Case Reports in Otolaryngology

Arteriovenous Malformation in the Auricle in a 59-Year-Old Woman, Junhui Jeong Volume 2021 (2021), Article ID 7438571, 3 pages

A Case of Nasopharyngeal Mycobacteriosis with Bony Erosion of the External Skull Base, Kohei Matsuo, Satoshi Tanaka, Masayuki Sakata, Hiroki Takeda, Akihiro Nagata, Masashi Mori, Rie Ito, Yoshifumi Yamamoto, Kiyonobu Ueno, and Atsuhiko Uno Volume 2021 (2021), Article ID 7500273, 4 pages

Deep Neck Infection: Atypical Presentation of Papillary Thyroid Cancer, Apichana Mahattanapreut, Rangsima Aroonroch, Chalermchai Chintrakarn, and Chutintorn Sriphrapradang Volume 2021 (2021), Article ID 1479201, 4 pages

Alobar Holoprosencephaly with Cebocephaly in a Neonate Born to an HIV-Positive Mother in Eastern Uganda, Franck Katembo Sikakulya, Sonye Magugu Kiyaka, Robert Masereka, and Robinson Ssebuufu Volume 2021 (2021), Article ID 7282283, 4 pages

ALK-Positive Anaplastic Large Cell Lymphoma: A Diagnostic Dilemma for the Otolaryngologist in a Resource Poor Setting, Nicholas Figaro, Rickhi Ramoutar, Rodolfo Arozarena, Dawn Meyers, and Solaiman Juman Volume 2021 (2021), Article ID 3756742, 6 pages

INI1-Intact Sinonasal Carcinoma with Rhabdoid Features, Erin Mulry, Danielle M. Blake, Poornima Hegde, and Todd E. Falcone Volume 2021 (2021), Article ID 6075130, 3 pages

Bilateral Recurrent Laryngeal Nerve Palsy following Total Thyroidectomy in Triple A Syndrome, an Unexpected but Critical Complication, Mathieu Chamberland, Marc-Antoine Poulin, and Danielle Beaudoin Volume 2021 (2021), Article ID 1315117, 3 pages

Importance of Imaging in Congenital Unilateral Vocal Fold Paralysis: A Case of Neck Neuroblastoma Presenting with Unilateral Vocal Fold Paralysis, W. X. Yeo, C. Y. Chan, and K. K. H. Tan Volume 2021 (2021), Article ID 7368567, 4 pages

A Rare Complication of Fine-Needle Aspiration of Neck Structures, Yazeed M. Qadadha, Nainika Nanda, Chad Ennis, and Timothy McCulloch Volume 2021 (2021), Article ID 8944119, 5 pages

Delayed-Onset Neuropathic Pain after Septoplasty, Foteini-Stefania Koumpa, Mark Ferguson, and Hesham Saleh Volume 2021 (2021), Article ID 9966318, 4 pages

Docosahexaenoic acid supplementation alleviates behavioral memory impairment caused via repeated administration of sevoflurane in aged rats

