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Abstract Background Mercury poisoning can occur as a result of occupational hazard or suicide attempt. This article presents a 36-year-old case admitted to emergency department (ED) due to exposure to metallic mercury. Case Presentatıon A 36-year-old woman presented to the ED with a three-day history of abdominal pain, diarrhea and fever. One week ago her daughter had brought mercury in the liquid form from the school. She had put it on the heating stove. One day later, her 14-month old sister baby got fever and died before admission to the hospital. Her blood pressure was 134/87 mmHg; temperature, 40.2°C; heart rate 105 bpm and regular; respiration, 18 bpm; O2 saturation, 96%. Nothing was remarkable on examination and routine laboratory tests. As serine or urinary mercury levels could not be tested in the city, symptomatic chelation treatment with N-acetyl cysteine (NAC) was instituted with regard to presumptive diagnosis and history. At the 7th day of admission she was discharged without any sequelae or complaint. At the discharge day blood was drawn and sent for mercury levels which turned out to be 30 μg/dL (normal range: 0 - 10 μg/dL). Conclusion Public education on poisoning and the potential hazards of mercury are of vital importance for community health.

Arsenic is a toxic and carcinogenic substance. Arsenic is known to have negative effects on male reproductive functions. In this study, protective effects of quercetin against arsenic-induced testicular damage in rats were investigated. In this study, 27 Sprague-Dawley male rats were divided into three groups. Control group (10 ml/kg/day SF), arsenic group (10 mg/kg/day sodium arsenite), arsenic + quercetin group (10 mg/kg/day sodium arsenite + 50 mg/kg/day quercetin). At the end of the 15 days, rats were sacrificed. Testis tissues were collected and stained with hematoxylin and eosin for histopathological analysis. Apoptotic cells were studied by using TUNEL assay. Cell proliferation was studied by PCNA method. The activities of superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) as well as malondialdehyde (MDA) were measured by spectrophotometry. As a result of exposure to arsenic in rat, our study showed that reduced germ cells and degeneration of seminiferous tubules, increase TUNEL-positive apoptotic cells in the walls of the seminiferous tubules and decreased PCNA-positive cells in testes by histopathological methods. After quercetin treatment, we have demonstrated that structural deterioration in testes was ameliorated, decreased TUNEL-positive apoptotic cells, increased PCNApositive cells. After arsenic exposure; decreased SOD, CAT and GSH-Px activities, increased in the MDA levels in testes tissues was detected by biochemical analyses. After quercetin administration, an increase of SOD, CAT and GSH-Px activity and a decrease of MDA levels were determined. These data suggested that quercetin has protective effects against arsenicinduced testicular damage by decreasing morphological damage, apoptosis, lipid peroxidation, and oxidative stress. [ABSTRACT FROM AUTHOR]

Aim: The protective effect of vitamin E (vit E) on cadmium (Cd) induced oxidative stress was studied in the blood of rats. Methods: The rats were randomly divided in to three experimental groups: Control, Cd treated and Cd + vit E treated, each containing 10 animals. The Cd treated and Cd + vit E treated groups were injected subcutaneously daily with CdCl2 dissolved in isotonic NaCl in the amount of 2 mL/kg for 20 days, resulting in a dosage of 0.49 mg Cd/kg/d. In addition, Cd + vit E treated group received intramuscular injection of 150 mg/kg vit E until the end of the study. Results: Cd treatment increased significantly malondialdehyde (MDA) levels and the antioxidant enzyme activities of superoxide dismutase (SOD), glutathione peroxidase (GSH-Px) and catalase (CAT) in plasma and erythrocytes compared to the control group. Cd + vit E treatment, decreased significantly elevated MDA levels in plasma and erythrocyte and also reduced significantly the enhanced antioxidant levels. Cd treatment increased significantly the activity of iron levels in the plasma compared to the control group. Cd + vit E treatment, decreased the activity of iron levels in the plasma compared to the Cd treated group. In the control group, the histology of erythrocytes was normal. In Cd treated group, there was marked membrane destruction and there were hemolytic changes in erythrocytes. In Cd + vit E treated group, these changes were less than Cd treated group. Conclussion: Our results show that vit E exerts a protective effect against cadmium toxicity. [ABSTRACT FROM AUTHOR]

Bacteria and fungi are natural sources of metabolites exhibiting diverse bioactive properties such as wound healing, antioxidative, antibacterial, antifungal, anti-inflammatory, antidiabetic, and anticancer activities. Two important groups of bacteria or fungi-derived metabolites with wound-healing potential are polysaccharides and peptides. In addition to bacteria-derived cellulose and hyaluronic acid and fungi-derived chitin and chitosan, these organisms also produce different polysaccharides (e.g., exopolysaccharides) with wound-healing potential. The most commonly used bacterial peptides in wound healing studies are bacteriocins and lipopeptides. Bacteria or fungi-derived polysaccharides and peptides exhibit both the in vitro and the in vivo wound healing potency. In the in vivo models, including animals and humans, these metabolites positively affect wound healing by inhibiting pathogens, exhibiting antioxidant activity, modulating inflammatory response, moisturizing the wound environment, promoting the proliferation and migration of fibroblasts and keratinocytes, increasing collagen synthesis, re-epithelialization, and angiogenesis. Therefore, peptides and polysaccharides derived from bacteria and fungi have medicinal importance. This study aims to overview current literature knowledge (especially within the past 5 years) on the in vitro and in vivo wound repair potentials of polysaccharides and peptides obtained from bacteria (Actinobacteria, Bacteroidetes, Cyanobacteria, Firmicutes, and Proteobacteria) and fungi (yeasts, filamentous microfungi, and mushrooms)., (© 2024 The Author(s). Journal of Basic Microbiology published by Wiley‐VCH GmbH.)

Extracellular aggregation of amyloid-beta (Aβ) in the brain plays a central role in the onset and progression of Alzheimer's disease (AD). Moreover, intraneuronal accumulation of Aβ via oligomer internalization might play an important role in the progression of AD. Deficient autophagy, which is a lysosomal degradation process, occurs during the early stages of AD. Tripeptidyl peptidase-1 (TPP1) functions as a lysosomal enzyme, and TPP1 gene mutations are associated with type 2 late infantile neuronal ceroid lipofuscinosis (LINCL). Nevertheless, there is little information about the role of TPP1 in the pathogenesis of AD; therefore, the present study aimed to measure the decrease in intraneuronal Aβ accumulation by a recombinant analog of the TPP1 enzyme, cerliponase alfa (CER) (Brineura®), and to determine whether autophagy pathways play a role in this decrease. In this study, endogenous Aβ accumulation was induced by fAβ 1-42 (a toxic fragment of full-length Aβ) exposure, and mouse hippocampal neuronal cells (HT-22) were treated with CER (human recombinant rhTPP1 1 mg mL -1 ). Soluble Aβ, TPP1, and the proteins involved in autophagy, including mammalian target of rapamycin (p-mTOR/mTOR), p62/sequestosome-1 (p62/SQSTM1), and microtubule-associated protein 1 A/1B-light chain 3 (LC3), were evaluated using western blotting. The sirtuin-1, beclin-1, and Atg5 genes were also studied using RT-PCR. Aβ and TPP1 localizations were observed via immunocytochemistry. CER reduced the Aβ load in HT-22 cells by inducing TPP1 expression and converting pro-TPP1 into the mature form. Furthermore, exposure to CER and fAβ 1-42 induced the autophagy-regulatory/related pathways in HT-22 cells and exposure to CER alone increased sirtuin-1 activity. Based on the present findings, we suggest that augmentation of TPP1 with enzyme replacement therapy may be a potential therapeutic option for the treatment of AD., Competing Interests: Declaration of competing interest The authors declare no conflict of interest. The funders had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript; or in the decision to publish the results., (Copyright © 2024 Elsevier Inc. All rights reserved.)

