Κυριακή 3 Οκτωβρίου 2021

Mini-Incision Parotidectomy-Our Technique

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Abstract

Traditional parotidectomy incision was devised by Blair (1912) which was modified by Bailey (1941). Over the years various approaches and techniques have evolved to improve the aesthetic outcome and at the same time for complete disease clearance with reduced complications. In this study, we evaluated the feasibility of our mini-incision parotidectomy technique along with the surgical and quality of life (QOL) outcomes. This prospective case series was conducted at Apollo Hospitals, Bangalore over a period of 2 years (June 2018-August 2020) and includes 20 patients. The surgical outcomes were assessed in terms of feasibility of mini-incision technique with respect to levels of parotid involved and functional outcomes in terms of presence or absence of complications like facial palsy (temporary or permanent), seroma and Frey's syndrome. Patient related quality of life (QOL) outcomes were assessed in terms of post-operative pain score, patient comfort score and cosmetic score by using numerical rating scale-11 (NRS-11). The mini-incision parotidectomy technique is feasible for lesions in all the parotid levels and conversion or lengthening of incision was not needed in any of the cases. 2(10%) patients had temporary facial palsy (House-Brackman grade III) which was recovered within 3 weeks after surgery. One patient (5%) with adenoid cystic carcinoma had permanent facial palsy. Out of 20 patients 2(10%) had seroma and 1(5%) patient presented with Frey's syndrome. Mean post-operative pain score at 0, 6 and 24 h were 4.8, 3.4 and 1.8 out of 10 respectively. Mean comfort score was 9 out of 10 and mean cosmetic score was 9.5 out of 10. Mini-incision parotidectomy technique can render improved functional as well as aesthetic outcomes after parotidectomy without compromising the surgical clearance of the disease process.

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A New Biomarker in Differentiation of Mucosal Chronic Otitis Media from Squamous Chronic Otitis Media: The Systemic Immune-Inflammation Index (SII)

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Abstract

The Systemic Immune-inflammation Index (SII) is a new biomarker based on the number of neutrophils, platelets, and lymphocytes in the Complete blood count, and is shown as diagnostic and prognostic in many diseases. Mucosal or Squamous COM differentiation is necessary preoperatively in chronic otitis media patients. The purpose of this study was to test the predictive value of inflammation markers to predict the differentiation of Mucosal COM and Squamous COM. Our aim is; using "SII" as a powerful test to differentiate cholesteatoma and active mucosal middle ear disease. In the present study, 300 patients who underwent mastoidectomy ± tympanoplasty between 2010 and 2020 were retrospectively evaluated. The patients were divided into two equal groups as clinical, microscopically, and pathologically Squamosal COM (Cholesteatoma) and Mucosal COM (Suppurative) (n = 150). Routine hemogram tests were performed for both groups. White blood cell, red blood cell, neutrophil, lymphocyte, and platelet numbers were calculated. The SII value was calculated manually according to the formula of "neutrophil × platelet/lymphocyte. There were a total of 300 patients who were aged 20–63 in both groups. A total of 130 of these patients were male (43%), and 170 (57%) were female. In terms of NLR and PLR, Group 2 (Mucosal COM) had higher values at statistically significant levels (p < 0.001, p < 0.001, respectively). In terms of SII, Group 2 (Mucosal COM) had higher values at statistically significant levels (p < 0.001). According to the results of the ROC Analysis in our series, it was found that NLR, PLR, and SII values were above the acceptable level, and were statistically significant (p < 0.001, p < 0.001, p < 0.001, respectively). The cut-off value of SII was 470.29, sensitivity was 65.8, and specificity was 34. According to our study, hig h SII values in COM differentiation are very important in diagnosing Mucosal COM. SII values can help to the diagnosis in Squamous COM/Mucosal COM differentiation. There is no current practical, inexpensive, and widespread laboratory test used in the Mucosal/Squamous COM differentiation. SII can be diagnostic, and determine the treatment in this differentiation. A great number of studies are needed for SII values to become standard in COM.

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Three‐dimensional (3D) reconstruction and navigation in robotic‐assisted partial nephrectomy (RAPN) for renal masses in the solitary kidney: a comparative study

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Abstract

Background

Numerous efforts were made to improve renal function and oncologic outcomes in surgery for patients with kidney cancer. We explored new robotic methods in solitary kidneys.

