histological changes of the female rat mammary gland during the fertile period with a special reference to E-cadherin expression

E-cadherin [E-cad] is a cell adhesion molecule, essential for the maintenance of the epithelial phenotype. The current study aimed at showing the histological changes and the pattern of E-cad expression in the female rat mammary gland during different stages of their fertile period microscopically and morphometrically. Thirty-five adult female albino rats [3-4 months old] were divided into seven groups [five rats each]: the rats in group I were not pregnant [resting] and groups II-VII were sacrificed at days 7 and 14 of each of their pregnancy, lactation, and weaning stages. The excised right inguinal mammary glands were processed for H and E and E-cad immunostaining. The sections were evaluated microscopically and morphometrically. The mammary gland of nonpregnant rats had abundant adipose connective tissue with few glandular elements. During pregnancy, there was a progressive increase in the alveoli, which became distended with milk, with prominent sac formation during lactation. The E-cad expression pattern was mainly observed as a strong positive linear membranous pattern in all borders of epithelial cell lining, whereas the myoepithelial cells were negative. These observations were found in different groups, except that of lactation, where the pattern was limited to the basolateral membranes of these epithelial cells. Morphometrically, the positive membranous epithelial cells for E-cad, its density area fraction and cytoplasmic positive reaction ranged from 7-83%, 3.9-6.8% and 0-7%, respectively in all groups. In late pregnancy, there was a marked increase in the negative epithelial cells [93%], with a significant decrease in density area fraction expression [3.9%], which was persistent during lactation. Positive E-cad expression of stromal cells was only observed during weaning. The E-cad was mainly localized to the membranes of epithelial cell lining and absent in myoepithelial cells. The quantitative E-cad expression can represent a tool that ensures qualitative microscopic observations during the fertile period

Ginkgo modulates noise induced hippocampal damage in male albino rats: a light and electron microscopic study

Noise has been a major problem to mankind and induces many auditory and extra-auditory hazards. This study was carried out to determine the injurious effects of noise on the hippocampus and to show whether Ginkgo biloba has any modulatory effect on hippocampal injury. Twenty-five adult male albino rats were divided into five groups: a control group; a noise group exposed to 100 dB of sound pressure level white noise 4h/day for 4 weeks; a protected group exposed to the same noise level with the administration of a G. biloba extract [50mg/kg daily] for 4 weeks; a recovery group, which was allowed to recover for 4 weeks after noise cessation; and a treated group, administered the same dose of G. biloba for 4 weeks after noise cessation. In the noise-exposed group, the pyramidal cell layer of CA1 and CA3 and the granular cell layer of the dentate gyrus [DG] showed a decrease in thickness compared with the control group, which showed loss and degeneration of many cells, and evidence of increased apoptosis. The protected and treated groups showed improvement in many parameters compared with the recovery group, that is, an increase in the thickness of CA1, CA3, and DG; increase in the surface area of cells; increased vascularity; and a statistically significant decrease in apoptosis compared with the recovery group. Noise exerted detrimental effects on cells of CA1, CA3, and DG of the hippocampus. Although partial spontaneous recovery may occur after cessation of noise exposure, the administration of G. biloba led to a marked decrease in the injurious effect of noise on the hippocampus. This might suggest the probable usefulness of G. biloba in reducing the central hazardous effects in individuals exposed to noise

possible protective role of selenium supplementation on the structure of trhe heart in an experimental model of chronic renal failure: a light and electron microscopic study

Chronic kidney disease [CKD] is a worldwide health hazard with significant morbidity and mortality especially due to cardiovascular complications. This study was conducted to investigate the histological effects of CKD on the structure of the heart and to show the possible protective role of selenium [Se] supplements. Twenty adult male Wistar albino rats were used in this study. They were divided into three groups: group I [the control group] was divided into two subgroups: IA [sham operated], which was subjected to sham operation, and IB [the negative control group], which was left untreated; group II [the nephrectomy group] was subjected to a five-sixth nephrectomy operation to induce renal failure; group III [the Se-treated group] was subjected to a five/sixth nephrectomy operation following which the rats were supplemented with sodium selenite at a dose of 0.04 mg/kg for 10 weeks. At the end of the experiment body weight [BW] and serum creatinine were measured. Heart specimens were processed for light and electron microscopic examination, and morphometric analysis was performed for area percentage of intercellular spaces and collagen fibers. Group II showed significant widening of the interfiber spaces with aggregation of adipocytes, extravasated RBCs, and lymphocytes. There was also significant increase in the area percentage of collagen fibers. Cardiac myocytes appeared swollen, pale, and degenerated, and electron microscopic findings pointed to endothelial dysfunction. Se administration led to significant improvement in BW, creatinine level, and cardiac fibrosis; yet, the heart showed focal pale vacuolated myocytes, wide interfiber spaces, and extravasated blood. CKD led to definite focal degeneration in the cardiac muscle fibers. Se with the dose given improved BW, creatinine level, and cardiac fibrosis but could not offer complete protection against cardiovascular complication