Background: Intima proliferation and in-stent restenosis is a challenging situation in interventional treatment of small vessel obstruction. Al/Al 2 O 3 nanowires have been shown to accelerate vascular endothelial cell proliferation and migration in vitro, while suppressing vascular smooth muscle cell growth. Moreover, surface modification of Al/Al 2 O 3 nanowires with poly[bis(2,2,2-trifluoromethoxy)phosphazene (PTFEP) coating enables further advantages such as reduced platelet adhesion. Therefore, the study's goal was to compare the biocompatibility of novel Al/Al 2 O 3  + PTFEP coated nanowire bare-metal stents to uncoated control stents in vivo using optical coherence tomography (OCT), quantitative angiography and histomorphometric assessment., Methods: 15 Al/Al 2 O 3  + PTFEP coated and 19 control stents were implanted in the cervical arteries of 9 Aachen minipigs. After 90 days, in-stent stenosis, thrombogenicity, and inflammatory response were assessed. Scanning electron microscopy was used to analyse the stent surface., Results: OCT analysis revealed that neointimal proliferation in Al/Al 2 O 3  + PTFEP coated stents was significantly reduced compared to control stents. The neointimal area was 1.16 ± 0.77 mm 2 in Al/Al 2 O 3  + PTFEP coated stents vs. 1.98 ± 1.04 mm 2 in control stents (p = 0.004), and the neointimal thickness was 0.28 ± 0.20 vs. 0.47 ± 0.10 (p = 0.003). Quantitative angiography showed a tendency to less neointimal growth in coated stents. Histomorphometry showed no significant difference between the two groups and revealed an apparent inflammatory reaction surrounding the stent struts., Conclusions: At long-term follow-up, Al/Al 2 O 3  + PTFEP coated stents placed in peripheral arteries demonstrated good tolerance with no treatment-associated vascular obstruction and reduced in-stent restenosis in OCT. These preliminary in vivo findings indicate that Al/Al 2 O 3  + PTFEP coated nanowire stents may have translational potential to be used for the prevention of in-stent restenosis., Competing Interests: Declaration of competing interest The following co-authors hold a patent which is related to the contents of the manuscript: Ayman Haidar, Michael Veith, Cenk Aktas, Hashim Abdul-Khaliq, Ali Awadelkareem. Patent title: Beschichtung oder mit einer Beschichtung versehener Körper sowie Verfahren zu deren Herstellung. DAKZ 10 2017 113 7580. 2018; Deutsches Patent- und Markenamt. https://register.dpma.de/DPMAregister/pat/register?AKZ=1020171137580. In addition to this we declare that we have no conflicts of interest to disclose regarding this publication. If any conflicts of interest arise during the course of the publication, we will promptly disclose them to the editor of the publication or to the appropriate parties., (Copyright © 2024 The Authors. Published by Elsevier Inc. All rights reserved.)

Designing an efficient, durable, and inexpensive bifunctional electrocatalyst toward oxygen evolution reactions (OER) and oxygen reduction reactions (ORR) remains a significant challenge for the development of rechargeable zinc-air batteries (ZABs). The generation of oxygen vacancies plays a vital role in modifying the surface properties of transition-metal-oxides (TMOs) and thus optimizing their electrocatalytic performances. Herein, a H 2 /Ar plasma is employed to generate abundant oxygen vacancies at the surfaces of NiCo 2 O 4 nanowires. Compared with the Ar plasma, the H 2 /Ar plasma generated more oxygen vacancies at the catalyst surface owing to the synergic effect of the Ar-related ions and H-radicals in the plasma. As a result, the NiCo 2 O 4 catalyst treated for 7.5 min in H 2 /Ar plasma exhibited the best bifunctional electrocatalytic activities and its gap potential between E j = 10 for OER and E 1/2 for ORR is even smaller than that of the noble-metal-based catalyst. In situ electrochemical experiments are also conducted to reveal the proposed mechanisms for the enhanced electrocatalytic performance. The rechargeable ZABs, when equipped with cathodes utilizing the aforementioned catalyst, achieved an outstanding charge-discharge gap, as well as superior cycling stability, outperforming batteries employing noble-metal catalyst counterparts., (© 2024 The Authors. Small published by Wiley‐VCH GmbH.)

This work studies the technological preparation conditions, morphology, structural characteristics and elemental composition, and optical and photoluminescent properties of GaSe single crystals and Eu-doped β -Ga 2 O 3 nanoformations on ε -GaSe:Eu single crystal substrate, obtained by heat treatment at 750-900 °C, with a duration from 30 min to 12 h, in water vapor-enriched atmosphere, of GaSe plates doped with 0.02-3.00 at. % Eu. The defects on the (0001) surface of GaSe:Eu plates serve as nucleation centers of β -Ga 2 O 3 :Eu crystallites. For 0.02 at. % Eu doping, the fundamental absorption edge of GaSe:Eu crystals at room temperature is formed by n = 1 direct excitons, while at 3.00 at. % doping, Eu completely shields the electron-hole bonds. The band gap of nanostructured β -Ga 2 O 3 :Eu layer, determined from diffuse reflectance spectra, depends on the dopant concentration and ranges from 4.64 eV to 4.87 eV, for 3.00 and 0.05 at. % doping, respectively. At 0.02 at. % doping level, the PL spectrum of ε -GaSe:Eu single crystals consists of the n = 1 exciton band, together with the impurity band with a maximum intensity at 800 nm. Fabry-Perrot cavities with a width of 9.3 μm are formed in these single crystals, which determine the interference structure of the impurity PL band. At 1.00-3.00 at. % Eu concentrations, the PL spectra of GaSe:Eu single crystals and β -Ga 2 O 3 :Eu nanowire/nanolamellae layers are determined by electronic transitions of Eu 2+ and Eu 3+ ions.

Introduction: Lipoxygenases (LOXs) have essential roles in stroke, atherosclerosis, diabetes, and hypertension. 12/15-LOX inhibition was shown to reduce infarct size and brain edema in the acute phase of experimental stroke. However, the significance of 12/15-LOX on neuroinflammation, which has an essential role in the pathophysiology of stroke, has not been clarified yet., Methods: In this study, ischemia/recanalization (I/R) was performed by occluding the proximal middle cerebral artery (pMCAo) in mice. Either the 12/15-LOX inhibitor (ML351, 50 mg/kg) or its solvent (DMSO) was injected i.p. at recanalization after 1 h of occlusion. Mice were sacrificed at 6, 24, and 72-h after ischemia induction. Infarct volumes were calculated on Nissl-stained sections. Neurological deficit scoring was used for functional analysis. Lipid peroxidation was determined by the MDA assay, and the inflammatory cytokines IL-6, TNF-alpha, IL-1beta, IL-10, and TGF-beta were quantified by ELISA. The inflammasome proteins NLRP1 and NLRP3, 12/15-LOX, and caspase-1 were detected with immunofluorescence staining., Results: Infarct volumes, neurological deficit scores, and lipid peroxidation were significantly attenuated in ML351-treated groups at 6, 24, and 72-h. ELISA results revealed that the pro-inflammatory cytokines IL-1beta, IL-6, and TNF-alpha were significantly decreased at 6-h and/or 24-h of I/R, while the anti-inflammatory cytokines IL-10 and TNF-alpha were increased at 24-h or 72-h of ML351 treatment. NLRP1 and NLRP3 immunosignaling were enhanced at three time points after I/R, which were significantly diminished by the ML351 application. Interestingly, NLRP3 immunoreactivity was more pronounced than NLRP1. Hence, we proceeded to study the co-localization of NLRP3 immunoreactivity with 12/15-LOX and caspase-1, which indicated that NLRP3 was co-localized with 12/15-LOX and caspase-1 signaling. Additionally, NLRP3 was found in neurons at all time points but in non-neuronal cells 72 h after I/R., Discussion: These results suggest that 12/15-LOX inhibition suppresses ischemia-induced inflammation in the acute and subacute phases of stroke via suppressing inflammasome activation. Understanding the mechanisms underlying lipid peroxidation and its associated pathways, like inflammasome activation, may have broader implications for the treatment of stroke and other neurological diseases characterized by neuroinflammation., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest. The reviewer EE declared a shared affiliation with the author KL to the handling editor at the time of review. The handling editor EK declared a past co-authorship with the author MY., (Copyright © 2023 Cakir-Aktas, Bodur, Yemisci, van Leyen and Karatas.)

