Three-dimensional printed heart models showed potential utility, especially in understanding the relationship between intraventricular communications and great vessels, as well as in simulation for creating intracardiac pathways.

Working hypotheses to solve the critical problems of the existing highly active anti-retroviral therapy were proposed. The study based on the hypotheses proved the validity of the hypotheses and resulted in the development of 2'-deoxy-4'-C-ethynyl-2-fluoroadenosine, a nucleoside reverse transcriptase inhibitor, with highly potent activity against all HIV-1, very favorable toxic profiles, and stability in plasma. The nucleoside will prevent or delay the emergence of drug-resistant HIV-1 variants and be an ideal therapeutic agent for both HIV-1 and HBV infections.

No abstract

The mid-term results of the surgical repair of functional single ventricle with supracardiac or infracardiac TAPVC are acceptable. The surgical treatment of patients with mixed TAPVC and with severe atrioventricular valve regurgitation is not promising, but can be improved.

Objective: Surgical outcomes of biventricular repair for hearts with hypoplastic left ventricle with congenital mitral valve stenosis are described. Serial changes of left ventricular geometry and clinical features after biventricular repair were reviewed. Methods: Eight patients with hypoplastic left ventricle and congenital mitral valve stenosis who underwent first surgical intervention for biventricular circulation in neonatal or infantile period between 2001 and 2014 comprise the study population. Serial change in left ventricular end-diastolic diameter, left ventricular mass index, and relative wall thickness after biventricular repair were evaluated by two-dimensional echocardiography. Results: The median Z-scores of left ventricular end-diastolic diameter and mitral valve diameter before the first surgical intervention were À3.0 (range, À4.8 to À2.0) and À1.0 (À2.9 to 2.1), respectively. Mitral valves were surgically treated in five patients; they were replaced in two and repaired in three patients. Left ventricular end-diastolic diameter Z-score at five years after biventricular repair was 0.1 (À3.0 to 1.0), which was significantly larger than before first surgical intervention (P ¼ .005). Left ventricular mass index, on the other hand, did not change, but relative wall thickness significantly decreased (P ¼ .009). Postoperative catheter study showed pulmonary hypertension with high left ventricular end-diastolic pressure in more than half of survivors. Conclusions: Left ventricle increased in size after the biventricular repair with appropriate mitral valve procedures before progression of pulmonary hypertension. Left ventricular mass, however, did not accompany the increase. Some patients may have suffered from mild, but certain restrictive left ventricular physiology and subsequent pulmonary hypertension as the result of abnormal remodeling process of the myocardium.

The midterm results of atrioventricular valve repair in patients with functional single ventricle were favorable; however, young and small patients, especially those with hypoplastic left heart syndrome, still had poor outcomes.

A working hypothesis to solve the critical problems of existing HAART was proposed. The study based on the hypothesis proved the validity of the hypothesis and resulted in the development of 2'-deoxy-4'-C-ethynyl-2-fluoro-adenosine (4'Ed2FA), a nucleoside reverse transcriptase inhibitor (NRTI) with highly potent activity against all HIV-1 strains, very favourable toxic profiles, and stability in plasma.

Tubular atrophy is a common pathological feature of kidney fibrosis. Although fibroblasts play a predominant role in tissue fibrosis, the role of repairing tubular epithelia in tubular atrophy is unclear. We demonstrated the essential role of focal adhesion kinase (FAK)-mediated intratubular epithelial-mesenchymal transition (EMT) in the pathogenesis of tubular atrophy after severe ischemia-reperfusion injury (IRI). Actively proliferating tubular epithelia undergoing intratubular EMT were noted in the acute phase of severe IRI, resulting in tubular atrophy in the chronic phase, reflecting failed tubular repair. Furthermore, FAK was phosphorylated in the tubular epithelia in the acute phase of severe IRI, and its inhibition ameliorated both tubular atrophy and interstitial fibrosis in the chronic phase after injury. In vivo clonal analysis of single-labeled proximal tubular epithelial cells after IRI using proximal tubule reporter mice revealed substantial clonal expansion after IRI, reflecting active epithelial proliferation during repair. The majority of these proliferating epithelia were located in atrophic and non-functional tubules, and FAK inhibition was sufficient to prevent tubular atrophy. In vitro, TGFβ induced FAK phosphorylation and an EMT phenotype, which was also prevented by FAK inhibition. In an in vitro tubular epithelia gel contraction assay, TGFβ treatment accelerated gel contraction, which was suppressed by FAK inhibition. In conclusion, injury-induced intratubular EMT is closely related to tubular atrophy in a FAK-dependent manner.