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.

Voluntary Cough Effectiveness and Airway Clearance in Neurodegenerative Disease

xlomafota13 shared this article with you from Inoreader Voluntary Cough Effectiveness and Airway Clearance in Neurodegenerative Disease Via swallowing exercises 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 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.

The Nonrecurrent Laryngeal Nerve Without Abnormal Subclavian Artery: Report of Two Cases and Review of the Literature

xlomafota13 shared this article with you from Inoreader The Nonrecurrent Laryngeal Nerve Without Abnormal Subclavian Artery: Report of Two Cases and Review of the Literature Via ear nose throat Ear Nose Throat J. 2021 Dec 22:1455613211056547. doi: 10.1177/01455613211056547. Online ahead of print. ABSTRACT As a variant of recurrent inferior laryngeal nerve (RILN), the nonrecurrent inferior laryngeal nerve (NRILN) is closely related to the occurrence of abnormal subclavian artery (ASA). The nonrecurrent inferior laryngeal nerve has been found in patients without arterial abnormalities, which is seen in the coexistence of NRILN and RILN, but it is easily confused with sympathetic-inferior laryngeal anastomosis branch (SILAB). We encountered 2 right NRILN patients without ASA during thyroid surgery. This article summarizes the characteristics of these cases and proposes methods to distinguish the coexistence of NRILN and RILN from SILAB. So far, 11 articles have reported 16 cases of NRILN without arterial abnormalities. In patients without artery abnormality, the vagus nerve could send out a descending branch NRILN at the bifurcation of the carotid artery and enter the larynx after anastomosis with RILN. Adequate dissection of the carotid sheath may avoid confusion with SILAB, and neural monitoring is also expected to provide a reference for the identification. PMID:34935547 | DOI:10.1177/01455613211056547 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.