comparative study between bilateral ligation of the ovarian and the uterine arteries on the structure and function of the ovary of adult white rabbit: histological and immunohistochemical study

Uterine artery embolization is an effective alternative to surgery in fibroids and postpartum hemorrhage aiming to preserve the uterus and fertility. To compare between the effect of bilateral uterine artery ligation and bilateral ovarian artery ligation on the ovarian structure and function in rabbits. Twenty-eight adult female nonpregnant white New Zealand rabbits were divided into four groups [seven rabbits each]: group A [control], B [sham], C [subjected to bilateral ovarian artery ligation], and group D [subjected to bilateral uterine artery ligation]. After 2 months, all groups received a single dose of human chorionic gonadotrophin to induce ovulation and were then sacrificed 2 days later. Follicle stimulating hormone [FSH], luteinizing hormone [LH], and 17-beta-estradiol were measured. Ovaries were extracted bilaterally, weighed, and processed for microscopic and immunohistochemical studies. Group C showed a significant increase in FSH and LH, whereas 17-beta-estradiol and ovarian weight were significantly decreased. Moreover, there were only a few peripherally situated atretic follicles with no primary oocytes. Extensive apoptosis affecting the entire ovarian structure was detected. However, group D showed a significant increase in FSH and LH, with a nonsignificant decrease in 17-beta-estradiol and ovarian weight. Ovaries of group D showed delayed ovarian atresia. Granulosa cells showed pyknotic nuclei. Some atretic follicles still contained primary oocyte surrounded by indented zona pellucida. Apoptosis was detected especially in granulosa cells and corpus luteum. Uterine artery shares in the blood supply of the ovary. A countercurrent pathway exists between the ovary and the uterus. Ligation of the uterine artery compared with the ovarian artery ligation induced a delayed atresia in the follicles with preservation of the primary oocytes. Thus, uterine artery embolization could anticipate ovarian failure and early menopause

Histological and immunohistochemical study of experimentally induced concussion on young rats' frontal cortex and the possible protective role of erythropoietin hormone supplementation

Introduction: Closed-head concussive injury is one of the most common causes of traumatic brain injury. Multiple concussions, especially in children, can result in cumulative damage and increased risk for neurodegenerative diseases in later life

Aim of the work: The aim of the work was to clarify the effect of repeated concussions on the frontal cortex architecture and to identify a new protective therapy that decreases the brain insult caused by repeated concussions

Materials and methods: Twenty male albino rats 17-19 days old were divided into four groups: group I [control group] included five rats. The remaining rats were subjected to repeated head concussions for 3 successive days and then divided equally into the following groups: in group II [concussion group], animals were sacrificed 24 h after the last concussion; in group III [recovery group], rats were sacrificed 10 days after the last concussion; and in group IV [treated group], rats received an erythropoietin [EPO] injection for 3 successive days after the last concussion and were then sacrificed. The frontal cortex was examined using histological and immunohistochemical techniques

Results: In the present study, it was found that after 24 h of repeated concussions, subpial cellular infiltration, edema, and congested blood vessels were detected. The frontal cortex neurons showed degenerative changes. A significant decrease in glial fibrillar acid protein [GFAP] and synaptophysin [SYN] immunoreactivity was also detected. The recovery group showed hypercellularity of the frontal cortex. Some neurons still showed degenerative changes. A significant increase in GFAP and SYN immunoreactivity was detected. In the EPO-treated group, neurons were more or less normal. A significant decrease in GFAP immunoreactivity with a significant increase in SYN reactivity was detected compared with the recovery group

Conclusion: Concussion induced degenerative changes in neurons, neuroglia, and synapses. Recovery decreased degenerative changes with marked gliosis. Treatment with EPO improved degeneration, gliosis, and synapses