Objective To observe the clinical effect of acupuncture combined with traditional Chinese medicine Tongluo huayu decoction on white matter damage in patients with occlusive cerebral infarction.MethodsA total of 76 patients with cerebral infarction with cerebral hemorrhage were enrolled in this study from April 2013 to January 2015.The random number table was divided into observation group and control group (38 cases).The control group was given routine western medicine treatment, the observation group on the basis of the control group plus traditional Chinese medicine tongluo huayu decoction, and with acupuncture treatment, the two groups were treated for 2 months, compare the effectiveness of treatment, analysis of the two groups before and after treatment platelet aggregation rate MAR (CDCA) and platelet-activated granule membrane glycoprotein 62P (CD62P), and the prognosis was analyzed by NIHSS, Montreal Metabolic Assessment Scale (MoCA) and Barthel Index (BI) Observe adverse reactions.ResultsThe effective rate of the observation group was 94.74% higher than that of the control group (78.95%, P< 0.05).After treatment, the expression of CD62P (21.87±1.55)%, MAR (35.23±1.62)% and NIHSS score (10.27±0.78) (P< 0.05).The incidence of adverse events was 13.16% in the observation group (25.04±1.11) and the BI index (88.15±1.20) were significantly higher than those in the control group (P< 0.05);There was no significant difference in the prevalence of adverse effects between 13.16% and 7.89%.ConclusionAcupuncture combined with traditional Chinese medicine Tongluo huayu decoction can effectively protect the white matter of patients with massive arterial occlusive cerebral infarction, improve its platelet CD62P, MAR and neurological function, cognitive function, improve the quality of life, and mild adverse reactions, it is worth in the clinical promotion application.

OBJECTIVETo study the metabolism of mangiferin by human intestinal bacteria in vitro.

METHODHuman intestinal bacteria and mangiferin were incubated under anaerobic conditions in vitro. The metabolite was separated and purified by D101 macroporous resin column and preparation high performance liquid chromatography, and its structure was identified by MS and NMR.

RESULTAfter 12 h incubation with human intestinal bacteria, the content of mangiferin metabolite reached the maximum, and it was determined as 1, 3, 6, 7-tetrahydroxyxanthen by MS and NMR.

CONCLUSIONMangiferin can be metabolized in vitro by human intestinal bacteria into its aglycone (1, 3, 6, 7-tetrahydroxyxanthen).

Bacteria ; metabolism ; Chromatography, High Pressure Liquid ; Humans ; Intestines ; microbiology ; Xanthones ; metabolism

Objective: To investigate the spectrum of gene mutations in adult patients with B-acute lymphoblastic leukemia (B-ALL), and to analyze the influences of different gene mutations on prognosis. Methods: DNA samples from 113 adult B-ALL patients who administered from June 2009 to September 2015 were collected. Target-specific next generation sequencing (NGS) approach was used to analyze the mutations of 112 genes (focused on the specific mutational hotspots) and all putative mutations were compared against multiple databases to calculate the frequency spectrum. The impact of gene mutation on the patients’ overall survival (OS) and recurrence free survival (RFS) was analyzed by the putative mutations through Kaplan-Meier, and Cox regression methods. Results: Of the 113 patients, 103 (92.0%) harbored at least one mutation and 29 (25.6%) harbored more than 3 genes mutation. The five most frequently mutated genes in B-ALL are SF1, FAT1, MPL, PTPN11 and NRAS. Gene mutations are different between Ph⁺ B-ALL and Ph^- B-ALL patients. Ph^- B-ALL patients with JAK-STAT signal pathway related gene mutation, such as JAK1/JAK2 mutation showed a poor prognosis compared to the patients without mutation (OS: P=0.011, 0.001; RFS: P=0.014,<0.001). Patients with PTPN11 mutation showed better survival than those without mutation, but the difference was not statistically significant (P value > 0.05). Besides, in Ph⁺ B-ALL patients whose epigenetic modifications related signaling pathway genes were affected, they had a worse prognosis (OS: P=0.038; RFS: P=0.047). Conclusion Gene mutations are common in adult ALL patients, a variety of signaling pathways are involved. The frequency and spectrum are varied in different types of B-ALL. JAK family gene mutation usually indicates poor prognosis. The co-occurrence of somatic mutations in adult B-ALL patients indicate the genetic complex and instability of adult B-ALL patients.

Alzheimer's disease (AD) is a leading cause of dementia in the elderly. Mitogen-activated protein kinase phosphatase 1 (MKP-1) plays a neuroprotective role in AD. However, the molecular mechanisms underlying the effects of MKP-1 on AD have not been extensively studied. MicroRNAs (miRNAs) regulate gene expression at the post-transcriptional level, thereby repressing mRNA translation. Here, we reported that the microRNA-429-3p (miR-429-3p) was significantly increased in the brain of APP23/PS45 AD model mice and N2A^APP AD model cells. We further found that miR-429-3p could downregulate MKP-1 expression by directly binding to its 3'-untranslated region (3' UTR). Inhibition of miR-429-3p by its antagomir (A-miR-429) restored the expression of MKP-1 to a control level and consequently reduced the amyloidogenic processing of APP and Aβ accumulation. More importantly, intranasal administration of A-miR-429 successfully ameliorated the deficits of hippocampal CA1 long-term potentiation and spatial learning and memory in AD model mice by suppressing extracellular signal-regulated kinase (ERK1/2)-mediated GluA1 hyperphosphorylation at Ser831 site, thereby increasing the surface expression of GluA1-containing α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPARs). Together, these results demonstrate that inhibiting miR-429-3p to upregulate MKP-1 effectively improves cognitive and synaptic functions in AD model mice, suggesting that miR-429/MKP-1 pathway may be a novel therapeutic target for AD treatment.