Association between Lipoprotein(a) concentration and adverse cardiac events in patients with coronary artery disease: An observational cohort study.

This prospective study investigated the association between lipoprotein (a) [Lp(a)] levels and adverse cardiac events in patients undergoing percutaneous coronary intervention (PCI) for coronary artery disease. Among 600 patients, 79.16 % were male. Kaplan Meier analysis revealed significantly higher incidence rates of cardiac death, major adverse cardiac events, myocardial infarction, revascularization and stroke in patients with elevated Lp(a) (≥30 mg/dL). The Cox Regression model identified Lp(a) ≥30 mg/dL as a significant risk factor for adverse events (HR: 4.2920; 95%CI: 2.58-7.120; p < 0.05). Elevated Lp(a) levels were associated with an increased risk of adverse cardiac events in coronary artery disease patients undergoing PCI.

Confounding Factors Responsible for Elevated Lp(a) Levels in Patients with Coronary Artery Disease.

BACKGROUND: Cardiovascular diseases (CVDs) are a leading cause of global mortality, motivating research into novel approaches for their management. Lipoprotein(a) (Lp(a)), a unique lipoprotein particle, has been implicated in atherosclerosis and thrombosis, suggesting its potential as a therapeutic target for CVDs. AIM: This study aimed to investigate the association of Lp(a) levels with various cardiovascular parameters and events among patients with confirmed cardiovascular disease. METHODOLOGY: A prospective study was conducted, enrolling 600 participants, predominantly comprising males (79%), with a mean age of 52.78 ± 0.412 years diagnosed with cardiovascular disease. The follow-up was done for 18 months. Patient demographics, blood investigations, and occurrence of major adverse cardiac events (MACE) were collected. SPSS version 21 was used to statistically analyze the relationships between elevated Lp(a) levels and factors such as age, glycated hemoglobin, mortality, MACE, cardiac death, target vessel revascularization, and stroke. RESULTS: The study revealed significant (P < 0.05) associations between elevated Lp(a) levels and advanced age, increased glycated hemoglobin levels, as well as occurrences of all-cause mortality, MACE, cardiac death, target vessel revascularization, and stroke. Notably, a significant (P < 0.05), association between high Lp(a) levels and acute coronary syndrome (ACS) emerged, suggesting Lp(a)'s role in advanced cardiac events. CONCLUSION: The findings highlight the potential significance of Lp(a) as a notable risk factor in cardiovascular health. The observed associations between elevated Lp(a) and adverse cardiovascular events, including ACS, underscore its pathogenic role. Consequently, this study supports the rationale for further research into Lp(a)-specific therapeutic interventions, offering substantial promise in refining the management strategies for cardiovascular diseases.

Can acid produced from probiotic bacteria alter the surface roughness, microhardness, and elemental composition of enamel? An in vitro study.

Probiotics are live microorganisms that upon administration in adequate amounts provide various health benefits to the host. Probiotics are "lactic acid-producing bacteria" as they release large amounts of organic acids, particularly lactic acids, in their surrounding environment. Although the acids produced by probiotics are beneficial for gastrointestinal and vaginal health, the acidogenic nature of probiotics has raised concerns among dental professionals, especially concerning their effect on the enamel and dentin. Previous studies have found that probiotics can lower the pH of the saliva and cause essential elements like Calcium and Phosphorus to leach from the enamel. This can alter the surface topography of enamel and increase the risk of enamel defects. Studies have also noted that probiotic bacteria can replace cariogenic bacteria and lower the risk of tooth decay. However, the effect of acid produced by probiotics on the enamel surface remains unclear. Hence, the present study aims to evaluate the effect of probiotics on the surface roughness, microhardness, and elemental composition of enamel compared to 0.1 M Lactic acid (demineralizing agent). Twenty enamel sections were randomly divided into groups and subjected to a pH cycling model using a probiotic suspension and 0.1 M lactic acid. The changes in the surface roughness, microhardness, surface morphology, and elemental composition of the enamel with regard to Carbon, Oxygen, Sodium, Hydrogen, Magnesium, Phosphorus, Fluoride, Chlorine, and Calcium of the enamel were evaluated before and after the emersion in both the groups. The results showed a significant increase in the mean surface roughness in the probiotic group before and after the exposure. The microhardness of the enamel decreased along with altered arrangement of the enamel prisms, increased striations, scratch marks, and pitting after exposure to the probiotic group. A decrease in the atomic/weight% for Calcium, Phosphorous, Fluoride, Aluminium, and Oxygen and an increase in the weight/atomic% for Carbon, Nitrogen, and Sodium were noted compared to the baseline in the probiotic solution. The results in the probiotic group were comparable to the 0.1 M lactic acids. The pH changed from 5.78 to 3.06 at the end of 24 h in the probiotic group. Based on these findings, we conclude that exposure to probiotics can affect microhardness and surface roughness and cause leaching of essential elements like Calcium and Phosphorous from the enamel.

