The Role of Meteorin-Like Peptide and Asprosin in Colon Carcinoma.

INTRODUCTION:  Colon cancer is one of the most frequent gastrointestinal system cancers on a global scale. Common colonoscopy tests have reduced the incidence of colorectal cancer (CRC). Although nutrition, microorganisms, and their metabolites are related to colon cancer, the exact mechanism of CRC is still not clear. For this reason, it is of great importance to elucidate the molecular mechanisms of colon oncogenesis. METHODS: This study was conducted retrospectively with samples obtained from the laboratory of Firat University Faculty of Medicine, Department of Pathology. A total of 30 patient samples were used. The control group consisted of healthy colon tissues from the same patients, and the other group consisted of colon carcinoma tissues from the same patients. Tissue samples of both groups were evaluated immunohistochemically with meteorin-like (METRNL) peptide and Asprosin. RESULTS: The immunoreactivity of METRNL was found to be lower in colon carcinoma tissues than in healthy colon tissues (0.2 ± 0.06 and 0.08 ± 0.03, respectively). Asprosin immunoreactivity was found to be higher in colon carcinoma tissues than in healthy colon tissues (0.4 ± 0.07 and 1.08 ± 0.15, respectively). CONCLUSION: As a result of this study, it was observed that there was a significant difference between healthy colon tissue and colon carcinoma tissue in terms of METRNL and Asprosin expression. Both proteins might be involved in the molecular mechanism of colon carcinoma. This situation is important in terms of diagnosis.

The protective effects of humanin in rats with experimental myocardial infarction: The role of asprosin and spexin.

Objective: In this study, by applying humanin (HN) before myocardial infarction (MI) in rats, its protection in MI and the possible roles in asprosin and spexin were investigated. Materials and methods: The rats were divided into 7 groups each with 6 rats (group I (control), group II (HN 48th hour), group III (HN 7th day), group IV (MI 48th hour), group V (MI 7th day), group VI (MI + HN 48th hour), group VII (MI + HN 7th day). To create MI, 200 mg/kg isoproterenol (ISO) was administered subcutaneously to the rats. 2 mg/kg HN was given intraperitoneally (ip) to rats alone and before MI. Molecular parameters asprosin and spexin were examined by immunohistochemical in heart tissue. Biochemical parameters (aspartate aminotransferase (AST), lactate dehydrogenase (LDH), creatine kinase MB (CK-MB), Troponin I) were studied in serum by enzyme-linked immunosorbent assay (ELISA) method. Results: It was found in the study that the levels of spexin elevated especially towards the 7th day after MI and decreased more significantly towards the 7th day, after HN application before MI. Asprosin elevated significantly towards the 7th day after MI and decreased especially on the 7th day after HN application before MI. Also, serum AST, LDH, CK-MB, and Troponin I levels tended to decrease and a significant decrease was detected in congested veins in the heart tissue at the 48th hour of MI and erythrocyte extravasation, congested veins and necrotic muscle fibers at the 7th day of MI in rats given HN before MI. Conclusion: It was concluded that HN has a cardioprotective effect in MI and asprosin and spexin might mediate this effect.

Pre-treatment of the beta3-adrenergic receptor agonist BRL37344 reduces in vivo myocardial ischemia/reperfusion injury by improving AMPK and SIRT1 activity and by suppressing mTOR and p70S6K signaling pathways

