Pub Date : 2024-11-01Epub Date: 2024-01-09DOI: 10.1080/10520295.2023.2276205
Suna Aydin, Faruk Kilinc, Kader Ugur, Mustafa Ata Aydin, Mehmet Hanifi Yalcin, Tuncay Kuloglu, Nalan Kaya Tektemur, Serdal Albayrak, Elif Emre, Meltem Yardim, Ramazan Fazil Akkoc, Serhat Hancer, İbrahim Sahin, Vedat Cinar, Taner Akbulut, Selcuk Demircan, Bahri Evren, Berrin Tarakci Gencer, Aziz Aksoy, Merve Yilmaz Bozoglan, İsa Aydemir, Suleyman Aydin
Metabolic syndrome (MetS) is a prevalent public health problem. Uric acid (UA) is increased by MetS. We investigated whether administration of UA and 10% fructose (F) would accelerate MetS formation and we also determined the effects of irisin and exercise. We used seven groups of rats. Group 1 (control); group 2 (sham); group 3 (10% F); group 4 (1% UA); group 5 (2% UA); group 6 (10% F + 1% UA); and Group 7, (10% F + 2% UA). After induction of MetS (groups 3 -7), Group 3 was divided into three subgroups: 3A, no further treatment; 3B, irisin treatment; 3C, irisin treatment + exercise. Group 4, 1% UA, which was divided into three subgroups: 4A, no further treatment; 4B, irisin treatment; 4C, Irisin treatment + exercise. Group 5, 2% UA, which was divided into three subgroups: 5A, no further treatment; 5B, irisin treatment; 5C, irisin treatment + exercise. Group 6, 10% F + 1% UA, which was divided into three subgroups: 6A, no further treatment; 6B, irisin treatment; 6C, irisin treatment + exercise. Group 7, 10% F + 2% UA, which was divided into three subgroups: 7A, no further treatment; 7B, irisin treatment; 7C, irisin treatment + exercise., İrisin was administered 10 ng/kg irisin intraperitoneally on Monday, Wednesday, Friday, Sunday each week for 1 month. The exercise animals (in addition to irisin treatment) also were run on a treadmill for 45 min on Monday, Wednesday, Friday, Sunday each week for 1 month. The rats were sacrificed and samples of liver, heart, kidney, pancreas, skeletal muscles and blood were obtained. The amounts of adropin (ADR) and betatrophin in the tissue supernatant and blood were measured using an ELISA method. Immunohistochemistry was used to detect ADR and betatrophin expression in situ in tissue samples. The duration of these experiments varied from 3 and 10 weeks. The order of development of MetS was: group 7, 3 weeks; group 6, 4 weeks; group 5, 6 weeks; group 4, 7 weeks; group 3, 10 weeks. Kidney, liver, heart, pancreas and skeletal muscle tissues are sources of adropin and betatrophin. In these tissues and in the circulation, adropin was decreased significantly, while betatrophin was increased significantly due to MetS; irisin + exercise reversed this situation. We found that the best method for creating a MetS model was F + UA2 supplementation. Our method is rapid and simple. Irisin + exercise was best for preventing MetS.
