Histology and histopathology最新文献

Hip osteoarthritis (HOA) is the most common hip joint disorder, accounting for approximately 27.9% of all cases of osteoarthritis (OA), often leading to total hip replacement (THR). In the last decades, femoroacetabular impingement (FAI) has been addressed as a significant etiological factor in the development of early-onset HOA, especially in young adults with non-dysplastic hips. FAI has been found to cause damage to all joint tissues, cartilage, labrum, and subchondral bone, thus underlining the importance of an early diagnosis and intervention to prevent progression to end-stage disease. This review aims to provide a comprehensive overview of the biochemical, morphological, and cellular alterations occurring in hip joint tissues in the presence of FAI. Understanding the early pathological changes is of crucial importance as they often precede radiographic signs of disease and may serve as valuable biomarkers for early detection and management of FAI and peri-arthritic conditions to delay or prevent the need for THR in younger populations.

Background: Stroke is a crucial cause of morbidity and mortality worldwide. The regulator of G protein signaling 14 (RGS14) plays important roles in mediating multiple signaling pathways and various pathophysiological processes. However, the function of RGS14 in cerebral ischemic reperfusion injury (CIRI) remains unknown.

Methods and results: In this study, the roles of RGS14 during CIRI were studied in terms of gain- and loss-of-function experiments. Using RT-PCR, western blot, and TCC, HE, TUNEL, immunofluorescence, immunohistochemical staining, etc., we found that RGS14 significantly improved CIRI by reducing inflammation and apoptosis in both a mouse model of transient middle cerebral artery occlusion (t/MCAO) and a primary neuronal model of oxygen-glucose deprivation/reperfusion (OGD/R). In addition, mechanism studies have shown that RGS14 acts by inhibiting the activation of the TAK1-JNK/p38 signaling pathway, which was further confirmed using the TAK1 inhibitor (iTAK1), 5Z-7-oxyzeaenol, during OGD/R treatment of AdshRGS14-infected primary neurons.

Conclusions: These findings imply that RGS14 is a novel negative regulator and may serve as a potential therapeutic target for CIRI.

The age-standardized point prevalence of global osteoarthritis (OA) has increased, and OA will not only lead to disability in patients but also to a greater psychological burden. In recent years, the focus of scientists on treating OA has turned to disease prevention and treatment of early OA. Previous studies have proved that WuFu Decoction (WFD) could protect chondrocytes, and the Chinese herbs in this prescription have shown anti-inflammatory effects. In this study, we built the OA rat model by the modified Hulth method, conducted research with WFD, and set D-Glucosamine sulfate as the positive control. It is proven that WFD improved the micromorphology and tissue damage of the knee joint, decreased the score of the Mankin and OARSI system, and inhibited the IL-1β, TNF-α, MMP-13, and CTX-1 levels in serum. Additionally, WFD treatment inhibited p-ERK1/2 levels and raised the mRNA and protein levels of TGF-β1, p-Smad2, p-Smad3, type II collagen (the gene is COL2A1), ALP, TRACP, and BMP7. Furthermore, TGF-β1 inhibitor (Decorin) reversed the improvement effect of WFD on OA, but ERK1/2 inhibitor (PD98059) promoted this improvement effect. Silencing TGFβR2 can reverse the protective effect of WFD on primary chondrocytes. It is suggested that WFD can improve OA and chondrocytes by regulating the TGF-β1/Smad and ERK1/2 pathways. This study also identified active ingredients, such as Fumaric acid, Glycyrrhizic acid, Albiflorin, and Isoliquiritigenin. It provides a basis for the clinical application of WFD and for the promotion and development of TCM.

Purpose: Synovial pathology impacts joint disease progression and clinical outcome. The goal of this study was to modify Krenn synovitis score for more accurate and comprehensive evaluation of common orthopaedic joint conditions.

Methods: A total of 31 synovial samples were collected during foot and ankle surgery. Synovial sections were stained with hematoxylin and eosin and picrosirius red. Immunohistochemistry for CD3 and α-smooth muscle actin (α-SMA) were performed for inflammatory infiltration and fibroblast activation. Synovitis was evaluated with Krenn synovitis score and a modified Krenn synovitis score (MKSS), where the original subcategories of inflammatory infiltration and stromal cellularity were replaced with the density of CD3⁺T cells and collagen intensity, respectively.

Results: Of 31 synovial samples, the average Krenn synovitis score was 1.5±1.3 and MKSS was 1.8±1.2 (p>0.05). The two scores were positively correlated in assessing synovial pathology (r=0.6; p<0.001). The dominant subcategory shifted from stromal cellularity (64%) in Krenn synovitis score to the density of CD3⁺T cells (80%) in MKSS. By MKSS classification, but not Krenn synovitis score, type III collagen intensity and the ratio of type III over type I collagen increased in the synovitis group. The density of α-SMA⁺cells did not correlate with the intensity of synovial collagen and was not different between synovitis and non-synovitis samples.