Glioblastoma is one of the most devastating neoplasms of the central nervous system. This study focused on the development of serum extracellular vesicle (EV)-based glioblastoma tumor marker panels that can be used in a clinic to diagnose glioblastomas and to monitor tumor burden, progression, and regression in response to treatment. RNA sequencing studies were performed using RNA isolated from serum EVs from both patients ( n = 85) and control donors ( n = 31). RNA sequencing results for preoperative glioblastoma EVs compared to control EVs revealed 569 differentially expressed genes (DEGs, 2XFC, FDR < 0.05). By using these DEGs, we developed serum-EV-based biomarker panels for the following glioblastomas: wild-type IDH1 (96% sensitivity/80% specificity), MGMT promoter methylation (91% sensitivity/73% specificity), p53 gene mutation (100% sensitivity/89% specificity), and TERT promoter mutation (89% sensitivity/100% specificity). This is the first study showing that serum-EV-based biomarker panels can be used to diagnose glioblastomas with a high sensitivity and specificity.

Low-density polyethylene (LDPE) films are widely used in packaging, insulation and many other commodity applications due to their excellent mechanical and chemical properties. However, the water-wetting and water-repellant properties of these films are insufficient for certain applications. In this study, bare LDPE and textured LDPE (T-LDPE) films were subjected to low-pressure plasmas, such as carbon tetrafluoride (CF 4 ) and hydrogen (H 2 ), to see the effect of plasma treatment on the wetting properties of LDPE films. In addition, the surface of the LDPE film was textured to improve the hydrophobicity through the lotus effect. The LDPE and T-LDPE films had contact angle (θ) values of 98.6° ± 0.6 and 143.6° ± 1.0, respectively. After CF 4 plasma treatments, the θ values of the surfaces increased for both surfaces, albeit within the standard deviation for the T-LDPE film. On the other hand, the contact angle values after H 2 plasma treatment decreased for both surfaces. The surface energy measurements supported the changes in the contact angle values: exposure to H 2 plasma decreased the contact angle, while exposure to CF 4 plasma increased the contact angle. Kinetic friction force measurements of water drops on LDPE and T-LDPE films showed a decrease in friction after the CF4 plasma treatment, consistent with the contact angle and surface energy measurements. Notably, the kinetic friction force measurements proved to be more sensitive compared to the contact angle measurements in differentiating the wetting properties of the T-LDPE versus 3× CF 4 -plasma-treated LDPE films. Based on Atomic Force Microscopy (AFM) images of the flat LDPE samples, the 3× CF4 plasma treatment did not significantly change the surface morphology or roughness. However, in the case of the T-LDPE samples, Scanning Electron Microscopy (SEM) images showed noticeable morphological changes, which were more significant at sharp edges of the surface structures.

Just as the shapes of snowflakes provide us with information on the temperature and humidity of the upper atmosphere, the characteristics of presolar grains in meteorites place limits on their formation environment in a stellar outflow. However, even in the case of well-characterized presolar grains consisting of a titanium carbide core and a graphitic carbon mantle, it is not possible to delimit their formation environment. Here, we have demonstrated the formation of core-mantle grains in gravitational and microgravity environments and have found that core-mantle grains are formed by a nonclassical nucleation pathway involving the three steps: (i) primary nucleation of carbon at a substantially high supersaturation, (ii) heterogeneous condensation of titanium carbide on the carbon, and (iii) fusion of nuclei. We argue that the characteristics of not only core-mantle grains but also other presolar and solar grains might be accurately explained by considering a nonclassical nucleation pathway.

This study aimed to determine the ability of bacteria to produce the chitinase enzyme, purify, and characterize the enzyme from the isolate with the best activity, and determine the use of this purified enzyme as a biocontrol agent. The chitinolytic bacterium was identified as Stenotrophomonas maltophilia . The chitinase enzyme was purified 1.4 times at a 30% ammonium sulfate concentration with a yield of 40.7%. Following partial purification, the enzyme was purified by ion-exchange chromatography using HiPrep Q XL 16/10 column and HiPrep™ 26/10 desalting column with 25.34% and 18.12% yields, respectively. It was calculated that the purified enzyme had a molecular weight of 52 kDa by sodium dodecyl sulfate-polyacrylamide gel electrophoresis. The optimum activity of the enzyme was determined at 50 °C and pH 7.0. Enzyme activity was most induced by Fe 2+ , while it was most inhibited by Zn 2+ at 5 mM concentration. K m and V max values of the enzyme for colloidal chitin were calculated as 1.6419 mg/mL and 16.129 U/mg, respectively. The purified chitinase was used as a biocontrol agent against the fungus Fusarium oxysporum and potato beetle Leptinotarsa decemlineata . The enzyme was shown to be effective in reducing the growth of fungus and causing disruption of the chitin structure of potato beetle.

Background: Understanding the secondary damage mechanisms of traumatic brain injury (TBI) is essential for developing new therapeutic approaches. Neuroinflammation has a pivotal role in secondary brain injury after TBI. Activation of NLRP3 inflammasome complexes results in the secretion of proinflammatory mediators and, in addition, later in the response, microglial activation and migration of the peripheral immune cells into the injured brain are observed. Therefore, these components involved in the inflammatory process are becoming a new treatment target in TBI. Dexmedetomidine (Dex) is an effective drug, widely used over the past few years in neurocritical care units and during surgical operations for sedation and analgesia, and has anti-inflammatory effects, which are shown in in vivo studies. The aim of this original research is to discuss the anti-inflammatory effects of different Dex doses over time in TBI., Methods: Brain injury was performed by using a weight-drop model. Half an hour after the trauma, intraperitoneal saline was injected into the control groups and 40 and 200 μg/kg of Dex were given to the drug groups. Neurological evaluations were performed with the modified Neurological Severity Score before being killed. Then, the mice were killed on the first or the third day after TBI and histopathologic (hematoxylin-eosin) and immunofluorescent (Iba1, NLRP3, interleukin-1β, and CD3) findings of the brain tissues were examined. Nonparametric data were analyzed by using the Kruskal-Wallis test for multiple comparisons, and the Mann-Whitney U-test was done for comparing two groups. The results are presented as mean ± standard error of mean., Results: The results showed that low doses of Dex suppress NLRP3 and interleukin-1β in both terms. Additionally, high doses of Dex cause a remarkable decrease in the migration and motility of microglial cells and T cells in the late phase following TBI. Interestingly, the immune cells were influenced by only high-dose Dex in the late phase of TBI and it also improves neurologic outcome in the same period., Conclusions: In the mice head trauma model, different doses of Dex attenuate neuroinflammation by suppressing distinct components of the neuroinflammatory process in a different timecourse that contributes to neurologic recovery. These results suggest that Dex may be an appropriate choice for sedation and analgesia in patients with TBI., (© 2021. Springer Science+Business Media, LLC, part of Springer Nature and Neurocritical Care Society.)

