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Introduction Interactions have been demonstrated between cigarette smoking (CS) and occupational exposures to several particles. This study tested the postulate that CS interacts with coal mine dust exposure to impact and change radiological and histological endpoints of coal mine dust lung disease. Methods A retrospective evaluation of coalminers with a high-resolution computed tomography (HRCT) of the chest was conducted at West Virginia University Hospital (2015- 2022). There was a consensus review of both radiology and histology findings and their comparative analysis with a non-miner surgical resection cohort collected from thoracic oncology clinic. Results The study cohort (n=556) was divided into groups: coal-/smoking- (8.3%), coal-/smoking+ (26.6%), coal+/smoking- (22.3%), and coal+/smoking+ (42.8%). Miners were older males with a median duration of coal mine work (CMW) of 30-years. Ever-smokers (66% of miner cohort and 76% of non-miner cohort) smoked 35 and 28 composite pack years (CPY) respectively, where miners had greater intensity of smoking (22 vs 18 cigarettes/day) compared to non-miners. On HRCT, 1/3 rd and 1/5 th of miners had simple and complicated coal workers’ pneumoconiosis (sCWP and cCWP), respectively. 35% of ever-smoking miners had radiologic patterns for probable usual interstitial pneumonitis, nonspecific interstitial pneumonitis, desquamative interstitial pneumonitis, and combined pulmonary fibrosis and emphysema. Radiologically, both coal-/smoking+ and coal+/smoking+ showed excessive emphysema (70-80%). Histologically, miners had more fibrosis (47% and 50% in coal+/smoking- and coal+/smoking+ vs. 11% and 28% in coal-/smoking- and coal-/smoking+). Never-smoking miners demonstrated more histological evidence of CWP than ever-smokers (60% and 27%); in addition, they had radiologic and histologic emphysema (30%), radiologic interstitial lung disease (ILD) (14.5%) and histologic evidence of fibrosis (47%). Ever-smokers demonstrated histologic emphysema more frequently (33% and 67% in coal+/smoking- and coal+/smoking+ vs. 24% and 72% in coal-/smoking- and coal-/smoking+). Logistic regression modeling showed the following associations: radiologic and histologic emphysema with CPY; histologic fibrosis, any ILD (not including RB-ILD), CPFE and anthracosis with both CPY and CMW; radiologic RB-ILD inclusive of small-opacities, cCWP with both CMW and silica; and sCWP and pulmonary artery dilation with CMW. Interestingly, CPY≥30 negatively correlated with radiologic cCWP and histologic CWP. Mortality was increased in smokers (14% and 29% in coal+/smoking- and coal+/smoking+ vs. 4% and 20% in coal-/smoking- and coal-/smoking+) with predictors being radiologic ILD, histologic CWP, and related co-morbid diseases including COPD, chronic kidney disease, and gastroesophageal reflux. Conclusion CS demonstrated a major impact on miners’ health including changing radiologic and histologic endpoints of interstitial lung diseases and emphysema.

Background The acquisition of resistance to chemotherapy is a major hurdle in the successful application of cancer therapy. Several anticancer approaches, including chemotherapies, radiotherapy, surgery and targeted therapies are being employed for the treatment of cancer. However, cancer cells reprogram themselves in multiple ways to evade the effect of these therapies, and over a period of time, the drug becomes inactive due to the development of multi‐drug resistance (MDR). MDR is a complex phenomenon where malignant cells become insensitive to anticancer drugs and attain the ability to survive even after several exposures of anticancer drugs. In this review, we have discussed the molecular and cellular paradigms of multidrug resistance in cancer. Recent Findings An Extensive research in cancer biology revealed that drug resistance in cancer is the result of perpetuated intracellular and extracellular mechanisms such as drug efflux, drug inactivation, drug target alteration, oncogenic mutations, altered DNA damage repair mechanism, inhibition of programmed cell death signaling, metabolic reprogramming, epithelial mesenchymal transition (EMT), inherent cell heterogeneity, epigenetic changes, redox imbalance, or any combination of these mechanisms. An inevitable cross‐link between inflammation and drug resistance has been discussed. This review provided insight molecular mechanism to understand the vulnerabilities of cancer cells to develop drug resistance. Conclusion MDR is an outcome of interplays between multiple intricate pathways responsible for the inactivation of drug and development of resistance. MDR is a major obstacle in regimens of successful application of anti‐cancer therapy. An improved understanding of the molecular mechanism of multi drug resistance and cellular reprogramming can provide a promising opportunity to combat drug resistance in cancer and intensify anti‐cancer therapy for the upcoming future.