{"title":"Effects of irisin and exercise on adropin and betatrophin in a new metabolic syndrome model.","authors":"Suna Aydin, Faruk Kilinc, Kader Ugur, Mustafa Ata Aydin, Mehmet Hanifi Yalcin, Tuncay Kuloglu, Nalan Kaya Tektemur, Serdal Albayrak, Elif Emre, Meltem Yardim, Ramazan Fazil Akkoc, Serhat Hancer, İbrahim Sahin, Vedat Cinar, Taner Akbulut, Selcuk Demircan, Bahri Evren, Berrin Tarakci Gencer, Aziz Aksoy, Merve Yilmaz Bozoglan, İsa Aydemir, Suleyman Aydin","doi":"10.1080/10520295.2023.2276205","DOIUrl":"10.1080/10520295.2023.2276205","url":null,"abstract":"<p><p>Metabolic syndrome (MetS) is a prevalent public health problem. Uric acid (UA) is increased by MetS. We investigated whether administration of UA and 10% fructose (F) would accelerate MetS formation and we also determined the effects of irisin and exercise. We used seven groups of rats. Group 1 (control); group 2 (sham); group 3 (10% F); group 4 (1% UA); group 5 (2% UA); group 6 (10% F + 1% UA); and Group 7, (10% F + 2% UA). After induction of MetS (groups 3 -7), Group 3 was divided into three subgroups: 3A, no further treatment; 3B, irisin treatment; 3C, irisin treatment + exercise. Group 4, 1% UA, which was divided into three subgroups: 4A, no further treatment; 4B, irisin treatment; 4C, Irisin treatment + exercise. Group 5, 2% UA, which was divided into three subgroups: 5A, no further treatment; 5B, irisin treatment; 5C, irisin treatment + exercise. Group 6, 10% F + 1% UA, which was divided into three subgroups: 6A, no further treatment; 6B, irisin treatment; 6C, irisin treatment + exercise. Group 7, 10% F + 2% UA, which was divided into three subgroups: 7A, no further treatment; 7B, irisin treatment; 7C, irisin treatment + exercise., İrisin was administered 10 ng/kg irisin intraperitoneally on Monday, Wednesday, Friday, Sunday each week for 1 month. The exercise animals (in addition to irisin treatment) also were run on a treadmill for 45 min on Monday, Wednesday, Friday, Sunday each week for 1 month. The rats were sacrificed and samples of liver, heart, kidney, pancreas, skeletal muscles and blood were obtained. The amounts of adropin (ADR) and betatrophin in the tissue supernatant and blood were measured using an ELISA method. Immunohistochemistry was used to detect ADR and betatrophin expression in situ in tissue samples. The duration of these experiments varied from 3 and 10 weeks. The order of development of MetS was: group 7, 3 weeks; group 6, 4 weeks; group 5, 6 weeks; group 4, 7 weeks; group 3, 10 weeks. Kidney, liver, heart, pancreas and skeletal muscle tissues are sources of adropin and betatrophin. In these tissues and in the circulation, adropin was decreased significantly, while betatrophin was increased significantly due to MetS; irisin + exercise reversed this situation. We found that the best method for creating a MetS model was F + UA2 supplementation. Our method is rapid and simple. Irisin + exercise was best for preventing MetS.</p>","PeriodicalId":8970,"journal":{"name":"Biotechnic & Histochemistry","volume":null,"pages":null},"PeriodicalIF":1.6,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71477688","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-11-01Epub Date: 2024-01-09DOI: 10.1080/10520295.2023.2300797
Chelsea Peeler, Christopher R Pitzer, Hector G Paez, Sheila Criswell
The application of most chemical fixatives, such as formalin, in the anatomic pathology laboratory requires safety training and hazardous chemical monitoring due to the toxicity and health risks associated with their use. Consequently, the use of formalin has been banned in most applications in Europe; the primary exception is its use in the histology laboratory in lieu of a suitable and safer alternative. Glyoxal based solutions, several of which are available commercially, are the most promising alternative fixatives, because they are based on a mechanism of fixation similar to that of formalin. Unlike formalin, however, glyoxal based solutions do not dissociate from water and therefore do not require ventilation measures such as a fume hood. A primary barrier to the adoption of commercially available glyoxal based solutions is their low pH, which can produce undesirable morphological and antigenic tissue alterations; however, a recently available neutral pH glyoxal product (glyoxal acid free) (GAF) has been developed to mitigate the challenges of low pH. We compared the morphology and histochemistry among tissues fixed in 10% neutral buffered formalin, a commercially available acidic glyoxal product (Prefer), and GAF. Tissues fixed in formalin and Prefer exhibited similar morphology and staining properties; tissues fixed with 2% GAF exhibited deleterious effects.