Aim: A requirement for nanoparticle (NP) research is visualization of particles within cells and tissues. Limitations of electron microscopy and low yields of NP fluorescent tagging warrant the identification of alternative imaging techniques. Method: Confocal reflectance microscopy (CRM) in combination with fluorescence imaging was assessed for visualizing rhodamine B-conjugated silver and fluorescein isothiocyanate-conjugated lipid core-stearylamine NP uptake in vitro and in vivo . Results: CRM successfully identified cellular uptake and blood-brain barrier penetration of NPs owing to their distinguishing refractive indices. NP-dependent reflectance signals in vitro were dose and incubation time dependent. Finally, CRM facilitated the distinction between nonspecific fluorescence signals and NPs. Conclusion: These findings demonstrate the value of CRM for NP visualization in tissues, which can be performed with a standard confocal microscope.

Objective: Movies are among the most widely used media for advertising, promotional, and sponsorship activities of the tobacco industry, and the industry has been making huge investments in this sector for many years. In this study, the effects of movie scenes depicting the use of tobacco products, and the possible effects of the laws governing such scenes, were examined., Material and Methods: The sample of the study consisted of 50 films, the first 2 of which were the most watched each year, between the years 1992 and 2016, according to the data of the Center for Turkish Cinema Studies and the boxofficeturkiye.com websites. The scenes depicting the use of tobacco products were analyzed using the data collection form developed by the researchers. Each movie was evaluated separately by 2 researchers., Results: A tobacco product was used in 82% of the 50 films watched. Men (87%), individuals between the ages of 25 and 64 (78.0%), and leading actors (40%) used more tobacco products, and the most frequently used product was the cigarette (93.1%). The number andduration of scenes containing tobacco was greater by 1.6 times before the first law was passed, and between the passage of the first law and the passage of the second law (P > .05, P > .05). The number and duration of the scenes decreased between the passage of the first and the second laws and after the second law was passed, by 3.6 and 5.3 times, respectively (P < .05, P < .05)., Conclusion: Consistent and comprehensive tobacco control policies have been effective in reducing the number of scenes that contain tobacco in the movies produced in Turkey. A comprehensive and multidisciplinary approach is required to overcome the tobacco industry's impact on cinema.

Aim: In this study, suppression of Aquaporin-4 (AQP4) synthesis via intracerebroventricular (i.c.v.) injection of antisense oligonucleotide after focal cortical contusion injury in mice was investigated., Material and Methods: 12-week female Swiss albino mice of 20-25 g were used to create a focal cortical contusion model by the weight drop method (35 grams blunt weight, 70 cm height) onto the parietal cortex after craniectomy. The sham group underwent craniectomy without trauma. In the control group, weight was dropped onto the parietal cortex immediately after Dulbecco\'s Modified Eagle Medium (DMEM) i.c.v. injection following craniectomy. In addition, 1 nM of aquaporin-4 (AQP4) antisense oligonucleotide (ASO) was injected via i.c.v route immediately after trauma (0 hours) and 4 hours after trauma. All animals underwent magnetic resonance (MR) imaging and were sacrificed at 24 h. Brain water content was determined using the wet/dry weight method., Results: In the sham group, the average percentage of brain water content was 77.75% compared to the control group with 79.87%. The difference was statistically significant (*p=0.017). In the therapy group, the average was 78.81% and significantly reduced compared to the control group (*p=0.026) at 0 hours. In the 4-hour treatment group, the average of 79.11% was not statistically significant (p=0.39). MR imaging findings also showed a substantial reduction in brain edema in the 0-hour treatment group. However, the 4-hour treatment results, when compared with the control trauma group, did not show a significant difference., Conclusion: This study demonstrated that AQP4 antisense oligonucleotide therapy, when administered early after diffuse traumatic brain injury, leads to a significant reduction in brain edema.

Traumatic brain injury (TBI) is one of the significant causes of death among young people worldwide. Doxycycline (DOX), an antibiotic with anti-inflammatory effects, has not been used as a therapeutic agent to modify the inflammatory response after the traumatic brain injury. In this study, intraperitoneal administration of DOX reduced significantly the acute inflammatory markers like IL-6 and CD3, microglial migration to the damaged area marked with Iba-1, and neuronal apoptosis assessed with TUNEL assay at 72 h after the trauma. The low dose, 10 mg/kg of DOX had a dominant anti-inflammatory effect; while the high dose, 100 mg/kg of DOX, was more effective in decreasing neuronal apoptosis. In early hours after the head trauma, use of a low dose (10 mg/kg) of DOX for decreasing the acute form of inflammation followed by a high dose (100 mg/kg) for the anti-apoptotic effects particularly in severe head traumas, would be a promising approach to alleviate the brain injury., (Copyright © 2021 Elsevier B.V. All rights reserved.)

Objectives: There is a delicate homeostatic balance between the central nervous system and immune system. Stroke triggers an immunodepressive state to suppress a potential immune reaction directed against neuroglial tissue; however, this supposedly protective response inadvertently results in an infection-prone, and thereby a pro-inflammatory setting. In this study, we assessed the magnitude of cerebral volume loss in the unaffected contralateral hemisphere following stroke, and determined its relationship with inflammatory cascades., Methods: The volume of the hemisphere contralateral to the ischemic insult was measured on admission and follow-up MRI's in 50 ischemic stroke patients. Information related to clinical features, infectious complications, and markers of inflammation (erythrocyte sedimentation rate, neutrophil/lymphocyte ratio, C-reactive protein) were prospectively collected, and their relationship with hemispheric volume change was evaluated using bivariate and multivariate statistics., Results: The contralateral hemisphere volume decreased by a median (interquartile range) of 14 (4-32) mL after a follow-up duration of 101 (63-123) days (p < .001); the volume reduction was 0.8 (0.2-1.8) % per month with respect to baseline. Old age, atrial fibrillation, stroke severity, C-reactive protein level, neutrophil/lymphocyte ratio, and development of infections during hospitalization were significantly associated with volume loss (p < .05). Stroke severity (NIHSS score or infarct volume) and inflammation related parameters (neutrophil/lymphocyte ratio or systemic infections) remained independently and positively associated with volume loss in multivariate regression models., Conclusions: Cerebral tissue changes following stroke are not limited to the ischemic hemisphere. Apart from stroke severity, a pro-inflammatory state and post-stroke infections contribute to cerebral volume loss in the non-ischemic hemisphere., (Copyright © 2020 Elsevier B.V. All rights reserved.)

