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Abstract Background Prior research has linked e-cigarette use with chronic obstructive pulmonary disease (COPD). We examined the relationship between e-cigarette use and COPD prevalence in older adults with varying cigarette use status. Methods Data from the 2020 National Health Interview Survey were used to estimate the association between each of 9 exposure categories based on cigarette use (never, former, current) and e-cigarette use (never, former, current), with respondent-reported physician-diagnosed COPD prevalence in individuals 40 years and older (N = 22,997). Weighted multivariable analysis accounted for cigarette pack years, age of cigarette smoking onset, race, income-to-poverty ratio, rurality, gender, age, and medical comorbidities. Sensitivity of results was tested in 3 separate models with addition of years since quit cigarettes, smoking intensity and duration. Results 39.7% of individuals reported ever smoking cigarettes and 10.2% reported ever using e-cigarettes. Among individuals with ever e-cigarette use, 88.5% also reported current or former cigarette smoking. The weighted prevalence of COPD was 7.2%; Among those who reported former cigarette smoking, the highest risk of COPD prevalence compared to never cigarette/never e-cigarette use was in those currently using e-cigarettes (adjusted risk ratio (ARR) 2.82, 95% confidence interval (CI) [1.5, 5.3]). The ARR for former cigarette/current e-cigarette use was significantly larger than the ARR for former cigarette/never e-cigarette use (p

Introduction Cigarette smoking and smoking-related lung disease are more common in rural (vs urban) areas of the United States (US). This study examined relationships between geographical location, cigarette risk perceptions, and current smoking among older adults who are at greatest risk of developing smoking-related lung disease. Methods The study was a secondary data analysis of 12126 respondents aged ≥40 years from Wave 5 of the Population Assessment of Tobacco and Health Study. Weighted descriptive statistics and Poisson regressions assessed current smoking (vs never or former) as a function of geographical location in a stepwise fashion, first unadjusted, then adjusting for sociodemographic characteristics, and finally for both sociodemographic characteristics and cigarette risk perceptions (4-item scale), in three separate models. Sensitivity analyses examined whether individual risk perceptions items had a greater impact on the association between geographical location and current smoking. Results Current smoking was more common among rural (20.6%) than urban (17.6%) residents. The risk ratio (RR) for rural (vs urban) residence on current smoking decreased from 1.17 (95% CI: 1.03–1.32) to 1.14 (95% CI: 1.01–1.29) to 1.08 (95% CI: 0.96–1.21) across the stepwise models. Lower cigarette risk perceptions confounded the rural-current smoking association and was an independent risk factor for smoking (adjusted RR, ARR=2.15; 95% CI: 1.94– 2.18). In sensitivity analyses, believing that cigarettes are very or extremely (vs somewhat, slightly, or not at all) harmful to health and agreeing (vs not agreeing) that secondhand smoke causes lung disease in people who do not smoke, confounded the rural-current smoking association whereas beliefs about smoking causing lung cancer or lung disease in people who smoke did not. Conclusions Lower cigarette risk perceptions among rural residents confounded the positive association between rural residence and current smoking. Results from sensitivity analyses highlight potential targets for communication campaigns aimed at promoting more accurate perceptions of the harmful health consequences of cigarette smoking.

Abstract Objective Assess the efficacy of single and multiple intra-articular injections of autologous adipose-derived stem cells (ASCs) and adipose-derived stromal vascular fraction (ADSVF) for the treatment of knee osteoarthritis (OA). Methods We conducted a thorough and systematic search of several databases, including PubMed, Embase, Web of Science, Cochrane Library, and ClinicalTrials.gov, to identify relevant studies. The included studies were randomized controlled trials (RCTs) that involved single or multiple intra-articular injections of autologous ASCs or ADSVF for the treatment of patients with knee osteoarthritis, without any additional treatment, and compared to either placebo or hyaluronic acid. Results A total of seven RCTs were analyzed in this study. The results of the meta-analysis show that compared to the control group, both single and multiple intra-articular injections of ASCs or ADSVF demonstrated superior pain relief in the short term (Z = 3.10; P

