Changes in Glial Fibrillary Acidic Protein-Immunoreactive Astrocytes in the Prefrontal Cortex of the Male Rat following Chronic Khat Use.

Background: Long-term khat consumption is associated with significant neurocognitive changes, which have been elucidated in behavioral studies. With current research showing the centrality of astrocytes and other glial cells in neuronal signaling, there is possibility that these cells are also affected by chronic khat use. There is little literature on the structural changes in the prefrontal cortex neuronal and astrocytic cytoarchitecture and morphometry in chronic khat users. Objective: The objective of this study was to describe the changes in astrocyte morphometry and structure in rats after long-term use of khat (miraa). Materials and Methods: Adult male Wistar rats, aged 2-3 months, weighing 200-300 g were randomized into four groups of 10 each (control, Group 1, Group 2, and Group 3) to correspond with those used as controls and those that received 500 mg/kg, 1000 mg/kg, and 2000 mg/kg body weight khat extracts, respectively. Fresh khat leaves were purchased from Maua market in Meru, and crude extract was prepared using lyophilization. The control rats were fed on normal diet, while the experimental groups were fed on normal diet and khat extracts using oral gavage for 6 weeks. The animals were sacrificed and their brains were removed. We performed immunohistochemical visualization of astrocytes using glial fibrillary acidic protein. Photomicrographs of the stained sections were transferred to ImageJ Fiji software to study the astrocyte density and astrocytic processes. We used Kruskal-Wallis test to correlate the four animal groups in terms of astrocyte densities. Results: We observed an increase in the average number of astrocytes with increasing doses of khat compared to controls, with those in Group 3 (2000 mg/kg) having an exuberant reactive astrocytosis. Further, escalating khat doses resulted in increased glial fibrillary acidic protein immunoreactivity in the nuclei and astrocytic processes, gliotic changes, and increased complexity of astrocytic processes. Conclusion: Chronic khat use, especially at high doses, results in reactive astrocytosis and astrogliosis, which may be part of the mechanisms involved in the cognitive changes associated with its use.

Topographic and Structural Anatomy of the Suspensory Ligament of the Penis: Implications for Phalloplasty.

BACKGROUND: The suspensory ligamentous system of the penis supports the penis when erect and plays a key role during coitus. These ligaments, which are prone to injury during coitus, are clinically important in penile reconstruction procedures. OBJECTIVES: The current study investigated the macro- and microanatomy of the suspensory ligamentous system of the penis to determine the origin, course, insertion, dimensions, and tissue composition of these ligaments, knowledge of which is vital for successful penile reconstruction procedures. METHODS: The study utilized a total of 49 cadavers. Gross anatomy dissection, MRI, and histological staining were performed to elucidate the topography, dimensions, and tissue composition of the suspensory ligaments of the penis. RESULTS: Three ligaments were observed to form the suspensory ligamentous system of the penis. The most superficial is the fundiform ligament, which consists of superficial bundles and deep median bundles, with the former arising from the Scarpa's fascia and the latter arising from the linea alba of the anterior abdominal wall; both inserted into the superficial fascia of the penis. The suspensory ligament of the penis arose from the pubic symphysis and inserted into the deep fascia (Buck's fascia) of the penis. The arcuate ligament arose from the body of the pubis and pubic symphysis and inserted into the Buck's fascia. The ligaments were determined to consist of adipose tissue, collagen fibers, elastic fibers and reticular fibers, in varying proportions. CONCLUSIONS: The suspensory ligaments of the penis exhibit a fan-like structure on the penis that allows the forward movement of the penis as a result of engorgement of the erectile bodies while simultaneously offering support.

Potential role of inducible nitric oxide synthase (iNOS) activity in testicular dysfunction following co-administration of alcohol and combination antiretroviral therapy (cART) in diabetic rats: an immunohistochemistry study.

