Anti-apoptotic Bcl-2 and proapoptotic Bax genes are the most significant genes that are involved in the regulation of apoptosis. Abnormal apoptotic activity in preeclampsia and gestational diabetes is caused by dysregulation of these genes. In this study; we examined Bcl-2 and Bax protein expressions using immunohistochemical techniques in human placental tissue samples from cases of gestational diabetes (n: 20) and preeclampsia (n: 20). It was observed that Bax expression showed positive reaction compared to Bcl-2 expression so; Bax protein was thought to be an effective marker in determining apoptotic changes in placentas with gestational diabetes and preeclampsia.

Introduction: We investigated the therapeutic effects of carvacrol in an experimental esophageal burn rat model with immunohistochemical techniques. Materials and Methods: Three groups were included in this study, composed of eight Wistar albino rats each. The control group was given 1 mL 0.9% (wt/vol) NaCl; esophageal burns were induced in groups 2 and 3 by administration of 1 mL 40% NaOH in the distal 2 cm of the esophagus. The treatment group was administered 75 mg/kg carvacrol in 2 mL 0.9% NaCl for 10 days. After a routine histological examination of the tissues, sections were stained with vascular endothelial growth factor (VEGF) and caspase-3 for immunohistochemical analysis and were examined under a light microscope. Results: In the control group, there were regular cells in the cornified epithelial tissue and cylindrical cells in the basal layer, which faced toward the apical surface in the mitotic phase. The burn group displayed wide degeneration, necrosis, and abundant apoptotic cells in the epithelial tissue as well as intense inflammatory cell infiltration. In the treatment group, there was an increase in mitotic activity in the basal cells of the epithelial layer and degenerative changes, but a preserved epithelial layer and significant cornified structures. The treatment group showed positive caspase-3 expression in some apoptotic cells within the epithelial layer and in connective tissue, and there were only a small number of degenerated cells in the muscle layer. Additionally, in the treatment group, VEGF expression was evident in small numbers of inflammatory cells in the papillary region of the epithelium, and in dilated vascular endothelial cells. Conclusions: Carvacrol may contribute to a reduction in fibrosis by decreasing inflammation and preventing cell apoptosis.

Rats are widely used laboratory animals and have several parasites. One of these are helminths, known not only to cause serious effects on the experimental results in healthy subjects, but also in subjects with heavy infections. One of the relatively pathologic helminth is Trichosomoides crassicauda, which lives in the nodules of the urinary bladder. It is known that diabetics are more prone to infections with several microorganisms. Observations in a diabetic rat bladder showed T. crassicauda eggs inside the transitional epithelium, and structural changes in the bladder epithelium were evident. Urinary-bladder tissues taken from streptozotocin-injected diabetic subjects and citrate buffer-injected control subjects were fixed, embedded in araldite and investigated under a light microscope. Distinct changes in the histological structure of a diabetic urinary bladder transitional epithelium were observed afterT. crassicauda infection. Many papillomas were formed and the epithelial tissues were completely degenerated. In addition, electron microscopic examinations also revealed degeneration of the subepithelial tissues.

Aim: Deltamethrin (DM) is an insecticide and is widely used around the world. Rosmarinic acid (RA) is found in herbs and spices in the Lamiaceae (mint) family and has antioxidant, antiinflammatory and antiapoptotic effects. We objective to examine the protecting efficacy of Rosmarinic acid in preventing the toxic effects of Deltamethrin. Material and Methods: In ours study we used 28 male rats. Group 1: Control group, Group 2: RA group, RA was given 20 mg/kg peroral (p.o.) for 7 days, Group 3: DM group, 35 mg/kg/dose of DM was given 24 hours before sacrification as a single dose by gavage, Group 4: RA+ DM group. Results: BUN, creatinine, AST and ALT values of the RA+DM group were lower than the DM group. TAS and TOS grades were higher in the DM group matched to the RA+DM group. The damage scores of the DM group were higher aacording as those of the RA+DM group. Conclusion: RA has been shown to have predicative influence in the therapy of deltamethrin-induced nephrotoxicity and hepatotoxicity.

Background: The objective of this study was to investigate if long term formaldehyde inhalation may effect periodontal membrane and alveolar bone loss leading to periodontitis. the negative effects of formaldehyde was described using vascular endothelial growth factor (VEGF), matrix metallopeptidase 2 (MMP2) and Osteonectin antibodies involved in the extracellular matrix and angiogenetic development. Materials and methods: Thirty adult Wistar albino rats were used in this study. Rats were divided into two groups, control (n:15) and formaldehyde administered group (n:15). Formaldehyde group was administered 10 ppm formaldehyde during 5 days a week for 8 hours by inhalation. Maxillary bone regions were dissected under anesthesia. After fixation in 10% formaldehyde solution, tissues were passed through graded ethanol series to obtain paraffin blocks. Five-micrometer histological sections were cut with RM2265 rotary microtome stained with Masson- Trichrome and VEGF, MMP2 and Osteonectin antibodies for -examination under Olympus BH-2 light microscopy. Results: The present study revealed that congestion in blood vessels, degeneration of collagen fibers and alveolar matrix around alveolar bone were observed to be more significant in formaldehyde group than the control group (P≤0.001 ). Interestingly, VEGF expression in the formaldehyde group was the most significant finding between the two groups (P<0.001). When compared inflammation, MMP2 and osteonectin expressions were significant (P<0.01) in the formaldehyde group. Conclusions: It was suggested that formaldehyde toxicity decreased the expression of MMP2 and in osteoblasts as well as affecting the retention of MMP levels in tooth cavity, which is very low in collagen fibers. But, vise versa for the expression of VEGF in dilated vascular endothelial cells and osteocytes in alveolar bone. As a conclusion,formaldehyde disrupts the periodontal membrane and may cause collagen fibers degeneration by affecting the alveolar bone matrix. Background: The objective of this study was to investigate if long term formaldehyde inhalation may effect periodontal membrane and alveolar bone loss leading to periodontitis. the negative effects of formaldehyde was described using vascular endothelial growth factor (VEGF), matrix metallopeptidase 2 (MMP2) and Osteonectin antibodies involved in the extracellular matrix and angiogenetic development. Materials and methods: Thirty adult Wistar albino rats were used in this study. Rats were divided into two groups, control (n:15) and formaldehyde administered group (n:15). Formaldehyde group was administered 10 ppm formaldehyde during 5 days a week for 8 hours by inhalation. Maxillary bone regions were dissected under anesthesia. After fixation in 10% formaldehyde solution, tissues were passed through graded ethanol series to obtain paraffin blocks. Five-micrometer histological sections were cut with RM2265 rotary microtome stained with Masson- Trichrome and VEGF, MMP2 and Osteonectin antibodies for -examination under Olympus BH-2 light microscopy. Results: The present study revealed that congestion in blood vessels, degeneration of collagen fibers and alveolar matrix around alveolar bone were observed to be more significant in formaldehyde group than the control group (P≤0.001 ). Interestingly, VEGF expression in the formaldehyde group was the most significant finding between the two groups (P<0.001). When compared inflammation, MMP2 and osteonectin expressions were significant (P<0.01) in the formaldehyde group. Conclusions: It was suggested that formaldehyde toxicity decreased the expression of MMP2 and in osteoblasts as well as affecting the retention of MMP levels in tooth cavity, which is very low in collagen fibers. But, vise versa for the expression of VEGF in dilated vascular endothelial cells and osteocytes in alveolar bone. As a conclusion,formaldehyde disrupts the periodontal membrane and may cause collagen fibers degeneration by affecting the alveolar bone matrix.