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BACKGROUND/AIMS: Polypharmacy is a common clinical problem with chronic diseases that can be associated with adverse patient outcomes. The present study aimed to determine the prevalence and patient-specific characteristics associated with polypharmacy in an ulcerative colitis (UC) population and to assess the impact of polypharmacy on disease outcomes.METHODS: A retrospective chart review of patients with UC who visited a tertiary medical center outpatient clinic between 2006 and 2011 was performed. Polypharmacy was defined as major ( ≥ 5 non-UC medications) or minor (2–4 non-UC medications). UC medications were excluded in the polypharmacy grouping to minimize the confounding between disease severity and polypharmacy. Outcomes of interest include disease flare, therapy escalation, UC-related hospitalization, and surgery within 5 years of the initial visit.RESULTS: A total of 457 patients with UC were eligible for baseline analysis. Major polypharmacy was identified in 29.8% of patients, and minor polypharmacy was identified in 40.9% of the population. Polypharmacy at baseline was associated with advanced age (P< 0.001), female sex (P= 0.019), functional gastrointestinal (GI) disorders (P< 0.001), and psychiatric disease (P< 0.001). Over 5 years of follow-up, 265 patients remained eligible for analysis. After adjusting for age, sex, functional GI disorders, and psychiatric disease, major polypharmacy was found to be significantly associated with an increased risk of disease flare (odds ratio, 4.00; 95% confidence interval, 1.66–9.62). However, major polypharmacy was not associated with the risk of therapy escalation, hospitalization, or surgery.CONCLUSIONS: Polypharmacy from non-inflammatory bowel disease medications was present in a substantial proportion of adult patients with UC and was associated with an increased risk of disease flare.
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Adult , Female , Humans , Ambulatory Care Facilities , Chronic Disease , Cohort Studies , Colitis, Ulcerative , Follow-Up Studies , Hospitalization , Polypharmacy , Prevalence , Retrospective Studies , Risk Factors , UlcerABSTRACT
Objective To explore the distribution of inflam m atory cells and positive expression of P-se-lectin glycoprotein ligand-1 (PSG L-1) in infant brainstem tissue from hand-foot-m outh disease related fatal brainstem encephalitis. Methods Tw enty brainstem sam ples from infants suffered from brainstem en-cephalitis w ere collected as the experim ental group. Ten brainstem sam ples from infants died of non-brain diseases and injuries w ere collected as the control group. The distribution of inflam m atory cells and the expression of PSG L-1 in the tw o groups w ere exam ined by im m unohistochem ical m ethod. The characteristics of the positive cells w ere observed. Results In brainstem tissue of the experim ental group, there w ere sleeve infiltrations of inflam m atory cells around the vessels and in the glial nodule. Microglia was the m ost and following was neutrophils around the vessels and in the glial nodule. There was a significant statistical difference am ong m icroglias, neutrophils and lym phocytes (P<0.05). There was no sleeve infiltration in the control group. PSG L-1 protein was expressed w idely in inflam m atory cells in the experim ental group, especially in the inflam m atory cells around the vessels and in the glial nodule. B ut PSG L-1 positive staining could be observed significantly less in the control group com paring with the experim ental group (P<0.05). Conclusion Microglia is the m ain type of inflam m atory cells involved in the progress of the fatal disease. Moreover, PSG L-1 could participate in the pathogenesis of hand-foot-m outh disease related fatal brainstem encephalitis.
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Objective To investigate the influence of carotid artery stenting (CS)of asymptomatic critical internal carotid artery (ICA)stenosis patients on cognitive function .Methods One hundred and fifty‐six asymptomatic patients with internal carotid arter‐y stenosis(carotid stenosis severity≥70% )were enrolled ,in whom CS was attempted .Functional assessments including alzheimer disease assessment scale‐cognitive subtest (ADAS‐Cog) ,mini‐mental state examination (MMSE) ,and trail making test A(TMTa) and B(TMTb) were done prior to 1 weeks and 3 months after the procedure .Results Successful CS was achieved in all of patients (100% ) ,only 1 patient was lost to follow‐up .There were significant improvement in ADAS‐Cog score(pre 6 .60 ± 2 .04 vs .post 5 .16 ± 1 .63 ,P<0 .01) ,MMSE score (pre 26 .32 ± 1 .06 vs .post 27 .05 ± 1 .46 ,P< 0 .01) ,TMTa (pre 108 .94 ± 17 .42 vs .post 94 .70 ± 20 .27 ,P<0 .01) ,TMTb (pre 178 .65 ± 21 .77 vs .post 148 .92 ± 23 .65 ,P<0 .01) .There was new cerebral infarction dur‐ing 3 months after surgery .Conclusion Asymptomatic critical internal carotid artery (ICA)stenosis may be one reason of cognitive impairment ,and successful CS could improve cognitive function in asymptomatic ICA stenosis .
