Decoding Gastric Cancer: Machine Learning Insights Into the Significance of COMMDs Family in Immunotherapy and Diagnosis.

Copper, an indispensable trace element for the human body, serves not only as a crucial auxiliary factor in redox reactions within the organism but also as a significant constituent of numerous key metabolic enzymes. The COMMD family plays a vital role in regulating copper at both the cellular and systemic levels, particularly in the realm of tumor research, an area notably deficient in gastric cancer investigations. With the advancement of precision medical techniques, individualized and precise screening and treatment have become paramount considerations in the contemporary medical landscape for gastric cancer therapy. In light of this, we meticulously scrutinized existing transcriptomic datasets for gastric cancer, validating the expression levels and prognostic value of COMMD family genes. Simultaneously, employing the ssGSEA algorithm, we devised the COMMDs score. Enrichment analysis, gene mutations, and clinical features were incorporated into the assessment of this score. Furthermore, we contextualized the COMMDs score within the framework of the immune microenvironment, evaluating the relationship between the COMMDs family and immune factors as well as immune cells. The results suggest a correlation between the COMMDs score and various immune-related features. Based on this foundation, multiple machine learning approaches indicated Logistic Regression, with a remarkable ROC of 0.972, as the optimal diagnostic model. To accentuate the translational medical value of the COMMDs family, we selected COMMD10 as a differential gene in gastric cancer for further validation. Functional experiments revealed a decline in the proliferative and migratory capabilities of gastric cancer cells upon silencing COMMD10. Additionally, through pathway intervention, we unveiled the PI3K-AKT pathway as a potential mechanism through which COMMD10 influences gastric cancer activity. In summary, our study affirms the prospective role of the COMMDs family as potential markers for the diagnosis and treatment of gastric cancer in the future.

Ethanol inhibits pancreatic acinar cell autophagy through upregulation of ATG4B, mediating pathological responses of alcoholic pancreatitis.

Excessive alcohol intake is a major risk factor for pancreatitis, sensitizing the exocrine pancreas to stressors by mechanisms that remain obscure. Impaired autophagy drives nonalcoholic pancreatitis, but the effects of ethanol (EtOH) and alcoholic pancreatitis on autophagy are poorly understood. Here, we find that ethanol reduces autophagosome formation in pancreatic acinar cells, both in a mouse model of alcoholic pancreatitis induced by a combination of EtOH diet and cerulein (a CCK ortholog) and in EtOH+CCK-treated acinar cells (ex vivo model). Ethanol treatments decreased pancreatic level of LC3-II, a key mediator of autophagosome formation. This was caused by ethanol-induced upregulation of ATG4B, a cysteine protease that, cell dependently, regulates the balance between cytosolic LC3-I and membrane-bound LC3-II. We show that ATG4B negatively regulates LC3-II in acinar cells subjected to EtOH treatments. Ethanol raised ATG4B level by inhibiting its degradation, enhanced ATG4B enzymatic activity, and strengthened its interaction with LC3-II. We also found an increase in ATG4B and impaired autophagy in a dissimilar, nonsecretagogue model of alcoholic pancreatitis induced by EtOH plus palmitoleic acid. Adenoviral ATG4B overexpression in acinar cells greatly reduced LC3-II and inhibited autophagy. Furthermore, it aggravated trypsinogen activation and necrosis, mimicking key responses of ex vivo alcoholic pancreatitis. Conversely, shRNA Atg4B knockdown enhanced autophagosome formation and alleviated ethanol-induced acinar cell damage. The results reveal a novel mechanism, whereby ethanol inhibits autophagosome formation and thus sensitizes pancreatitis, and a key role of ATG4B in ethanol's effects on autophagy. Enhancing pancreatic autophagy, particularly by downregulating ATG4B, could be beneficial in mitigating the severity of alcoholic pancreatitis.NEW & NOTEWORTHY Ethanol sensitizes mice and humans to pancreatitis, but the underlying mechanisms remain obscure. Autophagy is important for maintaining pancreatic acinar cell homeostasis, and its impairment drives pancreatitis. This study reveals a novel mechanism, whereby ethanol inhibits autophagosome formation through upregulating ATG4B, a key cysteine protease. ATG4B upregulation inhibits autophagy in acinar cells and aggravates pathological responses of experimental alcoholic pancreatitis. Enhancing pancreatic autophagy, particularly by down-regulating ATG4B, could be beneficial for treatment of alcoholic pancreatitis.

