Muzaffer Aydin Ketani

The role of estrogen receptors, erbB receptors, vascular endothelial growth factor and its receptors, and vascular endothelial growth inhibitor in the development of the rat mammary gland

We identified the localization and distribution of cell-specific epidermal growth factor receptors (EGFRs: erbB-1, erbB-2, erbB-3, erbB-4), vascular endothelial growth factor (VEGF), VEGF receptors [VEGFRs: VEGF-R1 (flt-1), VEGF-R2 (flk-1/KDR), VEGF-R3 (flt-4)], vascular endothelial growth inhibitor (VEGI), and estrogen receptor (ER), and determined whether or not these growth factors in rat mammary glands are functional. Thirty-five adult female Spraque-Dawley rats were randomly divided into five groups, each of which were at the 7th, 14th, and 21st day of pregnancy; 7th day post-delivery; and 7th day after weaning. It was determined that erbB, VEGF and its receptors, VEGI, and ER stained at different intensities. Intense staining was observed, in particular, in erbB receptors during pregnancy and involution, and also in VEGF and its receptors during lactation, while ER stained during the last periods of pregnancy and lactation. In conclusion, the expression of erbB, VEGF and its receptors, and ER were determined at varying intensities at different sites of the mammary gland during pregnancy, lactation, and involution periods.

Preliminary study of efficacy of hyaluronic acid on caustic esophageal burns in an experimental rat model.

BACKGROUND The aim of this study was to investigate the effectiveness of hyaluronic acid on the prevention of esophageal damage and stricture formation after experimental caustic (alkaline) esophageal injury in rats. MATERIALS AND METHODS Twenty-one Wistar albino rats were randomly divided into three groups. A caustic esophageal burn was created following the Gehanno model: Group l (n=7) underwent operation, but no injury; Group 2 (n=7) was injured and left untreated; and Group 3 (n=7) was injured and treated with hyaluronic acid, first topically and then orally by gavage (2×0.3mL; 12.5mg/mL for 7days). The caustic esophageal burn was created by instilling 25% NaOH into the distal esophagus. All rats were euthanized on day 22 for evaluation. The efficacy of hyaluronic acid treatment was assessed histopathologically and biochemically via blood determination of the total antioxidant status (TAS), total oxidant status (TOS), oxidative stress index (OSI), and sulfhydryl group (SH) and lipid hydroperoxidase (LOOH) levels. Statistical analyses were performed. RESULTS Weight gain was significantly lower in Group 2 than in the other two groups (P<0.05). The mean stenosis index, histopathologic damage score, TAS, TOS, OSI, and SH and LOOH levels were higher in Group 2 than in the other two groups. The mean stenosis index, inflammation, TAS, SH and OSI in Group 2 were significantly different than those in the other two groups (P<0.05). CONCLUSION Hyaluronic acid treatment is effective in treating damage and preventing strictures after caustic esophageal burn in rats.

Effect of oral tamoxifen on the healing of corrosive oesophageal burns in an experimental rat model

OBJECTIVES Corrosive oesophagitis is a common health problem in children. Scar tissue can develop during the recovery period, and as a result, serious narrowing of the oesophagus can develop, in turn causing morbidity and mortality. In previous studies, it was argued that tamoxifen (TAM) may have antifibrotic effects beyond its oestrogen antagonist or agonist properties. We aimed to examine the possible effects of TAM on fibrosis and stricture formation, which are complications of corrosive oesophagitis. METHODS Three study groups were formed as follows: a non-oesophageal burn group (NON-EB, n = 6), an oesophageal burn group (EB, n = 6) and an oesophageal burn + tamoxifen group (EB-TAM, n = 6). In the NON-EB rats, the oesophageal lumen was washed with 0.9% NaCl while, in the EB and EB-TAM rats, the distal oesophagus was burned with a 50% NaOH solution. After application of this solution to the EB-TAM group rats, 0.4 mg/kg/day of TAM was administered via gavage for 7 days. Twenty-two days later, the rat oesophagi were examined histopathologically for inflammation, granulation, collagen deposition and stenosis. RESULTS In the EB group rats, the inflammation, collagen deposition and stenosis scores increased compared with those of the other groups. In the EB-TAM group, these three scores were lower compared with those of the EB group rats, but higher compared with those of the NON-EB group rats. No significant difference was observed in the granulation scores between the EB and EB-TAM groups. It was also observed that the EB-TAM group rats gained more weight than those in the EB group. CONCLUSIONS According to the data obtained, TAM use prevents inflammation, collagenization and stricture development. TAM may be a useful medicine in the treatment of corrosive oesophagitis.

