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Unlocking the possibilities of therapeutic potential of silymarin and silibinin against neurodegenerative Diseases-A mechanistic overview

Ashique S, Mohanto S, Kumar N, Nag S, Mishra A, Biswas A, et al.

Eur J Pharmacol, 2024 Oct 15;981:176906.
PMID: 39154829 DOI: 10.1016/j.ejphar.2024.176906

Silymarin, a bioflavonoid derived from the Silybum marianum plant, was discovered in 1960. It contains C25 and has been extensively used as a therapeutic agent against liver-related diseases caused by alcohol addiction, acute viral hepatitis, and toxins-inducing liver failure. Its efficacy stems from its role as a potent anti-oxidant and scavenger of free radicals, employed through various mechanisms. Additionally, silymarin or silybin possesses immunomodulatory characteristics, impacting immune-enhancing and immune-suppressive functions. Recently, silymarin has been recognized as a potential neuroprotective therapy for various neurological conditions, including Parkinson's and Alzheimer's diseases, along with conditions related to cerebral ischemia. Its hepatoprotective qualities, primarily due to its anti-oxidant and tissue-regenerating properties, are well-established. Silymarin also enhances health by modifying processes such as inflammation, β-amyloid accumulation, cellular estrogenic receptor mediation, and apoptotic machinery. While believed to reduce oxidative stress and support neuroprotective mechanisms, these effects represent just one aspect of the compound's multifaceted protective action. This review article further delves into the possibilities of potential therapeutic advancement of silymarin and silibinin for the management of neurodegenerative disorders via mechanics modules.
Combinational effect of angiotensin receptor blocker and folic acid therapy on uric acid and creatinine level in hyperhomocysteinemia-associated hypertension

Singh Y, Samuel VP, Dahiya S, Gupta G, Gillhotra R, Mishra A, et al.

Biotechnol Appl Biochem, 2019 Sep;66(5):715-719.
PMID: 31314127 DOI: 10.1002/bab.1799

Homocysteine [HSCH2 CH2 CH(NH2 )COOH] (Hcy) is a sulfur-containing amino acid of 135.18 Da of molecular weight, generated during conversion of methionine to cysteine. If there is a higher accumulation of Hcy in the blood, that is usually above 15 µmol/L, it leads to a condition referred to as hyperhomocysteinemia. A meta-analysis of observational study suggested an elevated concentration of Hcy in blood, which is termed as the risk factors leading to ischemic heart disease and stroke. Further experimental studies stated that Hcy can lead to an increase in the proliferation of vascular smooth muscle cells and functional impairment of endothelial cells. The analyses confirmed some of the predictors for Hcy presence, such as serum uric acid (UA), systolic blood pressure, and hematocrit. However, angiotensin-converting enzyme inhibitors angiotensin-converting enzyme inhibitors (ACEIs) and angiotensin receptor blockers (ARBs) alone are inadequate for controlling UA and creatinine level, although the addition of folic acid may be beneficial in hypertensive patients who are known to have a high prevalence of elevated Hcy. We hypothesized that combination therapy with an ARB (olmesartan) and folic acid is a promising treatment for lowering the UA and creatinine level in hyperhomocysteinemia-associated hypertension.
A contemporary biological pathway of islet amyloid polypeptide for the management of diabetic dementia

Sah SK, Samuel VP, Dahiya S, Singh Y, Gilhotra RM, Gupta G, et al.

Chem Biol Interact, 2019 Jun 01;306:117-122.
PMID: 31004596 DOI: 10.1016/j.cbi.2019.04.022

Major challenges of dealing elder patients with diabetes mellitus (DM) are the individualization of consideration in persons with various comorbid types of conditions. In spite of the fact that microvascular and macrovascular problems associated with DM are well documented, there is only a few numbers of reports viewing different conditions, for example, cognitive dysfunction. Cognitive dysfunction is of specific significance due to its effect on self-care and quality of life. All in all, the etiology of cognitive dysfunction in the maturing populace is probably going to be the grouping of ischemic and degenerative pathology. It is likewise trusted that Hyperglycemia is engaged with the system of DM-related cognitive dysfunction. At present, it isn't certain in the case of enhancing glycemic control or utilizing therapeutic agents can enhance the risk of cognitive decay. Amylin was later characterized as an amyloidogenic peptide, confined from a beta cell tumor and called islet amyloid polypeptide (IAPP), and after that, amylin. Conversely, we investigate the beneficial role and hypothesizing the mechanism of amylin related expanding the level and activation of CGRP receptor to enhance the cognition declination amid diabetic dementia.
Current biological and pharmacological updates on wogonin

Rawat S, Gupta G, Pathak S, Singh SK, Singh H, Mishra A, et al.