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Objective To investigate the effect of intracarotid administration of bone marrow stem cells (BMSCs) on learning and memory abilities of vascular dementia (VD) rats and the variability of expressions of neuron-specific enolase (NSE) and S-100 protein in the serum.Methods BMNCs collected from clean juvenile male Wistar rat femur were isolated; after adherent culture,the 3-4th generation BMSCs were performed induced differentiation.Ninety Wistar rats (age:18 to 24 months old) were randomly divided into three groups:control group,model group and treatment group,and each group was further classified into three subgroups by means of survival times of 2,4 and 8 weeks,which means that every subgroup consisted often rats.All VD rats,which were modeled by modified Pulsinellis 4-vessel occlusion (4VO); and those in the treatment group were injected 0.5 mL 1.2×107/mL BMSCs into the internal carotid artery 24 after operation.The learning and memory abilities of each rat in all subgroups were analyzed by shuttle box testing and the NSE leves and S-100 protein in serum were detected by enzyme-linked immuno sorbent assay (ELISA).Results The mean active avoidance response (AAR) ratios of the rats in the three subgroups (survival time of 2,4,8 weeks) of the model group,were,respectively,lower than those of the control group (P＜0.05),and those of the treatment group were significantly higher than those of the model group (P＜0.05).The serum levels of NSE in the treatment group was significantly lower than that in the model group two weeks after operation (P＜0.05),but it reversed 4 and 8 weeks after operation.The S-100 protein expressions in the treatment group was statistically lower than that in the model group (P＜0.05),however,there is no significant difference between treatment group and control group (P＞0.05).Conclusion Intracarotid administration of BMSCs obviously improves the learning and memory abilities of the VD rats,remarkably reduces the serum levels of NSE and S-100 protein,and efficiently relieves the injury degree of neurons and glial cells,which indicates that BMSCs therapy has effective protection on neural regeneration,neuronal proliferation and synaptic connectivity.
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Objective To investigate the effect of the reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase on Toll-like receptor 4 (TLR4)-mediated proinflammatory phenotype of cultured vascular smooth muscle cells (VSMCs) in mice.Methods NADPH oxidase agonist platelet-derived growth factorBB (PDGF-BB) and inhibitor apocynin were used respectively to treat cultured VSMCs from C57BL/6J and TLR4-/-mice.The fluorescent probe 2',7'-dichlorodihydrofluorescein diacetate was used to detect the reactive oxygen species (ROS) level in VSMCs.An enzyme-linked immunosorbent assay was used to detect the expressions of interleukin (IL)-6,IL-1β,and tumor necrosis factor-α (TNF-α) in VSMCs.Tetrazolium blue staining and Boyden chamber assay were used to detect the proliferation and migration of VSMC.Results The ROS levels were increased in VSMCs both from C57BL/6J and TLR4-/-mice after PDGF-BB treatment,and this could be inhibited by apocynin.PDGF-BB pretreatment significantly upregulated the expressions of IL-6 (52.69 ±3.49 ng/ml vs.35.04 ±2.74 ng/ml; P =0.001),IL-1β (79.68 ±2.33 ng/ml vs.62.38 ±0.54 ng/ml;P=0.000),and TNF-α (218.35± 5.42 ng/mlvs.124.74± 4.59 ng/ml; P=0.000) in VSMCs from C57BL/6J mice,and the abilities of proliferation (1.69 ± 0.53 vs.1.04 ± 0.40; P =0.000) and migration (42.11 ±4.05 vs.1.69 ± 0.53; P =0.000) were increased significantly; apocynin pretreatment significantly inhibit the expressions of IL-6 (42.11 ± 4.05 ng/ml vs.52.69 ± 3.49 ng/ml; P =0.010),IL-1β (67.57 ± 1.36 ng/ml vs.79.68 ±2.33 ng/ml; P =0.000) and TNF-α (156.18 ± 6.98 ng/ml vs.218.35 ± 5.42 ng/ml;P =0.000),as well as proliferation (1.23 ±0.42 vs.1.69 ±0.53; P =0.000) and migration (42.11 ±4.05 vs.52.69 ± 3.49; P =0.000).While there were no significant changes in the expressions of IL-6,IL-1β,and TNF-α in VSMCs from TLR4-/-mice after PDGF-BB and apocynin pretreatment.Conclusions NADPH oxidase-derived ROS involved in the TLR4-mediated VSMC inflammatory phenotype as well as proliferation and migration,which may be the important mechanisms of its influencing on the occurrence and development of atherosclerosis.
