Introduction: Transient hypogammaglobulinemia of infancy (THI) is a heterogeneous disorder characterized by reduced serum immunoglobulin G (IgG) levels in early infancy. Objective: This study aimed to identify potential risk factors associated with THI. Methods: Children with THI and normoglobulinemic healthy children were compared by using a questionnaire that addressed possible risk factors. Results: In total, 108 participants were enrolled, 54 patients with THI and 54 healthy controls. The median age at diagnosis of the patients with THI was 17 months (range, 4-38 months), and 40 (74.1%) were boys. In the control group, the median age was 22 months (range, 16-61 months), and 27 (50.0%) were boys. Male sex (p = 0.004), cesarean section birth (p = 0.003), low maternal education (p = 0.001), low paternal education (p = 0.004), analgesic use during pregnancy (p = 0.001), antibiotic use during pregnancy (p = 0.001), multivitamin use during pregnancy (p = 0.001), gestational diabetes or preeclampsia (p = 0.039), smoking exposure (p = 0.001), atopic disease (p = 0.001), and familial atopy (p = 0.001) were associated with THI, whereas low socioeconomic level (p = 0.001) and breast-feeding for > 6 months (p = 0.032) were less likely in the THI group. Conclusion: There are several features of pregnancy history and family demographics that are associated with THI.

The apolipoprotein L1 (APOL1) G1 and G2 gene variants, highly prevalent among the African American population (rare in other racial groups), are linked to increased risk of kidney disease, sepsis, and potentially coronary heart disease (CHD). Their role in tobacco-related CHD remains unclear.

To investigate the effect of APOL1 risk variants on the association between tobacco smoking and prevalent CHD in African American adults.

We conducted a cross-sectional study involving 519 African American adults recruited through the University of California San Francisco Lipid Clinic. Using multivariable logistic regression, we assessed the association between tobacco smoking and CHD, overall and with its most severe subtype, myocardial infarction (MI), among all participants and APOL1 genotype subgroups.

Among participants, 41% were current (14%) or former (27%) smokers, 54% carried APOL1 risk variants (1 or 2 alleles), and 28% had CHD, including 16% having MI. Current smokers with APOL1 risk variants had 3.3 times higher odds of CHD compared to nonsmokers (95% CI: 1.6, 6.8), with the strongest effect observed in those with 2 risk alleles (odds ratio [OR]: 7.3, CI: 1.1, 48.6) and a substantial effect in carriers of a single risk allele (OR: 3.2, CI: 1.5, 7.2). Among non-carriers, current smoking was not significantly associated with CHD (OR: 1.3). A similar trend was observed for MI. Former smoking was associated with CHD (OR: 2.0), independent of APOL1 genotype.

African American smokers with APOL1 G1 and/or G2 risk variants may be at greater risk of CHD; this relationship appears to follow an additive model.

The purpose of this study was to investigate the association between cannabis use and postoperative complications following ankle and hindfoot arthrodesis.

A retrospective cohort study using a large national insurance database from 2010 to 2022 was conducted. All patients who underwent ankle or hindfoot arthrodesis with at least 2 years' follow-up were included. Patients were divided into 4 groups: cannabis-only users, tobacco-only users, cannabis and tobacco users, and nonuser controls. Groups were matched 1:4 with nonuser controls based on demographic variables and comorbidities. Also, both cannabis and tobacco users were matched 1:4 with tobacco-only users based on demographics and comorbidities. Medical complications within 90 days of surgery and surgery-specific complications within 2 years were compared between groups with multivariable logistic regressions.

Compared with nonuser controls, cannabis users only were not at increased risk of 90-day medical complications or 2-year surgical complications. Tobacco use alone was associated with increased risk of postoperative admission (OR 1.32, 95% CI 1.21-1.43) and emergency department (ED) utilization (OR 1.57, 95% CI 1.48-1.66) within 90 days as well as infection (OR 1.24, 95% CI 1.18-1.30), hardware removal (OR 1.12, 95% CI 1.07-1.18), nonunion (OR 1.33, 95% CI 1.27-1.40), and wound dehiscence (OR 1.38, 95% CI 1.27-1.49) within 2 years of surgery compared with nonuser controls. Compared with tobacco-only use, combined cannabis and tobacco use was associated with increased risk of ED visits within 90 days (OR 1.45, 95% CI 1.30-1.62) and nonunion within 2 years of surgery (OR 1.19, 95% CI 1.05-1.35).

These findings suggest that although cannabis use alone was not associated with a higher risk of postoperative complications, its concurrent use with tobacco was linked to greater rates of adverse outcomes.

Level III, retrospective case control study.

Smoking may increase levels of pro-inflammatory cytokines, which is an important contributor to rheumatoid arthritis (RA) pathogenesis.

The aim of this study was to describe the characteristics of RA patients who were smokers compared with non-smokers.

A total of 849 RA patients who were smokers out of a large RA cohort of 10,364 patients (8.2%) were compared to 924 age-, sex-, and body mass index-matched RA patients who were non-smokers. Patients were subjected to full history-taking and clinical examination. Laboratory tests such as rheumatoid factor (RF) and anti-cyclic citrullinated peptide (anti-CCP) were measured. The disease activity score 28 (DAS28) and the health assessment questionnaire (HAQ) score were assessed.

The mean age among smokers was 46.4 ± 11.3 years, the male-female ratio was 3:1, and the mean disease duration was 6.4 ± 6.2 years. There was a significantly higher frequency of diabetes mellitus, hypertension, and metabolic syndrome in smokers compared to non-smokers (13.7%, 17.1%, and 9.2% vs. 8.4%, 12.9%, and 3.5%; P < 0.0001, P = 0.01, P < 0.0001, respectively), while hypothyroidism was more common in non-smokers (P = 0.03). Rheumatoid nodules (P = 0.03), oral ulcers (P = 0.002), keratoconjunctivitis sicca (P = 0.043), and neurological manifestations (P = 0.002) were significantly more common in smokers, but the DAS28 was lower (4.2 ± 1.5 vs. 4.8 ± 2.5; P < 0.0001). RA-related changes were significantly more common in female smokers than in males. On regression analysis, none of the differences found in the comparison between smokers and non-smokers remained significant.

Smoking in RA patients was found to be associated with a higher frequency of traditional comorbidities, rheumatoid nodules, oral ulcers, sicca complex, and neurological manifestations, but a lower disease activity. There is an obvious sex-driven pattern, with clinical alterations occurring more frequently in female smokers. Higher RF, anti-CCP, and double seropositivity are more observable in males and positive antinuclear antibody in females.

The global incidence and prevalence of cardiometabolic disorders have risen significantly in recent years. Although lifestyle choices in adulthood play a crucial role in the development of these conditions, it is well established that events occurring early in life can have an important effect. Recent research on cardiometabolic diseases has highlighted the influence of sexual dimorphism on risk factors, underlying mechanisms, and response to therapies. In this narrative review, we summarize the current understanding of sexual dimorphism in cardiovascular and metabolic diseases in the general population and within the framework of the Developmental Origins of Health and Disease (DOHaD) concept. We explore key risk factors and mechanisms, including the influence of genetic and epigenetic factors, placental and embryonic development, maternal nutrition, sex hormones, energy metabolism, microbiota, oxidative stress, cell death, inflammation, endothelial dysfunction, circadian rhythm, and lifestyle factors. Finally, we discuss some of the main therapeutic approaches, responses to which may be influenced by sexual dimorphism, such as antihypertensive and cardiovascular treatments, oxidative stress management, nutrition, cell therapies, and hormone replacement therapy.

