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.

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.

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.

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.

Electrochemical monitoring of bronchial inflammation in pediatric athletes: A prospective study

xlomafota13 shared this article with you from Inoreader Electrochemical monitoring of bronchial inflammation in pediatric athletes: A prospective study Via Experimental and therapeutic medicine Exp Ther Med. 2022 Feb;23(2):180. doi: 10.3892/etm.2021.11103. Epub 2021 Dec 28. ABSTRACT The assessment of inflammation by accessible, reproducible and especially non-invasive methods is one of the main goals for numerous medical specialties. One variable for assessment is the fraction of nitric oxide in exhaled air (FeNO), which correlates with the inflammatory syndrome of the airways. The objective of the present study was the biochemical evaluation of FeNO in children practicing sports in Oltenia, Romania. Between January and December 2018, children practicing sports (football, track and field, judo, fencing, handball, volleyball and basketball) were enrolled in the study. The FeNO values were compared with the asthma history and with the spirometric evaluation. A total of 23 children without a previous asthma diagnosis exhibited positive spirometry results. The prevalence of the disease was 3.6% in the cohort, and FeNO dosing show ed higher values in the group at risk in children diagnosed with asthma, compared with that in children without this diagnosis. The children who performed outdoor sports (soccer, and track and field) had higher electrochemical levels of nitric oxide compared with those who performed indoor sports (mean, 29.70 vs. 20.56; P<0.0005), which led to the hypothesis that these children had an increased risk of developing bronchospasm. FeNO dosing can thus be a useful and easy-to-use tool in practice for assessing bronchial inflammation in children practicing various types of sports. The spirometric data of undiagnosed asthma patients from the present study may indicate that the disease is still underdiagnosed within Romania. PMID:3506 9861 | PMC:PMC8764892 | DOI:10.3892/etm.2021.11103 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

KDM2B overexpression prevents myocardial ischemia-reperfusion injury in rats through regulating inflammatory response via the TLR4/NF-κB p65 axis

xlomafota13 shared this article with you from Inoreader KDM2B overexpression prevents myocardial ischemia-reperfusion injury in rats through regulating inflammatory response via the TLR4/NF-κB p65 axis Via Experimental and therapeutic medicine Exp Ther Med. 2022 Feb;23(2):154. doi: 10.3892/etm.2021.11077. Epub 2021 Dec 17. ABSTRACT Histone modifier lysine-specific demethylase 2B (KDM2B) has been previously reported to activate the inflammatory response by transcription initiation of the IL-6 gene. However, the effects of KDM2B on the inflammatory response during myocardial ischemia-reperfusion (I/R) injury and corresponding mechanisms remain poorly understood. The present study aimed to investigate the role and mechanism of KDM2B in myocardial I/R injury. Therefore, a myocardial I/R injury model was established in rats through coronary artery ligation. Adeno-associated virus-encoding KDM2B and small interfering RNA-KDM2B were designed to determine the effects of KDM2B on myocardial I/R injury using H&E staining and a TUNEL assay in the myocardial tissues. Reverse transcription-quantitative PCR and western blotting were performed to detect the mRNA and protein expr ession levels of KDM2B, toll-like receptor 4 (TLR4), NF-κB p65 and NOD-, LRR- and pyrin domain-containing protein 3 (NLRP3). ELISA was used to detect the levels of TNF-α, IL-6 and IL-1β in the peripheral blood samples. Pathological analysis demonstrated that the cells in the model group were disordered, with a large area of necrosis and neutrophil infiltration. Knocking down KDM2B expression significantly upregulated the mRNA and protein expression levels of TLR4, NLRP3, NF-κB p65 and the ratio of phosphorylated (p)-p65 to p65. KDM2B knockdown also significantly increased the levels of IL-1β, IL-6 and TNF-α in the peripheral blood, which aggravated myocardial injury and promoted the apoptosis of myocardial cells. However, overexpression of KDM2B downregulated the mRNA and protein expression levels of TLR4, NLRP3, NF-κB P65, the ratio of p-p65 to p65 whilst reducing the levels of IL-1β, IL-6 and TNF-α in the peripheral blood, which markedly improved myocardial injury and sig nificantly inhibited the apoptosis of cells in myocardial tissue. In conclusion, the results indicated that overexpression of KDM2B may prevent myocardial I/R injury in rats by reducing the inflammatory response through regulation of the TLR4/NF-κB p65 axis. PMID:35069835 | PMC:PMC8753960 | DOI:10.3892/etm.2021.11077 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.