OBJECTIVETo compare the differences in the clinical efficacy on post-stroke speech disorder between scalp electric acupuncture (EA) under anatomic orientation combined with rehabilitation training and simple rehabilitation training.

METHODSSixty patients of post-stroke speech apraxia were randomized into an observation group and a control group, 30 cases in each one. In the observation group, under anatomic orientation, the scalp EA was adopted to the dominant hemisphere Broca area on the left cerebrum. Additionally, the speech rehabilitation training was combined. In the control group, the speech rehabilitation training was simply,used. The treatment lasted for 4 weeks totally. The speech movement program module in the psychological language assessment and treatment system of Chinese aphasia was used for the evident of efficacy assessment. The scores of counting, singing scale, repeating phonetic alphabet, repeating monosyllable and repeating disyllable were observed in the patients of the two groups. The assessment was done separately on the day of grouping and 4 weeks after treatment.

RESULTSIn 4 weeks of treatment, the scores of counting, singing scale, repeating phonetic alphabet, repeating monosyllable and repeating disyllable were all improved as compared with those before treatment in the two groups (all P<0. 001). The results in the observation group were better than those in the control group (all P< 0. 05). The total effective rate was 100. 0% (30/30) in the observation group, superior apparently to 53. 3% (16/30) in the control group (P<0. 001).

CONCLUSIONThe scalp EA under anatomic orientation combined with' speech rehabilitation training obviously improves speech apraxia in stroke patients so that the speech disorder cani be relieved. The efficacy is better than that in simple rehabilitation training.

Acupuncture Points ; Adolescent ; Adult ; Aged ; Apraxias ; etiology ; physiopathology ; rehabilitation ; therapy ; Electroacupuncture ; Female ; Humans ; Language ; Male ; Middle Aged ; Speech Disorders ; physiopathology ; rehabilitation ; therapy ; Speech Therapy ; Stroke ; complications ; Young Adult

Objective To compare the clinical efficacy and postoperative liver function in patients with primary hepatic carcinoma treated by transcatheter arterial chemoembolization(TACE) or TACE combined with portal vein chemoembolization.Methods 48 patients with primary hepatic carcinoma, randomly divided into 2 groups (hepatic artery group in 25 cases and dual interventional group in 23 cases),underwent interventional treatment.The hepatic artery group underwent conventional hepatic artery interventional therapy, while the dual interventional group underwent hepatic artery and portal vein interventional treatment.The postoperative clinical efficiency, liver volume and liver function between the two groups'' patients were compared.Results To the endpoint of observation,the clinical efficacy and tumor reduction degree of dual interventional group were better than that of hepatic artery group.Compared with hepatic artery group, the postoperative ALT, AST and TBIL of dual interventional group were higher on the first and third days.On the seventh and fourteenth days, the statistical difference was not significant.The volume of non-embolization part in dual interventional group was larger than that in preoperative volume to different degrees.The most obvious change of liver volume happened in the 4th weeks after treatment.There was no treatment-related death or severe adverse reaction in two groups.Conclusion The treatment of TACE combined with portal vein chemoembolization is a safe and effective method, which may effectively inhibit the growth and reduce the volume of tumor, and result in compensatory hypertrophy of non-embolization part.

