Αρχειοθήκη ιστολογίου

Αλέξανδρος Γ. Σφακιανάκης
ΩτοΡινοΛαρυγγολόγος
Αναπαύσεως 5
Άγιος Νικόλαος Κρήτη 72100
2841026182
6032607174

Τετάρτη 22 Δεκεμβρίου 2021

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

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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

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Primary hyperparathyroidism-related giant parathyroid adenoma (Review)

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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

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

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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

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

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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

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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

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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

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Voluntary Cough Effectiveness and Airway Clearance in Neurodegenerative Disease

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J Speech Lang Hear Res. 2021 Dec 22:1-19. doi: 10.1044/2021_JSLHR-21-00308. Online ahead of print.

ABSTRACT

PURPOSE: Voluntary cough dysfunction is highly prevalent across multiple patient populations. Voluntary cough has been utilized as a screening tool for swallowing safety deficits and as a target for compensatory and exercise-based dysphagia management. However, it remains unclear whether voluntary cough dysfunction is associated with the ability to effectively clear the airwa y.

METHOD: Individuals with neurodegenerative disorders performed same-day voluntary cough testing and flexible endoscopic evaluations of swallowing (FEES). Participants who were cued to cough after exhibiting penetration to the vocal folds and/or aspiration with thin liquids during FEES met inclusion criteria. One-hundred and twenty-three trials were blinded, and the amount of residue before and after a cued cough on FEES was measured with a visual analog scale. Linear and binomial mixed-effects models examined the relationship between cough airflow during voluntary cough testing and the proportion of residue expelled.

RESULTS: Peak expiratory flow rate (p = .004) and cough expired volume from the entire epoch (p = .029) were significantly associated with the proportion of aspiration expelled from the subglottis. Peak expiratory flow rate values of 3.00 L/s, 3.50 L/s, and 5.30 L/s provided high predicted probabilities that ≥ 25%, ≥ 50%, and ≥ 80% asp irate was expelled. Accounting for depth of aspiration significantly improved model fit (p < .001).

CONCLUSIONS: These findings suggest that voluntary cough airflow is associated with cough effectiveness to clear aspiration from the subglottis, although aspiration amount and depth may play an important role in this relationship. These findings provide further support for the clinical utility of voluntary cough in the management of dysphagia.

PMID:34936376 | DOI:10.1044/2021_JSLHR-21-00308

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

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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

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