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Brand new experience on molecular regulating biofilm formation inside plant-associated bacteria.
Antibiotic stability was demonstrated to be poor in rifampicin, rifabutin and doxycycylin. CONCLUSIONS pDST results in NTM for unstable antibiotics have to be interpreted with care. Combination of pDST and gDST will be useful for the guidance of antimicrobial therapy in MAC-disease. The ongoing outbreak of COVID-19 that began in Wuhan, China, has constituted a Public Health Emergency of International Concern, with cases confirmed in multiple countries. Currently, patients are the primary source of infection. We report a confirmed case of COVID-19 whose oropharyngeal swab test of SARS-CoV-2 RNA turned positive in convalescence. This case highlights the importance of active surveillance of SARS-CoV-2 RNA for infectivity assessment. OBJECTIVE The feasibility of the decontamination procedure for Legionella pneumophila of water systems in healthcare facilities varies by water purification and disinfection methods in each country. We evaluated the efficacy of feasible decontamination strategies in Japan. METHODS This study was conducted at Tokyo Medical University Hospital (1015 beds) between 2015 and 2018. Samples from the water system and cooling tower were cultured periodically. Hyper-chlorination of cool tap water (>0.2 ppm), increases in the temperature of hot water (>55 °C), and flushing were used as decontamination strategies. The case of healthcare-associated legionellosis was surveyed. Environmental and clinical isolates were genotyped. RESULTS 1439 environmental samples were collected; 19 (1.3%) samples tested positive for L. pneumophila from water faucets of patient rooms, toilets, waste rooms, and water sourced from wells. Genotyping of 12 isolates confirmed that the same strains were present in eight environmental isolates and two isolates from patients over three years. Although the environmental contamination of the water system was persistent, the number of positive locations of hospital environments gradually decreased; eight in 2015, four in 2016, three in 2017, and four in 2018, respectively. CONCLUSIONS Monitoring contamination, hyper-chlorination, controlling temperature, and flushing were effective as a Legionella decontamination strategy. OBJECTIVE This study was aimed to identify the residence of human fibrocartilage stem cells (hFCSCs), characterize their stem cell properties and investigate the functional mechanisms which regulate fibrocartilage stem cells (FCSCs) toward chondrogenic differentiation during cartilage homeostasis and repairing. METHODS Cytological characteristics of hFCSCs and human orofacial mesenchymal stem cells (hOFMSCs) were analyzed. Chondrogenic potential of hFCSCs was compared with hOFMSCs both in vitro and in vivo. Regulatory role of SOX9 during FCSCs chondrogenesis was studied by shRNA interference in vitro, and by GFP+ FCSCs treatment in rat condylar cartilage defect model. SOX9 expression was also examined in temporomandibular joint osteoarthritis (TMJOA) patients' cartilage surface. RESULTS hFCSCs exhibited typical mesenchymal stem cell characteristics, with significantly stronger chondrogenic capability compared to hOFMSCs. Moreover, hFCSCs showed remarkably increased expression of SOX9. During cartilage pellet culture, there was stronger SOX9 expression in hFCSCs than hOFMSCs. SOX9 shRNA interference downregulated chondrogenic capability of hFCSCs in vitro, as well as disrupting migration and chondrogenic differentiation of GFP+ FCSCs toward mature chondrocytes in rat condylar cartilage defect. Of note, SOX9 expression was also found suppressed in the condylar superficial zone of TMJOA patients. CONCLUSION We found the existence of FCSCs in human TMJ cartilage, and characterized their distinct stem cell features. SOX9 is essential for hFCSCs chondrogenic differentiation, and a comprehensive understanding of the regulatory role of SOX9 in hFCSCs would be important for exploring potential intervention strategy of condylar cartilage degradation during TMJ disorders. OBJECTIVES Osteophytes are common anatomical signs of advanced osteoarthritis. It remains unclear whether they develop from physio-molecular, and/or mechanical stimuli. This study examined the effects of mechanical impact on the knee joint periosteum leading to osteophyte formation. DESIGN Eighteen mature rats received one single impact load of 53 N (30 MPa) to the periosteum of the experimental medial femoral condyles. Contralateral knees were used as controls. Animals were sacrificed at 24 h, 3, 6 and 9 weeks post-impact. Distal femurs were harvested and prepared for histology. Hematoxylin and Eosin, and Masson's trichrome stained slides were examined by light microscopy. Nuclear density was quantified to assess the tissue reaction. RESULTS 24 h The synovium membrane, fibrous and cambium periosteum were damaged. Blood infiltration pooled in the impacted medial collateral ligament (MCL) region. Week 3 A cartilaginous tissue spur, chondrophyte, was found in every rat at the impacted site of the MCL. Chondrophytes were composed of fibrocartilage and cartilage matrix, with signs of cartilage mineralization and remodelling activity. Week 6 Chondrophytes presented signs of more advanced mineralisation, recognized as osteophytes. Week 9 Osteophytes appeared to be more mineralized with almost no cartilage tissue. CONCLUSIONS Osteophytes can be induced with a single mechanical impact applied to the periosteum in rat knees. These data indicate that a moderate trauma to the periosteal layer of the joint may play a role in osteophyte development. The significance of clonal evolution in myelofibrosis (MF) relapse remains poorly understood. Here, we performed panel sequencing in paired samples of 30 MF patients, who relapsed after allogeneic hematopoietic stem cell transplantation (alloSCT). We identified a median of 2 (0-12) mutations in a median of 2 (0-8) genes before alloSCT, while 2 (median, range 0-12) mutations were found in 2 (median, range 0-6) genes at relapse. Additional whole genome sequencing (n=6) did not elucidate additional molecular changes. Together, our data provide further evidence, here