Non-alcoholic fatty liver disease (NAFLD) is the most prevalent chronic liver disease worldwide. Cardiovascular disease (CVD) and NAFLD share multiple common risk factors. Life's Crucial 9 (LC9), a novel indicator for comprehensive assessment of cardiovascular health (CVH), has not yet been studied in terms of its association with or predictive value for NAFLD. This study analyzed data from 10,197 participants in the National Health and Nutrition Examination Survey (NHANES) from 2007 to 2018. The association between LC9 and NAFLD was assessed using weighted logistic regression, while weighted Cox proportional hazards models were applied to evaluate the relationship between LC9 and all-cause mortality among NAFLD patients. Restricted cubic spline (RCS) analysis was conducted to explore dose-response relationships, and Kaplan-Meier survival curves were utilized to examine differences in survival outcomes. Machine learning (ML) approaches were employed to construct predictive models, with the optimal model further interpreted using SHapley Additive exPlanations (SHAP). An increase of 10 points in LC9 was negatively associated with the risk of NAFLD (model 3: OR = 0.39, 95% CI = 0.36 - 0.42, P < 0.001) and all-cause mortality in NAFLD patients (model 3: HR = 0.78, 95% CI = 0.67 - 0.91, P < 0.001). A non-linear relationship was observed between LC9 and NAFLD (P < 0.0001 for nonlinearity). Among the eight ML models, the Support Vector Machine (SVM) demonstrated the best predictive performance (AUC = 0.873). SHAP analysis indicated that LC9 was the most significant predictor in the model. LC9 demonstrated a nonlinear negative association with NAFLD and a linear negative association with all-cause mortality in NAFLD patients. Maintaining a higher LC9 score may reduce the risk of NAFLD and all-cause mortality among NAFLD patients. The predictive model developed using Support Vector Machine (SVM) exhibited strong clinical predictive value, with LC9 being the most critical factor in the model, facilitating self-risk assessment and targeted intervention.

Childhood maltreatment is recognized as a risk factor for cognitive decline in adulthood. However, the mechanisms underlying this association, particularly the role of systemic inflammation, remain understudied. To address this gap, this study investigated the indirect effects of inflammation on the associations between childhood maltreatment and both episodic memory (EM) and executive functioning (EF) performance 10 years after inflammatory measurement in older adults. We selected 590 participants (Mage = 65.5 years) from the Midlife in the United States Study based on available childhood maltreatment, inflammation, and composite cognitive data. Spearman's rank correlations were calculated to test associations among childhood maltreatment, cognition, and inflammation. The results informed follow-up analyses testing the indirect effects of inflammation on the associations between childhood maltreatment and cognition. Correlations demonstrated that inflammation was associated with overall childhood maltreatment as well as with specific domains of childhood maltreatment (i.e., physical abuse, sexual abuse, emotional abuse, and physical neglect), ps = .002-.010. Inflammation was negatively associated with EF, p = .001, and EM, p = .028. Follow-up analyses revealed significant indirect pathways linking overall childhood maltreatment, β = -.0088, SE = 0.0058, 95% CI [-0.0223, -0.00000], to EM performance through inflammation, but no specific domain of maltreatment drove this association. The results suggest that inflammation may help explain links between childhood maltreatment exposure and EM deficits in adulthood. These results elucidate the importance of evaluating childhood maltreatment as a risk factor for later-life cognitive decline, particularly within the context of heightened inflammatory biomarkers.

Accumulating evidence suggest that Epstein-Barr virus (EBV) is crucial in the development of multiple sclerosis (MS), with inadequate infection control possibly contributing to disease onset. Past infectious mononucleosis (IM) has been found to interact with smoking, obesity, and sun exposure. We aimed to investigate potential interactions between a history of IM and the following risk factors for MS: passive smoking, alcohol consumption, fish consumption, vitamin D status, adolescent sleep duration and sleep quality.

We analyzed data from a Swedish population-based case-control study (3128 cases and 5986 controls). Subjects were categorized based on IM status and each exposure variable and compared regarding MS risk by calculating odds ratios (OR) with 95% confidence intervals (CI) using logistic regression models. Additive interaction between aspects of IM status and each exposure was assessed by calculating the attributable proportion due to interaction (AP) with 95% CI.

The OR of developing MS among those who reported a history of IM was 1.86 (95% CI 1.63-2.12), compared with those who had not suffered from IM. We observed synergistic effects between a history of IM and each exposure variable with respect to risk of MS, with significant APs ranging between 0.20 and 0.35.

The concept of EBV infection as a crucial factor for MS gains further support from our findings suggesting that MS risk factors synergize with a history of IM in disease development. Targeting modifiable MS risk factors that impede effective immune regulation of the virus holds promise for preventive interventions.

Secondhand smoke (SHS) may exacerbate the global disease burden, particularly in workplace settings. Observational studies have implicated SHS as a risk factor for various non-malignant digestive system diseases (NMDSD), yet establishing a causal relationship remains challenging. Therefore, we conducted a Mendelian randomization (MR) study to explore whether workplace exposure to SHS is associated with NMDSD.

This study utilized a secondary dataset analysis based on Genome-Wide association study (GWAS) summary data. Genetic variants associated with exposure to SHS in the workplace were used as instrumental variables. Genome-wide association study (GWAS) summary data for SHS were obtained from the UK Biobank. GWAS summary data for NMDSD were sourced from the FinnGen study, the International Inflammatory Bowel Disease Genetics Consortium (IIBDGC), and a large-scale study conducted in Japan. We employed inverse variance-weighted (IVW), MR-Egger, and weighted median methods for MR analysis. Additionally, sensitivity analyses were conducted to ensure the robustness of our findings.

According to the IVW model, SHS in the workplace was positively associated with ulcerative colitis (UC) (OR=2.03; 95% CI: 1.03-4.05; p=0.04). There was no evidence of horizontal pleiotropy biasing causality (p>0.05), and leave-one-out analysis confirmed the stability and robustness of this association.

Our study identifies an association between regular exposure to SHS in the workplace and an increased risk of ulcerative colitis. However, the potential influence of active smoking or exposure to SHS from other sources cannot be excluded. Further research is needed to confirm these findings.

Previous studies have found an association between ankylosing spondylitis (AS) and chronic obstructive pulmonary disease (COPD); however, no research has investigated this relationship using Mendelian randomization (MR).

This study employed a bidirectional two-sample MR approach to assess the causal connection between AS and COPD. The analysis utilized publicly available statistics on AS and COPD from the Genome-wide Association Study (GWAS). The primary MR method employed was Inverse-Variance Weighting (IVW), supplemented by additional MR methods such as weighted median, MR-Egger, simple mode, and weighted mode. Sensitivity analyses were also performed to evaluate the impact of heterogeneity and pleiotropy on the MR results.

