Effect of chronic nicotine administration on the anterior cingulate cortex [area 24a] of adult albino rats: a histological and immunohistochemical study

Nicotine is the principal active component in cigarettes and cigars. It was reported that tobacco smoking enhances the performance of cognitive processing. The anterior cingulate cortex plays an important role in attention and working memory performance. This study was conducted to demonstrate the effects of chronic administration of various nicotine doses on the structure of the ventral anterior cingulate cortex [area 24a] in adult rats, as well as study the effect of withdrawal of high doses of nicotine. A total of 48 adult male albino rats were used. They were divided into four groups. Group I [N=1 2] was considered the control group. Group II [n=12] rats were treated with 1 mg/kg nicotine subcutaneously for 2 months. Group III rats [n=24] were treated with 6 mg/kg nicotine subcutaneously for 2 months. Thereafter, half of the animals were sacrificed. Group IV [the recovered group] consisted of the remaining I 2 rats of group III that were kept for another 2 months without treatment and then sacrificed. Brains were processed to be studied using Einarson's gallocyanin stain, the Golgi-Cox method, transmission electron microscopy, and immunohistochemical study for glial fibrillary acidic protein [GFAP]. Further, the number of cells in the second and fifth layers of the cingulate cortex [area 24a] was measured and statistically analyzed for all the studied groups. Examination of the cingulate cortex [area 24a] in low-dose nicotine-treated rats [group II] revealed an increase in the branching of the dendrites of the pyramidal cells together with a relative increase in the density of the spines. An ultrastructural study showed the presence of numerous synaptic contacts between the nerve processes. In high-dose nicotine-treated rats [group III] the cells showed degenerative changes, which were more evident in pyramidal cells. These changes were associated with a marked reduction in the extension and branching of the dendrites. Dense GFAP immunostained fibers and cells could be seen particularly in layer I. In the recovered rats [group IV] most of the cells restored their normal appearance. Mild GFAP expression could be observed. An insignificant difference in the number of cells was also found in comparison with controls. The effect of nicotine on the organization of the anterior cingulate cortex [area 24a] was found to vary according to dose. Withdrawal of high doses of nicotine will result in a marked reduction in the structural impairment of neurons

Histological and immunohistochemical changes in placental chorionic villi of patients with poorly controlled gestational diabetes

Normal placental development is essential for normal fetal development. The placenta is a complex fetal organ that plays pleiotropic roles during fetal growth. It separates the maternal and the fetal circulation. The placenta is exposed to the regulatory influence of the hormones, cytokines, growth factors, and substrates present in the circulation, and thus may be affected by changes in any of these. Gestational diabetes is one of the most prevalent medical complications of pregnancy and may cause increased fetal wastage. To study the structural changes in the placental chorionic villi of women with poorly controlled gestational diabetes in comparison with metabolically normal pregnant women. The study was carried out on placentas from 22 full-term pregnant women. All the women delivered at 38-40 weeks of gestation. Ten placentas were from normal uncomplicated pregnancies [control group] and the other 12 were from gestational diabetic pregnancies [diabetic group]. The placentas were processed and examined using light and electron microscopy. An immunohistochemical study using S100 protein antibody was carried out. In comparison with the control group, the placentas of poorly controlled gestational diabetic mothers showed an increase in syncytial knots, partial shedding of trophoblastic microvilli, and thickening of the basement membrane of the trophoblast. Fibrinoid necrosis, villous fibrosis, and dilated congested fetal blood vessels were also observed. The frequent appearance of Hofbauer cells [placental macrophages] was observed in the diabetic placenta in comparison with the control placenta. Positive diabetic trophoblastic and stromal cells for S100 protein antibodies were observed. It is concluded that poor control of diabetes during gestation may result in structural changes in the placentas, which may contribute toward fetal complications. Further research in this field may help in finding a solution for the evaluation of the destructive changes in diabetic placenta in the initial stages of pregnancy