LncRNA LL22NC03-N14H11.1 promoted hepatocellular carcinoma progression through activating MAPK pathway to induce mitochondrial fission.

Involvement of long non-coding RNAs (lncRNAs) in hepatocarcinogenesis has been largely documented. Mitochondrial dynamics is identified to impact survival and metastasis in tumors including hepatocellular carcinoma (HCC), but the underlying mechanism remains poorly understood. This study planned to explore the regulation of lncRNA LL22NC03-N14H11.1 on HCC progression and mitochondrial fission. Dysregulated lncRNAs in HCC are identified through circlncRNAnet and GEPIA bioinformatics tools. Biological function of LL22NC03-N14H11.1 in HCC was detected by CCK-8 assay, flow cytometry analysis, transwell invasion, and wound healing assays. Molecular interactions were determined by RNA immunoprecipitation, RNA pull-down, and co-immunoprecipitation assays. Results showed that LL22NC03-N14H11.1 was upregulated in HCC tissues and cells. Functionally, LL22NC03-N14H11.1 contributed to cell proliferation, migration, invasion, and epithelial-to-mesenchymal transition (EMT) in HCC. Moreover, LL22NC03-N14H11.1 facilitated mitochondrial fission in HCC cells. Mechanistically, LL22NC03-N14H11.1 recruited Myb proto-oncogene (c-Myb) to repress the transcription of leucine zipper-like transcription regulator 1 (LZTR1), so as to inhibit LZTR1-mediated ubiquitination of H-RAS (G12V), leading to the activation of mitogen-activated protein kinase (MAPK) signaling and induction of p-DRP1 (Serine 616). In conclusion, this study firstly revealed that lncRNA LL22NC03-N14H11.1 promoted HCC progression through activating H-RAS/MAPK pathway to induce mitochondrial fission, indicating LL22NC03-N14H11.1 as a novel potential biomarker for HCC treatment.

Upregulated fractalkine levels in Chinese patients with lupus nephritis.

OBJECTIVE: To investigate the expression levels of fractalkine (FKN) mRNA in peripheral blood mononuclear cells (PBMCs) and FKN protein in serum of patients with lupus nephritis (LN) from China, and to evaluate the associations between the expression of FKN and systemic lupus erythematosus disease activity index 2000 (SLEDAI-2 K), anti-double-stranded DNA and complement proteins in LN patients. METHODS: Real-time quantitative polymerase chain reaction and enzyme-linked immunosorbent assay were used to detect the expression levels of FKN mRNA in PBMCs and FKN protein in serum separately from 105 patients with LN and 52 healthy controls. RESULTS: Serum level and mRNA level of FKN were significantly increased in LN patients when compared to controls (P < 0.001). Higher FKN levels were found in active LN patients and LN patients with renal damage when compared with inactive LN patients and LN patients without renal damage (P < 0.001). Higher serum FKN levels were detected in inactive LN patients in comparison with healthy controls (Z = -7.165, P < 0.001). The FKN expression levels were positively correlated with SLEDAI-2 K, and was associated with the presence of autoantibodies and negatively correlated with complement proteins C3 and C4 in LN patients. CONCLUSIONS: The results suggest that upregulation of FKN is associated with the pathogenesis and activity of LN in Chinese patients.

Lipopolysaccharide-Binding Protein Downregulates Fractalkine through Activation of p38 MAPK and NF-κB.