Lipoxygenases are a family of lipid-oxidizing enzymes, which generate eicosanoids and related compounds from arachidonic acid and other polyunsaturated fatty acids. These metabolites play important roles in physiology and pathogenesis of host defense mechanisms, cardiovascular diseases, cancer, inflammatory, allergic and neurodegenerative diseases. The 12/15-lipoxygenase (LOX) is special in that it can directly oxidize lipid membranes containing polyunsaturated fatty acids, without the preceding action of a phospholipase, leading to the direct attack on membranous organelles, such as mitochondria. The cytotoxic activity of human 12/15-LOX is up-regulated in neurons and endothelial cells especially after a stroke and thought to contribute to both neuronal cell death and blood-brain barrier leakage. The discovery of inhibitors that selectively target recombinant 12/15-LOX in vitro , as well as possessing activity against the murine orthologous ex vivo , could potentially support a novel therapeutic strategy for the treatment of stroke and other brain disorders related to 12/15-LOX. Here we reviewed 12/15-LOX chemistry shortly, and the diseases in which 12/15-LOX has a role in their pathophysiology and recent advances of 12/15-LOX inhibitors as a treatment option for neurological diseases., Competing Interests: Conflict of interest: The authors declare no competing interests., (Copyright: © 2019 Turkish Neuropsychiatric Society.)

Urethral stricture is a common disease with high recurrence rate. Several manipulations were defined to prevent the recurrence but the results were disappointing. This study aimed to evaluate the efficacy of triamcinolone and mitomycin-C on urethral stricture formation and their effect on inhibition of urethral fibrosis. A total of 24 New Zealand rabbits were divided into 3 groups. Urethras of rabbits were traumatized with pediatric resectoscope. Resection area was irrigated with 10mL saline, swapped with a cotton wool soaked with 0.5mg/mL MMC and injected by 40mg triamcinolone in groups 1, 2 and 3 respectively. Retrograde urethrogram was performed at 28th day of procedure and the urethra was removed for histopathologic evaluation. There were significant differences in urethral diameters and in lumen reduction rate between the control and study groups (p<0.001). Compared to control group, all treatment groups showed mild fibrosis, less collagen bundle irregularity, and lower numbers of fibroblasts (p=0.003). The Tunnel assay showed that the number of apoptotic cells in the submucosal connective tissue was quantitatively higher in control groups (p=0.034). In the view of efficacy and safety, MMC and triamcinolone have the potential to replace the use of stents, clean intermittent catheterization, or long term catheters following internal urethrotomy. There were no statistically significant differences between two agents in terms of preventing urethral stricture formation in the present study. Mitomycin C and triamcinolone decreased the recurrence rates of urethral stricture., Competing Interests: Conflict of interest: None declared., (Copyright® by the International Brazilian Journal of Urology.)

Porous polyethylene (Medpor®) is commonly used in craniofacial reconstructive surgery. Rapid vascularization and tissue incorporation are crucial for the prevention of migration, extrusion, and infection of the biomaterial. Therefore, we analyzed whether surface modification by plasma etching may improve the early tissue response to Medpor®. Medpor® samples were treated in a plasma chamber at low (20 W; LE-PE) and high energy levels (40 W; HE-PE). The samples and non-treated controls were implanted into mouse dorsal skinfold chambers to analyze angiogenesis, inflammation, and granulation tissue formation over 14 days using intravital fluorescence microscopy, histology, and immunohistochemistry. Scanning electron microscopy (SEM) analyses revealed that elevating energy levels of plasma etching progressively increase the oxygen surface content and surface roughness of Medpor®. This did not affect the leukocytic response to the implants. However, LE-PE and HE-PE samples exhibited an impaired vascularization. This was associated with a reduced formation of a collagen-rich granulation tissue at the implantation site. Additional in vitro experiments showed a reduced cell attachment on plasma-etched Medpor®. Thus, plasma etching may not be recommended to improve the clinical outcome of reconstructive interventions using Medpor®. However, it may be beneficial for temporarily implanted polyethylene-based biomedical devices for which tissue incorporation is undesirable. © 2015 Wiley Periodicals, Inc. J Biomed Mater Res Part B: Appl Biomater, 104B: 1738-1748, 2016., (© 2015 Wiley Periodicals, Inc.)

Objective: Testicular torsion is an emergency condition that causes testicular injury. Any treatment opportunity reducing the destructive effect of testicular torsion is important for the future life of patients. In this experimental study we investigated the protective effect of mannitol on ischemia-reperfusion (I/R) injury in a rat testes torsion model., Method: In total, 32 male Sprague Dawley rats were included. Four experimental groups included eight rats each. Group A was a sham group in which the right testis was brought out through a scrotal incision and then replaced in the scrotum without torsion. In Group B, the right testis was torsioned, by rotating 720° clockwise and fixed to the scrotum with no treatment. In Group C, the same testicular torsion process was performed with saline infusion just after testicular torsion. In group D, mannitol infusion was used just after testicular torsion. Testicles were detorsioned after 3 h and left inside for more than 2 h before orchiectomy. Histopathological, immunohistochemical, and biochemical analyses were performed., Results: Testicular architecture was disturbed significantly in the torsion groups without mannitol infusion. However, testicular tissue structure was significantly better in the mannitol-treated group, demonstrating a protective effect. Similar findings were also shown for the proliferating cell nuclear antigen (PCNA) index and antioxidant activity; both were higher in the mannitol group than in the no-treatment and saline groups (p < 0.01). The apoptotic index was also significantly lower in the mannitol-treated group compared with the no treatment and saline groups (p < 0.01)., Conclusions: The seminiferous tubule structure in testicular torsion without mannitol treatment was significantly disturbed, whereas the structural disruption was considerably less in the mannitol group. Mannitol treatment also decreased reactive oxygen radical levels significantly and was able to decrease apoptosis. These results were consistent with other organ model studies that evaluated the protective effects of mannitol treatment in I/R injury. Mannitol infusion had a protective effect against I/R injury in testicular torsion in rats. This experimental study may guide clinicians to evaluate the effectiveness of mannitol in human testicular torsion., (Copyright © 2016 Journal of Pediatric Urology Company. Published by Elsevier Ltd. All rights reserved.)

Cadmium (Cd) is a serious environmental and occupational contaminant and may represent a serious health hazard to humans and other animals. Cd is reported to induce the generation of reactive oxygen species, and induces testicular damage in many species of animals. The goal of our study was to examine the anti-apoptotic and anti-oxidant effects of caffeic acid phenethyl ester (CAPE) on Cd-induced oxidative stress, apoptosis, and testicular injury in rats. A total of 40 male Wistar albino rats were divided into four groups: control, CAPE alone, Cd-treated, and Cd-treated with CAPE; each group consisted of 10 animals. To induce toxicity, Cd (1 mg/kg body weight) was dissolved in normal saline and subcutaneously injected into rats for 30 days. The rats in CAPE-treated group were given a daily dose of 10 μmol/kg body weight of CAPE by using intraperitoneal injection. This application was continued daily for a total of 30 days. To date, no examinations of the anti-apoptotic and anti-oxidant properties of CAPE on Cd-induced apoptosis, oxidative damage, and testicular injury in rat testes have been reported. CAPE-treated animals showed an improved histological appearance and serum testosterone levels in Cd-treated group. Our data indicate a significant reduction in the number of apoptotic cells in testis tissues of the Cd-treated group with CAPE treatment. Moreover, CAPE significantly suppressed lipid peroxidation, compensated deficits in the anti-oxidant defenses in testes tissue resulted from Cd administration. These findings suggest that the protective potential of CAPE in Cd toxicity might be due to its anti-oxidant and anti-apoptotic properties, which could be useful for achieving optimum effects in Cd-induced testicular injury.

