0.05). Other raw scores of MMSE in the vascular dementia group were lower than those in the cerebral infarction group and the normal control group ( P 0.05). P 300 peak latency in the vascular dementia group prolonged significantly as compared with that in the cerebral infarction group and the normal control group ( P

Objective To investigate the characteristics of brain imaging and its relationship with the cognitive disorders in vascular dementia patients. Methods The volumes of cerebral lobes and hippocampus formation in 30 ischemic vascular dementia patients and 30 normal controls were measured with MRI based technique. The indices of ventricles and cerebral sulci in 30 ischemic vascular dementia patients and 30 patients with ischemic stroke were calculated with CT based technique. The cognitive functions were assessed by psychometric testing (Mini Mental State Examination MMSE, Brief Screening Scale for Dementia BSSD, Raven's Standard Progress Matric RSPM) in all subjects. Results The volumes of frontal and temporal lobes in vascular dementia patients were smaller than those in ischemic stroke patients and normal control subjects ( P 0.05). The decrease of the volumes of the frontal and temporal lobes were positively correlated with the decrease of MMSE and BSSD scores. The cognitive disorders were more severe in the ischemic vascular dementia patients with pathological foci in the frontal and temporal lobes, multiple infarcts, and the total volume of infarcts greater than 50 mm 3 ( P

Objective To investigate the involvement of sympathetic nerve system in the transmission of nociceptive information related to vascular headache. Methods Fos expression in the midbrain periaqueductal grey (PAG) induced by electrical stimulation of dural matter near the superior sagittal sinus (SSS) of the rat was determined before and after the extirpation of the superior cervical ganglion (SCG) using standard avidin-biotin immunohistochemistry. Results Fos immunoreactive positive neurons were detected in the ventrolateral PAG, and were bilateral symmetry. Fos expression was (133.3±12.5) in SCG extirpated group, and higher than that in sham-operated group (76.0±11.3). Conclusion The sympathetic system may be involved in the transmission of nociceptive information through PAG, associated with vascular headache such as migraine.

In recent years,many investigations manifested that cortical spreading depression was probably the physiologic foundation of migraine aura.The authors reviewd the relationship between migraine aura and cortical spreading depression.

Objective To explore the effects of flunarizine hydrochloride on plasma calcitonin gene-related pep-tide and substance P levels after CSD in a rat migraine model of cortical spreading depression (CSD). Methods Thirty adult rats were randomly and evenly divided into three groups:control Group, CSD group and flunarizine group. The CSD waves were evoked by application of potassium chloride on brain surface with filter paper. Funarizine hydrochloride was intravenously administered to rats five minutes prior to application of potassium chloride. The plasma levels of CGRP and SP were measured by using radioimmunity assay. Statistical analyses were performed using two-sample t test and analy-sis of variance. Results CSD waves were absent in control group whereas CSD waves were induced in CSD and flunari-zine groups. The latency of the first CSD wave was longer in flunarizine group (167.90 ± 25.18 s) than in CSD group (130.90 ± 13.30 s) (P<0.01). The number of CSD waves was smaller in flunarizine group (4.50 ± 1.84) than in CSD group (8.50 ± 2.07) (P<0.01). The amplitude of CSD waves was lower in flunarizine group (11.40 ± 4.12 mv) than in CSD group (24.40±3.57 mv) (P<0.01). The levels of CGRP and SP in both CSD group (CGRP, 32.95±11.61 pg/mL;SP, 27.80±7.51 pg/mL) and flunarizine group (CGRP, 25.13 ± 5.67 pg/mL; SP, 19.45 ± 6.10 pg/mL) were higher than in control group (CGRP, 14.44 ± 6.39 pg/mL; SP, 12.36 ± 4.22 pg/mL) (P<0.01). The levels of CGRP and SP in flunarizine group (CGRP, 25.13±5.67 pg/mL;SP, 19.45±6.10 pg/mL) were lower than those in CSD group (CGRP, 32.95±11.61 pg/mL;SP, 27.80± 7.51 pg/mL) (P<0.05). Conclusions Flunarizine hydrochloride can inhibit CSD and reduce the plama levels of CGRP and SP in the rat model of CSD.

