The active form of vitamin B12 (methylcobalamin) has been reported to be effective on sleep‐wake rhythm disorders. Previous studies, however, were performed under open trial, and the effect of vitamin B12 has not been properly evaluated. The aim of this double‐blind study was to investigate the efficacy of methylcobalamin on delayed sleep phase syndrome (DSPS). Methylcobalamin (3 mg/day) or placebo was administered for 4 weeks. The subjects were 50 patients with DSPS aged 13–55 years (26.8 ± 1.3), 27 of whom received the active drug while 23 received the placebo. No significant differences were observed between the 2 groups in subjective evaluations of mood or drowsiness during the daytime or in night sleep by sleep‐log evaluation. These results indicate that 3 mg methylcobalamin administered over 4 weeks is not an effective treatment for DSPS.
Background:Transforming growth factor-β1 (TGF-β1) has the potential to induce acute inflammation and apoptosis in lung epithelial cells and plays a central role in subsequent fibrosis.Aims:To examine a new anti-TGF-β1 therapy against lung injury and fibrosis, which comprises the transfection of soluble TGF type II receptor (sTGFRII) gene into skeletal muscles by in vivo electroporation.Methods:Soluble TGFRII was detectable between 1 and 14 days in the serum and significantly increased between 3 and 10 days after gene transfer into muscles. Based on these findings, the sTGFRII gene was injected at 3 days before or 4 days after the bleomycin instillation in order to examine the significance of TGF-β1 on the early inflammatory phase (day 0 to day 7) or the fibrotic phase (day 7 to day 14) in this model.Results:Transfection of sTGFRII gene at 3 days before or 4 days after bleomycin instillation significantly attenuated apoptosis, injury, and fibrosis at 7 or 14 days, respectively. This method does not require the use of viral vector or neutralising antibody, and it is therefore possible to avoid problems regarding the pathogenicity of the viral vector or immunocomplex.Conclusions:This novel anti-TGF-β1 strategy may have clinical application in the treatment of lung injury and fibrosis.
25-year-old man presented in 1998 with the complaint of progressive dyspnea on exertion and was admitted to hospital in August 1999. Cardiac catheterization revealed moderate pulmonary hypertension (PH; pulmonary artery pressure 61/33 mmHg). Congenital heart disease and left-sided heart failure were excluded by echocardiography. Collagen disease and liver disease were ruled out by negative results for the autoantibody test and liver function test. Furthermore, a perfusion lung scan did not show any perfusion defects, which excluded pulmonary thromboembolism as a cause of PH. 1 An acute challenge test with O2 inhalation or continuous infusion of epoprostenol (PGI2) under right heart catheterization showed a moderate decrease in pulmonary artery pressure. The patient then had a catheter implanted in superior vena cava and continuous infusion of epoprostenol was initiated, as well as home O2 therapy and an anticoagulation regimen with warfarin.Later, after the patient had been discharged, serial Doppler echocardiography revealed an increase in pulmonary pressure despite an increase in the dose of infused epoprostenol (maximum dose: 10 ng · kg -1 · min -1 ). The patient was readmitted in February 2000 because of exacerbation of the dyspnea on exertion. Physical examination showed an accentuated pulmonary component of the second heart sound and right ventricular heave. There was a prominent V wave of the jugular vein and hepatojugular reflux was observed. Marked hepatomegaly was also present, but without overt edema of the lower limbs. An electrocardiogram showed right ventricular hypertrophy with right heart strain and tachycardia. Right axis deviation and right ventricular hypertrophy had progressed between the initial and current admission (Fig 1). Circulation Journal Vol.67, September 2003Echocardiography showed an increase in pulmonary artery pressure and enlargement of both the right atrium and right ventricle with severe tricuspid regurgitation; left ventricular function was preserved. Measurement of arterial blood gases with inhalation of 15 L/min of O2 showed a pH of 7.437, CO2 tension of 24.4 mmHg and O2 tension of Circ J 2003; 67: 793 -795 (Received December 21, 2001; revised manuscript received April 8, 2002; accepted April 11, 2002 Pulmonary capillary hemangiomatosis (PCH) is a rare idiopathic lung disorder that occurs in young patients and leads to pulmonary hypertension (PH). It is difficult to diagnosis in the early stage and is often mistaken for primary PH; in almost all cases of PCH, the correct diagnosis is not made until autopsy. In the present case of PCH, the patient had severe pulmonary hypertension and died of respiratory failure. Pathologically, PCH is characterized by proliferation of benign thin-walled capillary sized blood vessels in the lung parenchyma. (Circ J 2003; 67: 793 -795)
Pulmonary hypertension (PH) sometimes occurs in patients with systemic lupus erythematosus (SLE). Wereport a case of 51-year-old-woman with PH associated with SLE. She had been diagnosed as SLE on the basis of pericardial effusion, hematological disorder, positive antinuclear anti-body, and hypocomplementemia.Despite minimal lupus activity, she had marked elevation of pulmonary arterial pressure (101/53 mmHg)and decreased cardiac index (1.5 //min/m2). Symptomsrelated to PHwere progressive under treatment with oral corticosteroids, oxygen, calcium antagonists, and warfarin. After 17 months of epoprostenol treatment, she died of pulmonary infarction. SLE-associated PHis often severe and progressive even in association with minimal activity. (Internal Medicine 41: 109-112, 2002)
SUMMARYThis report describes a 45-year-old Japanese man who had episodes of anginal chest pain on effort. Coronary arteriography in the baseline state revealed subtotal occlusion in the mid-portion of the left anterior descending coronary artery. After intracoronary infusion of an endothelium-dependent vasodilator, substance P, the subtotal occlusion was immediately abolished. We concluded that endothelium-dependent vasodilation evoked with substance P was present at the site where coronary vasospasm occurred spontaneously in our case. (Jpn Heart J 36: 111-114, 1995)
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