Spike protein has been established as one of the molecules playing a pivotal role in coronavirus infection. On its bases, several vaccines have been developed, passed preclinical and clinical stages, and reached medical practice at the early stages of the pandemic. It was found efficient enough to induce various types of immunoglobulins. However, the missense mutations made it necessary to develop new sequences with adjuvants to enhance the efficacy against a broad spectrum of SARS-CoV-2 and newly emerging variants. Some attempts were carried out to improve the vaccine efficiency by loading it into a delivery system, which caused a prolongation effect. In this paper, we reviewed data around spike protein-based vaccines in terms of their efficacy, which was analyzed based on enhanced quantities/titers of immunoglobulins/neutralizing antibodies. Our search on the PubMed database using ‘spike protein-based coronavirus vaccines’ keywords showed over 150 publications that were further filtered based on their relevance. Further, we added other relevant papers to support the expressed ideas. We compared the effects of various vaccines of different origins in clinical studies and animal experiments where relevant. The efficacy of adjuvants has been reviewed as a separate section. In several cases, we explained the significance of the spike protein trimeric structure. We also explained the essential role of mutation while developing protein vaccines. The contributions of adjuvants in inducing immune responses have been separated into one section. The outcomes of clinical studies were highlighted to prove their efficacies.
GPCRs are a class of membrane proteins that are essential to signal transduction, and this is a vital process in many different physiologies. The significant mortality rate and widespread occurrence of stroke highlight the need to accelerate the research to develop viable treatment agents. A promising prospect for the development of new treatment approaches is the increasing comprehension of the pathophysiology of stroke and the crucial roles played by GPCRs. Because of the blood clot, the glial cells’ vascular supply is abruptly cut off, which sets off a series of events that include inflammation and neuronal damage and ultimately lead to cell death. Numerous therapeutic treatments, including thrombolytic agents like tissue plasminogen activator and urokinase, have been discovered as potential neuroprotective medicines; however, their use is restricted because of the modest therapeutic window. Accepting that GPCRs are the pertinent factors in ischemic stroke, we explore the potential medicinal promise of GPCR-targeted treatments and the shortcomings that ought to be resolved in order to translate these discoveries to clinical cases.
Non-adherence to antidiabetic medication remains the major factor contributing to poor clinical outcomes among patients with type 2 diabetes mellitus (T2DM). This study was designed to investigate the cross-sectional association between psychological distress and medication adherence in T2DM patients. Participants were 100 adults with T2DM from a teaching hospital in South India. Psychological distress was assessed using the 12-item General Health Questionnaire (GHQ-12) and the 8-item Morisky Medication Adherence Scale (MMAS-8) was used to assess medication adherence. This study demonstrated that a high proportion of patients (70 %) with T2DM experience psychological distress. Higher self-reported distress was the strongest independent predictor of medication non-adherence (β = −0.1145; P=0.0002). The study highlights that psychological distress in T2DM patients meets important drug discovery criteria such as unmet medical need, disease prevalence, and success probability. Understanding the biological mechanisms that underpin psychological distress would aid in the development of mechanism-based therapies. Better integration of medical and psychosocial treatments in general medical practice may be important to improve treatment adherence and reduce disparities in chronic disease care.