EXCLI J, 2020;19:635-640.
PMID: 32536834
Fulltext Activation of TWEAK/Fn14 signaling suppresses TRAFs/NF-?B pathway in the pathogenesis of cancer

Gupta G, Kazmi I, Al-Abbasi FA, Singh Y, Roshan S, Rani S, et al.

EXCLI J, 2021;20:232-235.
PMID: 34121970 DOI: 10.17179/excli2021-3378
Fulltext Recent Developments in Diagnosis of Epilepsy: Scope of MicroRNA and Technological Advancements

Bandopadhyay R, Singh T, Ghoneim MM, Alshehri S, Angelopoulou E, Paudel YN, et al.

Biology (Basel), 2021 Oct 25;10(11).
PMID: 34827090 DOI: 10.3390/biology10111097

Epilepsy is one of the most common neurological disorders, characterized by recurrent seizures, resulting from abnormally synchronized episodic neuronal discharges. Around 70 million people worldwide are suffering from epilepsy. The available antiepileptic medications are capable of controlling seizures in around 60-70% of patients, while the rest remain refractory. Poor seizure control is often associated with neuro-psychiatric comorbidities, mainly including memory impairment, depression, psychosis, neurodegeneration, motor impairment, neuroendocrine dysfunction, etc., resulting in poor prognosis. Effective treatment relies on early and correct detection of epileptic foci. Although there are currently a few well-established diagnostic techniques for epilepsy, they lack accuracy and cannot be applied to patients who are unsupportive or harbor metallic implants. Since a single test result from one of these techniques does not provide complete information about the epileptic foci, it is necessary to develop novel diagnostic tools. Herein, we provide a comprehensive overview of the current diagnostic tools of epilepsy, including electroencephalography (EEG) as well as structural and functional neuroimaging. We further discuss recent trends and advances in the diagnosis of epilepsy that will enable more effective diagnosis and clinical management of patients.
A Rare Case of Brucellosis with Multivalvular Endocarditis and Complete Heart Block

Gothwal SK, Goyal K, Garg AS, Sahu BK, Agrawal M, Mishra A, et al.

Curr Cardiol Rev, 2024 Jul 03.
PMID: 38963101 DOI: 10.2174/011573403X290326240703100925

BACKGROUND: Brucellosis is a public health concern that affects multiple organs. However, cardiovascular problems arise infrequently, affecting fewer than 2% of cases, typically presenting as endocarditis.
CASE PRESENTATION: A 50-year male was admitted with low-grade fever, night sweats, weight loss (13 kg), malaise, and generalized weakness for the past 6 months. On clinical examination, he was febrile with 39.0°C, an average heart rate of 54 bpm, and 100/40 mmHg blood pressure. On cardiovascular examination, S1 and S2 were soft with pan systolic murmur present in the mitral area, and the early diastolic murmur was present in the left third intercostal space. Electrocardiography was suggestive of third-degree heart block with AV dissociation. Transthoracic echocardiography showed mobile vegetations attached to multiple valves- an aortic valve (18.2x11.9mm) and a mitral valve (2.9x7.5mm) with perivalvular abscess. He was given oral doxycycline (100mg B.D.) and rifampicin (600mg/day); the patient responded, but the AV block did not resolve.
CONCLUSION: This report has drawn attention to multivalvular involvement and cardiac rhythm abnormalities in Brucellosis (in this case, A.V. dissociation was present) because early diagnosis and treatment can cause a significant decrease in morbidity as well as mortality by appropriate treatment.
Monotherapy of RAAS blockers and mobilization of aldosterone: A mechanistic perspective study in kidney disease

Gupta G, Dahiya R, Singh Y, Mishra A, Verma A, Gothwal SK, et al.