Aim To design and synthesize new phenyloxyisobutyric acid analogues as antidiabetic compounds. Methods Eight new target compounds were synthesized by combination of lipophilic moieties and acidic moiety with nucleophilic replacement or Mitsunobu condensation. The eight compounds were confirmed by 1H NMR, 13C NMR, IR and MS. Results In vitro insulin-sensitizing activity (3T3-L1adipocyte) demonstrated, that the cultured glucose concentration of up-clear solution detected with GODpioglitazone, compounds A and B were added to the insulin-resistant system. Conclusion In vitro insulin-sensitizing activity of target compound A is in between that of rosiglitazone and pioglitazone, and activity of target compound B is slightly less than that of pioglitazone.

Objective To determine whether rizatriptan has an effect on cortical spreading depression (CSD) and c-Fos expression within periaqueductal grey (PAG) induced by CSD in rats. Methods The experimental SD rats were randomly divided into group A injected with KCl, group B KCl plus rizatriptan and group C NaCL The number and amplitude of CSD were recorded after KCl or NaCl injection. C-Fos positive neurons of different layer were identified by the immunohistochemical technique 2 hours after the first injection of KCl or NaCl. Results There was no CSD in group C. The number of CSD in group A ( 10.70±3.23 ) was significantly more than that in group B (6.10±2.56, t = - 3.528, P < 0.01 ). The amplitude of CSD in group A ( 17.33 (95% CI 11.45--23.11 ) mV) was significantly greater than that in group B (11.82 (95%CI 9.24--14.70) mV, Z= -4.360, P< 0.01). There were more cFos-like immnoreactive neurons in every layer in group A than in group C (P < 0.01 ) and in group B (P < 0.05 ). Conclusion Rizatriptan has an inhibitory effect on CSD, which might induce the headache through exciting the neurons in PAG.

OBJECTIVETo investigate the efficacy and safety of pegylated recombinant human granulocyte colony stimulating factor (PEG-rhG-CSF) in the salvage therapy for the grade IV neutropenia induced by concurrent chemoradiotherapy, and to provide evidence for its clinical rational application.

METHODS114 malignant tumor patients suffered with grade IV neutropenia induced by concurrent chemoradiotherapy were treated in the following groups. In the P-50 group, 42 patients received a single subcutaneous injection of 50 µg/kg PEG-rhG-CSF. In the P-100 group, 30 patients received a single subcutaneous injection of 100 µg/kg PEG-rhG-CSF. In the P+R group, 22 patients received a single subcutaneous injection of 50 µg/kg PEG-rhG-CSF and multiple subcutaneous injections of 5 µg×kg(-1)×d(-1) rhG-CSF, until the absolute neutrophil count (ANC) ≥ 2.0×10(9)/L. In the R group, 20 patients received multiple subcutaneous injections of 5 µg×kg(-1)×d(-1) rhG-CSF, until ANC ≥ 2.0×10(9)/L. The P-50, P-100 and P+R groups were experimental groups, and the R group was defined as control group. In each group, the neutrophil proliferation rate and the neutrophil counts at different time points, the period of neutropenia symptom relief, and the rate of adverse reactions induced by above drugs were analyzed.

RESULTSBoth neutrophil proliferation rates and neutrophil counts in the patients of experimental groups at different time points were significantly higher than those in the control group. In the experimental groups the period of the clinical effect began in 12-24 hours, and the conditions of neutropenia were improved in 36 hours. In the experimental groups, the period of the symptom relief such as fever and skeletal muscle pain was (30.00 ± 7.48) hours and (30.00 ± 5.10) hours, respectively, significantly shorter than (72.00 ± 17.89) hours and (59.00 ± 11.46) hours in the control group (P < 0.05). The adverse drug reaction rate was 26.1% in the experimental groups and 25.0% in the control group (P > 0.05).

CONCLUSIONSFor the treatment of grade IV neutropenia induced by concurrent chemoradiotherapy, PEG-rhG-CSF is effective and safe. The recommend dose of this drug for the salvage therapy for those patients is a single hypodermal injection of 50 µg/kg. Usually it becomes effective in 12-24 hours.

