Physiological research最新文献_第10页

Serotonin and Effort-Based Decision-Making: Dissociating Behavioral Effects of 8-OH-DPAT and PCPA. 羟色胺和基于努力的决策：8-OH-DPAT和PCPA的分离行为效应。

IF 1.9 4区医学

Physiological research Pub Date : 2024-11-19 DOI: 10.33549/physiolres.935468

D Kunčická, N Cmarková, S Ondráčková, D Kačer, D Rodriguez, K Valeš, J Svoboda, H Brožka, A Stuchlík

{"title":"Serotonin and Effort-Based Decision-Making: Dissociating Behavioral Effects of 8-OH-DPAT and PCPA.","authors":"D Kunčická, N Cmarková, S Ondráčková, D Kačer, D Rodriguez, K Valeš, J Svoboda, H Brožka, A Stuchlík","doi":"10.33549/physiolres.935468","DOIUrl":"10.33549/physiolres.935468","url":null,"abstract":"Effort-based decision-making is particularly relevant to psychiatric conditions where motivation deficits are prominent features. Despite its clinical significance, the neurochemical mechanisms of this cognitive process remain unclarified. This study explores the impact of serotonin synthesis inhibition (PCPA) and modulation of serotonin release and 5-HT1A receptor agonism (8-OH-DPAT) on effort-based decision-making in rats. Adult male rats were trained in a modified T-maze task where they could obtain a high reward for climbing a mesh barrier or a low reward for no extra effort. Following training, rats received either acute 8-OH-DPAT treatment or subchronic PCPA treatment and were tested on their choices between high- and low-effort arms. The goal-arm choices and goal-arm entrance latencies were recorded. Next, homovanillic acid and 5-hydroxyindoleacetic acid, metabolites of dopamine and serotonin, respectively, were quantified in the rats' prefrontal cortex, striatum, and hippocampus. 8-OH-DPAT significantly increased low-effort, low-reward choices and increased goal-arm latency. In contrast, PCPA treatment did not affect these measures. Both PCPA and 8-OH-DPAT significantly decreased 5-hydroxyindoleacetic acid levels in the prefrontal cortex and the hippocampus. 8-OH-DPAT treatment was also associated with decreased homovanillic acid levels in the hippocampus. Our findings suggest that the overall reduction of serotonin levels alone does not affect effort-based decision-making and highlights the possible role of the hippocampus and the 5-HT1A receptor in this cognitive process.","PeriodicalId":20235,"journal":{"name":"Physiological research","volume":"73 5","pages":"869-880"},"PeriodicalIF":1.9,"publicationDate":"2024-11-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11629953/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142668931","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

MiR-92a-3p Promotes Renal Injury and Fibrosis Through Facilitating M1 Macrophage Polarization via Targeting LIN28A. MiR-92a-3p 通过靶向 LIN28A 促进 M1 型巨噬细胞极化，从而促进肾损伤和纤维化

IF 1.9 4区医学

Physiological research Pub Date : 2024-11-15 DOI: 10.33549/physiolres.935305

M Xu, X Zeng, M Pan, R Chen, Y Bai, J He, C Wang, Y Qi, Q Sun, C Wang, N An

{"title":"MiR-92a-3p Promotes Renal Injury and Fibrosis Through Facilitating M1 Macrophage Polarization via Targeting LIN28A.","authors":"M Xu, X Zeng, M Pan, R Chen, Y Bai, J He, C Wang, Y Qi, Q Sun, C Wang, N An","doi":"10.33549/physiolres.935305","DOIUrl":"10.33549/physiolres.935305","url":null,"abstract":"Infiltrated and activated M1 macrophages play a role in kidney injury and fibrosis during chronic kidney disease (CKD) progression. However, the specific ways that M1 macrophage polarization contributes to renal fibrosis are not fully understood. The study seeks to investigate how miR-92a-3p regulates M1 macrophage polarization and its connection to renal fibrosis in the development of CKD. Our results revealed that miR-92a-3p overexpression increased M1-macrophage activation, iNOS, IL-6, and TNF-alpha expression in RAW264.7 upon LPS stimulation. LIN28A overexpression reversed these effects. Moreover, miR-92a-3p overexpression in RAW264.7 exacerbated NRK-52E cell apoptosis induced by LPS, but LIN28A overexpression counteracted this effect. MiR-92a-3p knockout in unilateral ureteral obstruction (UUO) C57BL/6 mice led to reduced renal infiltration and fibrosis, accompanied by decreased iNOS, alpha-SMA, IL-6, TNF-alpha, and increased LIN28A. In summary, our findings suggest that miR-92a-3p may play a role in promoting renal injury and fibrosis both in vitro and in vivo. This effect is potentially achieved by facilitating M1 macrophage polarization through the targeting of LIN28A.","PeriodicalId":20235,"journal":{"name":"Physiological research","volume":"73 5","pages":"755-767"},"PeriodicalIF":1.9,"publicationDate":"2024-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11629952/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142639584","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The Toxic Effect of Toluene on Ovarian Cells Can Be Prevented by the MicroRNA miR-152. 微核糖核酸 miR-152 可防止甲苯对卵巢细胞的毒性作用