Effect of photobiomodulation therapy on inflammatory cytokines in healing dynamics of diabetic wounds: a systematic review of preclinical studies.

CONTEXT: Delayed wound healing in diabetes mellitus (DM) is due to the overlapping phases of the healing process. The prolonged inflammation and altered levels of inflammatory cytokines lead to deformed cell proliferation. Photobiomodulation alleviates the expression of inflammatory cytokines and promotes tissue repair, thereby restoring the wound healing process. OBJECTIVE: To find out the effect of photobiomodulation therapy (PBMT) in the healing dynamics of diabetic wounds with particular emphasis on interleukin-6, interleukin-1ß, and tumour necrosis factor-α. METHODS: Scientific databases searched using keywords of the population: DM, intervention: PBMT, and outcomes: inflammatory cytokines. RESULTS: We have included five preclinical studies in the present systematic review for qualitative analysis. These studies evaluated the effect of PBMT at different wavelengths, dosage, and time on wound healing in DM. CONCLUSIONS: The systematic review concludes that PBMT regulates inflammatory cytokines levels, enhances cell proliferation, and migration, thereby improving the wound healing properties.

Effect of Photobiomodulation Therapy on Oxidative Stress Markers in Healing Dynamics of Diabetic Neuropathic Wounds in Wistar Rats.

BACKGROUND: Prolonged and overlapping phases of wound healing in diabetes are mainly due to the redox imbalance resulting in the chronicity of the wound. Photobiomodulation therapy works on the principle of absorption of photon energy and its transduction into a biological response in the living tissue. It alleviates the cellular responses, thereby improving the mechanism of wound healing in diabetes. OBJECTIVE: To find out the effect of photobiomodulation therapy of dosage 4 J/cm2 in the healing dynamics of diabetic neuropathic wounds in Wistar rats and its relation with oxidative stress markers. METHODOLOGY: Diabetes was induced using Streptozotocin of 60 mg/kg of body weight to eighteen female Wistar rats. Neuropathy was induced by the sciatic nerve crush injury followed by an excisional wound of 2 cm2 on the back of the animal. Experimental group animals were treated with dosage 4 J/cm2 of wavelength 655 and 808 nm, and control group animals were kept unirradiated. The biomechanical, histopathological, and biochemical changes were analysed in both groups. RESULTS: There was a reduction in mean wound healing time and an increased rate of wound contraction in the experimental group animals compared to its control group. The experimental group showed improved redox status, and histopathological findings revealed better proliferative cells, keratinisation, and epithelialization than un-irradiated controls. CONCLUSIONS: Photobiomodulation therapy of dosage 4 J/cm2 enhanced the overall wound healing dynamics of the diabetes-induced neuropathic wound and optimised the oxidative status of the wound, thereby facilitating a faster healing process.

Lifestyle Modification with Physical Activity Promotion on Leptin Resistance and Quality of Life in Metabolic Syndrome - A Systematic Review with Meta-Analysis.

OBJECTIVE: This study focused to systematically extract, summarize and analyse the data on the effect of lifestyle modification on leptin resistance and quality of life in metabolic syndrome. METHODS: The systematic search was done using PubMed, Cochrane Database, EMBASE, Science Direct, CINAHL, Springer link, Web of Science from 2000-2018. English language articles and quantitative studies focusing on leptin resistance and quality of life were included. Random effect analysis was adopted to pool data and estimate 95% CI. The meta-analysis was done separately for leptin resistance and quality of life which included a total of 9 studies on both RCTs and Non-RCTs. RESULTS: The meta-analysis of RCTs reported insignificant effect of lifestyle modification on leptin resistance in metabolic syndrome when compared to comparison group (-5.94(-14.28, 2.41). Two clinical trials showed a significant effect with pooled data (5.52(2.14, 8.91). Meta-analysis of RCTs focusing on quality of life showed significant effect on mental component (4.89 (0.16, 9.62) of quality of life (2.36 (-3.67, 8.39) when compared to comparison group. CONCLUSION: This meta-analysis suggested that lifestyle modification has a potential to improve leptin resistance and mental component of quality of life in metabolic syndrome. However, more clearly defined studies are required to come to a stronger conclusion.

Persistent attenuation of brain oxidative stress through aging in perinatal maternal separated rat pups supplemented with choline and docosahexaenoic acid or Clitoria ternatea aqueous root extract.

