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<p><b>OBJECTIVE</b>To observe the effects of L-carnitine treatment on serum levels of brain natriuretic peptide (BNP) and N-terminal pro-BNP (NT-proBNP) and cardiac function in children with heart dysfunction and severe hand-foot-mouth disease (HFMD).</p><p><b>METHODS</b>A total of 120 children with severe HFMD were enrolled and randomly and equally divided into routine treatment group and L-carnitine treatment group. Thirty healthy children served as the control group. HFMD patients were given anti-fever and antiviral treatment as the basic treatment, while the patients in the L-carnitine treatment group were given L-carnitine as an adjuvant treatment to the basic treatment. Treatment outcomes were observed in the two groups. For all the subjects, serum levels of BNP and NT-proBNP and cardiac function parameters including left ventricular ejection fraction (LVEF), fractional shortening (FS), and cardiac index (CI) were measured at different time points before and after treatment.</p><p><b>RESULTS</b>Before treatment, HFMD patients had significantly higher serum levels of BNP and NT-proBNP and heart rate but significantly lower LVEF, FS, and CI compared with the control group (P<0.05). After treatment, the L-carnitine treatment group had a significantly higher response rate than the routine treatment group (P<0.05). After 3 days of treatment, the serum levels of BNP and NT-proBNP, LVEF, FS, and CI were significantly reduced in the L-carnitine group (P<0.05); the L-carnitine group had significantly lower serum levels of BNP and NT-proBNP, LVEF, FS, and CI than the routine treatment group (P<0.05); there were no significant differences in the serum levels of BNP and NT-proBNP, LVEF, FS, or CI between the L-carnitine treatment and control groups (P>0.05). After 5 days of treatment, there were no significant differences in the serum levels of BNP and NT-proBNP, LVEF, FS, or CI between the L-carnitine treatment and routine treatment groups (P>0.05). Heart rate recovery was significantly slower in the routine treatment group than in the L-carnitine treatment group (P<0.05).</p><p><b>CONCLUSIONS</b>As an adjuvant therapy for severe HFMD, L-carnitine treatment has satisfactory short-term efficacy in reducing the serum levels of BNP and NT-proBNP and improving cardiac function, thus improving clinical outcomes.</p>
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<p><b>OBJECTIVE</b>To study the expression and significance of endothelial microparticles (EMPs) in children with Henoch-Schönlein purpura (HSP).</p><p><b>METHODS</b>A total of 100 previously untreated children with HSP were classified to Henoch-Schönlein purpura nephritis (HSPN) group (n=40) and non-nephritis group (n=60). Thirty healthy children who underwent physical examination were enrolled as control group. Serum levels of EMPs, T helper 17 cells (Th17), and interleukin-17 (IL-17) were compared between groups.</p><p><b>RESULTS</b>The HSPN and non-nephritis groups had significantly higher levels of Th17 and IL-17 than the control group, and the HSPN group had the highest levels (P<0.05). The HSPN and non-nephritis groups had a significantly higher level of EMPs than the control group, and the HSPN group had the highest level (P<0.05). In the HSPN group, the levels of Th17 and IL-17 were positively correlated with the level of EMPs (r=0.830 and 0.644 respectively; P<0.05).</p><p><b>CONCLUSIONS</b>EMPs play an important role in the pathogenesis of HSP. The increase in EMPs might be one of the reasons for renal involvement in children with HSP.</p>
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OBJECTIVE@#To determine the effect of gene silencing of cyclophilin B (CypB) on growth and proliferation of gastric cancer cells.@*METHODS@#CypB siRNA lentivirus (LV-CypB-si) and control lentivirus (LV-si-con) were produced. CypB expression in gastric cancer cell lines was detected by Western blot. BGC823 and SGC7901 cells were chosen to be infected with LV-si-con and LV-CypB-si, and stable transfectants were isolated. The cell groups transfected with LV-CypB-siRNA, LV-siRNA-con and transfected no carrier were served as the experimental group, the implicit control group and the blank control group respectively. MTT and colony formation assays were used to examine the effect of CypB on the cell growth and proliferation in vitro. Cell cycle was analyzed with flow cytometry. The expression of VEGFR of BGC823-si and SGC7901-si was detected by Western blot.@*RESULTS@#Gene silencing of CypB can inhibit gastric cancer cell growth, proliferation, cell cycle progress and tumorigenesis. CypB expression level was obviously higher in SGC7901 and BGC823 than MKN28 and GES. These two cell lines were infected with LV-si-con and LV-CypB-si respectively. MTT and cloney formation assays showed a significantly decreased rate of cell proliferation from the forth day or the fifth day in cells transfected with LV-CypB-si (P<0.05). Down-regulation of CypB resulted in slightly decreased percentage of S phase and increased percentage of G1 (P<0.05). These findings indicated that CypB could promote the G1-S transition of gastric cancer cell. In addition, the expression of VEGF of BGC823 and SGC7901 transfected with CypB siRNA was reduced in comparison with the implicit control group and the blank control group.@*CONCLUSIONS@#Gene silencing of CypB decreases gastric cancer cells proliferation and in vivo tumorigenesis. These findings indiccate CypB could be a potential biomarker and therapeutic target for gastric cancer.