BACKGROUND: LBP and fractalkine are known to be involved in the pathogenesis of ARDS. This study investigated the relationship between LBP and fractalkine in LPS-induced A549 cells and rat lung tissue in an ARDS rat model. METHODS: A549 cells were transfected with LBP or LBP shRNA plasmid DNA or pretreated with SB203580 or SC-514 following LPS treatment. An ARDS rat model was established using LPS with or without LBPK95A, SB203580, or SC-514 treatment. RT-PCR, western blotting, ELISA, immunofluorescence, coimmunoprecipitation, and immunohistochemical staining were used to study the expression of fractalkine and LBP and p38 MAPK and p65 NF-κB activities. RESULTS: LPS increased LBP and reduced fractalkine. LBP overexpression further decreased LPS-induced downregulation of fractalkine and p38 MAPK and p65 NF-κB activation; LBP gene silencing, SB203580, and SC-514 suppressed LPS-induced downregulation of fractalkine and p38 MAPK and p65 NF-κB activation in A549 cells. LBP and fractalkine in lung tissue were increased and decreased, respectively, following LPS injection. LBPK95A, SB203580, and SC-514 ameliorated LPS-induced rat lung injury and suppressed LPS-induced downregulation of fractalkine by decreasing phospho-p38 MAPK and p65 NF-κB. CONCLUSIONS: The results indicate that LBP downregulates fractalkine expression in LPS-induced A549 cells and in an ARDS rat model through activation of p38 MAPK and NF-κB.

Endothelial protein C receptor polymorphisms and risk of sepsis in a Chinese population.

Objective To examine the potential relationship of EPCR polymorphisms and the risk of sepsis in a Chinese population. Methods Snapshot SNP genotyping assays and DNA sequencing methods were used to detect polymorphisms of the EPCR gene, rs2069948C/T (2532C/T) and rs867186A/G (6936A/G), in 64 patients with sepsis and in 113 controls. Soluble EPCR (sEPCR) was measured by ELISA. Results There were significant differences in the allele and genotype frequencies of EPCR gene rs2069948C/T and allele frequencies of rs867186A/G between male and female patients and controls. Females carrying rs2069948 C/T genotype or T allele and males carrying rs867186 A allele were associated with a significantly increased risk of sepsis. Plasma sEPCR levels of sepsis patients were higher than controls and showed no correlation with EPCR gene polymorphisms. Conclusions EPCR polymorphisms may be associated with increased risk of sepsis, but this has no effect on the release of sEPCR in patients with sepsis.

Nur77 attenuates endothelin-1 expression via downregulation of NF-κB and p38 MAPK in A549 cells and in an ARDS rat model.

Acute respiratory distress syndrome (ARDS) is characterized by inflammatory injury to the alveolar and capillary barriers that results in impaired gas exchange and severe acute respiratory failure. Nuclear orphan receptor Nur77 has emerged as a regulator of gene expression in inflammation, and its role in the pathogenesis of ARDS is not clear. The objective of this study is to investigate the potential role of Nur77 and its underlying mechanism in the regulation of endothelin-1 (ET-1) expression in lipopolysaccharide (LPS)-induced A549 cells and an ARDS rat model. We demonstrate that LPS induced Nur77 expression and nuclear export in A549 cells. Overexpression of Nur77 markedly decreased basal and LPS-induced ET-1 expression in A549 cells, whereas knockdown of Nur77 increased the ET-1 expression. LPS-induced phosphorylation and nuclear translocation of NF-κB and p38 MAPK were blocked by Nur77 overexpression and augmented by Nur77 knockdown in A549 cells. In vivo, LPS induced Nur77 expression in lung in ARDS rats. Pharmacological activation of Nur77 by cytosporone B (CsnB) inhibited ET-1 expression in ARDS rats, decreased LPS-induced phosphorylation of NF-κB and p38 MAPK, and relieved lung, liver, and kidney injury. Pharmacological deactivation of Nur77 by 1,1-bis-(3'-indolyl)-1-(p-hydroxyphenyl)methane (DIM-C-pPhOH, C-DIM8) had no effect on ET-1 expression and lung injury. These results indicated that Nur77 decreases ET-1 expression by suppressing NF-κB and p38 MAPK in LPS-stimulated A549 cells in vitro, and, in an LPS-induced ARDS rat model, CsnB reduced ET-1 expression and lung injury in ARDS rats.

