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Objective To explore the biochemical indicators of patients with coronary slow flow phenomenon (CSFP) in high altitude areas and to analyze the risk factors of CSFP. Methods A total of 90 CSFP patients with no coronary artery stenosis were selected as the CSFP group (48 patients in high altitude area and 50 patients in low and middle altitude area）and 101 patients with normal blood flow were selected as the control group (50 patients in high altitude area and 51 patients in low and middle altitude area). The biochemical indicators of the patient's admission were obtained, and the high risk factors of CSFP were analyzed. Results ALT, GOT, Na, CK, CG, LDL-C, TG, and ET-1 in the CSFP group were significantly higher than those in the control group (P<0.05), while HDL-C and NO in the CSFP group were lower than those in the control group (P<0.05). CG, TG and ET-1 in the high altitude group were higher than those in the low and middle altitude group (P<0.05), while NO was lower than that in the low and medium altitude group (P<0.05). ET-1 and NO were independent influencing factors of CSFP (P<0.05). Conclusion Dyslipidemia can occur in patients with CSFP, especially in high altitude areas. The change of blood lipid level is an independent influencing factor of CSFP.
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Objective To explore the changes of type H vessel during the low bone mineral density caused by iron accumulation and discuss its clinical meaning.Methods Ten 8-week old male C57BL/6J mice were used for experiments,and randomly divided into two groups:control group and iron group,and 5 mice in each group.In the iron group,0.1 g/kg of iron dextran was injected intraperitoneally once a week for 8 weeks.The control group was injected with the same amount of saline.The femoral and tibial specimens were examined by microscopic CT scan and bone tissue type H vessel immunohistochemical staining.Liver tissue from the two groups were collected for the content of iron by atomic absorption spectroscopy.All experimental data were analyzed with t-test.Results The content of hepatic iron in mice was significantly higher than that in the control group,which indicating that the model was successfully established.The tibia specimens were collected for immunostaining.The vascular area of type H at metaphyseal regions is 11.24％± 1.76％ in iron group and 30.69％±2.78％ in control group,respectively.There is significant difference between the two groups (P＜0.005).The femur specimens were collected for Micro-CT scan,the value of bone mineral density (BMD),bone volume/tissue volume (BV/TV),trabecular thickness (Tb.Th),trabecular number (Tb.N) and trabecular separation (Tb.Sp) was (0.19±0.013) g/cm3,11.92％±1.199％,(35.66±2.684) μm,(2.36±0.429)/mm and (284.41±23.197) μm in iron group and (0.37±0.023) g/cm3,35.76％± 1.336％,(62.05±2.238) μm,(5.68± 1.039)/mm and (163.23± 13.203) μm in control group,respectively.The differences between the two groups were statistically significant (P＜0.05).Conclusion Iron accumulation can lead to low BMD and suppress type H vessel formation in bone,which might provide a new experimental value for mechanism research on osteoporosis caused by iron accumulation.
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OBJECTIVE:To explore the necessity of pharmaceutical care provided by clinical pharmacists during the use of ad-vertised drugs. METHODS:Through retrospectively analyzing drug advertisements permission number of which had been revoked issued by China Food and Drug Administration during Jan. 2013-Jun. 2015 statistically,the reasons for permission withdrawal were analyzed to put forward the focal point of pharmaceutical care development. RESULTS & CONCLUSIONS:A total of 46 items of permission number had been revoked,including 45 items of Chinese patent medicine (97.83%),1 item of western medicine (2.17%). The reasons for permission revoking mainly included overstating therapeutic efficacy without authorization,guaranteeing onset time,guaranteeing recovery in certain time,propagandizing drugs in the name of experts,etc. These drug advertisements sent relatively one-sided information so as to easily mislead patients and consumers to use drug irrationally. So,it is necessary to provide pharmaceutical care by clinical pharmacists about this kind of drug. The focal points of pharmaceutical care contain telling patients usage and dosage detailedly,and explaining possible ADR and relevant countermeasures;emphasizing different therapeutic efficacy,onset time and recovery time due to individual difference;strengthening prescription check and medication suitability ap-praisal,and so on.