Chemoradiotherapy ; Granulocyte Colony-Stimulating Factor ; genetics ; metabolism ; Humans ; Injections, Subcutaneous ; Leukocyte Count ; Neutropenia ; chemically induced ; Neutrophils ; Recombinant Proteins ; Salvage Therapy ; methods

Objective To explore the characteristics of myocardial injury in patients with acute myocardial infarction(AMI)complicated by pleural effusion and its effect on long-term prognosis.Methods It was a prospective single-center study.Patients with AMI who were admitted to hospital within 15 days from symptom onset and performed echocardiography and cardiac magnetic resonance imaging(CMR)during hospitalization were consecutively enrolled and assigned to the with-pleural effusion group and the without-pleural effusion group according to the echocardiography result.Baseline data,cardiac magnetic resonance myocardial injury index and echocardiography characteristics were compared between the two groups.The occurrence of major adverse cardiovascular and cerebrovascular events(MACCE)was recorded through outpatient follow-up and telephone follow-up,including all-cause death,re-infarction,revascularization,rehospitalization for congestive heart failure and stroke.Cox regression analysis was performed to analyze influencing factors of all-cause death.Results Among 211 patients,31(14.7%)patients had pleural effusion and 180(85.3%)had no pleural effusion.Compared with the group without pleural effusion,the left ventricular end-diastolic diameter was larger,and left ventricular ejection fraction assessed by echocardiography was lower in the group with pleural effusion(P＜0.05).There were no significant differences in infarct size,left ventricular end-diastolic volume,left ventricular end-systolic volume,left ventricular ejection fraction and the presence of microvascular obstruction and intramyocardial hemorrhage between the two groups in CMR(all P＞0.05).At a median follow-up of 31 months,MACCE occurred in 43(20.4%)patients,and there was no significant difference between the two groups(χ2=3.160,P=0.075).Six cases(2.8%)had all-cause death.The incidence of all-cause death was higher in the group with pleural effusion than that in the group without pleural effusion(9.7%vs.1.7%,P<0.05).There was no significant difference in the incidence of other adverse events between the two groups(P＞0.05).Multivariate Cox regression analysis showed that advanced age and presence of pleural effusion were independent risk factors of all-cause death during follow-up.Conclusion Patients with AMI combined with pleural effusion have more severe myocardial injury and higher all-cause mortality.

BACKGROUNDThe molecular and cellular origins of migraine headache are among the most complex problems in contemporary neurology. Up to now the pathogenesis of migraine still remains unclearly defined. The objective of this study was to explore new factors that may be related to the mechanism of migraine.

METHODSThe present study performed a comprehensive analysis of gene expression in the trigeminal nucleus caudalis induced by electrical stimulation of dura mater surrounding the superior sagittal sinus in conscious rats using microarray analysis followed by quantitative real-time reverse-transcribed polymerase chain reaction (qRT-PCR) verification. Student's two sample t-test was employed when two groups were compared. A P value <0.05 was considered to be statistically significant.

RESULTSComparing the placebo and the electrical stimulation groups, 40 genes were determined to be significantly differentially expressed. These significantly differentially expressed genes were involved in many pathways, including transporter activity, tryptophan metabolism, G protein signaling, kinase activity, actin binding, signal transducer activity, anion transport, protein folding, enzyme inhibitor activity, coenzyme metabolism, binding, ion transport, cell adhesion, metal ion transport, oxidoreductase activity, mitochondrion function, and others. Most of the genes were involved in more than 2 pathways. Of particular interest is the up-regulation of Phactr3 and Akap5 and the down-regulation of Kdr.

CONCLUSIONThese findings may provide important clues for a better understanding of the molecular mechanism of migraine.

Animals ; Dura Mater ; physiology ; Electric Stimulation ; Gene Expression ; physiology ; Male ; Microarray Analysis ; Migraine Disorders ; genetics ; Rats ; Rats, Sprague-Dawley ; Real-Time Polymerase Chain Reaction ; Superior Sagittal Sinus ; physiology