Effect of experimentally induced hypothyroidism during pregnancy and lactation on the retina of juvenile and adult albino rats and the possible role of thyroid hormone supplementation

Nervous system growth and differentiation are closely correlated with the presence of thyroid hormones in initial development stages. Hypothyroidism during the fetal and postnatal life results in an irreversible mental retardation syndrome. At the cellular level, T3 is known to act on neuronal, neuroretinogenesis, and glial lineages. In this study, we aimed to study the influence of hypothyroidism on retinal development in juvenile and adult rats and the effects of thyroid hormone supplementation on both periods of development. This study was conducted using 56 male albino rats. They were divided into three groups: group 1 [control group] included 24 animals, group 2 [juvenile group] included 16 animals whose mother received carbimazole [NeoMercazol] antithyroid drug at a dose of 0.02 mg/day/pregnant female during gestation and lactation, this group was further subdivided into subgroup 2a [hypothyroid juvenile animals] and subgroup 2b [thyroid hormone-supplemented juvenile animals], and group 3 [adult group] included 16 animals, this group was also further subdivided into subgroup 3a [hypothyroid adult animals] and subgroup 3b [thyroid hormone-supplemented adult animals]. At the end of the experiment, the animals were killed. Retinal specimens from all groups were processed for light and electron microscopic studies. Biochemical analysis was carried out to measure the serum levels of triiodothyronine, T4, growth hormone, and insulin growth factor-1. In addition, estimations of lipid peroxidation, catalase activity, and antioxidant enzymes were made. Statistical analysis was carried out to measure the retinal thickness. Light and electron microscopic studies showed that thyroid hormone deprivation altered the organization of the retina in juvenile and adult rats. These changes were apparent in the form of significant reduction in the retinal layer thickness. In addition, degenerative changes in some layers were observed. The group with thyroid hormone supplementation showed recovery of both structural changes and retinal thickness, this recovery was apparent in the juvenile group. Adult animals showed minimal recovery. Biochemical analysis of the serum of hypothyroid animals showed a significant increase in lipid peroxidation products and decease in the serum levels of antioxidants, growth hormone, and insulin growth factor-1, comparable with the controls. Administration of thyroid hormone significantly restored their levels especially in the juvenile group. Gestational and lactational hypothyroidism induced marked changes in the developing retina in juvenile and adult rats. These changes were mostly normalized by thyroid hormone administration especially in the juvenile group

Effect of vagus nerve stimulation on serum level of pentraxin-3 at focal transient cerebral ischemia and reperfusion in adult male new zealand rabbits

Regarding that oxidative stress, distinguished by the overproduction of reactive oxygen species [ROS], has been implicated in the pathophysiology of cerebral ischemia. Pentraxin-3 [PTX-3] plays an important role in innate immune responses and in inflammatory disease. However, no study has evaluated PTX3 in animal models with cerebral ischemia and reperfusion. Aim of the work: is to assess the anti-inflammatory and anti-oxidant effect of vagus nerve stimulation [VNS] on focal model of transient cerebral ischemia and reperfusion. Focal transient cerebral I/R was induced by occlusion of right common carotid artery [CCA] for 30 minutes followed by reperfusion for one hour. Stimulating electrodes were implanted on the cervical part of the right vagus nerve. VNS started 15 min after right CCA ligation and lasted 15 min after reperfusion and delivered for 30 s at every 5 min. All the procedures were duplicated but no stimulus was delivered in the control group. Serum level of pentraxin-3, lipid peroxide and total thiols were determined at baseline, at end of ischemia and at end of reperfusion and the animal decapitated and neuronal damage was evaluated. VNS causes reduction of the ischemic features with revival of the cell shape and size, increased serum levels of pentraxin-3 and total thiols whereas the level of lipid peroxide was diminished. The observed diversity in pentraxin-3, lipid peroxide and total thiols levels in cerebral I/R, which may reflect relative roles in the bioactivity of the animal. The anti-inflammatory and anti-oxidant role of vagus nerve stimulation in cerebral I/R in rabbits, may represent a marker of altered cerebral function, that provide potential therapeutic applications