Diabetes, alcohol abuse, and combination antiretroviral therapy (cART) use have been reported to cause multi-organ complications via induction of oxidative stress and inflammation. Moreover, these are the most common factors implicated in male reproductive dysfunctions. This study evaluated testicular oxidative stress, inflammation, apoptosis, and germ cell proliferation in diabetic rats receiving alcohol or cART and their combination. Thirty adult male Sprague Dawley rats were divided into five groups, each consisting of six rats; control, diabetic only (DM), diabetic treated with alcohol (DM + A), diabetic treated with cART (DM + cART), and diabetic treated with both alcohol and cART (DM + A + cART). After 90 days of treatment, the rats were terminated, and the testes were extracted and processed for immunohistochemistry analysis for oxidative stress, inflammatory cytokines, apoptosis, and cell proliferation marker. In comparison to the control, oxidative stress markers, inducible nitric oxide synthase (iNOS), malondialdehyde (MDA), and 8-hydroxydeoxyguanosine (8-OHDG) increased significantly in all treated groups. Expression of testicular proinflammatory cytokines, interleukin-1ß, and tumor necrosis factor-α was upregulated in all treated groups, but interleukin-6 was upregulated in DM, DM + cART, and DM + A + cART treated groups and was downregulated in the DM + A treated group. All treated animal groups showed an upregulation of apoptotic marker (caspase 3) and a downregulation of proliferation marker (Ki-67). However, Ki-67 staining intensity significantly increased in treated animals compared to the control. These findings suggest that diabetes, alcohol abuse, cART use, and their combination via iNOS activity upregulation can induce inflammation and oxidative stress in testicular tissue, stimulating germ cell apoptosis and proliferation inhibition leading to failure of spermatogenesis.

Neonatal Orally Administered Zingerone Attenuates Alcohol-Induced Fatty Liver Disease in Experimental Rat Models.

Alcohol intake at different developmental stages can lead to the development of alcohol-induced fatty liver disease (AFLD). Zingerone (ZO) possess hepato-protective properties; thus, when administered neonatally, it could render protection against AFLD. This study aimed to evaluate the potential long-term protective effect of ZO against the development of AFLD. One hundred and twenty-three 10-day-old Sprague-Dawley rat pups (60 males; 63 females) were randomly assigned to four groups and orally administered the following treatment regimens daily during the pre-weaning period from postnatal day (PND) 12-21: group 1-nutritive milk (NM), group 2-NM +1 g/kg ethanol (Eth), group 3-NM + 40 mg/kg ZO, group 4-NM + Eth +ZO. From PND 46-100, each group from the neonatal stage was divided into two; subgroup I had tap water and subgroup II had ethanol solution as drinking fluid, respectively, for eight weeks. Mean daily ethanol intake, which ranged from 10 to 14.5 g/kg body mass/day, resulted in significant CYP2E1 elevation (p < 0.05). Both late single hit and double hit with alcohol increased liver fat content, caused hepatic macrosteatosis, dysregulated mRNA expression of SREBP1c and PPAR-α in male and female rats (p < 0.05). However, neonatal orally administered ZO protected against liver lipid accretion and SREBP1c upregulation in male rats only and attenuated the alcohol-induced hepatic PPAR-α downregulation and macrosteatosis in both sexes. This data suggests that neonatal orally administered zingerone can be a potential prophylactic agent against the development of AFLD.

Co-administration of alcohol and combination antiretroviral therapy (cART) in male Sprague Dawley rats: A study on testicular morphology, oxidative and cytokines perturbations.

Alcohol consumption alongside combination antiretroviral therapy (cART) has attracted research interest, especially because of increasing male infertility. This study investigated the combined effects of alcohol and cART on testicular morphology, biomarkers of oxidative stress, inflammation, and apoptosis. Rats, weighing 330-370 g, were divided into four groups of six animals each; control, alcohol treated (A), cART, and alcohol plus cART treated (A+cART). Following 90 days treatment period, animals were euthanized, testis extracted, and routinely processed for histology and immunohistochemical analysis. Significantly decreased epithelial area fraction, increased luminal and connective tissue area fractions, and reduction of epithelial height and spermatocyte number, were recorded in the treated groups compared to control. Extensive seminiferous epithelial lesions including widened intercellular space, karyolysis, and sloughing of germinal epithelium were recorded in all the treated groups. Furthermore, upregulation of inducible nitric oxide synthase and 8-hydroxydeoxyguanosine, interleukin-6, and caspase 3 recorded in treated animals, was more significant in A+cART group. Also, the levels of interleukin-1ß and tumor necrosis factor-α were more elevated in A and cART treated groups than in A+cART, while MDA was significantly elevated in cART and A+cART treated groups compared to control group. Altogether, the results indicate testicular toxicity of the treatments. It is concluded that consuming alcohol or cART induces oxidative stress, inflammation, and apoptosis in testis of rats, which lead to testicular structural and functional derangements, which are exacerbated when alcohol and cART are consumed concurrently. The result will invaluably assist clinicians in management of reproductive dysfunctions in male HIV/AIDS-alcoholic patients on cART.

