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"Azmatullah, Syed"
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Pharmacological evaluation of newly synthesized organotin IV complex for antiulcer potential
The present study aims to investigate the newly synthesized organotin (IV) complex (2E, 2′E) dibutylstannanediyl bis (4-(4-nitrophenyl) amino)-4-oxobut-2-enoate (DTN) for its anti-ulcer potential. Characterization performed by carbon nuclear magnetic resonance spectroscopy proved that all values are in the expected ranges of the new compound. Gastroprotective activity of DTN was evaluated through
in-silico,
anti-
H. pylori,
in-vitro
,
in-vivo, and ex-vivo proteomic analysis.
In-silico
analysis shows that DTN possess stable binding with protein targets involved in gastric ulcer pathophysiology. DTN exhibited an inhibitory effect against 2,2-diphenyl-1-picrylhydrazyl,
H. pylori
and hydrogen potassium ATPase (H
+
/K
+
-ATPase). The antiulcer activity was performed using an ethanol-induced gastric ulcer model in rats. Anti-oxidant profile of DTN showed a significant increase in glutathione-S-transferase, glutathione and catalase levels whereas lipid peroxidation levels were reduced. Histopathological findings confirmed that DTN protected the gastric mucosa of rats. Inflammatory markers tumor necrosis factor-alpha, nuclear factor kappa B, cyclooxygenase-2, interleukin 6 and interleukin-1β were reduced and prostaglandin-E
2
restored expression of these cytokines in DTN pretreated animals when analyzed by using immunohistochemistry, enzyme-linked immunosorbent assay and western blot techniques. In real-time polymerase chain reaction technique, the expression of H
+
/K
+
-ATPase was downregulated in DTN pretreated group. DTN did not cause any mortality up to 400 mg/Kg. This study indicates that the newly synthesized compound DTN, possess stable binding against selected targets. DTN exhibits a gastro-protective effect, mediated via anti-
H. pylori,
H
+
/K
+
-ATPase inhibition, anti-oxidant and anti-inflammatory pathways, exploring its therapeutic potential in gastric ulcer management.
Journal Article
The Mechanism of Central and Peripheral Histamine Induced Hypothermia in the Rat
The effector mechanisms involved in the hypothermia resulting from systemic or central administration of histamine to the conscious rat, were unknown. It has been suggested that increased cutaneous heat loss may be involved. To establish the mechanism(s) by which histamine administration causes hypothermia, changes in body temperature, the cardiovascular system and several thermoregulatory effector mechanisms were studied following systemic or central histamine administration to the conscious rat restrained at ambient temperatures between 14°C and 26°C. Systemic histamine administration caused biphasic changes in body temperature. The initial hyperthermia, apparent at higher ambient temperatures, was associated with decreased cutaneous heat loss. The hypothermia, apparent at lower ambient temperatures, was associated with reduced oxygen consumption, respiratory rate and muscular activity. Non-shivering thermogenesis by brown adipose tissue and evaporative heat loss from the rat did not appear to be influenced by systemic histamine administration. The cardiovascular changes observed resembled those associated with hypovolaemic shock. High plasma histamine concentrations were observed following systemic histamine administration and the possibility of penetration into brain tissue was discussed. I.c.v. administration of histamine also caused hypothermia associated with reduced muscular activity. This effect was independent of a major change in blood pressure and no cutaneous vasodilatation was observed. The effect appeared to be mediated by histamine H1 receptors. I.c.v. administration of mepyramine and cimetidine also resulted in hypothermia associated with decreased muscular activity. The significance of these findings to thermoregulation is discussed.
Dissertation
Further evidence of biallelic NAV3 variants associated with recessive neurodevelopmental disorder with dysmorphism, developmental delay, intellectual disability, and behavioral abnormalities
Neuron navigators (NAVs) are cytoskeleton-associated proteins well known for their role in axonal guidance, neuronal migration, and neurite growth necessary for neurodevelopment. Neuron navigator 3 (NAV3) is one of the three NAV proteins highly expressed in the embryonic and adult brain. However, the role of the
NAV3
gene in human disease is not well-studied. Recently, five bi-allelic and three mono-allelic variants in
NAV3
were reported in 12 individuals from eight unrelated families with neurodevelopmental disorder (NDD). Here, we report five patients from three unrelated consanguineous families segregating autosomal recessive NDD. Patients have symptoms of dysmorphism, intellectual disability, developmental delay, and behavioral abnormalities. Exome sequencing (ES) was performed on two affected individuals from one large family, and one affected individual from each of the other two families. ES revealed two homozygous nonsense c.6325C > T; p.(Gln2109Ter) and c.6577C > T; p.(Arg2193Ter) and a homozygous splice site (c.243 + 1G > T) variants in the
NAV3
(NM_001024383.2). Analysis of single-cell sequencing datasets from embryonic and young adult human brains revealed that
NAV3
is highly expressed in the excitatory neurons, inhibitory neurons, and microglia, consistent with its role in neurodevelopment. In conclusion, in this study, we further validate biallelic protein truncating variants in
NAV3
as a cause of NDD, expanding the spectrum of pathogenic variants in this newly discovered NDD gene.
Journal Article
A comparison of fluoroquinolones versus other antibiotics for treating enteric fever: meta-analysis
Objectives To review evidence supporting use of fluoroquinolones as first line agents over other antibiotics for treating typhoid and paratyphoid fever (enteric fever).Design Meta-analysis of randomised controlled trials.Data sources Cochrane Infectious Diseases Group specialised register, CENTRAL (issue 4, 2007), Medline (1966-2007), Embase (1974-2007), LILACS (1982-2007), selected conferences, reference lists, and ongoing trial register (November 2007).Review methods Trials comparing fluoroquinolones with chloramphenicol, cephalosporins, or azithromycin in culture-proven enteric fever were included. Two reviewers extracted data and assessed methodological quality. Odds ratios with 95% confidence intervals were estimated. Trials recruiting over 60% children were analysed separately from trials on adults. Primary outcomes studied were clinical failure, microbiological failure, and relapse.Results Twenty trials were included. Trials were small and often of limited methodological quality. Only 10 trials concealed allocation and only three were blinded. In trials on adults, fluoroquinolones were not significantly different from chloramphenicol for clinical failure (594 participants) or microbiological failure (n=378), but reduced clinical relapse (odds ratio 0.14 (95% confidence interval 0.04 to 0.50), n=467, 6 trials). Azithromycin and fluoroquinolones were comparable (n=152, 2 trials). Compared with ceftriaxone, fluoroquinolones reduced clinical failure (0.08 (0.01 to 0.45), n=120, 3 trials) but not microbiological failure or relapse. Compared with cefixime, fluoroquinolones reduced clinical failure (0.05 (0.01 to 0.24), n=238, 2 trials) and relapse (0.18 (0.03 to 0.91), n=218, 2 trials). In trials on children infected with nalidixic acid resistant strains, older fluoroquinolones (ofloxacin) produced more clinical failures than azithromycin (2.67 (1.16 to 6.11), n=125, 1 trial), but there were no differences with newer fluoroquinolones (gatifloxacin, n=285, 1 trial). Fluoroquinolones and cefixime were not significantly different (n=82, 1 trial).Conclusions In adults, fluoroquinolones may be better than chloramphenicol for preventing clinical relapse. Data were limited for other comparisons, particularly for children.
Journal Article