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.

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.

Pediatric esophageal stenoses: Challenges and new surgical device promoting tension-free esophageal anastomosis

xlomafota13 shared this article with you from Inoreader Pediatric esophageal stenoses: Challenges and new surgical device promoting tension-free esophageal anastomosis Via Experimental and therapeutic medicine Exp Ther Med. 2022 Mar;23(3):220. doi: 10.3892/etm.2022.11144. Epub 2022 Jan 14. ABSTRACT Esophageal stenoses of childhood have a broad spectrum of underlying causes. Their treatment is usually minimally invasive by endoscopic means, but sometimes surgery is necessary in refractory cases. Techniques employed in the surgical treatment of esophageal strictures include resection of the stenotic esophageal segment or esophageal substitution procedures. Esophageal anastomosis has always been a challenge in pediatric surgery. Anastomosis complications are linked to anatomical, biological and technical aspects. Mechanical tension between esophageal ends is an important cause of complications including anastomotic leaks or dehiscence. Eleven cases of esophageal stenoses, surgically treated in the Pediatric Surgery Department of Emergency Clinical Hospital for Children 'Marie S. Curie' by a single team in 5 years, were included in the present s tudy. The results showed that, the main causes of esophageal stenosis were represented by corrosive esophageal injury in five cases, complications of esophageal atresia repair in three cases, congenital esophageal stenosis in two cases and chemotherapy-induced esophageal necrosis in acute lymphoblastic leukemia treatment in one case. The authors also designed and presented a device facilitating esophageal anastomosis under tension. Its principle involved temporary absorption of tension at secure points of the two esophageal pouches and reallocating it in equal amounts following anastomosis while decreasing any stretch-related tissue trauma. In conclusion, this auxiliary tool is beneficial for esophageal anastomosis; however, the standard steps of the esophageal anastomosis procedure should still be considered when necessary. PMID:35222697 | PMC:PMC8812146 | DOI:10.3892/etm.2022.11144 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

HMBOX1 attenuates LPS-induced periodontal ligament stem cell injury by inhibiting CXCL10 expression through the NF-κB signaling pathway

xlomafota13 shared this article with you from Inoreader HMBOX1 attenuates LPS-induced periodontal ligament stem cell injury by inhibiting CXCL10 expression through the NF-κB signaling pathway Via Experimental and therapeutic medicine Exp Ther Med. 2022 Mar;23(3):224. doi: 10.3892/etm.2022.11148. Epub 2022 Jan 17. ABSTRACT Homeobox containing 1 (HMBOX1) is a member of the homeobox transcription factor family that has been reported to serve an important role in numerous biological processes. The present study aimed to determine the role of HMBOX1 in the pathogenesis of periodontitis. Human periodontal ligament stem cells (hPDLSCs) were treated with liposaccharide (LPS) and transfected with a HMBOX1 overexpression (Ov-HMBOX1) plasmid or small interfering (si)-C-X-C motif chemokine ligand 10 (CXCL10) plasmids. The effects of Ov-HMBOX1 on cell proliferation, inflammation and apoptosis were subsequently investigated using Cell Counting Kit-8, ELISA for analysis of IL-6, TNF-α and IL-1β levels, TUNEL and western blotting assays for analysis of Bcl-2, Bax, cleaved caspase-3 and caspase-3 levels, respectively. Furthermore, the potential effects of HMBOX1 on the mRNA and p rotein levels of CXCL10 and the NF-κB signaling pathway were investigated by using reverse transcription-quantitative PCR and western blotting. Finally, the physiological processes of lipopolysaccharide (LPS)-induced hPDLSCs overexpressing HMBOX1 were assessed following treatment with phorbol 12-myristate 13-acetate (PMA), a NF-κB agonist. The results revealed that Ov-HMBOX1 transfection promoted proliferation whilst alleviating inflammation and apoptosis in LPS-induced hPDLSCs. Ov-HMBOX1 reduced the expression of CXCL10 by suppressing the NF-κB signaling pathway. PMA treatment inhibited the proliferation of LPS-induced hPDLSCs transfected with Ov-HMBOX1, which was reversed by transfection with si-CXCL10. In conclusion, results of the present study provided evidence that HMBOX1 can attenuate LPS-induced hPDLSC injury by downregulating CXCL10 expression via the NF-κB signaling pathway, which may provide a novel insight into the development of potentially novel treatment strategie s for periodontitis. PMID:35222701 | PMC:PMC8812104 | DOI:10.3892/etm.2022.11148 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.