Outcome measurement in adult flexor tendon injury: A systematic review

xlomafota13 shared this article with you from Inoreader Outcome measurement in adult flexor tendon injury: A systematic review Via Journal of plastic, reconstructive & aesthetic surgery : JPRAS J Plast Reconstr Aesthet Surg. 2021 Sep 20:S1748-6815(21)00423-X. doi: 10.1016/j.bjps.2021.08.033. Online ahead of print. ABSTRACT BACKGROUND: Defining the optimal, evidence-based management of flexor tendon injury remains challenging. Lack of consensus on which measures to use to assess the outcome of interventions is a key issue, especially with regard to patient-reported outcome measures (PROMs). This systematic review defines the landscape of outcome measurement in studies on interventions for flexor tendon injuries to guide future research. METHODS: A PRISMA-compliant systematic review was conducted using bespoke search strategies applied to MEDLINE, EMBASE, PsycINFO, CENTRAL, CINAHL and AMED. A protocol was developed and registered prospectively (CRD42020186780). We identified all studies describing adult patients undergoing interventions for acute hand flexor tendon injuries. RESULTS: Of the 4844 studies, 114 studies met the final inclusion criteria for evaluating the outcomes of 8127 participants with 9071 injured digits. Studies included 24 randomised controlled trials, 19 cohort studies and 61 case series. Nine different PROMs were used in 24 studies (22%): three site-specific PROMs, one generic quality-of-life measure and four visual analogue scales. Clinician-reported outcome measures were used in 103 studies (96%), such as the range of motion reported in 102 studies (94%). Adverse outcomes were reported in 96 studies (89%), with the most frequently reported adverse outcomes being tendon rupture and infection. Re-operation was reported in 21 studies (19%). The most frequently reported health economic outcome measure was the length of work absence, reported in ten studies (9%). CONCLUSIONS: There is variability in the use of outcome measures used to study interventions for flexor tendon injuries. An independent systematic review of the psychometric properties of the identified outcome measures and a specific multi-stakeholder consensus process may support optimal choice and standardisation for future studies. PMID:35219612 | DOI:10.1016/j.bjps.2021.08.033 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Facial nerve perineural spread from cutaneous squamous cell carcinoma of the head and neck: A single institution analysis of epidemiology, treatment, survival outcomes, and prognostic factors

xlomafota13 shared this article with you from Inoreader Facial nerve perineural spread from cutaneous squamous cell carcinoma of the head and neck: A single institution analysis of epidemiology, treatment, survival outcomes, and prognostic factors Via Head & Neck Abstract Background This study aimed to examine patients with facial nerve (VII) perineural spread (PNS) from cutaneous squamous cell carcinoma of the head and neck. Methods Retrospective analysis of patients managed by an Australian tertiary center between 2000 and 2019. Results Seventy three patients were included. Most presented with recurrent disease (89.0%) and simultaneous trigeminal nerve (V) involvement (67.1%). Of the 55 patients (75.3%) who received curative intent treatment, 48 received surgery plus/minus post-operative radiotherapy. In these patients, 5-year disease-free survival, disease-specific survival, and overall survival was 50.7%, 68.7%, and 58.1%, respectively. Pathological nodal disease, involved margins, increasing VII zonal extent, and concurrent zone 2 V PNS significantly worsened outcomes. Conclusion High rates of recurrent disease reflects the importance of adequate treatment of the primary. Surgery and post-operative radiotherapy remains the mainstay treatment. Outcomes are improved in early-stage disease and with clear surgical margins, reinforcing the need for prompt diagnosis and intervention. View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Application of a three-dimensional printed model to localize a cranial cerebrospinal fluid leak: a case report

xlomafota13 shared this article with you from Inoreader Application of a three-dimensional printed model to localize a cranial cerebrospinal fluid leak: a case report Via leak of cerebrospinal fluid J Int Med Res. 2022 Feb;50(2):3000605221078412. doi: 10.1177/03000605221078412. ABSTRACT Localization of defect sites is a major challenge for surgical repair of cerebrospinal fluid (CSF) leaks. Here, we report a case in which we applied a 3-dimensional (3D) printed model to accurately identify the defect sites and facilitate the successful repair of a cranial CSF leak. A 37-year-old female patient diagnosed with recurrent nasopharyngeal carcinoma suffered CSF rhinorrhea and severe bacterial meningitis. Lumbar drainage and antibiotic administration failed to control the condition. In addition to high resolution computed tomography and magnetic resonance imaging, we applied a 3D printed model of the skull to improve the understanding of the osseous destruction at the skull base and aid in accurately localizing the defect sites of the right middle fossa. Accordingly, a right temporalis pedicled flap combined with an autogenous fascia lata flap was applied to cover the defect sites. The leak stopped postoperatively, and meningitis was relieved by enhanced antibacterial treatment. As a complement to high resolution computed tomography and magnetic resonance imaging, a 3D printed model may improve localization of complex defect sites and surgical planning by allowing preoperative visualization of the skull condition. PMID:35220787 | DOI:10.1177/03000605221078412 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