Conclusion: While maintaining the concept and basic elements of the Krenn synovitis score, MKSS incorporated more details of synovial pathology, particularly inflammatory infiltration and fibrosis. It could provide a more comprehensive evaluation of synovial pathology in common orthopaedic joint conditions.

Polycystic Ovary Syndrome (PCOS) is a condition causing histopathological alterations in the ovarian stroma. Telocytes (TCs) are specialized interstitial/stromal cells present in the connective tissue of various organs. In this study, we investigated the presence and spatial organization of TCs in the ovaries of a rat model of PCOS induced by dehydroepiandrosterone (DHEA). The ovarian tissues from both PCOS and control groups were stained using hematoxylin-eosin (H&E), Bielschowsky's silver stain, methylene blue, and toluidine blue for light microscopy analysis, and scanned digitally. Ovaries were marked with double-labeled immunofluorescence with CD34/estrogen receptor-α (ER-α) and vimentin/progesterone receptor-A (PR-A) and evaluated with a confocal microscope. The ultrastructure and telopodes (TPs) of TCs were also examined by transmission electron microscopy. TCs were identified in both groups, localized within follicular walls, adjacent to follicles, in stromal regions distant from the follicles, and perivascular areas. CD34/ER-α and vimentin/PR-A cells were significantly increased in PCOS. In conclusion, TCs were preserved in the DHEA-induced PCOS model, and according to our quantitative analysis, their ultrastructural features were unaffected by the PCOS microenvironment. Our findings suggest a potential association between TCs and the pathophysiology of PCOS. Further studies are necessary to elucidate the functional relationship of TCs in the development and progression of PCOS.

Ocular adnexal lymphomas (OALs) are a heterogeneous group of malignant lymphoproliferative tumors originating from clonal proliferations of lymphocytes, with a multifactorial etiopathogenesis. They can be distinguished in primary, involving ocular adnexa, and secondary, affecting also an additional site. Pathologically OALs encompass four histological subtypes with different biological behaviour and prognosis. The diagnosis relies on clinical manifestations, imaging and histopathological examinations. Clinical symptoms are classified in ophthalmologic, often nonspecific, and constitutional, indicating a systemic involvement. As regards cross-sectional imaging, computed tomography (CT) and magnetic resonance imaging (MRI) play a complementary role, nevertheless MRI outperforms other imaging methods due to the possibility to perform functional techniques such as diffusion-weighted imaging (DWI) and perfusion-weighted imaging (PWI). At conventional MRI, OALs demonstrate iso- or hypointensity on T1-weighted and T2-weighted sequences relative to cerebral cortex; enhancement is usually homogeneous. PWI and particularly DWI can be useful in discriminating OALs from benign orbital lymphoproliferative disorders (OLPDs) and from other malignant intraorbital tumors, since OALs, due to their high cellularity, demonstrate diffusion restriction with considerably low apparent diffusion coefficient value. Biopsy is needed for final diagnosis and accurate subtyping and grading. Differential diagnosis of OALs, in addition to benign OLPDs, includes granulomatous diseases, metabolic diseases, epithelial neoplasms and metastases. Structured report can be useful to make reporting of imaging findings more accurate and to improve communication between ophthalmologist and radiologist; moreover, it can represent a valuable decision‑supporting tool to assist the multidisciplinary management of the disease. Treatment options include systemic chemotherapy, radiotherapy, immunotherapy and surgical excision.

Periostin is involved in airway remodeling, salivary tumors, and various otolaryngological diseases. D-β-aspartic acid is the major isomer of D-aspartic acid found in the tissues of elderly individuals. In this study, we investigated the expression and role of D-β-aspartic acid and periostin in the formation of benign parotid tumors. The data of 36 patients (16 male and 20 female) who underwent parotid tumor resection between April 2017 and March 2022 and were clinically and pathologically diagnosed as having benign parotid tumors were included in this study. The mean age of the patients was 59.2 (range 26-82) years. Tumors were histologically classified as pleomorphic adenomas, Warthin's tumors, basal cell adenomas, oncocytomas, and myoepitheliomas. Increased D-β-aspartic acid expression was observed in the epithelium and stroma of benign parotid tumors. In the epithelium, D-β-aspartic acid was found in 35 of 38 samples (92.1%). In the stroma, it was found in 19 of 38 samples (50.0%). In the stroma of benign parotid tumors, increased expression of periostin was found in 32 of 38 samples (84.2%). Four periostin expression patterns were observed in benign parotid tumors: negative, superficial, infiltrative, and diffuse. Statistically significant differences were found between the expression pattern of D-β-aspartic acid in the stroma and the histological classification of benign parotid gland tumors. In addition, a statistically significant difference was found between the expression patterns of D-β-aspartic acid and periostin in the stroma. Our results suggest that D-β-aspartic acid and periostin may be involved in the pathogenesis of benign parotid gland tumors.