Materials and Methods

We prospectively registered and included 16 patients in the 3D-RAPN group with a solitary kidney (anatomic or functional), and retrospectively identified 25 patients with a solitary kidney who received RAPN also operated by us for comparison.

Results

The rates of global clamping reduced in the 3D-RAPN group (37.5% VS 76%)while selective rates were higher (56.2% VS 20%) (p=0.028). The mean percentages of Scr increase (+20.2% VS +30.2%, p=0.045) and eGFR reduction ( -16.8% VS -27.1%) as well as rate of opening collecting systems (31.3% VS 72%, p=0.010) were lower in 3D-RAPN group.

Conclusions

3D-RAPN less impaired the renal function of patients with a solitary kidney and showed superiority or non-inferiority in other evaluation indexes compared to conventional RAPN.

This article is protected by copyright. All rights reserved.

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Molecular genotyping in refractory thyroid cancers in 2021: When, how and why? A review from the TUTHYREF network

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Bull Cancer. 2021 Sep 27:S0007-4551(21)00303-9. doi: 10.1016/j.bulcan.2021.06.009. Online ahead of print.

ABSTRACT

Refractory thyroid cancers include radio-iodine-refractory cancers, metastatic or locally advanced unresectable medullary and anaplastic thyroid cancers. Their management has been based for several years on the use of multi-target kinase inhibitors, with anti-angiogenic action, with the exception of anaplastic cancers usually treated with chemo- and radiotherapy. The situation has recently evolved due to the availability of molecular genotyping techniques allowing the discovery of rare but targetable molecular abnormalities. New treatment options have become available, more effective and less toxic than the previously available multi-target kinase inhibitors. The management of refractory thyroid cancers is therefore becoming more complex both at a diagnosis level with the need to know when, how and why to look for these mo lecular abnormalities but also at a therapeutic level, innovative treatments being hardly accessible. The cost of molecular analyzes and the access to treatments need also to be homogenized because disparities could lead to inequality of care at a national or international level. Finally, the strategy of identifying molecular alterations and treating these rare tumors reinforces the importance of a discussion in a multidisciplinary consultation meeting.

PMID:34593218 | DOI:10.1016/j.bulcan.2021.06.009

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Treatment of burn contractures with allogeneic human dermal fibroblasts improves Vancouver scar scale: A phase I/II trial

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J Plast Reconstr Aesthet Surg. 2021 Sep 17:S1748-6815(21)00405-8. doi: 10.1016/j.bjps.2021.08.018. Online ahead of print.

NO ABSTRACT

PMID:34593339 | DOI:10.1016/j.bjps.2021.08.018

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Redifferentiation of BRAF V600E-Mutated Radioiodine Refractory Metastatic Papillary Thyroid Cancer After Treatment With Dabrafenib and Trametinib

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Cureus. 2021 Aug 27;13(8):e17488. doi: 10.7759/cureus.17488. eCollection 2021 Aug.

ABSTRACT

Radioactive iodine-refractory metastatic differentiated thyroid cancer (RAIR) is associated with a poor prognosis. Multikinase inhibitors have demonstrated improvement in progression-free but not overall survival in such patients, but usage is limited by significant adverse effects and the development of resistance. Clinical research has demonstrated improvement in progression-free survival with the combined use of the BRAF/MEK inhibitor in patients with metastatic melanoma and anaplastic thyroid cancer with the BRAFV600E mutation and has shown promise in redifferentiation of BRAF-positive RAIR differentiated thyroid cancer. A 58-year-old woman went to her primary care physician for a growing mass on the left side of her neck. CT imaging noted a 6 x 8 x 6 cm mixed cystic and solid mass and lymphadenopathy. Core biopsy subsequently showed metastatic papillary thyroid cancer (Stage III, PT4a/PN1b), and she underwent a total thyroidectomy with left neck dissection. She then received 204mCi 131I post-total thyroidectomy. Unfortunately, her thyroglobulin continued to increase post-radioactive iodine (RAI) treatment, indicating persistent and/or recurrent thyroid cancer. An RAI-131 whole-body scan on the thyrogen protocol showed no significant RAI uptake. A fluorodeoxyglucose (FDG)-positron emission tomography (PET) CT scan was then performed, which sho wed recurrent metastatic disease with hypermetabolism noted in the left thyroid bed and FDG-avid bilateral cervical lymph nodes and pulmonary nodules. Given these findings, her cancer was classified as radioactive iodine refractory (RAIR). Molecular testing indicated the BRAFV600E mutation. After a discussion with the patient, it was decided to initiate therapy with a BRAF inhibitor (dabrafenib 150 mg twice a day) and MEK inhibitor (trametinib 2 mg once a day) in an attempt to redifferentiate RAIR. Repeat RAI-131 thyrogen whole body scan one month after initiation of therapy demonstrated left level 2 cervical lymphadenopathy radioiodine uptake. The patient subsequently received 216 mCi 131I treatment given evidence of redifferentiation. Her post-treatment scan indicated additional uptake in a left lower lobe pulmonary nodule as well as a left paratracheal mass indicating successful RAI-131 uptake by metastases. Her thyroglobulin level, six months post-RAI, decr eased to 4.0 indicating an encouraging response. Further surveillance, including imaging studies, is planned. This case illustrates the re-differential potential for dabrafenib and trametinib treatment in patients with BRAFV600E-mutated RAIR differentiated thyroid cancer. This therapy has been shown to be successful in small series of patients and could potentially be offered to RAIR patients with the BRAFV600E mutation as an alternative to multikinase treatment given its favorable side-effect profile.