LACTB suppresses carcinogenesis in lung cancer and regulates the EMT pathway

xlomafota13 shared this article with you from Inoreader LACTB suppresses carcinogenesis in lung cancer and regulates the EMT pathway Via Experimental and therapeutic medicine Exp Ther Med. 2022 Mar;23(3):247. doi: 10.3892/etm.2022.11172. Epub 2022 Jan 28. ABSTRACT Lung cancer causes thousands of deaths worldwide every year, and present therapeutics show little benefit for advanced-stage patients. Researchers do not know why and how lung cancer begins. Lactamase β (LACTB) is a tumor-suppressor in some cancers. However, its role in lung cancer is unknown. By analyzing the TCGA database and Kaplan-Meier Plotter database, LACTB was found to be downregulated in lung cancer tissues but the methylation level was increased. Patients with high LACTB expression exhibited improved survival. Then, in vitro assays demonstrated that LACTB overexpression inhibited cell migration and invasion, and induced apoptosis in H1299 and H1975 cells. Knockdown of LACTB caused the reverse effects. Moreover, a much higher apoptotic rate and more potent inhibitory effects on H1299 and H1975 cells wer e obtained when LACTB was combined with docetaxel. In addition, members of the epithelial-mesenchymal transition (EMT) signaling pathway were assessed using western blot analysis. The expression of E-cadherin was decreased while levels of N-cadherin and vimentin were increased after knockdown of LACTB in lung cancer cells. By contrast, overexpression of LACTB increased the level of E-cadherin but decreased N-cadherin and vimentin. Therefore, LACTB is a tumor suppressor in lung cancer that inhibits cell migration and invasion and induces cell apoptosis. Meanwhile, LACTB was found to strengthen the anticancer role of docetaxel and to suppress the EMT pathway in lung cancer. PMID:35222724 | PMC:PMC8815028 | DOI:10.3892/etm.2022.11172 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Estrogen downregulates TAK1 expression in human fibroblast-like synoviocytes and in a rheumatoid arthritis model

xlomafota13 shared this article with you from Inoreader Erratum: Estrogen downregulates TAK1 expression in human fibroblast-like synoviocytes and in a rheumatoid arthritis model Via Experimental and therapeutic medicine Exp Ther Med. 2022 Mar;23(3):225. doi: 10.3892/etm.2022.11149. Epub 2022 Jan 17. ABSTRACT [This corrects the article DOI: 10.3892/etm.2020.8848.]. PMID:35222702 | PMC:PMC8812110 | DOI:10.3892/etm.2022.11149 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Butorphanol reduces the neuronal inflammatory response and apoptosis via inhibition of p38/JNK/ATF2/p53 signaling

xlomafota13 shared this article with you from Inoreader Butorphanol reduces the neuronal inflammatory response and apoptosis via inhibition of p38/JNK/ATF2/p53 signaling Via Experimental and therapeutic medicine Exp Ther Med. 2022 Mar;23(3):229. doi: 10.3892/etm.2022.11151. Epub 2022 Jan 18. ABSTRACT Neuronal cell apoptosis is a complex pathophysiological change that occurs following spinal cord injury (SCI) and affects self-repair. Therefore, preventing neuronal cell apoptosis can promote the recovery of nerve function. The present study aimed to investigate the effects of butorphanol on neuronal inflammatory response and apoptosis. The effects of butorphanol on cell viability and pathway-related protein expression were first assessed using the CCK8 and western blot assays, respectively. Lipopolysaccharide (LPS) was used to establish models. The influences of additional anisomycin, an agonist of MAPK pathway, on cell viability, pathway-related protein expression and lactate dehydrogenase level were determined using the CCK8 assay, western blotting and assay kits, respectively. In addition, the roles of butorphanol and anisomycin in inflammato ry factor levels and cell apoptosis were determined using reverse transcription-quantitative PCR, TUNEL and western blot assays. Butorphanol was found to protect PC12 cells from the action of LPS on viability and effectively upregulated the p38/JNK/activation of transcription factor 2 (ATF2)/p53 protein expression levels. In addition, anisomycin could break the protective role of butorphanol in cell viability and the inhibitory roles in inflammatory response and apoptosis. To sum up, butorphanol reduces neuronal inflammatory response and apoptosis via inhibiting p38/JNK/ATF2/p53 signaling. The present findings may provide a new direction for the treatment for SCI. PMID:35222706 | PMC:PMC8815053 | DOI:10.3892/etm.2022.11151 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Long non-coding RNA ATB is associated with metastases and promotes cell invasion in colorectal cancer via sponging miR-141-3p