Boophone disticha attenuates five day repeated forced swim-induced stress and adult hippocampal neurogenesis impairment in male Balb/c mice.

Depression is one of the most common neuropsychiatric disorders and is associated with dysfunction of the neuroendocrine system and alterations in specific brain proteins. Boophone disticha (BD) is an indigenous psychoactive bulb that belongs to the Amaryllidacae family, which is widely used in Southern Africa to treat depression, with scientific evidence of potent antidepressant-like effects. The present study examined the antidepressant effects of BD and its mechanisms of action by measuring some behavioural parameters in the elevated plus maze, brain content of corticosterone, brain derived neurotropic factor (BDNF), and neuroblast differentiation in the hippocampus of Balb/c mice exposed to the five day repeated forced swim stress (5d-RFSS). Male Balb/c mice were subjected to the 5d-RFSS protocol to induce depressive-like behaviour (decreased swimming, increased floating, decreased open arm entry, decreased time spent in the open arms and decreased head dips in the elevated plus maze test) and treated with distilled water, fluoxetine and BD. BD treatment (10 mg/kg/p.o for 3 weeks) significantly attenuated the 5d-RFSS-induced behavioural abnormalities and the elevated serum corticosterone levels observed in stressed mice. Additionally, 5d-RFSS exposure significantly decreased the number of neuroblasts in the hippocampus and BDNF levels in the brain of Balb/c mice, while fluoxetine and BD treatment attenuated these changes. The antidepressant effects of BD were comparable to those of fluoxetine, but unlike fluoxetine, BD did not show any anxiogenic effects, suggesting better pharmacological functions. In conclusion, our study shows that BD exerted antidepressant-like effects in 5d-RFSS mice, mediated in part by normalizing brain corticosterone and BDNF levels.

Ethyl Acetate Fractions of Tectona Grandis Crude Extract Modulate Glucose Absorption and Uptake as Well as Antihyperglycemic Potential in Fructose-Streptozotocin-Induced Diabetic Rats.

Type 2 diabetes (T2D) is a global health challenge with increased morbidity and mortality rates yearly. Herbal medicine has provided an alternative approach to treating T2D with limited access to formal healthcare. Tectona grandis is being used traditionally in the treatment of diabetes. The present study investigated the antidiabetic potential of T. grandis leaves in different solvent extractions, and the crude extract that demonstrated the best activity was further fractionated through solvent-solvent partitioning. The ethyl acetate fraction of the ethanol crude extract showed the best antidiabetic activity in inhibiting α-glucosidase, delaying glucose absorption at the small intestine's lumen, and enhancing the muscle's postprandial glucose uptake. The ethyl acetate fraction was further elucidated for its ability to reduce hyperglycemia in diabetic rats. The ethyl acetate fraction significantly reduced high blood glucose levels in diabetic rats with concomitant modulation in stimulated insulin secretions through improved pancreatic ß-cell function, insulin sensitivity by increasing liver glycogen content, and reduced elevated levels of liver glucose-6-phosphatase activity. These activities could be attributed to the phytochemical constituents of the plant.

Non-Genetic-Induced Zebrafish Model for Type 2 Diabetes with Emphasis on Tools in Model Validation.

The unrelenting increase in the incidence of type 2 diabetes (T2D) necessitates the urgent need for effective animal models to mimic its pathophysiology. Zebrafish possess human-like metabolic traits and share significant genetic similarities, making them valuable candidates for studying metabolic disorders, including T2D. This review emphasizes the critical role of animal models in diabetes research, especially focusing on zebrafish as an alternative model organism. Different approaches to a non-genetic model of T2D in zebrafish, such as the glucose solution, diet-induced, chemical-induced, and combined diet-induced and glucose solution methods, with an emphasis on model validation using indicators of T2D, were highlighted. However, a significant drawback lies in the validation of these models. Some of these models have not extensively demonstrated persistent hyperglycemia or response to insulin resistance and glucose tolerance tests, depicted the morphology of the pancreatic ß-cell, or showed their response to antidiabetic drugs. These tools are crucial in T2D pathology. Future research on non-genetic models of T2D in zebrafish must extensively focus on validating the metabolic deficits existing in the model with the same metabolic defects in humans and improve on the existing models for a better understanding of the molecular mechanisms underlying T2D and exploring potential therapeutic interventions.