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Objective To investigate the efficacy of intra-arterial thrombolysis with stenting for acute cerebral infarction. Methods Using a prospective case-control design, 24 patients with acute cerebral infarction who remained angiostegnosis ( ＞ 50%) after intra-arterial thrombolysis were randomly divided into stent treatment group and drug treatment group. They were treated with stenting + drug treatment and conventional drug treatment. The rates of vascular complete revascularization and residual stenosis, and the modified Rankin scale scores at 3 months in both groups were evaluated. Results The rate of complete revascularization in the stent treatment group was significantly higher than that in the drug treatment group (54. 5% vs.0%,χ2 =6.382, P ＜0. 001), and the rate of residual stenosis was significantly lower than that in the drug treatment group ([4.5 ±5.2]% vs. [82. 5 ±10. 5]%, t =7.464, P＜0.001). The rate of favorable clinical outcome in the stent treatment group was significantly higher than that in the drug treatment group (100% vs. 76. 9%,χ2 = 14. 263, P = 0.038). Conclusion The efficacy of intra-arterial thrombolysis with stenting in the treatment of acute cerebral infarction is superior to that in the drug treatment group, and it is safer.
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Objective To observe the dynamic changes of serum inflammatory factors after vertebral artery stenting and to investigate its clinical significance. Methods A total of 48 patients treated with vertebral artery stenting were included, and 48 patients only received cerebral angiography were used as a control group. The levels of soluble intercellular adhesion molecule-1 (sICAM-1), high-sensitivity C-reactive protein (hs-CRP) and tumor-necrosis factor-α (TNF-α) were detected before procedure (angiography), at 24 h, 48 h, 3 d, and 1 and 3 weeks after procedure (angiography). Results The serum levels of hs-CRP (4. 85 ± 0. 53 mg/L vs. 2. 57 ±0. 36 mg/L,P＜0. 05), TNF-α (2.42 ±0. 34 μg/L vs. 1. 08 ±0. 37 μg/L,P ＜0. 05) and sICAM-1 (449.43 ± 47. 16 μg/L vs. 269. 15 ± 37. 46 μg/L, P ＜ 0. 05) at 24 hours after procedure in the stenting group were significantly elevated compared with those before procedure. The Hs-CRP level (6.24 ± 0.59 mg/L) reached the peak at 48 hours after procedure. At week 3 (2. 51 ±0.29 mg/L), it returned to the level before procedure (2. 57 ±0. 36 mg/L); TNF-α level reached the peak at day 3 (2.30 ± 0.25 μg/L), and it remained higher level at week 3 (1. 89 ±0. 13 μg/L); the sICAM-1 level continued to rise at week 3 (296. 95 ± 59. 72 μg/L). The serum hs-CRP, TNF-α and sICAM-1 levels at 24 hours after procedure in the stenting group were significantly higher than those (3. 25 ±0.40 mg/L、J. 18 ±0. 19 μg/L and 336. 57 ± 50. 18μg/L) in the control group (all P＜0.05). Conclusions The serum hs-CRP, TNF-α, sICAM-1 levels were significantly elevated after vertebral artery stenting. It was suggested that the stenting caused a longer duration of inflammatory response.
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Objective To study the prevalence and genotype of human parvovirus B19 virus among blood products and plasma pools in China. Methods B19 DNA derived from 16 lots of factor Ⅷ concentrate produced by 4 manufactures and 10 lots of plasma pools were detected by nested PCR. Phylogenetic comparison of the partial B19 sequences obtained from positive samples were performed by direct sequencing. Results Twelve of sixteen lots of factor Ⅷ concentrate and all of ten lots of plasma pools were contaminated by B19 DNA. By comparing the partial B19 sequences,all the isolated viruses were genotype Ⅰ and their nucleotides were high conserved with homology of 98. 3%-100%. Conclusion B19 genotype Ⅰ DNA has been detected in high prevalence in factor Ⅷ concentrate and plasma pools. The genetic diversities were shown to be very low.
