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Hede Alstrup opublikował 5 miesięcy, 2 tygodnie temu
Emerging evidence has started to scratch the surface of the participation of miRNAs and lncRNAs in the regulation of NLRP3. Xenografted mice-based studies have also enabled us to develop a better comprehension of interplay between miRNAs, lncRNAs and NLRP3. Hopefully, detailed analysis of contextual regulation of NLRP3 by oncogenic and tumor suppressor miRNAs, lncRNAs and circRNAs will be helpful in getting a step closer to the personalized medicine.Zebrafish (danio rerio) is a small, tropical freshwater teleost fish that belongs to the Cyprinidae family and lives in natural waters and rice fields in South Asia, North India, and Pakistan. Zebrafish has become a popular vertebrate model organism for biomedical research due to its numerous advantages such as their small size, short life cycle, accessibility in large numbers and inexpensive maintenance. In addition, fertilization happens externally in zebrafish and allows zebrafish to be manipulated directly. As another important advantage, the embryos are transparent thus the stages of development can be easily identified. Zebrafish can have multiple co-orthologs for human genes. In the 1930s, the zebrafish was first used as a model for developmental and embryological studies and in 1981, was introduced as a genetic model by Streisinger by force of developed genetic techniques in zebrafish such as cloning, mutagenesis and transgenesis. In the 1990s, various genetic manipulations were introduced. These improvements have contributed to the popularity of zebrafish. After that zebrafish was used in various research areas including genetics, biomedicine, neurobiology, toxicology, pharmacology as well as in human disease models. Zebrafish is also becoming a popular model organism in dental research. It is preferred in dental material toxicity studies and in research related to the genetic and molecular factors in tooth formation and craniofacial development. This review provides information on the use of zebrafish in dental research, focusing on tooth formation and dentition (pharyngeal dentition) of zebrafish and the dental research performed using zebrafish.Cancer is a therapeutically challenging disease because of its heterogeneous and multifaceted nature. Decades of research have sequentially and systematically enabled us to develop a sharper and better understanding of the heterogeneous nature of cancer. Genetic, genomic and proteomic studies have unraveled wide-ranging signaling cascades which play cornerstone role in disease onset and progression. More importantly, activation of pro-survival signaling and loss of apoptosis also play critical role in cancer progression. TRAIL-mediated signaling pathway has emerged as one of the most comprehensively analyzed cascade because of its exceptional ability to target cancer cells while leaving normal cells intact. TRAIL discovery and landmark achievements related to TRAIL/TRAIL-receptor signaling pathway attracted the attention of researchers. Therefore, scientists started to add missing pieces to an incomplete jig-saw puzzle and allowed contemporary researchers to conceptualize a better molecular snapshot of TRAIL-induced signaling in various cancers. Circumstantial evidence illuminated a functionally unique „push and pull” between anti-apoptotic and pro-apoptotic proteins in different cancers. Overexpression of anti-apoptotic proteins and inactivation of pro-apoptotic proteins shifted the balance towards loss of apoptosis. There has been a breakneck increase in the number of clinical trials related to TRAIL-based therapeutics which validate the true pharmacological potential of TRAIL-based therapeutics as effective anticancer agents. However, apart from advancements in our clinical understanding about the efficacy of TRAIL-based therapeutics, researchers have also faced setbacks in the field of translational medicine. Therefore, in this review, we have attempted to set spotlight on the most recent and landmark discoveries which have leveraged our understanding related to TRAIL-mediated signaling altogether to a new level.This experiment was performed to investigate the effect of paeonol on the proliferation, apoptosis, migration, invasion and glutamine of gastric cancer HGC-27 cells and its possible mechanism. For this purpose, the MTT method was used to detect cell viability; Flow cytometry experiment was used to detect cell apoptosis; Transwell chamber experiment was used to detect cell migration and invasion; Western blotting was used to detect the expression levels of MMP2 and MMP9 protein; The decomposition of glutamine was evaluated by detecting the expression levels of glutamine, glutamic acid and α-ketoglutarate (α-KG). This study used RT-PCR to detect the expression of circSFMBT2 and miR-665. The targeting relationship between circSFMBT2 and miR-665 was verified by the dual-luciferase report experiment and RIP experiment. Results showed that different concentrations of Paeonol could significantly inhibit the proliferation, migration, invasion and glutamine decomposition of HGC-27 cells, and induce cell apoptosis in a dose-dependent manner. In gastric cancer tissues and cells, the expression of circSFMBT2 was up-regulated, and the expression of miR-665 was down-regulated. Over-expression of circSFMBT2 could partially restore the effects of paeonol on the proliferation, apoptosis, migration, invasion and glutamine of HGC-27 cells. CircSFMBT2 could target and negatively regulate the expression of miR-665. Overexpression of miR-665 could partially restore the effects of Pae and circSFMBT2 on the proliferation, apoptosis, migration, invasion and glutamine of HGC-27 cells. It was concluded that paeonol can inhibit the proliferation, migration, invasion and