Female reproductive and hormonal factors and lung cancer mortality among never-smokers: A prospective cohort study of 287 408 Chinese women

There is growing, but inconsistent evidence suggesting oestrogen may play a key role in lung cancer development, especially among never-smoking women for whom lung cancer risk factors remain largely elusive. Using the China Kadoorie Biobank, a large-scale prospective cohort with 302 510 women aged 30 to 79 years recruited from 10 regions in China during 2004 to 2008, we assessed the risk of lung cancer death among self-reported never-smoking women who were cancer-free at baseline, in relation to age at menarche, age at menopause, time since menopause, prior use of oral contraceptives (OCP), number of livebirths, breastfeeding and age at first livebirth. Women were followed up to December 31, 2016 with linkage to mortality data. Hazard ratios (HR) and 95% confidence intervals (CI) were estimated using Cox regression, adjusting for key confounders including several socio-demographic, environmental and lifestyle factors. Among 287 408 never-smoking women, 814 died from lung cancer with a median follow-up of 10.3 years. Women who had used OCP within 15 years prior to baseline had a significantly higher hazard of lung cancer death compared with never-users: HR = 1.85 (95% CI: 1.14-3.00) and risk increased by 6% with each additional year of use: HR = 1.06 (1.01-1.10). Among parous women, the hazard of lung cancer death increased by 13% with each single livebirth: HR = 1.13 (1.05-1.23); and among post-menopausal women, the risk increased by 2% with each year since menopause: HR = 1.02 (1.01-1.04). These results suggest that reproductive factors which were proxies for lower endogenous oestrogen level, for example, longer duration of OCP use, could play a role in lung cancer development.     

HIV Protease: Historical Perspective and Current Research

The retroviral protease of human immunodeficiency virus (HIV) is an excellent target for antiviral inhibitors for treating HIV/AIDS. Despite the efficacy of therapy, current efforts to control the disease are undermined by the growing threat posed by drug resistance. This review covers the historical background of studies on the structure and function of HIV protease, the subsequent development of antiviral inhibitors, and recent studies on drug-resistant protease variants. We highlight the important contributions of Dr. Stephen Oroszlan to fundamental knowledge about the function of the HIV protease and other retroviral proteases. These studies, along with those of his colleagues, laid the foundations for the design of clinical inhibitors of HIV protease. The drug-resistant protease variants also provide an excellent model for investigating the molecular mechanisms and evolution of resistance.     

Drug‐induced photosensitivity: culprit drugs,potential mechanisms and clinical consequences

Drug‐induced photosensitivity, the development of phototoxic or photoallergic reactions due to pharmaceuticals and subsequent exposure to ultraviolet or visible light, is an adverse effect of growing interest. This is illustrated by the broad spectrum of recent investigations on the topic, ranging from molecular mechanisms and culprit drugs through epidemiological as well as public health related issues to long‐term photoaging and potential photocarcinogenic consequences. The present review summarizes the current state of knowledge on the topic while focusing on culprit drugs and long‐term effects. In total, 393 different drugs or drug compounds are reported to have a photosensitizing potential, although the level of evidence regarding their ability to induce photosensitive reactions varies markedly among these agents. The pharmaceuticals of interest belong to a wide variety of drug classes. The epidemiological risk associated with the use of photosensitizers is difficult to assess due to under‐reporting and geographical differences. However, the widespread use of photosensitizing drugs combined with the potential photocarcinogenic effects reported for several agents has major implications for health and safety and suggests a need for further research on the long‐term effects.     

Evaluation of Structured Assessment and Mediating Factors of Suicide-Focused Group Therapy for Veterans Recently Discharged from Inpatient Psychiatry

The current study investigated the impact of adding the Suicide Status Form (SSF) to a suicide-focused group therapy for veterans recently discharged from an inpatient psychiatry setting. A sample of 141 veterans was enrolled and randomized into a Usual Assessment Group Therapy or SSF-Assessment Group Therapy. Participants completed interviews at baseline, 1, and 3 months. No significant differences were observed between groups regarding group attendance (IRR?=?1.01, Std. Err?=?0.08, 95% CI?=?0.87, 1.18) or client satisfaction (β?=?0.23, Std. Err?=?0.66, p?=?0.73, d?=??.25). No main effects were observed across the study on secondary outcomes of interest for suicidal ideation and overall symptom distress, although participants in both treatment conditions reported significant improvements on these outcomes over the course of the study. Patients in the Usual Assessment Group Therapy demonstrated greater reductions in overall symptom distress across the 3-month follow-up window (β?=?6.08, Std. Err?=?2.04, p?=?0.003; f²?=?0.05). Follow-up path analyses revealed that more frequent session attendance was significantly related to less suicidal ideation at 1-month, higher working alliance between individual members and group facilitators was associated with greater suicidal ideation at 1-month, and higher group cohesion among group members at 1-month was significantly associated with less thwarted belongingness at 1-month. Although the SSF did not improve the impact of an existing suicide-focused group therapy, the study findings support future research on group treatments for suicidal veterans.     

Evaluation of renal markers of T1D in Sprague‐Dawley exposed to 2‐aminoanthracene

The incidence of type 1 diabetes (T1D) and its associated risks of chronic kidney disease or end‐stage renal disease development are on the rise. T1D is an autoimmune disease in which insulin‐producing beta cells are destroyed. Increased incidence of T1D has been suggested to be a result of environmental factors such as exposure to polycyclic aromatic hydrocarbons (PAHs). 2‐aminoanthracene (2AA) is a PAH that has been associated with the onset of early diabetic symptoms. This study was conducted to assess if 2AA dietary ingestion would induce T1D renal injuries. To accomplish study goals, Sprague‐Dawley rats were assigned into three 2AA dietary (0, 50, and 100 mg/kg‐2AA) ingestion groups for 12 weeks. Animals were evaluated for various morphometric indices, clinical markers, and gene expression. The rats in the 100 mg/kg group lost 5% less weight than the other treatment groups and converted roughly 3% more of their food intake into body mass. Renal histopathology indicated no significant difference between groups. The kidney weight per bodyweight of the 100 mg/kg treatment group was 30.1% greater than the control group. Creatinine concentration of the 100 mg/kg group was 46.2% greater than the control group. Serum glucose levels were significantly elevated in rats exposed to 2AA. On the contrary, serum albumin concentration was significantly reduced in 2AA‐treated rats. T1D and genetic markers of renal injury such as FABP1, SPP1, IL‐1B, and IL‐7 were elevated in treated groups. These results suggest that 2AA may induce the early diabetic renal injuries.