由于福尔马林等大多数化学固定剂的毒性和健康风险,在解剖病理实验室中使用福尔马林等化学固定剂需要接受安全培训和危险化学品监测。因此,在欧洲,福尔马林已被禁止用于大多数用途;主要的例外是在组织学实验室中使用福尔马林,以替代更安全的合适替代品。乙二醛溶液是最有前途的替代固定剂,因为它们的固定机理与福尔马林相似。但与福尔马林不同的是,乙二醛溶液不会从水中解离,因此不需要通风橱等通风措施。采用市售乙二醛溶液的一个主要障碍是其 pH 值较低,可能会产生不良的形态学和抗原性组织变化;不过,最近开发出了一种中性 pH 值的乙二醛产品(无乙二醛酸)(GAF),可以缓解 pH 值低带来的挑战。我们比较了用 10%中性缓冲福尔马林、市售酸性乙二醛产品(Prefer)和 GAF 固定的组织的形态和组织化学。用福尔马林和 Prefer 固定的组织显示出相似的形态和染色特性;而用 2% GAF 固定的组织则显示出有害影响。
{"title":"Histochemical and morphological evaluation of a glyoxal acid-free fixative.","authors":"Chelsea Peeler, Christopher R Pitzer, Hector G Paez, Sheila Criswell","doi":"10.1080/10520295.2023.2300797","DOIUrl":"10.1080/10520295.2023.2300797","url":null,"abstract":"<p><p>The application of most chemical fixatives, such as formalin, in the anatomic pathology laboratory requires safety training and hazardous chemical monitoring due to the toxicity and health risks associated with their use. Consequently, the use of formalin has been banned in most applications in Europe; the primary exception is its use in the histology laboratory in lieu of a suitable and safer alternative. Glyoxal based solutions, several of which are available commercially, are the most promising alternative fixatives, because they are based on a mechanism of fixation similar to that of formalin. Unlike formalin, however, glyoxal based solutions do not dissociate from water and therefore do not require ventilation measures such as a fume hood. A primary barrier to the adoption of commercially available glyoxal based solutions is their low pH, which can produce undesirable morphological and antigenic tissue alterations; however, a recently available neutral pH glyoxal product (glyoxal acid free) (GAF) has been developed to mitigate the challenges of low pH. We compared the morphology and histochemistry among tissues fixed in 10% neutral buffered formalin, a commercially available acidic glyoxal product (Prefer), and GAF. Tissues fixed in formalin and Prefer exhibited similar morphology and staining properties; tissues fixed with 2% GAF exhibited deleterious effects.</p>","PeriodicalId":8970,"journal":{"name":"Biotechnic & Histochemistry","volume":null,"pages":null},"PeriodicalIF":1.6,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139073339","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-11-01Epub Date: 2024-01-09DOI: 10.1080/10520295.2023.2273860
Valeriy Kalinin, Pavel Padnya, Ivan Stoikov
Romanowsky staining was an important methodological breakthrough in diagnostic hematology and cytopathology during the late 19th and early 20th centuries; it has facilitated for decades the work of biologists, hematologists and pathologists working with blood cells. Despite more than a century of studying Romanowsky staining, no systematic review has been published that explains the chemical processes that produce the "Romanowsky effect" or "Romanowsky-Giemsa effect" (RGE), i.e., a purple coloration arising from the interaction of an azure dye with eosin and not due merely to their simultaneous presence. Our review is an attempt to build a bridge between chemists and biomedical scientists and to summarize the available data on methylene blue (MB) demethylation as well as the related reduction and decomposition of MB to simpler compounds by both light and enzyme systems and microorganisms. To do this, we analyze modern data on the mechanisms of MB demethylation both in the presence of acids and bases and by disproportionation due to the action of light. We also offer an explanation for why the RGE occurs only when azure B, or to a lesser extent, azure A is present by applying experimental and calculated physicochemical parameters including dye-DNA binding constants and electron density distributions in the molecules of these ligands. Finally, we discuss modern techniques for obtaining new varieties of Romanowsky dyes by modifying previously known ones. We hope that our critical literature study will help scientists understand better the chemical and physicochemical processes and mechanisms of cell staining with such dyes.