Toxic effect of cisplatin on cerebellar cortex and spinal cord of adult male albino rat and the possible role of vitamin E: light and electron microscopic study

The nervous system is frequently the site of symptomatic toxicity of antineoplastic agents, cisplatin is a widely used potent chemotherapeutic agent that is highly neurotoxic. It has been proven that it is able to generate reactive oxygen species and inhibit the activity of antioxidant enzymes. This study was carried out to demonstrate the neurotoxic effects of cisplatin on the structure of adult rat cerebellum and spinal cord, and the role of vitamin E which has been shown to ameliorate hephro, oto and neurotoxicities induced by cisplatin. Thirty adult male albino rats weighing 200-250 gm were divided into three groups: Group one: kept as a control. Group two: animals treated with cisplatin at a dose of 4mg/kg twice weekly by intraperitoneal injection, for one month. Group three: animals treated with vitamin E at a dose of 100mg/kg by intramuscular injection in concomitant with cisplatin twice weekly for one month. Animals were sacrificed and their cerebella and spinal cords were processed for light and electron microscopy. Morphometrical and statistical study was done for the mean number, as well as the mean surface area of Purkinje cells and mean surface area of their nuclei. The histological approach revealed marked degenerative changes in the Purkinje cells and motor ceurons of cisplatin treated animals [Group II]. Some of these cells appeared irregular with deeply stained cytoplasm and pykontic nuclei. Ultrastructural examination showed Purkinje cells with cellular shrinkage, damaged organelles and irregular nuclei with electron dense karyoplasms. Significant degenerative changes in the motor neurons and blood capillaries of the anterior horn of the spinal cord in the same group were frequently observed. Morphometric evaluations demonstrated significant decrease in the mean number and the mean surface area of nuclei and cell bodies of Purkinje cells. These structural and morphometrical alterations were much less observed in concomitant use of vitamin E with cisplatin [Group III]. Cerebellum and spinal cord are considered the target areas of cisplatin neurotoxicity, while vitamin E, when used in combination with cisplatin displays a protective action against neurotoxicity

Effect of cisplatin on the cerebellar cortex and spinal cord of adult male albino rat and the possible role of vitamin e: light and electron microscopic study

The nervous system is frequently the site of symptomatic toxicity of antineoplastic agents. Cisplatin is a widely used potent chemotherapeutic agent that is highly neurotoxic. It has been proven that it is able to generate reactive oxygen species and inhibit the activity of antioxidant enzymes. This study was carried out to demonstrate the neurotoxic effects of cisplatin on the structure of adult rat cerebellar cortex and motor neurons of the anterior horn of the spinal cord and to evaluate the role of vitamin E which has been shown to ameliorate nephro, oto and neurotoxicities induced by cisplatin. Thirty adult male albino rats weighing 200-250 gm were divided into three groups: Group [I]: Kept as a control. Group [II]: Animals treated with cisplatin at a dose of 4 mg/kg twice weekly by intraperitoneal injection, for one month. Group [III]: Animals treated with vitamin E at a dose of 100 mg/kg by intramuscular injection in concomitant with cisplatin twice weekly for one month. Animals were sacrificed and their cerebellar cortex and spinal cords were processed for light and electron microscopy. Morphometrical and statistical study was done for the mean number, as well as the mean surface area of Purkinje cells and mean surface area of their nuclei. The histological approach revealed marked degenerative changes in the Purkinje cells and motor neurons of cisplatin treated animals [GII]. Some of these cells appeared irregular with deeply stained cytoplasm and pykontic nuclei. Ultrastructural examination showed Purkinje cells with cellular distortion, damaged organelles and irregular nuclei with electron dense karyoplasms. Degenerative changes in the motor neurons and blood capillaries of the anterior horn of spinal cord of the same group were frequently observed. Morphometric evaluations demonstrated significant decrease in the mean number and the mean surface area of nuclei and cell bodies of Purkinje cells. These structural and morphometrical alterations were much less observed in concomitant use of vitamin E with cisplatin [GIII]. Cerebellar cortex and spinal cord motor neurons are considered target areas of cisplatin neurotoxicity, while vitamin E, when used in combination with cisplatin displays a protective action against neurotoxicity

