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Tensins are focal adhesion proteins that regulate various biological processes, such as mechanical sensing, cell adhesion, migration, invasion, and proliferation, through their multiple binding activities that transduce critical signals across the plasma membrane. When these molecular interactions and/or mediated signaling are disrupted, cellular activities and tissue functions are compromised, leading to disease development. Here, we focus on the significance of the tensin family in renal function and diseases. The expression pattern of each tensin in the kidney, their roles in chronic kidney diseases, renal cell carcinoma, and their potentials as prognostic markers and/or therapeutic targets are discussed in this review.

Hypertension and type 2 diabetes mellitus (T2DM) are important, intertwined public health issues. People with both conditions face significantly elevated risks of cardiovascular (CV) and renal complications. To optimize patient care, a multidisciplinary expert panel met to review recent evidence on optimal blood pressure (BP) targets, implications of albuminuria, and treatment regimens for hypertensive patients with T2DM, with the aim of providing recommendations for physicians in Hong Kong. The panel reviewed the relevant literature, obtained by searching PubMed for the publication period from January 2015 to June 2021, to address five discussion areas: (i) BP targets based on CV/renal benefits; (ii) management of isolated systolic or diastolic hypertension; (iii) roles of angiotensin II receptor blockers; (iv) implications of albuminuria for CV/renal events and treatment choices; and (v) roles and tools of screening for microalbuminuria. The panel held three virtual meetings using a modified Delphi method to address the discussion areas. After each meeting, consensus statements were derived and anonymously voted on by every panelist. A total of 17 consensus statements were formulated based on recent evidence and expert insights regarding cardioprotection and renoprotection for hypertensive patients with T2DM.

Interstitial lung diseases in children are a diverse group in terms of etiology and pathogenesis. With advances in genetic testing, mutations in surfactant protein have now been identified as the etiology for childhood interstitial lung disease of variable onset and severity, ranging from fatal acute respiratory distress syndrome (RDS) in neonates to chronic lung disease in adults. We presented an 11-month-old girl with surfactant protein C deficiency and secondary pulmonary hypertension, successfully treated with hydroxychloroquine, and provided a detailed discussion of the clinical and diagnostic approach and management.

Eisenmenger syndrome (ES) refers to congenital heart diseases (CHD) with reversal flow associated with increased pulmonary pressure and irreversible pulmonary vascular remodeling. Previous reports showed limited therapeutic strategies in ES. In this study, 5 ES patients (2 males and 3 females), who had been followed regularly at our institution from 2010 to 2019, were retrospectively reviewed. We adopted an add-on combination of sildenafil, bosentan, and iloprost and collected the clinical characteristics and outcomes as well as findings of echocardiography, computed tomography, pulmonary perfusion-ventilation scans, positron emission tomography, and biomarkers. The age of diagnosis in these ES patients ranged from 23 to 54 years (38.2 ± 11.1 years; mean ± standard deviation), and they were followed for 7 to 17 years. Their mean pulmonary arterial pressure and pulmonary vascular resistance index were 56.4 ± 11.3 mmHg and 24.7 ± 8.5 WU.m 2 , respectively. Intrapulmonary arterial thrombosis was found in 4 patients, ischemic stroke was noted in 2 patients, and increased glucose uptake of the right ventricle was observed in 4 patients. No patient mortality was seen within 5 years of follow-up. Subsequently, 2 patients died of right ventricular failure, 1 died of sepsis related to brain abscess, and another died of sudden death. The life span of these patients was 44-62 years. Although these patients showed longer survival, the beneficial data on specific-target pharmacologic interventions in ES is still preliminary. Thus, larger trials are warranted, and the study of cardiac remodeling in ES from various CHD should be explored.

Pediatric pulmonary hypertension (PH) has a similar clinical presentation to the adult disease but is associated with several additional disorders and challenges that require a specific approach for their fulminant course. With improved care for premature infants, various forms of pulmonary vascular disease have been found in children that did not previously exist. Pediatric PH can begin in utero, resulting in pulmonary vascularity growth abnormalities that may persist into adulthood. Here, we retrospectively reviewed several unique pediatric PH cases from 2000 to 2020 at Kaohsiung Medical University Hospital, Taiwan, a tertiary teaching hospital. Their comorbidities varied and included surfactant dysfunction, bronchopulmonary dysplasia, premature closure of the ductus arteriosus, high levels of renin and aldosterone, and Swyer-James-Macleod syndrome. Their clinical profiles, radiological characteristics, echocardiography, pulmonary angiogram, and therapeutic regimens were recorded. Further, because the underlying causes of pediatric PH were complex and markedly different according to age, adult PH classification may not be applicable to pediatric PH in all settings. We also classified these cases using different systems, including the Panama classification and the Sixth World Symposium on PH, and compared their advantages and disadvantages.

Pulmonary hypertension (PH) is a severe progressive disease, and the uncontrolled proliferation of pulmonary artery smooth muscle cells (PASMCs) is one of the main causes. Mitofusin-2 (MFN2) profoundly inhibits cell growth and proliferation in a variety of tumor cell lines and rat vascular smooth muscle cells. Down-regulation of MFN2 is known to contribute to PH. Proteasome inhibitors have been shown to inhibit the proliferation of PASMCs; however, there is no study on the regulation of proteasome inhibitors through MFN-2 in the proliferation of PASMCs, a main pathophysiology of PH. In this study, PASMCs were exposed to hypoxic conditions and the expression of MFN2 and cleaved-PARP1 were detected by Western blotting. The effects of hypoxia and proteasome inhibitors on the cell viability of PASMC cells were detected by CCK8 assay. The results indicated that hypoxia increases the viability and reduces the expression of MFN2 in a PASMCs model. MFN2 overexpression inhibits the hypoxia-induced proliferation of PASMCs. In addition, proteasome inhibitors, bortezomib and marizomib, restored the decreased expression of MFN2 under hypoxic conditions, inhibited hypoxia-induced proliferation and induced the expression of cleaved-PARP1. These results suggest that bortezomib and marizomib have the potential to improve the hypoxia-induced proliferation of PASMCs by restoring MFN2 expression.

This paper considers scheduling of surgical operations across multiple operating rooms subject to the limited availability of anaesthetists. The objective is to construct a feasible operations schedule that has the minimum makespan, i.e., the completion time of all operations. We abstract the problem into a theoretical server scheduling problem and formulate it in a mathematical form by proposing an integer programming model. Due to the intractability of its computing time, we circumvent the exact approaches and develop two approximation methods. Then, the steepest descent search is adopted for improving the solutions. Computational study suggests that the proposed methods can produce quality solutions in a few seconds.