This study examined associations between established cigar use and prevalence and incidence of cardiovascular diseases (CVD; congestive heart failure, stroke, or heart attack/needed bypass surgery) among U.S. adults, 40 years or older. Using Waves 1–5 (2013–2019) of the Population Assessment of Tobacco and Health (PATH) Study, incidence (Nindividuals (Nind) = 6,692; Nobservations (Nobs) = 23,738) and prevalence (Nind = 7,819; Nobs = 33,952) of CVD outcomes were examined using weighted generalized estimating equations (WGEEs) among adults who were exclusive current/former established cigar smokers (ever cigar smokers who have smoked fairly regularly), exclusive current/former established cigarette smokers (lifetime smokers of 100 or more cigarettes), dual current/former established cigarette and cigar smokers compared with never smokers of cigars or cigarettes, adjusting for covariates. The population-averaged incidence of CVD from one wave to next among exclusive current/former established cigar smokers during a six-year period based on WGEEs was low (overall average rate of 3.0 %; 95 % CI: 1.2, 7.0). Compared with never users, exclusive current/former established cigar smokers (OR = 1.67, 95 % CI: 1.11, 2.51) and exclusive current/former established cigarette smokers (OR = 2.12, 95 % CI: 1.45, 3.09) were more likely to have any CVD outcome in unadjusted analyses. When adjusted for covariates, only exclusive current/former established cigarette use was associated with CVD outcomes (AOR = 1.60, CI: 1.07, 2.40). Results suggest that exclusive established use of cigars or duration of exclusive cigar use was not associated with lifetime CVD prevalence compared with never cigar or cigarette smokers, which is important in understanding health outcomes in cigar users.

The quality of ocular fundus photographs can affect the accuracy of the morphologic assessment of the optic nerve head (ONH), either by humans or by deep learning systems (DLS). In order to automatically identify ONH photographs of optimal quality, we have developed, trained, and tested a DLS, using an international, multicentre, multi-ethnic dataset of 5015 ocular fundus photographs from 31 centres in 20 countries participating to the Brain and Optic Nerve Study with Artificial Intelligence (BONSAI). The reference standard in image quality was established by three experts who independently classified photographs as of “good”, “borderline”, or “poor” quality. The DLS was trained on 4208 fundus photographs and tested on an independent external dataset of 807 photographs, using a multi-class model, evaluated with a one-vs-rest classification strategy. In the external-testing dataset, the DLS could identify with excellent performance “good” quality photographs (AUC = 0.93 (95% CI, 0.91–0.95), accuracy = 91.4% (95% CI, 90.0–92.9%), sensitivity = 93.8% (95% CI, 92.5–95.2%), specificity = 75.9% (95% CI, 69.7–82.1%) and “poor” quality photographs (AUC = 1.00 (95% CI, 0.99–1.00), accuracy = 99.1% (95% CI, 98.6–99.6%), sensitivity = 81.5% (95% CI, 70.6–93.8%), specificity = 99.7% (95% CI, 99.6–100.0%). “Borderline” quality images were also accurately classified (AUC = 0.90 (95% CI, 0.88–0.93), accuracy = 90.6% (95% CI, 89.1–92.2%), sensitivity = 65.4% (95% CI, 56.6–72.9%), specificity = 93.4% (95% CI, 92.1–94.8%). The overall accuracy to distinguish among the three classes was 90.6% (95% CI, 89.1–92.1%), suggesting that this DLS could select optimal quality fundus photographs in patients with neuro-ophthalmic and neurological disorders affecting the ONH.

Background: Neuronal apoptosis is a major contributor to Alzheimer’s disease (AD). Periodontitis is a significant risk factor for AD. The periodontal pathogens Porphyromonas gingivalis and Treponema denticola have been shown to initiate the hallmark pathologies and behavioral symptoms of AD. Studies have found that T. denticola infection induced Tau hyperphosphorylation and amyloid β accumulation in the hippocampi of mice. Aβ accumulation is closely associated with neuronal apoptosis. However, the roles of T. denticola in neuronal apoptosis remain unclear and its roles in AD pathology need further study. Objective: This study aimed to investigate whether oral infection with T. denticola induced alveolar bone loss and neuronal apoptosis in mice. Methods: C57BL/6 mice were orally administered with T. denticola, Micro-CT was employed to assess the alveolar bone resorption. Western blotting, quantitative PCR, and TUNEL staining were utilized to detect the apoptosis-associated changes in mouse hippocampi. N2a were co-cultured with T. denticola to verify in vivo results. Results: Mice infected with T. denticola exhibited more alveolar bone loss compared with the control mice. T. denticola oral infection induced neuronal apoptosis in hippocampi of mice. Consistent results of the apoptosis-associated protein expression were observed in N2a cells treated with T. denticola and Aβ1–42 in vitro. However, the Aβ inhibitor reversed these results, suggesting that Aβ1–42 mediates T. denticola infection-induced neuronal apoptosis. Conclusions: This study found that oral infected T. denticola caused alveolar bone loss, and induced neuronal apoptosis by promoting Aβ accumulation in mice, providing evidence for the link between periodontitis and AD.

