The aims of this study were to observe the effect of exercise therapy on the function of the knee joint and the levels of cytokines and cytokine-related genes, specifically tumor necrosis factor-α (TNF-α), high sensitivity C-reactive protein (hs-CRP) and matrix metalloproteinase-3 (MMP-3), in the synovial joints of patients with knee osteoarthritis (KOA) and to explore its mechanism of action. A total of 100 KOA patients were divided into a treatment group (n=50) and a control group (n=50) according to the order of admission. The patients in the treatment group were treated with diclofenac sodium combined with exercise therapy and the patients in the control group were treated with diclofenac sodium only. The function of the knee joint and the therapeutic efficacy was evaluated and the TNF-α, hs-CRP and MMP-3 levels in the synovial fluid were measured following 4 weeks of treatment. The results revealed that the knee joint index score and the TNF-α, hs-CRP and MMP-3 levels in the synovial fluid decreased significantly in the KOA patients of the two groups following treatment (P<0.05). Compared with the control group, the knee joint index score and the TNF-α, hs-CRP and MMP-3 levels in the synovial joints were lower and the therapeutic efficacy was increased in the patients of the treatment group (P<0.05). In brief, exercise therapy may decrease cytokine and cytokine-related gene levels in the synovial fluid and inhibit inflammatory factor-mediated cartilage degradation in KOA patients, thus, effectively improving the clinical symptoms of KOA.

Within the airway management field, simulation has been used as a tool of training for over 40 years. Simulation training offers a chance of active involvement for the trainees. It can effectively enhance and upgrade the knowledge and skills of the trainees in airway management, and subsequently decrease medical errors and improve patients' outcomes and safety through a variety of airway management training modalities, such as common airway skills, difficult airway management strategies, and crisis management skills. To perform simulation-based airway management training effectively, not only are task trainers and high-fidelity simulators required but also instructors with rich experience in airway management simulation training and optimal curriculum design are essential.

Liver disease is a serious problem affecting millions of people with continually increasing prevalence. Stem cell therapy has become a promising treatment for liver dysfunction. We previously reported on human minor salivary gland mesenchymal stem cells (hMSGMSCs), which are highly self-renewable with multi-potent differentiation capability. In this study, keratinocyte-like cells with self-regeneration and hepatic differentiation potential were isolated and characterized, and named human minor salivary gland epithelial progenitor cells (hMSG-EpiPCs). hMSG-EpiPCs were easily obtained via minor intraoral incision; they expressed epithelial progenitor/stem cell and other tissue stem cell markers such as CD29, CD49f, cytokeratins, ABCG2, PLET-1, salivary epithelial cell markers CD44 and CD166, and the Wnt target related gene LGR5 and LGR6. The cells were induced into functional hepatocytes in vitro which expressed liver-associated markers ALB, CYP3A4, AAT, and CK18. Upon transplantation in vivo, they ameliorated severe acute liver damage in SCID mice caused by carbon tetrachloride (CCl4) injection. In a two-thirds partial hepatectomy mouse model, the transplanted cells survived at least 4 weeks and exhibited hepatic potential. These findings demonstrate that hMSG-EpiPCs have potential as a cellular therapy basis for hepatic diseases, physiological and toxicology studies and regenerative medicine.

Ischemic stroke commonly affects older individuals in China and worldwide. Such events are caused by a blood clot that blocks a vessel supplying blood to the brain. However, the etiology and pathogenesis of ischemic stroke are not fully understood. Genetics may play an important role in these events; indeed, rapid progress through the Human Genome Project has allowed the localisation and identification of genes related to ischemic stroke (1). Some single-gene disorders such as Fabry disease and sickle cell disease include ischemic stroke as a feature of the disorder, while in other cases, genetic variants appear to increase individual susceptibility to ischemic events.Polymorphisms in the members of the integrin family of genes, specifically integrin alpha-2 (ITGA2) and integrin beta-3 (ITGB3), are associated with thrombotic and arterial atherosclerotic disease (2, 3). Integrins are adhesion molecules that promote platelet aggregation, contributing to the development of blood clots (4). This function makes them intriguing candidates for the pathogenesis of ischemic stroke. Several polymorphisms have been identified in ITGA2 and ITGB3, but two, a C807T polymorphism (rs1126643 in ITGA2) and a T176C polymorphism (rs5918 in ITGB3), are associated with myocardial infarction and cerebral infarction (5, 6). Reiner et al. (7) found that ITGA2 C807T polymorphism was correlated with cerebral stroke in young women, and thus proposed that the T allele might be a hereditary susceptibility allele predisposing young women t o cerebral stroke. Similarly, Maakaroun et al. (8) found, through investigation on the ITGA2 C807T polymorphism in young twins, that the 807T allele was more frequent in twins with stroke than in those without stroke. However, Nikolopoulos et al. (5) found no correlation between the ITGA2 C807T polymorphism and incidence of ischemic stroke. Because genetic polymorphisms can differ between races/ethnicities, and few studies have been performed to date on ITGA2 and ITGB3 polymorphisms and ischemic stroke, it remains unclear whether ITGA2 C807T is related to ischemic stroke (9).We hypothesised that polymorphisms in ITGA2 and ITGB3 could increase susceptibility to ischemic stroke in Background: Recent studies have reported contrasting results regarding the association of polymorphisms in two integrin genes, ITGA2 and ITGB3, with ischemic stroke. Aims: The present study aimed to investigate the correlation between the ITGA2 C807T and ITGB3 T176C polymorphic loci with ischemic stroke, as well as plasma lipid and lipoprotein levels. Study Design: Case control study. Methods: Human venous blood samples were collected from patients admitted for ischemic stroke (n=350, 'patients') and healthy individuals (n=300, 'controls'). Blood was genotyped at these loci by polymerase chain reaction-restriction fragment length polymorphism. Plasma lipid and lipoprotein levels were measured by routine enzymatic, masking, and turbidimetry methods. Results:As expected, total cholesterol, triglycerides, and low-density lipoprotein we...

