The muscular branching patterns of the ulnar nerve in fetal forearms

xlomafota13 shared this article with you from Inoreader The muscular branching patterns of the ulnar nerve in fetal forearms Via radiol anat Surg Radiol Anat. 2022 Jan 23. doi: 10.1007/s00276-021-02870-y. Online ahead of print. ABSTRACT OBJECTIVE: We aimed to present our findings systematically by examining the muscular branching patterns of the ulnar nerve (UN) in the forearms of fetuses. METHODS: This study was conducted on the 52 forearms of 26 formalin-fixed fetal cadavers with gestational ages varying between 19 and 37 weeks. The anatomical dissection was performed by using stereomicroscope with × 8 m agnification. The numbers of muscular branches leaving UN and their order of leaving main nerve were noted down. The findings were classified according to the muscles they reached, and branching typing was done. RESULTS: It was found that a total of 2-6 muscular branches left UN to reach flexor carpi ulnaris (FCU) and flexor digitorum profundus (FDP). UN was classified by separating into five main types according to the number of muscular branches, and these types were classified into 16 different branching patterns according to the order of branches leaving from the main trunk and going to FCU and FDP. The pattern where two branches left UN was classified as Type I (n = 6), three branches left was classified as Type II (n = 18), four branches left was classified as Type III (n = 24), five branches left was classified as Type IV (n = 3), and six branches left was classified as Type V (n = 1). Martin-Gruber connection occurred in 17 (32.7%) fetal forearms. CONCLUSION: We believe that the information that UN can demonstrate different branching patterns on the forearm can help the surgeons to prevent complications that may develop in potential nerve injury during the selection and transfer of relevant branch. PMID:35066639 | DOI:10.1007/s00276-021-02870-y View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Transplantation of IL-1β siRNA-modified bone marrow mesenchymal stem cells ameliorates type II collagen-induced rheumatoid arthritis in rats

xlomafota13 shared this article with you from Inoreader Transplantation of IL-1β siRNA-modified bone marrow mesenchymal stem cells ameliorates type II collagen-induced rheumatoid arthritis in rats Via Experimental and therapeutic medicine Exp Ther Med. 2022 Feb;23(2):139. doi: 10.3892/etm.2021.11062. Epub 2021 Dec 14. ABSTRACT Rheumatoid arthritis (RA) is a chronic autoimmune disease that causes erosion of articular cartilage and bone and has adverse effects on both patients and livestock animals. The aim of the present study was to investigate the role of interleukin-1β (IL-1β) in the pathogenesis of RA, and to further determine whether injection of IL-1β small interfering RNA (siRNA) or transplantation of IL-1β siRNA + bone marrow mesenchymal stem cells (BMSCs) can ameliorate RA in rats. A collagen-induced arthritis (CIA) rat model was established by injecting type II collagen for 4 weeks. Next, CIA rats were randomly divided into three groups and injected or transplanted with PBS, IL-1β siRNA and IL-1β siRNA + BMSCs for another 4 weeks. The CIA rat model was successfully established, as demonstrated by the higher toe swelling value, thymus and spleen/body weigh t, immobility time and serum IL-1β concentration, as well as lower body weight, climbing time and mRNA expression of programmed death-1 (PD-1), transforming growth factor-β1 (TGF-β1) and forkhead box protein 3 (Foxp3) in the spleen, compared with control rats. Furthermore, histopathology results demonstrated that joint swelling and redness were observed in the knee joints of CIA rats. H&E results revealed that CIA rats presented erosive destruction of the bone and ulceration of the articular cartilage. In addition, in vitro results demonstrated that IL-1β expression was successfully silenced after IL-1β siRNA transfection in lipopolysaccharide-stimulated BMSCs. When compared with the results of PBS rats, both IL-1β siRNA injection and IL-1β siRNA + BMSC transplantation significantly increased the body weight, climbing time and mRNA expression of PD-1, TGF-β1 and Foxp3 in the spleen, while significantly reduced the immobility time and serum IL-1β concentration. In addition, when compared with that of IL-1β siRNA injection, IL-1β siRNA + BMSC transplantation exhibited markedly higher therapeutic efficacy against CIA. These results demonstrated that higher IL-1β contributed to the pathogenesis of CIA, and that IL-1β siRNA injection ameliorated CIA, while its combination with BMSCs exerted synergistic effects, which may be beneficial against RA. PMID:35069820 | PMC:PMC8756407 | DOI:10.3892/etm.2021.11062 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Synergistic effect of Bruton's tyrosine kinase and TNF-α in the regulation of rheumatoid arthritis and underlying mechanisms