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OBJECTIVE@#To explore the role of miR-214 in the progression of hepatocellular carcinoma (HCC) and its inhibitory mechanisms in depressing the signaling pathway of β-catenin, this study was conducted.@*METHODS@#We ectopically expressed miR-214 in HepG2 cells to obtain cell lines Lv-miR-214-HepG2 and their control Lv-control-HepG2. Differences between the two cell lines were compared in cell growth, proliferation, colony forming ability and cell cycles. RT-PCR method was applied for the quantification of β-catenin mRNA expression. Western-blot method was applied for the determination of the protein level of β-catenin and their downstream targets (ie. Cyclin D1, c-Myc and TCF-1). The effect of miR-214 on cells was further explored through RNA interference and restoring miR-214 expression.@*RESULTS@#In comparison with negative (Lv-control-HepG2) and blank (HepG2) control, a significant inhibition of cell growth and proliferation caused by miR-214 was observed after 48∼72h of cell culture experiments (P0.05). By comparing to the RT-PCR and Western-blot results of control, the miR-214 treatment led to a slightly decrease in the β-catenin mRNA expression (P>0.05), but an extremely inhibition in the protein level of β-catenin and its downstream targets Cyclin D1, c-Myc, and TCF-1 (P<0.05).@*CONCLUSIONS@#miR-214 functions as a suppressor during the progression of HCC, and its inhibitory role was achieved by down-regulating β-catenin signaling pathway.
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Objective: To explore the role of miR-214 in the progression of hepatocellular carcinoma (HCC) and its inhibitory mechanisms in depressing the signaling pathway of β-catenin, this study was conducted. Methods: We ectopically expressed miR-214 in HepG2 cells to obtain cell lines Lv-miR-214-HepG2 and their control Lv-control-HepG2. Differences between the two cell lines were compared in cell growth, proliferation, colony forming ability and cell cycles. RT-PCR method was applied for the quantification of β-catenin mRNA expression. Western-blot method was applied for the determination of the protein level of β-catenin and their downstream targets (ie. Cyclin D1, c-Myc and TCF-1). The effect of miR-214 on cells was further explored through RNA interference and restoring miR-214 expression. Results: In comparison with negative (Lv-control-HepG2) and blank (HepG2) control, a significant inhibition of cell growth and proliferation caused by miR-214 was observed after 48~72h of cell culture experiments (P0/G1 phase [(70.32±3.12)%] but a lower proportion in S phase [(18.42±2.90)%] (P0.05). By comparing to the RT-PCR and Western-blot results of control, the miR-214 treatment led to a slightly decrease in the β-catenin mRNA expression (P>0.05), but an extremely inhibition in the protein level of β-catenin and its downstream targets Cyclin D1, c-Myc, and TCF-1 (P<0.05). Conclusions: miR-214 functions as a suppressor during the progression of HCC, and its inhibitory role was achieved by down-regulating β-catenin signaling pathway.
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Objective: To determine the effect of gene silencing of cyclophilin B (CypB) on growth and proliferation of gastric cancer cells. Methods: CypB siRNA lentivirus (LV-CypB-si) and control lentivirus (LV-si-con) were produced. CypB expression in gastric cancer cell lines was detected by Western blot. BGC823 and SGC7901 cells were chosen to be infected with LV-si-con and LV-CypB-si, and stable transfectants were isolated. The cell groups transfected with LV-CypB-siRNA, LV-siRNA-con and transfected no carrier were served as the experimental group, the implicit control group and the blank control group respectively. MTT and colony formation assays were used to examine the effect of CypB on the cell growth and proliferation in vitro. Cell cycle was analyzed with flow cytometry. The expression of VEGFR of BGC823-si and SGC7901-si was detected by Western blot. Results: Gene silencing of CypB can inhibit gastric cancer cell growth, proliferation, cell cycle progress and tumorigenesis. CypB expression level was obviously higher in SGC7901 and BGC823 than MKN28 and GES. These two cell lines were infected with LV-si-con and LV-CypB-si respectively. MTT and cloney formation assays showed a significantly decreased rate of cell proliferation from the forth day or the fifth day in cells transfected with LV-CypB-si (P1 (P1-S transition of gastric cancer cell. In addition, the expression of VEGF of BGC823 and SGC7901 transfected with CypB siRNA was reduced in comparison with the implicit control group and the blank control group. Conclusions: Gene silencing of CypB decreases gastric cancer cells proliferation and in vivo tumorigenesis. These findings indiccate CypB could be a potential biomarker and therapeutic target for gastric cancer.
