【摘要】 目的 探討指導性強化作業療法對腦卒中患者上肢運動功能障礙的療效，旨在提高患者的生活質量。 方法 2007年6月-2009年6月將68例腦卒中偏癱患者隨機分成治療組及對照組。治療組進行指導性強化作業療法，對照組采用傳統康復訓練。分別于治療前、治療后和治療后1、3個月應用MAL和Bathel指數對其進行評定。 結果 兩組MAL評分及Bathel指數在治療后均有所提高，治療組在治療后1、3個月的MAL評分及Bathel指數較治療前增加，有統計學意義（Plt;0.05）；對照組無差異。治療后1、3個月，兩組MAL評分及Bathel指數比較有統計學意義（Plt;0.05）。 結論 指導性強化作業療法作為一種新型的康復治療技術，能夠改善患者上肢運動功能及日常生活能力，提高生活質量，具有較高的臨床應用價值。【Abstract】 Objective To explore the efficacy of guiding intensified occupational therapy for ischemic stroke patients with upper motor dysfunction, aiming at improving the quality life of the patients. Methods From June 2007 to June 2009, sixty-eight patients with stroke were randomly divided into treatment group and control group. Treatment group was treated with guiding strengthen occupational therapy and control group with trandional therapy. The MAL and the Bathel index were used to evaluate before treatment, after treatment and 3 months after treatment respectively. Results The MAL score and Bathel index were improved after treatment. The MAL score and Bathel index of the treatment group immediately and in 3 months after treatment increased greatly, and there were statistical significance (Plt;0.05). There was no difference in the MAL score and Bathel index in the control group before and after treatment. The MAL score and Bathel index of two groups were statistically significant after 3 months treatment (Plt;0.05). Conclusion Guiding intensified occupational therapy as a new kind of rehabilitation techniques, can improve the function of upper movement and daily life, and improve the quality life. It had high value of clinical applications.
The incidence and mortality of acute lung injury (ALI)/acute respiratory distress syndrome (ARDS) are still very high, but stem cells show some promise for its treatment. Here we found that intratracheal administration of human umbilical cord-mesenchymal stem cells (UC-MSCs) significantly improved survival and attenuated the lung inflammation in lipopolysaccharide (LPS)-induced ALI mice. We also used the proteins-chip and bioinformatics to analyze interactions between UC-MSCs treatment and immune-response alternations of ALI mice. Then we demonstrated that UC-MSCs could inhibit the inflammatory response of mouse macrophage in ALI mice, as well as enhance its IL-10 expression. We provide data to support the concept that the therapeutic capacity of UC-MSCs for ALI was primarily through paracrine secretion, particularly of prostaglandin-E2 (PGE2). Furthermore, we showed that UC-MSCs might secrete a panel of factors including GM-CSF, IL-6 and IL-13 to ameliorate ALI. Our study suggested that UC-MSCs could protect LPS-induced ALI model by immune regulation and paracrine factors, indicating that UC-MSCs should be a promising strategy for ALI/ARDS.
Background
Methylenetetrahydrofolate reductase gene (MTHFR C677T and A1298C) and methionine synthase gene (MS A2756G) polymorphisms have shown an association with male infertility risk in several ethnic populations. Although several studies have evaluated these associations in Chinese populations, their small sample sizes and inconsistent outcomes have prevented strong conclusions. Therefore, the present meta-analysis was performed with published studies to evaluate the associations of the three single nucleotide polymorphisms (SNPs) and male infertility in a Chinese population.
Methods
We conducted a search of PubMed, Embase, Web of Science, Chinese National Knowledge Infrastructure (CNKI), China biology medical literature (CBM), VIP, and Chinese literature (Wan Fang) databases up to May 31, 2016. Odds ratios (ORs) and 95% confidence intervals (95% CIs) were used to assess the strength of associations with a random-effect model or a fixed-effect model based on the heterogeneity analysis results. Sensitivity analysis was used to confirm the reliability and stability of the meta-analysis.