xlomafota13 shared this article with you from Inoreader Synergistic effect of Bruton's tyrosine kinase and TNF-α in the regulation of rheumatoid arthritis and underlying mechanisms Via Experimental and therapeutic medicine Exp Ther Med. 2022 Feb;23(2):141. doi: 10.3892/etm.2021.11064. Epub 2021 Dec 14. ABSTRACT The presence of Bruton's tyrosine kinase (BTK) in macrophages has been recommended as a promising therapeutic target for rheumatoid arthritis (RA). In addition, activated macrophages in the inflamed joints of patients with RA can also produce a plethora of cytokines, such as TNF-α. The aim of the present study was to investigate the potential role of BTK and TNF-α in the regulation of RA. The results demonstrated that higher levels of BTK and TNF-α were observed in macrophages in inflamed RA joints compared with those in normal joint tissues. Subsequently, the role of BTK and TNF-α in the regulation of cellular process in inflammatory macrophages was analyzed. It was demonstrated that aberrant expression of BTK and TNF-α in inflammatory macrophages can lead to higher cell proliferation rates. Once the expression of BTK or TNF-α was restricte d by using short interfering (si)RNAs (siBTK or siTNF-α), the activity of inflammatory macrophages was significantly downregulated. Of note, when the expression of BTK and TNF-α was simultaneously decreased, the proliferation rate of inflammatory macrophages was inhibited to the greatest extent. Subsequently, the underlying mechanisms through which BTK and TNF-α can regulate RA were investigated. The results demonstrated that BTK mainly regulated the ERK/JNK pathway, while TNF-α mainly affected the inactive rhomboid protein 2/B-cell-activating factor pathway. Finally, animal experiments demonstrated that simultaneous silencing of both BTK and TNF-α can significantly alleviate the symptoms associated with RA. PMID:35069822 | PMC:PMC8756421 | DOI:10.3892/etm.2021.11064 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

MicroRNA-195-5p inhibits the progression of hemangioma via targeting SKI

xlomafota13 shared this article with you from Inoreader MicroRNA-195-5p inhibits the progression of hemangioma via targeting SKI Via Experimental and therapeutic medicine Exp Ther Med. 2022 Feb;23(2):165. doi: 10.3892/etm.2021.11088. Epub 2021 Dec 22. ABSTRACT Hemangioma (HA), which is characterized by aberrant endothelial cell proliferation in blood vessels, is a common tumor during infancy. MicroRNAs (miRNAs/miRs) collectively participate in the development of HA; however, the potential roles of miR-195-5p in HA are not completely understood. The aim of the present study was to investigate the roles of miR-195-5p in HA. In the present study, miR-195-5p was found to be downregulated in HA cells, such as the XPTS-1 human infantile hemangioma-derived endothelial cell line and the EOMA hemangioendothelioma cell line. Overexpression of miR-195-5p was shown to suppress HA cell viability, colony formation and proliferation, and induced HA cell apoptosis. Furthermore, miR-195-5p downregulated Bcl-2 expression and upregulated Bax and Bcl-2 expression levels. V-ski sarcoma viral oncogene homolog (SKI) was ident ified as a target of miR-195-5p. Co-transfection of miR-195-5p mimics and SKI 3'-untranslated region wild-type decreased HA cell luciferase activity. SKI overexpression alleviated the miR-195-5p-induced decrease in HA cell proliferation and increased HA cell apoptosis. In addition, the regulatory role of miR-195-5p on the expression of Bcl-2, Bax and poly(ADP-ribose) polymerase was reversed by SKI. Collectively, the results of the present study demonstrated that miR-195-5p suppressed HA progression and its effects were mediated via SKI. Therefore, the miR-195-5p/SKI axis may represent a novel therapeutic target for HA. PMID:35069846 | PMC:PMC8753966 | DOI:10.3892/etm.2021.11088 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Mucosal gene expression profile of stricturing Crohn's disease: A preliminary study