xlomafota13 shared this article with you from Inoreader Docosahexaenoic acid supplementation alleviates behavioral memory impairment caused via repeated administration of sevoflurane in aged rats Via Experimental and therapeutic medicine Exp Ther Med. 2022 Jan;23(1):46. doi: 10.3892/etm.2021.10968. Epub 2021 Nov 15. ABSTRACT Elderly patients often need repeated surgical intervention, so it is important to determine the impact of repeated exposure to anesthetics on learning and memory. Docosahexaenoic acid (DHA) is considered to be an essential nutrient for maintaining brain health. The aim of the present study was to explore the potential effects of DHA on memory impairment induced by repeated sevoflurane anesthesia in aged rats. A total of 54 Sprague Dawley aged rats (18 months) were randomly divided into the following six groups: i) Control group; ii) sevoflurane group (Sev, 2.5% for 5 min); iii) DHA group (3 g/kg); iv) Sev + DHA (0.3 g/kg) group; v) Sev + DHA (1 g/kg) group; and vi) Sev + DHA (3 g/kg) group. Morris water maze experiment was performed to evaluate the learning and memory ability of the rats following treatment. H&E staining was used to observe any histological changes. Superoxide dismutase, malondialdehyde and glutathione peroxidase levels were detected using ELISA. Immunohistochemistry and western blotting were used to determine nuclear factor erythroid-2-related factor 2 (Nrf2) and heme oxygenase 1 (HO-1) protein expression levels. Following repeated sevoflurane anesthesia, rats exhibited a prolonged escape latency. The number of times rats crossed the platform and the time spent in the target quadrant were also significantly reduced by repeated sevoflurane anesthesia. However, rats treated with Sev + DHA exhibited a reduced escape latency, whilst the number of times they crossed the platform and the time spent in the target quadrant increased compared with Sev treatment alone. Histopathological examination revealed that DHA treatment ameliorated the disordered neuron arrangement, deep staining of the neuronal nucleus pyknosis and cell edema observed in the brain tissue induced by repeated sevoflurane anesthesia. Furthermo re, the protein expression levels of Nrf2 and HO-1 were demonstrated to be significantly increased in rats treated with DHA and exposed to repeated sevoflurane anesthesia compared with those in untreated rats that underwent repeated sevoflurane anesthesia. In conclusion, the present study revealed that DHA exerted protective effects against impairments in learning and memory induced by repeated sevoflurane anesthesia in aged rats, which may be associated with the Nrf2/HO-1 signaling pathway. PMID:34934425 | PMC:PMC8652387 | DOI:10.3892/etm.2021.10968 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Role of methylene blue in detecting the sentinel lymph node in colorectal cancer: In vivo vs. ex vivo technique

xlomafota13 shared this article with you from Inoreader Role of methylene blue in detecting the sentinel lymph node in colorectal cancer: <em>In vivo</em> vs. <em>ex vivo</em> technique Via Experimental and therapeutic medicine Exp Ther Med. 2022 Jan;23(1):72. doi: 10.3892/etm.2021.10995. Epub 2021 Nov 24. ABSTRACT The identification of sentinel lymph nodes is a valuable oncological method, which aims at mapping lymphatic drainage and has the advantage of correctly staging the disease and assessing prognosis. Lymph node invasion is an important prognostic feature. In colorectal cancer, lymphadenectomy is not influenced by the positive or negative status of the sentinel lymph node. The identification of lymph nodes with possible invasion by staining the primary tumor with methylene blue can lead to improved staging and management. In other words, the consequent administration of neoadjuvant therapy (chemotherapy) to the appropriate patients may result in lower recurrence rates. Thus, the aim of the present study was to use methylene blue to identify the sentinel node/nodes in colorectal cancer and to determine whether the dye-capturing nodes were invaded by th e tumor. This is a non-randomized prospective study, in which 26 patients with colon cancer with surgical indication were enrolled. Two types of methods were utilized: in vivo (16 patients) and ex vivo (10 patients). The identification rate was 75% for the in vivo technique and 60% for the ex vivo technique, resulting in a 69.26% overall identification rate. Of 18 patients with sentinel lymph nodes identified using dye, routine histological examination detected metastases in 6 (33.33%) of these patients. In conclusion, further research should be conducted into how the clinical application of sentinel node detection can be employed in colorectal cancer. PMID:34934443 | PMC:PMC8649879 | DOI:10.3892/etm.2021.10995 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Insulin resistance quantified by the value of HOMA-IR and cardiovascular risk in patients with type 2 diabetes

