Histology and histopathology最新文献

{"title":"Time course analysis of changes in neuronal loss, oxidative stress, and excitotoxicity in gerbil hippocampus following ischemia and reperfusion under hyperthermic conditions.","authors":"Tae-Kyeong Lee, Dae Won Kim, Joon Ha Park, Choong-Hyun Lee, Se-Ran Yang, Myoung Cheol Shin, Moo-Ho Won, Jun Hwi Cho, Ji Hyeon Ahn","doi":"10.14670/HH-18-840","DOIUrl":"https://doi.org/10.14670/HH-18-840","url":null,"abstract":"<p><p>Oxidative stress and excitotoxicity are the major causes of neuronal death/loss in the brain following ischemia and reperfusion (IR). Hyperthermia is known to exacerbate ischemic neuronal damage; however, the underlying mechanisms remain unclear. This study investigated the mechanisms underlying neuronal damage caused by IR injury (IRI) under hyperthermic conditions in the gerbil hippocampal CA1 region. Gerbils were controlled at normothermia (37.5±0.2°C) or hyperthermia (39.5±0.2°C). After temperature control for 30 min, the animals received IRI (following 5 min of transient forebrain ischemia) or sham ischemia, and were subsequently sacrificed at 0, 3, 6, 12, 24, 48, and 120h after IRI. Neuronal death was examined using neuronal nuclear antigen immunohistochemistry and Fluoro-Jade B histofluorescence. Oxidative stress was analyzed by immunohistochemistry for 8-Hydroxy-2'-deoxyguanosine (8OHdG) and superoxide dismutase 2 (SOD2). Excitotoxicity was investigated by immunohistochemistry and western blotting for glutamate transporter 1 (GLT1). Immunohistochemical staining for glial fibrillary acidic proteins (GFAP) was performed to detect reactive astrogliosis. Loss of pyramidal neurons was detected earlier (48h post-IRI) in the hyperthermia-IRI group than in the normothermia-IRI group (120h post-IRI). Further, 8OHdG and SOD2 immunoreactivity in the hyperthermia-IRI group was significantly higher than that in the normothermia-IRI group. Changes in GLT1 immunoreactivity in both groups were biphasic, indicating that the immunoreactivity and protein levels were significantly lower in the hyperthermia-IRI group. GFAP immunoreactivity was enhanced following neuronal loss, indicating that the immunoreactivity was significantly higher in the hyperthermia-IRI group. Taken together, these results suggest that brain IR under hyperthermic conditions can aggravate neuronal damage in the hippocampal CA1 region through severe oxidative stress and excitotoxicity.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18840"},"PeriodicalIF":2.5,"publicationDate":"2024-10-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142619272","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}

{"title":"Ferroptosis: A key regulator and potential target for tissue injury.","authors":"Ruihan Liu, Qing Luo, Guanbin Song","doi":"10.14670/HH-18-838","DOIUrl":"https://doi.org/10.14670/HH-18-838","url":null,"abstract":"<p><p>The maintenance of iron homeostasis is essential for proper body function. A growing body of evidence suggests that iron imbalance is the common denominator in many tissue injuries, including acute, chronic, and reperfusion injuries. Ferroptosis, a novel form of programmed cell death due to metabolic abnormalities, has become increasingly recognized as an important process mediating the pathogenesis and progression of numerous tissue injuries, including cerebral, myocardial, lung, liver, kidney, and intestinal injuries. Therefore, a thorough understanding of the mechanisms involved in the regulation of ferroptosis might contribute to improvements in disease management. In this review, we summarize the importance of ferroptosis in various tissue injuries, discuss the potential targets of ferroptosis in the treatment of tissue injuries, and describe the current limitations and future directions of these novel treatment targets.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18838"},"PeriodicalIF":2.5,"publicationDate":"2024-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142619269","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}