{"title":"Romanowsky staining: history, recent advances and future prospects from a chemistry perspective.","authors":"Valeriy Kalinin, Pavel Padnya, Ivan Stoikov","doi":"10.1080/10520295.2023.2273860","DOIUrl":"10.1080/10520295.2023.2273860","url":null,"abstract":"<p><p>Romanowsky staining was an important methodological breakthrough in diagnostic hematology and cytopathology during the late 19<sup>th</sup> and early 20<sup>th</sup> centuries; it has facilitated for decades the work of biologists, hematologists and pathologists working with blood cells. Despite more than a century of studying Romanowsky staining, no systematic review has been published that explains the chemical processes that produce the \"Romanowsky effect\" or \"Romanowsky-Giemsa effect\" (RGE), i.e., a purple coloration arising from the interaction of an azure dye with eosin and not due merely to their simultaneous presence. Our review is an attempt to build a bridge between chemists and biomedical scientists and to summarize the available data on methylene blue (MB) demethylation as well as the related reduction and decomposition of MB to simpler compounds by both light and enzyme systems and microorganisms. To do this, we analyze modern data on the mechanisms of MB demethylation both in the presence of acids and bases and by disproportionation due to the action of light. We also offer an explanation for why the RGE occurs only when azure B, or to a lesser extent, azure A is present by applying experimental and calculated physicochemical parameters including dye-DNA binding constants and electron density distributions in the molecules of these ligands. Finally, we discuss modern techniques for obtaining new varieties of Romanowsky dyes by modifying previously known ones. We hope that our critical literature study will help scientists understand better the chemical and physicochemical processes and mechanisms of cell staining with such dyes.</p>","PeriodicalId":8970,"journal":{"name":"Biotechnic & Histochemistry","volume":null,"pages":null},"PeriodicalIF":1.6,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71477689","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
We investigated possible protective effects of chlorogenic acid (CGA) against cyclophosphamide (CP) induced hepatic injury in mice. We measured aminotransferase alanine transaminase (ALT) and aspartate transaminase (AST) levels in the serum. We assayed catalase (CAT), superoxide dismutase (SOD), reduced glutathione (GSH), glutathione peroxidase (GSH-Px) and malondialdehyde (MDA) in hepatic tissue. We assessed expression of nuclear transcription factor 2 (Nrf2) and Kelch sample related protein-1 (keap1) proteins in hepatic tissues using immunohistochemistry. The relative mRNA expression levels of heme oxygenase-1 (HO-1), NADH quinone oxidoreductase 1 (NQO1), tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) were determined using quantitative real-time polymerase chain reaction (qRT-PCR). Hematoxylin & eosin staining was used to assess liver histopathology. We found that administration of CGA prior to induction of injury by CP decreased serum ALT, AST and MDA expressions in hepatic tissue, while CAT, SOD, GSH and GSH-Px concentrations were increased. We found that hepatocytes of animals administered CGA gradually returned to normal morphology. CGA increased the protein expression of Nrf2 in murine hepatic tissue. Administration of CGA up-regulated mRNA expression levels of HO-1, NQO1, TNF-α and IL-6 in hepatic tissue. CGA exhibited a marked protective effect on CP induced liver injury in mice.
{"title":"Protective effects of chlorogenic acid against cyclophosphamide induced liver injury in mice.","authors":"Hao Hao, Youmei Xu, Rui Chen, Shanshan Qi, Xiang Liu, Beibei Lin, Xiaohua Chen, Xiaoying Zhang, Lijuan Yue, Chen Chen","doi":"10.1080/10520295.2023.2287452","DOIUrl":"10.1080/10520295.2023.2287452","url":null,"abstract":"<p><p>We investigated possible protective effects of chlorogenic acid (CGA) against cyclophosphamide (CP) induced hepatic injury in mice. We measured aminotransferase alanine transaminase (ALT) and aspartate transaminase (AST) levels in the serum. We assayed catalase (CAT), superoxide dismutase (SOD), reduced glutathione (GSH), glutathione peroxidase (GSH-Px) and malondialdehyde (MDA) in hepatic tissue. We assessed expression of nuclear transcription factor 2 (Nrf2) and Kelch sample related protein-1 (keap1) proteins in hepatic tissues using immunohistochemistry. The relative mRNA expression levels of heme oxygenase-1 (HO-1), NADH quinone oxidoreductase 1 (NQO1), tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) were determined using quantitative real-time polymerase chain reaction (qRT-PCR). Hematoxylin & eosin staining was used to assess liver histopathology. We found that administration of CGA prior to induction of injury by CP decreased serum ALT, AST and MDA expressions in hepatic tissue, while CAT, SOD, GSH and GSH-Px concentrations were increased. We found that hepatocytes of animals administered CGA gradually returned to normal morphology. CGA increased the protein expression of Nrf2 in murine hepatic tissue. Administration of CGA up-regulated mRNA expression levels of <i>HO-1</i>, <i>NQO1</i>, <i>TNF-α</i> and <i>IL-6</i> in hepatic tissue. CGA exhibited a marked protective effect on CP induced liver injury in mice.</p>","PeriodicalId":8970,"journal":{"name":"Biotechnic & Histochemistry","volume":null,"pages":null},"PeriodicalIF":1.6,"publicationDate":"2024-11-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"138450826","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-09-11DOI: 10.1080/10520295.2024.2390179