xlomafota13 shared this article with you from Inoreader Insulin resistance quantified by the value of HOMA-IR and cardiovascular risk in patients with type 2 diabetes Via Experimental and therapeutic medicine Exp Ther Med. 2022 Jan;23(1):73. doi: 10.3892/etm.2021.10996. Epub 2021 Nov 24. ABSTRACT Cardiovascular disease (CVD) is recognized as a leading cause of death worldwide. Obesity, dyslipidemia, insulin resistance (IR), interconnected pathological conditions constitute risk factors that are closely associated with CVD. The aim of the present study was to highlight the association of IR with cardiovascular risk (CVR). The epidemiological, cross-sectional, non-interventional study was conducted over 12 months (2019-2020) within a research grant and included a sample of 400 subjects divided into 2 subgroups: group 1 (control) subjects did not have diabetes (n=200) and group 2 had type 2 diabetes (T2DM) (n=200). The Framingham risk score (FRS) was calculated according to the 2008 general CVD risk model from the Framingham Heart Study. Subsequent to a correlation of the value of homeostasis model assessment of insulin resistance (HOMA-IR) wi th the degree of CVR, the IR was higher in both groups, and CVR also increased. After being quantified by the Spearman correlation coefficient, the correlation in group 2 was higher at 0.625 compared to group 1 where this coefficient had a value of 0.440. A high FRS (FRS of 20%) was significantly associated with IR. The results therefore show that HOMA-IR is an independent risk factor for high FRS. New therapies focused on decreasing IR may contribute to decreased CVD. PMID:34934444 | PMC:PMC8649857 | DOI:10.3892/etm.2021.10996 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Aggressive prolactinoma (Review)

xlomafota13 shared this article with you from Inoreader Aggressive prolactinoma (Review) Via Experimental and therapeutic medicine Exp Ther Med. 2022 Jan;23(1):74. doi: 10.3892/etm.2021.10997. Epub 2021 Nov 24. ABSTRACT Aggressive prolactinoma (APRL) is a subgroup of aggressive pituitary tumors (accounting for 10% of all hypophyseal neoplasia) which are defined by: invasion based on radiological and/or histological features, a higher proliferation profile when compared to typical adenomas and rapidly developing resistance to standard medication/protocols in addition to an increased risk of early recurrence. This is a narrative review focusing on APRL in terms of both presentation and management. Upon admission, the suggestive features may include increased serum prolactin with a large tumor diameter (mainly >4 cm), male sex, early age at diagnosis (<20 years), and genetic predisposition [multiple endocrine neoplasia type 1 (MEN1), aryl hydrocarbon receptor interacting protein (AIP), succinate dehydrogenase (SDHx) gene mutations]. Potenti al prognostic factors are indicated by assessment of E-cadherin, matrix metalloproteinase (MMP)-9, and vascular endothelial growth factor (VEGF) status. Furthermore, during management, APRL may be associated with dopamine agonist (DA) resistance (described in 10-20% of all prolactinomas), post-hypophysectomy relapse, mitotic count >2, Ki-67 proliferation index ≥3%, the need for radiotherapy, lack of response in terms of controlling prolactin levels and tumor growth despite multimodal therapy. However, none of these as an isolated element serves as a surrogate of APRL diagnosis. A fourth-line therapy is necessary with temozolomide, an oral alkylating chemotherapeutic agent, that may induce tumor reduction and serum prolactin reduction in 75% of cases but only 8% have a normalization of prolactin levels. Controversies surrounding the duration of therapy still exist; also regarding the fifth-line therapy, post-temozolomide intervention. Recent data suggest alternatives such as som atostatin analogues (pasireotide), checkpoint inhibitors (ipilimumab, nivolumab), tyrosine kinase inhibitors (TKIs) (lapatinib), and mTOR inhibitors (everolimus). APRL represents a complex condition that is still challenging, and multimodal therapy is essential. PMID:34934445 | PMC:PMC8652381 | DOI:10.3892/etm.2021.10997 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Reducing oxidative stress may be important for treating pirarubicin-induced cardiotoxicity with schisandrin B

