Effects of tongue strengthening exercises on tongue muscle strength: a systematic review and meta-analysis of randomized controlled trials.

Tongue strengthening exercise (TSE) has been proposed as an intervention to increase tongue strength and improve swallowing. However, clinical evidence of its effectiveness is lacking. In this review, seven databases were searched from inception to September 30, 2021 for randomized controlled trials that compared tongue strengths between the TSE intervention and control groups, obtained from maximal tongue elevation peak force in kilopascals (kPa). The Cochrane risk of bias tool was used for quality assessment. In total, 12 studies with 388 participants were included. The pooled meta-analysis demonstrated that the anterior tongue strength (ATS) (MD = 5.34 kPa; 95% CI 3.28-7.40; I2 = 71%) and posterior tongue strength (MD = 8.12; 95% CI 3.45-12.79; I2 = 90%) were significantly higher in the TSE intervention than that in the control group. Among healthy participants, subgroup analysis showed that TSE had improvements on ATS in all age groups, with the greatest improvement in old people (≥ 65 years) (MD = 8.01; 95% CI 4.39-11.64; I2 = 30%). Meta-regression analysis revealed a nonsignificant trend toward greater improvement on tongue strength with increasing TSE duration. This study provides positive evidence that TSE may be beneficial in improving tongue strength and could be applied for adults, especially healthy older adults.

Clinical and Hematological Predictors for Return of Spontaneous Circulation in Patients With Out-of-Hospital Cardiac Arrest.

BACKGROUND: To investigate the association of clinical and hematological parameters with return of spontaneous circulation (ROSC) in out-of-hospital cardiac arrest (OHCA). METHODS: Clinical data of successive non-traumatic adult OHCA patients with available laboratory data of complete blood count and peripheral blood smear at emergency department (ED) arrival were requested. Hematological parameters were collected and calculated, and logistic regression and survival analysis were performed for association of ROSC with the parameters. RESULTS: From December 2015 to December 2016, a total of 188 OHCA patients transported to our ED were enrolled. In ROSC group, neutrophil-to-lymphocyte ratio (NLR) and platelet-to-lymphocyte ratio (PLR) were signifi cantly higher and smudge cell count was signifi cantly lower when compared with non-ROSC group. In the univariate regression, NLR more than 2.0 (odds ratio [OR]: 2.40, 95% confi dence interval [CI]: 1.31-4.41; p = 0.004) and smudge cell count less than 0.45 °- 109/L (OR: 0.33, 95% CI: 0.15-0.71; p = 0.004) were signifi cantly associated with ROSC in OHCA. In logistic regression, bystander witnessed (OR: 3.15, 95% CI: 1.59-6.27; p = 0.001) and prehospital epinephrine use (OR: 2.15, 95% CI: 1.10-4.23; p = 0.026) were signifi cantly associated with ROSC in OHCA. NLR and smudge cell count were also seemingly related to ROSC in OHCA, but without statistical signifi cance. In survival analysis, neither NLR nor smudge cell count was associated with patient survival to discharge in OHCA. CONCLUSIONS: NLR and smudge cell count at ED arrival could be potential indicators of ROSC in OHCA.

Krüppel-like factor 10 upregulates the expression of cyclooxygenase 1 and further modulates angiogenesis in endothelial cell and platelet aggregation in gene-deficient mice.

Krüppel-like family is a group of zinc-finger transcription factors which play key regulatory roles in cellular growth, development, differentiation and vascularization. Recent studies have shown that one of the members, KLF10, is specifically involved in the process of angiogenesis by acting as a key transcriptional regulator of TGF-ß1 in pro-angiogenic cells differentiation and function. KLF10(-/-) mice also displayed impaired blood flow recovery after hindlimb ischemia. However, the mechanism of KLF10 induced angiogenesis is still not well understood. From ChIP-chip, which have been adopt to elucidate the novel target genes and signaling cascades of KLF10, COX-1 (also named as PTGS1) is one of the target genes that may be regulated by Klf10 through promoter binding. In order to investigate the function of KLF10/COX-1 axis, promoter activity, EMSA, ChIP-PCR and tube formation assays were serially performed. Our results demonstrated that KLF10 acts as a transcriptional activator on COX-1 promoter where overexpression of KLF10 induces COX-1 protein expression and mRNA expression in endothelial cells. It has been known that COX-1 is the key enzyme in prostaglandin biosynthesis which regulated angiogenesis in endothelial cells. Using tube formation assay, we further demonstrated that KLF10 overexpressed endothelial cells formed better organized three-dimensional tube structure in contrast to the control group did. To specifically investigate the role for KLF10 in angiogenesis, the its deficient mice exhibited decreased light transmission which represents the extend of platelet aggregation slowing down. Taken together, our results indicate an important role for KLF10 in angiogenesis through the activation of COX-1.

Krüppel-like factor 10 expression as a prognostic indicator for pancreatic adenocarcinoma.

