American Journal of PharmTech Research

The present study aimed to formulate and evaluate Clindamycin hydrochloride-loaded proniosomal gel for topical drug delivery with improved entrapment efficiency, controlled release, antimicrobial activity, and skin tolerability. The formulations were evaluated for preformulation properties, drug–excipient compatibility, entrapment efficiency, particle size, zeta potential, SEM, physicochemical properties, in-vitro drug release, release kinetics, antimicrobial activity, skin irritation, and stability. UV spectrophotometric analysis showed maximum absorption at 210 nm, with good linearity over 2–10 µg/ml (R² = 0.9992). FTIR studies indicated no significant incompatibility between Clindamycin hydrochloride and the selected excipients (Span 60, cholesterol, and soya lecithin). Among the prepared formulations, F6 was selected as the optimized formulation. It exhibited an entrapment efficiency of 86.7 ± 0.3%, particle size of 249.69 nm, PDI of 0.362, and zeta potential of 35.7 mV. SEM revealed discrete, approximately spherical vesicles. The optimized gel showed a pH of 6.45 ± 0.03, spreadability of 28.9 ± 0.05 g·cm/sec, viscosity of 8890 cps, and drug content of 85.7 ± 0.3%. In-vitro drug release reached 86.34% at 7 hours, following first-order kinetics (R² = 0.9901). The formulation demonstrated antimicrobial activity and caused no visible erythema or edema. Additionally, only minor changes in entrapment efficiency were observed during the four-week stability study. Overall, F6 demonstrated promising physicochemical properties, controlled drug release, antimicrobial activity, and topical tolerability.

Alzheimer’s Disease (AD) is a progressive neurodegenerative disease that results in the loss of memory, motor function, ability to think, and other basic functions required for day-to-day life. The causes of the disease are still being investigated, but scientists and researchers have mostly agreed on one of the major genetic contributions to the disease. The excess buildup of two proteins, Tau and β-amyloid, limits communication between nerve cells or neurons. The buildup of these proteins only increases with the progression of the disease. This paper will discuss the genetic causes of AD, the process behind the formation of neurofibrillary tangles and amyloid plaques, recent neuroimaging techniques that help diagnose the disease, current symptomatic treatments, and upcoming future treatments that may be able to slow the progression of the disease significantly. Patients with AD exhibit a substantial accumulation of amyloid-β (Aβ) plaques and neurofibrillary tangles (NFTs) within their brains, accompanied by a cascade of pathological processes such as neuroinflammation, synaptic dysfunction, mitochondrial and bio-energetic disturbances, as well as vascular abnormalities. Collectively these processes may ; https://doi.org/10.1038/s41392-024-01911-3 ultimately lead to the death of neurons.[3,4] AD can be categorized into two types: early-onset familial Alzheimer’s disease (FAD) and late-onset Alzheimer’s disease (LOAD). FAD is rare (approximately 5% of AD cases) with typical disease onset at 65 years or younger, usually caused by gene variants of amyloid pre cursor protein (APP), presenilin (PSEN1) and PSEN2. LOAD is more common (~ 95% of AD cases) with disease onset older than 65 years and is associated with a combination of genetic (such as apolipo-protein E ε4 allele), environmental, and lifestyle factors [5]. In addition to these pathological hall marks, multiple alterations converge in the pathogenesis of AD. Elevated levels of inflammatory markers in AD patients indicate that neuroinflammation plays a significant role in disease pathogenesis [6] additionally, mitochondrial defects have been implicated in the exhaustion of nerve cells [7]. The disease is further

Background: Cephalosporins and sulfonylureas represent clinically important drug classes used in the management of bacterial infections and type 2 diabetes mellitus, respectively. Their distinct molecular targets, pharmacokinetic properties, therapeutic benefits, and adverse-effect profiles illustrate fundamental principles of pharmacological selectivity and rational drug utilisation. Objective: This review examines the pharmacodynamics, pharmacokinetics, classification, therapeutic applications, mechanisms of resistance or treatment failure, safety considerations, and contemporary clinical relevance of cephalosporins and sulfonylureas. Methods: A narrative literature review was undertaken using established pharmacology literature, biomedical review articles, and accessible clinical reference sources. Relevant evidence was synthesised to explain the mechanisms of action, therapeutic positioning, drug interactions, and limitations of both classes. Results: Cephalosporins inhibit bacterial cell-wall synthesis through interactions with penicillin-binding proteins. Their antibacterial spectrum varies with molecular structure, generation, susceptibility patterns, and resistance mechanisms, including β-lactamase production and altered target proteins. Sulfonylureas stimulate pancreatic β-cell insulin secretion by binding sulfonylurea receptors associated with ATP-sensitive potassium channels. Although effective glucose-lowering agents, they can cause hypoglycaemia and weight gain, with risks influenced by renal function, nutrition, age, and concomitant medicines. Both classes require individualised selection, appropriate dosing, monitoring, and consideration of patient-specific factors. Conclusion: Rational use of these pharmacologically distinct agents depends on understanding their molecular mechanisms, therapeutic indications, limitations, and safety profiles. Antimicrobial stewardship and individualised diabetes management are essential to optimise clinical outcomes and minimise preventable harm. Keywords Antimicrobial stewardship; β-lactam resistance; insulin secretion; hypoglycaemia; rational pharmacotherapy.