Results
A total of nine studies, including 1,713 cases and 1,104 controls, were included in the metaanalysis. The pooled results indicated that the MTHFR C667T polymorphism was significantly associated with increased risk of male infertility in the Chinese population in the allele model (T vs. C: OR = 1.47, 95% CI = 1.32-1.63), the dominant model (TT + CT vs. CC: OR = 1.51, 95% CI = 1.30-1.77), the additive model (TT vs. CC: OR = 2.08, 95% CI = 1.68-2.58) and the recessive model (TT vs. CT+CC: OR = 1.58, 95% CI = 1.31-1.90), whereas the MTHFR A1298C and MS A2756G polymorphisms were not risk factors. There was no significant heterogeneity in any genotype contrasts among the studies. The sensitivity analysis indicated that the results of this meta-analysis were relatively stable.
Conclusion
This study suggests that the MTHFR C667T polymorphism may contribute to the genetic susceptibility to male infertility in the Chinese population, whereas MTHFR A1298C and MS A2756G polymorphisms may be unrelated to male infertility. Studies with larger sample sizes and representative population-based cases and well-matched controls are needed to validate our results.
Mandibular prognathism (MP) is considered to be a cranial-facial disorder resulting from the interaction between genes and environment. Recent studies have demonstrated that susceptible chromosomal regions and candidate genes may be responsible for MP. In this study, the authors present current views on the effect of genetic components in nonsystematic mandibular prognathism, in order to clarify the genetic etiology of MP. Data source were Electronic databases, manual searching, and reference lists checking, up to April 2016. Study selection, level of evidence assessment, and data extraction were done by 2 individuals in duplicate. Ninety-one studies were retrieved in initial electronic and manual search, and based on the established inclusion and exclusion criteria, 15 were selected for the review. In result, loci 1p36, 1q32.2, 1p22.3, 4p16.1, 6q25, 19p13, 14q24.3, 14q31.1, and 14q31.2 were thought to harbor genes that confer susceptibility to MP. Genes Matrilin-1, ADAMTS1, COL2A1, and EPB41 seemed to be strongly associated with MP while gene of growth hormone receptor was in dispute. Genetic components appeared to be associated with MP. However, in view of the variety of populations and results in related publications, further studies are necessary to clarify the genetic etiology of MP.
Tooth development involves epithelium invagination, mesenchyme aggregation, and epithelium-mesenchyme communication. A sophisticated signaling pathway network regulates the differentiation and crosstalk of multiple cell types in tooth germs and coordinates the broad spectrum of complex processes. MicroRNAs (miRNAs), a class of small non-coding RNA species that have been relatively well studied over the last few years, are now proposed as important regulators of tooth developmental signaling pathways as they repress cellular protein levels to provide a posttranscriptional gene regulation. In this review, we summarize the current knowledge of miRNA characteristics in regulating morphogenesis, amelogenesis, dentin formation, and tooth eruption and how they interplay with the signaling molecules during these processes. (C) 2016 Elsevier Ltd. All rights reserved.
AIM: To assess the neuro-protective effect of bone marrow mesenchymal stem cells (BMSCs) on retinal ganglion cells (RGCs) following optic nerve crush in mice.
METHODS: C56BL/6J mice were treated with intravitreal injection of PBS, BMSCs, BDNF-interference BMSCs (BIM), and GDNF-interference BMSCs (GIM) following optic nerve crush, respectively. The number of surviving RGCs was determined by whole-mount retinas and frozen sections, while certain mRNA or protein was detected by q-PCR or ELISA, respectively.
RESULTS: The density (cell number/mm(2)) of RGCs was 410.77 +/- 56.70 in the retina 21d after optic nerve crush without any treatment, compared to 1351.39 195.97 in the normal control (P<0.05). RGCs in BMSCs treated eyes was 625.07 +/- 89.64/mm(2), significantly higher than that of no or PBS treatment (P<0.05). While RGCs was even less in the retina with intravitreal injection of BIM (354.07 +/- 39.77) and GIM (326.67 +/- 33.37) than that without treatment (P<0.05). BMSCs injection improved the internal BDNF expression in retinas.
CONCLUSION: Optic nerve crush caused rust loss of RGCs and intravitreally transplanted BMSCs at some extent protected RGCs from death. The effect of BMSCs and level of BDNF in retinas are both related to BDNF and GDNF expression in BMSCs.