Objective:This work aims to investigate diallyl disulfide (DADS) inhibition of cell migration and invasion in human colon cancer SW480 cells through the Rac1-ADF/cofilin1 pathway. Methods:The potential of cell migration and invasion was examined by scratch healing assay and transwell membrane assay. The expression of Rac1-ADF/cofilin1 pathway was detected by RT-PCR and Western blot. Results:After the SW480 cells were treated with 40 and 50 mg·L-1 of DADS for 24 h, the number of transmembrane cells through the Matrigel obviously decreased by 57.12%and 64.59%, respectively (P<0.05). After cell treatment for 48 h, the cell migration rates were 23.23%and 12.87%, which were significantly lower compared with the control group (75.86%;P<0.05). After the cells were treated with 45 mg·L-1 of DADS for 24 and 48 h, the expression of Rac1, Rock1, PAK1, LIMK1, and destrin mRNA respectively decreased compared with the control group (P<0.05). However, no significant difference was observed in the expression of cofilin1 mRNA (P>0.05). After the treatment with 45 mg·L-1 of DADS for 6, 12, 24, and 48 h, the expression of Rac1, Rock1, PAK1, LIMK1, and Destrin proteins respectively decreased in a time-dependent manner compared with the control group (P<0.05). However, no significant differences were observed in the expression of the cofilin1 protein (P>0.05). Moreover, the expression of p-LIMK1 and p-cofilin1 notably decreased in a time-dependent manner (P<0.05). Conclusion:DADS inhibits cell migration and invasion, which is related to the down-regulation of Rac1, Rock1, PAK1, LIMK1, p-LIMK1, p-cofilin1, and destrin through the Rac1-ADF/cofilin1 pathway.

OBJECTIVE: To analyze the rate of 235delC mutation in GJB2 gene in patients with idiopathic sudden hearing loss, and to explore its possible correlation with pathogenesis of idiopathic sudden hearing loss. METHOD: Two hundred and thirty-four patients with diagnosis of idiopathic sudden hearing loss in otolaryngology department were recruited as experimental group. Eighty people with normal hearing level were enrolled as control group. Their peripheral blood samples were obtained and genomic DNA was extracted. Using polymerase chain reaction, the coding region of GJB2 gene was amplified, and 235delC mutation is screened for in GJB2 gene by restriction endonuclease. At same time the clinical data of 234 patients was collected to analyze. RESULT: In 234 cases of idiopathic sudden hearing loss, 5 cases were found to have heterozygous 235delC mutation, none of them harbored homozygous 235delC mutation, the 235delC mutation rate was 2.1% (5/234). No 235delC mutation was found in control group. The rate of 235delC mutation in two group showed no statistically significant difference (P > 0.05). CONCLUSION This research shows that the rate of 235delC mutation in GJB2 is low in patients with idiopathic sudden hearing loss, and suggest that 235delC mutation possible has no correlation with idiopathic sudden hearing loss.
Adolescent ; Adult ; Aged ; Child ; Connexin 26 ; Connexins ; genetics ; DNA Mutational Analysis ; Female ; Hearing Loss, Sudden ; genetics ; Humans ; Male ; Middle Aged ; Mutation ; Young Adult

OBJECTIVE: To investigate characteristics of molecular etiology of children with profound sensorineural hearing loss in Hubei province, and to provide reference for deafness treatment and genetic counseling. METHOD: Three hundred and six children with profound sensorineural hearing loss in Hubei province were enrolled, their genomic DNA were extracted from peripheral blood and a deafness gene test chip was used to screen nine hot spot mutation in the GJB2, GJB3, SLC26A4, and mitochondria 12SrRNA gene. All patients with SLC26A4 gene mutation were given temporal bone CT scan. RESULT: One hundred and thirty-two (43.14%) out of 306 children were found carrying at least one pathogenic gene mutation. The mutation rates of GJB2, SLC26A4 and mitochondria DNA 12SrRNA gene were 29.41% (90/306), 13.72% (42/306) and 0.65% (2/306), respectively. None out of 306 children was detected GJB3 gene mutation. Thirty-six patients carrying SLC26A4 gene mutation were detected enlarged vestibular aqueduct by CT scan. CONCLUSION Mutations of GJB2 and SLC26A4 gene are two major pathogenic gene for genetic hearing loss in children. 235delC mutation is the main mutation type, followed by IVS7-2A> G mutation type. The screening of SLC26A4 gene common mutations contribute to the diagnosis of enlarged vestibular aqueduct syndrome.
Adolescent ; Child ; Child, Preschool ; China ; Connexin 26 ; Connexins ; genetics ; DNA Mutational Analysis ; Deafness ; genetics ; Female ; Genetic Testing ; Humans ; Infant ; Male ; Membrane Transport Proteins ; genetics ; Mutation ; Oligonucleotide Array Sequence Analysis ; Sulfate Transporters