IF 1.9 4区医学

Physiological research Pub Date : 2024-11-15 DOI: 10.33549/physiolres.935386

A Sirotkin, Z Fabová, B Loncová, K Popovičová, M Bauer, A Harrath

{"title":"The Toxic Effect of Toluene on Ovarian Cells Can Be Prevented by the MicroRNA miR-152.","authors":"A Sirotkin, Z Fabová, B Loncová, K Popovičová, M Bauer, A Harrath","doi":"10.33549/physiolres.935386","DOIUrl":"10.33549/physiolres.935386","url":null,"abstract":"The potential of microRNAs to protect the female reproductive system from the toxic influence of oil-related environmental contaminants has not yet been examined. The aim of the present study was to examine the ability of the microRNA miR-152 to prevent the toxic effects of toluene on ovarian cells. Porcine ovarian granulosa cells transfected or not transfected with miR-152 mimics were cultured with or without toluene (0, 10 and 100 ng/ml). The expression of miR-152; cell viability; proliferation (accumulation of PCNA, cyclin B1 and BrdU); cytoplasmic/mitochondrial apoptosis (accumulation of bax and caspase 3); and release of progesterone, testosterone and estradiol were quantified via RT-qPCR, the Trypan blue exclusion test, quantitative immunocytochemistry, the BrdU assay and ELISA. The addition of toluene reduced cell viability, decreased the levels of all the measured markers of proliferation and the release of all the measured steroid hormones, and promoted the expression of apoptosis markers. Transfection of cells with miR-152 mimics increased the expression of miR-152, cell proliferation, and progesterone release but reduced apoptosis and the release of testosterone and estradiol. Moreover, miR-152 prevented or inhibited all the toluene effects in addition to its inhibitory effect on testosterone and estradiol release. The present results demonstrate that miR-152 can protect ovarian cells from the harmful influence of toluene.","PeriodicalId":20235,"journal":{"name":"Physiological research","volume":"73 5","pages":"791-799"},"PeriodicalIF":1.9,"publicationDate":"2024-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11629955/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142639587","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Trimethylamine Induced Chronic Kidney Injury by Activating the ZBP1-NLRP3 Inflammasome Pathway. 三甲胺通过激活 ZBP1-NLRP3 炎症体通路诱导慢性肾损伤