{"title":"Experimental murine models of interstitial cystitis/bladder pain syndrome: A review.","authors":"Tetsuichi Saito, Tomonori Minagawa, Naoki Yoshimura, Yi Luo, Yoshiyuki Akiyama","doi":"10.14670/HH-18-837","DOIUrl":"https://doi.org/10.14670/HH-18-837","url":null,"abstract":"<p><p>Interstitial cystitis/bladder pain syndrome (IC/BPS) is a chronic enigmatic disease of the urinary bladder characterized by persistent bladder/pelvic pain in conjunction with lower urinary tract symptoms. IC/BPS is categorized as either Hunner-type IC (HIC) or BPS based on the presence/absence of the Hunner lesion, a reddish mucosal lesion in the bladder. HIC and BPS present with similar symptoms, however, the etiologies are completely different. Recent evidence suggests that HIC is an immune-mediated inflammatory disease of the urinary bladder. In contrast, BPS, other forms of HIC lacking Hunner lesions, is a minimally inflamed condition comprising various clinical phenotypes. Based on this evidence, basic research into IC/BPS has shifted to target each subtype of IC/BPS. Today, experimental murine models of autoimmune cystitis are used for HIC research, whereas models related to neurophysiological and psychosocial dysfunctions have been developed for BPS research. This emerging concept of a subtype-tailored approach may contribute to a better understanding of the full picture of IC/BPS, thereby improving current clinical management strategies and the development of novel therapies.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18837"},"PeriodicalIF":2.5,"publicationDate":"2024-10-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142619267","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}

{"title":"Impact of 6-OHDA injection and microtrauma in the rat <i>substantia nigra</i> on local brain amyloid beta protein concentrations in the affected area.","authors":"Joshua A Roldán-Kalil, Sara E Vendrell-Gonzalez, Natalia Espinosa-Ponce, Jadier Colón-Vasques, Jescelica Ortiz-Rivera, Vassiliy Tsytsarev, Janaina M Alves, Mikhail Inyushin","doi":"10.14670/HH-18-836","DOIUrl":"10.14670/HH-18-836","url":null,"abstract":"<p><p>Amyloid beta peptides (Aβ) are key indicators of Alzheimer's disease and are also linked to cognitive decline in Parkinson's disease (PD) and other neurodegenerative disorders. This study explored the accumulation of Aβ in a standard 6-Hydroxydopamine (6-OHDA) model of PD. We unilaterally injected 6-OHDA into the <i>substantia nigra</i> of Wistar rats to induce dopaminergic cell degeneration and death, a characteristic of PD. The goal was to detect Aβ protein in tissues and blood vessels showing inflammation or degeneration from the 6-OHDA injection. Our results showed that 6-OHDA injection produced a statistically significant rise in Aβ concentration at the injection site 60 minutes after injection, which was slightly reduced 24 hours post-injection but still significantly higher than in controls. We also tried Gp120 injection in the same zone but it only produced effects comparable to control needle trauma. The presence of Aβ in tissues and blood vessel walls after injection was confirmed through ELISA tests and was supported by immunohistochemical staining of injection areas. We found that the increased Aβ concentration was visible in and around blood vessels and inside blood vessel walls, and also, to a lesser extent in some cells, most probably neurons, in the area. This research highlights the connection between dopaminergic cell poisoning and the accumulation of Aβ, offering insights into the progression of PD to cognitive disorders and dementia.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18836"},"PeriodicalIF":4.6,"publicationDate":"2024-10-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142603915","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}

