Τετάρτη 29 Σεπτεμβρίου 2021

An Endoscopic Endonasal Nasopharyngectomy with Posterolateral Extension

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J Neurol Surg B Skull Base
DOI: 10.1055/s-0041-1735557

Background Invasion depth influences the choice for extirpation of nasopharyngeal malignancies. This study aims to validate the feasibility of endoscopic endonasal resection of lesions with a posterolateral invasion. As a secondary goal, the study intends to propose a classification system of endoscopic endonasal nasopharyngectomy determined by the depth of posterolateral invasion. Methods Eight cadaveric specimens (16 sides) underwent progressive nasopharyngectomy using an endoscopic endonasal approach. Resection of the torus tubarius, Eustachian tube (ET), medial pterygoid plate and muscle, lateral nasal wall, and lateral pterygoid plate and muscle were sequentially performed to expose the fossa of Rosenmüller, petroclival region, parapharyngeal space (PPS), and jugular foramen, respectively. Results Technical feasibility of endonasal nasopharyngectomy toward a posterolateral direction was validated in all 16 sides. Nasopharyngectomy was classified into four types as follows: (1) type 1: resection restricted to the posterior or superior nasopharynx; (2) type 2: resection includes the torus tubarius which is suitable for lesions extended into the petroclival region; (3) type 3: resection includes the distal cartilaginous ET, medial pterygoid plate, and muscle, often required for lesions extending laterally into the PPS; And (4) type 4: resection includes the lateral nasal wall, pterygoid plates and muscles, and all the cartilaginous ET. This extensive resection is required for lesions involving the carotid artery or extending to the jugular foramen region. Conclusion Selected lesions with posterolateral invasion into the PPS or jugular foramen is amenable to a resection via expanded endonasal approach. Classification of nasopharyngectomy based on tumor depth of posterolateral invasion helps to plan a surgical approach.
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Georg Thieme Verlag KG Rüdigerstraße 14, 70469 Stuttgart, Germany

Article in Thieme eJournals:
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Superior Semicircular Canal Dehiscence Revision Surgery Outcomes: A Single Institution's Experience

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World Neurosurg. 2021 Sep 25:S1878-8750(21)01426-1. doi: 10.1016/j.wneu.2021.09.083. Online ahead of print.

ABSTRACT

BACKGROUND: Superior semicircular canal dehiscence (SSCD) is an abnormality of the otic capsule which normally overlies the superior semicircular canal. Surgical management is indicated in patients with persistent and debilitating symptoms. Given the complexity of the disease, there are patients who experience less favorable surgical outcomes and require revision surgery. The purpose of this study was to report to the rate of postoperative symptomatic improvement in patients who required revision surgery.

METHODS: A retrospective analysis of patients undergoing SSCD surgical repair at a single institution was performed. Information on patient demographics, primary and secondary surgical approaches, surgical outcomes, and follow-up length was collected.

RESULTS: 17 patients underwent 20 revision surgeries. There were eleven (65%) females and six (35%) males. Mean age of the cohorts was 50 years (range 30-68 years), and mean follow-up length was 6.8 months (range 0.1-31.1 months). Cerebrospinal fluid (CSF) leak was noted in 67% of cases. The greatest postoperative symptomatic resolution was reported in oscillopsia (100%), headache (100%), and internal sound amplification (71%), while the least postoperative symptomatic resolution was reported in tinnitus (42%), aural fullness (40%), and dizziness (29%).

CONCLUSION: Revision surgery can provide symptomatic improvement in select SSCD patients; however, patients should be cautioned about the possibility of less favorable outcomes than in index surgery. Revision surgeries are associated with a considerably higher rate of perioperative CSF leak.

PMID:34583007 | DOI:10.1016/j.wneu.2021.09.083

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hsa-miR-15b-5p regulates the proliferation and apoptosis of human vascular smooth muscle cells by targeting the ACSS2/PTGS2 axis

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Exp Ther Med. 2021 Nov;22(5):1208. doi: 10.3892/etm.2021.10642. Epub 2021 Aug 24.

ABSTRACT

A previous bioinformatic analysis from our group predicted that the interaction of microRNA (miRNA/miR)-15b with the acyl-CoA synthetase short chain family member 2 (ACSS2) gene was important for the development of abdominal aortic aneurysm (AAA). Apoptosis of aortic vascular smooth muscle cells (VSMCs) is a pathological feature of AAA. The present study aimed to explain the roles of miR-15b/ACSS2 in AAA by exploring their effects on the proliferation and apoptosis of aortic VSMCs. Human aortic VSMCs (T/G HA-VSMC cell line) were divided into six groups and were transfected with miR-15b-5p mimics, mimic negative control (NC), miR-15b-5p inhibitors, inhibitor NC, miR-15b-5p mimics+pcDNA3.1 and miR-15b-5p mimics+ACSS2-overexpessing vector. CCK-8 assay was used to determine cell proliferation. Annexin V-FITC/PI staining and flow cytometry assays were used to measure cell apoptosis. Dual-luciferase reporter assays were used to confirm the targeted relationship between miR-15b-5p and ACSS2. Reverse transcription-quantitative PCR and/or western blotting were used to examine the expression levels of miR-15b-5p, ACSS2 and prostaglandin-endoperoxide synthase 2 (PTGS2). Following transfection of T/G HA-VSMCs with mimics and inhibitors to respectively upregulate and downregulate miR-15b-5p, the results demonstrated that overexpression of miR-15b-5p inhibited cell proliferation and promoted cell apoptosis; silencing of miR-15b-5p obtained the opposite results. ACSS2 may be a direct target of miR-15b-5p, since the luciferase activity of a ACSS2 wild-type vector, but not that of a ACSS2 mutant reporter, was significantly inhibited by miR-15b-5p mimics compared with controls. Additionally, the expression levels of ACSS2 and its downstream gene PTGS2 were significantly reduced or increased following transfection with miR-15b-5p mimics or in hibitors, respectively. Furthermore, overexpression of ACSS2 reversed the antiproliferative and proapoptotic effects of miR-15b-5p mimics by blocking the production of PTGS2 protein. In conclusion, miR-15b-5p may promote the apoptosis and inhibit the proliferation of aortic VSMCs via targeting the ACSS2/PTGS2 axis. The present study provided preliminary evidence indicating that the miR-15b-5p/ACSS2/PTGS2 axis may be a potential target for the treatment of AAA.