on MF, that clonal evolution after alloSCT is limited and that alloSCT rather selects specific (sub)clones. Parkinson's disease (PD) is an age associated, progressive, second most common neurodegenerative disease, caused due to degeneration of dopaminergic neurons in the substantia nigra (SN). Various studies imply mitochondrial dysfunction, oxidative stress, altered degradation of misfolded proteins in PD pathogenesis. Ursolic acid (UA), a natural pentacyclic triterpenoid carboxylic acid, is reported to possess a number of biological activities viz. anti-oxidant, anti-inflammatory. The focus of our study was to assess the neuroprotective potential of UA against the rotenone induced pathophysiological alterations. In this study rats were subjected to stereotaxic bilateral injection of rotenone (12 µg/µl) in SN. Further, they were treated per-orally with UA (5 and 10 mg/kg) for 30 days. During the study, neurobehavioural studies comprising Rota-rod, open field and Barnes maze test (BMT) were conducted. At the end of 30 days, the antioxidant (Reduced glutathione, superoxide dismutase, catalase and lipid peroxidation), inflammatory (TNF-α) parameters, immunohistochemistry for TH positive neurons, Glial Fibrillary Acidic Protein (GFAP) and mitochondrial complex I and mitochondrial biogenesis (MB) were assessed. The results showed a significant amelioration in the motor deficits by UA which can be attributed to the protection of TH positive neurons degeneration. A significant improvement in the cognitive function due to UA was observed in BMT. Biochemically, the oxidative stress and inflammation triggered by rotenone was significantly diminished by UA. UA also significantly obviated the complex I inhibition and promoted MB. The preliminary results thus firmly advocate the neuroprotective potential of UA to prevent rotenone induced neurotoxicity in rats. Schizophrenia (SZ) and bipolar disorder (BD) are severe psychiatric diseases that are characterized by abnormalities of thought, behaviour, cognition and mood. The genetic findings obtained from past molecular genetics research failed to elucidate the molecular pathogenesis of SZ and BD and this situation showed that the risk factors for these diseases were not solely due to the DNA sequence. On the other hand, evidence from cell, animal and postmortem brain studies suggest that abnormal epigenetic mechanisms are important actors in the etiology of complex diseases such as SZ and BD. In this review, epigenetic evidences that obtained from DNA methylation, post-translational histone modifications and non-coding RNA studies in SZ and BD were summarized and the importance of this evidences for advances in the diagnosis and treatment of SZ and BD were discussed briefly. Major depressive disorder (MDD) affects people worldwide. MDD treatments include antidepressants, which involve a delayed onset of action, long-term treatment, side effects and, frequently, only partial efficacy. The lack of access to the living brain, and the complex and still poorly elucidated pathophysiology of MDD, hinders treatment development. There is not only a need for new treatment strategies, but also for new approaches to investigating the pathophysiology of MDD. Light therapy is a well-established treatment acting through the retina. Since the retina is part of the central nervous system, it has been suggested as a useful area for investigating mental illness. In this article, we will first set out the evidence that MDD affects the retina's structure and function. https://www.selleckchem.com/products/kaempferide.html We will then review studies evaluating the efficacy of light therapy in unipolar non-seasonal MDD. Finally, we discuss the disruption of melatoninergic pathways in MDD, its assessment through the retina and the treatment of this disruption with light therapy. Pain measures traditionally used in rodents record mere reflexes evoked by sensory stimuli; the results thus may not fully reflect the human pain phenotype. Alterations in physical and emotional functioning, pain-depressed behaviors and facial pain expressions were recently proposed as additional pain outcomes to provide a more accurate measure of clinical pain in rodents, and hence to potentially enhance analgesic drug development. We aimed to review how preclinical pain assessment has evolved since the development of the tail flick test in 1941, with a particular focus on a critical analysis of some nonstandard pain outcomes, and a consideration of how sex differences may affect the performance of these pain surrogates. We tracked original research articles in Medline for the following periods 1973-1977, 1983-1987, 1993-1997, 2003-2007, and 2014-2018. We identified 606 research articles about alternative surrogate pain measures, 473 of which were published between 2014 and 2018. This indicates that preclinical pain assessment is moving toward the use of these measures, which may soon become standard procedures in preclinical pain laboratories. Eukaryotic ribonucleotide reductases are iron-dependent enzymes that catalyze the rate-limiting step in the de novo synthesis of deoxyribonucleotides. Multiple mechanisms regulate the activity of ribonucleotide reductases in response to genotoxic stresses and iron deficiency. Upon iron starvation, the Saccharomyces cerevisiae Aft1 transcription factor specifically binds to iron-responsive cis elements within the promoter of a group of genes, known as the iron regulon, activating their transcription. Members of the iron regulon participate in iron acquisition, mobilization and recycling, and trigger a genome-wide metabolic remodeling of iron-dependent pathways. Here, we describe a mechanism that optimizes the activity of yeast ribonucleotide reductase when iron is scarce. We demonstrate that Aft1 and the DNA-binding protein Ixr1 enhance the expression of the gene encoding for its catalytic subunit, RNR1, in response to iron limitation, leading to an increase in both mRNA and protein levels. By mutagenesis of the Aft1-binding sites within RNR1 promoter, we conclude that RNR1 activation by iron depletion is important for Rnr1 protein and deoxyribonucleotide synthesis.
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