{"title":"USP33 promotes pulmonary microvascular endothelial cell pyroptosis by stabilizing TRAF2 through deubiquitination.","authors":"Jianping Liang, Junbo Chen, Pengfei Xu","doi":"10.14670/HH-18-835","DOIUrl":"10.14670/HH-18-835","url":null,"abstract":"<p><strong>Objective: </strong>Inhibiting the pyroptosis of human pulmonary microvascular endothelial cells (HPMECs) is a promising therapeutic modality for acute lung injury (ALI). Given the undefined effect of ubiquitin-specific protease 33 (USP33) and tumor necrosis factor receptor-associated factor 2 (TRAF2) on pyroptosis in lung injury, this study investigates their roles in the pyroptosis of HPMECs during ALI.</p><p><strong>Methods: </strong>The hypoxia/reoxygenation (H/R)-induced model was constructed in HPMECs. Cell viability, cytotoxicity, and cell death were determined by the cell counting kit-8 (CCK-8), Lactate dehydrogenase (LDH), and Hoechst-PI staining, respectively. Western blot and qRT-PCR were used to detect protein and gene expression levels of pyroptosis-related markers, respectively. The TRAF2 ubiquitination level was measured via immunoprecipitation.</p><p><strong>Results: </strong>USP33 and TRAF2 expressions were elevated in H/R-induced HPMECs. Knockdown of USP33 increased cell viability and inhibited cellular pyroptosis, accompanied by decreases in IL-1β, IL-18, and Caspase-1. USP33 stabilized TRAF2 by deubiquitination. TRAF2 overexpression reversed the effect of USP33 silencing on suppressing HPMEC pyroptosis.</p><p><strong>Conclusion: </strong>USP33 stabilizes TRAF2 by deubiquitination to promote HPMEC pyroptosis during ALI.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18835"},"PeriodicalIF":2.5,"publicationDate":"2024-10-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142590648","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}

{"title":"E2F1-induced upregulation of <i>TROAP</i> contributes to endometrial cancer progression.","authors":"Shanshan Wang, Yidan Sun, Minjing Guo, Ping Zhu, Beibei Xin","doi":"10.14670/HH-18-834","DOIUrl":"https://doi.org/10.14670/HH-18-834","url":null,"abstract":"<p><strong>Purpose: </strong>To investigate the role of Trophinin-associated protein (TROAP) in endometrial cancer (EC) progression and elucidate how the transcription factor E2F transcription factor 1 (E2F1) modulates EC by upregulating <i>TROAP</i> expression.</p><p><strong>Methods: </strong><i>TROAP</i> expression in EC tissues and cell lines was analyzed using bioinformatics databases, quantitative real-time polymerase chain reaction (qRT-PCR), western blot, and immunohistochemistry. <i>TROAP</i> was knocked down in EC cells to assess its effects on proliferation, migration, invasion, and glycolysis. Potential transcription factors regulating <i>TROAP</i> were identified, and the relationship between E2F1 and <i>TROAP</i> gene regulation was examined using dual luciferase assay. <i>In vivo</i> tumor growth was evaluated using a mouse xenograft model.</p><p><strong>Results: </strong><i>TROAP</i> was overexpressed in EC tissues and cell lines compared with normal controls. High <i>TROAP</i> expression correlated with poor differentiation, advanced stage, lymph node metastasis, and worse overall survival in EC patients. Knockdown of <i>TROAP</i> inhibited the proliferation, migration, invasion, and glycolytic capacity of EC cells. E2F1 was identified as a transcriptional activator of TROAP. E2F1 overexpression enhanced <i>TROAP</i> expression and promoted EC cell proliferation, migration, and glycolysis in a TROAP-dependent manner. <i>TROAP</i> knockdown suppressed tumor growth <i>in vivo</i>.</p><p><strong>Conclusion: </strong><i>TROAP</i> is transcriptionally activated by E2F1 and promotes EC progression by enhancing cell proliferation, metastasis, and glycolysis. The E2F1-TROAP axis may serve as a potential therapeutic target for EC treatment.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18834"},"PeriodicalIF":2.5,"publicationDate":"2024-10-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142582756","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}