IF 1.9 4区医学

Physiological research Pub Date : 2024-11-15 DOI: 10.33549/physiolres.935378

L Bai, Q Chen, Y Li, F Wu, M Jin, Y Chen, X Teng, S Jin, H Fan, Y Wu

{"title":"Trimethylamine Induced Chronic Kidney Injury by Activating the ZBP1-NLRP3 Inflammasome Pathway.","authors":"L Bai, Q Chen, Y Li, F Wu, M Jin, Y Chen, X Teng, S Jin, H Fan, Y Wu","doi":"10.33549/physiolres.935378","DOIUrl":"10.33549/physiolres.935378","url":null,"abstract":"Trimethylamine N-oxide (TMAO), a bioactive metabolite of gut microbes, plays a pivotal role in the pathogenesis of kidney diseases by activating programmed cell death (PCD) pathways. However, whether trimethylamine (TMA) contributes to chronic kidney injury and which kind of PCD is involved in TMA-induced chronic kidney injury has not been previously evaluated. To observe the effect of TMA, male C57BL/6J mice were randomly divided into two groups: the Control group and the TMA group. The mice in the TMA group were intraperitoneally injected with 100 micromol/kg/day TMA for three months, whereas the mice in the Control group were injected with normal saline for the same period. After three months, plasma creatinine and blood urea nitrogen levels, indicators of kidney function, increased significantly in the TMA group as compared with those in the Control group. Furthermore, Masson staining assay showed that TMA treatment led to a larger area of fibrosis than the Control group. TMA treatment did not change the Bax/Bcl-2 ratio, RIP1, RIP3 and MLKL phosphorylation, or iron and malondialdehyde levels in kidney tissues, indicating that apoptosis, ferroptosis and necroptosis were not involved in TMA-induced chronic kidney injury. However, compared with the Control group, TMA treatment significantly upregulated NLRP3, Caspase-1, IL-1beta, cleaved-Caspase 8, Caspase-8, and ZBP1 protein expression in kidney tissues. These results indicated that the ZBP1-NLRP3 inflammasome pathway was involved in TMA-induced chronic kidney injury. In conclusion, our studies revealed that the ZBP1-NLRP3 inflammasome may take part in the progression of TMA induced chronic kidney injury.","PeriodicalId":20235,"journal":{"name":"Physiological research","volume":"73 5","pages":"779-789"},"PeriodicalIF":1.9,"publicationDate":"2024-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11629947/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142639588","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Mechanistic Studies of Cyclooxygenase-2 (COX-2) in Skeletal Muscle Cells During Rotator Cuff Injury: An In Vitro Study. 肩袖损伤期间骨骼肌细胞中环氧化酶-2 (COX-2) 的机制研究：体外研究

IF 1.9 4区医学

Physiological research Pub Date : 2024-11-15 DOI: 10.33549/physiolres.935282

L Wang, M Wang, X Tang, M Zhang, K Zhang, B Gao

{"title":"Mechanistic Studies of Cyclooxygenase-2 (COX-2) in Skeletal Muscle Cells During Rotator Cuff Injury: An In Vitro Study.","authors":"L Wang, M Wang, X Tang, M Zhang, K Zhang, B Gao","doi":"10.33549/physiolres.935282","DOIUrl":"10.33549/physiolres.935282","url":null,"abstract":"The mechanism of rotator cuff injury remains to be elucidated. And COX-2 plays a dual role in skeletal muscle injury and regeneration, would be associated with the development of rotator cuff injury. Therefore, we chose human skeletal muscle cells (HSKMC) as an in vitro muscle tissue model and transfected lentivirus with overexpressed COX-2 to simulate the in vitro environment of rotator cuff injury. To investigate the specific molecular biological mechanism of COX-2, transcriptome sequencing (RNA-Seq) was used to analyze the differentially expressed mRNAs in HSKMC overexpressing COX-2. Enrichment analysis was performed to analyze these differentially expressed genes and real-time quantitative PCR (RT-qPCR) was used to examine the mRNA levels of genes induced by overexpression. Subsequently, the role of COX-2 in cell proliferation was confirmed by cell counting kit-8 (CCK-8), and focal adhesion kinase (FAK) and signal transducer and activator of transcription 3 (STAT3) phosphorylation induced by COX-2 was utilized by western blotting (WB). The results showed that total of 30,759 differentially expressed genes were obtained, and the expression of CYP4F3 and GPR87 was significantly increased. COX-2 could bind CYP4F3 and GPR87 and co-localize with them in the cytoplasm. Finally, COX-2 promoted the proliferation of human skeletal muscle cells by activating the FAK and STAT3 pathways.","PeriodicalId":20235,"journal":{"name":"Physiological research","volume":"73 5","pages":"769-778"},"PeriodicalIF":1.9,"publicationDate":"2024-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11629944/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142639583","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

POLG p.A962T Mutation Leads to Neuronal Mitochondrial Dysfunction That is Restored After Mitochondrial Transplantation. POLG p.A962T突变导致神经元线粒体功能障碍，线粒体移植后可恢复。

