Three-dimensional choroidal vascularity index and choroidal thickness in fellow eyes of acute and chronic primary angle-closure using swept-source optical coherence tomography.

AIM: To compare the three-dimensional choroidal vascularity index (CVI) and choroidal thickness between fellow eyes of acute primary angle-closure (F-APAC) and chronic primary angle-closure glaucoma (F-CPACG) and the eyes of normal controls. METHODS: This study included 37 patients with unilateral APAC, 37 with asymmetric CPACG without prior treatment, and 36 healthy participants. Using swept-source optical coherence tomography (SS-OCT), the macular and peripapillary choroidal thickness and three-dimensional CVI were measured and compared globally and sectorally. Pearson's correlation analysis and multivariate regression models were used to evaluate choroidal thickness or CVI with related factors. RESULTS: The mean subfoveal CVIs were 0.35±0.10, 0.33±0.09, and 0.29±0.04, and the mean subfoveal choroidal thickness were 315.62±52.92, 306.22±59.29, and 262.69±45.55 µm in the F-APAC, F-CPACG, and normal groups, respectively. All macular sectors showed significantly higher CVIs and choroidal thickness in the F-APAC and F-CPACG eyes than in the normal eyes (P<0.05), while there were no significant differences between the F-APAC and F-CPACG eyes. In the peripapillary region, the mean overall CVIs were 0.21±0.08, 0.20±0.08, and 0.19±0.05, and the mean overall choroidal thickness were 180.45±54.18, 174.82±50.67, and 176.18±37.94 µm in the F-APAC, F-CPACG, and normal groups, respectively. There were no significant differences between any of the two groups in all peripapillary sectors. Younger age, shorter axial length, and the F-APAC or F-CPACG diagnosis were significantly associated with higher subfoveal CVI and thicker subfoveal choroidal thickness (P<0.05). CONCLUSION: The fellow eyes of unilateral APAC or asymmetric CPACG have higher macular CVI and choroidal thickness than those of the normal controls. Neither CVI nor choroidal thickness can distinguish between eyes predisposed to APAC or CPACG. A thicker choroid with a higher vascular volume may play a role in the pathogenesis of primary angle-closure glaucoma.

Publication trends of primary angle-closure disease during 1991-2022: a bibliometric analysis.

AIM: To perform a bibliometric analysis in the field of primary angle-closure disease (PACD) research to characterize current global trends and compare contributions from different countries, institutions, journals, and authors. METHODS: All PACD-related publications from 1991 to 2022 from the Web of Science Core Collection database were extracted. Microsoft Excel and VOSviewer were used to collect publication data, analyze publication trends, and visualize relevant results. RESULTS: A total of 1721 publications with 34 591 citations were identified. China produced the most publications (554) while ranking third in citations (8220 times). The United States contributed the most citations (12 315 times) with publications (362) ranking second. The Investigative Ophthalmology Visual Science was the most productive journal concerning PACD, and Aung Tin was the author with the highest number of publications in the field. Keywords were classified into three clusters, epidemiology and pathogenesis research, optical coherence tomography (OCT) and other imaging examinations, and glaucoma surgery treatment. Genome-wide association, susceptibility loci, OCT, and combined phacoemulsification have become new hot research topics in recent years since 2015. CONCLUSION: China, the United States, and Singapore make the most outstanding contributions in the field of PACD research. OCT, combined phacoemulsification, and gene mutation-related study, are considered the potential focus for future research.

RTN4B-mediated suppression of Sirtuin 2 activity ameliorates ß-amyloid pathology and cognitive impairment in Alzheimer's disease mouse model.

