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Introduction: Esotropia is a form of strabismus, a condition characterized by the misalignment of the eyes. Specifically, esotropia refers to inward deviation of one or both eyes. It can manifest at different ages, ranging from infancy to adulthood, and can have varying degrees of severity. The false appearance of esotropia in the alignment of the visual axes is what defines pseudoesotropia. Halil Pasha was a Turkish painter known for his contributions to the art scene during the late 19th and early 20th centuries. His artistic talent, coupled with his influential position as a statesman, allowed him to leave a lasting impact on the cultural landscape of the Ottoman Empire. Methods: In the present study, artistic depictions of esotropia or pseudoesotropia in Halil Pasha's "Yaşlı Halayık" were evaluated. A comprehensive literature review on strabismus in medicine and art was conducted. Results: "Yaşlı Halayık", translated as "Old Servant Woman", is one of the iconic paintings of Turkish art. It reflects the social dynamics and lifestyle of the time, offering a glimpse into the lives of women serving in Ottoman households. When we examine this painting as a physician, the first thing we notice is the old woman's eyes. An eye misalignment in the left eye of the old servant woman is noticed. Discussion: In medical humanities, which are addressed in medical education, medicine and art intersect with different perspectives and understandings. Although the evaluation of medical scenes in artworks seems to have been first observed by an art historian, today physicians and medical students need to examine artworks more carefully and develop their observational skills. Iconodiagnosis is the medical analysis of artworks that looks for clinical signs suggestive of medical disorders and diseases. The application of iconodiagnosis in medical education is an alternative and stimulating way to exercise students' observation skills; not only the physical examination of the patient is important, but also the information obtained from their posture, clothing, general demeanour and even physical aids. [ABSTRACT FROM AUTHOR]

We aimed to observe the possible effects of melatonin (MLT) deprivation (pinealectomy) and exogenous MLT administration on pulmonary edema induced by alpha-naphthylthiourea (ANTU), a toxic chemical agent, in rats. Seventy animals were assigned to seven groups: control, sham pinealectomy (PINX), PINX, ANTU (10 mg/kg intraperitoneal on day 30), ANTU + MLT (10 mg/kg/day i.p. for 30 days), ANTU + PINX, and ANTU + PINX + MLT. In this study, pleural effusion (PE) formation, lung weight/body weight (LW/BW) and PE/BW ratios (fluid accumulation and weight values in the lungs) increase detected. Pre-ANTU MLT administration led to significant decreases in PE, LW/BW, and PE/BW levels. The inhibited glutathione (GSH) and superoxide dismutase (SOD) levels and high malondialdehyde (MDA) levels that ANTU increase lipid peroxidation in the study. MLT administration eliminated oxidative stress by reducing MDA and ameliorating GSH and SOD levels. Pre-ANTU MLT administration led to a significant decrease in interleukin-1 beta (IL-1β) and tumor necrosis factor-alpha (TNF-α) levels in the lung when compared to the ANTU group without MLT administration. Post-pinealectomy ANTU administration significantly increased IL-1β and TNF-α levels when compared to ANTU and MLT administration without pinealectomy. Diffused inflammatory cell infiltration, interstitial pulmonary edema, and histopathological congestion were observed after the administration of ANTU. Severity of the damage was elevated in the ANTU + PINX group. MLT treatment regressed pulmonary effusion and edema and improves lung structure. In brief, the findings suggested that MLT inhibited proinflammatory mediators and could serve as a therapeutic agent to prevent inflammatory disorders. [ABSTRACT FROM AUTHOR]

