ACUTE EFFECT OF VIBRATORY STIMULATION ON ELBOW JOINT FLEXOR PERFORMANCE

A novel design of vibratory stimulation training system was developed in this study. Each participant took a pre-test, before receiving treatment with 20 seconds of vibratory stimulation (VS) at a specific frequency and amplitude. The participants then took a post-test. Percentage improvement was then calculated by comparing the pre- and post-test values for each index. The experimental data were analyzed through a two-way repeated-measures ANOVA analysis, with the independent variables being vibratory frequency and amplitude and the dependent variables being EMG root mean square, maximal force, rate of force development, and average force. The optimal vibratory stimulation pattern was found from this study that being a 60% maximal force loading combined with VS at 2.5 Hz and 1 N amplitude sustained over 20 s

Targeting delivery of paclitaxel into tumor cells via somatostatin receptor endocytosis

AbstractBackground: The binding of somatostatin (SST) to endogenous G-protein-coupled receptors (SST receptors or SSTRs) is followed by internalization of SST, and, several reports have shown that a high density of SSTRs is present on most hormone-secreting tissue tumors. Facile synthesis of the long-acting SST analog, octreotide, has previously been described. Octreotide might be of practical value in developing tumor tracers and in serving as a carrier of cytotoxic antitumor drugs.Results: Fluorescein-labeled octreotide was internalized into the cytosol of human breast MCF-7 carcinoma cells via binding to SSTRs. Octreotide-conjugated paclitaxel (taxol) was created by coupling taxol–succinate to the amino-terminal end of octreotide. This conjugate retains the biological activity of taxol in inducing formation of tubulin bundles, eventually causing apoptosis of MCF-7 cells. Cytotoxicity of octreotide-conjugated taxol is mainly mediated by SSTR, as shown by the observation that octreotide pretreatment can rescue the induced cell death. In comparison with free taxol, this conjugate shows much less toxicity in Chinese hamster ovary cells.Conclusions: Octreotide-conjugated taxol exerts the same antitumor effect of free taxol on stabilizing microtubule formation and inducing cell death. This conjugate triggers tumor cell apoptosis mediated by SSTRs and is exclusively toxic to SSTR-expressing cells. Octreotide-conjugated taxol is less toxic to low-SSTR-expressing cells compared with free taxol. Our results strongly indicated that octreotide-conjugated taxol demonstrates cell selectivity and may be used as a targeting agent for cancer therapy

Dependent k-Set Packing on Polynomoids

Specialized hereditary systems, e.g., matroids, are known to have many applications in algorithm design. We define a new notion called d-polynomoid as a hereditary system (E, ? ? 2^E) so that every two maximal sets in ? have less than d elements in common. We study the problem that, given a d-polynomoid (E, ?), asks if the ground set E contains ? disjoint k-subsets that are not in ?, and obtain a complexity trichotomy result for all pairs of k ? 1 and d ? 0. Our algorithmic result yields a sufficient and necessary condition that decides whether each hypergraph in some classes of r-uniform hypergraphs has a perfect matching, which has a number of algorithmic applications

ESL Club & Women Speak: Our Second Home in America

SWOSU ESL Club Newsletter: Fall 2017 is the third issue of the newsletter for the English as a Second Language Club (ESL).https://dc.swosu.edu/esl/1002/thumbnail.jp

Ceftriaxone attenuates hypoxic-ischemic brain injury in neonatal rats

<p>Abstract</p> <p>Background</p> <p>Perinatal brain injury is the leading cause of subsequent neurological disability in both term and preterm baby. Glutamate excitotoxicity is one of the major factors involved in perinatal hypoxic-ischemic encephalopathy (HIE). Glutamate transporter GLT1, expressed mainly in mature astrocytes, is the major glutamate transporter in the brain. HIE induced excessive glutamate release which is not reuptaked by immature astrocytes may induce neuronal damage. Compounds, such as ceftriaxone, that enhance the expression of GLT1 may exert neuroprotective effect in HIE.</p> <p>Methods</p> <p>We used a neonatal rat model of HIE by unilateral ligation of carotid artery and subsequent exposure to 8% oxygen for 2 hrs on postnatal day 7 (P7) rats. Neonatal rats were administered three dosages of an antibiotic, ceftriaxone, 48 hrs prior to experimental HIE. Neurobehavioral tests of treated rats were assessed. Brain sections from P14 rats were examined with Nissl and immunohistochemical stain, and TUNEL assay. GLT1 protein expression was evaluated by Western blot and immunohistochemistry.</p> <p>Results</p> <p>Pre-treatment with 200 mg/kg ceftriaxone significantly reduced the brain injury scores and apoptotic cells in the hippocampus, restored myelination in the external capsule of P14 rats, and improved the hypoxia-ischemia induced learning and memory deficit of P23-24 rats. GLT1 expression was observed in the cortical neurons of ceftriaxone treated rats.</p> <p>Conclusion</p> <p>These results suggest that pre-treatment of infants at risk for HIE with ceftriaxone may reduce subsequent brain injury.</p

Exploring the heterogeneity of effects of corticosteroids on acute respiratory distress syndrome: a systematic review and meta-analysis

