Detection of progressive and regressive phase and LINE-1 retrotransposon in transfected dogs with transmissible venereal tumor during chemotherapy.

Canine transmissible venereal tumor (CTVT) is a tumor that commonly occurs in genital and extragenital sites of both genders. Long interspersed nuclear elements (LINE-1) retrotransposon has a pivotal role in allogenic transfection among uncontrolled dog populations. This study aimed to perform pathomorphological, immunohistochemical, and in situ polymerase chain reaction (PCR) evaluation of CTVT (n = 18) in transfected dogs during chemotherapy. Immunohistochemically, tumor phases were investigated by using specific markers (CD3, CD4, CD8, CD79, and transforming growth factor beta [TGF-ß]), and investigated an amplified specific sequence of TVT LINE-1 retrotransposon by in situ PCR. Polyhedral-shaped neoplastic cells that had large, round, hypo/hyperchromatic nuclei and eosinophilic cytoplasm were detected. All marker results were positive, especially in the early weeks of recovery. CD4 and TGF-ß markers were conspicuously positive at the initial stage. In situ PCR LINE-1 sequence was initially positive in only four cases. It is believed that the CD and TGF-ß markers provide phase identification at tumor initiation and during chemotherapy. It is thought that presence of T and B lymphocytes, which have roles in cellular and humoral immunity, is needed so that regression of the tumor is possible.

Exogenous ghrelin enhances endocrine and exocrine regeneration in pancreatectomized rats.

AIM: Ghrelin, the most important modulator of endocrine and exocrine pancreatic functions, has a role in the development of islets of Langerhans during embryogenesis. The aim of this study was to evaluate the effects of ghrelin on pancreatic regeneration in rats with 90% pancreatectomy. MATERIALS AND METHODS: Two- to 3-week-old Wistar rats were used in the study. After anesthesia, 90% pancreatectomy was performed. In the ghrelin group, 90% pancreatectomy was performed. Ten nanomoles per kilogram per day of ghrelin was administered intraperitoneally from the first postoperative day. In the antagonist group, 90% pancreatectomy was performed. From the first postoperative day, rats received the ghrelin receptor antagonists and substance P intraperitoneally at 1 mumol/kg. In the control group, 90% pancreatectomy was performed, and intraperitoneal saline was administered. The sham group did not receive pancreatectomy. Eight rats from each group were randomly selected and sacrificed on the second, third, and 30th days. RESULTS: Blood glucose levels in pacreatectomized rats were significantly higher than in rats in the sham group. The number of beta islet cells, serum insulin levels, and PDX-1 and cytokeratin staining scores decreased in rats with pancreatectomy when compared to the sham-group rats. In the ghrelin-receiving rats, blood glucose levels tended to decrease from the 15th postoperative day. Ghrelin treatment increased insulin levels, insulin-positive islet cell number, and 5-bromo-2-deoxyuridine and PDX-1 staining, whereas ghrelin antagonist administration resulted in significant decreases in these parameters. Ghrelin treatment significantly improved glucose tolerance test results. CONCLUSION: Exogenous ghrelin administration decreased blood glucose levels after 90% pancreatectomy by increasing islet cell numbers and enhancing endocrine and exocrine regeneration.

Protective effects of recombinant human granulocyte colony stimulating factor in a rat model of necrotizing enterocolitis.

The role of cytokines and growth factors in the pathophysiology of neonatal necrotizing enterocolitis (NEC) is not defined clearly yet. The aim of this study was to determine the effects of recombinant human granulocyte colony stimulating factor (G-CSF) on intestinal cells in hypoxia-induced experimental NEC in rats. The study was experimented on Sprague Dawley rat pups. Group 1 (untreated, n = 7) rats were subjected to hypoxia-reoxygenation (H/O) and then were returned to standard conditions. Group 2 (G-CSF treated, n = 7) rats were subjected to H/O, and then were treated with G-CSF (100 microg/kg enterally) for 5 days. Group 3 was served as nonhypoxic controls. All animals were killed on day five, and histological examination was performed on intestinal samples. There were no histopathological changes in the control group. The histological findings in untreated rats were similar to those seen in neonatal NEC, with destruction of villi and crypts with extension to the muscularis layer. Intestinal damage was mild in group 2 and these histological changes were better than group 1, and worse than group 3. The mean of histologic grade of group 1 was 2.4 (range 2-3), and in the group 2, it was 1.2 (range 0-2). A difference was found when two groups were compared with each other (P < 0.05). In an experimental model of NEC, G-CSF could have a protective effect on intestinal damage.

Chitosan microparticles containing plasmid DNA as potential oral gene delivery system.