Investigation of association between IL-8 serum levels and IL8 polymorphisms in Chinese patients with sepsis.

OBJECTIVE: To assess the clinical relevance of IL8 gene polymorphisms in patients with sepsis and its association with systemic IL-8 levels. METHODS: PCR and DNA sequencing were used to examine the polymorphism of IL8 in 152 patients with sepsis and in 199 healthy volunteers in China. The distribution frequencies of the genotype and allele were compared among different groups. The serum IL-8 was measured by ELISA and analyzed in relation to polymorphisms of IL8. RESULTS: The homozygote TT genotype and T allele of rs4073 (genotype: p=0.01, allele: p=0.002), the homozygote CC genotype and C allele (genotype: p=0.03, allele: p=0.003) of rs2227306, homozygote AA genotype and A allele of re1126647 (genotype: p=0.01, allele: p=0.002) were associated with susceptibility to sepsis in males. Serum IL-8 levels were significantly increased in patients with sepsis but showed no correlation with IL8 rs4073, rs2227306 and rs1126647 polymorphisms. CONCLUSIONS: The male population carrying the homozygote TT genotype and T allele of rs4073, the homozygote CC genotype and C allele of rs2227306 and homozygote AA genotype and A allele of rs1126647 are more susceptible to sepsis, suggesting there is a protective effect in females carrying these genotypes and alleles respectively. There was no association between rs4073, rs2227306 and rs1126647 polymorphisms and serum levels of IL-8 in patients with sepsis.

Transforming growth factor beta 1 induced endothelin-1 release is peroxisome proliferator-activated receptor gamma dependent in A549 cells.

BACKGROUND: Endothelin-1 (ET-1) is involved in pulmonary vascular remodeling. The aim of this study was to investigate the biochemical interactions between PPAR-γ, TGF-ß1 and ET-1 in vitro. METHODS: A549 cells were pre-treated with S2505 (10 µM), S2871 (10 µM) with/without SB203580 (10 µM) for 60 min following 2 h treatment with 10 ng/mL TGF-ß1. A549 cells were also transfected with positive or negative PPAR-γ plasmids for comparison. RT-PCR, ELISA, western blotting and confocal laser scanning microscopy (CLSM) were used to measure the relevant expression of mRNA, protein, mediators of pathways and nuclear factor translocation. RESULTS: SB203580 inhibited TGF-ß1 induced ET-1 expression in A549 cells. S2871 decreased PPAR-γ mRNA and increase TGF-ß1-induced ET-1 expression. S2871 increased phosphorylation of p38 MAPK and Smad2. Cells transfected with PPAR-γ negative plasmid increased TGF-ß1 induced ET-1 expression, and increased the expression of phospho-p38 MAPK and phospho-Smad2. S2505 increased PPAR-γ mRNA expression, suppressed the increased TGF-ß1-induced expression of ET-1. S2505 inhibited TGF-ß1 induced phosphorylation of p38 MAPK and Smad2, also the nuclear translocation of Smad2. Cells transfected with PPAR-γ positive plasmid reduced TGF-ß1-induced ET-1 expression, and inhibited the expression of phospho-p38 MAPK and phospho-Smad2. CONCLUSIONS: TGF-ß1 induced release of endothelin-1 is PPAR-γ dependent in cultured A549 cells.

Methylprednisolone attenuates lipopolysaccharide-induced Fractalkine expression in kidney of Lupus-prone MRL/lpr mice through the NF-kappaB pathway.