Background: NUT carcinoma (NC), formerly known as NUT midline carcinoma, is a rare but highly aggressive cancer. It is a poorly differentiated carcinoma characterized by rearrangements of the NUTM1 (nuclear protein in Testis) gene with a member of the bromodomain-containing protein (BRD) family gene, usually BRD4. There is limited knowledge about primary pulmonary NC till now. It is probably underestimated or underdiagnosed because of its poorly differentiated character, misleading immunophenotype, and wide range of differential diagnoses.

Method: We report here two cases of pulmonary NC with different clinicopathological and molecular presentations to draw attention to some atypical clinicopathologic features that can help clinicians and pathologists consider this rare entity.

Results: The first case shows a nested pattern with small, uniform, blue epithelioid cells and aberrant expression of neuroendocrine markers, which has a known BRD3::NUTM1 fusion accompanied by a novel IGR (downstream ROR2)::NUTM1 fusion. The second case demonstrates solid sheets and cords of eosinophilic epithelioid-polygonal cells with a mucoid stroma and TTF1 expression, which has a novel SPECC1::NUTM1 gene fusion accompanied by TP53 and JAK1 gene oncogenic variants.

Conclusion: As a result, our study contributes to expanding the variant spectrum of the NUTM1 gene. NUT carcinoma with different fusion partners seems to have unique clinicopathological characteristics, yet more cases need to accumulate experience.

Background and aims: This study aimed to investigate the mechanism and efficacy of chelerythrine (CHE) in treating carbon tetrachloride (CCl₄)-induced liver fibrosis, with a particular focus on the nuclear factor-erythroid-related factor-2 (Nrf2) and nuclear factor-kappa-B (NF-κB) signaling pathways.

Methods: Mice were induced with CCl₄ for eight weeks and categorized into the control group, CCl₄ model group, and CHE low (7 mg/kg/d, ig,), medium (14 mg/kg/d, ig), and high-dose (28 mg/kg/d, ig) groups with 10 animals in each group. Following CHE treatment, liver sample morphology was assessed using multiple immunohistochemistry, and serum biochemical indicators were measured. ELISA was used to determine IL-10, IL-1β, and TNF-α contents. Western blotting and RT-PCR were employed to analyze protein and mRNA levels of α-SMA, Col-I, fibronectin, Nrf2, HO-1, NQO1, GCLc, GCLm, NF-κB, p-NF-κB, IκBα, and p-IκBα. Nrf2 knockout mice were used to assess the impact of CHE on the Nrf2 signaling pathway.

Results: The findings demonstrated that CHE significantly ameliorated oxidative damage, inflammatory response, and liver fibrosis in CCl₄-induced mice. CHE treatment increased Nrf2 expression and its target proteins, including HO-1 and GCLc, an effect not observed in Nrf2 knockout mice. In addition, CHE reduced NF-κB expression levels.

Conclusions: These results suggest that CHE can alleviate liver fibrosis in CCl₄-induced mice by modulating NF-κB/IκBα and Nrf2 signaling pathways. These findings propose CHE as a potential novel anti-liver fibrosis drug.

Background: This study aimed to preliminarily explore the differences between paravaginal and central defect types of anterior vaginal wall prolapse based on DeLancey's pelvic floor theory.

Methods: Seventy-eight patients with normal, paravaginal, or central defect vaginal wall tissues were collected and stained using hematoxylin and eosin (HE) and immunofluorescence staining to analyze and identify the expression of vimentin and phosphohistone H3 (PH3). Ribonucleic acid from fresh tissues was extracted for transcriptome sequencing to analyze differences between paravaginal and central defect types of anterior vaginal wall prolapse.

Results: Significant differences were found in age, menopausal status, body mass index, pregnancy, and delivery among the control, paravaginal, and central defect groups. Histological analysis revealed that the distribution of interstitium in the normal HE staining group was compact and continuous. In the paravaginal defect interstitium, fiber morphology was altered, while central defect interstitial fibers were fragmented. PH3 expression was significantly lower in the central defect type than in the normal and paravaginal defect groups, suggesting degenerative lesions in the vaginal mucosa with central defects. Vimentin distribution in the normal group was tightly packed and continuous, whereas, in the paravaginal defect interstitium, vimentin filaments were fragmented into small spots and micro-aggregates. In the central defect interstitium, vimentin micro-aggregates exhibited altered coalescence and cell shape, appearing punctate. These findings indicated degenerative lesions in the anterior vaginal interstitium of both paravaginal and central defect types. KEGG enrichment analysis of differential genes revealed their involvement in proteinaceous extracellular matrix (ECM)-related signaling pathways, with increased expression of matrix metalloproteinase 13 (MMP13), MMP3, MMP12, and MMP7 in the paravaginal defect type compared with the central defect type.

Conclusion: The differences between paravaginal and central defect types of anterior vaginal wall prolapse may be related to the expression of MMP-related proteins; KEGG enrichment analysis of differential genes indicated that they were closely related to the protein ECM pathway. Moreover, delineative lesions appeared in the paravaginal defect interstitium, and degenerative lesions appeared in the central defect mucosa and interstitium, which further enriched the DeLancey three-level theory.