Sirtuin 2 (SIRT2) is an NAD+ dependent deacetylase that is the most abundant sirtuin protein in the brain. Accumulating evidence revealed the role of SIRT2 in a wide range of biological processes and age-related diseases. However, the pivotal mechanism of SIRT2 played in Alzheimer's disease (AD) remains unknown. Here, we report that pharmacological inactivation of SIRT2 has a beneficial effect in AD. The deacetylase inhibitor of SIRT2 rescued the cognitive impairment in amyloid precursor protein/presenilin 1 transgenic mouse (APP/PS1 mouse), and the BACE1 cleavage was weakened to reduce the ß-amyloid (Aß) production in the hippocampus. Moreover, we firstly identified that Reticulon 4B (RTN4B) played a crucial role between SIRT2/BACE1 regulation in AD. RTN4B, as a deacetylation substrate for SIRT2, the deacetylation by SIRT2 drived the ubiquitination and degradation of RTN4B and then the disturbed RTN4B interacted with and influenced the expression of BACE1. When we overexpressed RTN4B in neurons of the hippocampus in the AD mouse model, the abnormal Aß accumulation and cognitive impairment were ameliorated, consistent with the results of SIRT2 inhibition in vivo. Moreover, we showed that the regulatory effect of SIRT2 on BACE1 is dependent on RTN4B. When RTN4B was knocked down, the effects of SIRT2 inhibition on the BACE1 level, Aß pathology, and AD-liked behaviors were also blocked. Collectively, we provide evidence that SIRT2 may be a potential target for AD; the new found SIRT2/RTN4B/BACE1 pathological pathway is one of the critical mechanisms for the improvement of SIRT2 on AD.

[Characteristics of soil enzyme stoichiometry along an altitude gradient on Qinghai-Tibet Pla-teau alpine meadow, China]. / é’è—é«˜åŽŸé«˜å¯’è‰ç”¸ä¸åŒæµ·æ‹”åœŸå£¤é ¶åŒ–å­¦è®¡é‡ç‰¹å¾.

Soil enzymes play critical roles in material cycle and energy flow of ecosystems. Understanding soil enzyme activities is of great significance for exploring ecosystem functions. In this study, we investigated soil enzyme activities, stoichiometry and their driving factors at six different altitudes (4300-5100 m) on Qinghai-Tibet Plateau alpine meadow using Biolog microplate analysis. The results showed that ß-1,4-glucosidase (ßG) closely related to C cycle, ß-1,4-N-acetylglucosaminidase (NAG) and L-leucine aminopeptidase (LAP) closely related to N cycle and the activity of acid phosphatase (AP), which was closely related to P cycle, all exhibited unimodal trends with increasing altitude, with the order of 4800 m＞4950 m＞4400 m＞4650 m＞5100 m＞4300 m. Soil N:P enzyme activity ratio showed the same trend as soil enzyme activity, and reached the highest value at 4950 m, however, soil C:N and C:P enzyme activities ratios increased along the altitude. Pearson correlation analysis showed that SOC, TN and soil water content were significantly positively correlated with the activities of four types of enzymes. Mean annual precipitation was significantly negatively associated with the activities of NAG and AP. Mean annual precipitation, mean annual temperature, Shannon diversity, vegetation richness, vegetation coverage and TN affected ratios of soil C:P and N:P enzymes. Soil C:N activity ratio correlated with mean annual temperature, mean annual precipitation, vegetation richness, vegetation coverage, SOC and TN. In summary, soil enzyme activities and stoichiometry had remarkable difference along the altitude gradient on Qinghai-Tibet Plateau alpine meadow, with certain N limitation in high altitude areas. Soil water content, TN, SOC, mean annual precipitation and mean annual temperature were key factors driving such differences.

MiR-4673 Modulates Paclitaxel-Induced Oxidative Stress and Loss of Mitochondrial Membrane Potential by Targeting 8-Oxoguanine-DNA Glycosylase-1.