BACKGROUND: Fractalkine (FKN) is involved in the occurrence and development of human lupus nephritis. It is known to be upregulated by lipopolysaccharide (LPS) as a stimulus in vivo. MRL/lpr mice have been used as an in vivo model to study lupus nephritis. Methylprednisolone (MP) is used widely in the clinical treatment of progressive glomerular diseases such as lupus nephritis. The aim of this study is to explore the mechanism of LPS induced FKN expression and to determine whether other molecular mechanisms contribute to the signaling pathway of MP action in MRL/lpr mice. METHODS: Forty-eight female MRL/lpr mice at 12 weeks of age were randomly distributed into six groups. Each group received various treatments for 8 weeks by receiving twice weekly intraperitoneal injections of (1) MP (MP-treated mice), of (2) SC-514 (SC-514-induced mice), of (3) normal saline and a single injection of LPS (LPS-induced mice), of (4) MP and a single injection of LPS (LPS + MP mice), of (5) SC-514 and a single injection of LPS (LPS + SC mice) and of (6) normal saline (control mice). One-way ANOVA was used for data analysis and P value <0.05 was considered statistically significantly. RESULTS: The expression of FKN and NF-kappaB p65 mRNA was detected by qPCR. The expression of FKN protein and the activation of NF-kappaB p65 were detected by immunohistochemistry and western blots respectively. The expression of FKN in the kidney of LPS induced mice was significantly increased and this was mediated by increased expression of NF-κB p65 and an increase in NF-kappaB phospho-p65. MP reduced proteinuria and ameliorated the renal damage in MRL/lpr mice. MP as well as the NF-kappaB inhibitor, SC-514, inhibited the LPS-induced increase of expression of FKN and the activation of NF-kappaB. CONCLUSIONS: The results indicate that MP attenuates LPS-induced FKN expression in kidney of MRL/lpr mice through the NF-kappaB pathway.

The association of polymorphisms of TLR4 and CD14 genes with susceptibility to sepsis in a Chinese population.

BACKGROUND: Sepsis is now the leading cause of death in the non-cardiovascular intensive care unit (ICU). Recent research suggests that sepsis is likely to be due to an interaction between genetic and environmental factors. Genetic mutations of toll-like receptor 4 (TLR4) and cluster of differentiation 14 (CD14) genes are involved in the immune and (or) inflammatory response. These may contribute to the susceptibility to sepsis in patients. This study was designed to evaluate whether the TLR4 and cluster CD14 gene polymorphisms are associated with susceptibility to sepsis. METHODS: The single nucleotide polymorphisms (SNPs) of TLR4 (rs10759932, rs11536889, rs7873784, rs12377632, rs1927907, rs1153879) and CD14 (rs2569190 and rs2563298) in patients with sepsis and control subjects in the Guangxi Province were analyzed by using the polymerase chain reaction-single base extension (PCR-SBE) and DNA sequencing methods. RESULTS: The rs11536889 polymorphism in TLR4 and rs2563298 polymorphism in CD14 were significantly associated with the risk of sepsis when compared to the control group. The frequencies of rs11536889 and rs2563298 polymorphisms in the group with sepsis were higher than that in the control group (OR = 1.430, 95% CI, 1.032-1.981, P<0.05; OR = 2.454, 95% CI, 1.458-4.130, P<0.05, respectively). Followed up haplotype analysis suggested that there were two haplotypes in which increased risk factors for sepsis were indicated. CONCLUSIONS: The rs11536889 polymorphism in TLR4 and rs2563298 polymorphism in CD14, and two haplotypes were associated with increased susceptibility to sepsis.

Overexpression of Fas and FasL is associated with infectious complications and severity of experimental severe acute pancreatitis by promoting apoptosis of lymphocytes.

This study investigated the relationship of Fas and Fas ligand (FasL) expression and apoptosis of lymphocytes in relation to the pathogenic immune response and infectious complications observed in experimental severe acute pancreatitis in mice. Forty male Balb/c mice were randomly divided into control, mild (MAP), and severe acute pancreatitis (SAP) groups. Overexpression of Fas/FasL messenger ribonucleic acid (mRNA) and protein was observed in spleen-derived lymphocytes in SAP (p < 0.01). Apoptosis of these resulted in a depletion of circulating lymphocytes in this group (p < 0.05). A further significant change in the SAP group with infectious complications was observed. A positive relationship was found between the Fas/FasL expression and lymphocyte apoptosis, and negative relationships were observed between Fas/FasL expression and CD4(+) and CD19(+) lymphocytes and the CD4(+)/CD8(+) ratio in SAP mice (p < 0.01). The results suggest that the overexpression of Fas/FasL is associated with infectious complications and severity of experimental severe acute pancreatitis by promoting apoptosis of lymphocytes.