PMID:34584553 | PMC:PMC8422401 | DOI:10.3892/etm.2021.10642

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MicroRNA-22 inhibits cell growth and metastasis in breast cancer via targeting of SIRT1

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Exp Ther Med. 2021 Nov;22(5):1194. doi: 10.3892/etm.2021.10628. Epub 2021 Aug 19.

ABSTRACT

[This retracts the article DOI: 10.3892/etm.2017.4590.].

PMID:34584539 | PMC:PMC8422378 | DOI:10.3892/etm.2021.10628

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Neuroendocrine neoplasia and bone (Review)

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Exp Ther Med. 2021 Nov;22(5):1219. doi: 10.3892/etm.2021.10653. Epub 2021 Aug 26.

ABSTRACT

This is a narrative review focusing on neuroendocrine neoplasia (NEN) and bone status, in terms of metastases and osteoporosis/fractures. One fifth of NEN have skeletal dissemination, this affinity being regulated by intrinsic tumor factors such as the C-X-C chemokine receptor 4 (CXCR4). Bone colonization impairs the patient quality of life, representing a surrogate of reduced survival. Patients with NEN without bone metastases may exhibit low bone mineral density, perhaps carcinoid-related osteoporosis, yet not a standardized cause of osteoporosis. Case-finding strategies to address bone health in NEN with a good prognosis are lacking. Contributors to fractures in NEN subjects may include: menopausal status and advanced age, different drugs, induced hypogonadism, malnutrition, malabsorption (due to intestinal resection, carcinoid syndrome), hypo vitaminosis D, impaired glucose profile (due to excessive hormones such as glucagon, somatostatinoma or use of somatostatin analogues), various corticoid regimes, and high risk of fall due to sarcopenia. Pheocromocytoma/paraganglioma involve bone through malignant forms (bone is an elective site) and potential secondary osteoporosis due to excessive hormonal content and increased sympathetic activity which is a key player of bone microarchitecture/quality as reflected by low Trabecular Bone Score. Glucocorticoid osteoporosis is related to NEN-associated ectopic Cushing syndrome. Currently, there are a lack of studies to emphasis that excessive gut-derivate serotonin in NENs with carcinoid syndrome is a specific activator of bone loss thus a contributor to carcinoid-related osteoporosis.

PMID:34584564 | PMC:PMC8422397 | DOI:10.3892/etm.2021.10653

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Current research developments of patient-derived tumour xenograft models (Review)

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Exp Ther Med. 2021 Nov;22(5):1206. doi: 10.3892/etm.2021.10640. Epub 2021 Aug 24.

ABSTRACT

Patient-derived tumor xenograft (PDTX) models are established by transferring patient tumors into immunodeficient mice. In these murine models, the characteristics of the primary tumor are retained, including the microenvironment of tumor cell growth and histopathology. Due to this, it has become the most reliable in vivo human cancer model. However, the success rates differ by type of tumor, site of transplantation and tumor aggressiveness. Subcutaneous transplantation is a standard method for PDTX, and subrenal capsule transplantation improves the engraftment rate. Recently, PDTX models are frequently used in the fields of precision medicine, predictive biomarkers, evaluation of drug efficacy and preclinical research on tumor immunotherapeutic drugs. The aim of the present article was to review the establishment, clinical applications an d limitations of the PDTX model in tumor research.

PMID:34584551 | PMC:PMC8422395 | DOI:10.3892/etm.2021.10640

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The hair follicle‐psoriasis axis: Shared regulatory mechanisms and therapeutic targets

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Abstract

It has long been known that there is a special affinity of psoriasis for the scalp: Here, it occurs most frequently, lesions terminate sharply in frontal skin beyond the hair line and are difficult to treat. Yet, surprisingly, scalp psoriasis only rarely causes alopecia, even though the pilosebaceous unit clearly is affected. Here, we systematically explore the peculiar, insufficiently investigated connection between psoriasis and growing (anagen) terminal scalp hair follicles (HFs), with emphasis on shared regulatory mechanism and therapeutic targets. Interestingly, several drugs and stressors that can trigger/aggravate psoriasis can inhibit hair growth (e.g. beta-blockers, chloroquine, carbamazepine, interferon-alpha, perceived stress). Instead, several anti-psoriatic agents can stimulate hair growth (e.g., cyclosporine, glucocorticoids, dithranol, UV irradiation), while skin/HF trauma (Köbner phenomenon/depilation) favors the development of psoriatic lesions and induces anagen in "quiescent" (telogen) HFs.

On this basis, we propose two interconnected working models: a) the existence of a bidirectional "hair follicle-psoriasis axis", along which keratinocytes of anagen scalp HFs secrete signals that favor the development and maintenance of psoriatic scalp lesions and respond to signals from these lesions, and b) that anagen induction and psoriatic lesions share molecular "switch-on" mechanisms, which invite pharmacological targeting, once identified. Therefore, we advocate a novel, cross-fertilizing and integrative approach to psoriasis and hair research that systematically characterizes the "HF-psoriasis axis", focused on identification and therapeutic targeting of selected, shared signaling pathways in the future management of both, psoriasis and hair growth disorders.

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