Health-promoting benefits of lentils: Anti-inflammatory and anti-microbial effects.

This paper describes how lentils (Lens culinaris species) can positively affect health by reducing inflammation, providing antioxidants, and displaying antimicrobial properties. Lentils are rich in proteins, essential amino acids, minerals, and fibers, making them a valuable source of nutrition, particularly in low and middle-income countries. Lentils have many health benefits, including positive effects on diabetes management, support for cardiovascular health, and antioxidative properties. The antioxidative properties of lentils, attributed to their phenolic content, and their ability to inhibit inflammation-related enzymes are also discussed. We discuss the potential of lentils as a dietary tool in promoting immunity, reducing disease burdens, and preventing nutritional deficiencies. Overall, lentils are a highly nutritious food with various health benefits, including anti-inflammatory and antimicrobial effects. The fiber and protein content in lentils make them beneficial for weight management, blood sugar regulation, and supporting overall gut health. Furthermore, the slow rate at which lentils affect blood sugar levels, due to their low glycemic index, can be advantageous for individuals with diabetes.

Can adverse cardiac events of the COVID-19 vaccine exacerbate preexisting diseases?

INTRODUCTION: SARS-CoV-2 infection and COVID-19 vaccination can both lead to serious cardiac conditions such as myocarditis, arrhythmia, acute myocardial infarction, and coagulopathy. Further studies are needed to better understand the risks and benefits of COVID-19 vaccination, and to determine the best course of action for individuals with preexisting heart conditions. AREAS COVERED: The current knowledge and challenges in understanding vaccine-associated heart issues concerning the COVID-19 pandemic are briefly summarized, highlighting similar cardiac conditions caused by either SARS-CoV-2 infection or COVID-19 vaccination and the potential clinical impacts. EXPERT OPINION: The short-term risks of severe cardiovascular side effects following COVID-19 vaccination are relatively low. However, further studies are needed to determine whether adverse vaccination events outweigh the long-term benefits in specific groups of individuals. Since cardiac inflammation, blood pressure dysregulation, coagulopathy, acute myocardial infarction, or arrhythmia could be the consequences of either SARS-CoV-2 infection or COVID-19 vaccination, clinical questions should be asked whether the COVID-19 vaccine worsens the condition in persons with preexisting heart diseases. It is important to carefully assess the potential risks and benefits of COVID-19 vaccination, especially for individuals with preexisting heart conditions, and to continue monitoring and studying the long-term effects of vaccination on cardiovascular health.

Deciphering epithelial-to-mesenchymal transition in pancreatic cancer.

Epithelial to mesenchymal transition (EMT) is a complex cellular program that alters epithelial cells and induces their transformation into mesenchymal cells. While essential to normal developmental processes such as embryogenesis and wound healing, EMT has also been linked to the development and progression of various diseases, including fibrogenesis and tumorigenesis. Under homeostatic conditions, initiation of EMT is mediated by key signaling pathways and pro-EMT-transcription factors (EMT-TFs); however, in certain contexts, these pro-EMT regulators and programs also drive cell plasticity and cell stemness to promote oncogenesis as well as metastasis. In this review, we will explain how EMT and EMT-TFs mediate the initiation of pro-cancer states and how they influence late-stage progression and metastasis in pancreatic ductal adenocarcinoma (PDAC), the most severe form of pancreatic cancer.

Evaluation of Short-Term Side Effects Following the First Dose of COVID-19 Vaccines Among Physicians and Dentists: A Cross-Sectional Study from India.

Background: Efficacy and safety are fundamental for the development of successful COVID-19 vaccines. Vaccine-associated side effects influence vaccine hesitancy. This study investigated the prevalence, severity, and onset of side effects following the first dose of COVID-19 vaccines among physicians and dentists working in various healthcare settings across India. Methods: A cross-sectional survey collected self-report data from April to June 2021 on side effects following the first dose of the vaccine. An online validated questionnaire using the Google Docs® platform was circulated via email and social media platforms. Results: More than 40% of participants experienced at least one side effect after the first dose of vaccination; the most common were mild and resolved within three days after vaccination. More than 91% of respondents received the Covishield (AstraZeneca) vaccine; the most prevalent adverse effects were soreness of the injected arm (78.9%), tiredness (71.1%), and fever (54.9%). Logistic regression showed that women were almost 60% less likely to report side effects. Conclusion: Findings supported the safety of the first dose of the COVID-19 vaccine based on relatively few self-limiting side effects, mainly soreness of the injected arm and tiredness. Further research is needed to determine the long-term safety of COVID-19 vaccines, especially after booster doses.

NF1 loss of function as an alternative initiating event in pancreatic ductal adenocarcinoma.

A long-standing question in the pancreatic ductal adenocarcinoma (PDAC) field has been whether alternative genetic alterations could substitute for oncogenic KRAS mutations in initiating malignancy. Here, we report that Neurofibromin1 (NF1) inactivation can bypass the requirement of mutant KRAS for PDAC pathogenesis. An in-depth analysis of PDAC databases reveals various genetic alterations in the NF1 locus, including nonsense mutations, which occur predominantly in tumors with wild-type KRAS. Genetic experiments demonstrate that NF1 ablation culminates in acinar-to-ductal metaplasia, an early step in PDAC. Furthermore, NF1 haploinsufficiency results in a dramatic acceleration of KrasG12D-driven PDAC. Finally, we show an association between NF1 and p53 that is orchestrated by PML, and mosaic analysis with double markers demonstrates that concomitant inactivation of NF1 and Trp53 is sufficient to trigger full-blown PDAC. Together, these findings open up an exploratory framework for apprehending the mechanistic paradigms of PDAC with normal KRAS, for which no effective therapy is available.