Ischemia-induced stroke is the most common disease of the nervous system and is associated with a high mortality rate worldwide. Cerebral ischemia may lead to remote organ dysfunction, particular in the lungs, resulting in lung injury. Nowadays, bone marrow-derived mesenchymal stem cells (BMSCs) are widely studied in clinical trials as they may provide an effective solution to the treatment of neurological and cardiac diseases; however, the underlying molecular mechanisms remain unknown. In this study, a model of permanent focal cerebral ischemia-induced lung injury was successfully established and confirmed by neurological evaluation and lung injury scores. We demonstrated that the transplantation of BMSCs (passage 3) via the tail vein into the lung tissues attenuated lung injury. In order to elucidate the underlying molecular mechanisms, we analyzed the gene expression profiles in lung tissues from the rats with focal cerebral ischemia and transplanted with BMSCs using a Gene microarray. Moreover, the Gene Ontology database was employed to determine gene function. We found that the phosphoinositide 3-kinase (PI3K)-AKT signaling pathway, transforming growth factor-beta (TGF-beta) and platelet-derived growth factor (PDGF) were downregulated in the BMSC transplantation groups, compared with the control group. These results suggested that BMSC transplantation may attenuate lung injury following focal cerebral ischemia and that this effect is associated with the downregulation of TGF-beta, PDGF and the PI3K-AKT pathway.
Thoracoscopic intrathoracic esophagogastrostomy is a technically demanding operation; these technical requirements restrict the extensive application of minimally invasive Ivor Lewis esophagectomy. In an attempt to reduce the difficulty of this surgical procedure, we developed a modified anastomotic technique for thoracolaparoscopic Ivor Lewis esophagectomy. During the entirety of this modified approach, neither technically challenging operations such as intrathoracic suturing, or knotting, nor special instruments such as an OrVil system or a reversepuncture head are required. Between Octomber 2015 and January 2016, 15 consecutive patients with cancer in the distal third of the esophagus or the gastric cardia underwent this modified surgical procedure. The good short- term outcomes that were achieved suggest that the modified anastomotic technique is safe and feasible for thoracolaparoscopic Ivor Lewis esophagectomy.
Precision medicine is a new strategy that aims at preventing and treating human diseases by focusing on individual variations in people's genes, environment and lifestyle. Precision medicine has been used for cancer diagnosis and treatment and shows evident clinical efficacy. Rapid developments in molecular biology, genetics and sequencing technologies, as well as computational technology, has enabled the establishment of "big data", such as the Human Genome Project, which provides a basis for precision medicine. Head and neck squamous cell carcinoma (HNSCC) is an aggressive cancer with a high incidence rate and low survival rate. Current therapies are often aggressive and carry considerable side effects. Much research now indicates that precision medicine can be used for HNSCC and may achieve improved results. From this perspective, we present an overview of the current status, potential strategies, and challenges of precision medicine in HNSCC. We focus on targeted therapy based on cell the surface signaling receptors epidermal growth factor receptor (EGFR), vascular endothelial growth factor (VEGF) and human epidermal growth factor receptor-2 (HER2), and on the PI3K/AKT/mTOR, JAK/STAT3 and RAS/RAF/MEK/ERK cellular signaling pathways. Gene therapy for the treatment of HNSCC is also discussed.
Dental caries, trauma, and other possible factors could lead to injury of the dental pulp. Dental infection could result in immune and inflammatory responses mediated by molecular and cellular events and tissue breakdown. The inflammatory response of dental pulp could be regulated by genetic and epigenetic events. Epigenetic modifications play a fundamental role in gene expression. The epigenetic events might play critical roles in the inflammatory process of dental pulp injury. Major epigenetic events include methylation and acetylation of histones and regulatory factors, DNA methylation, and small non-coding RNAs. Infections and other environmental factors have profound effects on epigenetic modifications and trigger diseases. Despite growing evidences of literatures addressing the role of epigenetics in the field of medicine and biology, very little is known about the epigenetic pathways involved in dental pulp inflammation. This review summarized the current knowledge about epigenetic mechanisms during dental pulp inflammation. Progress in studies of epigenetic alterations during inflammatory response would provide opportunities for the development of efficient medications of epigenetic therapy for pulpitis.