xlomafota13 shared this article with you from Inoreader Mucosal gene expression profile of stricturing Crohn's disease: A preliminary study Via Experimental and therapeutic medicine Exp Ther Med. 2022 Feb;23(2):149. doi: 10.3892/etm.2021.11072. Epub 2021 Dec 16. ABSTRACT Intestinal strictures are an important complication of Crohn's disease (CD), with ~40% of patients developing symptomatic obstruction within 10 years of diagnosis. However, there is a paucity of research examining the mechanisms driving the development of fibrotic strictures in CD. The present study aimed to identify the mucosal markers associated with stricturing complications by examining the differences in the gene expression profiles of two patient cohorts: Patients diagnosed with inflammatory CD (n=12) and patients with stricturing CD (n=9). For each patient, a paired sample of inflamed and uninflamed mucosa was isolated and assessed by quantitative PCR using a large panel of genes associated with inflammatory bowel disease. The presents study revealed a significantly increased level of four genes in the mucosa of patients with strictures com pared with the inflammatory pattern of the disease: Formyl-peptide receptor 1 [P=0.019; fold change (FC)=11.6], C-C chemokine receptor type 1 (P=0.035; FC=5.44), IFN-γ-inducible protein 10 (P=0.037; FC=3.8) and C-C chemokine ligand 25 (P=0.048; FC=3.56). The augmented expression of these four genes in the CD stricturing phenotype, if confirmed in larger cohorts of patients, could help elucidate the mechanisms leading to disease-associated complications. PMID:35069830 | PMC:P MC8756406 | DOI:10.3892/etm.2021.11072 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Adult female acne: Clinical and therapeutic particularities (Review)

xlomafota13 shared this article with you from Inoreader Adult female acne: Clinical and therapeutic particularities (Review) Via Experimental and therapeutic medicine Exp Ther Med. 2022 Feb;23(2):151. doi: 10.3892/etm.2021.11074. Epub 2021 Dec 16. ABSTRACT Acne is a chronic inflammatory condition affecting the pilosebaceous unit that was traditionally viewed as a disease of the adolescence. However, over the past several years, an increasing number of adult women have been reported to suffer from this condition. The prevalence of adult female acne ranges between 12 and 54%. Two clinical types can be distinguished in this population, a 'retentional' and an 'inflammatory' type, which usually tend to overlap. In terms of evolution, three main subtypes can be identified: Persistent acne, which is the most frequent subtype, late-onset acne and recurrent acne. This type of acne is mainly mild-to-moderate in severity and may be refractory to conventional treatment. The etiopathogenesis is complex and has yet to be fully elucidated. It appears to involve an interaction among genetic predisposition, hormonal factors, and chronic activation of the innate immune system overlapping with external factors, such as daily stress, Western-type diet, use of tobacco and cosmetics. The treatment may be challenging and a holistic approach is required, with special attention to the individual needs and particularities of adult women. Both topical and systemic treatments are available, with hormonal therapies being of special value in this population. The aim of the present article was to provide up-to-date, evidence-based information on the clinical presentation, etiopathogenesis and treatment of adult female acne. PMID:35069832 | PMC:PMC8753972 | DOI:10.3892/etm.2021.11074 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Lectin-type oxidized LDL receptor 1 modulates matrix metalloproteinase 2 production in peri-implantitis

xlomafota13 shared this article with you from Inoreader Lectin-type oxidized LDL receptor 1 modulates matrix metalloproteinase 2 production in peri-implantitis Via Experimental and therapeutic medicine Exp Ther Med. 2022 Feb;23(2):171. doi: 10.3892/etm.2021.11094. Epub 2021 Dec 27. ABSTRACT Peri-implantitis is a disease in which inflammatory lesions that affect the surrounding soft and hard tissues develop. Matrix metalloproteinase 2 (MMP2) is hypothesized to be involved in this destructive process. However, the regulatory mechanism of action of MMP2 in the peripheral tissues of the implant are not fully understood. To determine the expression of MMP2 in peri-implantitis, peri-implant crevicular fluid (PICF) was collected from patients with peri-implantitis. The healthy volunteers' peripheral blood human macrophages infected with Porphyromonas gingivalis (P. gingivalis) were used as a cell model to explore the regulatory mechanism of MMP2 regarding dental implants. Western blotting, reverse transcription-quantitative PCR and immunofluorescence staining were used to measure the expression of MMP2 in the present study. MM P2 expression was increased in the PICF of the patients with peri-implantitis and in human macrophages infected with P. gingivalis. Lectin-type oxidized LDL receptor 1 (LOX-1) mediated the expression of MMP2 in human macrophages upon infection of P. gingivalis, whereas dendritic cell-associated c-type lectin-1 did not appear to be involved in this regulatory process. However, JNK and ERK1/2 were involved in P. gingivalis induced MMP2 expression. The results of this study showed that MMP2 was involved in peri-implantitis. MMP2 was upregulated by LOX-1 in a JNK and ERKk1/2 signaling dependent manner in the cell model. The LOX-1/MMP2 signaling pathway may thus be a potential target for management of peri-implantitis. PMID:35069852 | PMC:PMC8764579 | DOI:10.3892/etm.2021.11094 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.