Supplemental Digital Content is Available in the Text. Background: Optic disc drusen (ODD) represent an important differential diagnosis of papilledema caused by intracranial hypertension, but their distinction may be difficult in clinical practice. The aim of this study was to train, validate, and test a dedicated deep learning system (DLS) for binary classification of ODD vs papilledema (including various subgroups within each category), on conventional mydriatic digital ocular fundus photographs collected in a large international multiethnic population. Methods: This retrospective study included 4,508 color fundus images in 2,180 patients from 30 neuro-ophthalmology centers (19 countries) participating in the Brain and Optic Nerve Study with Artificial Intelligence (BONSAI) Group. For training and internal validation, we used 857 ODD images and 3,230 papilledema images, in 1,959 patients. External testing was performed on an independent data set (221 patients), including 207 images with ODD (96 visible and 111 buried), provided by 3 centers of the Optic Disc Drusen Studies Consortium, and 214 images of papilledema (92 mild-to-moderate and 122 severe) from a previously validated study. Results: The DLS could accurately distinguish between all ODD and papilledema (all severities included): area under the receiver operating characteristic curve (AUC) 0.97 (95% confidence interval [CI], 0.96–0.98), accuracy 90.5% (95% CI, 88.0%–92.9%), sensitivity 86.0% (95% CI, 82.1%–90.1%), and specificity 94.9% (95% CI, 92.3%–97.6%). The performance of the DLS remained high for discrimination of buried ODD from mild-to-moderate papilledema: AUC 0.93 (95% CI, 0.90–0.96), accuracy 84.2% (95% CI, 80.2%–88.6%), sensitivity 78.4% (95% CI, 72.2%–84.7%), and specificity 91.3% (95% CI, 87.0%–96.4%). Conclusions: A dedicated DLS can accurately distinguish between ODD and papilledema caused by intracranial hypertension, even when considering buried ODD vs mild-to-moderate papilledema. [ABSTRACT FROM AUTHOR]

Objective The pathological mechanism of osteoporosis (OP) involves increased bone resorption mediated by osteoclasts and decreased bone formation mediated by osteoblasts, leading to an imbalance in bone homeostasis. Identifying key molecules in osteoclast-mediated OP progression is crucial for the prevention and treatment of OP. Methods Differential expression analysis and weighted gene co-expression network analysis (WGCNA) were performed on the OP patient datasets from the GEO database. The results were intersected with the differential expression results from the osteoclast differentiation dataset to identify key genes. These key genes were then subjected to disease relevance analysis, and consensus clustering was performed on OP patient samples based on their expression profiles. The subgroups were analyzed for differences, followed by GO, KEGG, GSEA, and GSVA analyses, and immune infiltration. Finally, osteoclast differentiation model was constructed. After validating the success of the model using TRAP and F-actin staining, the differential expression of key genes was validated in vitro via Western blot. Results CTRL, ARHGEF5, PPAP2C, VSIG2, and PBLD were identified as key genes. These genes exhibited strong disease relevance (AUC > 0.9). Functional enrichment results also indicated their close association with OP and osteoclast differentiation. In vitro differential expression validation showed that during osteoclast differentiation, CTRL was downregulated, while ARHGEF5, PPAP2C, VSIG2, and PBLD were upregulated, with all differences being statistically significant (P < 0.05). Discussion Currently, there are no studies on the effects of these five genes on osteoclast differentiation. Therefore, it is meaningful to design in vivo and in vitro perturbation experiments to observe the impact of each gene on osteoclast differentiation and OP progression. Conclusion CTRL, ARHGEF5, PPAP2C, VSIG2, and PBLD show high potential as molecular targets for basic and clinical research in osteoclast-mediated OP. [ABSTRACT FROM AUTHOR]

INTRODUCTION Cigarette smoking and smoking-related lung disease are more common in rural (vs urban) areas of the United States (US). This study examined relationships between geographical location, cigarette risk perceptions, and current smoking among older adults who are at greatest risk of developing smoking-related lung disease. METHODS The study was a secondary data analysis of 12126 respondents aged ≥40 years from Wave 5 of the Population Assessment of Tobacco and Health Study. Weighted descriptive statistics and Poisson regressions assessed current smoking (vs never or former) as a function of geographical location in a stepwise fashion, first unadjusted, then adjusting for sociodemographic characteristics, and finally for both sociodemographic characteristics and cigarette risk perceptions (4-item scale), in three separate models. Sensitivity analyses examined whether individual risk perceptions items had a greater impact on the association between geographical location and current smoking. RESULTS Current smoking was more common among rural (20.6%) than urban (17.6%) residents. The risk ratio (RR) for rural (vs urban) residence on current smoking decreased from 1.17 (95% CI: 1.03-1.32) to 1.14 (95% CI: 1.01-1.29) to 1.08 (95% CI: 0.96-1.21) across the stepwise models. Lower cigarette risk perceptions confounded the rural-current smoking association and was an independent risk factor for smoking (adjusted RR, ARR=2.15; 95% CI: 1.94-2.18). In sensitivity analyses, believing that cigarettes are very or extremely (vs somewhat, slightly, or not at all) harmful to health and agreeing (vs not agreeing) that secondhand smoke causes lung disease in people who do not smoke, confounded the rural-current smoking association whereas beliefs about smoking causing lung cancer or lung disease in people who smoke did not. CONCLUSIONS Lower cigarette risk perceptions among rural residents confounded the positive association between rural residence and current smoking. Results from sensitivity analyses highlight potential targets for communication campaigns aimed at promoting more accurate perceptions of the harmful health consequences of cigarette smoking. [ABSTRACT FROM AUTHOR]

