Notes

Cost-Effectiveness Analysis involving High-Risk Groupings T . b Screening process within Malaysia.
Within the last 60 years, microbiological research has challenged many dogmas such as bacteria being unicellular microorganisms directed by nutrient sources; these investigations produced new dogmas such as cyclic diguanylate monophosphate (cyclic di-GMP) second messenger signaling as a ubiquitous regulator of the fundamental sessility/motility lifestyle switch on the single-cell level. Successive investigations have not yet challenged this view; however, the complexity of cyclic di-GMP as an intracellular bacterial signal, and, less explored, as an extracellular signaling molecule in combination with the conformational flexibility of the molecule, provides endless opportunities for cross-kingdom interactions. Cyclic di-GMP-directed microbial biofilms commonly stimulate the immune system on a lower level, whereas host-sensed cyclic di-GMP broadly stimulates the innate and adaptive immune responses. Furthermore, while the intracellular second messenger cyclic di-GMP signaling promotes bacterial biofilm formation and chronic infections, oppositely, Salmonella Typhimurium cellulose biofilm inside immune cells is not endorsed. These observations only touch on the complexity of the interaction of biofilm microbial cells with its host. In this review, we describe the Yin and Yang interactive concepts of biofilm formation and cyclic di-GMP signaling using S. Typhimurium as an example.In the present study, we found the expression of miR-15a-5p (miR-15a) was increased in glioma tissues, and we further explore the underlying mechanism of miR-15a in glioma progression. Microarray analysis used to identify the differentially expressed microRNAs (miRNAs) in glioma tissues. The expression of miR-15a in glioma tissues and cell lines was tested by qRT-PCR. Luciferase assay was used to determine the binding between miR-15a and Smad7. Wound healing and transwell assay were used to examine the role of miR-15a/Smad7 in SHG139 cells. Western blot was used to detect the protein level of Smad7 and epithelial-mesenchymal transition (EMT) markers. A tumor formation model in nude mice was established to measure the role of miR-15a in vivo. MiR-15a was significantly increased in glioma tissues and cells, which indicated a poor prognosis of glioma patients. MiR-15a mimics induced miR-15a level in SHG139 cells, and promoted the malignancy of SHG139 cells, while miR-15a inhibitor showed the opposite effects. Luciferase assay indicated that Smad7 was the direct target of miR-15a, and Smad7 was down-regulated in glioma tissues. Functional experiments revealed that miR-15a inhibitor inhibited the EMT pathway and the migration and invasion of glioma cells, but the silencing of Smad7 reversed the effects of miR-15a inhibitor in EMT pathway and glioma progression. Finally, we performed animal experiments to verify the role of miR-15a in vivo. Present study showed that deletion of miR-15a inhibited the activation of EMT signaling via targeting Smad7, thus suppressed the tumorigenesis and tumor growth of glioma.Atherosclerosis (AS) is a chronic disease of the arterial wall. The role of lncRNAs in AS has been acknowledged. This study investigated the role of lncRNA plasmacytoma variant translocation 1 (PVT1) in AS via the MAPK/NF-κB pathway. Serum samples were collected from AS and non-AS patients. Serum levels of PVT1, CRP, IL-6, IL-1β, and TNF-α were determined. AS mouse model was established and transfected with si-PVT1. Levels of TG, TC, HDL, LDL, MAPK, NF-κB, MMP-2, MMP-9, TIMP-1, and macrophage content were detected. Human arterial vascular smooth muscle cells (HA-VSMCs) induced by 50 mg/mL oxLDL were transfected with si-PVT1 or oe-PVT1 and added with MAPK inhibitor U0126. Viability, apoptosis, cell cycle, colony formation and DNA replication were assessed. Levels of apoptosis-related proteins were detected. Consequently, PVT1 was highly expressed in AS patients. Silencing PVT1 decreased levels of TG, TC, LDL, IL-6, IL-1β, TNF-α, MMP-2, MMP-9, CRP, TIMP-1, MAPK, and NF-κB, increased HDL, reduced atherosclerotic plaques and macrophage content in mice, inhibited viability, clones and EdU positive rates in HA-VSMCs, but promoted apoptosis and cell cycle arrest. Inhibition of MAPK/NF-κB pathway suppressed proliferation and promoted apoptosis of HA-VSMCs while PVT1 overexpression facilitated AS development. Briefly, silencing PVT1 inhibited AS development by downregulating MAPK/NF-κB pathway.
Cervical cancer is the most prevalent malignancy worldwide and propofol reportedly has anti-cancer efficiencies. Herein, we tried to address the potential anti-cancer effects of propofol in cervical carcinoma.

The suppression effects of propofol on the proliferation and invasion of cervical cancer cells were analyzed by Cell Counting Kit-8 (CCK-8), colony formation and Transwell invasion assay. The protein expressions of epithelial marker, E-cadherin and mesenchymal marker, N-cadherin were evaluated using western blot. The level of MIR155 host gene (MIR155HG) was determined by qRT-PCR assay. The anti-cancer impact of propofol on cervical cancer cells growth
was determined by means of xenograft tumor model and lung metastasis model.

, propofol inhibited the growth and colony-formation of cervical carcinoma cells. Meanwhile, propofol treatment reduced the invasive trait of cervical carcinoma cells. In addition, MIR155HG was identified to be distinctly upregulated in cervical carcinoma when compared within normal. Propofol treatment decreased the expression of MIR155HG in cervical cancer cells. Consistently, the results from
xenograft model indicated that propofol repressed cervical cancer cells growth and decreased the expression of MIR155HG
. Furthermore, reintroduction of MIR155HG into cervical cancer cells counteracted the inhibitory potency of propofol on the growth and aggressive phenotypes in cervical carcinoma cells.