The study included two datasets related to AS (ebi-a-GCST005529 and ukb-a-88) and two datasets related to COPD (ebi-a-GCST90018807 and finn-b-J10_COPD). In our forward MR, the analysis of ebi-a-GCST005529 dataset against ebi-a-GCST90018807 dataset showed that AS was associated with an increased risk of COPD (OR = 1.1326, 95% CI = 1.0181-1.2600, P = 0.0221). However, there was no causal relationship between AS and COPD in the rest of the dataset analyses. In reverse MR analysis, no causal effect between COPD and AS was found among the datasets.

Our research provided partial evidence to support the viewpoint that AS may increase the prevalence of COPD. AS may be a risk factor for COPD, however, further studies are needed to validate these results and elucidate the underlying mechanisms.

Cigarette smoking is posited as a potential factor in disrupting the balance of the human gut microbiota. However, existing studies with limited sample size have yielded inconclusive results.

Here, we assessed the association between cigarette smoking and gut microbial profile among Chinese males from four independent studies (N total = 3308). Both 16S rRNA and shotgun metagenomic sequencing methods were employed, covering 206 genera and 237 species. Microbial diversity and abundance were compared among non-smokers, current smokers, and former smokers.

Actinomyces[g], Atopobium[g], Haemophilus[g], Turicibacter[g], and Lachnospira[g] were found to be associated with smoking status (current smokers vs. non-smokers). Metagenomic data provided a higher resolution at the species level, particularly for the Actinomyces[g] branch. Additionally, serum γ-glutamylcysteine (γ-Glu-Cys) was found to have a potential role in connecting smoking and Actinomyces[g]. Furthermore, we revealed putative mediation roles of the gut microbiome in the associations between smoking and common diseases including cholecystitis and type 2 diabetes.

We characterized the gut microbiota profile in male smokers and further revealed their potential involvement in mediating the impact of smoking on health outcomes. These findings advance our understanding of the intricate association between cigarette smoking and the gut microbiome.

Metabolic dysfunction-associated steatotic liver disease (MASLD) is a prevalent chronic liver condition marked by excessive lipid accumulation in hepatic tissue. This disorder can lead to a range of pathological outcomes, including metabolic dysfunction-associated steatohepatitis (MASH) and cirrhosis. Despite extensive research, the molecular mechanisms driving MASLD initiation and progression remain incompletely understood. Oxidative stress and lipid peroxidation are pivotal in the "multiple parallel hit model", contributing to hepatic cell death and tissue damage. Gut microbiota plays a substantial role in modulating hepatic oxidative stress through multiple pathways: impairing the intestinal barrier, which results in bacterial translocation and chronic hepatic inflammation; modifying bile acid structure, which impacts signaling cascades involved in lipidic metabolism; influencing hepatocytes' ferroptosis, a form of programmed cell death; regulating trimethylamine N-oxide (TMAO) metabolism; and activating platelet function, both recently identified as pathogenetic factors in MASH progression. Moreover, various exogenous factors impact gut microbiota and its involvement in MASLD-related oxidative stress, such as air pollution, physical activity, cigarette smoke, alcohol, and dietary patterns. This manuscript aims to provide a state-of-the-art overview focused on the intricate interplay between gut microbiota, lipid peroxidation, and MASLD pathogenesis, offering insights into potential strategies to prevent disease progression and its associated complications.

Rheumatoid arthritis (RA) and chronic obstructive pulmonary disease (COPD) are prevalent and incapacitating conditions, sharing common pathogenic pathways such as tobacco use and pulmonary inflammation. The influence of respiratory conditions including COPD on RA has been observed, meanwhile RA may constituting one of the risk factors for COPD. It unclear that whether a bidirectional associate between RA and COPD. Our study aims to explore the bidirectional relationship between RA and COPD.

We systematically searched PubMed, Cochrane Library, and Embase for observational studies from the databases inception to February 20, 2024, utilizing medical subject headings (MeSH) and keywords. We included studies in which RA and COPD were studied as either exposure or outcome variables. Statistical analyses were conducted employing STATA software (version 14.0). The relationship was reported as odds ratios (OR) and corresponding 95% confidence intervals (CI). Publication bias was assessed using funnel plots and Egger's regression.

Nineteen studies with 1,549,181 participants were included. Risk of bias varied from low to moderate, with evidence levels rated as low or very low. Pooled analysis revealed a significant association between RA and increased COPD risk (OR=1.41, 95%CI 1.13 to 1.76, I2 = 97.8%, P=0.003). Subgroup analyses showed similar COPD risk elevations in both of genders, seropositive/seronegative RA, cohort and case control studies. Additionally, there was a significant RA risk increase among those with COPD (OR=1.36, 95%CI 1.05 to 1.76, I2 = 55.0%, P=0.022), particularly among females and seropositive RA, and cohort studies.

The meta-analysis identifies a significant bidirectional association between RA and COPD, emphasizing mutually increased risk. Recognizing this connection may can inform proactive approaches to disease prevention and management, potentially reducing the public health burden and improving quality of life.

https://www.crd.york.ac.uk/PROSPERO/, identifier CRD42024518323.

Rosacea can be seen in many patients nowadays, and the related causes are complex. Despite a certain association between smoking and rosacea being reported by several studies, the actual causality has not been established for the possible bias and confounders.

We used Mendelian randomization (MR) to evaluate a potential causal effect of smoking on rosacea risk. Statistics on smoking and rosacea were obtained from the FinnGen project and Neale Lab Consortium. The causal association was assessed by multiple methods including inverse variance weighted (IVW), MR Egger, weighted median, and weighted mode. Furthermore, sensitivity analyses were also conducted to address pleiotropy, along with the leave-one-out method.R version 4.2.3 was applied for the analyses.

The IVW estimation revealed that previous smoking has a deleterious effect on rosacea (odds ratio [OR] = 6.7729, 95% confidence interval [CI] = 1.5691-29.2356, p = 0.0104). By contrast, there was no statistically relationship between current smokers and rosacea (OR = 0.6180, 95% CI = 0.0605-6.3094, p = 0.6847). Results were similar in the analysis based on the weighted median method (previous smoking: OR = 8.6297, 95% CI = 1.0131-73.5071, p = 0.0486; current smoking: OR = 0.2896, 95% CI = 0.0106-7.9132, p = 0.4627). The stability of the causal effect estimates was supported by several sensitivity analyses and the leave-one-out method.

Our MR study found support forrosacea risk and previous smoking. Although no evidence was found to increase the risk of rosacea in current smokers, to prevent various diseases associated with smoking, the public should be encouraged to avoid smoking at the very beginning.