INTRODUCTION: Perinatal maternal separation stress (PMSS) induces brain lipid peroxidation and reduction in endogenous antioxidants. The present study was designed to assess the brain oxidative stress (MDA) and protein thiol levels through various stages of aging in PMSS rat pups supplemented with choline with docosahexaenoic acid (DHA) or Clitoria ternatea (Linn) aqueous root extract (CTR). MATERIAL AND METHODS: Study groups, control, PMSS, PMSS + choline with DHA, PMSS + CTR (n = 6/group) were included in the study. Pups of PMSS groups were separated from their mothers for a period of 6 h/day for 30 days. PMSS + supplemented groups were treated as appropriate during the same period. Rats were sacrificed on day 30, 60, 90, 210 and 360. Brains were processed for MDA and protein thiol levels. RESULTS: Brain MDA levels were significantly increased in PMSS rats at day 30, 60 (p < 0.001), 90 (p < 0.01) and attenuated in PMSS pups supplemented with choline with DHA and CTR at day 30, 60 (p < 0.01), 90 (p < 0.01, p < 0.05) and 360 (p < 0.001) when compared to the same in age-matched controls and PMSS rats, respectively. Alternatively, brain protein thiol levels in PMSS rats were reduced in all age groups when compared to the same in age-matched controls. A significant increase in brain thiol levels was observed in supplemented groups at day 60 (p < 0.01) and 210 (p < 0.01, p < 0.05) when compared to the same in age-matched PMSS rats. CONCLUSIONS: PMSS causes enhanced brain lipid peroxidation (MDA levels) and reduces endogenous antioxidants. Supplementation of choline and DHA or CTR during PMSS in rats persistently attenuates brain oxidative stress through aging.

Antarth, a polyherbal preparation protects against the doxorubicin-induced toxicity without compromising its Antineoplastic activity.

Doxorubicin (DOX), an anthracycline drug widely used for the treatment of various cancers, causes a cumulative dose-dependent cardiotoxicity that is characterized by an irreversible dilated cardiomyopathy and congestive heart failure. Antarth (ANT) a polyherbal preparation was evaluated for its cardioprotective properties against doxorubicin-induced cardiotoxicity in mice. Mice were treated with 25 mg/kg ANT orally once daily for 5 consecutive days before a single intraperitoneal injection of 15 mg/kg doxorubicin. The animals were killed 30 h after DOX treatment. DOX induced a significant elevation in the serum levels of glutamic pyruvic transaminase (GPT), glutamic oxaloacetic transaminase (GOT), creatine kinase (CK-MB) and lactate dehydrogenase (LDH), indicating its acute cardiotoxicity. The treatment of mice with ANT before DOX administration significantly reduced the serum levels of GPT, GOT, CK-MB and LDH indicating that ANT protected against the DOX-induced cardiotoxicity. Pretreatment of mice with 25 mg/kg ANT inhibited the DOX-induced decline in the antioxidant status. Intraperitoneal injection of 1.25 mg/kg DOX once daily for 9 consecutive days significantly improved the survival of mice bearing Ehrlich ascites carcinoma (EAC). Treatment of EAC with 25 mg/kg ANT alone did not affect the anticancer activity of DOX since ANT did not alter the tumor cell growth, the median survival time and average survival time of tumor bearing mice. The present study demonstrates that ANT protects mice against DOX-induced cardiotoxicity, without compromising the antineoplastic activity of DOX.

Antarth, a polyherbal preparation protects against the doxorubicin-induced toxicity without compromising its antineoplastic activity

Doxorubicin (DOX), an anthracycline drug widely used for the treatment of various cancers, causes a cumulative dose-dependent cardiotoxicity that is characterized by an irreversible dilated cardiomyopathy and congestive heart failure. Antarth (ANT) a polyherbal preparation was evaluated for its cardioprotective properties against doxorubicin-induced cardiotoxicity in mice. Mice were treated with 25 mg/kg ANT orally once daily for 5 consecutive days before a single intraperitoneal injection of 15 mg/kg doxorubicin. The animals were killed 30 h after DOX treatment. DOX induced a significant elevation in the serum levels of glutamic pyruvic transaminase (GPT), glutamic oxaloacetic transaminase (GOT), creatine kinase (CK-MB) and lactate dehydrogenase (LDH), indicating its acute cardiotoxicity. The treatment of mice with ANT before DOX administration significantly reduced the serum levels of GPT, GOT, CK-MB and LDH indicating that ANT protected against the DOX-induced cardiotoxicity. Pretreatment of mice with 25 mg/kg ANT inhibited the DOX-induced decline in the antioxidant status. Intraperitoneal injection of 1.25 mg/kg DOX once daily for 9 consecutive days significantly improved the survival of mice bearing Ehrlich ascites carcinoma (EAC). Treatment of EAC with 25 mg/kg ANT alone did not affect the anticancer activity of DOX since ANT did not alter the tumor cell growth, the median survival time and average survival time of tumor bearing mice. The present study demonstrates that ANT protects mice against DOX-induced cardiotoxicity, without compromising the antineoplastic activity of DOX.