Abstract This study aimed to investigate the role and signaling pathways of β3-AR in myocardial ischemia/reperfusion (I/R) injury, which is one of the leading causes of death worldwide. 47 male rats were randomly divided into two main groups to evaluate infarct size and molecular parameters. Rats in both groups were randomly divided into 4 groups. Control (sham), I/R (30 min ischemia/120 min reperfusion), BRL37344 (BRL) (A) (5 µg/kg single-dose pre-treatment (preT) before I/R) and BRL (B) (5 µg/kg/day preT for 10 days before I/R). Infarct size was determined with triphenyltetrazolium chloride staining and analyzed with ImageJ program. The levels of AMPK, SIRT1, mTOR, and p70SK6 responsible for cellular energy and autophagy were evaluated by western blot. Infarct size increased in the I/R group (44.84 ± 1.47%) and reduced in the single-dose and 10-day BRL-treated groups (32.22 ± 1.57%, 29.65 ± 0.55%; respectively). AMPK and SIRT1 levels were decreased by I/R but improved in the treatment groups. While mTOR and p70S6K levels increased in the I/R group, they decreased with BRL preT. BRL preT protects the heart against I/R injury. These beneficial effects are mediated in part by activation of AMPK and SIRT1, inhibition of mTOR and p70S6K, and consequently protected autophagy.

Effect of humanine on the Notch signaling pathway in myocardial infarction.

Background/aim: By applying humanin (HN) before myocardial infarction (MI), its protection in myocardial injury and the possible roles of its cellular mechanism in the Notch pathway were investigated. Materials and methods: The study was carried out at Firat University Experimental Research Center (12/24/2018-12/23/2019). Spraque-Dawley rats were divided into 10 groups: I (control) (n = 6), II (HN 6 h) (n = 6), III (HN 24 h) (n = 6), IV (HN day 7) (n = 6), V (MI 6 h) (n = 7), VI (MI 24 h) (n = 7), VII (MI day 7) (n = 7), VIII (MI+HN 6 h) (n = 7), IX (MI+HN 24 h) (n = 7), and X (MI+HN day 7) (n = 7). To create MI, 200 mg/kg of isoproterenol (ISO) was administered to the rats subcutaneously. Moreover, 252 µg/kg of HN was given intraperitoneally (ip) to the rats on its own and before MI. Molecular parameters Notch1, Notch2, Hes1, Hes2, Jagged1, Jagged2, DLL1, and DLL4 were examined using polymerase chain reaction in the heart tissue, Notch1, Hes1, and DLL4 were examined using western blot, while heart tissue was taken for histochemical examinations. Results: The mRNA expression levels of the Notch signaling members (Notch1, Notch2, Hes1, Hes2, Jagged1, Jagged2, DLL1, and DLL4) tended to decrease after MI. The Notch signaling members increased more significantly, especially toward day 7 after HN application before MI. In the western blot anylyses, the Notch1, Hes1, and DLL4 protein levels increased significantly toward day 7 in the groups given HN before MI. Moreover, the serum AST, LDH, CK-MB, and troponin I levels tended to decrease with the application of HN before MI and there was a significant decrease in edema, hemorrhage, and mononuclear cells in the heart tissue at 24 h post-MI and fibrosis on day 7 post-MI. Conclusion: HN administration before MI has a cardioprotective effect on rats via the Notch signaling pathway.

The Beneficial Effects of Fish Oil Following Cisplatin-Induced Oxidative and Histological Damage in Liver of Rats.

This study investigated the protective effect of fish oil (FO) on cisplatin (CP) toxicity in the rat liver. Twenty-eight rats were divided equally into four groups, with the first being a control group. The second group (CP group) was given 7 mg/kg of CP and the third group (FO group) was given 1 FO softgel/rat/day for 14 days. The rats in the fourth group (CP + FO group) were treated with both CP and FO at the above doses. CP treatment caused significant oxidative damage via an increase in thiobarbituric acid reactive substances (TBARS) and reduced antioxidant defenses through a decrease in the activities of catalase (CAT), superoxide dismutase (SOD), reduced glutathione (GSH), and glutathione peroxidase (GPx) in rat liver tissue. Also, CP caused histopathological abnormalities, including necrosis, in the liver tissue. However, concurrent FO treatment prevented the negative oxidative and histopathological effects of CP. In conclusion, CP treatment can cause hepatotoxicity in rats, but dietary supplementation with FO can attenuate the oxidative and histological changes caused by CP. Thus, FO may be useful in preventing CP-induced hepatotoxicity in cancer patients.