Abstract Context Sex differences exist in heart failure (HF) phenotypes, but there is limited research on the role of sex hormones in HF and its subtypes. Objective To examine the associations of total testosterone, dehydroepiandrosterone sulfate (DHEA-S), and sex hormone-binding globulin (SHBG) with incident HF, HF with preserved ejection fraction (HFpEF), and HF with reduced ejection fraction (HFrEF). Design Atherosclerosis Risk in Communities (ARIC) study (prospective cohort study). Median follow-up is 19.2 years. Setting General community. Participants 4107 men and 4839 postmenopausal women, with mean age of 63.2 (standard deviation [SD] 5.7) and 62.8 (5.5) years, respectively. Exposure Plasma sex hormone levels were measured at visit 4 (1996-1998). Main Outcome Measures Incident HF events were identified through hospital discharge codes and death certificates. Results The Hazard Ratios for HF associated with 1 SD decrease in log-transformed total testosterone, DHEA-S, and SHBG were 1.10 (95% confidence interval 1.03, 1.17), 1.07 (1.00, 1.15), and 1.04 (0.96, 1.11) in men, and 1.05 (0.99, 1.13), 1.17 (1.09, 1.24), and 0.93 (0.85, 1.01) in women, respectively. The associations between sex hormones with subtypes of HF had similar patterns but were attenuated and became statistically insignificant. Conclusion In this prospective cohort, lower levels of endogenous testosterone and DHEA-S in men and DHEA-S in postmenopausal women were associated with the development of HF. Similar directions of association in both sexes and both HF subtypes suggest that sex hormones play a role in the development of HF through common pathways regardless of sex.

Sex hormones may influence sex differences in cardiovascular disease (CVD). N-terminal pro-B-type natriuretic peptide (NT-proBNP), a predictor of CVD, is higher in women than men, which may relate to sex hormones. To evaluate whether total testosterone (T), bioavailable T, free T, estradiol, dehydroepiandrosterone (DHEA), and SHBG are associated with NT-proBNP. Cohort study. Cross-sectional sample included 2371 postmenopausal women and 2688 men free of CVD, of which 2041 women and 2348 men were included longitudinally. NT-proBNP at baseline (2000 to 2002) and one or more repeat NT-proBNPs (through 2012). Analyses adjusted for CVD risk factors. Women had higher NT-proBNP than men (median 79.9 vs 38.5 pg/mL). Cross-sectionally, higher bioavailable T, free T, DHEA, and lower SHBG levels were independently associated with lower NT-proBNP among both women and men (all P < 0.05). Higher total T in women and estradiol in men were also associated with lower NT-proBNP (both P < 0.05). Longitudinally, in women, higher total T, bioavailable T, free T, DHEA, and lower estradiol and SHBG were associated with greater 10-year increase in NT-proBNP (all P < 0.05). In men, higher free T and estradiol were associated with greater NT-proBNP increase (both P < 0.05). A more androgenic sex hormone pattern was inversely associated with NT-proBNP cross-sectionally and may contribute to sex differences in NT-proBNP. Longitudinally, a more androgenic sex hormone pattern was associated with greater increase in NT-proBNP in women, which may reflect a mechanism for CVD risk after menopause.