IF 1.9 4区医学

Physiological research Pub Date : 2024-11-15 DOI: 10.33549/physiolres.935313

W Hu, C Shi, H Guo, B Zhang

{"title":"POLG p.A962T Mutation Leads to Neuronal Mitochondrial Dysfunction That is Restored After Mitochondrial Transplantation.","authors":"W Hu, C Shi, H Guo, B Zhang","doi":"10.33549/physiolres.935313","DOIUrl":"10.33549/physiolres.935313","url":null,"abstract":"Mutations in DNA polymerase gamma (POLG) are known as the predominant cause of inherited mitochondrial disorders. But how these POLG mutations disturb mitochondrial function remains to be determined. Furthermore, no effective therapy, to date, has been reported for POLG diseases. Using differentiated SH-SY5Y cells, a human neuronal model cell line, the current study investigated whether the novel POLG variant p.A962T impairs mitochondrial function. This involved quantifying mitochondrial DNA (mtDNA) content using PCR and assessing the expression levels of the subunits of complex IV (COXI-IV), a complex I subunit NDUFV1 and Cytochrome C (Cyto C) release using Western blotting. Activities of mitochondrial complex I, II, and IV were measured using colorimetric assays. Mitochondrial membrane potential (delta Psim) and ATP were evaluated using fluorescence assays and luminescent assays, respectively. In addition, we investigated whether mitochondrial transplantation (MT) using Pep-1-conjugated mitochondria could compensate for mitochondrial defects caused by the variant in cells carrying mutant POLG. The results of this study showed that POLG p.A962T mutation resulted in mitochondrial defects, including mitochondrial DNA (mtDNA) depletion, membrane potential (delta Psim) depolarization and adenosine triphosphate (ATP) reduction. Mechanistically, POLG mutation-caused mtDNA depletion led to the loss of mtDNA-encoded subunits of complex I and IV and thus compromised their activities. POLG p.A962T mutation is a pathogenic mutation leading to mitochondrial malfunction and mtDNA depletion in neurons. Cell-penetrating peptide Pep-1-mediated MT treatment compensated for mitochondrial defects induced by these POLG variants, suggesting the therapeutic application of this method in POLG diseases.","PeriodicalId":20235,"journal":{"name":"Physiological research","volume":"73 5","pages":"801-808"},"PeriodicalIF":1.9,"publicationDate":"2024-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11629961/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142639585","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Supplementing With Which Form of Creatine (Hydrochloride or Monohydrate) Alongside Resistance Training Can Have More Impacts on Anabolic/Catabolic Hormones, Strength and Body Composition? 在进行阻力训练的同时补充哪种形式的肌酸（盐酸或一水肌酸）会对合成代谢/代谢激素、力量和身体成分产生更大影响？

IF 1.9 4区医学

Physiological research Pub Date : 2024-11-15 DOI: 10.33549/physiolres.935323

E Eghbali, H Arazi, K Suzuki

{"title":"Supplementing With Which Form of Creatine (Hydrochloride or Monohydrate) Alongside Resistance Training Can Have More Impacts on Anabolic/Catabolic Hormones, Strength and Body Composition?","authors":"E Eghbali, H Arazi, K Suzuki","doi":"10.33549/physiolres.935323","DOIUrl":"10.33549/physiolres.935323","url":null,"abstract":"The purpose of this study was to determine the effects of resistance training (RT) alongside creatine-hydrochloride (Cr-HCl) or creatine monohydrate (CrM) supplementation on anabolic/catabolic hormones, strength, and body composition. Forty participants with an age range of 18-25 years were randomly divided into four groups (n=10): RT+Cr-HCl (0.03 g.kg-1 of body mass), RT+CrM-loading phase (CrM-LP) (0.3 g.kg-1 of body mass for five days (loading) and 0.03 g.kg-1 body mass for 51 days (maintenance)), RT+CrM-without loading phase (CrM-WLP) (0.03 g.kg-1 body mass), and RT+placebo (PL). The participants consumed supplements and performed RT with an intensity of 70-85 % 1RM for eight weeks. Before and after the training and supplementation period, strength (1RM), body composition (percent body fat (PBF), skeletal muscle mass (SMM), muscular cross-sectional area (MCSA)) and serum levels of testosterone, growth hormone (GH), insulin-like growth factor-1 (IGF-1), cortisol, adrenocorticotropic hormone (ACTH), follistatin and myostatin were measured. The results showed that in the supplementation groups, strength, arm and thigh MCSA, and SMM significantly increased, and PBF significantly decreased (P</=0.05); this change was significant compared to the PL group (P</=0.05). In addition, the results showed a significant increase in GH, IGF-1 levels, the ratio of follistatin/myostatin, testosterone/cortisol (P</=0.05), and a significant decrease in cortisol and ACTH levels (P</=0.05) in the supplementation groups. Hormonal changes in GH, IGF-1, testosterone/cortisol, cortisol, and ACTH levels in the supplementation groups were significant compared to the PL group (P</=0.05). The results showed that CrM and Cr-HCl significantly enhanced the beneficial effects of RT on strength, hypertrophy, and hormonal responses, with Cr-HCl showing no benefit over CrM.","PeriodicalId":20235,"journal":{"name":"Physiological research","volume":"73 5","pages":"739-753"},"PeriodicalIF":1.9,"publicationDate":"2024-11-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11629957/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142639586","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Cadmium-Induced Hepatotoxicity in Mice - Prophylactic Supplementation of Quercetin Exerts Hepatoprotective Effect by Modulating PI3K/Akt/NF-kappaB Signaling Pathway. 镉诱导的小鼠肝毒性--预防性补充槲皮素可通过调节 PI3K/Akt/NF-kappaB 信号通路发挥保肝作用

