Sensory nerve endings in the human female umbilical skin: light and electron microscopic study

Sensory innervation consists of free nerve endings and endings terminated with corpuscular structures. Cutaneous innervation is closely associated with major skin functions such as wound healing, thermoregulation, and hair growth. Diminution in erotic sensation has been reported by some women after abdominal lipectomy. Hence, the lack of knowledge about the normal sensory distribution in the umbilical skin has been a problem. The purpose of this study was, therefore, to map the sensory innervation of the human umbilical skin using histological, immunohistochemical [S-100 protein], and ultrastructural techniques. Umbilical skin biopsies were obtained during surgical procedures for abdominal lipectomy in female participants. The specimens were processed for light and electron microscopic examinations. With light microscopy, abundant Meissner's, Ruffini, and innervated Merkel cells were observed. Numerous free nerve endings, comparable with those observed in male and female external genitalia, were observed surrounding the ducts and the acini of sweat glands. Pacinian corpuscles were also observed, but less frequently. Neurovascular bundles, closely related to those observed in female external genitalia, were also observed. The relatively dense sensory innervation in the umbilical skin that was comparable with that in lip, as well as in male and female external genitalia, can be correlated with the observed retardation in the erotic sensation in clinical studies after removal of a part of the umbilical skin. The frequently observed innervated Merkel cells and the widely scattered Meissner's corpuscles in the umbilical skin could explain the relatively high tactile sensation in this skin

Morphological changes induced in the brain of rats exposed prenatally to iron and the possible protective role of folic acid

Iron supplementation is recommended during pregnancy to meet the demands of both the mother and rapidly growing fetus. However, newborns and particularly preterm infants are highly susceptible to free radical oxidative damage resulting from iron. Folic acid supplementation is needed during pregnancy and it has been shown to reduce the tissue damage resulting from iron induced oxidative stress. Thirty pregnant female albino rats were used in this experiment and divided into three groups [A, B, C]. Group [A]: Was kept as control. Group [B]: Treated with iron gluconate orally in a dose of 50 mg/kg for eleven days [from day 6-16] of gestation. Group [C]: Treated with the same dose of iron glunonate concomitantly with folic acid in a dose of 5mg/kg for the same previous duration. Samples from the brain striatum of newborns were taken and processed for light and electron microscopic investigation. The light microscopic examination of striatal area of group [B] showed necrotic changes appeared in some neurons in the form of shrinkage and condensation in their nuclei, others appeared degenerated with irregular nuclear outline and multiple vacuoles in their cytoplasm. Aggregated glial cells were observed around the blood capillary and mitotic division could be detected in some of them. Enhanced level of glial fibrillary acidic protein [GFAP] was observed in comparison to control group. Multiple iron deposits in the cytoplasm of neurons and glial cells were observed in group [B] animals. Marked improvement was observed in both neurons and glial cells of group [C]. Electron microscopy revealed apoptotic changes affecting mainly glial cells and some neurons in group [B] associated with swelling of Golgi cisternae and vacuolated mitochondria. Marked improvement was observed in both neurons and glial cells of group [C]. These results indicate that folic acid appears to reduce the iron induced neuronal damage in the brain of newly born rats exposed prenatally to iron

Postnatal development of vomeronasal gland in the female cats. histological, ultrastructural and morphomertic studies

The VND consists of several structures which include the vomeronasal duct[VND], the vomeronasal glands[VNGs], vessels and nerves. It is the peripheral organ of the accessory olfactory system which detects some types of pheromones. Several studies are carried on the adult VNO however, no informations are available on the development of the VNGs in cat which represeni one of the examples of early odour perception. This work aim at investigating the development of the cat's VNGs using histological, histochemical, electron microscopic and morphometric techniques. A total number of 24 female cats of different ages was used in this study. The animals were equally divided into Jbur groups [GI, 0-1day, GTh 2 weeks, GIII: 1 month, GIV. 2 months,].After sacrifice, specimens were taken from the VNO for light and electron microscopic studies. with progress of age, the glandular end pieces and ducts gel more branched. Progressive increase in PAS reaction in VNGs with a mild increase in +ve reaction for Alcian blue occurred with development. However, the VND revealed +ve Alcian blue reaction at birth and the reaction increased with age progress. These .tIndings reflect the profuse secretion of neutral mucin and a limited acid mucin. Ultrastructurally the developing VNGs exhibited moderates dense cytoplasm containing basal RER and electeon dense secretory granules which predominant in GI, II. Both electron dense and electron lucent secretory granules get increased with age progress. The lamina propria contained collagen and reticular fibers which increased with age progress. No elastic fibers were present. Fenestrated blood capillaries,non myelinaled and mixed nerve bundles were present also in the surrounding C. T Statistical analysis with ANOVA test revealed a significant increase in count and size of the acini with progress of development. The morphological data in the present study confirm the functional capability of the VNGs at birth. It demonstrates marked postnatal development of the VNGs. The VNGs of the cat are formed of serous, mucous and mixed acini. Acid mucopolysaccharides appear to be produced mainly by the epitheliumn lining of the VND

Effect of fluoride on rat cerebellar cortex: light and electron microscopic studies