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Vascular dementia iS one of the common forms of dementia,and its occurrence is closely associated with cerebrovascular disease.There are abundant stem cells in cord blood that differentiate into neural stem cells.The studies of stem cell transplantation in the treatment of ischemic cerebrovascular disease and neurodegenerative diseases have achieved some results. Cord blood stem cells may also he used in the treatment of vascular dementia.
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Setting criterion of teaching system,improving examination methods and strengthening the cultivation of basic medical skills and practice ability might be beneficial to the increase of the practice quality.
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To study the current situation and affecting factors of bilingual teaching for Neurology,we investigated the students of a five-year medical undergraduade in clinical medicine with a questionaire.It will provide the data and reference to effectively improve bilingual teaching program for Neurology.
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<p><b>OBJECTIVE</b>To investigate the features of glutamate activity in the limbic system and the effects of glutamate on the activation of the hypothalamus-pituitary-adrenal (HPA) axis throughout both acute cerebral ischemia and reperfusion.</p><p><b>METHODS</b>The changes in glutamate content in the nervous cell gap, in corticotrophin releasing hormone (CHR) mRNA expression level in brain tissue, and in adrenocorticotropic hormone in blood plasma at different time-points after middle cerebral artery occlusion (MCAO) in rats were determined respectively with high-performance liquid chomatography (HPLC) and in situ hybridization.</p><p><b>RESULTS</b>Glutamate content in the hippocampus and the hypothalamus increased rapidly at ischemia 15 minutes, and reached peak value (the averages were 21.05 mg/g +/- 2.88 mg/g and 14.20 mg/g +/- 2.58 mg/g, respectively) at 1 hour after middle cerebral artery occlusion. During recirculation, it returned rapidly to the baseline level. At 24 hours after reperfusion, it went up once more, and remained at a relative high level until 48 hours after reperfusion, and then declined gradually. CRH mRNA expression levels in the temporal cortex, hippocampus and hypothalamus were enhanced markedly at 1 hour ischemia and were maintained until 96 hours after reperfusion. At the same time, adrenocorticotropic hormone level in plasma was relatively increased. In the peak stage of reperfusion injury, there was a significantly positive correlation (n = 15, r = 0.566, P < 0.05) of the glutamate contents in the hypothalamus with the number of cells positive for CRH mRNA expression level in the hypothalamus.</p><p><b>CONCLUSION</b>It is probable that the CRH system in the central nervous system is mainly distributed in the limbic system, and glutamate might be one of the trigger factors to induce excessive stress response in the HPA axis.</p>
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Animals , Male , Rats , Glutamic Acid , Hypothalamo-Hypophyseal System , Chemistry , Infarction, Middle Cerebral Artery , Metabolism , Limbic System , Chemistry , Pituitary-Adrenal System , Chemistry , Rats, Wistar , Reperfusion Injury , MetabolismABSTRACT
Objective To explore the changes and significance of somatostatin (SS) and acetylcholine (Ach) contents in vascular dementia rats. Methods Model of vascular dementia rats was established. Active avoidance responase (AAR) ratio was used as the index for the judgement of the learning and memory abilities of vascular dementia rats. The SS and Ach contents in different cerebral sections of rats with and without intervention of huperzine A were determined by radioimmunoassay. Results A remarkable decrease in SS and Ach contents was found in vascular dementia rats, which could be reversed by intervention of huperzine A. Conclusion The decreased SS content in cerebrum after ischemia is related with vascular dementia. SS may be involved in the pathological process of vascular dementia through the mutual regulation with Ach.
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Objective To observe the changes of cerebral CT and auditory event related potentials (ERP, P300) for finding the effective method for the comprehensive evaluation of the patients with Alzheimer's disease. Methods Cerebral CT, P300, and Mini Mental State Examination (MMSE) were employed to assess 30 patients with Alzheimer's disease. Results Latency and amplitude of wave of P300 in patients were prolonged and decreased, respectively. Cerebral CT found an obvious atrophy in the frontal and temporal lobes of cerebra. These changes were obviously correlated with the severity of dementia. Conclusion Using cerebral CT, P300, and MMSE can offer morphometric, functional and psychological information which is helpful for precise assessment of patients with Alzheimer's disease.