Spondyloarthritis (SpA) is a group of chronic inflammatory diseases affecting the spine and peripheral joints, causing pain, stiffness, and reduced mobility. This narrative review examines how lifestyle factors-specifically smoking, alcohol consumption, and unhealthy diet-contribute to the onset and progression of SpA. It highlights their impact on disease activity, comorbidities, radiographic damage, and treatment response. Therefore, healthcare providers are encouraged to support patients in making personalized lifestyle changes. These findings underscore the importance of a comprehensive approach to SpA management, integrating lifestyle modifications with conventional therapies for optimal disease control and improved outcomes.

Smoking is a significant risk factor for numerous diseases, including coronary artery disease (CAD). Chronic inflammation from smoking affects endothelial function and may alter adipokine secretion, particularly resistin, in perivascular adipose tissue (PVAT). This study investigated the association between resistin concentrations in PVAT and smoking status in CAD patients undergoing coronary artery bypass grafting (CABG).

The study included 110 patients with advanced CAD scheduled for CABG. Patients were categorized into never-smokers and ever-smokers, with the latter further divided into current and past smokers. Resistin concentrations in PVAT and plasma, along with plasma interleukin-6 (IL-6) and high-sensitivity C-reactive protein (hs-CRP) concentrations, were measured using ELISA.

Significant differences in PVAT resistin concentrations were observed between never-smokers and ever-smokers (p < 0.0001), as well as between never-smokers and both current (p < 0.0001) and past smokers (p < 0.0001). PVAT resistin concentrations correlated positively with the number of pack-years (p < 0.0001) and plasma resistin (p < 0.0001) and IL-6 concentrations (p < 0.0001). Plasma resistin, IL-6, and hs-CRP concentrations were higher in ever-smokers compared with never-smokers. Multiple regression analysis indicated that smoking is significantly correlated with higher PVAT resistin concentrations, with increased pack-years (p = 0.0002), higher plasma resistin concentrations (p < 0.0001), and IL-6 concentrations (p < 0.0001), all contributing to elevated PVAT resistin.

Smoking status in advanced CAD patients requiring CABG is positively associated with PVAT resistin concentrations, with a clear demonstration of dose-dependency.

The purpose of this review is to simplify and guide dentists through the main laboratory investigations frequently used in dentistry for diagnosis and patient management. It emphasizes the critical role of laboratory tests in dental practice, highlighting their significance for accurate diagnosis, effective treatment planning, and ongoing monitoring of oral health. Systemic conditions often manifest through oral symptoms, making laboratory assessments essential for identifying undiagnosed health issues that may impact dental treatment outcomes. A comprehensive literature search was conducted using PubMed and Google Scholar to gather relevant studies, ensuring a thorough examination of existing knowledge on the subject. This review defines commonly used laboratory tests, including complete blood count (CBC), coagulation tests, hemoglobin A1c (HbA1c), liver function tests, immunological assays, and microbiological and virological evaluations. Each test provides valuable insights into patient health, aiding in the detection of conditions such as anemia, diabetes, and liver disease, which can complicate dental procedures. By adopting an evidence-based, personalized approach to patient care, dental professionals can enhance safety and treatment success. This article underscores the necessity of integrating laboratory assessments into routine dental practice, promoting a holistic understanding of patient health and improving overall treatment outcomes.

In the last few years, immune checkpoint inhibitors (ICIs) improved treatment strategies for advanced non-small cell lung cancer (NSCLC) with no targetable driver mutations. Empirical evidence strongly suggests that males and females differ in outcomes following the use of ICIs for treatments of solid cancers. Women in fact exhibit greater humoral and cell-mediated immune responses and an even more advanced immune editing which plays an important role in controlling cancer rising and evolution. However, at present, no conclusive studies have addressed differences in response to ICIs regarding sex and, to note, reproductive status in women or autoimmune diseases in both sexes are often not recorded in clinical trials. Consequently, it can be argued that to assess cancer responses and study cancer spread, results of published studies in men may not unconditionally be applied on female patients treated with ICIs, and vice versa. In this chapter have been discussed recent data about gender differences in the immune system and in NSCLC patients treated with ICIs, highlighting sex as a key factor in evaluating different responses in the two sexes.

Autoimmune disorders are characterized by aberrant T cell and B cell reactivity to the body's own components, resulting in tissue destruction and organ dysfunction. Autoimmune diseases affect a wide range of people in many parts of the world and have become one of the major concerns in public health. In recent years, there have been substantial progress in our understanding of the epidemiology, risk factors, pathogenesis and mechanisms of autoimmune diseases. Current approved therapeutic interventions for autoimmune diseases are mainly non-specific immunomodulators and may cause broad immunosuppression that leads to serious adverse effects. To overcome the limitations of immunosuppressive drugs in treating autoimmune diseases, precise and target-specific strategies are urgently needed. To date, significant advances have been made in our understanding of the mechanisms of immune tolerance, offering a new avenue for developing antigen-specific immunotherapies for autoimmune diseases. These antigen-specific approaches have shown great potential in various preclinical animal models and recently been evaluated in clinical trials. This review describes the common epidemiology, clinical manifestation and mechanisms of autoimmune diseases, with a focus on typical autoimmune diseases including multiple sclerosis, type 1 diabetes, rheumatoid arthritis, systemic lupus erythematosus, and sjögren's syndrome. We discuss the current therapeutics developed in this field, highlight the recent advances in the use of nanomaterials and mRNA vaccine techniques to induce antigen-specific immune tolerance.

Cigarette smoking exacerbates respiratory diseases, while plant-derived polyphenols offer antioxidant and anti-inflammatory benefits. This study exploresd the effects of Rhoifolin (ROF), a polyphenol from Jordanian Teucrium polium, on lung health in rats exposed to tobacco smoke. Male rats were divided into two groups: one exposed to cigarette smoke (CS), and the other to ROF treatment alongside smoke exposure (CS/ROF). ROF was administered orally for 21 days before smoke exposure. Results showed smoke-induced lung inflammation and oxidative stress, mitigated by ROF treatment. Histological examination revealed smoke-related morphological changes in lung tissue. ROF treatment reduced oxidative stress and inflammation, as evidenced by decreased proinflammatory cytokines. In silico docking demonstrated ROF's potential as an inhibitor of proinflammatory cytokines. This study demonstrates the therapeutic potential of ROF and similar polyphenols in mitigating the harmful effects of cigarette smoke on lung health.

Systemic Immune-Inflammation Index (SII), calculated by (neutrophils count × platelet count)/lymphocytes count, is a novel index of the local immune response and systemic inflammation response. The SII has been shown to play an important role in the prognosis of many diseases, including cardiovascular diseases, cancer and COPD. However, its role in the prognosis of bronchiectasis remains unclear and requires further investigation. This study aimed to investigate the association between SII and readmissions in patients with acute exacerbations of bronchiectasis.

We conducted a retrospective cohort study of all bronchiectasis patients admitted to the respiratory ward in Beijing Chaoyang Hospital from January 2020 to January 2022. Patients were classified into four groups according to the quartiles of log2(SII) at admission. The primary endpoint was readmission at 1-year follow up. Univariate and multivariate cox regression models were applied to investigate the relationship between SII and readmissions at 1-year follow up in patients with bronchiectasis.