PMID:34595070 | PMC:PMC8465644 | DOI:10.7759/cureus.17488

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Conjunctivoductivo‐Dacryocystorhinostomy: A Novel Surgery for Intractable Canalicular Obstruction

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Se alleviates homocysteine-induced fibrosis in cardiac fibroblasts via downregulation of lncRNA MEG3

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Exp Ther Med. 2021 Nov;22(5):1269. doi: 10.3892/etm.2021.10704. Epub 2021 Sep 7.

ABSTRACT

Selenium (Se) is considered to have antioxidant properties, which are beneficial for heart condition. Hyperhomocysteinemia (HHCY) has been suggested to potentially lead to heart failure and is characterized by cardiac fibrosis; however, investigation on the role of Se and HHCY in cardiac fibrosis is rare. Since previous studies demonstrated the important role of the long non-coding RNA maternally expressed 3 (MEG3) in some heart diseases, the present study aimed to determine how Se and MEG3 might exert regulatory effects on HCY-induced fibrosis in cardiac fibroblasts (CFs). Mouse CFs were isolated and treated with HCY and Se. The expression of α-smooth muscle actin (α-SMA), collagen I and III was detected by western blotting to reflect CF fibrosis. Reverse transcription-quantitative PCR was performed to determine the expression levels of MEG3. I nflammation and oxidative stress responses were analyzed by measuring TNF-α, IL-1β (ELISA) and reactive oxygen species levels (using a commercial kit), respectively. Cell Counting Kit-8 was used to evaluate CF proliferation. Total and phosphorylated (p) expression of janus kinase 2 (JAK2) and signal transducer and activator of transcription 3 (STAT3) was evaluated by western blotting. CFs were transfected with adenovirus expressing MEG3 short-hairpin RNA to knock down MEG3 expression. Se treatment downregulated the expression level of MEG3 in HCY-stimulated CFs, whilst inhibiting the inflammatory and oxidative stress response. Furthermore, Se inhibited the increased proliferation of CFs following HCY treatment. In addition, MEG3-knockdown in CFs could improve fibrosis caused by HCY. Furthermore, the ratios of p-JAK2/JAK2 and p-STAT3/STAT3 were decreased following treatment with Se or MEG3 silencing. Taken together, the findings from the present study suggested that Se may alleviat e cardiac fibrosis by downregulating the expression of MEG3 and reducing the inflammatory and oxidative stress response in CFs. This suggests that Se may be a potential therapeutic option for treating cardiac fibrosis in the future.

PMID:34594406 | PMC:PMC8456485 | DOI:10.3892/etm.2021.10704

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Novel function of fluvastatin in attenuating oxidized low-density lipoprotein-induced endothelial cell ferroptosis in a glutathione peroxidase4- and cystine-glutamate antiporter-dependent manner

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Exp Ther Med. 2021 Nov;22(5):1275. doi: 10.3892/etm.2021.10710. Epub 2021 Sep 8.

