Periodontal treatment consists of active periodontal therapy (APT) and supportive periodontal therapy (SPT). Regular SPT is recommended to prevent and control the occurrence of periodontal disease following APT. A patient's compliance with SPT is considered one of the most important factors affecting long-term periodontal status. Tooth loss is generally considered the final outcome of periodontitis. This review aimed to analyze the relationship between patient compliance with regular SPT and tooth loss. The PRISMA (Preferred Reporting Items for Systematic Reviews and Meta-Analyses) guideline for systematic reviews was used. A search of articles was conducted using MEDLINE (PubMed) and other databases. Quality assessments of selected studies were performed. To assess the effect of compliance on tooth loss during SPT, pooled risk ratio of tooth loss (RRTL) was used as the primary outcome. Pooled risk difference of tooth loss (RDTL) and weighted mean difference of tooth loss rate (WDTLR) were used as secondary outcomes. Subgroup analysis and meta-regression were conducted to evaluate the effects of different variables. In total, 710 articles were screened. Eight studies, which had a regular-compliance (RC) group and an erratic-compliance (EC) group with at least a 5-y follow-up period, qualified for the meta-analysis. The risk of tooth loss in the RC group was significantly lower than that in the EC group (pooled RRTL: 0.56 [confidence interval (CI): 0.38, 0.82]; pooled RDTL: -0.05 [CI: -0.08, -0.01]). The definition of compliance was a variable significantly related to risk ratio of tooth loss. Patients in the RC group had significantly lower tooth loss rate during SPT than did patients in the EC group (WDTLR: -0.12 [CI: -0.19, -0.05]). Teeth have less risk of being lost if patients are more compliant with supportive periodontal therapy. However, unidentified variables causing data heterogeneity and affecting the risk of tooth loss may have been present. More well-controlled prospective studies are needed in the future.
Dendrimer-encapsulated nanoparticles are shown to be versatile catalysts for both the hydrogenation of styrene and Heck heterocoupling of iodobenzene and methacrylate in supercritical CO2 (scCO2).
The effects of malnutrition on outcomes in miliary tuberculosis (MTB) are not well described. The aim of the present study was to find predictors for the development of acute respiratory failure (ARF) and survival in MTB patients, focusing on parameters reflecting nutritional condition.Out of the patients from three hospitals who had microbiologically or histopathologically confirmed tuberculosis, 56 patients presenting with typical disseminated pulmonary nodules on radiographs were retrospectively enrolled. A four-point nutritional risk score (NRS) was defined according to the presence of four nutritional factors: low body mass index (BMI; ,18.5 kg?m The male to female ratio was 1:3. ARF developed in 25% of patients (14 out of 56), with a 50% fatality rate. A high NRS (o3 points) was an independent risk factor for the development of ARF and fatality. In 90-day survival analysis, ARF, severe lymphocytopenia, hypocholesterolaemia, low BMI and higher NRS were risk factors for poor outcome. In multivariate analysis, only high NRS was an independent risk factor for 90-day survival rate in patients with MTB.A high nutritional risk score was a good predictor of poor outcome in miliary tuberculosis patients. Additional approaches to recover the nutritional deficits may become a focus in future management of miliary tuberculosis.
Background:c-MYC copy number gain (c-MYC gain) has been associated with aggressive behaviour in several cancers. However, the role of c-MYC gain has not yet been determined in lung adenocarcinomas classified by genetic alterations in epidermal growth factor receptor (EGFR), KRAS, and anaplastic lymphoma kinase (ALK) genes. We investigated the clinicopathologic and prognostic significance of c-MYC gain for disease-free survival (DFS) and overall survival (OS) according to EGFR, KRAS, and ALK gene status and stages in lung adenocarcinomas.Methods:In 255 adenocarcinomas resected in Seoul National University Bundang Hospital from 2003 to 2009, fluorescence in situ hybridisation (FISH) with c-MYC probe and centromeric enumeration probe 8 (CEP8) was analysed using tissue microarray containing single representative core per each case. EGFR (codon 18 to 21) and KRAS (codon 12, 13, and 61) mutations were analysed by polymerase chain reaction and direct sequencing method from formalin-fixed, paraffin-embedded tissue sections. ALK rearrangement was determined by FISH method. c-MYC gain was defined as >2 copies per nucleus, chromosome 8 gain as ⩾3 copies per nucleus, and gain of c-MYC:CEP8 ratio (hereafter, c-MYC amplification) as ⩾2.Results:We observed c-MYC gain in 20% (51 out of 255), chromosome 8 gain in 5.5% (14 out of 255), c-MYC amplification in 2.4% (6 out of 255), EGFR mutation in 49.4% (118 out of 239), KRAS mutation in 5.7% (7 out of 123), and ALK rearrangement in 4.9% (10 out of 205) of lung adenocarcinomas. c-MYC gain was observed in 19% (22 out of 118) of patients with lung adenocarcinomas with an EGFR mutation, but not in any patients with a KRAS mutation, or an ALK rearrangement. c-MYC gain (but not chromosome 8 gain or c-MYC amplification) was an independent poor-prognostic factor in the full cohort of lung adenocarcinoma (P=0.022, hazard ratio (HR)=1.71, 95% confidence interval (CI), 1.08–2.69 for DFS; P=0.032, HR=2.04, 95% CI, 1.06–3.91 for OS), as well as in stage I subgroup (P=0.023, HR=4.70, 95% CI, 1.24–17.78 for DFS; P=0.031, HR=4.65, 95% CI, 1.15–18.81 for OS), and in EGFR-mutant subgroup (P=0.022; HR=2.14; 95% CI, 1.11–4.10 for DFS).Conclusions:c-MYC gain (but not chromosome 8 gain or c-MYC amplification) was an independent poor-prognostic factor for DFS and OS in lung adenocarcinomas, both in full cohort and stage I cancer, and possibly for DFS in EGFR-mutant adenocarcinomas. Additional studies are required to determine if patients with lung adenocarcinoma with c-MYC gain are candidates for additional first-line treatment to mitigate their increased risk for disease progression and death.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.