Altogether, these results indicated that propofol restrained the growth and invasion of cervical cancer cells partly via regulating MIR155HG expression.
Altogether, these results indicated that propofol restrained the growth and invasion of cervical cancer cells partly via regulating MIR155HG expression.Tissue inhibitor matrix metalloproteinase 1 (TIMP1) has been reported to act as a tumor oncogene in colon cancer. However, little is known about the biological role of TIMP1 in gastric cancer. In this study, we found that the expression of TIMP1 in GC tissues was upregulated compared with the normal gastric tissues. TIMP1 was confirmed as a direct target of miR-6745 and silencing TIMP1 mimicked the effects of miR-6745 in GC cells. Further mechanism studies have shown that miR-6745 inhibits the Wnt/β-catenin pathway by targeting TIMP1, thereby inhibiting cell proliferation, migration and invasion. In addition, through the analysis of GC tissues, a negative correlation between miR-6745 and TIMP1 was found in 42 GC tissues. Our findings indicate that the miR-6745-TIMP1 axis regulates Wnt/βcatenin signaling and participates in GC tumorigenesis and provide a potential therapeutic target for preventing GC progression.Esophageal squamous cell carcinoma (ESCC) is the most common and aggressive tumor worldwide, and the long-term survival of these patients remains poor. Three databases (GSE17351, GSE20347, and GSE100942) were obtained from Gene Expression Omnibus, and 193 differentially expressed genes including 56 upregulated and 137 downregulated genes were identified by paired test using limma R package. Then, functional enrichments by gene ontology and Kyoto Encyclopedia of Genes and Genomes analyses showed these genes were mainly related protein digestion and absorption, and IL-17 signaling pathway. We then constructed a protein-protein interaction network and cytoHubba module to determine the six hub genes and overall survival analysis of the six hub genes were evaluated by UALCAN and GEPIA2 analysis. Ultimately, the experimental results confirmed the KIF4A was overexpressed in the ESCC tissues and cell lines compared with the normal esophageal mucosal tissues and was linked to poor prognosis. Moreover, we also revealed that KIF4A facilitates proliferation, cell cycle, migration, and invasion of ESCC in vivo and in vitro. Overall, these findings demonstrated that KIF4A could serve as diagnostic and prognostic biomarkers and may help facilitate therapeutic targets in ESCC patients.Összefoglaló. A dystrophia myotonica (DM) multiszisztémás, autoszomális domináns módon öröklődő, többségében felnőttkori izombetegség, melynek incidenciája 1 8000. A betegség kapcsán fellépő izomszöveti degeneráció a harántcsíkolt izomszövet átépülése mellett a szívizomszövetet is érinti, ami fontos oki szerepet játszik az érintett betegek csökkent várható élettartamában. A DM-ben szenvedők halálozásának közel egyharmadáért a cardiovascularis okok tehetők felelőssé. Esetriportunkban egy 52 éves, korábban kritikus bradycardia és I. fokú atrioventricularis blokk miatt pacemakerimplantáción átesett, DM-mel diagnosztizált nőbeteg kardiológiai utánkövetését mutatjuk be. Ipatasertib mouse A hirtelen szívhalál rizikóstratifikációja céljából elvégzett invazív elektrofiziológiai vizsgálat során kamrafibrilláció lépett fel, így a korábban implantált pacemakerelektródák mellé sokkelektróda került beültetésre, a pacemakerkészüléket implantálható kardioverter-defibrillátorra (ICD) cseréltük. Az 1 éves ICD-kontrollvizsgálat során azt találregistered. A shock electrode was added to the previously implanted pacemaker, enabling defibrillation in case of detection of a sustained ventricular arrhythmia. During the 1-year follow-up, 22 episodes of sustained ventricular tachycardia were identified, with the device successfully terminating the malignant arrhythmias. Our case shows that electrophysiological study and the succeeding implantation of an implantable cardiac defibrillator is highly important in identifying and terminating ventricular arrhythmias in high-risk DM patients. Orv Hetil. 2021; 162(46) 1856-1858.Összefoglaló. Manapság, a COVID-19-járvány közepette, a megfelelő kézmosás segít megelőzni vagy legalábbis lassítani a fertőző betegségek, például a SARS-CoV-2-fertőzés terjedését. A kézmosás rutinjának megfelelő oktatás multilaterális tevékenységet igényel, amely a fiatalok ismeretén, egészségmagatartásán, attitűdjein, tapasztalatain és motivációján alapul. A TANTUdSZ Ifjúsági Egészségnevelési Program kortársoktató pedagógiai és egészségtudományi egyetemi karok hallgatóival, valamint középiskolai kortárssegítőkkel és mintegy 3000, magyarországi óvodás, általános és középiskolás diák bevonásával valósult meg, különböző egészségfejlesztési területeken. A vizsgálatok egyik célja az oktatási program hatékonyságának értékelése érdekében a gyermekek kézhigiénés ismereteinek és készségeinek elemzése és összehasonlítása volt a beavatkozások előtt és után. A jelen közleményben ismertetett longitudinális felmérés alsó tagozatos tanulók (n = 165) kézmosási készségének és attitűdváltozásainak rövid és hosszú távú változását értékeli három időpontban.
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