A total of 521 patients were included in our study. The median (IQR) SII at admission were 506.10 (564.84). Patients with higher SII tended to be older, male, past and current smokers, have lower BMI, and more dyspnea symptoms. They also had higher inflammatory markers and received a greater spectrum of antibiotics and more intravenous glucocorticoids. Higher SII at admission were independently associated with readmission in patients with acute exacerbations for bronchiectasis following confounder adjustment (OR =1.007; 95% CI, 1.003-1.011; p <0.001).

Patients with elevated SII levels were typically older males, often smokers, with lower BMI and increased dyspnea. They received more antibiotics and intravenous glucocorticoids. Higher SII at admission are associated with readmission in patients with acute exacerbations of bronchiectasis. SII has potential clinical value as a predictive biomarker for clinical outcomes in bronchiectasis, offering a valuable tool for management strategies.

Despite the protective nature of the blood-brain barrier (BBB) and brain-protecting tissues, some types of CNS injury or stress can cause cerebral cytokine production and profound alterations in brain function. Neuroinflammation, which can also be accompanied by increased cerebral cytokine production, has a remarkable impact on the pathogenesis of many neurological illnesses, including loss of BBB integrity and ischemic stroke, yet effective treatment choices for these diseases are currently lacking. Although little is known about the brain effects of Metformin (MF), a commonly prescribed first-line antidiabetic drug, prior research suggested that it may be useful in preventing BBB deterioration and the increased risk of stroke caused by tobacco smoking (TS). Therefore, reducing neuroinflammation by escalating anti-inflammatory cytokine production and declining pro-inflammatory cytokine production could prove an effective therapeutic strategy for ischemic stroke. Hence, the current investigation was planned to explore the potential role of MF against stroke and TS-induced neuroinflammation and reactive oxygen species (ROS) production. Our studies revealed that MF suppressed releasing pro-inflammatory mediators like tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) by aiming at the nuclear factor kappa B (NF-κB) signaling pathway in primary neurons and astrocytes. MF also upregulated anti-inflammatory mediators, like interleukin-10 (IL-10), and interleukin-4 (IL-4), by upregulating the Nrf2-ARE signaling pathway. Adolescent mice receiving MF along with TS exposure also showed a notable decrease in NF-κB expression compared to the mice not treated with MF and significantly decreased the level of TNF-α, IL-1β, MCP-1, and MIP-2 and increased the levels of IL-10 and IL-4 through the activation of Nrf2-ARE signaling pathway. These results suggest that MF has anti-neuroinflammatory effects via inhibiting NF-κB signaling by activating Nrf2-ARE. These studies support that MF could be a strong candidate drug for treating and or preventing TS-induced neuroinflammation and ischemic stroke.

Earlier studies suggested a potential association between tobacco smoking and nickel sensitization, but little is known about other contact allergens.

To investigate the association of smoking status and contact sensitizations as well as subtypes of dermatitis, and to analyse the sensitization profiles of tobacco smokers.

Within the Information Network of Departments of Dermatology (IVDK), we performed a cross-sectional multicentre pilot study comprising 1091 patch-tested patients from 9 departments, comparing 541 patients with a history of cigarette smoking (281 current and 260 former smokers) with 550 never-smokers.

We could not confirm the previously reported association between nickel sensitization and tobacco smoking. Moreover, sensitizations to other allergens, including colophony, fragrance mix I, Myroxylon pereirae and formaldehyde, were not increased in cigarette smokers compared with never smokers. Hand dermatitis (50.6% vs. 33.6%) and occupational cause (36.2% vs. 22.5%) were significantly more frequent among cigarette smokers compared with never-smokers as shown by non-overlapping 95% confidence intervals.

Although our study does not allow a firm conclusion on whether smoking status contributes to certain contact sensitizations, it confirms an association of smoking with hand dermatitis and occupational cause.

The prevalence and disease burden of chronic inflammatory diseases (CIDs) are predicted to rise. Patients are commonly treated with biological agents, but the individual treatment responses vary, warranting further research into optimizing treatment strategies. This study aimed to compare the clinical treatment responses in patients with CIDs initiating biologic therapy based on smoking status, a notorious risk factor in CIDs. In this multicentre cohort study including 233 patients with a diagnosis of Crohn's disease, ulcerative colitis, rheumatoid arthritis, axial spondyloarthritis, psoriatic arthritis or psoriasis initiating biologic therapy, we compared treatment response rates after 14 to 16 weeks and secondary outcomes between smokers and non-smokers. We evaluated the contrast between groups using logistic regression models: (i) a "crude" model, only adjusted for the CID type, and (ii) an adjusted model (including sex and age). Among the 205 patients eligible for this study, 53 (26%) were smokers. The treatment response rate among smokers (n = 23 [43%]) was lower compared to the non-smoking CID population (n = 92 [61%]), corresponding to a "crude" OR of 0.51 (95% CI: [0.26;1.01]) while adjusting for sex and age resulted in consistent findings: 0.51 [0.26;1.02]. The contrast was apparently most prominent among the 38 RA patients, with significantly lower treatment response rates for smokers in both the "crude" and adjusted models (adjusted OR 0.13, [0.02;0.81]). Despite a significant risk of residual confounding, patients with CIDs (rheumatoid arthritis in particular) should be informed that smoking probably lowers the odds of responding sufficiently to biological therapy. Registration: Clinical.Trials.gov NCT03173144.

Rheumatoid arthritis (RA) is considered a multifactorial condition where interaction between the genetic and environmental factors lead to immune dysregulation causing autoreactivity. While among the various genetic factors, HLA-DR4 and DQ8, have been reported to be the strongest risk factors, the role of various environmental factors has been unclear. Though events initiating autoreactivity remain unknown, a mucosal origin of RA has gained attention based on the recent observations with the gut dysbiosis in patients. However, causality of gut dysbiosis has been difficult to prove in humans. Mouse models, especially mice expressing RA-susceptible and -resistant HLA class II genes have helped unravel the complex interactions between genetic factors and gut microbiome. This review describes the interactions between HLA genes and gut dysbiosis in sex-biased preclinical autoreactivity and discusses the potential use of endogenous commensals as indicators of treatment efficacy as well as therapeutic tool to suppress pro-inflammatory response in rheumatoid arthritis.

Sexual minorities (SMs; e.g., lesbian, gay, bisexual, and other non-heterosexual individuals) are more likely to be current alcohol drinkers than their heterosexual peers while separately experiencing elevated inflammation. Yet, little research has assessed the association between alcohol use and inflammation among subgroups of SMs, let alone potential differences among people with multiple marginal identities (e.g., race/ethnicity and sexual identity). Data came from the National Health and Nutrition Survey 2015-2016. Survey-weighted multivariable linear regression analysis was used to assess the relationship between alcohol use categories, heavy episodic drinking, and log-CRP (C-reactive protein). Models were stratified by sexual identity to determine whether associations between alcohol use and inflammation or between race/ethnicity and inflammation differed by sexual identity. Among 3220 participants, 1000 (36.8%) reported light alcohol use, 870 (32.0%) reported moderate use, and 483 (17.8%) reported heavy use. Mean raw CRP was 4.1 mg/L (SD = 8.1). The association between race/ethnicity and CRP differed in stratified relative to non-stratified models with key differences in CRP among individuals with multiple marginalized identities. We also observed that while the "classic" J-shaped relationship between alcohol use and systemic inflammation persists among heterosexuals in this sample, it does not hold among subgroups of sexual minorities. In particular, bisexuals who report heavy alcohol use, compared to non-users, experience significantly elevated CRP. Finally, we did not observe any association between heavy episodic drinking and CRP among subgroups of sexual minorities. Future studies assessing alcohol and biomarker data need to strive to include subgroups of sexual minorities and people with multiple marginal identities to better target behavioral and biomedical interventions aimed at reducing health disparities.