David G Hicks,Bradley M Turner
Ground breaking advances in medicine, driven in part by major technologic developments in molecular biology have led us to a new model for cancer care that has been termed personalized, or precision medicine. Precision medicine is a model for making medical decisions that employs an innovative clinical approach and advanced tumor testing methods that are tailored to understanding an individual patient's tumor biology and the molecular drivers of their disease. This medical model includes a combination of diagnostic testing and specific treatment options that can be offered to patients at presentation and in theory throughout the course of their disease as new mutations arise with the development of disease recurrence. Although the precision medicine model offers incredible potential to transform cancer care, these advances are only meaningful when they reach the correct patients. The evolving paradigm of precision medicine is changing the practice of pathology, and the pathology community needs to be mindful of these changes because every tissue specimen represents a patient's life, and those patients are depending on the pathology community to handle their tissue correctly. The diagnostic tests performed in the pathology laboratory for precision medicine are increasingly complex, and pathologists along with the entire laboratory and clinical communities need to take steps to ensure that the right diagnosis is given to the right patient to inform the right treatment options, at the right time, along every step of the continuum of care for cancer patients. While hormone receptors and human epidermal growth factor receptor 2 (HER2) overexpression and/or amplification have been the mainstay for risk-stratification, and treatment decision making in breast cancer since the early 2000's, the seminal work on gene expression by Perou and colleagues in the early 2000's opened the door for molecular testing in the prognostic and predictive assessment of breast cancer. Molecular testing is now part of the standard of care in the precision medicine model for breast cancer care. In this article, the reader will gain a better understanding of how the lack of standardization of pre-analytic factors has the potential to negatively impact the quality of the tissue specimen for downstream biomarker and molecular testing, which ultimately can negatively affect patient care. The reader will also gain insight into the current climate surrounding molecular testing in breast cancer.
{"title":"Optimized biomarker evaluation and molecular testing in the era of breast cancer precision medicine.","authors":"David G Hicks,Bradley M Turner","doi":"10.1080/10520295.2024.2390179","DOIUrl":"https://doi.org/10.1080/10520295.2024.2390179","url":null,"abstract":"Ground breaking advances in medicine, driven in part by major technologic developments in molecular biology have led us to a new model for cancer care that has been termed personalized, or precision medicine. Precision medicine is a model for making medical decisions that employs an innovative clinical approach and advanced tumor testing methods that are tailored to understanding an individual patient's tumor biology and the molecular drivers of their disease. This medical model includes a combination of diagnostic testing and specific treatment options that can be offered to patients at presentation and in theory throughout the course of their disease as new mutations arise with the development of disease recurrence. Although the precision medicine model offers incredible potential to transform cancer care, these advances are only meaningful when they reach the correct patients. The evolving paradigm of precision medicine is changing the practice of pathology, and the pathology community needs to be mindful of these changes because every tissue specimen represents a patient's life, and those patients are depending on the pathology community to handle their tissue correctly. The diagnostic tests performed in the pathology laboratory for precision medicine are increasingly complex, and pathologists along with the entire laboratory and clinical communities need to take steps to ensure that the right diagnosis is given to the right patient to inform the right treatment options, at the right time, along every step of the continuum of care for cancer patients. While hormone receptors and human epidermal growth factor receptor 2 (HER2) overexpression and/or amplification have been the mainstay for risk-stratification, and treatment decision making in breast cancer since the early 2000's, the seminal work on gene expression by Perou and colleagues in the early 2000's opened the door for molecular testing in the prognostic and predictive assessment of breast cancer. Molecular testing is now part of the standard of care in the precision medicine model for breast cancer care. In this article, the reader will gain a better understanding of how the lack of standardization of pre-analytic factors has the potential to negatively impact the quality of the tissue specimen for downstream biomarker and molecular testing, which ultimately can negatively affect patient care. The reader will also gain insight into the current climate surrounding molecular testing in breast cancer.","PeriodicalId":8970,"journal":{"name":"Biotechnic & Histochemistry","volume":null,"pages":null},"PeriodicalIF":1.6,"publicationDate":"2024-09-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142187810","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-08-23DOI: 10.1080/10520295.2024.2389517