[Objective] To evaluate the clinical efficacy and safety of propranolol in treating infantile hemangiomas.[Methods] Ninety children with hemangioma collected from July 2010 to November 2011 were recruited in this study.Oral propranolol was given at a dose of 1.5-2.0 mg/kg per day,and the dose was adjusted according to the growth of body weight.Patients were revisited every month for the observation of appearance of hemangioma.The following parameters,including blood glucose,alanine transarninase,aspartate aminotransferase,urea nitrogen,creatinine,creatine kinase,heart rate,blood pressure,electrocardiogram and ultrasound image of hemangioma,were monitored before and after the administration of propranolol.[Results] A rapid halt in haemangioma proliferation was seen in 91.1％ (82/91) of the patients within 24-48 hours after the administration of popranolol.After 1-10 months of treatment,haemangioma shrunk by 0-25％ with a lightening of lesional color in 8.0％ (7/88) of the patients,by 26％-50％ with an obvious lightening of lesional color in 39.8％ (35/88),by 51％-75％ with a marked lightening of lesional color in 26.1％ (23/88),and 26.1％ (23/88)of the patients achieved a shrinkage of more than 75％ or fading of lesional color.The 7-8 months of treatment leaded to the best outcome,followed by 5-6 months,3-4 months,and 1-2 months,of treatrnent.No rebound was observed in patients who stopped the treatment at 10 months to l year and 4 months of age.Usually during early stage of the therapy,some of the patients suffered from reduced diastolic blood pressure,sleep disorder,loose stools,hypoglycemia,cold extremities,bronchial hyperreactivity,elevated alanine transaminase/aspartate aminotransferase or creatine kinase isoenzyme,most of which were tolerable and relieved with or without symptomatic treatment.[Conclusion]s Propranolol can suppress the growth and accelerate the regression of hemangiomas in proliferative phase,and also can promote the subsidence of hemangiomas in regressive phase.The side effects of propranolol are usually mild,but still need close monitoring.

Mitochondrial DNA (mtDNA) common deletion (CD) plays a significant role in aging and age-related diseases. In this study, we used D-galactose (D-gal) to generate an animal model of aging and the involvement and causative mechanisms of mitochondrial damage in such a model were investigated. Twenty 5-week-old male Sprague-Dawley rats were randomly divided into two groups: D-gal group (n=10) and control group (n=10). The quantity of the mtDNA CD in the hippocampus was determined using a TaqMan real-time PCR assay. Transmission electron microscopy was used to observe the mitochondrial ultrastructure in the hippocampus. Western blot was used to detect the protein levels of NADPH oxidase (NOX) and uncoupling protein 2 (UCP2). We found that the level of mtDNA CD was significantly higher in the hippocampus of D-gal-induced aging rats than in control rats. In comparison with the control group, the mitochondrial ultrastructure in the hippocampus of D-gal-treated rats was damaged, and the protein levels of NOX and UCP2 were significantly increased in the hippocampus of D-gal-induced aging rats. This study demonstrated that the levels of mtDNA CD and NOX protein expression were significantly increased in the hippocampus of D-gal-induced aging rats. These findings indicate that NOX-dependent reactive oxygen species generation may contribute to D-gal-induced mitochondrial damage.