Nausea and vomiting in pregnancy (NVP) have been proposed to have a prophylactic function. In this review, I re-examine NVP from an evolutionary perspective in light of new research on NVP. First, current evidence suggests that the observed characteristics of NVP does not align well with a prophylactic function. Further, NVP is typically associated with high costs for pregnant women, while moderate-to-severe NVP is associated with increased risks of poorer foetal/birth outcomes. In contrast, mild NVP limited to early pregnancy may associate with improved foetal outcomes-indicating a potential evolutionary benefit. Second, researchers have recently identified growth differentiation factor 15 (GDF15) to cause NVP, with implications that low-levels of pre-conception GDF15 (associated with lower cellular stress/inflammation) may increase risks/symptoms of NVP. If so, NVP in contemporary post-industrialized populations may be more severe due to environmental mismatch, and the current symptomology of NVP in such populations should not be viewed as a typical experience of pregnancy.

Observational studies have indicated a link between autoimmune liver diseases (AILD) and chronic hepatitis B (CHB) through observational studies. The association between AILD and CHB remains indeterminate.

A two-sample Mendelian randomization (MR) analysis was conducted to scrutinize the causal nexus between AILD and CHB utilizing summary statistics derived from extensive genome-wide association studies (GWASs) in European populations. The primary statistical methodology employed was the inverse variance-weighted (IVW) method to deduce the causal connection of AILD on CHB. This study incorporated primary biliary cholangitis (PBC), primary sclerosing cholangitis (PSC), and autoimmune hepatitis (AIH) as subtypes of AILD. Additionally, we conducted a multivariable MR (MVMR) analysis to account for the potential confounding effects of smoking, alcohol consumption, body mass index (BMI), and some autoimmune diseases.

Our MR investigation encompassed a cohort of 725,816 individuals. The MR analysis revealed that genetically predicted PSC significantly correlated with a reduced risk of CHB (IVW OR = 0.857; 95%CI: 0.770-0.953, P = 0.005). Conversely, the reverse MR analysis suggested that genetic susceptibility to PSC might not modify the risk of CHB (IVW OR = 1.004; 95% CI: 0.958-1.053, P = 0.866). Genetically proxied PBC and AIH exhibited no discernible causal association with CHB in the MR analysis using the IVW method (P = 0.583; P = 0.425). The MVMR analysis still indicated a decreased risk of CHB associated with PSC (OR = 0.853, P = 0.003).

Our study elucidates a causal relationship between PSC and a diminished risk of CHB.

Surgical excision of the primary tumor represents the most frequent and curative procedure for solid malignancies. Compelling evidence suggests that, despite its beneficial effects, surgery may impair immunosurveillance by triggering an immunosuppressive inflammatory stress response and favor recurrence by stimulating minimal residual disease. In addition, many factors interfere with the immune effectors before and after cancer procedures, such as malnutrition, anemia, or subsequent transfusion. Thus, the perioperative period plays a key role in determining oncological outcomes and represents a short phase to circumvent anesthetic and surgical deleterious factors by supporting the immune system through the use of synergistic pharmacological and non-pharmacological approaches. In line with this, accumulating studies indicate that anesthetic agents could drive both protumor or antitumor signaling pathways during or after cancer surgery. While preclinical investigations focusing on anesthetics' impact on the behavior of cancer cells are quite convincing, limited clinical trials studying the consequences on survival and recurrences remain inconclusive. Herein, we highlight the main factors occurring during the perioperative period of cancer surgery and their potential impact on immunomodulation and cancer progression. We also discuss patient management prior to and during surgery, taking into consideration the latest advances in the literature.

The therapeutic effectiveness of immune checkpoint inhibitors (ICIs) in bladder cancer varies among individuals. Identifying reliable predictors of response to these therapies is crucial for optimizing patient outcomes.

This retrospective study analyzed 348 bladder cancer patients treated with ICIs, with additional validation using data from 248 patients at our institution who underwent PD-L1 immunohistochemical staining. We examined patient smoking history, clinicopathological characteristics, and immune phenotypes. The main focus was the correlation between smoking history and immunotherapy outcomes. Multivariate logistic and Cox proportional hazard regressions were used to adjust for confounders.

The study cohort comprised 348 bladder cancer patients receiving ICIs. Among them, 116 (33.3%) were never smokers, 197 (56.6%) were former smokers (median pack-years = 28), and 35 (10.1%) were current smokers (median pack-years = 40). Analysis revealed no statistically significant difference in overall survival across different smoking statuses (objective response rates were 11.4% for current smokers, 17.2% for never smokers, and 22.3% for former smokers; P = 0.142, 0.410, and 0.281, respectively). However, a notable trend indicated a potentially better response to immunotherapy in former smokers compared to current and never smokers. In the validation cohort of 248 patients from our institution, immunohistochemical analysis showed that PD-L1 expression was significantly higher in former smokers (55%) compared to current smokers (37%) and never smokers (47%). This observation underscores the potential influence of smoking history on the tumor microenvironment and its responsiveness to ICIs.

In conclusion, our study demonstrates the importance of incorporating smoking history in predicting the response to immunotherapy in bladder cancer patients, highlighting its role in personalized cancer treatment approaches. Further research is suggested to explore the comprehensive impact of lifestyle factors on treatment outcomes.

Despite the success of antiretroviral therapy (ART), people living with HIV (PLWH) suffer from a high burden of pulmonary diseases, even after accounting for their smoking status. Cytotoxic CD8 T-cells are likely implicated in this phenomenon and may act as a double-edged sword. While being essential in viral infection control, their hyperactivation can also contribute to lung mucosal tissue damage. The effects of HIV and smoking on pulmonary mucosal CD8 T-cell dynamics has been a neglected area of research, which we address herein.

Bronchoalveolar lavage (BAL) fluid were obtained from ART-treated PLWH (median duration of supressed viral load: 9 years; smokers: n = 14; non-smokers: n = 21) and HIV-uninfected controls (smokers: n = 11; non-smokers: n = 20) without any respiratory symptoms or active infection. Lymphocytes were isolated and CD8 T-cell subsets and homing markers were characterized by multiparametric flow cytometry.

Both smoking and HIV infection were independently associated with a significant increase in frequencies of total pulmonary mucosal CD8 T-cell. BAL CD8 T-cells were primarily CD69 + expressing CD103 and/or CD49a, at least one of the two granzymes (GzmA/GzmB), and little Perforin. Higher expression levels of CD103, CD69, and GzmB were observed in smokers versus non-smokers. The ex vivo phenotype of GzmA + and GzmB + cells revealed increased expression of CD103 and CXCR6 in smokers, while PLWH displayed elevated levels of CX3CR1 compared to controls.