Selçuk Kaplan, Bilge Aydın Türk, Ebru Elibol, Gürkan Özbey, Tekin Ekinci
The present study aimed to investigate the histopathological effects of obstetric gel (OG) on vaginal tissue. In this study, 21 female Wistar albino rats were divided into three groups, comprising seven animals in each group. The first group (group 1) was the control group, the second group (group 2) was the physiological saline (PS) group, and the third group (group 3) was the OG group. In group 1, dilatation was performed using Hegar dilators from Hegar 5 to Hegar 10 without any vaginal application. In group 2, the vagina was washed with a PS-filled applicator. In group 3, the vagina was washed with an OG-filled applicator and Hegar dilators were used to achieve vaginal dilatation. In the group of OG-applied rats, there was an increase in mast cell infiltration, tissue epithelial thickness, and fibrillin-1 levels of the mucosa in the vaginal tissue. The present study is the first to investigate the histopathological effects of OG used for vaginal tissue dilatation in rats. OGs have no early effectiveness in preventing the damage caused by compression of the vaginal wall; however, OGs may have a protective effect against pelvic floor pathologies.
本研究旨在探讨产科凝胶(OG)对阴道组织的组织病理学影响。本研究将 21 只雌性 Wistar 白化大鼠分为三组,每组 7 只。第一组(第一组)为对照组,第二组(第二组)为生理盐水组,第三组(第三组)为产道凝胶组。第一组使用 Hegar 5 至 Hegar 10 号扩张器进行扩张,不进行任何阴道应用。在第二组中,使用充满 PS 的涂抹器清洗阴道。在第 3 组中,使用充满 OG 的涂抹器清洗阴道,并使用 Hegar 扩张器进行阴道扩张。在涂抹 OG 的大鼠组中,肥大细胞浸润、组织上皮厚度和阴道组织粘膜的纤维素-1 水平均有所增加。本研究首次调查了用于大鼠阴道组织扩张的 OG 的组织病理学影响。OG对预防阴道壁受压造成的损伤没有早期效果;但OG可能对盆底病变有保护作用。
{"title":"Histopathologic effects of obstetric gel on the vaginal tissue: in vaginal trauma formed rat model.","authors":"Selçuk Kaplan, Bilge Aydın Türk, Ebru Elibol, Gürkan Özbey, Tekin Ekinci","doi":"10.1080/10520295.2024.2389517","DOIUrl":"https://doi.org/10.1080/10520295.2024.2389517","url":null,"abstract":"<p><p>The present study aimed to investigate the histopathological effects of obstetric gel (OG) on vaginal tissue. In this study, 21 female Wistar albino rats were divided into three groups, comprising seven animals in each group. The first group (group 1) was the control group, the second group (group 2) was the physiological saline (PS) group, and the third group (group 3) was the OG group. In group 1, dilatation was performed using Hegar dilators from Hegar 5 to Hegar 10 without any vaginal application. In group 2, the vagina was washed with a PS-filled applicator. In group 3, the vagina was washed with an OG-filled applicator and Hegar dilators were used to achieve vaginal dilatation. In the group of OG-applied rats, there was an increase in mast cell infiltration, tissue epithelial thickness, and fibrillin-1 levels of the mucosa in the vaginal tissue. The present study is the first to investigate the histopathological effects of OG used for vaginal tissue dilatation in rats. OGs have no early effectiveness in preventing the damage caused by compression of the vaginal wall; however, OGs may have a protective effect against pelvic floor pathologies.</p>","PeriodicalId":8970,"journal":{"name":"Biotechnic & Histochemistry","volume":null,"pages":null},"PeriodicalIF":1.6,"publicationDate":"2024-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142035130","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2024-08-23DOI: 10.1080/10520295.2024.2389535
Leica Barnhart, Chloe Balzer, Sheila Criswell
Helicobacter pylori, a curved bacterial rod and causative agent of peptic ulcer and gastric adenocarcinoma, is found as an infectious agent in the stomach of over half of the global population. H. pylori has been identified in oral biofilms and its presence in adenotonsillar tissues has been suggested, with variations in testing methodology both proving and disproving its presence. The current study employed 119 formalin-fixed paraffin-embedded tonsillar tissues from an adult population (n=86) in a major metropolitan city with immunohistochemistry procedures using a monoclonal antibody to determine the incidence of H. pylori in the tonsils. H. pylori was identified in 72.1% of the patients and was associated with Actinomyces spp. in 92.0% of those cases. The high incidence of H. pylori in patients undergoing tonsillectomy suggests that H. pylori may be a contributing factor for tonsillitis and tonsillar hypertrophy. Furthermore, the reservoir for H. pylori in the tonsils may explain why some persons remain refractory to antibiotic treatment for gastric H. pylori.