The potential of chitosan as a polycationic gene carrier for oral administration has been explored since 1990s. Chitosan has been shown to effectively bind DNA in saline or acetic acid solution and protect DNA from nuclease degradation. In this study, pDNA (plasmid DNA) was encapsulated in chitosan microparticles. Chitosan-DNA microparticles were prepared using a complex coacervation process and stability of plasmid DNA was investigated in this complex. The chitosan-DNA microparticles could protect the encapsulated plasmid DNA from nuclease degradation. Release of pDNA from microparticles was studied in simulated gastric, simulated intestinal medium and acidic PBS (phosphate buffer saline) (pH 4.5) buffer at 37 degrees C, and released pDNA was assayed spectrophotometrically. In vitro release of pDNA from chitosan microparticles was dependent on pH, as the pH of the release medium increased release profile decreased. In in vivo-animal studies blue color was observed with X-gal (4-chloro-5-bromo-3-indolyl-beta-galactosidase) staining of histological stomach and small intestine sections after oral administration of pDNA-chitosan microparticles as an indicator of exogeneous gene expression.

The effects of aflatoxin B1 on the development of kwashiorkor in mice.

Seventy Swiss albino mice (6-week-old male) were selected for the investigation into aflatoxin B1's role in the cause of kwashiorkor. The mice were divided randomly into four groups. They were grouped within each group by being fed either low or normal protein level diets supplemented with very small amounts of aflatoxin B1 (0.5 microg/day). The control groups were fed aflatoxin B1-free diets containing either normal or low protein levels. All groups were monitored for 7 weeks. The increase in body weight was found to be low in groups I and II, given diets contaminated with aflatoxin B1. Although groups II and IV, which were given low dietary protein, showed remarkable decreases in serum total protein and albumin levels (group II: total protein 4.1 +/- 0.1 g/dL, albumin 2.6 +/- 0.8 g/dL and group IV: total protein 4.6 +/- 1.3 g/dL, albumin 2.8 +/- 0.82 g/dL) when compared with the groups fed a normal dietary protein level (group I: total protein 5.9 +/- 1.3g/dL, albumin 3.4 +/- 0.7g/dL and group III: total protein 5.4 +/- 1.6g/dL, albumin 3.5 +/- 1.2g/dL; P < 0.05). The statistical difference between these two groups was found not to be significant (P > 0.05). However, decreases in total protein and albumin levels were a little more prominent in group II. In addition, histopatological changes of the liver was remarkable in the group fed a low protein diet and aflatoxin B1 when compared with the group fed only a low protein diet and no aflatoxin B1. More significantly, however, was the increase in liver weight in both groups fed a low protein diet (groups II and IV). Our conclusion is that aflatoxin B1 could not have contributed to the development of kwashiorkor.

[The beneficial effect of selenium against induction of squamous cell carcinoma of the tongue in rabbits]. / Tavsanda yassi epitel hücreli dil kanseri modelinde selenyumun yararli etkisi.

OBJECTIVES: In a rabbit model of squamous cell carcinoma of the tongue, we monitored histopathologic changes and assessed the effect of selenium against carcinogenesis. STUDY DESIGN: The study included 36 male albino New Zealand rabbits. To induce squamous cell carcinoma of the tongue, 9,10-dimethyl-1,2-benzanthracene (DMBA)-acetone solution was applied three times a week for a duration of 20 weeks under anesthesia with xylazine hydrochloride and ketamine. The rabbits were randomly assigned to receive either pure tap water (24 rabbits) or tap water supplemented with 4 ppm sodium selenite (12 rabbits). One rabbit in each group was sacrificed at the end of 4, 8, 12 and 16 weeks, and the remaining rabbits at the end of 20 weeks for macroscopic and microscopic examination of the tongue. RESULTS: By week 20, two rabbits in the selenium group, and nine rabbits receiving tap water died from acute necrotizing bronchopneumonia due to pasteurellosis. Dysplasia was significantly less in selenium-receiving rabbits (16.7% vs 66.7%, p < 0.0001), and its development manifested a delayed onset. Carcinoma in situ was detected in 25% of tap water-receiving rabbits that remained alive by week 19 to 20, while none of the rabbits had carcinoma in situ in the selenium group. CONCLUSION: Our data demonstrate that selenium has an inhibitory and preventive effect against chemically-induced rabbit tongue carcinogenesis.

A case of aspergillosis in a broiler breeder flock.

A case of aspergillosis in a broiler breeder flock having respiratory and nervous system problems caused by Aspergillus fumigatus and Aspergillus niger is documented. Dyspnea, hyperpnea, blindness, torticollis, lack of equilibrium, and stunting were observed clinically. On postmortem examination of the affected birds, white to yellow caseous nodules were observed on lungs, thoracic air sacs, eyes, and cerebellum. Histopathologic examination of lungs and cerebellum revealed classic granulomatous inflammation and cerebellar lesions, necrotic meningoencephalitis, respectively. No lesions were noted in the cerebrum histopathologically. Aspergillus hyphae were observed in stained sections prepared from lesioned organs. Fungal spores and branched septate hyphae were observed in direct microscopy. Aspergillus fumigatus and A. niger were isolated from the inoculations prepared from the suspensions of organs showing lesions.