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.

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.

P2X7R antagonist protects against renal injury in mice with adriamycin nephropathy

xlomafota13 shared this article with you from Inoreader P2X7R antagonist protects against renal injury in mice with adriamycin nephropathy Via Experimental and therapeutic medicine Exp Ther Med. 2022 Feb;23(2):161. doi: 10.3892/etm.2021.11084. Epub 2021 Dec 21. ABSTRACT Activation of the purinergic P2X7 receptor (P2X7R) has been associated with the development of experimental nephritis. Therefore, the current study aimed to explore the mechanism of P2X7R in renal injured mice with adriamycin (ADR) nephropathy. The protective effect of a P2X7R antagonist on the kidneys of mice with ADR nephropathy was also evaluated. Nephropathy was induced by a single intravenous injection of ADR (10.5 mg/kg). A total of 6 h before the model was established, the P2X7R antagonist A438079 (100, 200 and 300 µmol/kg) was injected into the mice, which was subsequently administered daily for 1 week by intraperitoneal injection. Subsequently, all mice were sacrificed, after which blood, 24 h-urine and the kidneys were collected. The levels of albumin (ALB) and total cholesterol (TC) in the serum, along with urine protein content at 24 h were determined using an automatic biochemical analyzer. The levels of IL-1β and IL-18 were additionally detected in the renal tissues by ELISA. Moreover, the expression of P2X7R, oxidized (ox)-low density lipoprotein (LDL), C-X-C motif chemokine ligand 16 (CXCL16), Bax, caspase-3 and NLRP3 in renal tissues was detected by immunohistochemistry. Apoptosis in the renal tissues was observed using the TUNEL assay. The results demonstrated that compared with the control group, decreased weight, increased proteinuria, decreased serum ALB and increased serum TC was observed in the ADR group. The expression of IL-1β, IL-18, P2X7R, ox-LDL, CXCL16, Bax, caspase-3 and NLRP3, as well as cellular apoptosis in the renal tissues of the ADR group, was significantly increased in the ADR group compared with the control. However, compared with the ADR group, the changes in all indices in the ADR + A438079 groups were attenuated. Overall, P2X7R, ox-LDL and CXCL16 may be associated with ADR nephropa thy, while inhibition of P2X7R may reduce the expression of ox-LDL by downregulating the CXCL16 pathway to alleviate kidney injury in mice with ADR nephropathy. Furthermore, activated P2X7R may promote the release of inflammatory cytokines IL-1β and IL-18 through the downstream P2X7R/NLRP3 pathway and upregulate the expression of Bax and caspase-3 to promote apoptosis, which participates in the process of ADR nephropathy. Inhibiting P2X7R may also reduce the release of IL-1β and IL-18 by downregulating the P2X7R/NLRP3 pathway, downregulating the expression of Bax and caspase-3, and reducing apoptosis, thereby alleviating kidney injury in mice with ADR nephropathy. PMID:35069842 | PMC:PMC8753981 | DOI:10.3892/etm.2021.11084 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.

Potential biomarkers of acute myocardial infarction based on co-expression network analysis

xlomafota13 shared this article with you from Inoreader Potential biomarkers of acute myocardial infarction based on co-expression network analysis Via Experimental and therapeutic medicine Exp Ther Med. 2022 Feb;23(2):162. doi: 10.3892/etm.2021.11085. Epub 2021 Dec 21. ABSTRACT Acute myocardial infarction (AMI) is a common cause of death in numerous countries. Understanding the molecular mechanisms of the disease and analyzing potential biomarkers of AMI is crucial. However, specific diagnostic biomarkers have thus far not been fully established and candidate regulatory targets for AMI remain to be determined. In the present study, the AMI gene chip dataset GSE48060 comprising blood samples from control subjects with normal cardiac function (n=21) and patients with AMI (n=26) was downloaded from Gene Expression Omnibus. The differentially expressed genes (DEGs) between the AMI and control groups were identified with the online tool GEO2R. The co-expression network of DEGs was analyzed by calculating the Pearson correlation coefficient of all gene pairs, mutual rank screening and cutoff threshold screening. Subsequently, the Gene Ontology (GO) database was used to analyze the genes' functions and pathway enrichment of genes in the most important modules was performed. Kyoto Encyclopedia of Genes and Genomes (KEGG) Disease and BioCyc were used to analyze the hub genes in the module to determine important sub-pathways. In addition, the expression of hub genes was confirmed by reverse transcription-quantitative PCR in AMI and control specimens. In the present study, 52 DEGs, including 26 upregulated and 26 downregulated genes, were identified. As key hub genes, three upregulated genes (AKR1C3, RPS24 and P2RY12) and three downregulated genes (ACSL1, B3GNT5 and MGAM) were identified from the co-expression network. Furthermore, GO enrichment analysis of all AMI co-expression network genes revealed functional enrichment mainly in 'RAGE receptor binding' and 'negative regulation of T cell cytokine production'. In addition, KEGG Disease and BioCyc analysis indicated functional enrichment of the genes RPS24 a nd P2RY12 in 'cardiovascular diseases', of AKR1C3 in 'cardenolide biosynthesis', of MGAM in 'glycogenolysis', of B3GNT5 in 'glycosphingolipid biosynthesis' and of ACSL1 in 'icosapentaenoate biosynthesis II'. In conclusion, the hub genes AKR1C3, RPS24, P2RY12, ACSL1, B3GNT5 and MGAM are potential markers of AMI, and have potential application value in the diagnosis of AMI. PMID:35069843 | PMC:PMC8753964 | DOI:10.3892/etm.2021.11085 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Bacterial endocarditis masked by COVID-19: A case report

