As the validity of climate change is tossed around like a political football, its effects on the health of the current and future populations continue to worsen. The effects are being seen across the globe, and they have social, ecological, and biological health implications. Populations are aging at rapid rates, creating larger demographics of people with social and physical dependency. This, combined with the current social and health inequity, will result in an increased burden of temperature-related morbidity and mortality on the elderly and racial minorities through the biological effects of extreme temperature. Cardiovascular disease is the number one killer in the world and will especially see sharp increases, as temperature rise exacerbates its effects. The extreme temperature from climate change is also negatively affecting agriculture and the symbiosis between humans and the environment, impacting not only our food systems, but our safety nets too. All these three components (social, ecological, and biological) interact and influence one another. This literature review analyzes the current research into these areas and describes their interplay, while suggesting novel approaches to address the impact climate change is having and will have on the health of the world.

Owing to the rapid and unplanned urbanization, varying use of lands, and an exponential rise in trade and global travel, the number of opportunities for a vector contact with humans has significantly increased. In fact, the recent global estimates depict that in excess of four-fifth of the world's population is at risk of at least one or more vector-borne diseases (VBDs). All these factors together justify the need for an urgent and a holistic approach to minimize the incidence and impact of VBDs. Systematic analyses of the existing vector control measures indicate that there is an immense scope to ameliorate the impact of vector control. In conclusion, there is a big-time need for having a collaborative and coordinated response for the containment of VBD worldwide, and thus, all the stakeholders should work together for the achievement of the same.

Objective: Patients with hyperuricemia is often associated with hyperlipidemia. Therefore, the relationship between serum apolipoprotein A1 (Apo-A1) and serum uric acid (UA) level was studied. Methods: Seventy-three patients with gout, 43 patients with hyperuricemia, and 70 healthy controls were enrolled in the study. The liver and kidney function, blood glucose, blood lipid and other biochemical indicators were detected, and Apo-A1 content was detected by enzyme-linked immunosorbent assay. Results: 73 patients with gout, 43 patients with hyperuricemia, and 70 healthy controls were included in the study. None of the patients had diabetes, hypertension, coronary heart disease, or other chronic diseases. There was no difference in blood lipids among the three groups. The lower expressed Apo-A1 was validated in the hyperuricemia group and gout group (P < 0.001). Among all patients, Apo-A1 levels were negatively correlated with plasma UA level (R² = −0.4925, P < 0.0001). Conclusion: It was confirmed that Apo-A1 was related to the change of plasma UA level to some extent.

Purpose: Ectopic adrenocorticotropic hormone (ACTH)-secreting syndrome (EAS) is a relatively rare disease. EAS could not be inhibited by endogenous or exogenous glucocorticoid, which may be its most important characteristic. We aimed to explore the expression of glucocorticoid receptor (GR) in small cell lung cancer (SCLC) with or without EAS. Materials and Methods: In this study, we first reported one patient with EAS caused by SCLC, and we examined the expression of ACTH and GR on pulmonary tissue in normal people and SCLC patients with or without EAS. Results: Immunochemistry analysis showed that there was no obvious difference in the expression of GR in SCLC without EAS compared with normal people. While in the EAS patient, GR expression was absent in the tissue. Conclusions: Therefore, our study found that lower expression of GR in small cell lung cancer (SCLC) with EAS, which may contribute to the no inhibition by endogenous or exogenous glucocorticoid.