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In this study, it was aimed to examine the effects of U rtica dioica L. ( UD) that has antioxidant feature in the experimental testicular I/R model in rats in terms of anti-apoptotic and antioxidative effects. In our study, 24 male rats were divided into three groups: control group, I/R group and I/R + UD (2 mg kg−1) group. Seminiferous tubule calibre measurement, Johnson score, haematoxylin-eosin staining, proliferative cell nucleus antigen ( PCNA) immunohistochemical staining and TUNEL as histopathological have been conducted. The structural deterioration in the testicular on I/R group has reduced after the treatment of UD. Our data indicate a significant reduction in the activity of in situ identification of apoptosis using terminal dUTP nick end labelling ( TUNEL), and there was a rise in the expression of proliferating cell nuclear antigen ( PCNA) in testis tissues of UD-treated rats in the I/R group. The I/R + UD group showed a decrease in malondialdehyde levels and an increase in the activities of superoxide dismutase, catalase and glutathione peroxidase in comparison with the I/R group. It could be concluded that protective effects of UD on the I/R testicles are via reduction of histological damage, apoptosis, oxidative stress and lipid peroxidation. [ABSTRACT FROM AUTHOR]

This study investigated the effect of quercetin on changes in testes due to arsenic exposure. Twenty-seven male rats were divided into three groups: control (10 ml kg−1 day−1 saline), arsenic (10 mg kg−1 day−1 sodium arsenite) and arsenic + quercetin (arsenic + 50 mg kg−1 day−1 quercetin). The rats were sacrificed at the end of 15-day experiment. There was no difference between control group and arsenic group in body weight gain, testicular weight and serum total testosterone level. Quercetin treatment did not cause a significant difference in these parameters. In the arsenic group rats, we determined deterioration in the structure of seminiferous tubules, a decrease in the number of spermatogenic cells, an increase in the number of apoptotic cells, a decrease in the number of PCNA-positive cells, a decrease in SOD, CAT and GSH-Px activities, and an increase in the MDA level in testicular tissue. In all these changes, arsenic+quercetin group showed an improved compared to arsenic group. The amount of arsenic increased in the arsenic group was compared to the control group, and there was no difference between arsenic group and arsenic + quercetin group in the amount of arsenic. In conclusion, quercetin prevented arsenic-induced testicular damage with its anti-apoptotic and antioxidant effects. [ABSTRACT FROM AUTHOR]

Copyright of European Poultry Science / Archiv für Geflügelkunde is the property of Verlag Eugen Ulmer and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

Copyright of Journal of Microscopy is the property of Wiley-Blackwell and its content may not be copied or emailed to multiple sites or posted to a listserv without the copyright holder's express written permission. However, users may print, download, or email articles for individual use. This abstract may be abridged. No warranty is given about the accuracy of the copy. Users should refer to the original published version of the material for the full abstract. (Copyright applies to all Abstracts.)

The aim of this study was to investigate the protective effects of fish omega-3 (n-3) fatty acids on doxorubicin (DOX)-induced acute cardiotoxicity. A total of 24 rats were divided into three groups: control, DOX-treated, and DOX treated with fish n-3 fatty acids. Control group received 0.4 ml/kg/day of saline intragastrically. The rats in the fish n-3 fatty acid-pretreated group were given 400 mg/kg/day fish n-3 fatty acids for 30 days by intragastric intubation. To induce acute cardiotoxicity, DOX (30 mg/kg) was injected intraperitoneally by a single dose and the rats were killed after 48 h. DOX treatment caused severe damage in heart tissues. Disorganization of myocardial muscle fibers, myofibrillar loss, and cardiotoxic myocardial fibers with cytoplasmic vacuoles were seen. Fish n-3 fatty acid-treated rats showed an improved histological appearance in the DOX-treated group. Our data indicate a significant reduction in the activity of terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick end labeling in cardiomyocytes of the DOX-treated group with fish n-3 fatty acids therapy. The DOX-treated with fish n-3 fatty acids group showed a significant decrease in malondialdehyde levels, and an increase in superoxide dismutase and glutathione peroxidase activities in comparison with the DOX-treated group. This study showed that fish n-3 fatty acids may be a suitable cardioprotector against acute toxic effects of DOX. [ABSTRACT FROM AUTHOR]

Among the family of stainless steels, cast austenitic stainless steels (CASSs) are preferably used due to their high mechanical properties and corrosion resistance. These steels owe their properties to their microstructural features consisting of an austenitic matrix and skeletal or lathy type δ-ferrite depending on the cooling rate. In this study, the solidification behavior of CASSs (304L and 316L grades) was studied using ThermoCalc software in order to determine the solidification sequence and final microstructure during cooling. Theoretical findings were supported by the microstructural examinations. For the mechanical characterization, not only hardness measurements but also tribological studies were carried out under dry sliding conditions and worn surfaces were examined by microscopy and 3D profilometric analysis. Results were discussed according to the type and amount of microstructural features.

Acute pharyngitis in adults is primarily a viral infection; only about 10% of cases are of bacterial etiology. Most cases of bacterial pharyngitis are caused by group A beta-hemolytic streptococci (GABHS). One laboratory method for the diagnosis of GABHS is rapid antigen diagnostic testing (RADT), which can be processed during an emergency department visit and which has become a popular alternative to throat swab cultures. We conducted a study to define the sensitivity and specificity of RADT, using throat culture results as the gold standard, in 100 emergency department patients who presented with symptoms consistent with streptococcal pharyngitis. We found that RADT had a sensitivity of 68.2% (15 of 22), a specificity of 89.7% (70 of 78), a positive predictive value of 65.2% (15 of 23), and a negative predictive value of 90.9% (70 of 77). We conclude that RADT is useful in the emergency department when the clinical suspicion is GABHS, but results should be confirmed with a throat culture in patients whose RADT results are negative. [ABSTRACT FROM AUTHOR]

The liver has long been identified as a target organ of arsenic exposure. Arsenic is a potent environmental toxicant and its accumulation in the liver causes hepatotoxicity. In our study, the investigation of effects of melatonin on arsenic-induced liver damage in rats was planned. In our study, 27 male rats were divided into three groups: control (saline, 5 ml/kg/day, intragastrically), arsenic (sodium arsenite, 5 mg/kg/day, intragastrically), and arsenic+melatonin (sodium arsenite, 5 mg/kg/day, intragastrically and melatonin, 25 mg/kg/day, intraperitoneally) group. At the end of 15 days, the rats were weighed and sacrificed then liver tissues were collected. Superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidise (GSH-Px) activities as well as malondialdehyde (MDA) levels were determined by spectrophotometry. The amount of arsenic in liver tissue was analyzed by Inductively Coupled Plasma/Optical Emission Spectrometer (ICP-OES). There were no significant differences in respect to weights of rats among the groups. Arsenic significantly decreased the enzyme activities of SOD, CAT, and GSH-Px as well as increased the levels of MDA in liver tissues. Melatonin treatments significantly increased of reduced SOD, CAT, and GSH-Px enzyme activities and decreased the elevated tissue MDA levels in liver tissues. The amount of arsenic in liver tissues significantly increased in arsenic group. There were no significant differences in respect to the amount of arsenic in liver tissues between the arsenic group and melatonin group. These data suggested that melatonin has beneficial effects against arsenic-induced liver damage by decreasing oxidative stress and lipid peroxidation. [ABSTRACT FROM AUTHOR]

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.)