BACKGROUND: Our previous study identified a novel microRNA, miR-4673, which is upregulated in A549 cells exposed to paclitaxel (PTX). In this study, we investigated the role of miR-4673 in PTX-induced cytotoxicity. METHODS: 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay, apoptosis assay, 5,5',6,6'-Tetrachloro-1,1',3,3'-tetraethyl-imidacarbocyanine iodide (JC-1) staining and 2',7'-Dichlorofluorescein (DCFH) staining were used to evaluate cell viability, apoptosis, mitochondrial membrane potential (MMP) loss and reactive oxygen species (ROS) generation in A549 and H1299 cells. Bioinformatics analysis and Luciferase reporter assay were used to explore whether 8-oxoguanine-DNA glycosylase-1 (OGG1) is a target gene of miR-4673. RESULTS: Enforced expression of miR-4673 decreased cell viability and increased PTX-induced apoptosis, MMP loss and reactive oxygen species (ROS) generation in A549 and H1299 cells. Bioinformatics analysis, which was used to identify potential target of miR-4673, revealed a binding site of miR-4673 in 3'UTR of OGG1. Luciferase reporters assays showed that miR-4673 specifically binds to 'CUGUUGA' in 3'UTR of OGG1. Enforced expression of miR-4673 decreased accumulation of OGG1. In addition, silencing OGG1 enhanced inhibitory effects of PTX on apoptosis, MMP loss and ROS generation, which is similar to effects of miR-4673. Moreover, enforced expression of OGG1 compromised promoting effects of miR-4673 on PTX-induced apoptosis, MMP loss and ROS generation. CONCLUSION: miR-4673 modulates PTX-induced apoptosis, MMP loss and ROS generation by targeting OGG1.

microRNA-506 regulates proliferation, migration and invasion in hepatocellular carcinoma by targeting F-spondin 1 (SPON1).

Our previous study indicates microRNA-506 (miR-506) is downregulated in hepatocellular carcinoma (HCC). In the current study, we investigate the effects of miR-506 on proliferation, migration and invasion in HCC. We report that enforced expression of miR-506 inhibits proliferation, migration and invasion in vitro, and suppresses tumor growth in vivo. Conversely, suppression of miR-506 exhibits promoting effects on proliferation, migration and invasion in vitro, and on tumor growth in vivo. In addition, miR-506 binds to the 3'UTR of F-spondin 1(SPON1), and enforced expression of miR-506 decreases accumulation of SPON1. Moreover, enforced expression of SPON1 and suppression of SPON1 alleviates effects of miR-506 mimics and inhibitors on proliferation, migration and invasion in vitro, respectively. In conclusion, microRNA-506 regulates proliferation, migration and invasion in HCC by targeting SPON1.

FBXO31 promotes cell proliferation, metastasis and invasion in lung cancer.

FBXO31 is a member of F-box family which is involved in diverse biological functions and development of disease. Recent reports in breast cancer, hepatocellular carcinoma and ovarian cancer demonstrated inhibitory effect of FBXO31 on proliferation and tumorigenesis. However, the function of FBXO31 is not analyzed in lung cancer so far. In this study, we reported that expression of FBXO31 was higher in lung cancer tissues compared with non-cancerous lung tissues, and that higher expression of FBXO31 was significantly associated with tumor size, tumor infiltration, clinical stages and lymph node metastasis. In addition, exogenous expression of FBXO31 promoted cell growth, metastasis and invasion in A549 cells. Conversely, silencing FBXO31 by specific siRNA caused inhibitory effect on cell growth, metastasis and invasion. Moreover, tumorigenicity assays in nude mice showed FBXO31 promoted tumor growth in vivo. In conclusion, our data suggest FBXO31 promotes cell proliferation, metastasis and invasion in lung cancer.

Serum soluble CD40 is associated with liver injury in patients with chronic hepatitis B.

Soluble cluster of differentiation 40 (sCD40) is proteolytically cleaved from membrane-bound CD40 and binds to CD154, thereby inhibiting CD40-CD154-mediated immune responses. The aim of the present study was to clarify the role of sCD40 in chronic hepatitis B (CHB). The sCD40 levels in sera from 132 patients with CHB and 33 healthy individuals were retrospectively measured. sCD40 concentrations in patients with CHB were higher than those in healthy controls, and sCD40 levels correlated positively with serum levels of the liver dysfunction biomarkers alanine transaminase (ALT) and aspartate transaminase (AST). sCD40 concentrations increased with a rise in the severity of liver necroinflammation and fibrosis. Patients with >75% liver tissue staining positive for hepatitis B virus (HBV) antigen expression showed significantly lower sCD40 levels than those who stained negative for the HBV antigen. The area under the receiver operating characteristic curve of sCD40 was greater than that of ALT and AST; thus, sCD40 levels have a high diagnostic accuracy for detecting severe liver inflammation in patients with CHB, and could serve as an immunological marker of hepatic tissue injury.

