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.

Transoral robotic surgery for the identification of unknown primary head and neck squamous cell carcinomas: Its effect on the wait and the weight

xlomafota13 shared this article with you from Inoreader Transoral robotic surgery for the identification of unknown primary head and neck squamous cell carcinomas: Its effect on the wait and the weight Via Head & Neck Abstract Background Neck carcinoma of unknown primary (CUP) is a frequent scenario. Transoral robotic mucosectomies (TORM) of pharynx have increased rate of primary identification, but come with cost of treatment delay. Methods We reviewed patients who underwent CUP protocol from 2014 to 2020. Patients with cervical nodes carcinoma and failure to localize a primary source were classified as CUP. We determined primary identification rate and postoperative complications. Results We included 65 patients underwent TORM. Surgical approach consisted of lingual and/or palatine tonsillectomies. The primary detection rate was 49.2%. Average weight reduction was 2.5 ± 4.3 kg. The average number of days from consultation to definitive treatment was 52.2 ± 18.3. Conclusion A systematic approach to patients with CUP showed a promising primary identification rate compared to panendoscopy alone. TORM carries a small risk of complications. The benefits of primary identification must be weighed with the morbidity and delay to definitive treatment. View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Cancer stem cell markers CD44v9+/CD133- are associated with low apoptosis in both sporadic and ulcerative colitis-associated colorectal cancers

xlomafota13 shared this article with you from Inoreader Cancer stem cell markers CD44v9+/CD133- are associated with low apoptosis in both sporadic and ulcerative colitis-associated colorectal cancers Via Cellular and Molecular Biology Histol Histopathol. 2022 Feb 28:18445. doi: 10.14670/HH-18-445. Online ahead of print. ABSTRACT OBJECTIVE: To elucidate tumor cell behavior associated with cancer stem cell (CSC) marker expression, the expression of CD133, CD44v9, and ALDH1A1, which are considered markers of CSCs, was examined in sporadic and ulcerative colitis (UC)-associated colorectal tumors. METHODS: A total of 23 cases of sporadic colorectal cancer and 44 cases of adenoma were collected. Additionally, 22 cancer lesions and 38 dysplasia lesions were selected from 28 colectomy cases of UC with neoplastic lesions. Lesions were examined by immunohistochemistry using primary antibodies against CD133, CD44v9, ALDH1A1, Ki-67, cleaved-Caspase 3, and p53. RESULTS: CD133, CD44v9, and ALDH1A1 showed higher expression in both sporadic and UC-associated tumors than in the normal mucosa. ALDH1A1 expression in sporadic cancer was higher in the right colon than in the left colon (p=0.0089). ALDH1A1 expression in UC-associated cancer was higher in those with longer disease duration than in those with shorter disease duration (p=0.019). The CD44v9+/CD133- region had fewer cleaved-Caspase 3 positive cells in both sporadic and UC-associated cancers. In sporadic cancer, CD133+/ALDH1A1+ regions had fewer apoptotic cells than CD133+/ALDH1A1- regions, while CD133+/ALDH1A1- regions were less proliferative than CD133+/ALDH1A1+ regions in UC-associated cancer. CONCLUSION: CD44+/CD133- regions were commonly associated with low apoptosis in sporadic and UC-associated cancers; thus, these were considered target areas for CSCs. Additionally, the combination of markers comprising CSCs may differ between sporadic and UC-associated cancers. PMID:35224715 | DOI:10.14670/HH-18-445 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Ventriculoperitoneal Shunt Alone for Cerebrospinal Fluid Rhinorrhea With Neuroendocrine Alterations in Idiopathic Intracranial Hypertension: A Case Report and Literature Review

xlomafota13 shared this article with you from Inoreader Ventriculoperitoneal Shunt Alone for Cerebrospinal Fluid Rhinorrhea With Neuroendocrine Alterations in Idiopathic Intracranial Hypertension: A Case Report and Literature Review Via leak of cerebrospinal fluid Front Neurol. 2022 Feb 10;13:809224. doi: 10.3389/fneur.2022.809224. eCollection 2022. ABSTRACT Spontaneous skull base cerebrospinal fluid (CSF) leaks due to idiopathic intracranial hypertension (IIH) are a rare entity. Patients often present with CSF rhinorrhea, recurrent meningitis, chronic headache, and visual defects, while few patients have been reported to present with neuroendocrine alterations. Endonasal endoscopic repair is the first-line treatment for these leaks at present. However, the relatively high risk of recurrence remains the main cause of reoperation because of elevated intracranial pressure (ICP) after endoscopic surgery and absence of postoperative ICP management. A shunting procedure may stop CSF leakage or relieve symptoms in complex cases, and this is presently well-known as the last-line therapy for CSF liquorrhea. We describe a 29-year-old woman with spontaneous CSF rhinorrhea and neuroendocrine alterations due to II H, and with no previous history of trauma, tumor, or nasal surgery. The bone defect in the skull base became implicated when the site of the leak was detected by cranial magnetic resonance imaging and computed tomography (CT). The patient was successfully managed via ventriculoperitoneal shunt (VPS) alone without endoscopic repair, and neuroendocrine alterations resolved after the shunting procedure. PMID:35222246 | PMC:PMC8866819 | DOI:10.3389/fneur.2022.809224 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.

Vitamin D3 promotes autophagy in THP-1 cells infected with Mycobacterium tuberculosis

xlomafota13 shared this article with you from Inoreader Vitamin D3 promotes autophagy in THP-1 cells infected with <em>Mycobacterium tuberculosis</em> Via Experimental and therapeutic medicine Exp Ther Med. 2022 Mar;23(3):240. doi: 10.3892/etm.2022.11165. Epub 2022 Jan 25. ABSTRACT Tuberculosis (TB) is a major disease that causes mortality worldwide. The lethality of this disease is a result of the contagious bacteria Mycobacterium tuberculosis (M.tb). Infection can inhibit phagosomal maturation, with M.tb mainly attacking macrophages and inhibiting autophagy and apoptosis. Vitamin D has been used to treat tuberculosis, whereby the active metabolite, 1,25-dihydroxyvitamin D, may enhance the immune response to M.tb. Moreover, macrophages infected with M.tb have a high demand for Ca2+. However, the mechanisms by which vitamin D3 protects against and treats TB remain unclear. In the present study, MTT assay showed that vitamin D3 decreased the viability of THP-1 cells in a dose- and time-dependent manner. Autophagy-related factors in THP-1 cells infected with M.tb were analyzed by w estern blotting and RT-qPCR and the results demonstrated that vitamin D3 significantly increased the expression level of p62, LC3Ⅱ/LC3Ⅰ, Beclin-1, ATG-5 and AMPK in THP-1 cells following M.tb infection. The Ca2+ concentration assay demonstrated that vitamin D3 may promoted cellular autophagy by inhibiting the concentration of Ca2+. Furthermore, the effect of vitamin D3 on M.tb infection was also assessed using Balb/c mice; pulmonary injury was assessed by H&E staining of the lungs tissue. The results demonstrated that vitamin D3 markedly attenuated cellular damage caused by M.tb infection. In conclusion, the present study indicated that vitamin D3 may activate cell autophagy signals by inhibiting the concentration of Ca2+. These data may improve understanding of the effect of vitamin D3 on M.tb infection and help determine the underlying mechanism of vitamin D3 to alleviate and treat the inflammatory response cause d by TB. PMID:35222717 | PMC:PMC8815057 | DOI:10.3892/etm.2022.11165 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.