In this study 8 patients with Alport's syndrome are presented. The ocular manifestations of these patients were retinal flecks, macular depigmentation, microspherophakia and anterior lenticonus. One patient revealed bilateral macular hole which was an unusual feature. Four patients had renal biopsies with the characteristic electron microscopic changes of the disease. According to these findings our conclusion is that Alport's syndrome is a disorder of selected basement membranes.
We investigated the ultrastructural effects of the organophosphate compound methamidophos and treatment with atropine and pralidoxime (2-PAM) on rat kidneys. Male Wistar albino rats were assigned to four groups. Group 1 received 30 mg/kg methamidophos, the LD50 for this compound in rats, via oral gavage. Group 2 received only physiologic saline. Group 3 rats received 30 mg/kg methamidophos and were treated with 2-PAM and atropine via intraperitoneal injection when cholinergic symptoms were noted. Group 4 served as a control, and received physiologic saline in equivalent volumes and routes to Group 3. Kidney tissues were prepared for electron microscopic studies. No ultrastructural changes were detected in Group 1 after acute poisoning with methamidophos and in Group 3 treated with antidotes after poisoning. Acute organophosphate poisoning and antidotal treatment in this model are not associated with histopathological changes in the rat kidney but the models with different organophosphate compounds, by administrating the different dosages, may be more illuminative in explaining the effects of these chemicals in kidney.
Our results indicate the curative role of vitamin D treatment on the androgen excess in PCOS rat model which causes abnormalities in ovarian morphology and functions. Vitamin D has positive effects on the hormonal and structural changes observed in PCOS, but it has been concluded that long-term use may be more beneficial.
The sodium-potassium activated and magnesium dependent adenosine-5'-triphosphatase (Na(+)-K(+)/Mg(+2) ATPase EC.3.6.1.3.) activity and lipid peroxidation and early ultrastructural findings were determined in rat brain at the acute stage of ischaemia produced by permanent unilateral occlusion of the middle cerebral artery (MCA). The effects of the pretreatment with intravenous high-dose methylprednisolone (MP) on these biochemical indices and ultrastructural findings were also evaluated in the same model. The rats were divided into four groups. In group I, 10 rats were used to determine Na(+)-K(+)/Mg(+2) ATPase activity and the extent of lipid peroxidation by measuring the malondialdehyde (MDA) content and normal ultrastructural findings. In group II on 20 rats, only subtemporal craniectomy was done in order to determine the effects of the surgical procedure on these indices and findings. This group was treated intravenously with saline solution before occlusion. In group III with MCA occlusion, saline solution was administered intravenously to 20 rats in the same amount of methylprednisolone used in group IV, ten minutes before the occlusion. In Group IV, a single high-dose (30 mg/kg) of methylprednisolone was administered intravenously, ten minutes before occlusion in 20 rats. After occlusion of the middle cerebral artery, Na(+)-K(+)/Mg(+2) ATPase activity was decreased promptly in the first ten minutes in the ischaemic hemisphere and remained at a lower level than the contralateral hemispheres in the same group and the normal levels in group I, during 120 minutes of ischaemia. A single dose methylprednisolone pretreatment prohibited the inactivation of Na(+)-K(+)/Mg(+2) ATPase. On the other hand, there was significant difference in malondialdehyde content between group I and group III. Malondialdehyde levels were significantly increased following ischaemia and a non-significant increase was observed in the contralateral hemisphere. Methylprednisolone treatment significantly decreased malondialdehyde content on the side of the ischaemic hemisphere. We conclude that there is a positive relationship between membrane-bound enzyme Na(+)-K(+)/Mg(+2) ATPase activity, malondialdehyde content and early ultrastructural changes in the treated group with MP. These data suggest that the pretreatment injection of high doses (30 mg/kg) methylprednisolone contribute to the protection of the brain from ischaemia with stabilization of the cell membrane by effecting the lipid peroxidation and the activation of Na(+)-K(+)/Mg(+2) ATPase.
In the present study the effects of β-adrenergic antagonist and α-adrenergic agonist drugs on rabbit corneas were evaluated in vivo by using transmission electron microscopy. Twenty-four New Zealand albino rabbits were divided into six groups according to the drug applied. The rabbits to which only balanced salt solution (BSS) or BSS and benzalkonium chloride (BAC) were applied were taken as the control groups. The other four groups consisted of the rabbits to which Timoptic 0.5%, Betagan 0.5%, Betoptic 0.5% and Iopidine 1% were applied, respectively. All of drugs were instilled topically twice daily for 6 weeks. In the BSS group, all layers of the cornea were ultrastructurally normal. In the BSS and BAC group slight epithelial and endothelial changes were found. However, in the other groups, loss of microvilli, increase in glycogen particles, nuclear indentation, widening of the intercellular spaces and cytoplasmic vacuolization in epithelium were observed. No significant abnormality was found in the basal lamina, stroma and Descemet’s membrane. Slight ultrastructural changes were noted in the endothelium such as vacuolization due to dilatation of the endoplasmic reticulum cisternae and focal cytoplasmic lytic areas. The results of this study indicate that various ultrastructural changes occur in groups treated with antiglaucomatous drug and that topical treatment with timolol and apraclonidine for 6 weeks is more toxic to the rabbit cornea than levobunolol and betaxolol.
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