xlomafota13 shared this article with you from Inoreader Bacterial endocarditis masked by COVID-19: A case report Via Experimental and therapeutic medicine Exp Ther Med. 2022 Feb;23(2):186. doi: 10.3892/etm.2021.11109. Epub 2021 Dec 30. ABSTRACT Infective endocarditis represents a rare complication among patients infected with severe acute respiratory syndrome coronavirus-2 (SARS-CoV-2); it is often a nosocomial infection and the symptomatology can be masked by respiratory failure symptoms from SARS-CoV-2 bronchopneumonia. Management of patients with severe forms of SARS-COV-2 infection who also have associated infective endocarditis is very difficult, especially in mono-specialty hospitals (such as infectious diseases hospitals) where access to cardiological investigations is limited. The current study presents the case of a 73-year-old woman with increased cardiovascular risk (high blood pressure, diabetes mellitus and obesity), with uninvestigated ischaemic heart disease, who was admitted to the Department of Infectious Diseases in the Clinical Infectious Diseases Hospital (Constanta, Romania) due to SARS-CoV-2. Although the evolution was initially favorable, the condition of the patient significantly deteriorated on the 14th day of hospitalization due to the development of Enterococcus faecium infective endocarditis. Despite the therapy, the evolution was fulminant. Infection with coronavirus disease 2019 can result in numerous comorbidities, which cause higher mortality rates than in the general population. PMID:35069867 | PMC:PMC8764899 | DOI :10.3892/etm.2021.11109 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Intestinal ischemia-reperfusion induces the release of IL-17A to regulate cell inflammation, apoptosis and barrier damage

xlomafota13 shared this article with you from Inoreader Intestinal ischemia-reperfusion induces the release of IL-17A to regulate cell inflammation, apoptosis and barrier damage Via Experimental and therapeutic medicine Exp Ther Med. 2022 Feb;23(2):158. doi: 10.3892/etm.2021.11081. Epub 2021 Dec 17. ABSTRACT Intestinal ischemia-reperfusion (I/R) injury promotes the release of IL-17A, and previous studies have indicated that TGF-β activated kinase 1 (TAK1) is an important signaling molecule in the regulatory function of IL-17A. The present study aimed to explore the potential effects of IL-17A release in intestinal I/R injury, and to investigate the underlying regulatory mechanisms. Initially, the expression levels of TAK1 and JNK in a hypoxia/reoxygenation model were determined, and the effects of TAK1-knockdown on JNK phosphorylation and the viability, inflammation, apoptosis and barrier function of Caco-2 cells were assessed using Cell Counting Kit-8, reverse transcription-quantitative PCR, TUNEL and transepithelial electrical resistance assays, respectively. Subsequently, an antibody targeting IL-17A was used, and the effects of the IL-17A antibod y on the expression levels of TAK1 as well as cell viability, inflammation, apoptosis and barrier function were determined. The results of the present study demonstrated that TAK1-knockdown markedly reduced JNK phosphorylation and improved the levels of cell viability, inflammation, apoptosis and barrier function via the MAPK signaling pathway. In addition, treatment with the IL-17A antibody inhibited the expression of TAK1, and reversed the aforementioned effects of TAK1 on Caco-2 cells. In conclusion, intestinal I/R induces the release of IL-17A to regulate cell viability, inflammation, apoptosis and barrier damage via the TAK1/MAPK signaling pathway. PMID:35069839 | PMC:PMC8753980 | DOI:10.3892/etm.2021.11081 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

The Effect of (Val)ganciclovir on Hearing in Congenital Cytomegalovirus: A Systematic Review

xlomafota13 shared this article with you from Inoreader The Effect of (Val)ganciclovir on Hearing in Congenital Cytomegalovirus: A Systematic Review Via The Laryngoscope Objective To search for existing evidence of a beneficial effect of (val)ganciclovir on hearing in children with congenital cytomegalovirus (cCMV) infection and to identify future research questions. Study Design Systematic review following the Preferred Reporting Items for Systematic Reviews and Meta-Analyses guidelines, searches were performed in PUBMED, EMBASE, and WEB OF SCIENCE on December 15, 2021. Methods Studies providing ear-specific hearing results after treating children with cCMV-related hearing loss with (val)ganciclovir were retained. A meta-analysis [Peto odds ratio (OR), Review Manager 5.3] was performed to compare hearing outcome between treated and untreated children. The National Institutes of Health tool was used for quality assessment and heterogeneity was assessed with I 2 statistics. Results Eighteen studies with a total of 682 treated patients were included for the systematic review. Our meta-analysis showed that treating symptomatic children with hearing loss resulted in more hearing improvement [Peto OR 7.72, 95% confidence interval (CI) 3.08–19.34] and less hearing deterioration (Peto OR 0.23, 95% CI 0.10–0.57). Relative to an improvement and deterioration rate of 9.4% and 28.2% in an untreated group, the rate of the treated group was 44.5% and 6.3%, respectively. Conclusions There is sufficient evidence in literature to support treatment with (val)ganciclovir of children with symptomatic cCMV and hearing loss. However, still today, there is insufficient evidence of the potential beneficial role of (val)ganciclovir on hearing outcome of children with isolated hearing loss, late-onset hearing loss, and asymptomatic cCMV. The urgent need for future prospective, randomized clinical trials still exists. A standardization of definitions and treatment protocols would create uniformity in future studies. Laryngoscope, 2022 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.