The effects of novokinin, an AT2 agonist, on blood pressure, vascular responses, and levels of ADMA, NADPH oxidase, and Rho kinase in hypertension induced by NOS inhibition and salt.

BACKGROUND/AIM: The effects of AT2 receptor agonist novokinin on blood pressure, eNOS, NADPH oxidase, protein arginine methyltransferases (PRMTs), and Rho kinase in hypertension were investigated. Furthermore, in isolated thoracic aorta rings, contractile and dilator responses were studied. MATERIALS AND METHODS: To develop hypertension, L-NAME was administered intraperitoneally and salt was given with tap water (1%) for 4 weeks. Novokinin was administered intraperitoneally for the last 2 weeks. Blood pressures were measured using the tail-cuff method and enzyme levels by real-time polymerase chain reaction in aortic tissues. RESULTS: Blood pressure increased significantly in hypertensive rats. Novokinin reduced the blood pressure in the hypertensive group. While the contractile responses to increasing doses of angiotensin II were increased, vascular reactivity (Emax) and sensitivity (EC50) to acetylcholine were decreased in hypertensive rats. In novokinin-treated hypertensive groups, the EC50 value decreased and the Emax value for acetylcholine significantly increased. The levels of Rho kinase and PRMT expression increased and the level of eNOS expression decreased in the hypertensive group. In novokinin-treated rats, ADMA, NADPH oxidase, and Rho kinase tended to decreased, but these changes did not reach statistical significance. CONCLUSION: Although further studies are needed to determine its effectiveness, the AT2 agonist novokinin may be a novel agent that is promising in terms of protective effects for the treatment of hypertension.

2,3,7,8-Tetrachlorodibenzo-p-dioxin-induced hypertension: the beneficial effects of melatonin.

OBJECTIVE: The purpose of the present study was to evaluate the effects of melatonin on biochemical and cardiovascular changes resulting from exposure to 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), a polychlorinated dibenzo-para-dioxin. METHODS: A total of 24 Sprague-Dawley rats were divided equally into the following four groups: (1) control group was administered with 0.5 mL corn oil by gavage and 0.5 cc vehicle of melatonin (proportionally nine parts physiological serum + one part ethyl alcohol) intraperitoneally for 4 weeks, (2) the melatonin group was given 5 mg/kg/day melatonin intraperitoneally for 4 weeks, (3) the TCDD group was given 500 ng/kg/day TCDD by gavage for 4 weeks and (4) the TCDD + melatonin group was given TCDD (500 ng/kg/day) by gavage and melatonin (5 mg/kg/day) intraperitoneally simultaneously for 4 weeks. Systolic blood pressure was evaluated by the tail-cuff method. Vascular responses to phenylephrine and acetylcholine were evaluated in the isolated thoracic aortas. RESULTS: TCDD not only augmented the systolic blood pressure but also increased the contractile responses to phenylephrine in aorta. Melatonin reversed the blood pressure augmented by TCDD and decreased the contractile responses to phenylephrine in aorta. TCDD induced an increase in the malondialdehyde levels in kidney tissue and melatonin did not change it. Therefore, TCDD caused a decrease in glutathione levels in kidney tissues and melatonin reversed it. CONCLUSION: Present data demonstrated that TCDD may lead to an increase in blood pressure via increased renal oxidative stress and vascular reactivity. However, melatonin might ameliorate the blood pressure disturbed by TCDD in part by decreasing the oxidant activity induced by TCDD.

Rare and challenging extra-axial brain lesions: CT and MRI findings with clinico-radiological differential diagnosis and pathological correlation.

