A prospective study on the efficacy of oral estrogen in female patients with acromegaly

Pituitary - To evaluate the efficacy and safety of oral estrogen therapy in female patients of childbearing age with uncontrolled acromegaly and to verify the significance of the presence of...     

2D shear wave elastography in evaluation of prognostic factors in breast cancer

Purpose

To evaluate the reproducibility of the 2D shear wave elastography (2D-SWE) method and to identify the prognostic factors of breast lesions.

Methods

In this prospective study, 44 female patients were consecutively included from January 2020 to September 2021. All patients showing visible masses at B-mode ultrasound underwent to clinical evaluation, followed by qualitative and quantitative 2D-SWE by two different operators with over 15-year and 2-year experience, respectively. Subsequently, patients underwent to surgical treatment after core needle biopsy. Reproducibility of qualitative and quantitative 2D-SWE was evaluated by Cohen’s kappa and intraclass correlation coefficient (ICC). Clinical, imaging, and histopathological data and 2D-SWE evaluations were analysed with Spearman's rank correlation test.

Results

The mean age of the patients was 55 years?±?12. The mean histological and ultrasound tumour size of were 23.1 mm?±?13.2 and 17.2 mm?±?10.2, respectively. The interobserver agreement showed a good reproducibility limited to the qualitative evaluation colour maps (Cohen’s kappa?=?0.603) and to the quantitative evaluation E ratio (ICC?=?0.771). Correlation analysis between the ultrasound and 2D-SWE values and the clinical-pathological parameters showed a significant relationship between E ratio and Elston–Ellis grading (P?<?0.030) and between tumour size and Elston–Ellis grading (P?<?0.041).

Conclusion

The 2D-SWE has shown good reproducibility among operators with different experience. It could be a promising tool in the evaluation of some prognostic factors in ultrasound visible breast cancer.

     

Myocardial dysfunction and abnormal left ventricular exercise response in autonomic diabetic patients

In diabetic patients, the pathophysiologic mechanisms of exercise-induced left ventricular (LV) dysfunction remain controversial. In this study, the role of myocardial contractility recruitment in determining an abnormal LV response to isometric or dynamic exercise has been investigated in 14 diabetic patients with autonomic dysfunction. Ischemic heat disease was excluded by the absence of LV wall motion abnormalities induced by isotonic and isometric exercise and by coronary angiography. Left ventricular and myocardial function were studied at rest, and during isometric and isotonic exercise, by two-dimensional echocardiography; moreover, recruitment of an inotropic reserve was assessed by postextra-systolic potentiation at rest and at peak handgrip. An abnormal response of LV ejection fraction to isometric (9/14) or to dynamic (8/14) exercise was frequent in study patients. In these patients, baseline myocardial contractility was normal, and the significant increase in ejection fraction by postextrasystolic potentiation indicated a normal contractile reserve (65 ± 7% vs. 74 ± 6%, p=0.001). Nevertheless, the downward displacement of LV ejection fraction-systolic wall stress relationships during exercise suggests an inadequate increase in myocardial contractility. However, the abnormal ejection fraction at peak handgrip was completely reversed by postextrasystolic potentiation (67 ± 6% vs. 58.1 ± 10%, p=0.008), a potent inotropic stimulation independent of the integrity of adrenergic cardiac receptors. A defective inotropic recruitment, despite the presence of a normal LV contractile reserve, plays an important role in deexercise LV dysfunction in diabetic patients with autonomic neuropathy.     

Human respiratory syncytial virus N,P and M protein interactions in HEK-293T cells

Characterization of Human Respiratory Syncytial Virus (HRSV) protein interactions with host cell components is crucial to devise antiviral strategies. Viral nucleoprotein, phosphoprotein and matrix protein genes were optimized for human codon usage and cloned into expression vectors. HEK-293T cells were transfected with these vectors, viral proteins were immunoprecipitated, and co-immunoprecipitated cellular proteins were identified through mass spectrometry. Cell proteins identified with higher confidence scores were probed in the immunoprecipitation using specific antibodies. The results indicate that nucleoprotein interacts with arginine methyl-transferase, methylosome protein and Hsp70. Phosphoprotein interacts with Hsp70 and tropomysin, and matrix with tropomysin and nucleophosmin. Additionally, we performed immunoprecipitation of these cellular proteins in cells infected with HRSV, followed by detection of co-immunoprecipitated viral proteins. The results indicate that these interactions also occur in the context of viral infection, and their potential contribution for a HRSV replication model is discussed.     

Mental Health Service Users’ Perceptions of Stigma,From the General Population and From Mental Health Professionals in Mexico: A Qualitative Study

Community Mental Health Journal - Negative attitudes towards people with mental health disorders have been widely studied and identified in the general population, and even within health care...     

Mutations in protein N-arginine methyltransferases are not the cause of FTLD-FUS

The nuclear protein fused in sarcoma (FUS) is found in cytoplasmic inclusions in a subset of patients with the neurodegenerative disorder frontotemporal lobar degeneration (FTLD-FUS). FUS contains a methylated arginine–glycine–glycine domain that is required for transport into the nucleus. Recent findings have shown that this domain is hypomethylated in patients with FTLD-FUS. To determine whether the cause of hypomethylation is the result of mutations in protein N-arginine methyltransferases (PRMTs), we selected 3 candidate genes (PRMT1, PRMT3, and PRMT8) and performed complete sequencing analysis and real-time polymerase chain reaction mRNA expression analysis in 20 FTLD-FUS cases. No mutations or statistically significant changes in expression were observed in our patient samples, suggesting that defects in PRMTs are not the cause of FTLD-FUS.