This study aimed to investigate the protective effects of melatonin against arsenic-induced apoptosis and oxidative stress in rat testes. A total of 27 male rats were divided into 3 groups: control (saline: 5 ml kg(-1) day(-1), intragastrically), arsenic (sodium arsenite (NaAsO2): 5 mg kg(-1) day(-1), intragastrically), and arsenic + melatonin (sodium arsenite (NaAsO2): 5 mg kg(-1) day(-1), intragastrically and melatonin: 25 mg kg(-1) day(-1), intraperitoneally) group. At the end of 30 days, the rats were killed under anesthesia. Histopathological examination showed that testicular injury mediated by arsenic was ameliorated by the administration of melatonin. The number of apoptotic germ cell was increased, and the number of proliferating cell nuclear antigen (PCNA)-positive germ cell was decreased in testis after arsenic administration. Our data indicate a significant reduction in the activity of terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labeling, and there was a rise in the expression of PCNA in testis of arsenic + melatonin group. The decreased superoxide dismutase, catalase, and glutathione peroxidase activities as well as increased malondialdehyde levels in testis due to arsenic administration were also counteracted by melatonin. These data suggested that melatonin has beneficial effects against arsenic-induced testicular damage by decreasing morphological damage, germ cell apoptosis, lipid peroxidation, and oxidative stress. Our results suggest that melatonin plays a protective role against arsenic-induced testicular apoptosis and oxidative stress., (© The Author(s) 2013.)

Objective: To evaluate the preventive effect of phosphodiesterase type 5 inhibitor (tadalafil) on the formation of urethral stricture after urethral injury., Materials and Methods: A total of 28, 4-month-old male New Zealand rabbits were included and divided into 3 groups. Group 1 was a sham group with 8 rabbits that underwent only urethroscopy. Group 2 was a nontreatment group with 10 rabbits that underwent urethral electrocoagulation without any treatment. Group 3 was the treatment group with 10 rabbits that underwent urethral electrocoagulation with systemic tadalafil treatment. After 30 days of follow-up, urethroscopy and retrograde urethrography were performed to evaluate the morphological changes in the urethra. The urethra tissues were examined with standard light microscopy by a histologist, and apoptosis was evaluated by the terminal dUTP nick end-labeling assay., Results: Urethral diameters in group 1, group 2, and group 3 were 9.14 ± 0.73 mm, 3.52 ± 1.2 mm, and 7.68 ± 1.14 mm, respectively. The differences in urethral diameters were statistically significant between groups (P < .01). Collagen deposition in submucosal connective tissue was significantly less in the tadalafil group vs the nontreatment group. The numbers of apoptotic cells in submucosal connective tissue were also quantitatively higher in urethral stricture groups compared to the sham group., Conclusion: Tadalafil treatment had a protective effect against the formation of urethral stricture in rabbit model. This treatment can be a promising opportunity for urethral stricture and must be supported by clinical studies., (Copyright © 2016 Elsevier Inc. All rights reserved.)

Objective: To determine the role of cyclooxygenase (COX) expression in the urothelium of the urinary bladder during radiation injury caused by pelvic radiotherapy for cancer therapy., Study Design: Twenty-four male Swiss Albino mice were separated into 4 groups. The first group was the control group (Group 1) and the second, third, and fourth groups were euthanized after 24 hours (Group 2), 48 hours (Group 3), and 7 days (Group 4), respectively. A single-fractioned 10 Gy of ionizing radiation was applied to all mice's pelvic zone with Co-60. Bladders were removed completely from the pelvic region. Histochemical analysis using hematoxylin and eosin and immunohistochemical analysis using anti-COX-1 and COX-2 antibodies were performed on tissue samples. The immunoreactivities of the urinary bladder were quantified using H-score measurement, and statistical comparison was performed., Results: In the immunohistochemical examination the COX-1 immunoreactivities were found to be higher in the urothelium of the bladder in the radiation exposed groups than in the normal control group (group 1) (p < 0.005). Additionally, high immunoreactivity of COX-2 molecule was established in groups 2, 3, and 4 of radiation groups as compared to group 1 (p < 0.005) in examination of the urothelium. COX-1 and COX-2 immunoreactivities in the submucosa were detected higher in group 4 than in the other groups (p < 0.005)., Conclusion: COX-1 and COX-2 expressions in the urothelium and subepithelium of the urinary bladder were investigated in mice during the acute radiation response. The expression of COX-1 and COX-2 in the urothelium seems to prevent bladder damage from radiation, supplying differentiation and restoration of the urothelium.

Objective: To investigate the reaction of versican and heparin-binding EGF-like growth factor (HB-EGF) molecule concentrations to acute radiation exposure in normal bladder and rectal tissue samples in order to gain more insight into the effects of cancer radiotherapy., Study Design: Four groups with 6 male adult Swiss Albino mice per group were investigated. The mice bladder and rectum tissue samples were subjected to a 10-Gy single-dose radiation exposure in the pelvic region with a Co-60 teletherapy device and investigated 1, 2, and 7 days after radiation exposure, with 1 reference group which was not exposed to radiation., Results: In the immunohistochemical examination of the tissue samples with anti-versican and anti-HB-EGF primary antibodies was observed a statistically significant increase 7 days after radiation exposure., Conclusion: The observed increase of versican and HB-EGF concentrations in the normal tissue matrix after radiation exposure may play a role in the side effects of radiotherapy.

The goal of this study was to examine the neuroprotective effect of ebselen against intracerebroventricular streptozotocin (ICV-STZ)-induced oxidative stress and neuronal apoptosis in rat brain. A total of 30 adult male Sprague-Dawley rats were randomly divided into 3 groups of 10 animals each: control, ICV-STZ, and ICV-STZ treated with ebselen. The ICV-STZ group rats were injected bilaterally with ICV-STZ (3 mg/kg) on days 1 and 3, and ebselen (10 mg/kg/day) was administered for 14 days starting from 1st day of ICV-STZ injection to day 14. Rats were killed at the end of the study and brain tissues were removed for biochemical and histopathological investigation. Our results demonstrated, for the first time, the neuroprotective effect of ebselen on Alzheimer's disease (AD) model in rats. Our present study, in ICV-STZ group, showed significant increase in tissue malondialdehyde levels and significant decrease in enzymatic antioxidants superoxide dismutase and glutathione peroxidase in the frontal cortex tissue. The histopathological studies in the brain of rats also supported that ebselen markedly reduced the ICV-STZ-induced histopathological changes and well preserved the normal histological architecture of the frontal cortex tissue. The number of apoptotic neurons was increased in frontal cortex tissue after ICV-STZ administration. Treatment of ebselen markedly reduced the number of degenerating apoptotic neurons. The study demonstrates the effectiveness of ebselen, as a powerful antioxidant, in preventing the oxidative damage and morphological changes caused by ICV-STZ in rats. Thus, ebselen may have a therapeutic value for the treatment of AD., (© The Author(s) 2013.)

The purpose of the present investigation was to evaluate cadmium (Cd)-induced neurotoxicity in hippocampal tissues and beneficial effect of quercetin (QE) against neuronal damage. A total of 30 male rats were divided into 3 groups: control, Cd-treated, and Cd + QE-treated groups. After the treatment, the animals were killed and hippocampal tissues were removed for biochemical and histopathological investigation. Cd significantly increased tissue malondialdehyde (MDA) and protein carbonyl (PC) levels and also decreased superoxide dismutase (SOD) and catalase (CAT) enzyme activities in hippocampal tissue compared with the control. Administration of QE with Cd significantly decreased the levels of MDA and PC and significantly elevated the levels of antioxidant enzymes in hippocampal tissue. In the Cd-treated group, the neurons of both tissues became extensively dark and degenerated with pyknotic nuclei. The morphology of neurons in Cd + QE group was well protected, but not as neurons of the control group. The caspase-3 immunopositivity was increased in degenerating neurons of the Cd-treated group. Treatment of QE markedly reduced the immunoreactivity of degenerating neurons. The results of the present study show that QE therapy causes morphologic improvement in neurodegeneration of hippocampus after Cd exposure in rats., (© The Author(s) 2013.)