Bacterial toxins are widespread in the environment as well as in the digestive system of humans and animals. Toxin from Gram-negative bacteria (endotoxin or lipopolysaccharide; LPS) has a life-long programming effect on reproduction in rats, but the mediators have not been well-documented, so we investigated the effects of LPS on the timing of puberty in female rats. Because the levels of nitric oxide (NO) and interleukin 1β (IL-1β) increase following injection of LPS, we injected neonates (post-natal day (pnd) 7) with LPS, with or without NO or IL-1β inhibitors. Half of the prepubescent (pnd 30) animals received an additional LPS injection. Vaginal opening, number of ovarian follicles, and serum anti-LPS antibodies were determined. A single LPS injection was sufficient to reduce the primordial follicle pool, but puberty was delayed when rats received 2 LPS injections (at pnd 7 and 30). NO or IL-1β inhibitors improved both of these parameters, suggesting that the early detrimental effects of LPS on puberty and primordial follicle pool are mediated by NO and IL-1β. Key words: lipopolysaccharide, puberty, ovarian function, IL-1β, nitric oxide, female rats. Les toxines bacteriennes sont repandues dans l'environnement et dans le systeme digestif des humains et des animaux. On sait que la toxine des bacteries negatives a Gram (endotoxine ou lipopolysaccharide; LPS) exerce un effet de programmation sur la reproduction des rats qui dure toute la vie, mais ses mediateurs ne sont pas bien documentes. Puisque les niveaux d'oxyde nitrique (NO) et d'interleukine 1β (IL-1β) augmentent a la suite d'une injection de LPS, les auteurs ont examine les effets d'une injection neonatale de LPS (jour 7 postnatal) en presence ou non d'inhibiteurs de NO ou d'IL-1β, sur la maturation pubertaire de rats femelles. La moitie des animaux a recu une injection supplementaire de LPS en periode pre-pubertaire (jour 30 postnatal). L'ouverture vaginale, le nombre de follicules ovariens et la presence d'anticorps anti-LPS dans le serum ont ete determines. Une injection unique de LPS suffisait a reduire le pool de follicules primordiaux mais la puberte n'etait retardee que chez les rates ayant recu deux injections de LPS, aux jours 7 et 30 postnataux. Les inhibiteurs amelioraient les deux parametres, suggerant que les effets nocifs precoces du LPS sur la puberte et le pool de follicules primordiaux passent par l'intermediaire du NO et de l'IL-1β. [Traduit par la Redaction] Mots-cles: lipopolysaccharide, puberte, fonction ovarienne, IL-1β, oxyde nitrique, rats femelles., Introduction The environmental chemicals that have an impact on human health are not only man-made or man-introduced agents (Rylander 2002); humans are continuously exposed to toxins originating from microorganism-associated molecular [...]

Aim: Cancer is one of the most common health problems in the world. Music is a therapy method that creates positive changes in human behavior. This study aims to examine the effects of Turkish and Western classical music on MCF-7, SKOV-3, PC-3, U87, and COLO741 cancer cell lines. Material and Methods: Group 1: No sound, Group 2: Turkish classical music (ney), Group 3: Western classical music (piano), and Group 4: Western classical music (violin). After listening to the cancer cells for 40 min, the audio files were interrupted for 1h, and then music was played for another 40 min. The effect of music on the proliferation of cancer cells was determined by WST-1 cell viability analysis. Statistical analyzes were performed with the SPSS program. Results: There was no statistically significant difference between the groups that were applied music once in only the MCF-7 breast cancer cells and the control group (p>0.05). A statistically significant decrease was detected in cell viability when the control group and the other groups that were applied to music twice were compared (p<0.05). For other cancer cell lines except (please the SKOV-3 ovarian cancer cells, it was determined that music application once also caused a statistically significant decrease in cell viability (p<0.05). Conclusion: We determined that classical music effectively reduced and suppressed the number of cancer cells. According to the data, Turkish and Western classical music can be used to support the treatment in of cancer patients. [ABSTRACT FROM AUTHOR]

Aim: Breast cancer is the most common malignancy in women. This disease is a critical public health problem and further research at the molecular level would define its prognosis and specific treatment. Phenformin is an antidiabetic agent. Recent studies showed that it should be considered as a potential agent for the prevention and treatment of cancer cell lines. This study aimed to investigate the antiproliferative effect of phenformin on MDA-MB-231 and MCF-7 breast cancer cell lines. Materials and Methods: MDA-MB-231 and MCF-7 breast cancer cell lines were used in the study. Experimental groups; control group, 1 μM, 2.5 μM, and 5 μM phenformin administered groups were planned. WST-1 analysis was performed to evaluate the viability of cells 24 h after the treatments. Statistical analysis was carried out using the SPSS 17.0 statistical program. p<0.05 was considered to indicate a statistically significant difference. Results: In the MDA-MB-231 breast cancer cell line, there were statistically significant differences among all groups (p<0.05, for all), except between the 1 μM phenformin-treated and control groups (p>0.05). In the MCF-7 breast cancer cell line; there were statistically significant differences between the control group and 5 μM phenformin-treated, and between 1 μM phenformin-treated and 5 μM phenformin-treated (p<0.05, for all) groups. Conclusion: Phenformin seems to exert antiproliferative effects on MDA-MB-231 and MCF-7 breast cancer cell lines. It was observed that the antiproliferative effect was stronger in the MDA-MB-231 cell line. It showed a stronger antiproliferative effect in the MDAMB-231 cell line of antiproliferative effect. [ABSTRACT FROM AUTHOR]