IF 1.9 4区医学

Physiological research Pub Date : 2024-11-12 DOI: 10.33549/physiolres.935252

L Liu, Q Zhao, J Huang, S Lei

{"title":"Cadmium-Induced Hepatotoxicity in Mice - Prophylactic Supplementation of Quercetin Exerts Hepatoprotective Effect by Modulating PI3K/Akt/NF-kappaB Signaling Pathway.","authors":"L Liu, Q Zhao, J Huang, S Lei","doi":"10.33549/physiolres.935252","DOIUrl":"10.33549/physiolres.935252","url":null,"abstract":"This current study seeks to examine the pre-protective function of Quercetin in Cadmium (Cd)-induced liver damage, along with its modulation of the PI3K/Akt/NF-kappaB signaling pathway. A total of 60 male C57BL/6J mice were randomly assigned to four groups: control (C), quercetin (Q, 100 mg/kg/day), Cd (Cd, 2.5 mg/kg/day), and quercetin and Cd (Q+Cd). Before receiving Cd treatment, quercetin was administered intragastrically for 4 weeks. In the present study, liver markers, oxidative stress parameters, pro-inflammatory cytokines, liver histopathology, apoptotic markers and PI3K/Akt/NF-kappaB signaling molecules were examined. We observed that the body weight of the Cd-treated mice dramatically rise after 4 weeks of quercetin pre-administration, and the Cd concentration was significantly decreased. Liver function markers like alanine transaminase (ALT), aspartate transaminase (AST), alkaline phosphatase (ALP), and lactate dehydrogenase (LDH) were significantly reduced in quercetin treatment in Cd-induced mice. Additionally, we observed that quercetin reduced Cd-mediated liver injury in mice by assessing the level of malondialdehyde (MDA), and the activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), and glutathione (GSH) concentrations and the histological alterations. By monitoring tumor necrosis factor-alpha (TNF-alpha), interleukin-6 (IL-6), and interleukin-1beta (IL-1beta), quercetin successfully reduced the inflammatory cytokines that the Cd metal caused in the liver. Additionally, in the liver tissues of Cd-mediated, quercetin could enhance the expression of Bcl-2 and decrease the expression of p-Akt, p-PI3K, Bax, Caspase-9, Caspase-3, NF-kappaB. In conclusion, quercetin protects against Cd induced liver injury via several pathways, including oxidative stress, inflammation and apoptosis, and its protective effect correlates with antioxidant activity.","PeriodicalId":20235,"journal":{"name":"Physiological research","volume":"73 5","pages":"703-716"},"PeriodicalIF":1.9,"publicationDate":"2024-11-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11629949/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142626595","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Anti-Müllerian Hormone Can Help With Predicting Ovarian Failure for Premenopausal Women Who Have Undergone Ablative Radioiodine Treatment for Thyroid Cancer. 抗缪勒氏管激素有助于预测因甲状腺癌接受放射性碘消融治疗的绝经前妇女的卵巢功能衰竭。

