Screening for musculoskeletal problems in children using a questionnaire

Background

On April 1, 2016, the Ministerial ordinance was enforced, and musculoskeletal examination of the extremities was made mandatory. From 2008, the University of us started musculoskeletal direct examination. To expand the examination, from 2016, we started to use the marksheet-type questionnaire. This study aimed to report the results of a musculoskeletal examination and investigate the association between musculoskeletal examination and age/gender and reports the reliability of the collected questionnaire data.

Augmentation of intrarenal angiotensin II levels in uninephrectomized aldosterone/salt-treated hypertensive rats; renoprotective effects of an ultrahigh dose of olmesartan.

Recent studies have suggested that aldosterone plays a role in the pathogenesis of renal injury. In this study, we investigated whether local angiotensin II (Ang II) activity contributes to the progression of renal injury in aldosterone/salt-induced hypertensive rats. Uninephrectomized rats were treated with 1% NaCl in a drinking solution and one of the following combinations for 6 weeks: vehicle (2% ethanol, s.c.; n=9), aldosterone (0.75 mug/h, s.c.; n=8), aldosterone+Ang II type 1 receptor blocker olmesartan (10 mg/kg/day, p.o.; n=8), or aldosterone+olmesartan (100 mg/kg/day, p.o.; n=9). Aldosterone/salt-treated hypertensive rats exhibited severe proteinuria and renal injury characterized by glomerular sclerosis and tubulointerstitial fibrosis. Aldosterone/salt-induced renal injury was associated with augmented expression of angiotensin converting enzyme and Ang II levels in the renal cortex and medullary tissues. Renal cortical and medullary mRNA expression of transforming growth factor-beta (TGF-beta) and connective tissue growth factor (CTGF) as well as the collagen contents were increased in aldosterone/salt-treated hypertensive rats. Treatment with olmesartan (10 or 100 mg/kg/day) had no effect on blood pressure but attenuated proteinuria in a dose-dependent manner. Olmesartan at 10 mg/kg/day tended to decrease renal cortical and medullary Ang II levels, TGF-beta and CTGF expression, and collagen contents; however, these changes were not significant. On the other hand, an ultrahigh dose of olmesartan (100 mg/kg/day) significantly decreased these values and ameliorated renal injury. These data suggest that augmented local Ang II activity contributes, at least partially, to the progression of aldosterone/salt-dependent renal injury.     

CT findings in panacinar emphysema]

We analyzed the CT images (in vivo) of 5 lobes (right middle lobe, 1; left lower lobe, 1; right lower lobe, 3) with panacinar emphysema (PAE) obtained at autopsy or thoracotomy for solitary lung tumor. The lobes were inflation-fixed by the method of Heitzman and sliced axially for a CT-pathologic correlative study. One lobe with mild PAE had normal appearance on CT; however, the other four lobes with PAE demonstrated low-attenuation areas (LAAs) of various shapes and sizes on CT. LAAs were locally distributed on CT slices in one lobe, dominant in the inner zones in two lobes, and diffuse in one lobe. Relatively normal to diminished vasculature was observed within the LAAs of four lobes. These CT findings differed significantly from those of centriacinar emphysema (CAE) as reported in other studies. We conclude that CT is useful in the clinical diagnosis of PAE and its differentiation from CAE.     

Thoracoscopic closure of a congenital partial pericardial defect

We describe our technique for performing direct thoracoscopic closure of a congenital partial pericardial defect, which was successfully employed in a 15-year-old boy. This is the first such report of a procedure that is noninvasive and may therefore become the treatment of choice for patients with a small congenital pericardial defect.     

A case of mitral valve replacement with autologous pulmonic valve in congenital mitral stenosis

A one-year-old infant with congenital mitral stenosis and pulmonary hypertension underwent by mitral valve replacement with his pulmonic valve autograft and pulmonary tract reconstruction with heterogeneous pericardial conduit. His postoperative hemodynamics data showed that left atrial pressure decreased and pulmonary hypertension continued. Echocardiography showed that the implanted autograft functioned properly. On the seventh postoperative day, he died of pulmonary hypertension. In case with congenital mitral stenosis with the small mitral annulus and the small left ventricular cavity, it is difficult to perform mitral valve replacement by commercially available mechanical or tissue valves. Because these valves are not suitable for the small mitral annulus. The mitral valve replacement with pulmonic valve autograft is recommended in such a case with the congenital mitral stenosis.