Five miRNAs as novel diagnostic biomarker candidates for primary nasopharyngeal carcinoma.

MicroRNAs (miRNAs) play an essential role in the development and progression of nasopharyngeal carcinomas (NPC). Despite advances in the field of cancer molecular biology and biomarker discovery, the development of clinically validated biomarkers for primary NPC has remained elusive. In this study, we investigated the expression and clinical significance of miRNAs as novel primary NPC diagnostic biomarkers. We used an array containing 2, 500 miRNAs to identify 22 significant miRNAs, and these candidate miRNAs were validated using 67 fresh NPC and 25 normal control tissues via quantitative real-time PCR (qRT-PCR). Expression and correlation analyses were performed with various statistical approaches, in addition to logistic regression and receiver operating characteristic curve analyses to evaluate diagnostic efficacy. qRT-PCR revealed five differentially expressed miRNAs (miR-93-5p, miR-135b-5p, miR-205-5p and miR-183-5p) in NPC tissue samples relative to control samples (p<0.05), with miR-135b-5p and miR-205-5p being of significant diagnostic value (p<0.01). Moreover, comparison of NPC patient clinicopathologic data revealed a negative correlation between miR-93-5p and miR- 183-5p expression levels and lymph node status (p<0.05). These findings display an altered expression of many miRNAs in NPC tissues, thus providing information pertinent to pathophysiological and diagnostic research. Ultimately, miR-135b-5p and miR-205-5p may be implicated as novel NPC candidate biomarkers, while miR- 93-5p, miR-650 and miR-183-5p may find application as relevant clinical pathology and diagnostic candidate biomarkers.

Human umbilical cord blood mesenchymal stem cell transplantation suppresses inflammatory responses and neuronal apoptosis during early stage of focal cerebral ischemia in rabbits.

AIM: Human umbilical cord blood mesenchymal stem cells (hUCB-MSCs) have been shown to ameliorate cerebral ischemia in animal models. In this study we investigated the effects of hUCB-MSCs on inflammatory responses and neuronal apoptosis during the early stage of focal cerebral ischemia in rabbits. METHODS: Focal cerebral ischemia was induced in male New Zealand rabbits by occlusion of MCA for 2 h. The blood samples were collected at different time points prior and during MCAO-reperfusion. The animals were euthanized 3 d after MCAO, and the protein levels of IL-1ß, IL-6, IL-10 and TNF-α in the serum and peri-ischemic brain tissues were detected using Western blot and ELISA, respectively. Inflammatory cell infiltration, neuronal apoptosis and neuronal density were measured morphologically. hUCB-MSCs (5 × 10(6)) were iv injected a few minutes after MCAO. RESULTS: The serum levels of IL-1ß, IL-6 and TNF-α were rapidly increased, and peaked at 2 h after the start of MCAO. hUCB-MSC transplantation markedly and progressively suppressed the ischemia-induced increases of serum IL-1ß, IL-6 and TNF-α levels within 6 h MCAO-reperfusion. Focal cerebral ischemia decreased the serum level of IL-10, which was prevented by hUCB-MSC transplantation. The expression of IL-1ß, IL-6, IL-10 and TNF-α in the peri-ischemic brain tissues showed similar changes as in the serum. hUCB-MSC transplantation markedly suppressed the infiltration of inflammatory cells, and increased the neuronal density around the ischemic region. Furthermore, hUCB-MSC transplantation significantly decreased the percentage of apoptosis around the ischemic region. CONCLUSION: hUCB-MSCs transplantation suppresses inflammatory responses and neuronal apoptosis during the early stage focal cerebral ischemia in rabbits.