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<p><b>OBJECTIVE</b>To study the expression of tau-related protein in spinal cord of Chinese patients with Alzheimer's disease.</p><p><b>METHODS</b>Gallays-Braak stain and immunohistochemical study for tau protein (AT8) were carried out in the spinal cord tissue (T2, T8, T10, L2 and S2 segments) of 3 Chinese patients with Alzheimer's disease. Seven age-matched cases without evidence of dementia or neurologic disease were used as controls.</p><p><b>RESULTS</b>Neurofibrillary tangles were identified in the neurons of anterior horn in 2 Alzheimer's disease cases but none was observed in the controls. Tau-positive axons and astroglia were detected in all Alzheimer's disease cases. Tau immunoreactivity in spinal cord of the patients correlated with that in brain tissue.</p><p><b>CONCLUSION</b>The expression of tau-related protein is demonstrated in the spinal cord of Alzheimer's disease patients suggesting that axonal transport defect may play a role in the pathogenesis of Alzheimer's disease.</p>
Subject(s)
Aged , Humans , Male , Alzheimer Disease , Metabolism , Pathology , Axonal Transport , Axons , Metabolism , Pathology , Neurofibrillary Tangles , Metabolism , Pathology , Phosphorylation , Spinal Cord , Metabolism , Pathology , tau Proteins , MetabolismABSTRACT
Objective To investigate the epidemiological,genealogic characteristic,familial history of the families with fatal familial insomnia,its clinical and pathological features as well as the heredity rule of related genes.Methods 135 familial members of 7 eras were studied.Vein blood samples from patients as well as from some familial members were collected.PRNP gene was studied with PCR,its serial was determined and then authenticated with Nsp I.Brain tissue was obtained for neuropathological test and PrPSc test with Western blot method.Results Clinical symptoms of the 2 diagnosed cases were typical.11 familial members died of similar neural disease.32 samples of their familial members,codon at D178N of PRNP of 11 members was mutated,with mutation rate as 34.38% while D129N showed as methionine.Brain tissue of both probands denaturalized into spongiform and the nerve fiber was absent but PrPSc protein was identified.Conclusion Genealogy was described in the family with fatal familial insomnia since the patients had typical clinical symptoms and pathological characteristics.It seemed necessary to confirm cases of fatal familial insomnia and their genealogy with epidemiological data and to investigate its gene characteristics as well as with neuropathological and Western blot tests.
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<p><b>OBJECTIVE</b>To study the possible effect of tetracycline on protease-resistant activity in vitro and infectivity in vivo of a scrapie strain 263K.</p><p><b>METHODS</b>Scrapie pathogens were incubated with tetracycline at different concentrations for various periods of time and protease-resistant PrP signals were evaluated with proteinase K-treatment and Western blots. The preparations treated with tetracycline were intracerebrally inoculated into golden hamsters and typical TSE manifestations were noted. PrPSc in brain tissues of the infected animals was detected by PrP specific Western blot assays.</p><p><b>RESULTS</b>Protease-resistant PrP was significantly reduced in or removed from the preparations treated with tetracycline in a dose-dependant manner. Compared with the control group after incubated for 53.75 +/- 0.50 days, the preparations treated with 5 mmol/L and 20 mmol/L tetracycline prolonged the incubation time of 61.5 +/- 1.73 and 59.5 +/- 0.58 days (P < 0.05).</p><p><b>CONCLUSION</b>Treatment of scrapie pathogen 263K with tetracycline reduces or removes its protease-resistant activity in vitro.</p>
Subject(s)
Animals , Cricetinae , Brain , Pathology , Peptide Hydrolases , Metabolism , PrPSc Proteins , Metabolism , Virulence , Scrapie , Pathology , Tetracycline , Pharmacology , Time FactorsABSTRACT
<p><b>OBJECTIVE</b>To investigate the value of transarterial chemoembolization (TACE) using mixed emboli for hepatocellular carcinoma (HCC).</p><p><b>METHODS</b>188 patients with HCC were divided into two groups according to the treatment modality: 103 patients in group A treated by routine iodine embolus agent; 85 patients in group B by mixed iodine embolus agent (ultra-liquified iodinized oil + gelatin sponge + chemotherapeutic agents). The pattern of the arrested iodine deposition in the tumor, response, resectability during follow-up, pathological changes, survival and complications in the two groups were analyzed and compared.</p><p><b>RESULTS</b>The pattern of full-and-dense iodine deposition in the tumor and the response rate (CR + PR) were 59.2% and 32.0% in group A, 89.4% and 56.5% in group B. Surgical resection after TACE was possible in 5.8% (6/103) of group A versus 15.3% (13/85) of group B. Complete tumor necrosis was observed in 1.0% and 4.7% in groups A and B, respectively. 1-, 2- and 3-year actual survival rates were 57.7%, 42.8% and 8.4% in group A, and 79.8%, 55.3%, 38.5% in group B. The difference in results between the two groups was statistically significant, however, the incidence of complication in the two groups was similar.</p><p><b>CONCLUSION</b>Transarterial chemoembolization with mixed iodine emboli is more effective than with the routine iodine emboli in the treatment of bulky or nodular hepatocellular carcinoma rich in blood supply. Mixed iodine emboli is tolerable without increase in severe complications.</p>