Mitochondrial DNA (mtDNA) common deletion (CD) plays a significant role in aging and age-related diseases. In this study, we used D-galactose (D-gal) to generate an animal model of aging and the involvement and causative mechanisms of mitochondrial damage in such a model were investigated. Twenty 5-week-old male Sprague-Dawley rats were randomly divided into two groups: D-gal group (n=10) and control group (n=10). The quantity of the mtDNA CD in the hippocampus was determined using a TaqMan real-time PCR assay. Transmission electron microscopy was used to observe the mitochondrial ultrastructure in the hippocampus. Western blot was used to detect the protein levels of NADPH oxidase (NOX) and uncoupling protein 2 (UCP2). We found that the level of mtDNA CD was significantly higher in the hippocampus of D-gal-induced aging rats than in control rats. In comparison with the control group, the mitochondrial ultrastructure in the hippocampus of D-gal-treated rats was damaged, and the protein levels of NOX and UCP2 were significantly increased in the hippocampus of D-gal-induced aging rats. This study demonstrated that the levels of mtDNA CD and NOX protein expression were significantly increased in the hippocampus of D-gal-induced aging rats. These findings indicate that NOX-dependent reactive oxygen species generation may contribute to D-gal-induced mitochondrial damage.
Aging ; metabolism ; physiology ; Animals ; Galactose ; adverse effects ; metabolism ; Hippocampus ; metabolism ; physiology ; Male ; Mitochondria ; metabolism ; physiology ; NADPH Oxidases ; metabolism ; Oxidative Stress ; physiology ; Rats ; Rats, Sprague-Dawley

Objective To analyze clinicopathological characteristics and the potential risk-related factors of female breast hyperplasia in different age groups.Method From Jan 2015 to Dec 2016,patients diagnosed with breast hyperplasia in 12 hospitals were evaluated.All patients completed the self-designed questionnaires on women'health,including basic demographic information,clinic examination information,radiologic information and pathologic results.The patients were divided into a young group (＜ 45 years old) and an elderly group (from 45 to 75 years old).Results There were 3 684 cases of breast hyperplasia,including 2 291 cases in young group and 1 393 cases in elder group,respectively Clinically breast pain type were most commonly observed in both young and older groups (50.3％ vs.42.7％,P ＜ 0.001).While pathological research based on biopsy showed that breast adenopathy were the most common changes in both groups (67.9％ vs.61.7％,P ＜0.001).More breast cancer cases were identified in elder group than that in young group,especially in clinically lump type patients (9.4％ vs.4.2％,P ＜ 0.001).Compared with elder group,patients in young group have different distribution characteristics regarding to fertility factors,lifestyle factors and psychology scale including anxiety and depression.Conclusion Distributions of clinicopathological characteristics and risk factors of female breast hyperplasia differ across different age groups.

Objective:To investigate the relationship between single nucleotide polymorphism (SNPs) of Zeste homolog enhancer 2 (EZH2) gene and the risk of breast cancer.Methods:Recruiting 1 039 breast cancer patients and 1 040 controls at 22 referral hospitals nationwide in China, the genotype distribution of 3 SNPs loci of EZH2 genes was observed to detect the correlation between different genotypes and the risk of breast cancer genotypes EZH2 expression in breast cancer tissues and its correlation with patient prognosis were analyzed using breast cancer data from the database.Results:EZH2 rs6464926 CC genotype was compared with TT genotype (TT vs. CC: OR=1.362, 95% CI: 1.063-1.746, P=0.015) and dominant model (TC+TT vs .CC: OR=1.22, 95% CI: 1.004-1.483, P=0.045) .In women with BMI ≥24 kg/m 2, the TC genotype ( P=0.050), TT genotype ( P=0.025) and dominant model (TC+TT, P=0.021) of rs6464926 locus were significantly different from CC genotype in cancer risk. rs6464926 was correlated with EZH2 gene expression ( P=6.89E-47). EZH2 gene is highly expressed in breast cancer tissues, and patients with high expression were associated with shorter OS ( HR=1.27, P=0.013), DMFS ( HR=1.37, P<0.01), and RFS ( HR=1.44, P<0.01). Conclusions:The polymorphism rs6464926 of EZH2 gene is associated with breast cancer susceptibility in Chinese women. rs6464926 might regulate breast cancer risk and prognosis by changing EZH2 expression.