There are many kinds of extra-axial brain tumors and tumor-like lesions, and definitive diagnosis is complicated in some cases. In this pictorial essay, we present rare and challenging extra-axial brain lesions including neuroenteric cyst, primary leptomeningeal melanomatosis, isolated dural neurosarcoidosis, intradiploic epidermoid cyst, ruptured dermoid cyst, intraventricular cavernoma, and cavernous hemangioma of the skull with imaging findings and clinico-radiological differential diagnosis, including the pathologic correlation. Familiarity with these entities may improve diagnostic accuracy and patient management.

Effects of rosuvastatin on ADMA, rhokinase, NADPH oxidase, caveolin-1, hsp 90 and NFkB levels in a rat model of myocardial ischaemia-reperfusion.

AIM: Endothelial dysfunction, oxidative stress and inflammation are among the most important mechanisms of ischaemia-reperfusion (I/R) injury. Besides their cholesterol-lowering effects, statins are known to provide protection against myocardial dysfunction and vascular endothelial injury via nitric oxide-dependent mechanisms. The aim of this study was to investigate the effects of rosuvastatin on certain intermediates involved in the generation of nitric oxide (asymmetrical dimethyl arginin, ADMA, caveolin-1 and hsp 90), oxidative stress (rhokinase, NADPH oxidase) and inflammation (NFkB), using an in vivo model of myocardial infarction in the rat. METHODS: Adult male Sprague Dawley rats were divided into three groups (control, I/R and I/R after 15 days of rosuvastatin administration). Reperfusion was applied for 120 min following left anterior descending coronary artery ischaemia for 30 min. Caveolin-1, hsp 90 and NFkB levels were evaluated with the quantitative reverse transcriptase polymerase chain reaction (qRT-PCR) and ADMA, rhokinase and NADPH oxidase levels were evaluated with ELISA. RESULTS: While NFkB and hsp 90 levels were higher in the I/R group, their levels were significantly lower in the rosuvastatin group. While ADMA and NADPH oxidase levels significantly increased with I/R, they were lower in the rosuvastatin-treated group, but not statistically significant. Rhokinase levels were significantly lower in the rosuvastatin group. Caveolin-1 levels were not different between the groups. CONCLUSION: Our results suggest that ADMA, rhokinase, NADPH oxidase, hsp 90 and NFkB could facilitate I/R injury, and rosuvastatin significantly reduced levels of these parameters. These results indicate that rosuvastatin may have a protective role in I/R injury via mechanisms targeting inflammation, endothelial dysfunction and oxidative stress.

Evaluation of demographic characteristics, and general disease state of patients affliated with home health care unit of Malatya State Hospital.

OBJECTIVE: Home Health Care Unit a unit provides health services for elderly, bedridden and individuals with chronic diseases at home along within the frame of the diagnosis, and treatments of the relevant experts. Therefore, it is intended to reduce the probable physical and emotional burden related to the patient that arise by commuting to the hospital, to increase the number of empty beds for other patients and to improve the living standard by reducing the risk of hospital infection. In this study, the demographic characteristics of housebound patients, their general disease and its relationship with age and gender was investigated. METHODS: The following study was performed on 626 active patients of Malatya State Hospital Home Health Care Unit from January to November 2014. Data were analyzed using Microsoft Excel Program. RESULTS: The study included 60.5% (n=379) female and 39.5% (n=247) male patients. The highest group consisted of patients with 80 years or above 37.7% (n=236). Cerebrovascular disease (CVD) (n=95; 25.0%), senility (n=56; 14.8%) and Alzheimer's disease (n=50; 13.2%) were commonly observed in women. Male patients had CVD (n=54; 21.8%), femur fracture or gonarthrosis which required surgery (n=28; 11.3%), and fracture due to trauma or traffc accidents (n=28; 11.3%), senility and Alzheimer's disease (n=218.5%). CONCLUSION: In recent years home health care units became even more important after the gradual increase in the elderly population and injuries due to accidents. This study can help to provide home health care units in a more effcient manner by educating the staff and relatives who take care of the patients.