Insurance type is associated with appropriate use of surgical and adjuvant care for differentiated thyroid carcinoma

xlomafota13 shared this article with you from Inoreader Insurance type is associated with appropriate use of surgical and adjuvant care for differentiated thyroid carcinoma Via radioactive iodine Surgery. 2021 Sep 30:S0039-6060(21)00794-7. doi: 10.1016/j.surg.2021.07.038. Online ahead of print. ABSTRACT BACKGROUND: We aimed to characterize the association between differentiated thyroid cancer (DTC) patient insurance status and appropriateness of therapy (AOT) regarding extent of thyroidectomy and radioactive iodine (RAI) treatment. METHODS: The National Cancer Database was queried for DTC patients diagnosed between 2010 and 2016. Adjusted odds ratios (AOR) for AOT, as defined by the American Thyroid Association guidelines, and hazard ratios (HR) for overall survival (OS) were calculated. A difference-in-differences (DD) analysis examined the association of Medicaid expansion with outcomes for low-income patients aged <65. RESULTS: A total of 224,500 patients were included. Medicaid and uninsured patients were at increased risk of undergoing inappropriate therapy, including inappropriate lobectomy (Medicaid 1.36, 95% confidence interval [CI]: 1.21-1.54; uninsured 1.30, 95% CI: 1.05-1.60), and under-treatment with RAI (Medicaid 1.20, 95% CI: 1.14-1.26; uninsured 1.44, 95% CI: 1.33-1.55). Inappropriate lobectomy (HR 2.0, 95% CI: 1.7-2.3, P < .001) and under-treatment with RAI (HR 2.3, 95% CI: 2.2-2.5, P < .001) were independently associated with decreased survival, while appropriate surgical resection (HR 0.3, 95% CI: 0.3-0.3, P < .001) was associated with improved odds of survival; the model controlled for all relevant clinico-pat hologic variables. No difference in AOT was observed in Medicaid expansion versus non-expansion states with respect to surgery or adjuvant RAI therapy. CONCLUSION: Medicaid and uninsured patients are at significantly increased odds of receiving inappropriate treatment for DTC; both groups are at a survival disadvantage compared with Medicare and those privately insured. PMID:34600741 | DOI:10.1016/j.surg.2021.07.038 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Days alive and out of hospital following transoral robotic surgery: Cohort study of 262 patients with head and neck cancer

xlomafota13 shared this article with you from Inoreader Days alive and out of hospital following transoral robotic surgery: Cohort study of 262 patients with head and neck cancer Via Head & Neck Abstract Background Days alive and out of hospital (DAOH) is a validated outcome in clinical trials, since it reflects procedure-associated morbidity and mortality. Transoral robotic surgery (TORS) has become a widely adopted procedure with increasing demand for knowledge and data on morbidity. Methods Retrospective single-center assessment of a prospective TORS database comprising patients treated for malignancy between 2013 and 2018 using DAOH to describe procedure- and disease-related morbidity the first 12-postoperative months. Results For 262 patients, median DAOH365 was 357 days (IQR 351–360). Indications for TORS were (i) primary curative resection (61%), (ii) salvage resection (15%), and (iii) diagnostic work-up of cancer of unknown primary in the head and neck (24%). Median DAOH365 was 359 days (IQR 351–361 days), 348 days (IQR 233–355), and 357 days (351–361), respectively. Pneumonia had the highest impact in DAOH365 reduction. Conclusion Total median DAOH365 after TORS was 357 days. The main cause leading to DAOH365 reduction was pneumonia. View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Auditory, Visual, and Cross-Modal Mismatch Negativities in the Rat Auditory and Visual Cortices