The present study aimed to analyze the effects of pinealectomy and crocin treatment in isoproterenol-induced myocardial damage. Seventy rats were divided into seven groups: control, sham control, pinealectomy (PNX), isoproterenol (ISO; 85 mg/kg on the 29th and 30th days of the experiment, subcutaneous injection), PNX + ISO, PNX + crocin (50 mg/kg/day for 30 days, intragastric administration), and PNX + ISO + crocin. PNX procedure was performed on the first day of the study. A significant increase was observed in serum cardiac damage markers (CK-MB, Troponin I) after ISO administration. ISO administration led to a significant increase in cardiac oxidative stress parameters, such as malondialdehyde (MDA) and total oxidant status (TOS), while it led to a decrease in antioxidant defense system parameters, such as reduced glutathione (GSH), superoxide dismutase (SOD), catalase (CAT) and total antioxidant status (TAS) when compared to control groups. Elevated MDA and TOS levels were observed, while reduced SOD and CAT activities, and decreased GSH and TAS levels were observed in the group that underwent PNX and ISO administration when compared to the PNX group. Furthermore, in the PNX + ISO + Crocin group, SOD and CAT activities, and GSH and TAS levels ameliorated and MDA and TOS levels were reduced with the crocin treatment when compared to the PNX + ISO group. Also, marked increases were observed in serum cardiac markers, histopathological and immunohistochemical findings after the crocin treatment. All findings demonstrated that crocin could be employed as a cardioprotective agent due to its antioxidant, anti-inflammatory, and anti-apoptotic properties. [ABSTRACT FROM AUTHOR]

The aim of the present study was to investigate the therapeutic and protective effects of linalool against doxorubicin (DOX)-induced kidney injury. Forty-eight Wistar rats were divided into 8 groups as follows; Control, DOX [20 mg/kg, intraperitoneal (ip) single dose DOX], linalool (LIN50 and LIN100; 50 mg/kg and 100 mg/kg linalool via ip for 5 days, respectively), DOX + LIN50 and DOX + LIN100 (20 mg/kg single dose of DOX via ip on first day and 50 mg/kg and 100 mg/kg linalool via ip, respectively), LIN50 + DOX and LIN100 + DOX (50 mg/kg and 100 mg/kg linalool via ip for 5 days, respectively and 20 mg/kg single dose of DOX via ip on fifth day). Doxorubicin led to a significant increase in the level of malondialdehyde (MDA) in the kidney, whereas superoxide dismutase (SOD), catalase (CAT) and reduced glutathione (GSH) levels decreased remarkably when compared with control. On the other hand, LIN supplementation before and after DOX treatment led to a significant decrease in MDA and also increases in SOD, CAT and GSH levels. DOX caused significant increases in the levels of blood urea nitrogen (BUN) and creatinine (Cr) levels in the plasma, while LIN supplementation as a therapeutic and preventive agent led to significant decreases in BUN and Cr levels. The current study demonstrated that LIN supplementation after or before DOX treatment can led to therapeutic and preventive effects against DOX-induced renal damage. [ABSTRACT FROM AUTHOR]

Ranolazine is beneficial when given as an adjunct to treatment in symptomatic angina pectoris. Therefore, it may be useful to evaluate the effect of ranolazine on cardiovascular endothelial cells in hypoxic conditions that may resemble decreased oxygen delivery during angina pectoris. In this study, chemical hypoxia caused by exposure of Human Umbilical Vein Endothelial Cells (HUVECs) to different concentrations of cobalt chloride (CoCl2) (100 µM - 1000 µM) for 24 and 48 h was evaluated. In this chemical hypoxia model, HIF-1alpha and eNOS were measured semi-quantitatively by immunocytochemistry. Activation of the intracellular MAPK and PI3K pathways was evaluated by flow cytometry. During chemical hypoxia, HIF-1alpha was increased in a CoCl2 concentration-dependent manner; however, eNOS did not change significantly. In the presence of 10 µM ranolazine, HIF-1alpha increased in cells exposed to 1000 µM CoCl2 for 24 h, whereas HIF-1alpha decreased in cells exposed to 1000 µM CoCl2 for 48 h. Endothelial cell viability decreased with a high concentration of CoCl2. Ranolazine (1 µM, 10 µM) added to the medium failed to restore cell viability as measured by WST-1. The proportional percentage of cells in which only the MAP kinase pathway was activated increased during chemical hypoxia. Although ranolazine could reduce HIF-1alpha levels in the 48hour group, it had no beneficial effect on CoCl2 toxicity. [ABSTRACT FROM AUTHOR]

