Acupuncture Therapy ; instrumentation ; methods ; standards ; China ; Humans ; Moxibustion ; instrumentation ; methods ; standards ; Needles ; standards ; Reference Standards

Objective To analyze and compare the incidence of diarrhea between cerebral hemorrhage and infarction. Method We observed and compared the time when diarrhea occurred in both 147 cases of cerebral hemorrhage patients and 142 cases of cerebral infarction patients by using statistical methods. Result The incidence of diarrhea in former group was 36.05%, and that of latter was 16.91%. Conclusions The incidence in patients with diarrhea of cerebral hemorrhage was markedly higher than that of patients with cerebral infarction. This may attribute to the higher intracranial pressure in cerebral hemorrhage patients than that of cerebral infarction ones. The complications of reduction of immune function,intestinal infection and hypoproteinemia may be the other factors resulting in the higher incidence of diarrhea in cerebral hemorrhage patients than that of cerebral infarction ones.

Objective:To study the relationship between Fc? receptor ⅢB(Fc? RⅢB) genotype and severe chronic periodontitis or generalized aggressive periodontitis.Methods:DNA from 35 subjects with severe chronic periodontitis,25 with generalized aggressive periodontitis and 95 of periodontal healthy controls were sampled by buccal swab and extracted using Chlex-100 method.Polymerase chain reaction with sequence specific primers (PCR-SSP)was carried out to determine the Fc?RIIIB genotype.The data were analyzed with ? 2 test. Results: NA1/NA2 heterozygote was the predominant genotype in the 3 groups.No statistically differences of Fc?RIIIB genotype distribution were found between any two of the stuied groups.The gene frequencies of NA1 and NA2 were 0.6 and 0.4 respectively.Conclusion:No direct relationship exists between Fc?RⅢB genotype and the occurrence of severe chronic periodontitis and generalized aggressive periodontitis according to the present study.

ABSTRACT:Objective To investigate the effect and mechanism of anthocyanin on hepatic ischemia reperfusion injury in rats .Methods Totally 30 SD rats were randomly divided into sham group ,model group and anthocyanin group (n=10 in each) .Hepatic ischemia was constructed in model group and anthocyanin group by ligating left middle lobe of liver vascular branches for 90 min . Anthocyanin was administered at 90 min before ischemia by intraperitoneal injection at the concentration of 100 mg/kg for rats in anthocyanin group .Rats in model group and sham group were injected with the same dosage of normal saline at the same time .Serum and liver tissues were collected at 4 h after reperfusion by putting the rats to death .The expressions of ALT ,AST ,IL‐6 ,IL‐1βand TNF‐αin the serum were examined by ELISA .The pathological changes of liver tissue were evaluated by HE .The mRNA levels of IL‐6 ,IL‐1βand TNF‐αwere measured by RT‐PCR .The content of MDA was examined by TBA . The activities of CAT ,GPx and SOD were evaluated by xanthine oxidase method and the expression of p‐JAK2 ,p‐STAT3 ,JAK2 ,STAT3 and P53 were measured by Western blot .Results Compared with those in the sham group ,the activities of ALT and AST ,the expressions of p‐JAK2 ,p‐STAT3 ,P53 ,IL‐6 ,IL‐1β,TNF‐α and the content of MDA as well as the pathological changes of the liver in model group were significantly increased . However ,the activities of CAT ,GPx and SOD in model group were decreased and the expressions of JAK2 and STAT3 between the two groups did not differ .Compared with those in model group ,the activities of ALT and AST ,the expressions of p‐JAK2 ,p‐STAT3 ,P53 ,IL‐6 ,IL‐1β,TNF‐α,the content of MDA and the pathological changes of the liver in anthocyanin group were significantly decreased . But the activities of CAT , GPx and SOD in anthocyanin group were increased and the expressions of JAK 2 and STAT3 between the two groups did not differ , either .Conclusion Anthocyanin pretreatment can significantly decrease hepatic ischemia/reperfusion injury by suppressing oxidative stress and inflammation ,and the mechanism may be associated with reducing JAK2/STAT3/P53 signaling activation .

Animals ; Neurotransmitter Agents ; metabolism ; Rabbits ; Syncope, Vasovagal ; metabolism ; physiopathology

China ; epidemiology ; Cross-Sectional Studies ; Female ; Health Status ; Humans ; Male ; Occupational Health

Catecholamines ; blood ; cerebrospinal fluid ; metabolism ; Child ; Humans ; Neuropeptides ; blood ; cerebrospinal fluid ; metabolism ; Neurotransmitter Agents ; blood ; cerebrospinal fluid ; metabolism ; Syncope, Vasovagal ; blood ; cerebrospinal fluid ; metabolism ; physiopathology

Adolescent ; Child ; Child, Preschool ; Chyle ; Female ; Humans ; Infant ; Male ; Pericardial Effusion ; diagnosis ; therapy ; Radiography, Thoracic

Adult ; Female ; Humans ; Male ; Middle Aged ; Palatine Tonsil ; surgery ; Tonsillectomy ; instrumentation ; methods

This study examined the effect of astilbin on the proliferation of rat aortic smooth muscle cells (RASMCs) induced by angiotensin II (AngII) and explored the possible mechanisms. Cell proliferation model of RASMCs was induced by treatmente with AngII. Cells were randomly divided to 8 groups. Normally cultured VSMCs serves as blank control group; in AngII model group, cells were treated with AngII at 10(-7) mol/L; in three astilbin groups, cells were treated with 10, 15, 30 mg/L of astilbin; in three AngII+astilbin groups, cells were treated with AngII (at 10(-7) mol/L) and astilbin at 10, 15, 30 mg/L. Cell proliferation ability was detected by MTT method and the cell cycles and proliferation index were flow cytometrically determined. The expression of c-myc mRNA was assessed by using reverse transcription polymerase chain reaction (RT-PCR), and the expression of NF-κB in RASMCs was immunocytochemically observed. Our results showed that MTT metabolism in RASMCs in the basic and AngII stimulated situation was inhibited by astilbin, and the cells numbers of G(0)/G(1) phase were increased and that of G(2)/S phase were decreased markedly. Not only highly expression of c-myc gene stimulated by AngII could be inhibited by Astilbin significantly, but also the expression of NF-κB protein can be down regulated by Astilbin. We are led to conclude that astilbin astilbin can inhibit the AngII-mediated proliferation of RASMCs by blocking the transition of RASMCs from G(0)/G(1) phase to S phase and by down-regulating the expression of NF-κB, c-myc gene.