Neonatal Oral Administration of Chrysin Prevents Long-Term Development of Non-Alcoholic Fatty Liver Disease in a Sexually Dimorphic Manner in Fructose Nurtured Sprague Dawley Rats.

High-fructose diets are linked with the development of non-alcoholic fatty liver disease (NAFLD), the management of which is a burden to society. Interventions with phytochemicals in the early postnatal period may prevent fructose-induced NAFLD later in adulthood. We investigated the protective potential of chrysin against fructose-induced NAFLD. Four-day-old male and female suckling Sprague Dawley rats (N = 112) were randomly grouped and orally gavaged daily with distilled water (negative Control-Cn + W), chrysin(Chr-100 mg/kg), fructose-solution (Fr-20% w/v), and Chr + Fr between postnatal day (PND) 4 and 21 and then weaned onto normal rat chow and plain drinking water to PND 55. From PND 56 to 130, half of the rats continued on plain water, and the rest had Fr as drinking fluid. Terminally, the liver tissue was collected, and the lipid content was determined and histologically assessed for NAFLD. Dietary Fr induced an increased hepatic lipid content (p = 0.0001 vs. Cn + W) both sexes, and it was only attenuated by neonatal Chr in female rats (p < 0.05). Histologically, there was increased microvesicular steatosis (p = 0.0001 vs. Cn + W) in both sexes, and it was prevented by neonatal Chr (p > 0.05). Fr caused macrovesicular steatosis (p = 0.01 vs. Cn + W) in females only, and chrysin did not prevent it (p > 0.05). Fr induced hepatocellular hypertrophy, and inflammation was observed in females only (p = 0.01 vs. Cn + W), and this was prevented by Chr (p > 0.05). The collagen area fraction was increased by Fr (p = 0.02 (males) and p = 0.04 (females) vs. Cn + W, respectively; however, chrysin did not prevent this (p > 0.05). Neonatal chrysin prevented some of the deleterious effects of the high-fructose diet on the liver, suggesting that chrysin should be further explored as a strategic prophylactic neonatal intervention against high-fructose-diet-induced NAFLD.

Coadministration of ARV (Atripla) and Topiramate disrupts quail cardiac neural crest cell migration.

INTRODUCTION: Congenital anomalies such as ventricular septal defects and truncus communis have been reported with the prenatal use of antiretroviral therapy. The mechanism of antiretroviral therapy teratogenicity is unclear and is therefore the focus of this study. Some human immunodeficiency virus patients on antiretrovirals are placed on antiepileptic drugs which are also teratogenic. The interactive effects arising from this therapeutic combination may affect their teratogenic propensity through their effects on neural crest cell migration. METHODS: Appropriately cultured neural crest cells from dissected neural tubes of 32-hr old quail embryos exposed to culture media containing peak plasma levels of Atripla, Topiramate and the combination of both were studied. Distance of migration of neural crest cells was measured using the migration assay and the cells were stained with rhodamine phalloidin to evaluate the cell actin. Also quail neural crest cells were brought into suspension and microinjected into chick hosts to determine the migration of the cells to the interventricular septum. RESULTS: Migration of cultured neural crest cells was extensive in the control cultures, but inhibited in the treated groups. The experimental cultures showed a disarray of actin cytoskeleton contrary to normal distribution of actin filaments in controls. Significantly, few quail neural crest cells migrated to the interventricular septum of chick host embryos compared to the control cultures. The coadministration of topiramate with antiretroviral therapy does not seem to affect the activity of the antiretroviral drug. CONCLUSION: These results indicate that Atripla and Topiramate cause ventricular septal defects by inhibiting the migration of cardiac neural crest cells.

