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Periodontitis is caused by pathogenic subgingival microbial biofilm development and dysbiotic interactions between host and hosted microbes. A thorough characterization of the subgingival biofilms by deep amplicon sequencing of 121 individual periodontitis pockets of nine patients and whole metagenomic analysis of the saliva microbial community of the same subjects were carried out. Two biofilm sampling methods yielded similar microbial compositions. Taxonomic mapping of all biofilms revealed three distinct microbial clusters. Two clinical diagnostic parameters, probing pocket depth (PPD) and clinical attachment level (CAL), correlated with the cluster mapping. The dysbiotic microbiomes were less diverse than the apparently healthy ones of the same subjects. The most abundant periodontal pathogens were also present in the saliva, although in different representations. The single abundant species Tannerella forsythia was found in the diseased pockets in about 16-17-fold in excess relative to the clinically healthy sulcus, making it suitable as an indicator of periodontitis biofilms. The discrete microbial communities indicate strong selection by the host immune system and allow the design of targeted antibiotic treatment selective against the main periodontal pathogen(s) in the individual patients.Graves' disease (GD) is a clinical syndrome with an enlarged and overactive thyroid gland, an accelerated heart rate, Graves' orbitopathy (GO), and pretibial myxedema (PTM). GO is the most common extrathyroidal complication of GD. GD/GO has a significant negative impact on the quality of life. GD is the most common systemic autoimmune disorder, mediated by autoantibodies to the thyroid-stimulating hormone receptor (TSHR). It is generally accepted that GD/GO results from complex interactions between genetic and environmental factors that lead to the loss of immune tolerance to thyroid antigens. However, the exact mechanism is still elusive. Systematic investigations into GD/GO animal models and clinical patients have provided important new insight into these disorders during the past 4 years. These studies suggested that gut microbiota may play an essential role in the pathogenesis of GD/GO. Antibiotic vancomycin can reduce disease severity, but fecal material transfer (FMT) from GD/GO patients exaggerates the disease in GD/GO mouse models. There are significant differences in microbiota composition between GD/GO patients and healthy controls. [https://www.selleckchem.com/products/arq531.html Nemtabrutinib datasheet] Lactobacillus, Prevotella, and Veillonella often increase in GD patients. The commonly used therapeutic agents for GD/GO can also affect the gut microbiota. Antigenic mimicry and the imbalance of T helper 17 cells (Th17)/regulatory T cells (Tregs) are the primary mechanisms proposed for dysbiosis in GD/GO. Interventions including antibiotics, probiotics, and diet modification that modulate the gut microbiota have been actively investigated in preclinical models and, to some extent, in clinical settings, such as probiotics (Bifidobacterium longum) and selenium supplements. Future studies will reveal molecular pathways linking gut and thyroid functions and how they impact orbital autoimmunity. Microbiota-targeting therapeutics will likely be an essential strategy in managing GD/GO in the coming years.The mammalian gut microbial community, known as the gut microbiota, comprises trillions of bacteria, which co-evolved with the host and has an important role in a variety of host functions that include nutrient acquisition, metabolism, and immunity development, and more importantly, it plays a critical role in the protection of the host from enteric infections associated with exogenous pathogens or indigenous pathobiont outgrowth that may result from healthy gut microbial community disruption. Microbiota evolves complex mechanisms to restrain pathogen growth, which included nutrient competition, competitive metabolic interactions, niche exclusion, and induction of host immune response, which are collectively termed colonization resistance. On the other hand, pathogens have also developed counterstrategies to expand their population and enhance their virulence to cope with the gut microbiota colonization resistance and cause infection. This review summarizes the available literature on the complex relationship occurring between the intestinal microbiota and enteric pathogens, describing how the gut microbiota can mediate colonization resistance against bacterial enteric infections and how bacterial enteropathogens can overcome this resistance as well as how the understanding of this complex interaction can inform future therapies against infectious diseases.<br /><br /> As a consequence of the epidemiological transition, multimorbidity has been identified as a critical public health challenge in India. The majority of the studies in the domain are grounded on hospital-based data or are based on small sample size, findings from which can only be generalized to a specific sub-group. These studies recommend exploring multimorbidity holistically at a national level to ensure adequate healthcare management in the country. Therefore, the present study examines the pattern and correlates of single and multimorbidity over the past two decades in India.<br /><br /> The study utilized data on 397901, 257519, and 399705 individuals from 52nd (1994-1995), 60th (2004-2005), and 75th (2018) rounds of cross-sectional data from the National Sample Survey (NSS). Univariate, bivariate, and multivariable statistical methods were applied to draw inferences from the data. The findings depict an increase in single and multimorbidity burden over individuals' age and NSS rounds.<br /><br /> Hypertension and diabetes were the fastest-growing morbidities over time. Higher education, urban residence, and belonging to an affluent class were significantly associated with both single and multimorbidity occurrence over time.