Rationale: It is not certain the extent to which childhood smoking adds chronic obstructive pulmonary disease (COPD) risk independent of lifetime cigarette exposure. Objectives: We examined the association between age started smoking cigarettes regularly, current smoking status, smoking history, and risk of COPD. Methods: Cross-sectional survey of U.S. adults ⩾40 years old in the 2020 National Health Interview Survey. Respondents who were ever cigarette smokers were asked when they began smoking regularly. Multivariable analysis assessed self-report of COPD diagnosis as a function of age started smoking (<15 yr vs. ⩾15 yr) adjusting for current smoking, cigarette pack-years, and covariates. Measurements and Main Results: Overall, 7.1% reported that they had COPD, 2.6% for never-smokers compared with 23.1% and 11.6% for smoking onset <15 and ⩾15 years, respectively. Persons who began smoking regularly at <15 years of age had higher pack-years of smoking (median, 29 vs. 15, respectively), and higher smoking intensity (median, 20 cigarettes/d for <15 yr vs. 10 cigarettes/d for ⩾15 yr for current smokers). In the multivariable analysis, the relative risk for COPD among childhood smokers was 1.41 (95% confidence interval, 1.22-1.63) compared with later-onset smokers. Substituting smoking duration for pack-years confounded the association between current smoking and COPD but did not change the childhood smoking estimate. In a stratified analysis, higher risk for childhood smoking was found at all current smoking intensity levels. Conclusions: Among adults aged ⩾40 years, one-fifth of childhood smokers have COPD. Lifetime cigarette smoking explained some but not all of the higher risk. If replicated, this suggests a lung development window of enhanced vulnerability to cigarette smoking. [ABSTRACT FROM AUTHOR]

Objective • Smoking stands as a significant factor contributing to aberrations in bone metabolism, while microRNAs are intricately linked to the regulation of bone metabolism. This study aimed to identify cotinine- responsive microRNAs (miRNAs) and downstream regulatory pathways of their target genes involved in the regulation of osteoblastic cells, providing a foundation for new treatments targeting miRNAs for the bone metabolism imbalance induced by smoking. Methods • Primary osteoblastic cells of Sprague-Dawley rats were cultured through a modified enzymatic digestion method from the cranial bone of neonatal rats and stimulated with a high concentration of cotinine (1000 ng/ mL) for 7 days. Then, miRNA gene chip technology was utilized to detect the changes in miRNA expression profiles in cotinine-stimulated osteoblastic cells, and differential expression profiles of cotinine-responsive miRNAs in osteoblastic cells were identified. Real-time polymerase chain reaction was used to detect the levels of significantly differentially expressed miRNAs in rat osteoblastic cells. Gene ontology (GO) and Kyoto encyclopedia of Genes and Genomes (KEGG) pathway analyses were utilized to predict target genes of these miRNAs to reveal the potential biological functions and pathways. Results • We identified 6 statistically differentially expressed miRNAs in the miRNA microarray analysis, of which 3 were upregulated and 3 were downregulated. We chose bone metabolism-related miRNAs as the miRNAs of interest. Quantitative real-time polymerase chain reaction was used to detect the expression levels of the differentially expressed miRNAs, and only miR-210 was significantly upregulated (3.34-fold), consistent with the microarray data. GO and KEGG pathway analyses of predicted miR-210 target genes revealed that miR-210 might participate in numerous signaling pathways, such as the RAS, Rap, PI3K-Akt, and calcium signaling pathways. Conclusion • We found that the strongly upregulated miR-210 may play an important regulatory role in osteoblast cells’ biological behavior and bone formation function. The GO analysis results showed that miR-210 mainly involved protein binding, transporter activity, growth factor binding, and ion channel activity. According to the results of the KEGG analysis, miR-210 might negatively regulate the PI3K-Akt signaling pathway, thus affecting the proliferation of osteoblastic cells. These findings suggest that miR-210 may be a potential target for regulating the imbalance of bone metabolism caused by smoking, offering a new direction for clinical treatment of patients with bone metabolism-related diseases. [ABSTRACT FROM AUTHOR]