xlomafota13 shared this article with you from Inoreader Erratum: Long non-coding RNA ATB is associated with metastases and promotes cell invasion in colorectal cancer via sponging miR-141-3p Via Experimental and therapeutic medicine Exp Ther Med. 2022 Mar;23(3):238. doi: 10.3892/etm.2022.11163. Epub 2022 Jan 24. ABSTRACT [This corrects the article DOI: 10.3892/etm.2020.9391.]. PMID:35222715 | PMC:PMC8815047 | DOI:10.3892/etm.2022.11163 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Metformin reduces chondrocyte pyroptosis in an osteoarthritis mouse model by inhibiting NLRP3 inflammasome activation

xlomafota13 shared this article with you from Inoreader Metformin reduces chondrocyte pyroptosis in an osteoarthritis mouse model by inhibiting NLRP3 inflammasome activation Via Experimental and therapeutic medicine Exp Ther Med. 2022 Mar;23(3):222. doi: 10.3892/etm.2022.11146. Epub 2022 Jan 17. ABSTRACT Osteoarthritis (OA) is an age-related degenerative disease, and its incidence is increasing with the ageing of the population. Metformin, as the first-line medication for the treatment of diabetes, has received increasing attention for its role in OA. The purpose of the present study was to confirm the therapeutic effect of metformin in a mouse model of OA and to determine the mechanism underlying the resultant delay in OA progression. The right knees of 8-week-old C57BL/6 male mice were subjected to destabilization of the medial meniscus (DMM). Metformin (200 mg/kg) was then administered daily for 4 or 8 weeks. Safranin O-fast green staining, H&E staining and micro-CT were used to analyse the structure and morphological changes. Immunohistochemical staining was used to detect type II collagen (Col II), matrix metalloproteinase 13 (MMP-13), NO D-like receptor protein 3 (NLRP3), caspase-1, gasdermin D (GSDMD) and IL-1β protein expression. Reverse transcription-quantitative PCR was used to detect the mRNA expression of NLRP3, caspase-1, GSDMD and IL-1β. Histomorphological staining showed that metformin delayed the progression of OA in the DMM model. With respect to cartilage, metformin decreased the Osteoarthritis Research Society International score, increased the thickness of hyaline cartilage and decreased the thickness of calcified cartilage. Regarding the mechanism, in cartilage, metformin increased the expression of Col II and decreased the expression of MMP-13, NLRP3, caspase-1, GSDMD and IL-1β. In addition, in subchondral bone, metformin inhibited osteophyte formation, increased the bone volume fraction (%) and the bone mineral density (g/cm3), decreased the trabecular separation (mm) in early stage of osteoarthritis (4 weeks) but the opposite in an advanced stage of osteoarthritis (8 weeks). Overall, metformin inhibited the activation of NLRP3 inflammasome, decreased cartilage degradation, reversed subchondral bone remodelling and inhibited chondrocyte pyroptosis. PMID:35222699 | PMC:PMC8812147 | DOI:10.3892/etm.2022.11146 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Circular RNA, hsa_circRNA_102049, promotes colorectal cancer cell migration and invasion via binding and suppressing miRNA-455-3p

xlomafota13 shared this article with you from Inoreader Circular RNA, hsa_circRNA_102049, promotes colorectal cancer cell migration and invasion via binding and suppressing miRNA-455-3p Via Experimental and therapeutic medicine Exp Ther Med. 2022 Mar;23(3):244. doi: 10.3892/etm.2022.11169. Epub 2022 Jan 27. ABSTRACT Colorectal cancer (CRC) is the second most prevalent malignant gastrointestinal tumor type worldwide, displaying poor prognosis. Accumulating studies have reported the significance of circular RNAs (circRNAs) and microRNAs (miRNAs) in CRC carcinogenesis and development. At present, the functions and mechanisms of action underlying the circular RNA, hsa_circRNA_102049, in CRC are not completely understood. The present study aimed to establish the involvement of hsa_circRNA_102049 in CRC, as well as the associated mechanisms. The expression levels of hsa_circRNA_102049 and miRNA-455-3p were measured in CRC cell lines and tissues via reverse transcription-quantitative PCR. CRC progression was evaluated by performing Cell Counting Kit-8, flow cytometry, wound healing and Transwell invasion assays. The results demonstrated that hsa_circRNA_102049 was h ighly expressed in both CRC tissues and cell lines, which was associated with enhanced CRC cell proliferation, migration and invasion. Furthermore, miR-455-3p expression was downregulated in CRC cells and served as a target of has_circRNA_102049, which was validated by performing the dual luciferase reporter assay. hsa_circRNA_102049 knockdown significantly increased miR-455-3p expression, which was significantly reversed by co-transfection with the miR-455-3p inhibitor. Notably, miRNA-455-3p overexpression alleviated hsa_circRNA_102049-mediated induction of CRC cell proliferation, migration and invasion. The present study clearly demonstrated that miRNA-455-3p was a target of hsa_circRNA_102049. Moreover, the results indicated that the circular RNA, hsa_circRNA_102049, may function as a tumor promoter in CRC via directly sponging miRNA-455-3p. PMID:35222721 | PMC:PMC8815054 | DOI:10.3892/etm.2022.11169 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Managing Cachexia in Head and Neck Cancer: a Systematic Scoping Review