<br /><br /> The burden of single and multimorbidity increases over time among India's older adults. Therefore, there is an urgent need to recuperate chronic disease management strategies for older adults in the Indian healthcare infrastructure.<br /><br />The burden of single and multimorbidity increases over time among India's older adults. Therefore, there is an urgent need to recuperate chronic disease management strategies for older adults in the Indian healthcare infrastructure.<br /><br /> There is limited knowledge on how the prevalence of multimorbidity varies within and across major Canadian urban centres. The objective of this study was to investigate the between-neighbourhood variation in the prevalence of multimorbidity in Canada's large urban centres, controlling for compositional effects associated with individual-level demographic and socioeconomic factors.<br /><br /> Cross-sectional data from the 2015-2018 cycles of the Canadian Community Health Survey (CCHS) were pooled at the microdata level. Respondents (20years and older) residing in one of the 35 census metropolitan areas (CMAs) were included (<br /><br /> = 100,803). Census tracts (CTs) were used as a measure of neighbourhood. To assess the between-neighbourhood differences in multimorbidity prevalence, we fitted three sequential random intercept logistic regression models.<br /><br /> During the 2015-2018 period, 8.1% of residents of large urban centres had multimorbidity. The results from the unadjusted model indicate that 13.4% of the total individual imorbidity, even after accounting for overall characteristics of the CMAs in which these neighbourhoods are located, as well as individual-level factors.<br /><br /> Chronic pain is often experienced alongside other long-term conditions (LTCs), yet our understanding of this, particularly in relation to multimorbidity (≥2 LTCs) is poor. We aimed to examine associations between the presence/extent of chronic pain with type/number of LTCs experienced.<br /><br /> We examined the relationship between number/type of LTCs (N = 45) in UK Biobank participants (n = 500,295) who self-reported chronic pain lasting ≥3 months in seven body sites or widespread. Relative risk ratios (RRR) for presence/extent of chronic pain sites were compared using logistic regression adjusted for sociodemographic (sex/age/socioeconomic status) and lifestyle factors (smoking/alcohol intake/BMI/physical activity).<br /><br /> 218,648 participants self-reported chronic pain. Of these, 69.1% reported ≥1 LTC and 36.2% reported ≥2 LTCs. In 31/45 LTCs examined, &gt;50% of participants experienced chronic pain. Chronic pain was common with migraine/headache and irritable bowel syndrome where pain is a primary symptom, but also with mental health conditions and diseases of the digestive system. Participants with &gt;4 LTCs were over three times as likely to have chronic pain (RRR 3.56, 95% confidence intervals (CIs) 3.44-3.68) and 20 times as likely to have widespread chronic pain (RRR 20.13, 95% CI 18.26-22.19) as those with no LTCs.<br /><br /> Chronic pain is extremely common across a wide range of LTCs. People with multimorbidity were at higher risk of having a greater extent of chronic pain. These results show that chronic pain is a key factor for consideration in the management of patients with LTCs or multimorbidity.<br /><br />Chronic pain is extremely common across a wide range of LTCs. People with multimorbidity were at higher risk of having a greater extent of chronic pain. These results show that chronic pain is a key factor for consideration in the management of patients with LTCs or multimorbidity.<br /><br /> This study aimed to compare the efficacy of transarterial chemoembolization (TACE) plus sorafenib (TACE-S) to TACE plus lenvatinib (TACE-L) for the treatment of HCC with portal vein tumor thrombus (PVTT).<br /><br /> This cohort study recruited patients from September 2017 to September 2020.A total of 59 and 57 consecutive patients were treated with TACE-L and TACE-S, respectively.<br /><br /> Before propensity score matching (PSM), comparing TACE-L to TACE-S, the median overall survival (OS) time was 16.4 months and 12.7 months, respectively [hazard ratio (HR) 1.34; 95% confidence interval (CI) 0.81-2.20; <br /><br /> = 0.25]. The median progression-free survival (PFS) time was 8.4 months and 7.43 months, respectively (HR 1.54; 95% CI 0.98-2.41; <br /><br /> = 0.081). After PSM, the median OS time was 18.97 months and 10.77 months, respectively (HR 2.21; 95% CI 1.12-4.38; <br /><br /> = 0.022); the median PFS time was 10.6 months (95% CI 6.6-18.0 months) and 5.4 months (95% CI 4.2-8.1 months), respectively (HR 2.62; 95% CI 1.43-4.80; <br /><br /> = 0.002). After PSM, the overall response rate (ORR) was 66.8% vs. 33.3% [odds ratio (OR) 0.85; 1.05-6.90; <br /><br /> = 0.037].<br /><br /> Both TACE-L and TACE-S are safe, well-tolerated treatments for HCC with PVTT. In HCC with PVTT, TACE-L was significantly superior to TACE-S with respect to OS, PFS, and ORR. A larger-scale randomized clinical trial is needed.<br /><br />Both TACE-L and TACE-S are safe, well-tolerated treatments for HCC with PVTT. In HCC with PVTT, TACE-L was significantly superior to TACE-S with respect to OS, PFS, and ORR. A larger-scale randomized clinical trial is needed.[This corrects the article DOI 10.3389/fonc.2020.01378.].We present a case series of 13 consecutive patients with prostate cancer treated with low-dose-rate (LDR) brachytherapy, utilizing SpaceOAR Vue™, the recent iodinated iteration of the SpaceOAR™ hydrogel rectal spacer. Low- and favorable intermediate-risk patients receiving monotherapy and unfavorable intermediate- and high-risk patients undergoing a brachytherapy boost were included. Permanent brachytherapy can result in subacute and late rectal toxicity, and precise contouring of the anterior rectal wall and posterior aspect of the prostate is essential for accurate dosimetry to confirm a safe implant. Clearly visible on non-contrast CT imaging, SpaceOAR Vue™ can substantially aid in post-implant contouring and analysis. Not previously described in the literature in the context of LDR brachytherapy, we demonstrate the added clinical benefit of placing a well-visualized rectal spacer.