Chem Biol Interact, 2020 Feb 01;317:108975.
PMID: 32032593 DOI: 10.1016/j.cbi.2020.108975

In patients with acute kidney injury progressively converting into chronic kidney disease (CKD), proteinuria and high blood pressure predict progression to end-stage renal disease (ESRD). Although, Renin-angiotensin-aldosterone system (RAAS) regulates blood pressure and kidney disease through both direct and indirect mechanisms. RAAS blockers that act at the level of angiotensin or lower in the cascade can cause compensatory increases in the plasma renin and angiotensin II level. Here, in this review article, we are exploring the evidence-based on RAAS blockade action releases of aldosterone and hypothesizing the molecular mechanism for converting the acute kidney injury into chronic kidney disease to end-stage renal disease.
Role of the Serine/Threonine Kinase 11 (STK11) or Liver Kinase B1 (LKB1) Gene in Peutz-Jeghers Syndrome

Altamish M, Dahiya R, Singh AK, Mishra A, Aljabali AAA, Satija S, et al.

Crit Rev Eukaryot Gene Expr, 2020;30(3):245-252.
PMID: 32749111 DOI: 10.1615/CritRevEukaryotGeneExpr.2020033451

Peutz-Jeghers syndrome (PJS) is a well-described inherited syndrome, characterized by the development of gastrointestinal polyps and characteristic mucocutaneous freckling. PJS is an autosomal prevailing disease, due to genetic mutation on chromosome 19p, manifested by restricted mucocutaneous melanosis in association with gastrointestinal (GI) polyposis. The gene for PJS has recently been shown to be a serine/threonine kinase, known as LKB1 or STK11, which maps to chromosome subband 19p13.3. This gene has a putative coding region of 1302 bp, divided into nine exons, and acts as a tumor suppressor in the hamartomatous polyps of PJS patients and in the other neoplasms that develop in PJS patients. It is probable that these neoplasms develop from hamartomas, but it remains possible that the LKB1 or STK11 locus plays a role in a different genetic pathway of tumor growth in the cancers of PJS patients. This article focuses on the role of LKB1 or STK11 gene expression in PJS and related cancers.
Fulltext Influenza seasonality and vaccination timing in tropical and subtropical areas of southern and south-eastern Asia

Saha S, Chadha M, Al Mamun A, Rahman M, Sturm-Ramirez K, Chittaganpitch M, et al.

Bull World Health Organ, 2014 May 01;92(5):318-30.
PMID: 24839321 DOI: 10.2471/BLT.13.124412

OBJECTIVE: To characterize influenza seasonality and identify the best time of the year for vaccination against influenza in tropical and subtropical countries of southern and south-eastern Asia that lie north of the equator.
METHODS: Weekly influenza surveillance data for 2006 to 2011 were obtained from Bangladesh, Cambodia, India, Indonesia, the Lao People's Democratic Republic, Malaysia, the Philippines, Singapore, Thailand and Viet Nam. Weekly rates of influenza activity were based on the percentage of all nasopharyngeal samples collected during the year that tested positive for influenza virus or viral nucleic acid on any given week. Monthly positivity rates were then calculated to define annual peaks of influenza activity in each country and across countries.
FINDINGS: Influenza activity peaked between June/July and October in seven countries, three of which showed a second peak in December to February. Countries closer to the equator had year-round circulation without discrete peaks. Viral types and subtypes varied from year to year but not across countries in a given year. The cumulative proportion of specimens that tested positive from June to November was > 60% in Bangladesh, Cambodia, India, the Lao People's Democratic Republic, the Philippines, Thailand and Viet Nam. Thus, these tropical and subtropical countries exhibited earlier influenza activity peaks than temperate climate countries north of the equator.
CONCLUSION: Most southern and south-eastern Asian countries lying north of the equator should consider vaccinating against influenza from April to June; countries near the equator without a distinct peak in influenza activity can base vaccination timing on local factors.
Fulltext Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)1

Klionsky DJ, Abdel-Aziz AK, Abdelfatah S, Abdellatif M, Abdoli A, Abel S, et al.

Autophagy, 2021 Jan;17(1):1-382.
PMID: 33634751 DOI: 10.1080/15548627.2020.1797280

In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes. These guidelines are not meant to be a dogmatic set of rules, because the appropriateness of any assay largely depends on the question being asked and the system being used. Moreover, no individual assay is perfect for every situation, calling for the use of multiple techniques to properly monitor autophagy in each experimental setting. Finally, several core components of the autophagy machinery have been implicated in distinct autophagic processes (canonical and noncanonical autophagy), implying that genetic approaches to block autophagy should rely on targeting two or more autophagy-related genes that ideally participate in distinct steps of the pathway. Along similar lines, because multiple proteins involved in autophagy also regulate other cellular pathways including apoptosis, not all of them can be used as a specific marker for bona fide autophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field.