xlomafota13 shared this article with you from Inoreader Auditory, Visual, and Cross-Modal Mismatch Negativities in the Rat Auditory and Visual Cortices Via cortical auditory Front Hum Neurosci. 2021 Sep 17;15:721476. doi: 10.3389/fnhum.2021.721476. eCollection 2021. ABSTRACT When the brain tries to acquire an elaborate model of the world, multisensory integration should contribute to building predictions based on the various pieces of information, and deviance detection should repeatedly update these predictions by detecting "errors" from the actual sensory inputs. Accumulating evidence such as a hierarchical organization of the deviance-detection system indicates that the deviance-detection system can be interpreted in the predictive coding framework. Herein, we targeted mismatch negativity (MMN) as a type of prediction-error signal and investigated the relationship between multisensory integration and MMN. In particular, we studied whether and how cross-modal information processing affected MMN in rodents. We designed a new surface microelectrode array and simultaneously recorded visual and auditory evoked pote ntials from the visual and auditory cortices of rats under anesthesia. Then, we mapped MMNs for five types of deviant stimuli: single-modal deviants in (i) the visual oddball and (ii) auditory oddball paradigms, eliciting single-modal MMN; (iii) congruent audio-visual deviants, (iv) incongruent visual deviants, and (v) incongruent auditory deviants in the audio-visual oddball paradigm, eliciting cross-modal MMN. First, we demonstrated that visual MMN exhibited deviance detection properties and that the first-generation focus of visual MMN was localized in the visual cortex, as previously reported in human studies. Second, a comparison of MMN amplitudes revealed a non-linear relationship between single-modal and cross-modal MMNs. Moreover, congruent audio-visual MMN exhibited characteristics of both visual and auditory MMNs-its latency was similar to that of auditory MMN, whereas local blockage of N-methyl-D-aspartic acid receptors in the visual cortex diminished it as well as visual MMN. These results indicate that cross-modal information processing affects MMN without involving strong top-down effects, such as those of prior knowledge and attention. The present study is the first electrophysiological evidence of cross-modal MMN in animal models, and future studies on the neural mechanisms combining multisensory integration and deviance detection are expected to provide electrophysiological evidence to confirm the links between MMN and predictive coding theory. PMID:34602996 | PMC:PMC8484534 | DOI:10.3389/fnhum.2021.721476 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Massive Cervical Lymphadenopathy Post-COVID-19 Vaccination

xlomafota13 shared this article with you from Inoreader Massive Cervical Lymphadenopathy Post-COVID-19 Vaccination Via ear nose throat Ear Nose Throat J. 2021 Oct 2:1455613211048984. doi: 10.1177/01455613211048984. Online ahead of print. ABSTRACT The coronavirus disease 2019 (COVID-19) is a global pandemic caused by severe acute respiratory syndrome coronavirus 2. Rapid spread with rampant growth of cases and deaths brought forth an urgent need for novel therapies including vaccinations. The mRNA vaccines for COVID-19 disease have been implemented at an unprecedented scale in an effort to combat the unrelen ting pandemic. Such a massive scale vaccination program is bound to coincide with adverse events related to treatment. We present a case of massive cervical lymphadenopathy in a 58-year-old male patient post-Moderna COVID-19 vaccination. Additional investigations did not identify malignancy and he was diagnosed with vaccine-related lymphadenopathy. Patient significantly improved with corticosteroid treatment within 2 days of admission. Lymphadenopathy is reported as the second most common local reaction to the Moderna vaccine. Promoting knowledge of this side effect, particularly in the setting widespread vaccination efforts, would allow for better management of cases, especially in relation to oncologic patients. PMID:34601889 | DOI:10.1177/01455613211048984 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Solitary neurofibroma in the external auditory canal

xlomafota13 shared this article with you from Inoreader Solitary neurofibroma in the external auditory canal Via ear nose throat Ear Nose Throat J. 2021 Oct 2:1455613211048978. doi: 10.1177/01455613211048978. Online ahead of print. ABSTRACT Significance Statement: Neurofibromas, derived from perineural cells, are usually benign in the nervous system. Although neurofibromas are common in the head and neck, they rarely affect the external auditory canal (EAC), and few cases have been reported. We describe a case of a solitary EAC neurofibroma with otoscopy, radiological imaging, a surgical approa ch, and an uneventful outcome. PMID:34601890 | DOI:10.1177/01455613211048978 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Mangiferin inhibits hypoxia/reoxygenation-induced alveolar epithelial cell injury via the SIRT1/AMPK signaling pathway