Mucin profiles of the abomasum in bulls and rams: A comparative study.

Many pathogens require direct binding to mucosal cells to cause an infection. The mucosal epithelium of the digestive tract, which is covered by a mucin layer, fulfills several protective functions that are essential to maintaining the health of the digestive tract. Mucins are glycoproteins, which are found on membranes and in mucus gels and protect the underlying mucosal cells. Both membrane‐associated mucins and secreted mucins are critical components of mucosal defense. The aim of this study was to determine the localization and expression of mucin profile of the abomasum via histochemistry and immunohistochemistry. The abomasums of 20 bulls and 20 rams were evaluated. Histochemical examination showed that neutral and acidic mucins were present in the mucosa and the glands of the pars cardiaca, fundus, and pars pylorica of the abomasums of both bulls and rams. However, the expression of acidic mucins was weak in the superficial glands and strong in the deep glands of the abomasum of rams. In both bulls and rams, MUC1, MUC5AC, and MUC6 were expressed in the glandular epithelial cells in all regions of the abomasum. Interestingly, while MUC2 was not expressed in the pars cardiaca and fundus, it was weakly expressed in the parietal cells of the pars pylorica in both species. In conclusion, the presence of neutral and acidic mucins and MUC1, MUC2, MUC5AC, and MUC6 proteins in luminal epithelial and glandular cells of abomasum in the bulls and rams support the hypothesis that mucins play a key role in the protection of the abomasal mucosa against infectious agents.

Distribution of CD68-, CD8-, MHCI- and MHCII-positive cells in the bull and ram testis and epididymis

The mammalian testis possesses a special immunological environment because of its properties of remarkable immune privilege and effective local innate immunity. The testicular immune privilege protects immunogenic germ cells from systemic immune attack, and local innate immunity is important in preventing testicular microbial infections. Thus, this study aimed to immunohistochemically demonstrate the distribution and localization of CD68‐, CD8‐, MHCI‐ and MHCII‐positive immune cells in the testes and epididymes. Negative immunoreactivity was detected in the seminiferous tubule epithelium and peritubular myoid cells of the testes upon staining in CD68, CD8 and MHC Class I. Positive CD68 immunoreaction was determined in the Sertoli cells and some Leydig cells. The detection of positive cells for CD8 clearly indicated the presence of lymphocytes. Furthermore, the staining with MHCI intensity was ascertained to vary from weak to moderate in the Sertoli and Leydig cells and connective tissue cells. MHCII‐positive immunoreactivity was determined in myoid cells and Leydig cells in the interstitial area. The epithelium of the epididymis showed positive staining for CD68 and CD8, but the stroma displayed a rather weak staining. In the ram epididymis, neither intraepithelial nor interstitial positive reaction was observed for MHCI. In the epididymis, the basal cells displayed a stronger staining for MHCII. In conclusion, these cells not only contribute to local immunity through their direct effects on the quality of fertility in males, but also contribute either directly or indirectly to immune privilege by minimizing the development of both autoimmune reactions and potentially harmful risks.

Morphological Changes Caused by Streptozotocin-Induced Diabetes in the Healthy Gingiva of Rats

BACKGROUND AND OBJECTIVE Epidemiologic and clinical studies have indicated that diabetes is a risk factor for periodontal disease progression. The aim of the present study was to evaluate the morphological changes of gingiva in streptozotocin diabetic rats. MATERIAL AND METHODS 30 male Wistar rats that weighed 250-300 g were used in this study. The animals were randomly divided into 2 groups, one with streptozotocin-induced diabetes and another one with healthy (non-diabetic) animals. All rats were sacrificed after 21 days, and their maxillary first molars with surrounding tissues were observed morphological analyses. RESULTS In this study, it was observed that the epithelial thickness was greater in the diabetes group, compared to the control group. The statistical comparison of the diabetes and control groups for the thickness of each of the layers of the epithelium demonstrated that the thickness of the keratinized (corneum), granular and basal layers had significantly increased in the diabetic animals. Furthermore, the diabetes group displayed a decrease in the height of the connective tissue papillae, which was found to be statistically insignificant. Another important finding detected in the diabetes group was the congestion of the gingival capillaries, which showed that blood circulation is impaired in diabetes cases. CONCLUSION On the basis of the results obtained in this study, it was concluded that streptozotocin-induced diabetes may increase predisposition to periodontal disease by causing morphological changes in the periodontal tissues.