Administration of ursolic acid to new-born pups prevents dietary fructose-induced non-alcoholic fatty liver disease in Sprague Dawley rats.

Overconsumption of fructose time dependently induces the development of non-alcoholic fatty liver disease (NAFLD). We investigated whether ursolic acid (UA) intake by new-born rats would protect against fructose-induced NAFLD. One hundred and seven male and female Sprague Dawley rat pups were randomly grouped and gavaged (10 ml/kg body weight) with either 0.5% dimethylsulphoxide (vehicle control), 0.05% UA, 50% fructose mixed with UA (0.05%) or 50% fructose alone, from postnatal day 6 (P6) to P20. Post-weaning (P21-P69), the rats received normal rat chow (NRC) and water to drink. On P70, the rats in each group were continued on water or 20% fructose to drink, as a secondary high fructose diet during adulthood. After 8 weeks, body mass, food and fluid intake, circulating metabolites, visceral adiposity, surrogate markers of liver function and indices of NAFLD were determined. Food intake was reduced as a result of fructose feeding in both male and female rats (p < 0.0001). Fructose consumption in adulthood significantly increased fluid intake and visceral adiposity in female rats (p < 0.05) and had no apparent effects in male rats (p > 0.05). In both sexes of rats, fructose had no significant (p > 0.05) effects on body mass, circulating metabolites, total calorie intake and surrogate markers of hepatic function. Fructose consumption in both early life and adulthood in female rats promoted hepatic lipid accumulation (p < 0.001), hypertrophy, microvesicular and macrovesicular steatosis (p < 0.05). Early-life UA intake significantly (p < 0.001) reduced fructose-induced hepatic lipid accumulation in both male and female rats. Administration of UA during periods of developmental plasticity shows prophylactic potential against dietary fructose-induced NAFLD.

ß-Sitosterol mitigates the development of high-fructose diet-induced nonalcoholic fatty liver disease in growing male Sprague-Dawley rats.

Fructose contributes to the development of nonalcoholic fatty liver disease (NAFLD). ß-Sitosterol (Bst), a naturally occurring phytosterol, has antihyperlipidaemic and hepatoprotective properties. This study interrogated the potential protective effect of ß-sitosterol against NAFLD in growing rats fed a high-fructose diet, modelling children fed obesogenic diets. Forty-four 21 day old male rat pups were randomly allocated to and administered the following treatments for 12 weeks: group I, standard rat chow (SRC) + plain drinking water (PW) + plain gelatine cube (PC); group II, SRC + 20% w/v fructose solution (FS) as drinking fluid + PC; group III, SRC + FS + 100 mg/kg fenofibrate in a gelatine cube; group IV, SRC + FS + 20 mg/kg ß-sitosterol gelatine cube (Bst); group V, SRC + PW + Bst. Terminally, the livers were dissected out, weighed, total liver lipid content determined, and histological analyses done. Harvested plasma was used to determine the surrogate biomarkers of liver function. The high-fructose diet caused increased (p < 0.05) hepatic lipid (total) accretion (>10% liver mass), micro- and macrovesicular hepatic steatosis, and hepatic inflammation. ß-Sitosterol and fenofibrate prevented the high-fructose diet-induced macrovesicular steatosis and prevented the progression of NAFLD to steatohepatitis. ß-Sitosterol can prospectively be used to mitigate diet-induced NAFLD.

Quercetin administration post-weaning attenuates high-fructose, high-cholesterol diet-induced hepatic steatosis in growing, female, Sprague Dawley rat pups.