INTRODUCTION: The effectiveness of corticosteroid therapy on the mortality of acute respiratory distress syndrome (ARDS) remains under debate. We aimed to explore the grounds for the inconsistent results in previous studies and update the evidence. METHODS: We searched MEDLINE, Cochrane Central Register of Controlled Trials and Web of Science up to December 2013. Eligible studies included randomized clinical trials (RCTs) and cohort studies that reported mortality and that had corticosteroid nonusers for comparison. The effect of corticosteroids on ARDS mortality was assessed by relative risk (RR) and risk difference (RD) for ICU, hospital, and 60-day mortality using a random-effects model. RESULTS: Eight RCTs and 10 cohort studies were included for analysis. In RCTs, corticosteroids had a possible but statistically insignificant effect on ICU mortality (RD, −0.28; 95% confidence interval (CI), −0.53 to −0.03 and RR, 0.55; 95% CI, 0.24 to 1.25) but no effect on 60-day mortality (RD, −0.01; 95% CI, −0.12 to 0.10 and RR, 0.97; 95% CI, 0.75 to 1.26). In cohort studies, corticosteroids had no effect on ICU mortality (RR, 1.05; 95% CI, 0.74 to 1.49) but non-significantly increased 60-day mortality (RR, 1.30; 95% CI, 0.96 to 1.78). In the subgroup analysis by ARDS etiology, corticosteroids significantly increased mortality in influenza-related ARDS (three cohort studies, RR, 2.45, 95% CI, 1.40 to 4.27). CONCLUSIONS: The effects of corticosteroids on the mortality of ARDS differed by duration of outcome measures and etiologies. Corticosteroids did not improve longer-term outcomes and may cause harm in certain subgroups. Current data do not support routine use of corticosteroids in ARDS. More clinical trials are needed to specify the favorable and unfavorable subgroups for corticosteroid therapy

B-Cell Lymphoma 6 (BCL6) Is a Host Restriction Factor That Can Suppress HBV Gene Expression and Modulate Immune Responses

Hepatitis B virus (HBV) infection causes acute and chronic liver inflammation. Recent studies have demonstrated that some viral antigens can suppress host innate and adaptive immunity, and thus lead to HBV liver persistency. However, the cellular factors that can help host cells to clear HBV during acute infection remain largely unknown. Here, we used HBV-cleared and HBV-persistent mouse models to seek for cellular factors that might participate in HBV clearance. HBV replicon DNA was delivered into the mouse liver by hydrodynamic injection. RNA-Seq analysis was conducted to identify immune-related genes that were differentially expressed in HBV-persistent and HBV-cleared mouse models. A cellular factor, B cell lymphoma 6 (BCL6), was found to be significantly upregulated in the liver of HBV-cleared mice upon HBV clearance. Co-expression of BCL6 and a persistent HBV clone rendered the clone largely cleared, implicating an important role of BCL6 in controlling HBV clearance. Mechanistic studies demonstrated that BCL6 functioned as a repressor, binding to and suppressing the activities of the four HBV promoters. Correspondingly, BCL6 expression significantly reduced the levels of HBV viral RNA, DNA, and proteins. BCL6 expression could be stimulated by inflammatory cytokines such as TNF-α; the BCL6 in turn synergized TNF-α signaling to produce large amounts of CXCL9 and CXCL10, leading to increased infiltrating immune cells and elevated cytokine levels in the liver. Thus, positive feedback loops on BCL6 expression and immune responses could be produced. Together, our results demonstrate that BCL6 is a novel host restriction factor that exerts both anti-HBV and immunomodulatory activities. Induction of BCL6 in the liver may ultimately assist host immune responses to clear HBV

Non-Intrusive Adaptation: Input-Centric Parameter-efficient Fine-Tuning for Versatile Multimodal Modeling

Large language models (LLMs) and vision language models (VLMs) demonstrate excellent performance on a wide range of tasks by scaling up parameter counts from O(10^9) to O(10^{12}) levels and further beyond. These large scales make it impossible to adapt and deploy fully specialized models given a task of interest. Parameter-efficient fine-tuning (PEFT) emerges as a promising direction to tackle the adaptation and serving challenges for such large models. We categorize PEFT techniques into two types: intrusive and non-intrusive. Intrusive PEFT techniques directly change a model's internal architecture. Though more flexible, they introduce significant complexities for training and serving. Non-intrusive PEFT techniques leave the internal architecture unchanged and only adapt model-external parameters, such as embeddings for input. In this work, we describe AdaLink as a non-intrusive PEFT technique that achieves competitive performance compared to SoTA intrusive PEFT (LoRA) and full model fine-tuning (FT) on various tasks. We evaluate using both text-only and multimodal tasks, with experiments that account for both parameter-count scaling and training regime (with and without instruction tuning)

Konsep Demokrasi Politik Dalam Islam

Coexistence of chronic rhinosinusitis (CRS) with asthma appears to impair asthma control. Type-2 innate lymphoid cells (ILC2s) respond to the cytokines of thymic stromal lymphopoietin (TSLP), interleukin (IL)-25 and IL-33, thus contributing to airway diseases such as CRS and asthma. We investigate whether the augmented Th2-cytokines in CRS might be related to sinonasal tract ILC2s corresponding to enhanced IL-25, IL-33 and TSLP release in severe asthmatics, and be involved in asthma control. Twenty-eight asthmatics (12 non-severe and 16 severe) with CRS receiving nasal surgery were enrolled. The predicted FEV1 inversely associated with CRS severity of CT or endoscopy scores. Higher expression of Th2-driven cytokines (IL-4, IL-5, IL-9, and IL-13), TSLP, IL-25 and IL-33 in nasal tissues was observed in severe asthma. Severe asthmatics had higher ILC2 cell counts in their nasal tissues. ILC2 counts were positively correlated with Th2-cytokines. Nasal surgery significantly improved asthma control and lung function decline in severe asthma and CRS. The higher expression of IL-33/ILC2 axis-directed type 2 immune responses in nasal tissue of CRS brought the greater decline of lung function in severe asthma. ILC2-induced the upregulated activity of Th2-related cytokines in asthmatics with CRS may contribute to a recalcitrant status of asthma control