IF 1.9 4区医学

Physiological research Pub Date : 2024-11-12 DOI: 10.33549/physiolres.935247

B Havlínová, I Součková, K Kopořivová, J Doležal

{"title":"Anti-Müllerian Hormone Can Help With Predicting Ovarian Failure for Premenopausal Women Who Have Undergone Ablative Radioiodine Treatment for Thyroid Cancer.","authors":"B Havlínová, I Součková, K Kopořivová, J Doležal","doi":"10.33549/physiolres.935247","DOIUrl":"10.33549/physiolres.935247","url":null,"abstract":"Differentiated thyroid carcinoma is the most common endocrinological malignancy with an increasing incidence over the last 30 years, with women being more frequently affected. In indicated cases, total thyroidectomy followed by adjuvant radioiodine administration is performed, despite current trends towards less aggressive treatment. We would like to investigate the possible adverse effects of radioiodine (RAI) on ovarian function using a simple serum biomarker. Anti-Müllerian hormone (AMH) appears to be the best endocrine marker for assessing physiological age-related oocyte loss for healthy women. The aim of our ongoing prospective study is to determine serum AMH to estimate ovarian reserve for premenopausal women treated with RAI. Over the course of one year, 33 serum samples from women with thyroid cancer and 3 serum samples from healthy women were examined. AMH levels were compared before radioiodine treatment and at regular intervals after treatment. Mean of the AMH level was 5.4 ng/ml (n=33) prior to RAI. The average level of AMH decreased to 1.8 ng/ml in 4-6 months after treatment. In 22.2 % of patients AMH dropped to 0 ng/ml from a non-zero value. Thereafter, we observed an increase in AMH, the average value was 2.7 ng/ml in 8-12 months. We demonstrated a significant decrease in AMH shortly after radioiodine treatment and a subsequent trend of increase at one year after treatment. Consequently, predicting the adverse effects of radioiodine by assessing a serum biomarker could help to select an appropriate treatment strategy for young women planning pregnancy.","PeriodicalId":20235,"journal":{"name":"Physiological research","volume":"73 5","pages":"729-737"},"PeriodicalIF":1.9,"publicationDate":"2024-11-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11629958/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142626593","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Reproductomics: Exploring the Applications and Advancements of Computational Tools. 生殖组学：探索计算工具的应用和发展。

IF 1.9 4区医学

Physiological research Pub Date : 2024-11-12 DOI: 10.33549/physiolres.935389

P Sengupta, S Dutta, F Liew, A Samrot, S Dasgupta, M A Rajput, P Slama, A Kolesarova, S Roychoudhury

{"title":"Reproductomics: Exploring the Applications and Advancements of Computational Tools.","authors":"P Sengupta, S Dutta, F Liew, A Samrot, S Dasgupta, M A Rajput, P Slama, A Kolesarova, S Roychoudhury","doi":"10.33549/physiolres.935389","DOIUrl":"10.33549/physiolres.935389","url":null,"abstract":"Over recent decades, advancements in omics technologies, such as proteomics, genomics, epigenomics, metabolomics, transcriptomics, and microbiomics, have significantly enhanced our understanding of the molecular mechanisms underlying various physiological and pathological processes. Nonetheless, the analysis and interpretation of vast omics data concerning reproductive diseases are complicated by the cyclic regulation of hormones and multiple other factors, which, in conjunction with a genetic makeup of an individual, lead to diverse biological responses. Reproductomics investigates the interplay between a hormonal regulation of an individual, environmental factors, genetic predisposition (DNA composition and epigenome), health effects, and resulting biological outcomes. It is a rapidly emerging field that utilizes computational tools to analyze and interpret reproductive data, with the aim of improving reproductive health outcomes. It is time to explore the applications of reproductomics in understanding the molecular mechanisms underlying infertility, identification of potential biomarkers for diagnosis and treatment, and in improving assisted reproductive technologies (ARTs). Reproductomics tools include machine learning algorithms for predicting fertility outcomes, gene editing technologies for correcting genetic abnormalities, and single cell sequencing techniques for analyzing gene expression patterns at the individual cell level. However, there are several challenges, limitations and ethical issues involved with the use of reproductomics, such as the applications of gene editing technologies and their potential impact on future generations are discussed. The review comprehensively covers the applications and advancements of reproductomics, highlighting its potential to improve reproductive health outcomes and deepen our understanding of reproductive molecular mechanisms.","PeriodicalId":20235,"journal":{"name":"Physiological research","volume":"73 5","pages":"687-702"},"PeriodicalIF":1.9,"publicationDate":"2024-11-12","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11629954/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142626608","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

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