Effect of human umbilical cord blood mesenchymal stem cell transplantation on neuronal metabolites in ischemic rabbits.

BACKGROUND: Because there is little research on the effects of transplanted stem cells on neuronal metabolites in infarct areas, we transplanted human umbilical cord blood mesenchymal stem cells (hUCB-MSCs) into cerebral ischemic rabbits and examined the neuronal metabolites. RESULTS: Rabbits (n = 40) were equally divided into sham, middle cerebral artery occlusion (MCAO), hUCB-MSC, and saline groups. The rabbit ischemic model was established by MCAO. The effects of hUCB-MSC transplantation were assessed by proton magnetic resonance spectroscopy (1H-MRS), neurological severity scores (NSSs), infarct area volume, neuronal density, and optical density (OD) of microtubule-associated protein 2 (MAP2)-positive cells. We also evaluated complete blood cell counts(CBCs) and serum biochemical parameters. NSSs in the hUCB-MSC group at 7 and 14 days after reperfusion were lower than in MCAO and saline groups (p < 0.05). Compared with MCAO and saline groups at 2 weeks after MCAO, the infarction volume in the hUCB-MSC group had decreased remarkably (p < 0.05). Significant neuronal metabolic changes occurred in the infarct area at 24 h and 2 weeks after MCAO. 1H-MRS revealed an elevation in the lactate (Lac)/creatine including phosphocreatine (Cr) ratio and a decrease in the N-acetylaspartate (NAA)/Cr and choline-containing phospholipids (Cho)/Cr ratios at 24 h after MCAO in the MCAO group (p < 0.01). Compared with saline and MCAO groups at 24 h and 2 weeks after MCAO, NAA/Cr and Cho/Cr ratios had increased significantly, whereas the Lac/Cr ratio had decreased significantly in the hUCB-MSC group (p < 0.01). Neuronal density and OD of MAP2-positive cells in the MCAO group were significantly lower than those in the sham group, whereas the neuronal density and OD of MAP2-positive cells in the hUCB-MSC group were higher than those in MCAO and saline groups (p < 0.05). CBCs and biochemical parameters were unchanged in the MCAO group at 24 h and 2 weeks after hUCB-MSC transplantation. CONCLUSIONS: Transplanted hUCB-MSCs might ameliorate ischemic damage by influencing neuronal metabolites in the infarct area, providing additional evidence for neuroprotection by stem cells. No significant changes were observed in CBCs or serum biochemical parameters, suggesting that intravenous infusion of hUCB-MSCs is safe for rabbits in the short-term.

Hepatoprotective effects of baicalein against CCl4-induced acute liver injury in mice.

AIM: To investigate the hepatoprotective effect of baicalein against carbon tetrachloride (CCl4)-induced liver damage in mice. METHODS: Mice were orally administered with baicalein after CCl4 injection, and therapeutic baicalein was given twice a day for 4 d. The anti-inflammation effects of baicalein were assessed directly by hepatic histology and serum alanine aminotranferease and aspartate aminotransferase measurement. Proliferating cell nuclear antigen was used to evaluate the effect of baicalein in promoting hepatocyte proliferation. Serum interleukin (IL)-6, IL-1ß and tumor necrosis factor-α (TNF-α) levels were measured by enzyme-linked immunosorbent assay and liver IL-6, TNF-α, transforming growth factor-α (TGF-α), hepatocyte growth factor (HGF) and epidermal growth factor (EGF) genes expression were determined by quantitative real-time polymerase chain reaction. RESULTS: CCl4-induced acute liver failure model offers a survival benefit in baicalein-treated mice. The data indicated that the mRNA levels of IL-6 and TNF-α significantly increased within 12 h after CCl4 treatment in baicalein administration groups, but at 24, 48 and 72 h, the expression of IL-6 and TNF-α was kept at lower levels compared with the control. The expression of TGF-α, HGF and EGF was enhanced dramatically in baicalein administration group at 12, 24, 48 and 72 h. Furthermore, we found that baicalein significantly elevated the serum level of TNF-α and IL-6 at the early phase, which indicated that baicalein could facilitate the initiating events in liver regeneration. CONCLUSION: Baicalein may be a therapeutic candidate for acute liver injury. Baicalein accelerates liver regeneration by regulating TNF-α and IL-6 mediated pathways.

