http://localhost:80/xmlui/handle/123456789/13307 2026-04-24T18:18:13Z 2026-04-24T18:18:13Z Zafar, Saba Rasul, Akhtar Iqbal, Muhammad Shahid Rasool, Maria Ahmed, Bilal Qadir, Muhammad Imran http://localhost:80/xmlui/handle/123456789/13441 2022-10-20T10:00:06Z 2021-01-16T00:00:00Z

Title: Nanobiotechnology: Cradle for revolution in drug carrier systems Authors: Zafar, Saba; Rasul, Akhtar; Iqbal, Muhammad Shahid; Rasool, Maria; Ahmed, Bilal; Qadir, Muhammad Imran Abstract: : The role of nanobiotechnology in the treatment of diseases is limitless. In this review we tried to focus main aspects of nanotechnology in drug carrier systems for treatment and diagnosis of various diseases such as cancer, pulmonary diseases, infectious diseases, vaccine development, diabetes mellitus and the role of nanotechnology on our economy and its positive social impacts on our community. We discussed here about the different “Biotechnano Strategies” to develop new avenues and ultimately improve the treatment of multiple diseases.

2021-01-16T00:00:00Z Ilahi, Ikram Taqweem Ul Haq http://localhost:80/xmlui/handle/123456789/13440 2022-10-20T09:59:43Z 2021-01-16T00:00:00Z

Title: Role of Kisspeptin-GPR54 system in regulation of reproductive functions in human and other mammals Authors: Ilahi, Ikram; Taqweem Ul Haq Abstract: Kisspeptin is a 54- amino acid peptide that acts as a ligand of a receptor called GPR54 which is basically a transmembrane receptor that spins seven times across the cell membrane and coupled with G-protein. Kisspeptin regulates the development of reproductive functions and the onset of puberty in human and other mammals by acting at the brain, hypothalamus, pituitary and gonad levels of reproductive axis. Kisspeptin is also involved in regulation of trophoblastic invasion during pregnancy, ovulation, and sperm hyperactivation. Inactivating mutations in human kisspeptin gene (KISS1) cause idiopathic hypogonadotropic hypogonadism. Some mutations in human kisspeptin receptor gene (KISS1R) make the receptor inactive which result in idiopathic hypogonadotropic hypogonadism. Some mutations in human KISS1R gene make the receptor prematurely activated and result in the development of central precocious puberty. Central precocious puberty is also caused by some mutations in human KISS1 gene that make the kisspeptin resistant to degradation. This leads to an increased basal kisspeptin level and subsequently the development of central precocious puberty. Higher kisspeptin level has been detected in the serum and plasma of central precocious puberty patients, which suggest that serum or plasma kisspeptin level can be used as a marker for diagnosis of central precocious puberty.

2021-01-16T00:00:00Z Altaf, Iqbal Azmat, Rafia http://localhost:80/xmlui/handle/123456789/13439 2022-10-20T09:59:03Z 2021-01-16T00:00:00Z

Title: IR study of degradation of acetaminophen by iron nano-structured catalyst Authors: Altaf, Iqbal; Azmat, Rafia Abstract: Full degradation of acetaminophen (paracetamol) in aqueous solution was investigated at room temperature through heterogeneous iron nano-structured as catalyst in this article. Iron Nano-structured was prepared through simple hydrothermal processes using Iron oxide (Fe2O3) as precursor. The catalytic activity of as prepared Nano-catalyst (NC) was investigated in the degradation of the acetaminophen as an environmental pollutant, commonly called paracetamol, under different operating parameters like pH, dosages of acetaminophen and dose of NC. Remarkable differences in IR spectra were observed after reaction which showed complete degradation of 15 ppm of Acetaminophen using 0.1 g of nano-structured with the recovery of NC followed by its activity four times with full catalytic performance

2021-01-16T00:00:00Z Zaidi, Syeda Nuzhat Fatimah Usman, Sheikh Muhammad http://localhost:80/xmlui/handle/123456789/13437 2022-10-20T09:58:14Z 2021-01-16T00:00:00Z

Title: Salicylic acid attenuates gentamicin-induced nephrotoxicity in rabbits Authors: Zaidi, Syeda Nuzhat Fatimah; Usman, Sheikh Muhammad Abstract: Gentamicin (GM) is a generally utilized as an antibiotic against dangerous and life threatening contaminations, yet its value is restricted by the development of nephrotoxicity. The present investigation was intended to decide the defensive impact of salicylic acid (SA) in gentamicin-induced nephrotoxicity in rabbits. Quantitative assessment of gentamicin-induced structural changes and level of functional modifications in the kidneys were performed by biochemical examinations keeping in mind the end goal is to decide the potential protective impacts of SA co-administration with gentamicin. Gentamicin was seen to cause a serious nephrotoxicity which was proved by a plasma urea, plasmacreatinine, plasma uric acid, plasma Na+ , plasma K+ , intra-erythrocyte Na+ and intra-erythrocyte K+ levels. On the other hand, simultaneous SA administration protected kidney tissue against the oxidative damage and the nephrotoxic effect caused by GM treatment. The outcomes from our investigation show that SA supplement lessens oxidative-stress related to renal damage by reducing oxygen free radicals in gentamicin-treated rabbits.

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