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.

Protective effects of syringic acid on inflammation, apoptosis and intestinal barrier function in Caco-2 cells following oxygen-glucose deprivation/reoxygenation-induced injury

xlomafota13 shared this article with you from Inoreader Protective effects of syringic acid on inflammation, apoptosis and intestinal barrier function in Caco-2 cells following oxygen-glucose deprivation/reoxygenation-induced injury Via Experimental and therapeutic medicine Exp Ther Med. 2022 Jan;23(1):66. doi: 10.3892/etm.2021.10989. Epub 2021 Nov 23. ABSTRACT Syringic acid (SA) is an abundant phenolic acid compound that has been demonstrated to yield therapeutic benefits in myocardial and renal ischemia/reperfusion (I/R). However, the role of SA in intestinal I/R injury is unclear. Thus, the present study aimed to investigate the protective effect of SA against intestinal I/R injury. Caco-2 cells were incubated with different doses of SA before oxygen-glucose deprivation/reoxygenation (OGD/R) induction. The viability of Caco-2 cells, the activity of lactate dehydrogenase (LDH), the production of pro-inflammatory cytokines and the levels of reactive oxygen species, superoxide dismutase and malondialdehyde were measured. Apoptosis was evaluated using a TUNEL assay and western blotting. Transepithelial electrical resistance and western blotting were performed to evaluate intestinal barrier function in Caco -2 cells. The present study revealed that pretreatment with SA significantly increased cell viability and reduced LDH release in Caco-2 cells subjected to OGD/R treatment. In addition, SA suppressed OGD/R-induced inflammatory responses by reducing pro-inflammatory cytokine levels. Furthermore, the levels of oxidative stress and apoptosis were ameliorated by SA. SA also alleviated the intestinal barrier disruption exhibited by Caco-2 cells after OGD/R injury. Overall, the present study revealed that SA may potentially protect Caco-2 cells from OGD/R injury, and that this effect may be attributed to its anti-inflammatory and anti-apoptotic activities, as well as its ability to protect the function of the intestinal barrier. PMID:34 934437 | PMC:PMC8649867 | DOI:10.3892/etm.2021.10989 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.

Primary hyperparathyroidism-related giant parathyroid adenoma (Review)

xlomafota13 shared this article with you from Inoreader Primary hyperparathyroidism-related giant parathyroid adenoma (Review) Via Experimental and therapeutic medicine Exp Ther Med. 2022 Jan;23(1):88. doi: 10.3892/etm.2021.11011. Epub 2021 Nov 26. ABSTRACT Primary hyperparathyroidism (PHPT), an endocrine condition caused by a parathyroid adenoma (PTA) in 80-85% of the cases, has shifted in the modern era to a mildly symptomatic phenotype due to the prompt recognition of hypercalcemia and to a minimally invasive surgical approach which has a curative potential. Clinical complications of PHTH are either related to high calcium or parathyroid hormone [also parathormone (PTH)] or both, while the originating tumor typically is small, without local mass effects. A distinct entity is represented by giant PTA (GPTA) which is considered at a weight of more than 3 (3.5) grams. The present article is a review of the literature involving practical points of non-syndromic PHPT-related GPTA. Most authors agree that pre-operatory calcium and PTH are higher in GPTA vs. non-GPTA. However, the clinical presentation of PHPT may be less severe, probably due to local mass effects that bring the patient to an early medical evaluation. Age distribution, sex ratio, rate of successful pre-operatory location do not differ from non-giant PTA. Hypovitaminosis D is more frequent in PTA of higher dimensions. Post-operative hypocalcemia, but not recurrent/persistent PHPT, is expected, even hungry bone disease. A higher rate of atypia is described although the tumor is mostly benign. Unusual presentations such as cystic transformation, initial diagnosis during pregnancy or auto-infarction have been reported. The ectopic localization of PTA presented in almost 15% of all cases may also be found in GPTA. What are the exact cutoffs for defining GPTA is still an open issue. PMID:34934453 | PMC:PMC8652388 | DOI:10.3892/etm.2021.11011 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.

Necrotizing fasciitis of the chest wall: A clinical case report and literature review

xlomafota13 shared this article with you from Inoreader Necrotizing fasciitis of the chest wall: A clinical case report and literature review Via Experimental and therapeutic medicine Exp Ther Med. 2022 Jan;23(1):90. doi: 10.3892/etm.2021.11013. Epub 2021 Nov 26. ABSTRACT Necrotizing fasciitis of the chest wall is a very rare pathology, but with significant mortality, representing a therapeutic challenge. All international reports indicate the need for early diagnosis and an aggressive medical-surgical attitude in order to improve the prognosis. In addition to a review of literature, we present a case developed secondary to a thoracic pleural drainage for pyopneumothorax associated with significant bronchopleural fistula in a destroyed tuberculous left lung. Along with medical treatment, extensive surgical debridement was required. Despite drainage incisions and negative pressure wound therapy (NPWT), the evolution of the fasciitis was difficult, due to bronchopleurocutaneous fistula. Thus, the Azorin procedure (transcervical mediastinoscopic closure of the left main bronchus) was performed. Once this procedure was completed, the inflammatory phenomena were controlled which allowed for a second step consisting of left pneumonectomy, with the application of specific methods for the prevention of bronchial fistula. The clinical case was a therapeutic challenge requiring a complex, staged, multidisciplinary approach due to both the immunocompromised terrain and the severity of the lesions. In conclusion, early recognition and aggressive and combined application of medical and surgical treatment methods can ensure therapeutic success. PMID:34934455 | PMC:PMC8652382 | DOI:10.3892/etm.2021.11013 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.