{"title":"The role of the Ki-67 labelling index as an independent prognostic factor in indonesian glioma patients.","authors":"Ery Kus Dwianingsih, Sofia Pranacipta, Emilia Theresia, Sekar Safitri, Rachmat Andi Hartanto, Rusdy Ghazali Malueka","doi":"10.14670/HH-18-833","DOIUrl":"https://doi.org/10.14670/HH-18-833","url":null,"abstract":"<p><strong>Introduction: </strong>Gliomas are the most common type of brain tumor. However, interpreting glioma morphology is subjective, and identifying mitosis can be challenging. This can impact the determination of the patient's tumor grade, therapy, and prognosis. In addition, the Ki-67 expression level, which reflects the tumor cells' ability to proliferate, is closely related to the patient's survival. This study aims to find a correlation between Ki-67 expression and the overall survival (OS) of glioma patients in the Indonesian population.</p><p><strong>Methods: </strong>Ninety-one glioma patients from Sardjito General Hospital were collected for formalin-fixed embedded paraffin (FFPE) samples, and the Ki-67 labeling index (LI) was calculated by determining the percentage of labeled nuclei per 1000 cells using a 40x objective lens in a randomized area (average method). The OS was calculated from the day of pathology diagnosis until death or the last follow-up (for censored cases). Kaplan-Meier survival analysis was used to analyze the OS.</p><p><strong>Results: </strong>Individuals aged ≥60 with high-grade tumors, infratentorial gliomas, and a Ki-67 LI ≥10% had a shorter OS. The p-values associated with these factors were 0.001, 0.018, and 0.006, respectively. In multivariate analysis, age and tumor grade did not significantly correlate with OS.</p><p><strong>Conclusion: </strong>Glioma patients with a Ki-67 LI ≥10% have a significantly shorter OS than those with a lower Ki-67 LI, indicating that Ki-67 LI is an independent prognostic factor in Indonesian glioma patients.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18833"},"PeriodicalIF":2.5,"publicationDate":"2024-10-15","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142576044","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}

{"title":"Aerobic exercise remodels gut microbiota to alleviate cerebral ischemia-reperfusion injury.","authors":"Mingjin Zhu, Jiajie Zhu, Jiafei Pan, Rui Fu, Guoyuan Pan, Jie Zhang","doi":"10.14670/HH-18-832","DOIUrl":"10.14670/HH-18-832","url":null,"abstract":"<p><p>Aerobic exercise exhibits a neuroprotective role against cerebral ischemia-reperfusion (I/R) injury, and the present study explored the underlying mechanisms. Adult Sprague-Dawley rats (n=87) were used in the study, and cerebral I/R injury in rats was modeled using middle cerebral artery occlusion and reperfusion (MCAOR), followed by interval aerobic exercise training at a moderate intensity. Colonization with gut microbiota from the trained rats was performed on MCAOR rats. Neurobehavioral assessments were performed. Cerebral infarction and neuronal damage were detected by tissue staining and molecular experiments. Gut microbiota composition was analyzed by 16S rRNA gene sequencing. Neuroinflammation was detected using an enzyme-linked immunosorbent assay. Aerobic exercise ameliorated neurological deficit, spontaneous locomotor activity, and spatial learning and memory impairment in MCAOR rats (<i>P</i><0.001). Further, aerobic exercise decreased infarct volume, attenuated neuronal damage, increased SYN1 and PSD95 expression, as well as reduced neuroinflammation by upregulating IL-10 and downregulating IL-6, TNF-α, IL-17, and TGF-β in MCAOR rats (<i>P</i><0.05). Aerobic exercise altered gut microbiota composition in MCAOR rats. Gut microbiota colonization in rats alleviated cerebral I/R injury by reducing neurological deficit scores, promoting spontaneous locomotor activity, decreasing infarct volume, elevating SYN1 and PSD95 expression, and improving neuroinflammation (<i>P</i><0.05). In conclusion, aerobic exercise remodeled the gut microbiota in rats to attenuate cognitive dysfunction and neuroinflammation after cerebral I/R.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18832"},"PeriodicalIF":2.5,"publicationDate":"2024-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142619265","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}