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Objective To investigate the characteristics of cognitive impairment in patients with type 2 diabetes mellitus (T2DM),and to analyze the correlation of T2DM with its risk factors and serum insulin like growth factor-1 (IGF-1) levels Methods A total of 78 hospitalized patients with T2DM at our hospital from November 2011 to March 2012 were divided into the cognitive impairment group (n=39) and the non-cognitive impairment group (n=39) according to Montreal Cognitive Assessment (MoCA) scores,and general clinical data were collected.Levels of blood lipids,glycosylated hemoglobin (HbAlc),fasting blood glucose (FBG),fasting blood insulin (FBI) and other biochemical indicators were detected,insulin resistance index (HOMA-IR) scores were calculated,and serum IGF-1 levels were determined by the enzyme-linked immunosorbent assay (ELISA).Results The education levle was (8.94±4.13) years for the cognitive impairment group and (12.65[2.50) years for the non-cognitive impairment group,and there was a statistically significant difference between the two groups (P=0.004).HbAlc levels were (9.69 ± 1.25) and (7.96 ± 1.31) for the cognitive impairment group and the non-cognitive impairment group,respectively,and were statistically difference between the two groups (P =0.001).Serum IGF-1 levels were (122.60±11.56) mmol/L and (139.32±9.57) mmol/L in the cognitive impairment group and the non-cognitive impairment group,respectively,and had a statistically significant difference between the two groups (P =0.037).Additionally,compared with the non-cognitive impairment group,scores on visuospatial ability,naming,language,abstraction,delayed recall and orientation were lower in the cognitive impairment group (P＜[0.05 or 0.01).Moreover,MoCA scores were negatively correlated with TC,LDL-C,TG,HbAlc,FBI levels and HOMA IR (r=0.498,-0.411,0.414,-0.452,-0.449,-0.539,respectively,P＜0.05 for all),and positively correlated with education lcvcl and IGF 1 level (r=0.579 and 0.491,respectively,P＜0.05 for both) Conclusions Cognitive impairment caused by T2DM is prominent in visuospatial ability,language,memory and executive functions,and is closely related to poor education,poor glycemic control,dyslipidemia and insulin resistance.Furthermore,decreased serum IGF-1 levels might be a risk factor for diabetic cognitive impairment.
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To investigate the effect of monoamine oxidase inhibitor tranylcypromine (TCP) on the differentiation of human U251 glioma cells, we treated U251 cells with TCP and/or 100 nmol/L histone deacetylase inhibitor trychostatin A (TSA). The differentiation of U251 cells was observed with inverted microscopy. The cell proliferation and cell cycle distribution were determined by MTT assay and flow cytometry, respectively. Apoptosis was observed by Hoechst 33258 staining. The levels of differentiation-related genes were assessed by real-time PCR and Western blotting. TCP-induced differentiation was characterized by typical morphological changes, inhibition of cellular proliferation, accumulation of cells in the G1 phase of the cell cycle, decreased expression of the pluripotency transcription factors Oct4 and Sox2, and increased expression of glial fibrillary acid protein (GFAP). The combination of TCP and TSA treatment also triggered an over-expression of GFAP. These findings suggest that TCP may induce differentiation of U251 glioma cells, and the differentiation process may be promoted by histone deacetylase inhibitor TSA.
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Humans , Brain Neoplasms , Pathology , Cell Line, Tumor , Cell Transformation, Neoplastic , Glioma , Pathology , Histone Deacetylase Inhibitors , Pharmacology , Hydroxamic Acids , Pharmacology , Monoamine Oxidase Inhibitors , Pharmacology , Tranylcypromine , PharmacologyABSTRACT
ObjectiveTo investigate the effect of soluble β-amyloid protein (Aβ) oligomers on the expression levels of insulin signaling transduction cascades-associated proteins including insulin receptor ( InsR),insulin receptor substrate-Ⅰ( IRS-Ⅰ) and protein kinase B (PKB) of rat hippocampal neurons,and the pathogenesis of Alzheimer's disease (AD) in depth.MethodsSoluble Aβ oligomers (5 μl) were injected into the lateral ventriculus of the AD group by a microinjector under the stereotaxic apparatus.Normal saline solution ( NS,5 μl) was injected into the NS group in the same way,and the control group received the puncture without injection. It was repeated after 1 week and the behavior of all rats was evaluatedbyY-mazetestafter2weeks.Thenhippocampuswasremovedandunderwent immunohistochemical staining to detect the expression of proteins associated.ResultsCompared with the other groups,learning and memory ability of the Aβ-treated rats were impaired.To be specific,the times of learning were increased and the times of memory were decreased. However,there was no significant difference between the NS group and the control group.Besides,the expression levels of InsR,IRS-Ⅰ,and PKB were decreased in AD group showing that a mean optical density of staining on these proteins ( InsR:0.12 ± 0.0l ; IRS-Ⅰ:0.14 ± 0.02; PKB:0.12 ± 0.03 ) was reduced in contrast with that in the NS group and the control group.Whereas there was no significant difference between the NS group (0.40 ± 0.02,0.39 ± 0.06,0.38 ± 0.03,mean difference:- 0.13,- 0.13,- 0.17,all P ＜ 0.05 ) and the control group (0.38 ± 0.07,0.35 ± 0.03,0.35 ± 0.06,mean difference:- 0.15,- 0.07,- 0.73,all P ＜ 0.05 ).ConclusionsSoluble Aβ1-42 induced learning and memory disability of the rats.The mechanism might be that Aβ can lead to disorders of the insulin signaling transduction pathway of hippocampal neurons and decrease the expression levels of the proteins in the pathway.