BACKGROUND: Fructose and cholesterol-rich diets have been implicated in the upsurge of metabolic syndrome (MetS). Phytochemicals are being explored as alternatives for the prevention and management of MetS. Thirty-six 21-day-old, female Sprague Dawley rats fed a high-fructose, high-cholesterol diet post-weaning were used to investigate the prophylactic potential of quercetin. Group 1 was given standard rat chow (SRC); Group 2: SRC and quercetin (75 mg kg-1 daily); Group 3: SRC and fenofibrate (100 mg kg-1 daily); Group 4 was given a high cholesterol diet (HCD) (2% added dietary cholesterol in SRC), 20% fructose drinking solution (FS); Group 5 was given HCD, 20% FS and quercetin (75 mg kg-1 daily); Group 6: HCD, 20% FS and fenofibrate (100 mg kg-1 daily). Rats were fed ad libitum for 8 weeks, euthanized, and blood and liver samples were collected. RESULTS: The HCD and FS significantly increased (P < 0.05) absolute and relative liver masses and serum cholesterol. Fasting blood glucose, serum triglycerides, alanine transaminase, creatinine, and urea were not significantly different (P > 0.05) between groups. The HCD and FS significantly increased liver lipid yield compared to the SRC and rats receiving SRC with fenofibrate (P < 0.05). Quercetin or fenofibrate together with HCD and FS attenuated the diet-induced increase in liver lipids by approximately 50%, although this was not statistically significant. Liver macro- and micro-steatosis scores were significantly increased (P < 0.05) in rats receiving HCD and FS. Quercetin or fenofibrate administration together with HCD and FS significantly decreased (P < 0.05) liver macro-steatosis scores. CONCLUSION: The prophylactic effect of quercetin on fructose and cholesterol diet-induced liver lipid accumulation may be exploited in the fight against non-alcoholic fatty liver disease (NAFLD). © 2019 Society of Chemical Industry.

The long-term protective effects of neonatal administration of curcumin against nonalcoholic steatohepatitis in high-fructose-fed adolescent rats.

There is an increased prevalence of nonalcoholic steatohepatitis (NASH) in adolescents. The suckling period is developmentally plastic, affecting later health outcomes. We investigated whether neonatal administration of curcumin would provide protection against the development of NASH later in adolescence in rats fed a high-fructose diet. From postnatal day (PN) 6 to PN 21, the pups (N = 128) were allocated to four groups and orally gavaged daily with either 0.5% dimethyl sulfoxide solution (vehicle control), curcumin (500 mg·kg-1 ), fructose (20%, w/v) or curcumin and fructose combined. All the pups were weaned and half the rats in each group had tap water, whereas the other received fructose (20%) as their drinking fluid ad libitum for 6 weeks. The rats' liver NASH scores, lipid content, and RNA gene expression ratios of AMPKα and TNFα were determined. Hepatic lipid content was similar across the treatment groups in the males (P > 0.05, ANOVA). In the females, the hepatic lipid content in the treatment groups ranged from 2.7 to 4.3%. The livers of male and female rats that had fructose either as neonates and/or postweaning had significantly marked inflammation (P = 0.0112, Kruskal-Wallis) and fibrosis (P < 0.0001, ANOVA) which were attenuated by curcumin. The hepatic gene expression ratios for AMPKα in both sexes were significantly downregulated (P < 0.0001, ANOVA), whereas the expression ratios of TNFα were significantly upregulated (P < 0.0001) in rats fed a high-fructose diet pre and/or postweaning compared to the other groups. Neonatal curcumin administration is a potential natural pharmacological candidate for the prevention of NASH.

Quantitative analysis of age and life-history stage related changes in DCX expression in the male Japanese quail (Cortunix japonica) telencephalon.

Most avian neurogenesis studies focused on the song control system and little attention has been given to non-song birds such as the Japanese quail. However, the only few neurogenesis studies in quails mainly focused on the sex steroid sensitive areas of the brain such as the medial preoptic and lateral septal nuclei. Despite the important role the quail telencephalon plays in filial imprinting and passive avoidance learning, neurogenesis in this structure has been completely overlooked. The aim of this study was therefore to quantitatively determine how DCX expression in the Japanese quail telencephalon changes with post hatching age (3-12 weeks) and life history stage. In this study, DCX was used as a proxy for neuronal incorporation. Bipolar and multipolar DCX immunoreactive cells were observed in the entire telencephalon except for the entopallium and arcopallium. In addition, DCX expression in all the eight telencephalic areas quantified was strongly negatively correlated with post-hatching age. Furthermore, numbers of bipolar and multipolar DCX immunoreactive cells were higher in the juvenile compared to subadult and adult quails. In conclusion, neuronal incorporation in the quail telencephalon is widespread but it declines with post hatching age. In addition, the most dramatic decline in neuronal incorporation in the telencephalic areas quantified takes place just after the birds have attained sexual maturity.

Age-related changes in Ki-67 and DCX expression in the BALB/ c mouse (Mus Musculus) brain.