Phosphate Dysregulation and Metabolic Syndrome.

Phosphorus is one of the most abundant minerals in the human body. It is essential for almost all biochemical activities through ATP formation, intracellular signal transduction, cell membrane formation, bone mineralization, DNA and RNA synthesis, and inflammation modulation through various inflammatory cytokines. Phosphorus levels must be optimally regulated, as any deviations may lead to substantial derangements in glucose homeostasis. Clinical studies have reported that hyperphosphatemia can increase an individual's risk of developing metabolic syndrome. High phosphate burden has been shown to impair glucose metabolism by impairing pancreatic insulin secretion and increasing the risk of cardiometabolic disorders. Phosphate toxicity deserves more attention as metabolic syndrome is being seen more frequently worldwide and should be investigated further to determine the underlying mechanism of how phosphate burden may increase the cardiometabolic risk in the general population.

Interactions between FGF23 and vitamin D.

Fibroblast growth factor-23 (FGF23) controls the homeostasis of both phosphate and vitamin D. Bone-derived FGF23 can suppress the transcription of 1α-hydroxylase (1α(OH)ase) to reduce renal activation of vitamin D (1,25(OH)2D3). FGF23 can also activate the transcription of 24-hydroxylase to enhance the renal degradation process of vitamin D. There is a counter-regulation for FGF23 and vitamin D; 1,25(OH)2D3 induces the skeletal synthesis and the release of FGF23, while FGF23 can suppress the production of 1,25(OH)2D3 by inhibiting 1α(OH)ase synthesis. Genetically ablating FGF23 activities in mice resulted in higher levels of renal 1α(OH)ase, which is also reflected in an increased level of serum 1,25(OH)2D3, while genetically ablating 1α(OH)ase activities in mice reduced the serum levels of FGF23. Similar feedback control of FGF23 and vitamin D is also detected in various human diseases. Further studies are required to understand the subcellular molecular regulation of FGF23 and vitamin D in health and disease.

Prevalence of COVID-19 vaccine reactogenicity among Bangladeshi physicians.

Increased COVID-19 vaccine hesitancy presents a major hurdle in global efforts to contain the COVID-19 pandemic. This study was designed to estimate the prevalence of adverse events after the first dose of the Covishield (AstraZeneca) vaccine among physicians in Bangladesh. A cross-sectional study was conducted using an online questionnaire for physicians (n = 916) in Bangladesh. Physicians who received at least one dose of the COVID-19 vaccine were included. The study was carried out from April 12 to May 31, 2021. More than 58% of respondents (n = 533) reported one or more adverse events. Soreness of the injected arm (71.9%), tiredness (56.1%), fever (54.4%), soreness of muscles (48.4%), headache (41.5%) and sleeping more than usual (26.8%) were the most commonly reported adverse events. Most vaccine-related reactogenicities were reported by the younger cohorts (<45 years). The majority of respondents reported severity of reactogenicity as "mild," experienced on the day of vaccination, and lasting for 1-3 days. The most common reactogenicity was pain at the injection site; the second most common was tiredness. Almost half (49.2%) of the physicians took acetaminophen (paracetamol) to minimize the effects of vaccine reactogenicity. Multivariate logistic regression analyses showed that physicians with diabetes and hypertension (OR = 2.729 95% CI: 1.282-5.089) and asthma with other comorbidities (OR = 1.885 95% CI: 1.001-3.551) had a significantly higher risk of vaccine-related reactogenicities than physicians without comorbidities. Further safety studies with larger cohorts are required to monitor vaccine safety and provide assurance to potential vaccine recipients.

Zinc and its role in vitamin D function.

Zinc is an essential mineral with an important relationship with vitamin D. Studies have found that reduced blood zinc levels could predict vitamin D deficiency in adolescent girls, while zinc supplementation increased vitamin D levels in postmenopausal women. In vitro studies using human peritoneal macrophages have found that zinc induced the release of calcitriol (1,25-dihydroxycholecalciferol). Zinc also acts as a cofactor for vitamin D functions, as the transcriptional activity of vitamin D-dependent genes relies on zinc to exert pleiotropic functions, including mineral ion regulation. Vitamin D could also induce zinc transporters to regulate zinc homeostasis. Together, zinc and vitamin D in adequate concentrations help maintain a healthy musculoskeletal system and beyond; however, deficiency in either of these nutrients can result in various disorders affecting almost all body systems. This brief article will focus on the role of zinc in vitamin D functions.

Phosphate Metabolism: From Physiology to Toxicity.

Systemic phosphate homeostasis is tightly controlled by the delicate cross-organ talk among intestine, kidney, bone, and parathyroid glands. The endocrine regulation of phosphate homeostasis is primarily mediated by fibroblast growth factor 23 (FGF23), vitamin D, and parathyroid hormone (PTH). Bone-derived FGF23 acts on the proximal tubular epithelial cells of the kidney to partly maintain the homeostatic balance of the phosphate. FGF23, through binding with its cell surface receptors in the presence of klotho, can activate downstream signaling kinases to reduce the functionality of the sodium-phosphate (NaPi) co-transporters of the kidney to influence the systemic phosphate homeostasis. Given the complexity of molecular regulation of phosphate homeostasis, providing information on all aspects of its homeostatic control in a single volume of a book is an overwhelming task. As the Editor, I have organized the chapters that I believe will provide necessary information on the physiologic regulation and pathologic dysregulation of phosphate in health and diseases. Readers will be able to use this volume as a quick reference for updated information on phosphate metabolism without prior acquaintance with the field.