[Comparison of intraocular pressure reducing effects of three prostaglandin eyedrops in open-angle glaucoma].

OBJECTIVE: To compare the efficacy of latanoprost, travoprost and bimatoprost given in the evening on the 24-hour intraocular pressure (IOP) curve in open-angle glaucoma patients. METHODS: It was a case-control study. Patients with primary open-angle glaucoma were selected for the present study. Twenty-one, 22 and 20 patients were treated once daily with latanoprost, travoprost and bimatoprost for 4 weeks, respectively. Before and four weeks after the treatment, IOP was measured by masked evaluators at 8AM, 10AM, noon, 2PM, 4PM, 6PM, 8PM, 10PM, midnight, 2AM, 4AM and 6AM. Repeated measure analysis of variance was used to compare the IOP responses to the drug regimens for the entire circadian curve. Analysis of variance was used to compare the circadian variations of intraocular pressure. RESULTS: The IOPs of all patients in these 3 groups decreased markedly after 4 weeks. The daily average IOP (mean ± standard deviation) in the latanoprost group decreased from (18.9 ± 2.1) mm Hg (1 mm Hg = 0.133 kPa) to (15.3 ± 2.7) mm Hg, and the extent of the decrease was 19.0%. IOP in the travoprost group decreased from (19.1 ± 3.1) mm Hg to (15.3 ± 2.1) mm Hg, with a decrease of 19.4%. IOP in the bimatoprost group decreased from (18.6 ± 1.9) mm Hg to (14.9 ± 1.9) mm Hg, with a decrease of 19.9%. The effectiveness of the treatments did not differ significantly between these three groups (F = 1.501, P = 0.110). The descending percentage compared with circadian variation ranges before treatment in patients with latanoprost, travoprost and bimatoprost was 31.0%, 31.1% and 31.9%, respectively. In comparison of these three groups, the circadian variations of intraocular pressure did not differ significantly (F = 0.286, P = 0.752). CONCLUSIONS: This study demonstrated that latanoprost, travoprost and bimatoprost are all effective in reducing IOP over the 24-hour curve in primary open-angle glaucoma. On the basis of our data, there was no statistically significant difference in the IOP reduction between these three drugs.

FBXO31 is down-regulated and may function as a tumor suppressor in hepatocellular carcinoma.

The F-box protein family member FBXO31 has rarely been studied in human hepatocellular carcinoma (HCC). This study was designed to investigate the expression profile of FBXO31 in HCC and the possibility that FBXO31 might function as a tumor suppressor in HCC cell lines. We report that FBXO31 is strongly down-regulated in HCC cell lines and specimens. Ectopic expression of FBXO31 inhibited cell proliferation and colony formation in HepG2 and Hep3B cells. The endogenous expression of FBXO31 was fluctuated through cell cycle in the HepG2 cells with maximal expression from late G2 to early G1 phase. Ectopic expression of FBXO31 in HepG2 resulted in the accumulation of cells at the G1 phase of the cell cycle. Possible mechanism might be cyclin D1 degradation mediate by FBXO31 through ubiquitin ligase pathway. Ectopic overexpression of FBXO31 resulted in down-regulation of cyclin D1 which leads to the accumulation of cells at the G1 phase of the cell cycle. Cytoplasmic location of FBXO31 was consistent with cyclin D1 degradation in cytoplasm. Together, our findings suggested that down-regulation of FBXO31 might function as a tumor suppressor in HCC.

[Expression of S100A6 in primary and metastatic human gastric cancer].