ABSTRACT

Oxidized low-density lipoprotein (ox-LDL) induces endothelial cell apoptosis and dysfunction. Statins are drugs that are clinically used to lower serum cholesterol levels, and they have been shown to exert vascular protective effects. In the present study, human umbilical vein endothelial cells were transfected with scramble control siRNA or siRNA specific for glutathione peroxidase (GPx)4 or cystine-glutamate antiporter (xCT). MTT, Matrigel and Transwell assays were used to evaluate cell proliferation, tube formation and migration, respectively. The levels of TNF-α, IL-α, 4-hydroxynonenal, GPx4 and xCT expression were detected by western blot analysis. It was demonstrated that ox-LDL promoted cytokine production and reduced the proliferation, migration and angiogenesis of endothelial cells. It was also observed that ox-LDL decreased GPx4 and xC T expression and induced ferroptosis. Furthermore, the inhibition of ferroptosis by deferoxamine mesylate attenuated ox-LDL-induced endothelial cell dysfunction and restored ox-LDL-decreased GPx4 and xCT expression. Consistent with these results, GPx4 and xCT knockdown by siRNA transfection aggravated ox-LDL-induced endothelial cell dysfunction and inhibition of proliferation. To the best of our knowledge, the present study was the first to discover that fluvastatin may protect endothelial cells from ox-LDL-induced ferroptosis and dysfunction. Furthermore, knockdown of GPx4 and xCT expression blunted the protective effects of fluvastatin on ox-LDL-treated endothelial cells. These data indicated a novel function of fluvastatin in the protection of endothelial cells from ox-LDL-induced ferroptosis, the mechanism of which involves the regulation of GPx4 and xCT.

PMID:34594412 | PMC:PMC8456483 | DOI:10.3892/etm.2021.10710

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Association between obesity and iron deficiency (Review)

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Exp Ther Med. 2021 Nov;22(5):1268. doi: 10.3892/etm.2021.10703. Epub 2021 Sep 7.

ABSTRACT

Obesity is a risk factor for several comorbidities and complications, including iron deficiency anemia. Iron deficiency anemia is a serious global public health problem, with a worldwide prevalence. The high prevalence of obesity in combination with iron deficiency incidence observed in different age and sex categories suggests an association between obesity and iron status. Obesity may disrupt iron homeostasis, resulting in iron deficiency anemia. The association between obesity and iron deficiency may be due to increased hepcidin levels mediated by chronic inflammation. Hepcidin is a small peptide hormone that functions as a negative regulator of intestinal iron absorption. Significant body weight loss in overweight and obese individuals decreases chronic inflammation and serum hepcidin levels, resulting in improved iron status due to increased iron absorption. However, further randomized controlled trials are required to confirm this effect.

PMID:34594405 | PMC:PMC8456489 | DOI:10.3892/etm.2021.10703

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miR-122-5p downregulation attenuates lipopolysaccharide-induced acute lung injury by targeting IL1RN

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Exp Ther Med. 2021 Nov;22(5):1278. doi: 10.3892/etm.2021.10713. Epub 2021 Sep 8.

ABSTRACT

MicroRNAs (miRs) and inflammatory cytokines can induce acute lung injury (ALI), which can develop into acute respiratory distress syndrome in severe cases. Previous research has revealed that miR-122-5p participates in the development of ALI, and that its expression is positively associated with ALI. However, the mechanism by which miR-122-5p contributes to ALI remains to be determined. In the current study, TargetScan and dual luciferase reporter gene assays were used to confirm that IL-1 receptor antagonist (IL1RN) was a target of miR-122-5p. Subsequently, by referring to previous literature, a lipopolysaccharide (LPS)-induced ALI cell model was established. A549 cells were transfected with mimic control or miR-122-5p mimics for 24 h, and 10 µg LPS was used to treat the transfected cells for 12 h. The results revealed that miR-122-5p mimics dec reased cell viability and promoted apoptosis. Lactate dehydrogenase (LDH) release assays indicated that miR-122-5p mimics increased LDH release. ELISA demonstrated that miR-122-5p mimics promoted TNF-α, IL-1β and IL-6 expression levels. A549 cells were transfected with inhibitor control, miR-122-5p inhibitor, miR-122-5p inhibitor + control-small interfering (si)RNA or miR-122-5p inhibitor + IL1RN-siRNA for 24 h, after which the cells were treated with 10 µg LPS for 12 h. The results revealed that the effects of the miR-122-5p inhibitor were the opposite of those of the miR-122-5p mimic. All the effects of miR-122-5p inhibitor on LPS-treated A549 cells were significantly reversed by IL1RN-siRNA. Overall, the results highlighted miR-122-5p as a potential novel target for the treatment of ALI.

PMID:34594415 | PMC:PMC8456493 | DOI:10.3892/etm.2021.10713

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