Histological investigation of the impact of streptozotocin-induced experimental diabetes on the healthy gingivae of rats

This study was aimed at the histological investigation of the impact of experimental diabetes on the healthy gingiva of rats. Thirty male Wistar rats were used in this study. The animals were randomly divided into two groups (n = 15) prior to the experiment. Group 1 experimental diabetes was created by streptozotocin injection in 15 rats. Group 2 comprised the control group (15 rats). On the 7th, 14th and 21st days after the induction of diabetes by streptozotocin, five animals from each group were euthanized by cardiac puncture. The gingiva of the maxillary left first molar tooth of the sacrificed animals was extracted for histological examination. Histological examination demonstrated that, when compared to the control group, the diabetes group displayed marked hyperkeratosis and parakeratosis of the gingival epithelium on day 21 post-induction. Furthermore, the diabetes group presented with an increased number of inflammatory cells and vasodilatation of the capillaries, in comparison to the controls. The overall evaluation of the findings obtained in this study suggested that diabetes alone could cause changes in the periodontium and affect periodontal health.

The Effects of Sialoadenectomy and Epidermal Growth Factor on Gingival Tissue in Rats: An Ultrastructural Study

ABSTRACT Submandibular salivary glands (SMGs) synthesize, accumulate and secrete a large amount of epidermal growth factor (EGF) in rats. EGF stimulates cell proliferation and differentiation by binding to its reseptors (EGFR). The aim of the present study was to mimic an endogenous epidermal growth factor deficiency through sialoadenectomy in paralel to exogenous EGF administration and to observe the ultrastructural changes in rat gingival tissue, employing electron microscopy. Thirty adult female Wistar albino rats were divided randomly into three groups: a control group (n:10), a sialoadenectomy group (n:10) and a sialoadenectomy group to which an EGF was administered (n:10). The experimental groups of rats were subjected to sialoadenectomy in order to create EGF deficiency. After 27 days both control and experimental rat groups were euthanized by pentobarbital and their gingival tissue was removed. Tissue samples from gingiva were processed for ultrastructural study. Electron microscopic evaluation indicated that while in the control group gingival tissues showed a normal appearance changes were observed in the experimental groups. We observed a partial degeneration of the epithelial cell junctions. Widespread crystolisis was also observed in a group of mitochondria. It is concluded that epidermal growth factor deficiency achieved by sialoadenectomy caused ultrastructural changes in gingival epithelium.

Epidermal Growth Factor Receptor (EGFR) Immunolocalization in the Sialoadenectomized Rat Ovaries

ABSTRACT Intra-ovarian regulation of follicular maturation is modulate by various factors. Among these, Epidermal growth factor (EGF) is vital factor. Epidermal growth factor (EGF) have potent mitogenic effects on granulosa and theca cells. The aim of present study was to investigate the effects of sialoadenectomy on the distrubution of immunoreactive epidermal growth factor receptor (EGFR) in the rat ovaries. Twenty Adult female Wistar albino rats were divided into two groups, a control and one experimental groups. The experimental groups of rats were subjected to sialoadenectomy in order to create EGF deficiency. After 60 days of sialoadenectomy (EGF deficiency) and control group rats were killed by pentobarbital and their ovaries removed. The sections were stained with APAAP immunohistochemical staining for evaluation using a light microscope. A statistically significant reduced body weight was noted in the experimental groups of rats when compared to the control group. This marked EGFR immunoreactivity was maintained in control rat ovaries, whereas it deacreased in sialoadenectomized rat ovaries. In conclusion, the present study indicated that there is paralel relationship between ovary follicule cells EGFR immunolocalization and EGF deficiency.