Road crashes in Adelaide metropolitan region, the consequences of COVID-19.

Background: Many countries instituted lockdown rules as the COVID-19 pandemic progressed, however, the effects of COVID-19 on transportation safety vary widely across countries and regions. In several situations, it has been shown that although the COVID-19 closure has decreased average traffic flow, it has also led to an increase in speeding, which will indeed increase the severity of crashes and the number of fatalities and serious injuries. Methods: At the local level, Generalized linear Mixed (GLM) modelling is used to look at how often road crashes changed in the Adelaide metropolitan area before and after the COVID-19 pandemic. The Geographically Weighted Generalized Linear Model (GWGLM) is also used to explore how the association between the number of crashes and the factors that explain them varies across census blocks. Using both no-spatial and spatial models, the effects of urban structure elements like land use mix, road network design, distance to CBD, and proximity to public transit on the frequency of crashes at the local level were studied. Results: This research showed that lockdown orders led to a mild reduction (approximately 7%) in crash frequency. However, this decrease, which has occurred mostly during the first three months of the lockdown, has not systematically alleviated traffic safety risks in the Greater Adelaide Metropolitan Area. Crash hotspots shifted from areas adjacent to workplaces and education centres to green spaces and city fringes, while crash incidence periods switched from weekdays to weekends and winter to summer. Implications: The outcomes of this research provided insights into the impact of shifting driving behaviour on safety during disorderly catastrophes such as COVID-19.

Lung fibrosis: Post-COVID-19 complications and evidences.

BACKGROUND: COVID 19, a lethal viral outbreak that devastated lives and the economy across the globe witnessed non-compensable respiratory illnesses in patients. As been evaluated in reports, patients receiving long-term treatment are more prone to acquire Pulmonary Fibrosis (PF). Repetitive damage and repair of alveolar tissues increase oxidative stress, inflammation and elevated production of fibrotic proteins ultimately disrupting normal lung physiology skewing the balance towards the fibrotic milieu. AIM: In the present work, we have discussed several important pathways which are involved in post-COVID PF. Further, we have also highlighted the rationale for the use of antifibrotic agents for post-COVID PF to decrease the burden and improve pulmonary functions in COVID-19 patients. CONCLUSION: Based on the available literature and recent incidences, it is crucial to monitor COVID-19 patients over a period of time to rule out the possibility of residual effects. There is a need for concrete evidence to deeply understand the mechanisms responsible for PF in COVID-19 patients.

New Insights into the Clinical Implications of Yes-Associated Protein in Lung Cancer: Roles in Drug Resistance, Tumor Immunity, Autophagy, and Organoid Development.

Despite significant innovations in lung cancer treatment, such as targeted therapy and immunotherapy, lung cancer is still the principal cause of cancer-associated death. Novel strategies to overcome drug resistance and inhibit metastasis in cancer are urgently needed. The Hippo pathway and its effector, Yes-associated protein (YAP), play crucial roles in lung development and alveolar differentiation. YAP is known to mediate mechanotransduction, an important process in lung homeostasis and fibrosis. In lung cancer, YAP promotes metastasis and confers resistance against chemotherapeutic drugs and targeted agents. Recent studies revealed that YAP directly controls the expression of programmed death-ligand 1 (PD-L1) and modulates the tumor microenvironment (TME). YAP not only has a profound relationship with autophagy in lung cancer but also controls alveolar differentiation, and is responsible for tubular structure formation in lung organoids. In this review, we discuss the various roles and clinical implications of YAP in lung cancer and propose that targeting YAP can be a promising strategy for treating lung cancer.