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.

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.

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.

Therapeutic effect and mechanism of 4-phenyl butyric acid on renal ischemia-reperfusion injury in mice

xlomafota13 shared this article with you from Inoreader Therapeutic effect and mechanism of 4-phenyl butyric acid on renal ischemia-reperfusion injury in mice Via Experimental and therapeutic medicine Exp Ther Med. 2022 Feb;23(2):144. doi: 10.3892/etm.2021.11067. Epub 2021 Dec 15. ABSTRACT The aim of the present study was to explore the effects and possible mechanism of 4-phenylbutyric acid (4-PBA) on renal ischemia-reperfusion injury (RIRI) in mice. A RIRI model of HK-2 cells was constructed using hypoxia/reoxygenation (H/R) treatment. Dexmedetomidine and 4-PBA were used to treat the cells before and after modeling. Apoptosis and expression levels of cyclophilin D (CypD), cytochrome c, eukaryotic translation initiation factor 2α (eIF2α), glucose-regulated protein 78 (GRP78), intercellular adhesion molecule (ICAM)-1 and vascular adhesion molecule (VCAM)-1 were measured using flow cytometry, western blotting and immunohistochemistry. The renal volume, weight and renal arterial resistance index (RRI) were determined using the renal ischemia model. Compared with untreated model cells, 4-PBA treatment significantly decreased ap optosis and the expression levels of CypD, Cytochrome c, eIF2α and GRP78 in HK-2 cells. There was no significant change in renal volume and weight after modeling, but RRI was significantly decreased after 4-PBA treatments in the model. Western blotting and immunohistochemistry analysis demonstrated that 4-PBA treatment also significantly decreased the expression of ICAM-1 and VCAM-1. Overall, 4-PBA had a therapeutic effect on RIRI in mice. This protection may be mediated by decreasing the expression levels of CypD, Cytochrome c, eIF2α and GRP78, and subsequent reduction of cellular oxygen free radicals and apoptosis, leading to an alleviated endoplasmic reticulum stress response and RIRI. PMID:35069825 | PMC:< a href="https://www.ncbi.nlm.nih.gov/pmc/PMC8756420/?utm_source=Inoreader&utm_medium=rss&utm_content=1ba2t84FK1dz-fAY5g7-lbp7yzA9oSsgU2XptRGyGkyx-wIkEA&ff=20220125000243&v=2.17.5" target="_blank" rel="noopener" class="underlink bluelink">PMC8756420 | DOI:10.3892/etm.2021.11067 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.

Analysis of long-term anatomic results of radical mastoidectomy

xlomafota13 shared this article with you from Inoreader Analysis of long-term anatomic results of radical mastoidectomy Via Experimental and therapeutic medicine Exp Ther Med. 2022 Feb;23(2):156. doi: 10.3892/etm.2021.11079. Epub 2021 Dec 17. ABSTRACT A long-term, retrospective, non-controlled study was performed on the drainage results of mastoidectomy (both radical and modified radical) and the relevant statistical factors that could influence the anatomic outcome were defined. The present study took into consideration the same cohort of 200 patients we have communicated with before in our previous studies concerning the long-term functional results of mastoidectomy and long-term results of ossicular replacement with biovitroceramic prosthesis. The patients were clinically followed for the same period of 8.12 years. The drainage (anatomic) results, similar to previously published functional results, were defined by analytical function of the severity and the period of evolution of disease. The main goal was to define the situations and factors (presence of complications, type of disease, type of tympanic perforation or status of ossicular chain) that influenced the drainage results that could provide us with some type of anatomical prognosis. The follow-up started at the moment of complete epithelization for each cavity as time represents the main study comparison criteria. Drainage failure was assessed by the number of otorrhea episodes. It was concluded that practically and ideally, a maximum of 84% of the mastoid and petrous cells can be cleaned out. The results of 78% drainage success are congruent to this theory. The remaining 16% of cells may contain irreversible lesions. PMID:35069837 | PMC:PMC8753967 | DOI:10.3892/etm.2021.11079 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Portal vein reconstruction with interposition of cryopreserved aortic graft: A case report and literature review

xlomafota13 shared this article with you from Inoreader Portal vein reconstruction with interposition of cryopreserved aortic graft: A case report and literature review Via Experimental and therapeutic medicine Exp Ther Med. 2022 Feb;23(2):184. doi: 10.3892/etm.2021.11107. Epub 2021 Dec 30. ABSTRACT Pancreatic cancer is one of the most aggressive malignancies with poor rates of survival especially in the event radical procedures are not feasible. However, improvements in surgical techniques have led to the successful association of vascular resection followed by reconstruction without a significant increase in the rates of postoperative complications. In the present article, we present the case of a 49-year-old patient diagnosed with pancreatic head cancer invading the portal vein. After discussing with the patient the risks and the benefits of the surgical procedure, the patient was submitted to pancreatoduodenectomy en bloc with portal vein resection while the continuity of the portal vein was reestablished by using a cadaveric graft originating from the abdominal aorta. The postoperative outcome was uneventful. In conclusion, in selected c ases, arterial cadaveric grafts may be used in order to establish the continuity of the portal vein with good results. However, it should be emphasized that these are demanding procedures which should be carefully analyzed before deciding upon the opportunity for performing them. PMID:35069865 | PMC:PMC8764900 | DOI:10.3892/etm.2021.11107 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

p-Coumaric acid suppresses reactive oxygen species-induced senescence in nucleus pulposus cells

xlomafota13 shared this article with you from Inoreader p-Coumaric acid suppresses reactive oxygen species-induced senescence in nucleus pulposus cells Via Experimental and therapeutic medicine Exp Ther Med. 2022 Feb;23(2):183. doi: 10.3892/etm.2021.11106. Epub 2021 Dec 30. ABSTRACT p-Coumaric acid (PCA) is a phenolic acid that is widely present in numerous plants and human diets. Studies have demonstrated the antioxidant and anti-senescence effects of PCA in different cell types. However, the anti-senescence effects of PCA in nucleus pulposus (NP) cells have remained to be determined. In the present study, reverse transcription-quantitative PCR was used to measure the gene expression of Cyclooxygenase-2 (Cox-2), inducible nitric oxide synthase (iNOS), p53, p16, aggrecan and collagen-2 in NP cells. Immunofluorescence staining was used to evaluate the protein expression of p53, p16 and collagen-2 in NP cells. In addition, cell cycle of NP cells was measured by flow cytometry. β-galactosidase staining were used to investigate the senescence of NP cells. Preliminary results indicated that PCA suppressed ROS-induced senescence i n NP cells via both the p16 and p53 pathways. NP cells were pretreated with PCA at a concentration of 10 or 50 µg/ml prior to stimulation with 200 µM hydrogen peroxide (H2O2). Pretreatment with PCA significantly inhibited H2O2-induced cell cycle arrest in a dose-dependent manner. PCA also reduced the gene expression of Cox-2, iNOS, p53 and p16 induced by H2O2. By contrast, aggrecan and collagen-2 expression in NP cells was upregulated after PCA treatment. Furthermore, PCA suppressed H2O2-induced changes in the protein expression of p16, p53 and collagen-2. H2O2 stimulation of NP cells increased senescence-associated β-galactosidase (SA-β-gal) activities, while PCA treatment markedly reversed these SA-β-gal activities. Collectively, the present results indicated that PCA attenuated H2O2-induced oxidative stress and cellular senescence, suggesting a potential therapeutic utility of PCA in intervertebral disc degeneration. PMID:35069864 | PMC:PMC8764901 | DOI:10.3892/etm.2021.11106 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.