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<p><b>OBJECTIVE</b>To investigate the association between non-syndromic cleft lip with or without cleft palate (NSCL/P) and environmental factors in Ningxia population.</p><p><b>METHODS</b>This case-control study involved 453 NSCL/P patients and 452 normal newborns from Ningxia. A questionnaire focusing on various factors, including family history, pregnancy reaction, drug use during pregnancy, and infections, was used and responses were analyzed through Chi-square test and Logistic regression analysis with SPSS 16.0.</p><p><b>RESULTS</b>The constituent ratio of different types of NSCL/P was cleft lip∶cleft lip and palate∶cleft palate equal to 1︰2.02︰1.51. Logistic regression analysis revealed that abnormal pregnancy, infection, abortion, drugs, drinking, smoking, and living near factories likely increased the risk of NSCL/P (P<0.05). Single fetus, pregnancy-related nausea, vomiting, parents' moderate tastes, and eating soy foods and fruits decreased the risk of NSCL/P (P<0.05).</p><p><b>CONCLUSIONS</b>The incidence of NSCL/P should be reduced to enhance the conditions of women during pregnancy by maintaining a balanced diet and avoiding infections, abortion, drugs, and negative habits. .</p>
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Female , Humans , Infant, Newborn , Pregnancy , Case-Control Studies , China , Epidemiology , Cleft Lip , Epidemiology , Cleft Palate , Epidemiology , Diet , Incidence , Parents , SmokingABSTRACT
Objective To investigate the neuroprotective effect of Dengzhan Shengmai capsule (DZSM) in rat cerebral ischemia-reperfusion injury and to explore the mechanism. Methods Rats were divided into Sham group, MCAO group, DZSM group, carbenoxolone (CBX) group and DZSM + CBX group. Each group was assessed for neurological function , infarct volume and the expression of Caspase-3 48 h after reperfusion. Connexin 43 (Cx43) expression of MCAO group was detected 3, 12, 24, 48 h after reperfusion. Results There were lower neurological deficit scores , infarct volume and the expression of Caspase-3 in DZSM , CBX and DZSM + CBX group 48 h after reperfusion when compared with those in MCAO group (P < 0.05) but Cx43 expression level in each group increased after reperfusion at each time point (P < 0.05). Expression of Cx43 was lower in DZSM, CBX and DZSM + CBX group than that in MCAO group (P < 0.05). Lower expression of Cx43 was also seen in CBX and DZSM + CBX group when compared with that in DZSM group (P < 0.05). Conclusion DZSM capsule can improve neurological function , reduce infarct volume and inhibit the expression of Caspase-3. The mechanism may be related to its inhibition of Cx43 expression.
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[ ABSTRACT] AIM:To investigate the effect of triptolide on the inhibition of microglial activation in 1-methyl-4-phenyl pyridinium ( MPP+)-induced hemiparkinson disease rats.METHODS:The rat model of Parkinson disease was es-tablished by intranigral injection of MPP +.The rats were randomly divided into sham group, MPP+group, triptolide group and vehicle group.The survival of dopaminergic neurons was detected by the immunofluorescence of tyrosine hydroxylase ( TH) in the substantia nigra ( SN) .The activation of microglia was determined by immunofluorescence of OX-42 ( micro-glia marker) in the SN.The expression of chemokine receptor CX3CR1 in SN was measured by Western blotting.RE-SULTS:Intranigral injection of MPP+increased the fluorescence intensity of the microglial marker, and promoted DA neu-ron degenerative death.Immunohistological analysis showed that the OX-42 density was decreased (P<0.01) and tyrosine hydroxylase (TH) positive neurons were increased in the triptolide group (P<0.01).The expression of CX3CR1 was lower in triptolide group than that in model group (P<0.05).CONCLUSION:Triptolide may improve PA neurons func-tion in MPP+-induced rats through inhibiting CX3CR1 expression and microglial activation.
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OBJECTIVE:To optimize the extraction technology of total saponins from Coreopsis tinctoria. METHODS:Etha-nol leaching technology was adopted. Based on single factor test,the extraction technology was optimized by orthogonal test using extraction temperature,ethanol volume fraction,extraction time,solid-liquid ratio as factors,extraction rate of total saponins as in-dex. The optimized technology was validated. RESULTS:The optimal technology was that ratio of solid to liquid was 1:30 (C. tinctoria-60% ethanol),extracting for 2 h at 50 ℃. Validation test showed that average extraction rate of total saponins was 6.8%(RSD=0.85%,n=3). CONCLUSIONS:The optimized technology can be used for the extraction of total saponins from C. tinc-toria and keep stable.
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AIM:To investigate the integrative treatment of both coenzyme Q 10 ( CoQ10 ) and minocycline in the rats intranigrally intoxicated with 1-methyl-4-phenylpyridinium ( MPP+) .METHODS:The rat model of Parkinson disease ( PD) was established by intranigral microinjection of MPP +.The degree of microglial activation was measured by immuno-fluorescent density of OX-42 ( a microglia marker ) in the substantia nigra ( SN) .The number of viable dopaminergic neurons was determined by counting the tyrosine hydroxylase ( TH) positive neurons in the SN .The behavioral performances were re-vealed with the number of apomorphine-induced rotations , score of forelimb akinesia and vibrissae-elicited forelimb placing a-symmetry.RESULTS:Pretreatment with CoQ10 or intracerebroventricular (icv) posttreatment with minocycline alone pro-vided partial attenuation against MPP +-induced locomotor defects .Integrative therapy provided enhanced beneficial effects , and resulted in a significant attenuation of locomotor disability than any single therapy (all P<0.01).The results of immu-nohistological analysis showed that the TH positive neurons were maximally protected by integrative therapy compared with minocycline group and CoQ 10 group (P<0.01) .CONCLUSION:The integrative therapy of CoQ 10 combined with minocy-cline may offer additional therapeutic benefit to MPP +-induced hemiparkinson rat model .Such neuroprotective strategy of tar-geting different aspect of the neurodegenerative phenotypes may highlight a new therapeutic strategy for future management of PD.
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Endoplasmic reticulum(ER)stress can be caused by disturbances in the function of the ER with the accumulation of misfolded proteins.The ER response is characterized by unfolded protein response(UPR)causing translational attenuation,induction of ER chaperones and degradation of misfolded proteins.In case of prolonged or aggravated ER stress,cellular signals leading to apoptosis are activated.ER stress has been suggested to be involved in human neurodegenerative diseases,such as Alzheimer's disease,Parkinson's disease,and amyotrophic lateral sclerosis,as well as other disorders.Here we will discuss the neurotoxic effect of ER stress in these three major neurodegenerative diseases,and highlight current knowledge in this field that may reveal novel insight into disease mechanisms and help to design better therapies for these disorders.