Several studies have identified age as one of the strongest regulators of neurogenesis in the mammalian brain. However, previous age-related studies focused mainly on changes in neurogenesis during different stages of adulthood and did not describe changes in neurogenesis through the different life history stages of the animal. The aim of this study was therefore to determine time course changes in neurogenesis in the male BALB/c mouse brain at postnatal ages 1 week to 12 weeks, spanning juvenile, sub adult and adult life history stages. To achieve this, Ki-67 and DCX immunohistochemistry was used to assess changes in cell proliferation and neuronal incorporation respectively. Ki-67 expression was mainly observed in the olfactory bulb, rostral migratory stream, sub ventricular zone of lateral ventricle and the sub granular zone of the dentate gyrus. In addition, fewer Ki-67 positive cells were also observed in the neocortex, cerebellum and tectum. DCX was expressed in similar regions as Ki-67 except for the cerebellum and tectum. Expression of both Ki-67 and DCX sharply decreased with advancing age or life history stages in the sub ventricular zone, rostral migratory stream and sub granular zone of the BALB/c mouse brain. Neurogenesis therefore persists throughout all life history stages in the BALB/c mouse brain although it decreases with age.

Changes in neurogenesis with post­hatching age in the male Japanese quail (Cortunix japonica) brain.

Most avian neurogenesis studies have previously focused on the song control system and little attention has been given to non­song birds. The objective of this study was to assess changes in neurogenesis associated with post­hatching age (3­12 weeks) in the Japanese quail brain using proliferating cell nuclear antigen (PCNA) and doublecortin (DCX) immunohistochemistry. PCNA­immunoreactive (ir) cells were observed mainly in the olfactory bulb ventricular zone, telencephalic ventricular zones and cerebellum. Fewer PCNA­ir cells were also observed in the hypothalamus, thalamus and bed nucleus of the stria terminalis. In telencephalic ventricular zones, PCNA­ir cells were concentrated ventrally and dorsally adjacent to the mesopallium and medial striatum, respectively. DCX­ir cells were observed in the olfactory bulb, telencephalon and cerebellum. Furthermore, DCX­ir cells were scattered throughout the pallium except in the entopallium and arcopallium, septal nuclei and striatum. Fewer DCX­ir cells were also observed in the hippocampus and bed nucleus of stria terminalis. The density of PCNA­ir cells and DCX­ir cells in all brain areas declined with post­hatching age. In conclusion, cell proliferation appears to be restricted to the ventricular zones whereas neuronal recruitment is more widespread in the olfactory bulb, telencephalon and cerebellum. Postnatal neuronal incorporation appears to be absent in the diencephalon and mesencephalon.

Terminalia Sericea aqueous leaf extract protects growing wistar rats against fructose-induced fatty liver disease.

Background Terminalia sericea (T. sericea) is traditionally used to treat stomach ailments, infections, hypertension and diabetes mellitus. Previous in vitro studies have reported that T. sericea has lipolytic properties. This study interrogated the effects of T. sericea on linear growth, development of fatty liver disease, viscera morphometry and health of growing rats fed a 12% fructose solution (FS). Methods Thirty 21-day old male Wistar rat pups were randomly allocated to five treatments: group I - plain gelatine cubes (PGC) + plain tap water (PW), group II - 12% FS + PGC, group III - gelatine cubes containing fenofibrate (Feno) at a dose of 100 mg/kg body + FS, group IV - gelatine cubes containing the low dose (100 mg/kg body mass per day) of the T. sericea extract (TsL) + FS, group V - gelatine cubes containing the high dose (400 mg/kg body mass per day) of the T. sericea extract (TsH) + FS. Following 12 weeks of feeding, the rats were fasted overnight, euthanized and plasma and viscera harvested for analysis. Results Consumption of fructose resulted in significantly increased (p<0.05) liver lipid content and caused macrovesicular steatosis. The T. sericea extracts at 400 mg/kg per day suppressed the fructose-induced liver lipid accumulation and macrovesicular steatosis similarly to 100 mg/kg per day of Feno. Conclusions These findings suggest that the aqueous T. sericea leaf extract at 400 mg/kg per day could potentially protect against fructose-induced lipid accumulation as well as macrovesicular steatosis.