xlomafota13 shared this article with you from Inoreader Mangiferin inhibits hypoxia/reoxygenation-induced alveolar epithelial cell injury via the SIRT1/AMPK signaling pathway Via Experimental and therapeutic medicine Exp Ther Med. 2021 Nov;22(5):1220. doi: 10.3892/etm.2021.10654. Epub 2021 Aug 26. ABSTRACT Lung ischemia-reperfusion injury (LIRI) is one of the complications that can occur after lung transplantation and may lead to morbidity and mortality. Mangiferin (MAF) is a naturally occurring glucosyl xanthone that has been documented to possess anti-inflammatory, immunomodulatory and potent antioxidant effects. The purpose of the present study was to investigate the effect of MAF on LIRI using a hypoxia-reoxygenation (H/R) cell model. In the present study, the viability of lung alveolar epithelial cells (A549) and H/R-A549 were detected by MTT assay. ELISA was used to evaluate the expression levels of IL-6 and IL-1β. TUNEL assay and western blotting were used to evaluate the apoptosis. In addition, H/R-A549 cells were treated with sirtinol, which is known inhibitor of sirtuin 1 (SIRT1) activity, to determine the effects of MAF on proteins asso ciated with the SIRT1/5'AMP-activate protein kinase (AMPK) signaling pathway using western blotting. The results showed that 20 µM MAF exerted a protective effect on A549 cells against H/R mediating no clear cytotoxic effects. In terms of inflammation, MAF reduced IL-6, IL-1β, cyclooxygenase-2 and inducible nitric oxide synthase expression, which was accompanied by activation of the SIRT1/AMPK signaling pathway. In addition, compared with those in the group treated with sirtinol, expression of SIRT1, Bcl-2 and AMPK activity were elevated in MAF-treated H/R-A549 cells, whereas the expression of Bax, cleaved caspase-3 and cleaved caspase-9 was suppressed. TUNEL analysis of H/R-A549 cells treated with MAF in combination with sirtinol revealed that treatment with sirtinol blocked the SIRT1/AMPK signaling pathway and increased the apoptosis rate compared with the MAF group. Taken together, results of the present study revealed that MAF could inhibit lung H/R cell injury through the SIR T1/AMPK signaling pathway. PMID:34603517 | PMC:PMC8453333 | DOI:10.3892/etm.2021.10654 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Resolvin D2 suppresses NLRP3 inflammasome by promoting autophagy in macrophages

xlomafota13 shared this article with you from Inoreader Resolvin D2 suppresses NLRP3 inflammasome by promoting autophagy in macrophages Via Experimental and therapeutic medicine Exp Ther Med. 2021 Nov;22(5):1222. doi: 10.3892/etm.2021.10656. Epub 2021 Aug 26. ABSTRACT Inflammasome, a multiprotein complex that regulates interleukin (IL)-1β secretion and pyroptosis, participates in numerous inflammatory diseases, including sepsis, atherosclerosis and type-2 diabetes. Investigating the inflammasome regulation is therefore crucial to understand the inflammasome activation and develop treatment for the related diseases. In addition, it remains unknown how the inflammasome is naturally suppressed during the inflammatory process. The present study aimed to investigate the role of resolvin D2 (RvD2), an innate suppressor of inflammation produced from essential ω3-polyunsaturated fatty acids, in the activation of the inflammasome via in vitro and in vivo experiments. The effects of RvD2 on the cytokine production of inflammasome-related peritonitis were determined, and the NLRP3 inflammasome activation was investigated in the presence of RvD2. Moreover, the potential mechanisms underlying RvD2 in NLRP3 inflammasome regulation through autophagy and proteasome were investigated. The results of the present study demonstrated that RvD2 suppressed inflammasome-mediated peritonitis in vivo and regulated the NLR family pyrin domain containing 3 (NLRP3) inflammasome, but not in absent in melanoma 2 (AIM2), NLR family CARD domain containing 4 (NLRC4) inflammasomes. Mechanistically, RvD2 was found to promote the degradation of NLRP3 through autophagy, and the inhibition of autophagy could reverse the RvD2-mediated suppression of NLRP3 inflammasome in vitro and partially reverse the inflammasome-mediated peritonitis in vivo. In summary, the present study reported the negative regulation of NLRP3 inflammasome activation by RvD2. The findings from this study may extend the knowledge of the innate regulation of inflammasome and highlight a possible target for inflammasome-r elated diseases. PMID:34603519 | PMC:PMC8453332 | DOI:10.3892/etm.2021.10656 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Resolvin D2 suppresses NLRP3 inflammasome by promoting autophagy in macrophages