Deregulation of transforming growth factor (TGF)-ß function is a common feature of pancreatic cancer, rendering these cancers unresponsive to TGF-ß-stimulated growth inhibition. Recent findings have supported a primary role for Krüppel-like factor 10 (KLF10) as an important transcription factor involved in mediating TGF-ß1 signaling. The aim of this study was to evaluate the correlation between KLF10 expression and the clinical and pathologic features of pancreatic cancer. Tissue specimens from patients with pancreatic adenocarcinoma were retrospectively collected for immunohistochemical analysis. To demonstrate that Klf10 expression was primarily regulated by methylation status, the Klf10 promoter was examined by methylation-specific PCR using a pancreatic cancer cell line (Panc-1). DNA methyltransferase (DNMT) inhibitor and small-interfering RNA depletion of DNMT genes were used to reverse KLF10 expression in the Panc-1 cells. In parallel, DNMT1 expression was evaluated in the pancreatic cancer tissue specimens. In 95 pancreatic cancer tissue specimens, KLF10 expression was inversely correlated with pancreatic cancer stage (P = 0.01). Multivariable analysis revealed that, in addition to the presence of distant metastasis at diagnosis (P = 0.001 and 0.001, respectively), KLF10 was another independent prognostic factor related to progression-free and overall survival (P = 0.018 and 0.037, respectively). The loss of KLF10 expression in advanced pancreatic cancer is correlated with altered methylation status, which seems to be regulated by DNMT1. Our results suggest that KLF10 is a potential clinical predictor for progression of pancreatic cancer.

Klf10 induces cell apoptosis through modulation of BI-1 expression and Ca2+ homeostasis in estrogen-responding adenocarcinoma cells.

Estrogen stimulates cell growth and inhibits apoptosis through estrogen receptor-mediated mechanisms in many cell types. Remarkably, there is another dimension to estrogen action by which apoptosis is induced in breast cancer cells. While these mechanisms are not yet completely understood, finding the molecules involved has paved the way for the development of a new drug group. Using ChIP-chip, we have demonstrated that Klf10, a Krüppel-like zinc finger transcription factor, which was induced in response to estrogen, directly modulates the transcription of BI-1 (Bax inhibitor-1; also called the testis-enhanced gene transcript, TEGT). Eventually, the estrogen induced Klf10 and then suppresses BI-1 transcription. The estrogen/Klf10/BI-1 interrelationship was further confirmed using BI-1 promoter and EMSA assays. The estrogen-elicited reduction of BI-1 promoter activity was significantly reversed when the Klf10 binding element was mutated to abolish Klf10 binding. A si-Klf10 antisense-oligo nucleotide was also able to restore BI-1 promoter activity to its pre-estrogen-treatment level. BI-1 is known to regulate stress via the endoplasmic reticulum; in this context down-regulation of BI-1 is able to cause Ca(2+) release and trigger an apoptosis pathway in breast cancer. In our study, Klf10 not only suppressed cellular BI-1 expression but also increased the cytosolic Ca(2+) concentration, eventually causing apoptotic cell death. Based on these results, we suggest the pathway by which estrogen induces apoptosis is possibly through an up-regulation of Klf10 that decreases BI-1 and finally increases the concentration of cytoplasmic calcium.

Use of the duplex TaqMan PCR system for detection of Shiga-like toxin-producing Escherichia coli O157.

Real-time PCR assays have been applied for the detection and quantification of pathogens in recent years. In this study two combinations of primers and fluorescent probes were designed according to the sequences of the rfb(Escherichia coli O157) and stx2 genes. Analysis of 217 bacterial strains demonstrated that the duplex real-time PCR assay successfully distinguished the Escherichia coli O157 serotype from non-E. coli O157 serotypes and that it provided an accurate means of profiling the genes encoding O antigen and Shiga-like toxin 2. On the other hand, bacterial strains that lacked these genes were not detected by this assay. The quantitative ranges of the real-time PCR assay for these two genes were linear for DNA concentrations ranging from 10(3) to 10(9) CFU/ml of E. coli O157:H7 in pure culture and milk samples. The real-time PCR allowed the construction of standard curves that facilitated the quantification of E. coli O157:H7 in feces and apple juice samples. The detection sensitivity of the real-time PCR assay ranged from 10(4) to 10(9) CFU/g (or 10(4) to 10(9) CFU/ml) for feces and apple juice and 10(5) to 10(9) CFU/g for the beef sample without enrichment. After enrichment of the food samples in a modified tryptic soy broth, the detection range was from 10(0) to 10(3) CFU/ml. The real-time PCR assays for rfb(E. coli) (O157) and stx2 proved to be rapid tests for the detection of E. coli O157 in food matrices and could also be used for the quantification of E. coli O157 in foods or fecal samples.

Isolation and identification of Escherichia coli O157:H7 in a Taiwanese patient with bloody diarrhea and acute renal failure.

Escherichia coli O157:H7 is a frequent foodborne pathogen in many developed countries. Outbreaks of this infection have been reported in countries all over the world. The first clinical case of E. coli O157:H7 infection from Taiwan was reported in a 6- year-old boy who had returned from USA in August 2001. In this paper, we describe the results of the isolation and identification of this strain, and molecular typing for comparison with previously reported strains. Biochemical and molecular biological tests were used to confirm that this patient, who developed bloody diarrhea and kidney failure as a result of the infection, was indeed infected with E. coli O157:H7. None of the patients' close contacts were affected. Molecular typing by use of pulsed-field gel electrophoresis revealed this clinical strain to have a unique genotype, which is different from all available clinical strains reported from Japan and environmental strains reported from Taiwan. America Type Culture Collection reference strains and an out-break strain from USA had the nearest relationships with this clinical isolate. Molecular typing showed that this infection by E. coli O157:H7 was not derived from the local environmental strains and was acquired during overseas travel.