Cadmium (Cd), an environmental and industrial pollutant, generates free radicals responsible for oxidative stress. Cd can also lead to various renal toxic damage such as the proximal tubules and glomerulus dysfunction. Thymoquinone (TQ) is the main constituent of the essential oil obtained from black seeds (Nigella sativa) and has various pharmacological effects. The aim of the present study was to examine the nephroprotective, anti-oxidant, and anti-apoptotic effect of the TQ against Cd-induced nephrotoxicity. A total of 24 male Wistar albino rats were divided into three groups: control, Cd-treated, and Cd-treated with TQ; each group contain eight animals. The Cd-treated group was injected subcutaneously with CdCl2 dissolved in saline in the amount of 2 ml/kg/day for 30 days, resulting in a dosage of 1 mg/kg Cd. The rats in TQ-treated groups were given TQ (50 mg/kg body weight) once a day orally together with first Cd injection during the study period. The histopathological studies in the kidney of rats also showed that TQ markedly reduced the toxicity of Cd and preserved the normal histological architecture of the renal tissue. Immunohistochemical analysis revealed that TQ significantly decreased the Cd-induced over expression of nuclear factor-κB in renal tissue. Furthermore, TQ treatment resulted in decreased the number of apoptotic cells. TQ significantly suppressed lipid peroxidation, compensated deficits in the anti-oxidant defenses (reduced superoxide dismutase, glutathione peroxidase and catalase activities) in renal tissue resulted from Cd administration. These findings suggest that the nephroprotective potential of TQ in Cd toxicity might be due to its anti-oxidant and anti-apoptotic properties, which could be useful for achieving optimum effects in Cd-induced nephrotoxicity.

Objective: The aim of this study was to investigate the role of quercetin on cadmium-induced oxidative stress, testicular damage, and apoptosis in rat testes., Study Design: The rats were randomly allotted into 1 of 3 experimental groups: control, cadmium-treated, and cadmium-treated with quercetin; each group con- tained 10 animals. Control animals received daily injec- tions of the saline vehicle alone. The cadmium-treated group was injected subcutaneously with cadmium chloride (CdCl2) dissolved in saline at a dose of 2 mL/kg/ day for 30 days, resulting in a dosage of 1 mg/kg cadmium. The rats in quercetin-treated groups were given quercetin (15 mg/kg body weight) once a day i.p., starting 2 days prior to the cadmium injection during the study period. All animals were sacrificed and testes tissues were removed for histopathological and biochemical (malondialdehyde [MDA], superoxide dismutase [SOD], glutathione peroxidase [GSH-Px], and serum testosterone levels) investigation., Results: The mean seminiferous tubule diameter, Johnsen's mean testicular biopsy score values, biochemical parameters (MDA, SOD, GSH-Px, and serum testosterone levels), and amount of germ cell apoptosis were significantly decreased in the cadmium-treated groups as compared to the control group. Furthermore, the quercetin-treated animals showed improved histological and biochemical parameters in the cadmium-treated group., Conclusion: The present study showed that quercetin treatment protected testes against toxic effects of cadmium. We believe that further preclinical research into the utility of quercetin may indicate its usefulness as a potential treatment for spermatogenesis after testicular injury caused by cadmium-treated rats.

We aimed to investigate the preventive effect of Infliximab (IFX), a tumor necrosis factor (TNF)-α inhibitor, on bleomycin (BLC)-induced lung fibrosis in rats. Rats were assigned into four groups as follows: I-BLC group, a single intra-tracheal BLC (2.5 mg/kg) was installed; II-control group, a single intra-tracheal saline was installed; III-IFX + BLC group, a single-dose IFX (7 mg/kg) was administered intraperitoneally (i.p.), 72 h before the intra-tracheal BLC installation; IV-IFX group, IFX (7 mg/kg) was administered alone i.p. on the same day with IFX + BLC group. All animals were sacrificed on the 14th day of BLC installation. Levels of tumor necrosis factor (TNF)-α, transforming growth factor (TGF)-β, interleukin (IL)-6, periostin, YKL-40, nitric oxide (NO) in rat serum were measured, as well as, myeloperoxidase (MPO), superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) activity, and reduced glutathione (GSH), hydroxyproline, malondialdehyde (MDA) content in lung homogenates. Lung tissues were stained with hematoxylin and eosin (H&E) for quantitative histological evaluation. The inducible nitric oxide synthase (iNOS) expression and cell apoptosis in the lung tissues were determined quantitatively by immunohistochemical staining (INOS) and by TUNNEL staining, respectively. BLC installation worsened antioxidant status (such as SOD, CAT, GPx, GSH, MPO), while it increased the serum TNF-α, TGF-β, IL-6, periostin, YKL-40, and lipid peroxidation, and collagen deposition, measured by MDA and hydroxyproline, respectively. IFX pretreatment improved antioxidant status as well as BLC-induced lung pathological changes, while it decreased the TNF-α, TGF-β, IL-6, periostin, YKL-40, lipid peroxidation and collagen deposition. Finally, histological, immunohistochemical, and TUNNEL evidence also supported the ability of IFX to prevent BLC-induced lung fibrosis. The results of the present study indicate that IFX pretreatment can attenuate BLC-induced pulmonary fibrosis.

We aimed to investigate the protective role of thymoquinone (TQ) by targeting its antiapoptotic and antioxidant properties against kidney damage induced by arsenic in rats. We have used the 24 male Sprague-Dawley rats. Rats were divided into three groups. Physiological serum in 10 mL/kg dose as intragastric was given to the control group. Sodium arsenite (10 mg/kg, intragastric by gavage for fifteen days) was given to the arsenic group. Sodium arsenite (10 mg/kg, intragastric by gavage for fifteen days) and TQ (10 mg/kg, intragastric by gavage for 15 days) was given to the arsenic + TQ group. After 15 days, the animals' kidneys were taken theirs, then we have performed histological and apoptotic assessment. Superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GSH-Px) enzyme activities and malondialdehyde (MDA) levels have examined as the oxidative stress parameters. We have determined the levels of arsenic. Increased renal injury and apoptotic cells have been detected in the arsenic group. Degenerative changes in the arsenic + TQ group were diminished. Although the MDA levels were augmented in the arsenic group, SOD, CAT and GSH-Px enzyme activities were lessened than the other groups. Our findings suggest that TQ may impede the oxidative stress, the cells have been damaged and also the generation of apoptotic cells arisen from arsenic. TQ plays a protective role against arsenic-induced toxicity in kidney and may potentially be used as a remedial agent.