Fluoride accumulation in the brain of experimental animals was particularly observed in the hippocampus. It caused altered neuronal and cerebrovascular integrity, abnormal behavioral patterns and metabolic brain lesions. Fluoride affected indeed the cerebellar development in mice but its effect on adult rat cerebellar cortex is something awaits further investigation. Is to define the effects of fluorosis on the histological structure of adult rat cerebellar cortex. A total number of 40 adult female albino rats were used. They were divided into two groups [20 animals each]. Group I: Was kept as control group, received distilled water orally daily by gastric tube for 2 months. Group II: Received sodium fluoride orally [dissolved in distilled water] at a dose of 12 mg/Kg body weight for two months. Samples from cerebella were taken and processed for light and electron microscopic investigation. After fluoride treatment, features of neurodegeneration were observed. The Purkinje cells appeared shrunken, deeply stained, with multilayer disposition, which was confirmed by morphometric evaluation of the Purkinje cell layer thickness. Ultrastructurally, increased infolding of nuclear envelope, mitochondrial alterations, dilated Rough endoplamic reticulum cisternae and clusters of vesicles near the Golgi bodies were observed. Apoptotic granule cells accumulated in a clumping manner, Bergmann astrocytes with features of increased activity, dilated and congested blood capillaries were noticed. GFAP positive cells were more abundant and appeared larger in the three cortical layers of treated animals associated with positive reaction for inducible nitric oxide synthase [iNOS] compared to negative reaction in control animals. The cerebellar cortex was particularly susceptible to sodium fluoride- induced oxidative stress and could contribute to the development of neurodegenerative diseases

Aging of the olfactory system of male rats a histological and ultrastructural study I-olfactory and vomerosensory epithelia

In the present study, age-related histological, histochemical, and ultrastructural changes in both the olfactory epithelium [OE] and the vomeronasal organ [VNO] have been investigated. A total number of 30 albino rats were used in this study Animals were divided equally into two groups; [adult group] and [aged group]. The OE of the aged animals was reduced in thickness, with a relative disturbance in the zonal arrangement of its layers and invaded by acini of Bowman's glands. A basal nuclear-free zone and apical pale cells were also observed within the aged OE. Both mitotic figures and apoptotic bodies were seen in the aged OE. Periodic acid schief-Alcian blue [PAS-AB,] reaction revealed an increase in the PAS-reaction both in the apical and basal parts of the aged OE. Alkaline phosphatase reaction showed a marked reduction in the enzyme activity within the basal cell layer with the appearance of scattered positive cells with the aged OE. On the other hand an increase in the enzyme activity of Bowman 'S glands was observed. The most frequent ultrastructural finding within the aged OE was the accumulation of dense inclusion bodies within the mature ORNs. Less frequently filamentous inclusions were also detected. SEM investigation revealed reduction in the olfactory area and shortening in the olfactory cilia. In aged animals the vomerosensory cells showed vacuolated cytoplasm. Intraepithelial blood capillaries appeared irregular. Histochemically, the PAS-reaction was increased in the apical processes of the supporting cells and reduced in the VS cells whereas alkaline phosphatase along the apical surface was not affected. Ultrastructurally, vomerosensory cells exhibited dilatation of most organelles mainly sER and Golgi bodies, numerous clear vesicles of variable sizes, multiple electron-dense inclusions and lipofuscin granules. VNO are more vulnerable to the aging process than the OE. Sensory cells in particular are more affected than other cell types

Apoptosis in the gastric ulceration "Shay rat model": rol of IL-6 modulation by the cytoprotectant compper-glycinate and-nicotinate complexes

So far, the mechanism[s] of the very promising gastric antiulcerogenic acting: copper-nicotinate and copper-glycinate complexes is not yet completely understood. It could be hypothesized that modulation of IL-6 and apoptosis may elucidate one aspect of a common mechanism ['s of their action. Shay Rat" pyloric ligation gastric ulcer model was utilized in this study. To/al IL-6 in gastric juice and blood serum was measured by an ELISA assay. Total DNA content and its percentage of fragmentation in gastric juice and Caspase-3 activity in the non glandular stomach mucosal scraping were measured calorimetrically in the four studied groups [I: control ulcerated untreated, II: ulcerated-treated with copper-glycinate, III: ulcerated treated with copper-nicotinate and, IV. ulcerated treated with Omeprazole therapeutic control ,16 rats each].There was highly significant reduction in the levels of each of IL-6 in gastric juice, serum of treated rats [P<0. 001], fragmented DNA, and similar reduction in the caspase-3 activity [P<0.001] amongst the different treatments compared to untreated rats. Histopathological examination revealed discontinuation of the lining epithelium by aggregated lymph follicles and/or inflammatory cells infiltration ,dilated and congested blood vessels and apoptotic changes affecting epithelial cells mainly, all significantly but differentially prevented by treatments. This study showed for the first time that gastric ulceration augmented IL-6 and promoted caspase-3 activity as a marker for apoptosis confirmed by DNA fragmentation and histopathology in the used "Shay Rat" gastric ulcer model .Ali parameters were greatly alleviated by treatments, with stronger equ1otent ability for each of the copper complexes used compared to the clinical gold-standard treatment of/he disease, omeprazole