No abstract

We have analytically solved the radial Schrödinger equation with inverted Woods-Saxon and Manning-Rosen Potentials. With the ansatz for the wave function, we obtain the generalized wave function and the negative energy spectrum for the system.

The antiretroviral is a non-nucleoside reverse transcriptase inhibitor of human immunodeficiency virus type 1. This study was undertaken to investigate the effect of nevirapine (NVP) administration on gastric acid secretion, pepsin secretion, mucosal secretion, intestinal motility, and transit using apparently healthy albino Wistar rats. Eighty albino Wistar rats (50-125 g body weight) from the start of the experiment were used for the study. Rats in the control group were fed normal rodent chow, while the NVP group was fed by gavage NVP (0.4 mg/kg body weight) two times daily (07:00 and 18:00 hours) in addition to normal rodent chow for 12 weeks. All animals were allowed free access to clean drinking water. Mean basal gastric output and peak acid output following histamine administration in the NVP-treated group were significantly higher (p < 0.001, respectively) compared to the control. Following cimetidine administration, there was significant decrease (p < 0.001) in peak acid output in the NVP-treated group compared to the control. The concentration of gastric pepsin, adherent mucus secretion, and mean value for ulcer score were significantly higher (p < 0.001) compared to their control group, respectively. There were significant increases (p < 0.05, respectively) in intestinal motility and basal contraction (p < 0.05) and increase in intestinal transit of the ileum of NVP-treated rats compared to their control, respectively. Results of the study suggest that NVP administration might provoke gastric ulceration in rats which may be caused by high pepsin, high basal acid output, and increased intestinal motility and transit.

Summary:The comparative effects of chronic (28 days) consumption of kola nut and its active constituent, caffeine diets on locomotor behaviour and body weights in mice were investigated. 30 adult Swiss white mice (15-30g body weight), were used for the study. The open field-maze was employed for the evaluation of locomotor behaviour. Mice in the control group (n = 10) were fed normal rodent chow, mice in the kola nut-fed group (n = 10) were fed kola diet (25% wt/wt of rodent chow) while those in the caffeine-fed group (n = 10) were fed caffeine diet (0.66% wt/wt of rodent chow) for 4 weeks. All animals were allowed free access to clean drinking water. Daily food intake, water intake and body weight change were also measured. Daily food intake in the kola nut and caffeine-fed group of mice was significantly (P<0.001 respectively) lower than the control. There was also a significant (P<0.001) decrease in daily water intake in the caffeine-fed group compared to the control whereas, the apparent decrease of water intake in the kola nut-fed group was not significantly different from the control. Body weight change was also significantly (P<0.001 and P<0.05 respectively) lower in the kola nut and caffeine-fed groups of mice when compared to the control. The frequency of rearing in the open field was significantly (P<0.01) lower in the caffeine-fed group of mice when compared to the control. The frequency of grooming was also significantly (P<0.05) lower in the caffeine-fed group of mice when compared to the control. There was also a significant (P<0.05) decrease in the frequency of light-dark transitions in the light/dark transition box for the caffeine-fed group when compared to the control. The results showed that chronic consumption of kola nut and caffeine diets caused decrease in food intake and body weight. Consumption of caffeine-diet also significantly decreased water intake and locomotor activity. The effect of kola nut-diets on water intake and locomotor activity was not significant. Hence, the effect of kola nut on locomotor behaviour and water intake may not be due to caffeine only.

Asymptomatic and early clinical stages of Parkinson's disease (PD) have been linked with comorbid non‐motor symptoms including dysfunction of the gastrointestinal (GI) tract. Notwithstanding, neuroprotective and gastroprotective effects of Ginkgo biloba supplements (GBS) have been investigated independently. Hence, whether GBS‐mediated GIT‐protective capacity could be helpful in PD via gut–brain anti‐inflammatory signaling still remains unknown. Treatment with GBS significantly repressed the motor behavioral and neuromuscular deficits and prevented loss of striatal dopaminergic loss by improving the level of tyrosine hydroxylase enzyme and suppressing synucleinopathy development. Striatal neurons and ileal epithelial injury following intraperitoneal rotenone administration were accompanied with oxidoinflammatory/nitroinflammatory stress and marked inhibition of cholinergic transmission. Moreover, there was increased striatal executioner caspase‐3 and decreased nuclear factor erythroid‐2‐related factor 2 (Nrf2) immunoexpression, loss of striatal pyramidal neuron with a marked decrease in length and width of the dendritic spines as well as significant hyperplasia of cryptal cells in the ileal epithelial tissues, all which were reversed by the pretreatment + concurrent (Pre‐CONC) and concurrent (CONC) GBS treatment pattern. In sum, we proved the potential dual effects of GBS in preventing both dopaminergic neural‐related impairments and gut wall abnormalities linked with PD.