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Objective To investigate the roles of differentiation and proliferation related proteins in neural stem cells (NSCs) in rats treated with L monosodium glutamate (MSG). Methods Tissue proteins were extracted from the rat forebrain. Western blotting was used to investigate the changes of differentiation and proliferation related proteins in NSCs in rats treated with MSG. Results Compared with those in rats of the normal control group, the related proteins (Notch1, hes5, Mash1, and NeuroD) in NSCs were significantly decreased in MSG rats at 30 and 60 d, especially for Notch1 and hes5 ( P
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Objective To explore the changes of differentiation and proliferation of neural stem cells in rats treated with corticosterone (CORT). Methods Adult SD rats were administered with CORT (10 mg?kg -1 ?d -1 ) by consecutive subcutaneous injection for 14 days. Single and double immunohistochemical stainings were used to identify the neural stem cells and differentiated neural cells in adult rats. Results Compared with that in the normal control group, the number of BrdU immunohistofluorescence positive cells and BrdU+NF200, BrdU+NeuroD, BrdU+GFAP double immunostaining positive cells in the cerebral cortex, hippocampus, and hypothalamus were markedly decreased ( P
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Objective To explore the roles of expression of brain derived neurotrophic factor (BDNF) in the brain of old rats after chronic cerebral perfusion deficiency in the pathogenesis of vascular dementia. Methods Rat model of vascular dementia was established by modified Pulsinelli 4 vessel occlusion (4VO) and divided into 3d (3 d), 1 week (1 w), 2 weeks (2 w), 4 weeks (4 w) and 2 months (2 m) groups. Computer controlled initiative avoidance response shuttle box system was used to test the learning and memory capacity of rats. Immunohistochemical method was used to examine the expression of BDNF in CA1 region of the hippocampus and cortex of temporal and frontal lobe. Results Compared with those in control group, BDNF positive cells in CA1 region were decreased significantly in 4VO 1 w group ( P 0 05). Compared with those in the control group, BDNF positive cells in the cortex of temporal and frontal lobe were increased significantly in 4VO 3 d group ( P
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Objective To observe the protective effect of edaraven on brain tissue and the therapeutic mechanism in rats following intracerebral hemorrhage(ICH).Methods In this series,96 Sprague-Dawley rats were divided into three groups at random(n=32 in each group):sham-operative group,ICH model group and edaraven therapy group.ICH model was induced by infusion of autologous whole blood into the caudate-putamen.Rats in sham-operative group were treated the same as above,but no blood injected.Rats in edaraven therapy group were treated with edaraven(3 mg/kg)by peritoneal injection 30 min before operation and once per 12 hours after operation.These rats were killed at 6,24,72,and 168 h after neurologic impairment test with Longa criteria.Brain water content was measured by dry-wet weight method.Malondialdehyde and TNF-alpha in the vicinity of the hematoma were measured by thio-barbituric acid method and ELISA respectively.Results Compared with sham operative group,neurologic impairment score,brain water content,malondialdehyde and TNF-alpha in brain tissues were obviously higher in ICH model group(P
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Objective To explore the effects of erythropoietin (EPO) on the proliferation and differentiation of neural stem cells and on the cognition function of vascular dementia (VD) rats. MethodsTotally 45 Sprague-Dawlev (SD) rats were randomly and equally divided into the sham control group, the VD group, and the treatment group. The VD rat model was established by performing cerebral ischemia/reperfusion repeatedly and given an intraperitoneal injection sodium nitroprusside. The rats from the treatment group received an introperitoneal injection of EPO after the establish of VD model, and the animals from the others were treated with normal saline. The learning-memory abilities were measured by using computerized shuttle-training case and the proliferation and differentiation of neural stem cells were detected by immunofluorescence staining. ResultsThe active avoidance reaction (AAR) ratio in the VD group was significantly decreased compared with the sham control group (P
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Objective To detect the expression of TNF α and ICAM 1 in cerebral ischemia reperfusion injury. To explore their probable modulation mechanism.Methods Immunohistochemistry was used to examine the expression of TNF α and ICAM 1.The MPO activity was determined by spectrophotometry.Result The expression of TNF α and ICAM 1 were obviously rised after cerebral ischemia reperfusion (P< 0.05).Conclusion The up regulation of TNF α and ICAM 1 after cerebral ischemia reperfusion induced the accumulation of leukocytes, which involved in ischemia reperfusion injury mechanism. TNF α play an important role in expression of ICAM 1.