xlomafota13 shared this article with you from Inoreader Reducing oxidative stress may be important for treating pirarubicin-induced cardiotoxicity with schisandrin B Via Experimental and therapeutic medicine Exp Ther Med. 2022 Jan;23(1):68. doi: 10.3892/etm.2021.10991. Epub 2021 Nov 23. ABSTRACT The cardiotoxicity of pirarubicin (THP) seriously affects its clinical application, which cannot be ignored. The antioxidant effect of schisandrin B (SchB) has been extensively reported in the context of dietotherapy. However, whether this antioxidant effect can protect the heart from THP damage remains unknown. The aim of the present study was to investigate whether the antioxidant effect of SchB can antagonize the cardiotoxicity of THP. Changes in electrocardiogram (ECG), echocardiography and serum lactate dehydrogenase, brain natriuretic peptide, creatine kinase MB and cardiac troponin T levels were used to detect the degree of cardiac damage. The levels of superoxide dismutase (SOD), malondialdehyde, catalase and total antioxidant capacity in the serum and heart were measured to observe the oxidative stress state of rats. Primary cardiomyocytes were cultured, and cell viability and reactive oxygen species (ROS) production were detected. Western blotting was used to detect the expression levels of SOD2, NOX2, pro/cleaved-caspase3 and Bcl-2/Bax in heart tissue and primary cardiomyocytes to verify the related signaling pathways. THP-treated rats showed a range of cardiac damage, including an abnormal ECG, echocardiography and myocardial enzymes. In the cellular experiments, cell viability decreased and ROS increased. However, this damage was alleviated after SchB treatment. Further studies demonstrated that SchB antagonized THP cardiotoxicity via its antioxidant effect. In conclusion, SchB protects the heart from THP damage in rats, and the mechanism may be closely associated with its antioxidant effect. PMID:34934439 | PMC:PMC8649856 | DOI:10.3892/etm.2021.10991 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Pathological complete response following cisplatin or carboplatin-based neoadjuvant chemotherapy for triple-negative breast cancer: A systematic review and meta-analysis

xlomafota13 shared this article with you from Inoreader Pathological complete response following cisplatin or carboplatin-based neoadjuvant chemotherapy for triple-negative breast cancer: A systematic review and meta-analysis Via Experimental and therapeutic medicine Exp Ther Med. 2022 Jan;23(1):91. doi: 10.3892/etm.2021.11014. Epub 2021 Nov 26. ABSTRACT The addition of platinum compounds to standard neoadjuvant chemotherapy (NACT) for triple-negative breast cancer (TNBC) is highly controversial. Platinum agents, such as cisplatin and carboplatin, are DNA-damaging agents which exhibit activity in breast cancer, particularly in the TNBC subgroup. In order to assess the efficacy of each most representative platinum agent (cisplatin and carboplatin) in patients with TNBC treated with NACT, the present study performed a systematic review and meta-analysis of all available published studies on TNBC. A search of PubMed was performed to identify studies that investigated platinum-based NACT in patients with TNBC. The primary endpoints were the pooled rate of the pathological complete response (pCR) between cisplatin vs. carboplatin-based NACT. A total of 24 studies were selected (17 studies for carboplati n and 6 studies for cisplatin and 1 study with both carboplatin and cisplatin, with 20 prospective studies) for the analysis of 1,711 patients with TNBC. Overall, the pooled rate of pCR in patients treated with platinum-based NACT was 48%. No significant differences were observed between the rates of pCR obtained under carboplatin vs cisplatin treatment. The carboplatin pCR rate was 0.470 [95% confidence interval (CI), 0.401-0.539], while the cisplatin pCR rate was 0.473 (95% CI, 0.379-0.568). The comparison between these two categories revealed no significant differences (P=0.959). In the whole, the present study demonstrates that neoadjuvant platinum-based chemotherapy improves the pCR rate in patients with TNBC, regardless of the platinum agent used. Carboplatin may thus represent a viable option due to its more favorable toxicity profile. PMID:34934456 | PMC:PMC8652390 | DOI:10.3892/etm.2021.11014 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Stomatin-knockdown effectively attenuates sepsis-induced oxidative stress and inflammation of alveolar epithelial cells by regulating CD36