xlomafota13 shared this article with you from Inoreader Resolvin D2 suppresses NLRP3 inflammasome by promoting autophagy in macrophages Via Experimental and therapeutic medicine Exp Ther Med. 2021 Nov;22(5):1222. doi: 10.3892/etm.2021.10656. Epub 2021 Aug 26. ABSTRACT Inflammasome, a multiprotein complex that regulates interleukin (IL)-1β secretion and pyroptosis, participates in numerous inflammatory diseases, including sepsis, atherosclerosis and type-2 diabetes. Investigating the inflammasome regulation is therefore crucial to understand the inflammasome activation and develop treatment for the related diseases. In addition, it remains unknown how the inflammasome is naturally suppressed during the inflammatory process. The present study aimed to investigate the role of resolvin D2 (RvD2), an innate suppressor of inflammation produced from essential ω3-polyunsaturated fatty acids, in the activation of the inflammasome via in vitro and in vivo experiments. The effects of RvD2 on the cytokine production of inflammasome-related peritonitis were determined, and the NLRP3 inflammasome activation was investigated in the presence of RvD2. Moreover, the potential mechanisms underlying RvD2 in NLRP3 inflammasome regulation through autophagy and proteasome were investigated. The results of the present study demonstrated that RvD2 suppressed inflammasome-mediated peritonitis in vivo and regulated the NLR family pyrin domain containing 3 (NLRP3) inflammasome, but not in absent in melanoma 2 (AIM2), NLR family CARD domain containing 4 (NLRC4) inflammasomes. Mechanistically, RvD2 was found to promote the degradation of NLRP3 through autophagy, and the inhibition of autophagy could reverse the RvD2-mediated suppression of NLRP3 inflammasome in vitro and partially reverse the inflammasome-mediated peritonitis in vivo. In summary, the present study reported the negative regulation of NLRP3 inflammasome activation by RvD2. The findings from this study may extend the knowledge of the innate regulation of inflammasome and highlight a possible target for inflammasome-r elated diseases. PMID:34603519 | PMC:PMC8453332 | DOI:10.3892/etm.2021.10656 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

MicroRNA-92b promotes cell proliferation and invasion in osteosarcoma by directly targeting Dickkopf-related protein 3

xlomafota13 shared this article with you from Inoreader MicroRNA-92b promotes cell proliferation and invasion in osteosarcoma by directly targeting Dickkopf-related protein 3 Via Experimental and therapeutic medicine Exp Ther Med. 2021 Nov;22(5):1258. doi: 10.3892/etm.2021.10693. Epub 2021 Sep 3. ABSTRACT [This retracts the article DOI: 10.3892/etm.2017.5356.]. PMID:34603526 | PMC:PMC8453327 | DOI:10.3892/etm.2021.10693 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Antibodies against thyroid-stimulating hormone receptor cause maternal-neonatal transmission of Graves' Disease