{"title":"Prevalence of <i>Helicobacter pylori</i> in routine adult tonsillectomies.","authors":"Leica Barnhart, Chloe Balzer, Sheila Criswell","doi":"10.1080/10520295.2024.2389535","DOIUrl":"https://doi.org/10.1080/10520295.2024.2389535","url":null,"abstract":"<p><p><i>Helicobacter pylori</i>, a curved bacterial rod and causative agent of peptic ulcer and gastric adenocarcinoma, is found as an infectious agent in the stomach of over half of the global population. <i>H. pylori</i> has been identified in oral biofilms and its presence in adenotonsillar tissues has been suggested, with variations in testing methodology both proving and disproving its presence. The current study employed 119 formalin-fixed paraffin-embedded tonsillar tissues from an adult population (n=86) in a major metropolitan city with immunohistochemistry procedures using a monoclonal antibody to determine the incidence of <i>H. pylori</i> in the tonsils. <i>H. pylori</i> was identified in 72.1% of the patients and was associated with <i>Actinomyces spp</i>. in 92.0% of those cases. The high incidence of <i>H. pylori</i> in patients undergoing tonsillectomy suggests that <i>H. pylori</i> may be a contributing factor for tonsillitis and tonsillar hypertrophy. Furthermore, the reservoir for <i>H. pylori</i> in the tonsils may explain why some persons remain refractory to antibiotic treatment for gastric <i>H. pylori</i>.</p>","PeriodicalId":8970,"journal":{"name":"Biotechnic & Histochemistry","volume":null,"pages":null},"PeriodicalIF":1.6,"publicationDate":"2024-08-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142035131","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Hesperetin, a citrus flavonoid, has been a widely studied anticancer agent against many types of cancers, but the exact mechanism of efficacy is still unrevealed. Therefore, this study has attempted to delineate the mechanical aspect of hesperetin's anticancer efficacy against colon cancer using immunoblotting, scanning, and transmission electron microscopic studies. The treatment with hesperetin (25 and 50 µM) has significantly (p < 0.0001) curbed down the proliferation and cell viability of HCT-15 cells in a concentration as well as time dependent manner. Hesperetin was able to achieve this through the induction of caspase-dependent apoptosis. Moreover, hesperetin effectively inhibited phosphorylation of Akt with a parallel increase in PTEN expression thereby inhibiting the PI3K signaling axis, which contributes to the suppression of proliferation. In addition, hesperetin enhanced autophagy through dephosphorylating mTOR, one of the downstream targets of Akt with simultaneous acceleration in Beclin-1 and LC3-II expression levels. Interestingly, hesperetin enhanced the effects of Akt inhibitor LY294002 and mTOR inhibitor rapamycin. This study documented the potential of hesperetin to induce apoptosis through simultaneous acceleration over the autophagic process in colon cancer cells. Thus, hesperetin played a beneficial therapeutic role in preventing colon carcinoma growth by regulating the Akt and mTOR signaling axis.