xlomafota13 shared this article with you from Inoreader Stomatin-knockdown effectively attenuates sepsis-induced oxidative stress and inflammation of alveolar epithelial cells by regulating CD36 Via Experimental and therapeutic medicine Exp Ther Med. 2022 Jan;23(1):69. doi: 10.3892/etm.2021.10992. Epub 2021 Nov 23. ABSTRACT Sepsis-induced acute lung injury is a type of lung disease with a high fatality rate that is characterized by acute inflammation. In the present study, the underlying role and potential mechanism of the stomatin (STOM) protein were investigated in lipopolysaccharide (LPS)-induced oxidative stress and inflammation in a mouse lung epithelial cell line, MLE-12. The expression levels of STOM and CD36 were measured using reverse transcription-quantitative PCR and western blotting. Subsequently, the expression levels of STOM and CD36 in LPS-treated MLE-12 cells were knocked down or overexpressed, respectively, via transfection with a small interfering RNA-STOM or a CD36-overexpression vector. An RNA immunoprecipitation (RIP) assay was used to determine the interaction between STOM and CD36, while Cell Counting Kit-8 assay and ELISA were performed to dete ct cell viability and oxidative stress, respectively. Moreover, western blotting and ELISA kits were used to detect the expression levels of associated inflammatory factors. The results of the present study demonstrated that STOM expression was upregulated in MLE-12 cells treated with LPS compared with the untreated control group. According to the Search Tool for the Retrieval of Interacting Genes/Proteins database, it was predicted that STOM and CD36 had the ability to interact with each other. The predicted binding between STOM and CD36 was verified using a RIP assay. The results demonstrated that STOM positively regulated the expression of CD36. Moreover, in LPS-treated MLE-12 cells, STOM-knockdown reversed the inhibitory effects of LPS on cell viability, and the promoting effects of LPS on oxidative stress and inflammation. These aforementioned changes were alleviated by the overexpression of CD36. To conclude, the results of the present study revealed that STOM may interact wit h CD36 to affect the levels of oxidative stress and inflammation in LPS-treated MLE-12 cells. PMID:34934440 | PMC:PMC8649852 | DOI:10.3892/etm.2021.10992 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

Paeoniflorin inhibits proliferation and promotes autophagy and apoptosis of sweat gland cells

xlomafota13 shared this article with you from Inoreader Paeoniflorin inhibits proliferation and promotes autophagy and apoptosis of sweat gland cells Via Experimental and therapeutic medicine Exp Ther Med. 2022 Jan;23(1):53. doi: 10.3892/etm.2021.10975. Epub 2021 Nov 16. ABSTRACT Axillary bromhidrosis is sweat excreted by apocrine glands in the armpits, mouth corners and other parts. The clinical manifestation includes excessive sweating and heavy odor, leading to the growth of bacteria and skin disease. The present study investigated the mechanism underlying the effect of paeoniflorin (PF) in the treatment of bromhidrosis. PF was injected into the feet of rats, and the foot skin was dissected for histological analysis. Primary human sweat gland cells (hSGCs) were isolated from patients with bromhidrosis. After 24 h treatment with PF or 3-methyladenine, the production of reactive oxygen species (ROS), autophagy, apoptosis, proliferation and cell cycle distribution were determined. PF induced nuclear pyknosis in rat SGCs. In vitro PF treatment inhibited cell proliferation with a 25% inhibitory concentration of 9.530 � �M. Treatment with 9.530 µM PF for 24 h significantly increased apoptosis, ROS production and autophagy in hSGCs. PF promoted LC3B and Beclin 1 expression, but inhibited p62, phosphorylated (p)-PI3K and p-Akt expression. 3-methyladenine treatment reversed PF-induced changes in hSGCs. PF-induced inhibition of hSGC proliferation was associated with ROS production, apoptosis, and autophagy. These findings provide a basis for treating bromhidrosis. PMID:34934430 | PMC:PMC8652401 | DOI:10.3892/etm.2021.10975 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

