Agminated fibroblastic connective tissue nevus in a 1‐year‐old boy

Fibroblastic connective tissue nevus (FCTN) is a benign cutaneous mesenchymal lesion characterized by proliferation of CD34‐positive fibroblastic/myofibroblastic spindle‐shaped cells. We report a case of agminated FCTN on the right lower abdomen of a 1‐year‐old boy.     

The diagnostic value of image guided percutaneous fine needle aspiration biopsy in equivocal mediastinal masses

Background and aims The aim of this study was to assess the diagnostic value of image guided percutaneous fine needle aspiration (FNA) biopsy in equivocal mediastinal masses.Patients Sixty-six patients with an equivocal mediastinal mass who underwent FNA biopsy between 1993 and 2003 were eligible for final analysis. The cytological and definitive diagnosis of masses were grouped as primary 22 (33%)−30 (46%) and secondary (metastatic) neoplasms 18 (27%)−18 (27%) and nonneoplastic lesions 20 (30%)−18 (%27) respectively.Results The diagnostic accuracy (%95 C.I.) of FNA biopsy for primary mediastinal neoplasms, secondary neoplasms and nonneoplastic lesions were found to be 93.3 (83.8–98.2)%, 100 (95.1–100)%, 93.3 (83.8–98.2)%, respectively.Conclusion Image guided percutaneous FNA biopsy is a safe and highly accurate diagnostic method for equivocal mediastinal masses.     

The use of frame fixation in the management of open distal extensor mechanism avulsion fracture in a dislocated knee

An avulsion fracture of the tibial tubercle is a common injury in traffic accident. If the fracture is closed, then a comparatively good prognosis can be expected through reinforcement of the bone via osteosynthesis and the use of artificial ligaments. In this case, an open wound was observed in the tibial tubercle, and the wound was so polluted that the healing process was significantly delayed. It was therefore difficult to provide simultaneous surgical treatment and so three operations were required to perform the reconstruction of the extensor mechanism. The reconstruction of extensor mechanism and the frame fixation between the patella and tibia was performed. Six months after the injury, the patient was able to walk without aid, had a range of movement from 5°to 130°, and did not show any indications of ADL disorder. Using this method of frame fixation between the patella and tibia proved to be an effective technique for the reconstruction of the open knee extension mechanism injury.     

Pressure overload-induced transient oxidative stress mediates perivascular inflammation and cardiac fibrosis through angiotensin II.

Oxidative stress is implicated in the pathogenesis of various cardiovascular diseases. We have shown that in Wistar rats with a suprarenal aortic constriction (AC), pressure overload-induced transient perivascular inflammation (monocyte chemoattractant protein-1 [MCP-1] induction and macrophage accumulation) in the early phase is the determinant of reactive myocardial fibrosis and resultant diastolic dysfunction in the late phase. Thus, we investigated the role of reactive oxygen species production in cardiac remodeling in AC rats. Superoxide production and the footprint of lipid peroxidation were assessed using dihydroethidium staining and immunohistostaining against 4-hydroxy-2-nonenal (4-HNE), respectively. In sham rats, dihydroethidium and 4-HNE signals were scarcely found in the heart. At day 3, AC rats showed dihydroethidium signals mainly in the intramyocardial arterial wall, whereas modest 4-HNE staining was observed diffusely in the myocardium. These signals declined to lower levels by day 14 despite sustained hypertension. Chronic administration of a subdepressor dose of an angiotensin II type 1 receptor blocker candesartan reduced the pressure overload-induced dihydroethidium and 4-HNE signals at day 3. Moreover, candesartan decreased MCP-1 induction and macrophage infiltration at day 3 and prevented myocardial fibrosis at day 14, without affecting left ventricle and myocyte hypertrophy. In conclusion, acute pressure overload induced self-limited superoxide production mainly in the vascular wall. The reactive oxygen species production would contribute to the perivascular inflammation and subsequent myocardial fibrosis. Angiotensin II was suggested to have a pressure-independent effect on the reactive oxygen species production.     

Increased expression of gp91phox homologues of NAD(P)H oxidase in the aortic media during chronic hypertension: involvement of the renin-angiotensin system.

Although vascular cells express multiple members of the Nox family of nicotinamide adenine dinucleotide phosphate (NAD(P)H) oxidase, including gp91phox, Nox1, and Nox4, the reasons for the different expressions and specific roles of these members in vascular injury in chronic hypertension have remained unclear. Thus, we quantified the mRNA expressions of these NAD(P)H oxidase components by real-time polymerase chain reaction and evaluated superoxide production and morphological changes in the aortas of 32-week-old stroke-prone spontaneously hypertensive rats (SHRSP) and age-matched Wistar Kyoto rats (WKY). The aortic media of SHRSP had an approximately 2.5-fold greater level of Nox4 mRNA and an approximately 10-fold greater level of Nox1 mRNA than WKY. The mRNA expressions of gp91phox and p22phox in SHRSP and WKY were comparable. SHRSP were treated from 24 weeks of age for 8 weeks with either high or low doses of candesartan (4 mg/kg/day or 0.2 mg/kg/day), or a combination of hydralazine (30 mg/kg/day) and hydrochlorothiazide (4.5 mg/kg/day). The high-dose candesartan or the hydralazine plus hydrochlorothiazide decreased the blood pressure of SHRSP to that of WKY, whereas the low-dose candesartan exerted no significant antihypertensive action. Media thickening and fibrosis, as well as the increased production of superoxide in SHRSP, were nearly normalized with high-dose candesartan and partially corrected with low-dose candesartan or hydralazine plus hydrochlorothiazide. These changes by antihypertensive treatment paralleled the decrease in mRNA expression of Nox4 and Nox1. These results suggest that blood pressure and angiotensin II type 1 receptor activation are involved in the up-regulation of Nox1 and Nox4 expression, which could contribute to vascular injury during chronic hypertension.