{"title":"Hesperetin regulates PI3K/Akt and mTOR pathways to exhibit its antiproliferative effect against colon cancer cells.","authors":"Gowrikumar Saiprasad, Palanivel Chitra, Ramar Manikandan, Arunagirinathan Koodalingam, Ganaspasam Sudhandiran","doi":"10.1080/10520295.2024.2382764","DOIUrl":"https://doi.org/10.1080/10520295.2024.2382764","url":null,"abstract":"<p><p>Hesperetin, a citrus flavonoid, has been a widely studied anticancer agent against many types of cancers, but the exact mechanism of efficacy is still unrevealed. Therefore, this study has attempted to delineate the mechanical aspect of hesperetin's anticancer efficacy against colon cancer using immunoblotting, scanning, and transmission electron microscopic studies. The treatment with hesperetin (25 and 50 µM) has significantly (p < 0.0001) curbed down the proliferation and cell viability of HCT-15 cells in a concentration as well as time dependent manner. Hesperetin was able to achieve this through the induction of caspase-dependent apoptosis. Moreover, hesperetin effectively inhibited phosphorylation of Akt with a parallel increase in PTEN expression thereby inhibiting the PI3K signaling axis, which contributes to the suppression of proliferation. In addition, hesperetin enhanced autophagy through dephosphorylating mTOR, one of the downstream targets of Akt with simultaneous acceleration in Beclin-1 and LC3-II expression levels. Interestingly, hesperetin enhanced the effects of Akt inhibitor LY294002 and mTOR inhibitor rapamycin. This study documented the potential of hesperetin to induce apoptosis through simultaneous acceleration over the autophagic process in colon cancer cells. Thus, hesperetin played a beneficial therapeutic role in preventing colon carcinoma growth by regulating the Akt and mTOR signaling axis.</p>","PeriodicalId":8970,"journal":{"name":"Biotechnic & Histochemistry","volume":null,"pages":null},"PeriodicalIF":1.6,"publicationDate":"2024-08-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142016295","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
This study investigated whether abemaciclib (ABE) administration had any adverse effects on ovarian and sex hormones in female rats, and the protective effect of curcumin. Forty female rats were equally divided into the sham control, DMSO, curcumin (CMN), ABE, and ABE+CMN groups. Pharmaceuticals were administered by gavage daily for 28 days. Serum sex hormones were measured in an autoanalyzer operating with a microparticle immunoassay method. In addition, histopathological examination and 8-OHdG expression were performed on the ovarian tissue. Progesterone and testosterone levels were significantly decreased, while estradiol levels were significantly increased, in the ABE group compared to the sham and DMSO groups. In addition, there were significant differences in sex hormone levels in the CMN and/or CMN+ABE groups compared to the ABE group. There was decreased expression of 8-OHdG in the ABE+CMN group compared to the ABE or CMN only groups. This study exhibited that ABE administration can adversely affect functions and histology of the ovarian tissue, but CMN therapy may be protective against the adverse effects on ovarian in ABE-induced rats.
{"title":"Effect of abemaciclib and curcumin administration on sex hormones, reproductive functions, and oxidative DNA expression in rats.","authors":"Zübeyir Huyut, Bünyamin Uçar, Kenan Yıldızhan, Fikret Altındağ, Mehmet Tahir Huyut","doi":"10.1080/10520295.2024.2389524","DOIUrl":"https://doi.org/10.1080/10520295.2024.2389524","url":null,"abstract":"<p><p>This study investigated whether abemaciclib (ABE) administration had any adverse effects on ovarian and sex hormones in female rats, and the protective effect of curcumin. Forty female rats were equally divided into the sham control, DMSO, curcumin (CMN), ABE, and ABE+CMN groups. Pharmaceuticals were administered by gavage daily for 28 days. Serum sex hormones were measured in an autoanalyzer operating with a microparticle immunoassay method. In addition, histopathological examination and 8-OHdG expression were performed on the ovarian tissue. Progesterone and testosterone levels were significantly decreased, while estradiol levels were significantly increased, <b>in the ABE</b> group compared to the sham and DMSO groups. In addition, there were significant differences in sex hormone levels in the CMN and/or CMN+ABE groups compared to the ABE group. There was decreased expression of 8-OHdG in the ABE+CMN group compared to the ABE or CMN only groups. This study exhibited that ABE administration can adversely affect functions and histology of the ovarian tissue, but CMN therapy may be protective against the adverse effects on ovarian in ABE-induced rats.</p>","PeriodicalId":8970,"journal":{"name":"Biotechnic & Histochemistry","volume":null,"pages":null},"PeriodicalIF":1.6,"publicationDate":"2024-08-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142016294","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}