Aims Visceral adipose tissue (AT) promotes inflammation and may be associated with disease progression in heart failure with preserved ejection fraction (HFpEF). We characterized regional AT distribution in HFpEF patients and controls and analysed associations with co‐morbidities and exercise tolerance. Methods and results Magnetic resonance imaging was performed to quantify epicardial, liver, abdominal, and thigh skeletal muscle AT. We assessed New York Heart Association (NYHA) class, 6 min walk distance, and global well‐being score. Multivariable linear regression models adjusting for body surface area were used. We studied 55 HFpEF patients (41 women, mean age 67 ± 11 years) and 33 controls (21 women, mean age 57 ± 10 years). Epicardial AT (median [interquartile range] 4.6 [2.0] vs. 3.2 [1.4] mm, P < 0.001), thigh intermuscular fat (11.0 [11.5] vs. 5.0 [2.7] cm2, P < 0.001) and liver fat fraction (6.4% [6.1] vs. 4.1% [5.5], P = 0.001) were higher in HFpEF patients than controls. Women with HFpEF had higher abdominal and thigh subcutaneous AT than men. Greater thigh intermuscular fat was associated with higher blood pressure (β [SE] 0.73 [0.17], P < 0.001) and diabetes (odds ratio [95% confidence interval] 1.2 [1.0–1.5], P = 0.03). Greater thigh intramuscular fat was associated with both worse NYHA class (β [SE] 2.7 [1.0], P = 0.01) and shorter 6 min walk distance (β [SE] −4.1 [1.9], P = 0.03), and greater epicardial AT (β [SE] −0.2 [0.1], P < 0.001) and liver fat fraction (β [SE] −0.4 [0.2], P = 0.04) were associated with lower global well‐being score. Conclusions Heart failure with preserved ejection fraction patients have increased epicardial, liver, and skeletal muscle fat compared with controls out of proportion to their increased body size, and adiposity was associated with worse NYHA class and exercise tolerance in HFpEF. These results provide the basis for further investigation into the effect of interventions to reduce regional AT distribution in relation to HFpEF symptoms and pathophysiology.

The rising prevalence of colorectal cancer (CRC) may be attributed to various nutritional and behavioural factors, making both factors as important topics for discussion to the layman and the oncology community. To explore additional dietary risk factors, other than those already known, according to the Ayurvedic perspective in CRC patients. Detail dietary data was collected from 420 patients of CRC and 116 healthy volunteers registered at our institute with the help of a food frequency questionnaire. Descriptive analysis was done by plotting radar charts, whereas the logistic regression models were used to calculate the adjusted Odd Ratios (ORs) associated with consumption of green chilli, red chilli powder and curd, individually and in combinations. The controls in the present study were younger, had more males, the majority of them belonged to middle- and lower-income groups and had a family history of cancer as compared with cohort of case studies. Green chilli consumption was found to be the maximum within the lower-income group (n = 18, 66.67%), while that of red chilli (n = 150, 48.23%), and curd (n = 107, 34.04%) within the middle class. Maximum consumption of green chillies (Males n = 48, 29.27%; Females n = 36, 21.95%), red chillies (Males n = 40, 29.85%; Females n = 16, 24.61%) and curd (Males n = 31, 28.97%) was observed in the age group 46 to 60 irrespective of sex. Tobacco was found to be the most common addiction in all groups. The maximum number of patients frequently consuming these three dietary items presented majorly with rectal cancer, and liver metastasis and were in advanced grade and stage of cancer. Curd and curd with red chilli powder had a significant association with the development of CRC with an OR of 2.7280 (95% CI 1.6346 to 4.5531) and 5.0806 (95% CI 2.4015 to 10.7485), respectively, which was highly significant (p < 0.0001). Green chilli was notably an associated risk with an OR of 2.0095 (95% CI 1.3258 to 3.0458), which was also statistically significant (p = 0.001). Red chilli powder and green chilli with curd had ORs as 1.6917 (95% CI 1.1105 to 2.5771) and 2.1778 (95% CI 1.1591 to 4.0918) with p = 0.0144 and 0.0156, respectively. In the present study, green chilli, red chilli, and curd are identified as additional dietary risk factors for colorectal cancers, owing to their ability to produce chronic inflammation leading to various inflammatory conditions including cancer.

ObjectiveTo evaluate the feasibility and safety of umbilical cord milking (UCM) in neonates who are depressed at birth.Study designThis is a quasi-randomized, non-blinded, controlled trial on infants (≥35 weeks) who were depressed at birth. UCM (cord milked three times) was performed during the even months and the neonates born during the odd months were in the control group. Primary outcome was feasibility and safety.ResultsA total of 101 infants were enrolled (50 UCM group and 51 control group) between January 2015 and October 2016. UCM was performed in 95% of infants (59/62) who qualified to receive UCM. There were no significant differences in resuscitation delay, resuscitation efforts, and short-term outcomes between the two groups.ConclusionsUCM is feasible for term and late preterm infants who are depressed at birth. A larger clinical trial is needed to evaluate long-term benefits of UCM in neonates with HIE.