OBJECTIVE: Some members of the S100 gene family have been suggested to be associated with cancer development and metastasis. Our previous cDNA micro-array studies have showed S100A6 expression is elevated in gastric cancer compared with that in paired normal mucosa. To validate our previous results and further investigate the possible role of S100A6 gene in gastric cancer, we carried out this detailed S100A6 expression analysis in more matched gastric cancer samples. METHODS: S100A6 expression was detected in 20 paired fresh surgical samples of gastric tumor tissue and matched non-cancerous mucosa by QRT-PCR. A gastric cancer tissue microarray (TMA) containing 1020 duplicate matched normal mucosa, gastric cancer tissue and metastatic lymph node tissue cores from 208 gastric cancer patients was constructed. S100A6 expression was detected by immunohistochemistry and the correlation between S100A6 expression with clinicopathological factors and survival was analyzed. RESULTS: As quantitated by QRT-PCR, S100A6 transcript level was elevated in 73.7% of the primary cancer lesions with an average 2.25-fold up-regulation than that in matched non-neoplastic mucosa. As displayed by immunohistochemistry, the positive rate of S100A6 in non-neoplastic mucosa, tumor lesions and metastatic lymph nodes was 34.3%, 84.1% and 90.9%, respectively. S100A6 expression level in cancer and metastatic lymph node was significantly higher than their matched non-neoplastic mucosa (P < 0.05). 65.5% of patients showed an increased S100A6 expression in cancer tissue compared with that in matched normal mucosa. S100A6 overexpression was associated with larger tumor size and deeper invasion (P = 0.022 and P = 0.009). No evidence was found for an association between S100A6 expression level and other variables, including tumor grade, nodal metastases, and TNM stage. There was no association between S100A6 expression level and survival. But compared with paired non-neoplastic mucosa, an increased S100A6 expression in tumor lesion predicated a decreasing suvival if compared with a decreased S100A6 expression, though the difference was statistically not significant. CONCLUSION: Elevated expression of S100A6 gene may be an early event in the development and progression of gastric cancer. Further study of this gene may be helpful for understanding the nature of gastric carcinoma.

[Influence of dendritic cell infiltration on prognosis and biologic characteristics of progressing gastric cancer].

OBJECTIVE: To study the relation between dendritic cell (DC) infiltration and clinicopathologic parameters, biologic characteristics and prognosis of progressing gastric cancer. METHODS: The development of apoptotic cell death (apoptotic index, AI) in 61 progressing gastric carcinoma tissues was analyzed by terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate biotin nick end labeling (TUNEL) method. The PCNA labeling index (PCNA-LI), density of dendritic cells in the tumor were detected by immunohistochemical method by the LSAB kit using antibody against S-100 protein and PC-10. RESULTS: DC infiltration was negatively correlated with lymph node metastasis, clinical stage and PCNA-LI, but positively with AI. The DCs in gastric cancer groups with and without lymph node metastasis were (5.63 +/- 4.37)/HPF and (8.51 +/- 5.57)/HPF with difference significant (P < 0.05). The DC infiltration in I, II, III stage lesions were (11.23 +/- 6.05)/HPF, (6.28 +/- 4.37)/HPF and (5.53 +/- 5.19)/HPF also with differences significant (P < 0.01). The PCNA-LI was significantly higher in the low DC group (57.10% +/- 14.18%) than that of high DC group (48.15% +/- 10.59%, P < 0.01). AI findings were 3.77% +/- 1.26% and 2.95% +/- 1.07% in the high and low DC groups (P < 0.01). A positive correlation was observed between DC infiltration and AI (r = 0.39, P < 0.01) whereas a negative correlation between DC infiltration and PCNA-LI (r = -0.47, P < 0.01). The prognosis of high DC infiltration patients was significantly better than those with low ones. CONCLUSION: The infiltrating dendritic cells in and around tumor, representing the local immune status of the host, may play an important role in immunological defense mechanism of host versus tumor. Dendritic cells may inhibit the proliferation and induce the apoptosis of the tumor cells, thus affecting the clinical features and improve the prognosis of gastric carcinoma.