The present study was carried out to evaluate the neuroprotective effect of quercetin (QE) in protecting the cadmium (Cd)-induced neuronal injury in frontal cortex of rats. A total of 30 adult male Sprague-Dawley rats were randomly divided into three groups of 10 animals each: control, Cd treated and Cd treated with QE. The Cd-treated group was injected subcutaneously with cadmium chloride (CdCl2) dissolved in saline at a dose of 2 ml/kg/day for 30 days, resulting in a dosage of 1 mg/kg Cd. The rats in QE-treated groups were given QE (15 mg/kg body weight) once a day intraperitoneally starting 2 days prior to Cd injection, during the study period. Rats were sacrificed at the end of the study and the frontal cortex tissues were removed for biochemical and histopathological investigation. To date, there is no available information on the effect of QE on neuronal injury after Cd exposure. Rats intoxicated with Cd for 30 days, significantly increased tissue malondialdehyde (MDA) levels and significantly decreased enzymatic antioxidants superoxide dismutase, glutathione peroxidase and catalase in the frontal cortex tissue. Administration of QE with Cd significantly diminished the levels of MDA and significantly elevated the levels of enzymatic antioxidants in the frontal cortex tissue. The histopathological studies in the brain of rats also supported that QE markedly reduced the Cd-induced histopathological changes and well preserved the normal histological architecture of the frontal cortex tissue. The caspase-3 immunopositivity was increased in degenerating neurons of the Cd group. Treatment with QE markedly reduced the immunoreactivity of degenerating neurons. In conclusion, the results of the current study suggest that QE may be beneficial in combating the Cd-induced neurotoxicity in the brain of rats. We believe that further preclinical research into the utility of QE may indicate its usefulness as a potential treatment for neurodegeneration after Cd exposure in rats., (© The Author(s) 2013.)

Purpose: The aim of this study was to compare the proliferation and attachment behavior of fibroblasts and epithelial cells on differently structured abutment materials., Materials and Methods: Three different surface topographies were prepared on zirconia and titanium alloy specimens and defined as follows: machined (as delivered without further surface modification), smooth (polished), and rough (sandblasted). Energy-dispersive X-ray spectroscopy, topographical analysis, and water contact angle measurements were used to analyze the surface properties. Fibroblasts (HGF1) and epithelial cells (HNEpC) grown on the specimens were investigated 24 hours and 72 hours after seeding and counted using fluorescence imaging. To investigate adhesion, the abundance and arrangement of the focal adhesion protein vinculin were evaluated by immunocytochemistry., Results: Similar surface topographies were created on both materials. Fibroblasts exhibited significant higher proliferation rates on comparable surface topographies of zirconia compared with the titanium alloy. The proliferation of fibroblasts and epithelial cells was optimal on different substrate/topography combinations. Cell spreading was generally higher on polished and machined surfaces than on sandblasted surfaces. Rough surfaces provided favorable properties in terms of cellular adhesion of fibroblasts but not of epithelial cells., Conclusions: Our data support complex soft tissue cell-substrate interactions: the fibroblast and epithelial cell response is influenced by both the material and surface topography., (© 2014 Wiley Periodicals, Inc.)

A novel synthesis of a nanostructured cell adhesive surface is investigated for future stent developments. One-dimensional (1D) Al2O3 nanostructures were prepared by chemical vapor deposition of a single source precursor. Afterwards, recombinant filamentous bacteriophages which display a short binding motif with a cell adhesive peptide (RGD) on p3 and p8 proteins were immobilized on these 1D Al2O3 nanostructures by a simple dip-coating process to study the cellular response of human endothelial EA hy.926. While the cell density decreased on as-deposited 1D Al2O3 nanostructures, we observed enhanced cell proliferation and cell-cell interaction on recombinant phage overcoated 1D Al2O3 nanostructures. The recombinant phage overcoating also supports an isotropic cell spreading rather than elongated cell morphology as we observed on as-deposited Al2O3 1D nanostructures.

Background: In the present study, the protective and therapeutic effects of quercetin (QE) on renal injury induced by methotrexate (MTX) have been examined., Materials and Methods: A total of 24 male rats were divided into the following three groups: control group, MTX group, and MTX + QE group. Rats in MTX group received 20 mg/kg of single dose of MTX, while those in MTX + QE group received 20 mg/kg of single dose MTX, in addition to 15 mg/kg of QE administered 30 min prior to MTX and in the following 5-day period as a single daily dose. At the end of the experimental period, renal tissues were removed for histopathological and biochemical assessments., Results: Light microscopic examination showed a disruption of the renal structure in rats in MTX group in the form of tubular degeneration and dilation, with shedding of the tubular epithelial cells into the lumen. QE treatment was associated with less marked degenerative changes, with a similar histological appearance to that of controls. Furthermore, QE treatment resulted in decreased the number of apoptotic cells. Biochemical assessments showed significantly higher malondialdehyde (MDA) levels in MTX group as compared to control and MTX + QE groups. superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) levels showed a significant decrease in MTX group as compared to controls. However, QE significantly suppressed MDA level, compensated deficits in the anti-oxidant defenses [reduced SOD, GSH-Px, and CAT levels] in kidney tissue resulted from MTX administration., Conclusions: In conclusion, renal toxic effects of MTX may be alleviated by QE.

The goal of this study was to evaluate the possible protective effects of melatonin against cholestatic oxidative stress, liver damage and hepatocyte apoptosis in the common rats with bile duct ligation (BDL). A total of 24 male Wistar albino rats were divided into three groups: control, BDL and BDL + received melatonin; each group contains eight animals. Melatonin-treated BDL rats received daily melatonin 100 mg/kg/day via intraperitoneal injection. The application of BDL clearly increased the malondialdehyde (MDA) levels and decreased the superoxide dismutase (SOD) and glutathione (GSH) activities. Melatonin treatment significantly decreased the elevated tissue MDA levels and increased the reduced SOD and GSH enzyme levels in the tissues. The changes demonstrate that the bile duct proliferation and fibrosis in expanded portal tracts include the extension of proliferated bile ducts into lobules, mononuclear cells and neutrophil infiltration into the widened portal areas as observed in the BDL group. The data indicate that melatonin attenuates BDL-induced cholestatic liver injury, bile duct proliferation and fibrosis. The α-smooth muscle actin (α-SMA) and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL)-positive cells in the BDL were observed to be reduced with the melatonin treatment. These results suggest that administration of melatonin is a potentially beneficial agent to reduce liver damage in BDL by decreasing oxidative stress., (© The Author(s) 2012.)

To date, there is no available information on the protective effect of onion (Allium cepa) extract (AcE) on cadmium (Cd)-induced cardiotoxicity. The present study was performed to assess the possible antioxidant and anti-apoptotic roles of AcE in Cd-induced cardiotoxicity in rats. A Cd group was injected subcutaneously with CdCl2 dissolved in saline at a dose of 2 ml/kg/day for 30 days, resulting in a dosage of 1 mg/kg Cd. The rats in the AcE-treated group were given 1 ml of AcE via intragastric intubation for 30 days. The rats intoxicated with Cd for 30 days showed increased tissue malondialdehyde (MDA) levels and decreased levels of the enzymatic antioxidants superoxide dismutase (SOD), glutathione peroxidase (GSH-Px), and catalase (CAT) in cardiac tissue. AcE attenuated these adverse effects of Cd. After Cd exposure, histological abnormalities were observed, including myofibrillar loss, vacuolization of cytoplasm and irregularity of myofibrils. These histological alterations were effectively attenuated by the treatment with AcE. Furthermore, our data indicate a significant reduction of apoptosis in the cardiomyocytes of the Cd group treated with AcE therapy. Animal studies show antioxidant effects of AcE. But to date, no study reported the effect of AcE on biochemical and histopathological changes due to Cd induced on rat heart. Our study showed that AcE therapy reduced Cd-induced oxidative stress and apoptosis, possibly through its antioxidant and anti-apoptotic activity.