[Detection of FasL mRNA, sFasL and their regulatory effect on T lymphocyte subsets in patients with severe acute pancreatitis].

OBJECTIVE: To investigate the levels of FasL mRNA in peripheral blood mononualear cells (PBMCs), serum soluble Fas ligand (sFasL) and their regulatory effect on T lymphocyte subsets in patients with severe acute pancreatitis (SAP). METHODS: Forty-eight patients with pancreatitis were randomly divided into two groups: 20 cases with SAP and 28 cases with mild acute pancreatitis (MAP). Twenty-eight healthy volunteers were selected as control group. The expression of FasL mRNA in PBMCs was detected by real-time quantitative PCR(qRT-PCR), and serum sFasL was measured by ELISA. T lymphocyte subsets in peripheral blood were detected by flow cytometry. RESULTS: Compared with control group and MAP group, FasL mRNA of PBMCs and serum sFasL increased significantly in SAP group (P<0.05), a little increase in MAP group, and there was no significant difference between MAP group and control group (P>0.05). The CD4(+) T cell ratio, CD4(+)/CD8(+) ratio decreased significantly in SAP group (P<0.05) vs control group and MAP group), and they were found negatively related to FasL mRNA, serum sFasL level. CONCLUSION: The SAP patients showed the significantly increased FasL mRNA of PBMCs and serum sFasL and decreased CD4(+) T-cell ratio, CD4(+)/CD8(+) ratio. FasL may mediate the apoptosis of T lymphocytes.

The role of Fas expression on the occurrence of immunosuppression in severe acute pancreatitis.

BACKGROUND: Severe acute pancreatitis (SAP) is a dangerous illness with high mortality where most patients do not die of excessive inflammation, but die of immunosuppression and multiple infections at a later stage. The mechanism of immunosuppression in SAP is unknown. AIM: The purpose of this study was to analyze the role of Fas expression on the occurrence of immunosuppression in patients with SAP. METHODS: Forty-eight patients with pancreatitis were divided into two groups: 20 cases with SAP (7 cases with sepsis, 13 cases without sepsis) and 28 cases with mild acute pancreatitis (MAP). Twenty-eight healthy volunteers were selected as controls. Fas mRNA expression in peripheral blood was detected by qPCR and Fas protein of lymphocyte membranes; T lymphocyte subsets and expression of monocyte Human leukocyte antigen DR (HLA-DR) in peripheral blood were detected by flow cytometry. RESULTS: Compared with MAP and control groups, expression level of Fas mRNA and lymphocyte Fas protein in peripheral blood were significantly increased in the SAP group (all P < 0.01). There was a further significant increase in the SAP group with sepsis compared to those without sepsis (all P < 0.01). The CD4(+) T cell ratio, CD4(+)/CD8(+) ratio and monocyte HLA-DR expression in the SAP group were decreased significantly compared with MAP and control groups (all P < 0.01). Significant negative relationships were observed between Fas mRNA expression and CD4(+) T-cell ratio, CD4(+)/CD8(+) ratio, and monocyte HLA-DR expression in SAP patients with sepsis (all P < 0.05). CONCLUSIONS: The results suggest that expression level of Fas is related to severity and immune status of pancreatitis. Overexpression of Fas may lead to the occurrence of immunosuppression and sepsis.

[Blood and renal fractalkine expression in patients with lupus nephritis and its significance].