glutamine decomposition of gastric cancer HGC-27 cells via circSFMBT2/miR-665 axis, and also induce cell apoptosis.There are very scanty reports on gastro-intestinal stromal tumors (GISTs), a very common tumor of mesenchymal cells in GIT track primary resistance to imatinib. This comprehensive study identifies the prevalence, clinical presentation and GIST genotype association in the imatinib naïve population. Prospectively a record of anthropometric, baseline demographic data and clinical details for the patients diagnosed with GIST were scrutinized. Pathological information included the presence or absence of necrosis, tumor size, mitotic counts, immune-histochemical staining for CD 34, CD 117 and DOG1 was performed using biopsy sample. Selected exon genes of KIT, PDGFRA and BRAF were amplified and subjected to mutation analysis by direct sequencing. Appropriate statistical analyses were performed. The male/female ratio was 1.81 among 54 patients with GIST. The mean GIST size was comparatively bigger in females (2.49±0.855) than males (2.26±1.13). The stomach was the most common site for GIST followed by the Small bowel and rectum. The majority of the tumours were spindle cell. This study reports 12 different types of mutation among 39 KIT, 8 PDGFRA and 7 BRAF mutations. In KIT, the most prevalent was exon 11 mutation with the KITdelinc557/558 (14/30) being the major exon 11 type mutation. In PDGRFA, five exons 18 with p.D842V substitution and three exons 12 deletion mutation was reported. Seven patients had strong or diffuse BRAF staining having V600E type mutation as major BRAF type mutation. Drug-resistant GIST due to acquired mutations remains a serious issue, therefore genetic information of such mutational related to drug-resistant may provide the imperative clue for diagnosis and clinical treatment. These mutations are pivotal for prognosis and associated with imatinib as not all of them but only a few are reported resistant to the imatinib.To analyze the occurrence of resistant bacterial infection in patients undergoing cardiac surgery hospitalized in the surgical specialty hospital, in Erbil city, Iraq. A prospective study was done on a total of 138 patients operated and hospitalized in an intensive care unit and surgical wards. Bacterial isolates identification was done according to cultural characteristics, microscopic examination, some biochemical tests, analytic Profile Index 20E& API Staph, confirmed with VITEK® 2 compact system (BioMérieux). Antimicrobial susceptibility for disc diffusion tested to 17 antimicrobial agents. Resistance isolates were confirmed phenotypically for carbapenemase by Rapidec Carba NP Test (bioMe´rieux SA, Marcy-l’E´toile, France) for ESBLs producers by ESBL screening test VITEK 2 system. Molecularly blaIMP blaTEM, blaKPC, AmpC and blaCTX-M were detected by PCR. In 134 patients, 28.3% of patients got infected post-operatively. The most frequent source of isolation was from ICU patients (75%). Isolated bacteri%) out of 13 Staph. aureus isolates were harboring it. Finally, 3(60%) out of 5 E. coli isolates harboring both AmpC and bla-CTX-M genes. Cardiac surgery patients wound show increasingly emerging strains of ESBL-producing gram-negative bacteria K. pneumonia, P. aeruginosa and E. coli especially patients prolonged in the intensive care unit.Oral cancer (OC) is a common malignant tumor in oral surgery, which is prone to metastasis and the prognosis is not optimistic. Long-non-coding RNA (lncRNA) is a kind of endogenous transcripts with more than 200bp in length, lack of specific and complete open reading frame, and does not have the function of protein-coding. Studies have found that it can regulate gene expression at many levels, such as epigenetic level, transcriptional level and post-transcriptional level, thus affecting the occurrence and development of diseases. Recent studies have shown that the occurrence, development, of oral cancer, are associated with lncRNA. In this research, we found that lncRNA SNHG1 was up-regulated in oral cancer. Knockdown of lncRNA SNHG1 would inhibit the proliferation of oral cancer cells. Then we revealed a new mechanism that lncRNA SNHG1 regulated the growth of oral cancer via controlling the miR-421/HMGB2 axis, which provided new therapy for patients with oral cancer.This study aimed to evaluate the maternal and fetal results in women undergoing antihypertensive therapy (low aspirin or labetalol) with mild to severe chronic hypertension relative to women without medicines. This randomized multi-center clinical trial was performed with random division into three groups of 393 pregnant women with mild to moderate chronic hypertension. From the beginning of the pregnancy to the end of the puerperium, the low dosage aspirin group (n = 129), the labetalol group (n = 127), and the drug-free or control group (n = 126) reported both mother and child results. Major variations in the presence of severely motherly hypertension, pre-eclampsia, renal failure, ECG shifts, and cardiovascular rupture between treatment groups (low doses of aspirin and labetalol) and control groups were noted. Repeated placenta and blood pressure control hospitalizations. (P<0.001) in the control group more often (untreated). The new babies were more vulnerable to gestational age (SGA), neonatal hypotension, neonatal Hyperbilirubinemia, and ICU (p <0.001 in contrast with the low-dose aspirin and control groups). In the control group, the proportion of premature babies was considerably higher than in the treatment group (p<0,05). A mild to moderate persistent high blood pressure during pregnancy therapy helps minimize mother and child occurrence. The use of labetalol is correlated with a higher incidence of SGA, neonatal hypotension, and neonatal hyperbilirubinemia relative to low-dose aspirin or control group.