Introduction:Hepatotoxicity is a major complication of acetaminophen (APAP), a widely used analgesic and antipyretic drug. Resveratrol (RSV) is a naturally occurring diphenol and it has anticancer, antioxidant, and anti-inflammatory properties.Objectives: In this study, the beneficial effects of RSV on APAP-induced hepatotoxicity was investigated in rats.Materials and methods: Group 1: Ethanol, Group 2: Saline, Group 3: RSV (10 mg/kg/ip), Group 4: APAP (1000 mg/kg/ip/single dose), Group 5: APAP+RSV (20 min after administration of APAP). The rats were sacrificed 24 h after administration of APAP. Light and electron microscopic changes were evaluated. Levels of malondialdehyde (MDA) and glutathione (GSH), catalase (CAT), and superoxide dismutase (SOD) activities were determined in liver tissue.Results: Rats of the ethanol, saline, and RSV groups did not present any histopathological alterations. In the APAP group, we observed vascular congestion, necrosis, inflammation, sinusoidal dilatation, and loss of glycogen content. In the APAP+RSV group, these changes were markedly reduced. iNOS immunostaining showed very weak positive stained hepatocytes the sections of control, saline, and RSV groups. However, in the APAP group, iNOS immunostaining was most evident in pericentral hepatocytes. In the same areas in APAP+RSV group, intensity of iNOS immunostaining decreased. A significant increase in MDA and decreases in GSH level, CAT, and SOD activity indicated that APAP-induced hepatotoxicity was mediated through oxidative stress. Significant beneficial changes were noted in tissue oxidative stress indicators in rats treated with RSV.Conclusion: These biochemical, histopathological, and ultrastructural findings revealed that RSV reduced the severity of APAP-induced alterations in liver. [ABSTRACT FROM PUBLISHER]

Inflammation in the liver is an extraintestinal manifestation that is frequently seen during inflammatory bowel diseases (IBD). The authors investigated histopathologycal, ultrastructural and antioxidant effects of dexmedetomidine (Dex) on liver during trinitrobenzene sulfonic acid (TNBS)-induced inflammatory bowel disease. Thirty-two BALB/c mice were divided ( n = 8) as follows: control; Dex (dexmedetomidine) (30 μg/kg) for 6 days; TNBS 150 μL, TNBS + ethanol (50% w/v) intrarectally; TNBS + Dex. The histopathological and ultrastructural changes were evaluated. The levels of malondialdehyde ( MDA), activity of antioxidant enzymes (GPx and SOD) were measured in liver tissue. Induction of colitis induced histopathological and ultrastructural changes of damage in liver. Those changes were markedly reduced in the TNBS + Dex group and that reduction was even significant in comparison to the TNBS group. MDA levels were significantly higher in the TNBS group and dexmedetomidine significantly elevated SOD levels in the TNBS + Dex group. These results suggest that the administration of dexmedetomidine reduces the histopathological and ultrastructural damage and increases the defense capacity against oxidative damage on liver in this IBD mice model. [ABSTRACT FROM AUTHOR]

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: The study aimed to determine the CCl4-induced liver fibrosis model in pinealectomized rats and biochemically, immunohistochemically, and histopathologically investigate the therapeutic effect of melatonin on liver fibrosis. The surgical procedure for pinealectomy was performed at the beginning of the study, and the sham and pinealectomized rats were administered CCl4 dissolved in corn oil (1:1) alone every other day to induce liver fibrosis or together with melatonin (10 mg/kg) therapy for 15 days. Melatonin is an essential therapeutic agent and offers an alternative therapeutic strategy in CCl4-induced liver fibrosis by suppressing inflammation, oxidative stress, and the TGF-β1 signaling pathway. Treatment with melatonin ameliorated CCl4-induced liver fibrosis by restoring hepatocellular damage and reducing plasma AST, ALT, and ALP values. Melatonin increases the activity of SOD and CAT, which are important enzymes for antioxidant defence, and raises GSH levels, which further enhances antioxidant function. Also, melatonin reduced hepatic inflammation (IL-6 and IL-1β) and oxidative stress indices. Moreover, histopathological changes and immunohistochemical expression of TGF-β1 were restored following melatonin supplementation in the CCl4-induced liver fibrosis model in pinealectomized rats. Our study shows that melatonin supplementation has a beneficial effect in protecting the liver fibrosis induced by CCl4 in pinealectomized rats. [ABSTRACT FROM AUTHOR]

