mobility in vitro was examined by the Boyden chamber assay. Nude mice metastasis models were established by abdominal cavity transfer method. Tumour growth was evaluated by immunohistochemistry with proliferating cell nuclear antigen (PCNA). RESULTS: Knockdown of fascin1 expression in MKN45 cells resulted in decreased cellular proliferative and migratory abilities. In vitro, the cloning efficiency of siFascin1 cells (34.2%) was significantly lower compared to that in NT (78.5%) (p < 0.05). The migration rate in siFascin1 cells was significantly decreased (33.7%) compared with NT cells (89.4%) (p < 0.05). In vivo, the cell proliferation rate was lower in siFascin1 cells (25.8%) compared to that in NT (75.0%) (p < 0.05). The number of tumour clones in the liver was significantly lower in siFascin1 cells (2.0 +/- 1.1) compared to that in NT (5.1 +/- 1.6) (p < 0.05). CONCLUSIONS: Our study demonstrates that down-regulation of fascin1 suppresses the proliferation and migration of gastric cancer cells MKN45, suggesting that fascin1 siRNA may offer a novel potential gene therapy approach for human gastric cancer with fascin1 over-expression.

Specific activation of 2'-5'oligoadenylate synthetase gene promoter by hepatitis C virus-core protein: a potential for developing hepatitis C virus targeting gene therapy.

AIM: To examine whether 2'-5'oligoadenylate synthetase (OAS) gene promoter can be specifically activated by hepatitis C virus (HCV)-core protein. METHODS: Human embryo hepatic cell line L02 was transfected with pcDNA3.1-core plasmid and selected by G418. Expression of HCV-core was detected by reverse transcription polymerase chain reaction and Western blotting. The OAS promoter sequence was amplified from the genomic DNA and inserted into pGL3-basic vector. The resultant pGL3-OAS-Luci plasmid was transiently transfected into L02/core cells and luciferase activity was assayed. RESULTS: L02/core cell line stably expressing HCV-core protein was established. The pGL3-OAS-Luci construct exhibited significant transcriptional activity in the L02/core cells but not in the L02 cells. CONCLUSION: HCV-core protein activates the OAS gene promoter specifically and effectively. Utilization of OAS gene promoter would be an ideal strategy for developing HCV-specific gene therapy.

Expression of semaphorin 5A and its receptor plexin B3 contributes to invasion and metastasis of gastric carcinoma.

AIM: To investigate the protein and mRNA expression of semaphorin 5A and its receptor plexin B3 in gastric carcinoma and explore its role in the invasion and metastasis of gastric carcinoma. METHODS: Expression of semaphorin 5A and its receptor plexin B3 in 48 samples of primary gastric carcinoma, its corresponding non-neoplastic mucosa, and matched regional lymph node metastasis was assayed by reverse transcription-polymerase chain reaction (RT-PCR), real-time RT-PCR and Western blotting. RESULTS: The protein and mRNA expression of semaphorin 5A and its receptor plexin B3 increased gradually in non-neoplastic mucosa, primary gastric carcinoma and lymph node metastasis (P < 0.05). Moreover, the expression of semaphorin 5A was closely correlated with that of plexin B3. CONCLUSION: Semaphorin 5A and its receptor plexin B3 play an important role in the invasion and metastasis of gastric carcinoma.

[Advances in the studies of postmortem interval estimation by the levels of chemical components in human vitreous humor after death].

Estimation of postmortem interval (PMI) is one of the problems that need to be solved for forensic examination of the dead body. Accurate estimation of PMI has great values to criminal investigation and trial. The levels of chemical components in human vitreous humor are changed with time after death, which can help estimate the PMI. The levels of certain chemical components, such as potassium, magnesium, ammonia, urea, creatinine, uric acid, hypoxanthine, lactic acid and so on, in human vitreous humor will gradually increase with time after death, while others such as calcium, sodium, enzymes, glucose, vitamin C and so on will decrease. The updates and advances in those studies were reviewed in this article.