Smoking and HIV could promote cytotoxic CD8 T-cell retention in small airways through different mechanisms. Smoking likely increases recruitment and retention of GzmB + CD8 Trm via CXCR6 and CD103. Heightened CX3CR1 expression could be associated with CD8 non-Trm recruitment from the periphery in PLWH.

Exposure to cigarette smoke directly damages the lungs and causes lung inflammation. The anti-inflammatory properties of edible bird's nest (EBN) have been reported. We aimed to determine the effect of EBN on pneumonia in a mouse model exposed to cigarette smoke. Fifty BALB/c mice were randomly divided into control, model, positive drug, low-dose EBN, and high-dose EBN groups (n = 10 each). Except for the control group, the mice in each group were exposed to four cigarettes once a day for 8 days. In addition, we validated the effects of EBN on A549 cells and investigated the mechanism by which EBN alleviates lung inflammation. Edible bird's nest (EBN) could alleviate the structural damage of lung tissue and the smoke-induced inflammatory response in mice. The best effect was observed at the high dose of EBN (0.019 g). The mice treated with EBN had a stronger ability than those in the model group to resist cigarette smoke stimulation, as indicated by a decrease in serum and lung inflammatory markers (interleukin 6 [IL-6], tumor necrosis factor-α [TNF-α], and interleukin 8 [IL-8]), an increase in serum interleukin 10 (IL-10) levels, and a decrease in the expression of inflammasome NOD-like receptor pyrin 3 (NLRP3). In addition, our cell experiments showed that EBN attenuated cigarette smoke-induced pulmonary inflammation mainly by inhibiting the tumor necrosis factor receptor 1 (TNFR1)/nuclear factor-kappa B (NF-κB)/NLRP3 pathway. These findings provide theoretical evidence for the positive nutritional qualities of EBN for the lung by demonstrating that it inhibits the TNFR1/NF-κB/NLRP3 signaling pathway, which prevents the development of cigarette smoke-induced pulmonary inflammation.

Graves' disease (GD) is the most common cause of hyperthyroidism while Hashimoto or autoimmune thyroiditis is the most common cause of hypothyroidism. Spontaneous hypothyroidism may develop after successful medical treatment of GD in up to 20% of cases. This report presents a gentleman who is a known smoker and was diagnosed with GD at the age of 64 years. He was counseled about smoking cessation and started with medical treatment using carbimazole (CBZ). He was adequately controlled using medical treatment, yet he continued to smoke. After 2 years of medical treatment, CBZ was stopped due to developing hypothyroidism on the minimum dose of treatment. Celebrating the discontinuation of treatment, the patient decided to quit smoking. One month later, he was euthyroid; however, 4 months later, he developed overt hypothyroidism. He received levothyroxine replacement therapy and titrated to achieve euthyroidism and remained on levothyroxine for more than 5 years. The possibility that quitting smoking may have triggered the development of hypothyroidism was raised due to the coincidence of developing hypothyroidism only 4 months after quitting smoking. Current smoking is associated with a higher risk of developing both GD and Graves' orbitopathy. Quitting smoking is associated with a higher risk of developing new-onset thyroid autoimmunity. Quitting smoking is also associated with a sevenfold higher risk of autoimmune hypothyroidism especially in the first year of smoking cessation. Involved mechanisms may include a sudden increase in oxidative stress, a sudden increase in iodide delivery to thyroid follicles, or promoting T-helper 1-mediated autoimmune thyroiditis after quitting smoking. The present case suggests that quitting smoking may be a triggering factor for the development of hypothyroidism following successful medical treatment of GD, a phenomenon that may affect one-fifth of GD patients without previously reported triggers.

The detrimental effects of smoking are multisystemic and its effects on the eye health are significant. Smoking is a strong risk factor for age-related nuclear cataract, age-related macular degeneration, glaucoma, delayed corneal epithelial healing and increased risk of cystoid macular edema in patients with intermediate uveitis among others. We aimed to characterize the aqueous humor (AH) proteome in chronic smokers to gain insight into its perturbations and to identify potential biomarkers for smoking-associated ocular pathologies. Compared to the control group, chronic smokers displayed 67 (37 upregulated, 30 downregulated) differentially expressed proteins (DEPs). Analysis of DEPs from the biological point of view revealed that they were proteins involved in complement activation, lymphocyte mediated immunity, innate immune response, cellular oxidant detoxification, bicarbonate transport and platelet degranulation. From the molecular function point of view, DEPs were involved in oxygen binding, oxygen carrier activity, hemoglobin binding, peptidase/endopeptidase/cysteine-type endopeptidase inhibitory activity. Several of the upregulated proteins were acute phase reactant proteins such as clusterin, alpha-2-HS-glycoprotein, fibrinogen, alpha-1-antitrypsin, C4b-binding protein and serum amyloid A-2. Further research should confirm if these proteins might serve as biomarkers or therapeutic target for smoking-associated ocular diseases.

Inflamm-aging is associated with the rate of aging and is significantly related to diseases such as Alzheimer's disease, Parkinson's disease, atherosclerosis, heart disease, and age-related degenerative diseases such as type II diabetes and osteoporosis. This study aims to evaluate the safety and efficiency of autologous adipose tissue-derived mesenchymal stem cell (AD-MSC) transplantation in aging-related low-grade inflammation patients.

This study is a single-group, open-label, phase I clinical trial in which patients treated with 2 infusions (100 million cells i.v) of autologous AD-MSCs were initially evaluated in 12 inflamm-aging patients who concurrently had highly proinflammatory cytokines and 2 of the following 3 diseases: diabetes, dyslipidemia, and obesity. The treatment effects were evaluated based on plasma cytokines.

During the study's follow-up period, no adverse effects were observed in AD-MSC injection patients. Compared to baseline (D-44), the inflammatory cytokines IL-1α, IL-1β, IL-8, IL-6, and TNF-α were significantly reduced after 180 days (D180) of MSC infusion. IL-4/IL-10 at 90 days (D90) and IL-2/IL-10 at D180 increased, reversing the imbalance between proinflammatory and inflammatory ratios in the patients.

AD-MSCs represent a potential intervention to prevent age-related inflammation in patients.

ClinicalTrials.gov number is NCT05827757, first registered on 13th Oct 2020.

Active smoking is a well-established risk factor for developing Crohn's disease (CD) and negatively impacts overall disease progression. Patients who start or continue smoking after CD diagnosis are at risk for poor outcomes, higher therapeutic requirements, and have higher rates of relapse. However, it remains unclear if the exposure to smoking leads to increased sequencing through treatment therapies, especially biologics.