Physical exercise could cause muscle and tissue damage due to increase in the formation of free oxygen radicals during exercise. The aim of the present study was to investigate the effect of crocin on parameters associated with oxidative stress in recovery from acute swimming exercise in rats. Rats were divided into eight groups; Normal Control (NC: untreated and did not swim), Crocin Control (CC: received crocin and did not swim), Exercise-1 (Exe-1: untreated and swam), Exercise-24 (Exe-24: untreated and swam), Exercise-48 (Exe-48: untreated and swam), Exercise+Crocin-1 (Exe-Cro-1: received crocin and swam), Exercise+Crocin-24 (Exe-Cro-24: received crocin and swam), Exercise+Crocin-48 (Exe-Cro-48: received crocin and swam). AST, ALP, LDH, CK, XO enzymes levels increased after swimming in untreated and crocin-treated groups, but there was a less increase in crocin-treated groups. The highest MDA levels in serum were determined in Exe-1 compared with all other groups. There was significant difference between control and exercise groups in MDA level (p = 0.033). In contrast, there was significant difference between control and exercise groups in GSH level (p < 0.001). In addition, crocin given to swimming rats significantly increased GSH levels (p < 0.05) and decreased MDA levels when compared with untreated exercise groups. In conclusion, crocin is able to protect liver and skeletal muscle tissue against exercise-induced oxidative damage by preventing reactive oxygen species (ROS) production.

Aim: To investigate the potential role of oxidative stress and the possible therapeutic effects of N-acetyl cysteine (NAC), amifostine (AMF) and ascorbic acid (ASC) in methotrexate (MTX)-induced hepatotoxicity., Methods: An MTX-induced hepatotoxicity model was established in 44 male Sprague Dawley rats by administration of a single intraperitoneal injection of 20 mg/kg MTX. Eleven of the rats were left untreated (Model group; n = 11), and the remaining rats were treated with a 7-d course of 50 mg/kg per day NAC (MTX + NAC group; n = 11), 50 mg/kg per single dose AMF (MTX + AMF group; n = 11), or 10 mg/kg per day ASC (MTX + ASC group; n = 11). Eleven rats that received no MTX and no treatments served as the negative control group. Structural and functional changes related to MTX- and the various treatments were assessed by histopathological analysis of liver tissues and biochemical assays of malondialdehyde (MDA), superoxide dismutase (SOD), catalase, glutathione (GSH) and xanthine oxidase activities and of serum levels of aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase and total bilirubin., Results: Exposure to MTX caused structural and functional hepatotoxicity, as evidenced by significantly worse histopathological scores [median (range) injury score: control group: 1 (0-3) vs 7 (6-9), P = 0.001] and significantly higher MDA activity [409 (352-466) nmol/g vs 455.5 (419-516) nmol/g, P < 0.05]. The extent of MTX-induced perturbation of both parameters was reduced by all three cytoprotective agents, but only the reduction in hepatotoxicity scores reached statistical significance [4 (3-6) for NAC, 4.5 (3-5) for AMF and 6 (5-6) for ASC; P = 0.001, P = 0.001 and P < 0.005 vs model group respectively]. Exposure to MTX also caused a significant reduction in the activities of GSH and SOD antioxidants in liver tissues [control group: 3.02 (2.85-3.43) μmol/g and 71.78 (61.88-97.81) U/g vs model group: 2.52 (2.07-3.34) μmol/g and 61.46 (58.27-67.75) U/g, P < 0.05]; however, only the NAC treatment provided significant increases in these antioxidant enzyme activities [3.22 (2.54-3.62) μmol/g and 69.22 (61.13-100.88) U/g, P < 0.05 and P < 0.01 vs model group respectively]., Conclusion: MTX-induced structural and functional damage to hepatic tissues in rats may involve oxidative stress, and cytoprotective agents (NAC > AMF > ASC) may alleviate MTX hepatotoxicity.