Abstract The present study entails the systematic development and validation of a stability-indicating RP-HPLC method for the analysis of sitagliptin and ertugliflozin in a fixed-dose combination. Analytical quality by design (AQbD) concepts were used to define critical method variables, employing Pareto risk assessment and a Placket-Burman screening design, preceded by a Box-Behnken design with response surface analysis to optimise critical method parameters such as % acetonitrile (X1), buffer pH (X2) and column oven temperature (X3). Multiple response optimisation (Derringer’s desirability) of variables was accomplished by studying critical analytical attributes, such as resolution, retention time and theoretical plates. The title analytes were separated effectively on a PRONTOSIL C18 column at 37 °C using a mobile phase of acetonitrile:acetate buffer, pH 4.4 (36:64 percent v/v), pumped at a flow rate of 1 mL/min, and UV detection at 225 nm. Linearity was observed over a concentration range of 25-150 µg/mL and 3.75-22.5 µg/mL at retention times of 2.82 and 3.92 min for sitagliptin and ertugliflozin, respectively. The method obeyed all validation parameters of the ICH Q2(R1) guidelines. The proposed robust method allows the study of the selected drugs in pharmaceutical dosage forms as well as in drug stability studies under various stress conditions.

RESUMEN: A pesar de los efectos reportados del tabaco sin humo (TS) sobre el periodonto y la alta prevalencia del uso de TS en poblaciones rurales y en hombres, los estudios sobre este tema específico son limitados. El propósito de esta investigación transversal fue medir el producto final de la peroxidación lipídica (como producto final del estrés oxidativo), es decir, malondialdehído (MDA) en la saliva de pacientes con gingivitis, periodontitis crónica y evaluar la influencia del tabaco sin humo en el malondialdehído salival (S-MDA). Se incluyeron en el estudio un total de 30 pacientes con gingivitis, 30 con periodontitis crónica y 30 masticadores de tabaco sin humo con periodontitis crónica y 30 sujetos periodontalmente sanos. Se registraron el índice de placa (PI), el índice gingival (GI), la profundidad de la bolsa de sondeo (PD) y la pérdida de adherencia clínica (CAL), seguidos de la recogida de muestras de saliva estimuladas. Los niveles de MDA en saliva se evaluaron mediante espectrofotometría UV. Hubo un aumento estadísticamente significativo en los niveles de MDA en saliva en gingivitis, periodontitis crónica y en masticadores de tabaco sin humo con periodontitis crónica en comparación con el grupo sano. Los niveles más altos de MDA en saliva en el grupo de gingivitis, periodontitis crónica y masticadores de tabaco sin humo con periodontitis crónica reflejan un aumento de la actividad de los radicales de oxígeno durante la inflamación periodontal.

ABSTRACT: Despite the reported effects of smokeless tobacco (ST) on the periodontium and high prevalence of ST use in rural populations and in males studies on this specific topic are limited. The purpose of this cross-sectional investigation was to measure lipid peroxidation (as an end product of oxidative stress) end product i.e. Malondialdehyde (MDA) in saliva of patients with gingivitis, chronic periodontitis and to assess the influence of smokeless tobacco on Salivary Malondialdehyde (S-MDA). Total 30 patients with gingivitis, 30 with chronic periodontitis and 30 Smokeless Tobacco Chewers with Chronic Periodontitis and 30 periodontally healthy subjects were included in the study. Plaque Index (PI), Gingival Index (GI), Probing Pocket Depth (PD), and Clinical Attachment Loss (CAL) were recorded followed by stimulated Saliva sample collection. Salivary MDA Levels were assessed by UV Spectrophotometry. There was a statistically significant increase in the salivary MDA levels in gingivitis, chronic periodontitis and in smokeless tobacco chewers with chronic periodontitis when compared with healthy group. Higher salivary MDA levels in gingivitis group, chronic periodontitis, and smokeless tobacco chewers with chronic periodontitis reflects increasedoxygen radical activity during periodontal inflammation.

Resumen El síndrome respiratorio agudo severo coronavirus 2 (SARS-CoV-2) que causa la enfermedad por coronavirus (COVID-19) ha provocado una crisis en la salud global. Antes de la llegada de esta pandemia, se tenia una carga importante de enfermedad cardiovascular a nivel mundial. Con la introducción del nuevo virus, el mundo ahora se enfrenta a un doble peligro. Los primeros informes han sugerido un mayor riesgo de muerte en personas con trastornos cardio-metabólicos de base. Los efectos causados por el COVID-19, en el sistema cardiovascular aun no están bien determinados, sin embargo, el conocimiento sobre otras epidemias virales previamente ocurridas en el mundo, sugieren que estas infecciones pueden desencadenar síndromes coronarios agudos, arritmias e insuficiencia cardíaca a través de mecanismos directos e indirectos. En este artículo, nuestro objetivo fue analizar los efectos y los posibles mecanismos subyacentes de COVID -19, así como las posibles implicaciones de los tratamientos dirigidos contra este virus en el sistema cardiovascular.

Abstract Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) which causes coronavirus disease 2019 (COVID-19) has resulted in a global health crisis. Prior to the arrival of this viral pandemic, the world was already plagued with a significant burden of cardiovascular disease. With the introduction of the novel virus, the world now faces a double jeapordy. Early reports have suggested an increased risk of death in individuals with underlying cardio-metabolic disorders. The exact effects of COVID-19 on the cardiovascular system are not well determined, however lessons from prior viral epidemics suggest that such infections can trigger acute coronary syndromes, arrhythmias and heart failure via direct and indirect mechanisms. In this article, we aimed to discuss the effects and potential underlying mechanisms of COVID -19 as well as potential implications of treatments targeted against this virus on the cardiovascular system.

Abstract Interleukin 17(IL-17) is a pro-inflammatory cytokine produced mainly by Th17 cells. The present study was undertaken to investigate a possible association between IL-17 A genetic polymorphism at (-197A/G) and susceptibility to chronic and localized aggressive periodontitis (LAgP) in an Indian population. The study was carried out on 105 subjects, which included 35 LAgP patients, 35 chronic periodontitis patients and 35 healthy controls. Blood samples were drawn from the subjects and analyzed for IL-17 genetic polymorphism at (-197A/G), by using the polymerase chain reaction-restriction fragment length polymorphism method. A statistically significant difference was seen in the genotype distribution among chronic periodontitis patients, LAgP patients and healthy subjects. There was a significant difference in the distribution of alleles among chronic periodontitis patients, LAgP patients and healthy subjects. The odds ratio for A allele versus G allele was 5.1 between chronic periodontitis patients and healthy controls, and 5.1 between LAgp patients and healthy controls. Our study concluded that IL-17 A gene polymorphism at (-197A/G) is linked to chronic periodontitis and LAgP in Indian population. The presence of allele A in the IL-17 gene polymorphism (-197A/G) can be considered a risk factor for chronic periodontitis and LAgP.