Single nucleotide polymorphisms in the promoter region of interleukin-18 (IL-18), an inflammatory cytokine, have been linked to susceptibility to many diseases, including cancer and immune dysfunction. Here, we explored the potential association between the IL-18 -607C/A (rs1946518) promoter region polymorphism and susceptibility to ischemic stroke (IS). This locus was amplified from peripheral blood samples of 386 IS patients (cases) and 364 healthy individuals (controls) by the polymerase chain reaction with sequence-specific primers. Significant differences were observed by the χ2 test in the -607C/A (rs1946518) genotype and allele frequencies between cases and controls (P < 0.05). Furthermore, after excluding for age, gender, smoking status, and hypertension, logistic regression indicated that IS susceptibility of -607C carriers increased 1.6 times (OR = 1.601, 95%CI = 1.148-2.233, P = 0.006) compared to -607A carriers. Additionally, similar increases in IS risk were noted for male patients or patients less than 65 years old. In conclusion, IL-18 -607C/A (rs1946518) promoter polymorphism is associated with IS susceptibility, and the C allele may confer increased IS risk.

Background Alzheimer’s disease (AD) is an age-related neurodegenerative disease and exercises might mitigate the progression of AD. This investigation aimed to manifest the potential mechanism of exercises in AD. Methods Morris water maze (MWM) test was conducted to evaluate the cognitive function in APP/PS1 mice. Quantitative real-time PCR was performed to detect the expression of HOTAIR and miR-130a-3p. The enzyme-linked immunosorbent assay was applied to appraise the concentration of IL-1β, IL-6, and TNF-α. A luciferase report experiment was implemented to substantiate the relationship between miR-130a-3p and HOTAIR. Results Exercises contributed to the elevated expression of HOTAIR. The findings of MWM implied HOTAIR inhibited the impacts of voluntary exercises on escape latency, distance moved, percentage of time spent in the target quadrant, platform crossing times, and inflammation. MiR-130a-3p mediated the function of HOTAIR on cognitive ability and inflammation. Conclusion HOTAIR participated in the regulation of exercises on AD by sponging miR-130a-3p.

Dexmedetomidine (DEX) suppresses inflammatory responses and protects against organ injury. The aim of the present study was to investigate the effect of DEX on airway hyperresponsiveness (AHR) and allergic airway inflammation, as well as its underlying mechanism of action in a murine model of ovalbumin (OVA)-induced asthma. A total of 30 female BALB/c mice were divided into 6 groups (n=5 mice/group): Control, OVA, OVA + DEX (20, 30 or 50 µg/kg) and OVA + TAK-242 [a toll-like receptor 4 (TLR4) inhibitor]. The mice were intraperitoneally injected with 20, 30 or 50 µg/kg DEX 1 h before OVA challenge. AHR to inhaled methacholine (Mch) was measured, and the mice were sacrificed 24 h after the last challenge. AHR following Mch inhalation was measured using the FlexiVent apparatus. Hematoxylin and eosin, periodic acid-Schiff and Wright-Giemsa staining was performed to evaluate inflammatory cell infiltration in the lung tissue. The levels of IL-4, IL-5 and IL-13 in the bronchoalveolar lavage fluid were analyzed using ELISA, and their mRNA expression levels in the lung tissue were examined using reverse transcription-quantitative PCR. The protein expression of TLR4, NF-κB and phosphorylated (p) NF-κB in the lung tissue was also detected using immunohistochemistry. In the murine OVA-induced asthma model, DEX decreased AHR following Mch inhalation and reduced the infiltration of inflammatory cells. IL-4, IL-5 and IL-13 levels in the bronchoalveolar lavage fluid were significantly lower following DEX treatment. Furthermore, DEX treatment inhibited the expression of TLR4, NF-κB and p-NF-κB in the lung tissue and exhibited a similar effect to TAK-242 treatment. In conclusion, DEX may attenuate AHR and allergic airway inflammation by inhibiting the TLR4/NF-κB pathway. These results suggested that DEX may represent a potential anti-inflammatory agent for the treatment and management of patients with asthma.

Introduction: Exercise is effective in Alzheimer's disease (AD), which is characterized by neuro-degenerative progress with increasing morbidity. The present study aimed to explore whether HOTAIR participated in the regulation of exercise in AD. Material and methods: A relative expression of serum HOTAIR was detected using quantitative real-time polymerase chain reaction (PCR). The diagnostic significance of HOTAIR on distinguishing AD patients was evaluated by receiver operating characteristic (ROC) curve. Correlations between HOTAIR expression and Mini-Mental State Examination (MMSE) score or Alzheimer's Disease Assessment Scale-Cognitive (ADAS-Cog) score were analyzed with Pearson's test. Logistic regression analysis was applied to investigate factors as independent indicators for HOTAIR expression.Results: In AD patients, the expression of HOTAIR was increased, and it could function as a diagnostic marker in AD patients. The expression of HOTAIR was associated with MMSE score and ADAS-Cog score in AD patients before exercise. Exercise ameliorated the cognitive impairment and reduced the relative serum expression of HOTAIR. Exercise was proved to be an independent indicator of HOTAIR expression. Conclusions: HOTAIR was a possible biomarker for indicating AD patients, and it was correlated with MMSE scores and ADAS-Cog results. Exercise might moderate AD progress via controlling HOTAIR.