Comparative study on the effect of long-term administration of non-steroidal anti-inflammatory drugs meloxicam and ketoprofen on the structure of the kidney and gastric mucosa in the adult albino rats

Ketoprofen is a widely used drug related to the group of the traditional non selective non-steroidal anti-inflamatory drugs [NSAIDs]. Meloxicam is related to the group of the cyclooxygenase-2 [COX-2] selective inhibitors which is a newer version of NSAIDs. To demonstrate and compare the effects of long-term administration of meloxicam and ketoprofen on the structure of the kidney and gastric mucosa in the healthy adult rats. A total number of 36 adult male albino rats were used in this study. They were equally divided into three groups. Group I was considered as a control. Group II included the rats treated with ketoprofen in a dose of 1mg/kg orally once daily for 10 weeks by a gastric tube, Group III included the rats treated with meloxicam in a dose of 0.2 mg/kg orally once daily for 10 weeks via gastric tube. At the end of the experiment animals were sacrificed and specimens of the kidney and stomach were processed for light and scanning electron microscopic studies. Some kidney specimens were also processed to be studied by transmission electron microscopy. The diameter of renal corpuscles was measured in the three studied groups and statistically analyzed. In ketoprofen treated rats [group II] the renal corpuscles exhibited marked shrinkage of glomeruli. Many renal tubules appeared to be lined with damaged epithelium. Ultrastructural study of the lining cells of the proximal and distal convoluted tubules revealed that the degenerative changes involved both the nucleus and the cytoplasmic organelles. The interstitial tissue had focal areas of fibrosis. In the meloxicam treated rats [group III], there was little shrinkage of the glomeruli. However, the interstitial tissue showed heavy cellular infiltration. SEM study revealed an enlargement of the processes of the podocytes with loss of their pedicles. The gastric mucosa in group II showed an extensive damage to the surface epithelial cells in the form of ulcers while in group III there was patchy areas of epithelial destruction. This study demonstrated that long-term administration of COX-2 selective inhibitors exerted deleterious effects on the kidney comparable to those exerted by the nonselective NSAIDs. However, their damaging effect on the gastric mucosa appeared to be less than the nonselective NSAIDs but it was not abolished

Histological, immunohistochemical and quantitative analysis of collagen in patients with direct inguinal hernia

Abnormal collagen metabolism is thought to play an important role in the development of abdominal hernia. This is underlined by detection of altered collagen metabolism and structural changes of the tissues in patients with inguinal hernia. Was to study collagen synthesis defect in patients with direct inguinal hernia. Specimens were obtained from skin, transversalis fascia and sacs from forty two adult male patients with direct inguinal hernia and from 30 control adult patients without hernia during appendectomy. Sections from the specimens were stained with haematoxylin and eosin and Masson's trichrome stains, for light microscope. Furthermore, immunohistochemical study for collagen type III and histological quantitative analysis of total collagen were done. Other specimens were processed for electron microscopic study. Histological study of the tissues of patients with direct inguinal hernia revealed that the collagen fibers appeared loosely packed, widely separated and there was decrease in bundle formation. The immunohistochemical study showed an increase in type III collagen fibrils in comparison to that of controls. Also, there was a significant decrease in the amount of total collagen content compared to the control group. The electron microscopic study revealed degenerative changes in the fibroblasts associated with loosely packed collagen fibrils. These changes were detected in all studied tissues. We concluded that the substitution of collagen type I by collagen type III that has less tensile strength predisposes to development of direct inguinal hernia. We also concluded that inguinal hernia may be a local manifestation of a systemic disorder of collagen metabolism