OBJECTIVE: To investigate the expression of fractalkine (FKN) in the blood and renal tissues of patients with lupus nephritis and explore its significance. METHODS: According to the pathological classification, 48 patients with lupus nephritis were divided into mild group (22 cases) and severe group (26 cases), with 26 healthy subjects as the control group. RT-PCR and enzyme-linked immunosorbent assay were employed to detect the expression of FKN mRNA and protein in the blood of the subjects, and FKN expression and localization in the renal tissue of the patients with lupus nephritis were detected using immunohistochemical staining. RESULTS: The patients in both the mild and severe groups showed significantly increased expression of blood FKN mRNA and protein compared with the normal controls, and the increase was more obvious in severe cases (P<0.01). In the renal tissues of the patients, FKN was located mainly in the cytoplasm of the glomerular podocytes and renal tubular epithelial, and the number of positive glomerular cells number was significantly greater in severe cases than in the mild cases (P<0.01); FKN expression in the cortical interstitium did not show a significant difference between the 3 groups. CONCLUSION: FKN expression in the blood and glomeruli of patients with lupus nephritis is related to the severity of renal pathologies.

[Echo-tracking technology for evaluating the impact of blood pressure on vascular endothelial function].

OBJECTIVE: To evaluate the effect of blood pressure on vascular endothelial function using echo-tracking (ET) technology. METHODS: Thirty hypertensive (HP) patients, 30 subjects with high normal blood pressure (HN), and 30 normotensive control (NC) subjects were enrolled in this study. For each subject, conventional two-dimensional ultrasound was performed to measure the intima-media thickness (IMT), and an ET system was utilized to assess the carotid elasticity (Ep, ß, AC, AI, and PWVß). RESULTS: As the blood pressure increased, IMT, Ep, ß, AI, and PWVß values all increased and AC value decreased. Before excluding the confounding factors, the difference in IMT, Ep, ß, AC, AI, and PWVß values were significant between the 3 groups. After excluding the confounding factors, only PWVß value was significantly different between HN group and NC group; but between HP and NC group and between HP and HN group, the other parameters still showed significant differences. Systolic blood pressure had significant influences on IMT, Ep, AC, AI, and PWVß values, diastolic blood pressure significantly affected AI value, and pulse pressure significantly affected Ep and ß values. CONCLUSION: High normal blood pressure has no obvious effects on vascular function, and blood pressure is an independent risk factor of vascular endothelial dysfunction only in the stage of early hypertention. In early atherosclerosis, systolic blood pressure is the most significant factors affecting vascular endothelial function, followed by pulse pressure and diastolic blood pressure.

[Effects of matrine on proliferation and telomerase activity of colon cancer SW1116 cells].

OBJECTIVE: To investigate the effects of matrine on proliferation and telomerase activity of colon cancer SW1116 cells. METHODS: The proliferation inhibitory rate was evaluated by MTT assay. The telomerase activity was analyzed by TRAP-ELISA, and the expression of hTERT mRNA was determined by semi-quantitative RT-PCR. RESULTS: Matrine displayed strong proliferation inhibitory effect in a dose-and-time-dependent manner against SW1116 cells. Compared with control group, the telomerase activity and the expression of hTERT mRNA decreased significantly (P < 0.05 or P < 0.01) in matrine group. CONCLUSION: Matrine can inhibit the telomerase activity by depressing the expression of hTERT in SW1116 cells and inhibiting cell proliferation.

[Alteration of serum lipids in patients with acute leukemia and its clinical significance].

To explore the clinical significance on alteration of serum lipids in acute leukemia (AL) patients, the level of serum lipids was monitored in 86 AL cases by using of automatic biochemical analyzer. The results showed that TG was significantly higher (P < 0.05) while TC, LDL-C and HDL-C were obviously lower (P < 0.05) in AL patients than those in normal controls. After chemotherapy, TG decreased but TC, LDL-C and HDL-C were still higher (P < 0.05) as comparing to pre-treatment in complete remission cases. There were no changes of those parameters in non-remission patients. It is concluded that determination of serum lipids level in AL patients is a simple and important accessory index to evaluate curative effect and monitor patient's condition.