{"title":"Associations between BCL-2 expression and different histopathological prognostic factors in different molecular subtypes of invasive breast carcinoma of no special type.","authors":"Wael Abdo Hassan, Mohamed El-Assmy, Ahmed Kamal ElBanna, Ihab Harbieh, Noha Noufal, Hany Lotfy, Tarek Abdelaziz Hasan Shemais, Ossama Ashour Haikal, Mostafa Magdy Saber, Rehab Ibrahim Ali","doi":"10.14670/HH-18-831","DOIUrl":"https://doi.org/10.14670/HH-18-831","url":null,"abstract":"<p><strong>Background: </strong>Breast cancer is heterogeneous and the existing prognostic classifiers are limited in accuracy, leading to the unnecessary treatment of numerous women. B-cell lymphoma 2 (BCL-2), an anti-apoptotic protein, has been proposed as a marker of poor prognosis, associated with resistance to therapy in most tumor types expressing BCL-2. In breast cancer, however, BCL-2 expression has been reported to be a favorable prognostic factor. This study aimed to describe the association between BCL-2 and other well-known pathological prognostic markers among different molecular sub-types of invasive breast carcinoma of no special type (IBC; NST).</p><p><strong>Methods: </strong>BCL-2 expression, as well as that of estrogen receptor (ER), progesterone receptor (PR), and human epidermal growth factor receptor 2 (HER2), were immunohistochemically (IHC) evaluated and compared with other pathological factors, including tumor size, grade, tumor-infiltrating lymphocytes (TILs), lymph-vascular invasion (LVI), and lymph node (LNd) metastasis, in 128 breast cancer cases diagnosed with IBC; NST. Moreover, we analyzed the correlation between BCL-2 expression and relapse-free survival (RFS) in all patients over a two-year period.</p><p><strong>Results: </strong>We found that BCL-2 expression had different pathological prognostic factor associations with different molecular subtypes of breast carcinoma. In the luminal A (i.e., hormonal receptor-positive and HER2-negative) and triple-negative subtypes, the expression of BCL-2 in tumor cells was significantly associated with tumor size, tumor grade, and TILs. BCL2-positive expression in luminal IBC; NST patients resulted in a significantly favorable two-year survival.</p><p><strong>Conclusion: </strong>BCL-2 expression in IBC; NST has different prognostic effects depending on the molecular subtype of the cancer. In cancers with a HER2-enriched phenotype, BCL-2 expression was a marker of poor prognosis, while in cancers with a hormone receptor-positive phenotype, BCL-2 expression had a better prognostic impact.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18831"},"PeriodicalIF":2.5,"publicationDate":"2024-10-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142567908","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}

{"title":"Does old-to-young kidney transplantation rejuvenate old donor kidneys?","authors":"Mayumi Takahashi-Kobayashi, Kunio Kawanishi, Joichi Usui, Satoshi Yamazaki, Surya V Seshan, Kunihiro Yamagata","doi":"10.14670/HH-18-829","DOIUrl":"https://doi.org/10.14670/HH-18-829","url":null,"abstract":"<p><strong>Background: </strong>The number of older organ donors is increasing due to the aging population. Aged kidneys often face problems such as delayed graft function but previous murine experiments suggested the possibilities of rejuvenation, for example, in a parabiosis setting between old and young mice. To investigate kidney-graft rejuvenation, we compared an old-to-young (O-Y) patient transplantation group and a transplantation group with donors/recipients of approx. the same age (SA) with the renal senescence marker p16 in kidney biopsy samples at baseline and one year post-transplantation.</p><p><strong>Methods: </strong>We retrospectively analyzed our hospital's 32 cases of living-donor ABO-compatible transplants performed between 2013-2020. Both the baseline and one-year biopsy (n=9) or only the baseline biopsy (n=32) were analyzed. We divided the nine cases into an O-Y group (donors' median age 68 yrs, recipients 41, difference -27) and an SA group (donors' median age 53 yrs, recipients 51.5, difference -3.5). p16 was stained with the clones JC8 and E6H4 to determine the precise p16-positive rate.</p><p><strong>Results: </strong>The 32 baseline biopsies' p16-positive rate was weakly related to donor age, suggesting that the p16-positive rate can help evaluate kidney senescence. The (n=5) O-Y group's p16-positive rates were at baseline 0.08 and one year 0.12; the (n=4) SA group's rate was 0.03 at both baseline and one year.</p><p><strong>Conclusions: </strong>No kidney rejuvenation was observed, even when old donor kidneys went to young recipients.</p>","PeriodicalId":13164,"journal":{"name":"Histology and histopathology","volume":" ","pages":"18829"},"PeriodicalIF":2.5,"publicationDate":"2024-10-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142545179","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}