xlomafota13 shared this article with you from Inoreader Antibodies against thyroid-stimulating hormone receptor cause maternal-neonatal transmission of Graves' Disease Via Experimental and therapeutic medicine Exp Ther Med. 2021 Nov;22(5):1253. doi: 10.3892/etm.2021.10688. Epub 2021 Sep 3. ABSTRACT The present study aimed to investigate whether the thyroid-stimulating hormone receptor (TSHR) autoantibodies (Ab) from mothers with Graves' disease (GD) could cause neonatal thyroid disease and the underlying mechanisms of this. An adenovirus expressing the TSHR A-subunit and a control adenovirus expressing β-galactosidase was constructed by Beijing Sino Geno Max Co., Ltd. The sequences were subsequently verified and amplified via PCR. A GD model was established in female BALB/c mice (n=90) by three intramuscular injections of a TSHR-expressing adenovirus (Ad-TSHR). Mice injected with Ad-β-galactosidase served as a sham immunization group. The immunized females were paired with unimmunized males to generate offspring. The serum levels of TSHR-Ab and thyroxine (T4) of mothers and neonates were measured after delivery. Breast milk was collected f rom the stomachs of neonatal mice to determine the TSHR-Ab levels. The positive rate of serum TSHR-Ab (>0.3 IU/l) in the TSHR group was 99% (89/90) and 0% in the sham group. The mother mice in the TSHR group had elevated serum T4 levels and the thyroid pathological features of Graves' hyperthyroidism.GD mice gave birth to smaller newborns with thyroid pathological changes and higher serum levels of TSHR-Ab and T4, compared to the offspring in the sham group. The TSHR-Ab levels in breast milk from the GD mice declined with time. Mice immunized with Ad-TSHR exhibited the clinicopathological features of human GD and give birth to neonates with thyroid disease at birth. PMID:34603521 | PMC:PMC8453324 | DOI:10.3892/etm.2021.10688 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Quercetin suppresses inflammatory cytokine production in rheumatoid arthritis fibroblast-like synoviocytes

xlomafota13 shared this article with you from Inoreader Quercetin suppresses inflammatory cytokine production in rheumatoid arthritis fibroblast-like synoviocytes Via Experimental and therapeutic medicine Exp Ther Med. 2021 Nov;22(5):1260. doi: 10.3892/etm.2021.10695. Epub 2021 Sep 6. ABSTRACT Rheumatoid arthritis (RA) is a chronic, progressive and systemic autoimmune disease mainly characterized by symmetric multijoint synovitis. Quercetin has anti-inflammatory, anti-oxidation and immune regulation activities, and therefore shows high medicinal value. The present study aimed to observe the effect of quercetin on fibroblast-like synoviocytes (FLSs) in RA. Rheumatoid arthritis fibroblast-like synoviocytes (RAFLSs) were pretreated with 50 nmol/l quercetin for 2 h and were then stimulated using TNF-α for 24 h for subsequent experiments. RAFLSs were transfected with short interfering (si)-X-inactive specific transcript (XIST), microRNA (miR)-485 mimic, miR-485 inhibitor or si-PSMB8 or combination. ELISA, PCR and western blotting was used to evaluate the effect of quercetin on RAFLSs treated with TNF-α. It was revealed that quercetin inhib ited the production of inflammatory cytokines and the expression of XIST in RAFLSs induced by TNF-α. Bioinformatics analysis indicated that XIST acted as a sponge for miR-485 and that proteasome subunit β type-8 (PSMB8) was a direct target of miR-485. Moreover, PSMB8 functioned as a suppressor in inflammatory cytokine production of RAFLSs induced by TNF-α. Overall, quercetin was observed to inhibit the production of inflammatory cytokines and the expression of XIST in RAFLSs induced by TNF-α. Moreover, XIST-silencing could suppress the inflammatory reaction by sponging miR-485 in cells treated with TNF-α. Altogether, quercetin could suppress the development of RA in vitro. PMID:34603528 | PMC:PMC8453329 | DOI:10.3892/etm.2021.10695 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.