The Study of Prospective Adult Research Cohort with IBD (SPARC IBD) registry has been collecting patient-reported outcomes data in real-time, as well as laboratory, endoscopic, and pathologic samples from 17 tertiary referral centers since 2016. In this study, we conducted a retrospective review of the SPARC clinical registry collected between December 2016 and January 2021 from 1 participating site, the University of Maryland School of Medicine's Inflammatory Bowel Disease Program. A total of 619 patients were enrolled in the SPARC IBD database. Four hundred twenty-five patients with CD were included for initial review of completeness of data; of these, 144 patients were excluded due to missing data on smoking status and/or biologic treatment, resulting in a final cohort of 281 patients. We collected and analyzed baseline demographic and clinical characteristics. The final cohort was categorized into 3 exposure groups: current, former, and never smokers. Our outcome of interest was number biologics used, categorized into 3 groups: 0, 1, or ≥2 biologics.

One hundred seventy-two never smokers, 70 former smokers, and 39 current smokers were identified. Current, former, and never smokers had no statistically significant differences in number of biologics used (ie, biologic sequencing). However, statistically significant independent risk factors for increased sequencing of biologics were identified. These risk factors included female sex, ileocolonic disease location, younger age at diagnosis, and prolonged disease duration; none of these factors remained significant in adjusted analyses.

To date, this is the first study assessing the association of smoking and sequencing of biologics. Although current or former smokers were not found to sequence through more biologics when compared with never smokers, smoking is a well-established risk factor for poor health outcomes, and efforts should be made to counsel patients to quit. Further, additional research must be done to stratify risk to patients based on amount of tobacco exposure.

To compare presence and levels of serum cytokines in smokers and non-smokers with periodontitis following periodontal therapy.

Thirty heavy smokers and 30 non-smokers with stage III or IV periodontitis were included in this prospective cohort study. Clinical data and blood serum were collected at baseline (T0), after step I-III (T1), and after 12 months step IV periodontal therapy (T2). Cytokine IL-1β, IL-6, IL-8, TNF-α, IL-10, and IP-10 levels were measured using multiplex kit Bio-Plex Human Pro™ Assay. Linear regression models with cluster robust variance estimates to adjust for repeated observations were used to test intra- and intergroup levels for each marker, IL-6 and IL-8 defined as primary outcomes.

Clinical outcomes improved in both groups following therapy (p < 0.05). IL-6 levels increased with 75.0% from T0-T2 among smokers (p = 0.004). No significant intra- or intergroup differences were observed for IL-8. Higher levels of TNF-α (44.1%) and IL-10 (50.6%) were detected in smokers compared with non-smokers at T1 (p = 0.007 and p = 0.037, respectively). From T1-T2, differences in mean change over time for levels of TNF-α and IL-10 were observed in smokers compared with non-smokers (p = 0.005 and p = 0.008, respectively).

Upregulated levels of serum cytokines in smokers indicate a systemic effect of smoking following periodontal therapy. Differences in cytokine levels between smokers and non-smokers demonstrate a smoking induced modulation of specific systemic immunological responses in patients with severe periodontitis.

Smoking history is a heterogeneous situation for different populations, and numerous studies suggest that smoking cessation is conducive to reduce the mortality of lung cancer. However, no quantitative meta-analysis regarding smoking cessation duration based on different populations has demonstrated it clearly.

We systematically searched four electronic databases (PubMed, Embase, the Cochrane Central Register of Controlled Trials, and Scoups) till February 2023. Eligible studies reported the association between lung cancer survival and duration of smoking cessation. Additionally, we stratified the study population according to whether they had lung cancer at the time they quit smoking. Studies were pooled with the random-effects model.

Out of the 11,361 potential studies initially identified, we included 24 studies involving 969,560 individuals in our analysis. Lung cancer mortality varied across two groups: general quitters and peri-diagnosis quitters. For general quitters, those who had quit smoking for less than 10 years exhibited an RR of 0.64 (95% CI [0.55-0.76]), while those who quit for 10-20 years had an RR of 0.33 (0.25-0.43), over 20 years had an RR of 0.16 (0.11-0.24), and never-smokers had an RR at 0.11 (0.07-0.15). Among peri-diagnosis quitters, the 1-year Overall Survival (OS) showed an RR of 0.80 (0.67-0.96), the 2-year OS had an RR of 0.89 (0.80-0.98), the 3-year OS had an RR of 0.93 (0.84-1.03), and the 5-year OS had an RR of 0.85 (0.76-0.96).

Earlier and longer smoking cessation is associated with reduced lung cancer mortality, no matter in which cessation stage for two different populations.

Secondary metabolites from medicinal plants have a well-established therapeutic potential, with many of these chemicals having specialized medical uses. Isoflavonoids, a type of secondary metabolite, have little cytotoxicity against healthy human cells, making them interesting candidates for cancer treatment. Extensive research has been conducted to investigate the chemo-preventive benefits of flavonoids in treating various cancers. Biochanin A (BA), an isoflavonoid abundant in plants such as red clover, soy, peanuts, and chickpeas, was the subject of our present study. This study aimed to determine how BA affected glucose-6-phosphate dehydrogenase (G6PD) in human lung cancer cells. The study provides meaningful insight and a significant impact of BA on the association between metastasis, inflammation, and G6PD inhibition in A549 cells. Comprehensive in vitro tests revealed that BA has anti-inflammatory effects. Molecular docking experiments shed light on BA's high binding affinity for the G6PD receptor. BA substantially decreased the expression of G6PD and other inflammatory and metastasis-related markers. In conclusion, our findings highlight the potential of BA as a therapeutic agent in cancer treatment, specifically by targeting G6PD and related pathways. BA's varied effects, which range from anti-inflammatory capabilities to metastasis reduction, make it an appealing option for future investigation in the development of new cancer therapeutics.

To investigate the impact of smoking on clinical outcomes after repair of supraspinatus tendon in patients who had an intact repair found on postoperative magnetic resonance imaging.

Patients who received primary complete repair of supraspinatus tendon tear between 2014 and 2020 were retrospectively identified. Patients were excluded if a postoperative magnetic resonance imaging scan was not available or if the follow-up was less than 2 years. Visual analog score (VAS), American Shoulder and Elbow Surgeons (ASES) score, and active forward flexion were assessed at the 2-year follow-up. The percentage of patients acquiring minimal clinically important difference (MCID) was reported.

One hundred primary supraspinatus tendon repairs were included. The healing rate was 77% in smokers and 90% in nonsmokers. Smoking was the independent predictor of a poorer 2-year VAS (P < .001) and ASES (P < .001) scores. Significant improvement in clinical outcomes was observed between preoperation and the 2-year follow-up, regardless of the integrity of the repair or smoking status (P < .001). When the repaired tendon was intact, nonsmokers had a greater chance of achieving MCID in 2-year VAS and ASES scores than smokers. Ninety-nine percent of nonsmokers, compared with 82% of smokers, achieved MCID in VAS at the 2-year follow-up (P = .023). The corresponding figures for ASES were 98% and 71%, respectively (P = .004).

In this study, smoking was associated with poorer clinical outcomes, including a greater 2-year VAS pain score and a lower 2-year ASES score, when compared with nonsmokers, even in cases in which there was no full-thickness retear of the repaired supraspinatus tendon.

Level III, retrospective cohort study.