In vitro and in vivo effects of AVA4746, a novel competitive antagonist of the ligand binding of VLA-4, in B-cell acute lymphoblastic leukemia

xlomafota13 shared this article with you from Inoreader <em>In vitro</em> and <em>in vivo</em> effects of AVA4746, a novel competitive antagonist of the ligand binding of VLA-4, in B-cell acute lymphoblastic leukemia Via Experimental and therapeutic medicine Exp Ther Med. 2022 Jan;23(1):47. doi: 10.3892/etm.2021.10969. Epub 2021 Nov 15. ABSTRACT Treatment of resistant or recurrent acute lymphoblastic leukemia (ALL) remains a challenge. It was previously demonstrated that the adhesion molecule integrin α4, referred to hereafter as α4, mediates the cell adhesion-mediated drug resistance (CAM-DR) of B-cell ALL by binding to vascular cell adhesion molecule-1 (VCAM-1) on bone marrow stroma. In addition, it was previously observed that the blockade of α4 with natalizumab or inhibition using the small molecule antagonist TBC3486 sensitized relapsed ALL cells to chemotherapy. However, α4-targeted therapy is not clinically available for the treatment of leukemia to date. In the present study, the use of a novel non-peptidic small molecule integrin α4 antagonist, AVA4746, as a potential new approach to combat drug-resistant B-ALL was explored. An in vitro co-culture = model of primary B- ALL cells and an in vivo xenograft model of patient-derived B-ALL cells were utilized for evaluation of AVA4746. VLA-4 conformation activation, cell adhesion/de-adhesion, endothelial tube formation, in vivo leukemia cell mobilization and survival assays were performed. AVA4746 exhibited high affinity for binding to B-ALL cells, where it also efficiently blocked ligand-binding to VCAM-1. In addition, AVA4746 caused the functional de-adhesion of primary B-ALL cells from VCAM-1. Inhibition of α4 using AVA4746 also prevented angiogenesis in vitro and when applied in combination with chemotherapy consisting of Vincristine, Dexamethasone and L-asparaginase, it prolonged the survival of ~33% of the mice in an in vivo xenograft model of B-ALL. These data implicate the potential of targeting the α4-VCAM-1 interaction using AVA4746 for the treatment of drug-resistant B-lineage ALL. PMID:34934426 | PMC:PMC8652384 | DOI:10.3892/etm.2021.10969 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

MiR-194-3p modulates the progression of colorectal cancer by targeting KLK10

xlomafota13 shared this article with you from Inoreader MiR-194-3p modulates the progression of colorectal cancer by targeting KLK10 Via Cellular and Molecular Biology Histol Histopathol. 2021 Dec 22:18413. doi: 10.14670/HH-18-413. Online ahead of print. ABSTRACT BACKGROUND: A rich history of studies have manifested the importance of miRNAs to cancer progression, while miR-194-3p has been seldom explored. OBJECTIVE: The purpose of this study is to unearth the way the KLK10/miR-194-3p axis modulates colorectal cancer (CRC). METHODS: Differentially expressed genes of CRC in TCGA database were analyzed. Western blot and qRT-PCR were employed to test protein and mRNA expressions of two researched genes. Their targeting was confirmed using dual-luciferase. Biological behaviors of cells were tested by a series of cellular functional assays. RESULT: Remarkably low miR-194-3p expression and high KLK10 expression were observed in cancer cells. Overexpressing miR-194-3p hindered the progression of CRC cells. Overexpression of miR-194-3p significantly weakened the promoting effect of upregulat ed KLK10 on cell migration, invasion and proliferation. Their targeting was verified by dual -luciferase assay. Therefore, miR-194-3p hindered cell behaviors of CRC through KLK10. CONCLUSION: This investigation casts new light on the treatment of CRC through the KLK10/miR-194-3p axis. PMID:34935123 | DOI:10.14670/HH-18-413 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.