xlomafota13 shared this article with you from Inoreader Managing Cachexia in Head and Neck Cancer: a Systematic Scoping Review Via swallowing exercises Adv Ther. 2022 Feb 27. doi: 10.1007/s12325-022-02074-9. Online ahead of print. ABSTRACT INTRODUCTION: Patients with head and neck cancer (HNC) are usually confronted with functional changes due to the malignancy itself or its treatment. These factors typically affect important structures involved in speech, breathing, chewing, swallowing, and saliva production. Consequently, the intake of food will be limited, which further contributes to loss of body weight and muscle mass, anorex ia, malnutrition, fatigue, and anemia. This multifactorial condition can ultimately lead to cancer cachexia syndrome. This study aims to examine the treatment of cachexia in HNC patients. METHODS: We systematically searched OvidMedline, PubMed, Scopus, and Web of Science for articles examining the treatment of cachexia in HNC. RESULTS: A total of nine studies were found, and these suggested interventions including nutritional, pharmacologic, therapeutic exercise, and multimodal approaches. The nutritional intervention includes essential components such as dietary counseling, oral nutritional supplements, and medical nutritional support. Individualized nutritional interventions include oral, enteral (feeding tubes i.e., percutaneous endoscopic gastrostomy [PEG], nasogastric tube [NGT]) and parenteral nutrition. The pharmacologic interventions aim at increasing the appetite and weight of cachectic patients. Therapeutic exercise and increased physical activity can help to e nhance the synthesis of muscle protein, reducing inflammation and the catabolic effects of cachexia syndrome. CONCLUSION: Owing to the multifactorial nature of this syndrome, it is expected that the management approach should be multi-interventional. Early implementation of these interventions may help to improve survival and quality of health and life of cachectic HNC patients. PMID:35224702 | DOI:10.1007/s12325-022-02074-9 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Scalar position, dislocation analysis and outcome in CI reimplantation due to device failure

xlomafota13 shared this article with you from Inoreader Scalar position, dislocation analysis and outcome in CI reimplantation due to device failure Via http://link.springer.com/journal/405,European archives of oto-rhino-laryngology,The European Federation of Oto-Rhino-Laryngological Societies (EUFOS) : affiliated with the German Society for Oto-Rhino Eur Arch Otorhinolaryngol. 2022 Feb 28. doi: 10.1007/s00405-022-07315-9. Online ahead of print. ABSTRACT OBJECTIVE: Due to increasing indication for cochlear implantation (CI), reimplantation and technical upgrades their consequences are a special focus in CI surgery research. The aim of this study is to examine the indication and influences on both morphological position of the electrode array and audiological outcome following reimplantation. DESIGN: This is a retrospective analysis of adult CI patients reimplanted between 2004 and 2019. We evaluated the scalar position in pre- and postoperative cone beam computed tomography (CBCT) after CI and reimplantation and examined the indication for and the audiological outcome following reimplantation. RESULTS: The reimplanted patients showed stable and comparable audiological results for monosyllables and numbers for best fitted situation before and following reimplantation. Tec hnical upgrades did not result in a significant improvement of speech perception. CBCT scans of reimplanted ears did not show significant increased rates of scalar dislocation or partial insertion. CONCLUSION: Even with a technical upgrade, reimplantation does not improve speech perception outcome in CI patients. Therefore, the indication to reimplant should be approved critically. Reimplantation does not lead to a significantly increased risk for partial insertion, scalar dislocation or diminished electrode array insertion angle. PMID:35226182 | DOI:10.1007/s00405-022-07315-9 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.