Flame retardance-donated lignocellulose nanofibers (LCNFs) by the Mannich reaction with (amino-1,3,5-triazinyl)phosphoramidates and their properties.

Nitrogen/phosphorus-containing melamines (NPCM), a durable flame-retardant, were prepared by the successive treatment of ArOH (Ar = Br n C6H5-n , n = 0, 1, 2, and 3) with POCl3 and melamine monomer. The prepared flame-retardants were grafted through the CH2 unit to lignocellulose nanofibers (LCNFs) by the Mannich reaction. The resulting three-component products were characterized using FT-IR (ATR) and EA. The thermal behavior of the NPCM-treated LCNF fabric samples was determined using TGA and DSC analyses, and their flammability resistances were evaluated by measuring their Limited Oxygen Index (LOI) and the UL-94V test. A multitude of flame retardant elements in the fabric samples increased the LOI values as much as 45 from 20 of the untreated LCNFs. Moreover, the morphology of both the NPCM-treated LCNFs and their burnt fabrics was studied with a scanning electron microscope (SEM). The heat release lowering effect of the LCNF fabric against the water-based paint was observed with a cone calorimeter. Furthermore, the mechanical properties represented as the tensile strength of the NPCM-treated LCNF fabrics revealed that the increase of the NPCM content in the PP-composites led to an increased bending strength with enhancing the flame-retardance.

Cardiac tamponade due to rupture of coronary artery fistulas with a giant aneurysm containing a free floating ball thrombus: a case report.

A 76-year-old woman was admitted to our hospital with cardiac tamponade. Chest computed tomography revealed a large tumor adjacent to the pulmonary artery, the center of which was demonstrated as a high density area without contrast medium. Coronary angiography revealed a large aneurysm consisting of coronary artery fistulas. An afferent vessel connected tangentially to the surface of the aneurysm, so blood flowed around along the inner wall of the aneurysm. A filling defect was demonstrated in the center of the aneurysm that indicated a thrombus. The cause of cardiac tamponade was seemed to be bleeding of the coronary artery fistulas. Coil embolization was performed, but recanalization occurred. Therefore, ligature of the fistulas and aneurismal resection were performed using a cardiopulmonary bypass. A fresh floating thrombus was found in the aneurysm.

Effects of ghrelin administration on left ventricular function, exercise capacity, and muscle wasting in patients with chronic heart failure.

BACKGROUND: Ghrelin is a novel growth hormone-releasing peptide that also induces vasodilation, inhibits sympathetic nerve activity, and stimulates feeding through growth hormone-independent mechanisms. We investigated the effects of ghrelin on left ventricular (LV) function, exercise capacity, and muscle wasting in patients with chronic heart failure (CHF). METHODS AND RESULTS: Human synthetic ghrelin (2 microg/kg twice a day) was intravenously administered to 10 patients with CHF for 3 weeks. Echocardiography, cardiopulmonary exercise testing, dual x-ray absorptiometry, and blood sampling were performed before and after ghrelin therapy. A single administration of ghrelin elicited a marked increase in serum GH (25-fold). Three-week administration of ghrelin resulted in a significant decrease in plasma norepinephrine (1132+/-188 to 655+/-134 pg/mL; P<0.001). Ghrelin increased LV ejection fraction (27+/-2% to 31+/-2%; P<0.05) in association with an increase in LV mass and a decrease in LV end-systolic volume. Treatment with ghrelin increased peak workload and peak oxygen consumption during exercise. Ghrelin improved muscle wasting, as indicated by increases in muscle strength and lean body mass. These parameters remained unchanged in 8 patients with CHF who did not receive ghrelin therapy. CONCLUSIONS: These preliminary results suggest that repeated administration of ghrelin improves LV function, exercise capacity, and muscle wasting in patients with CHF.

Repeated inhalation of adrenomedullin ameliorates pulmonary hypertension and survival in monocrotaline rats.

Adrenomedullin (AM) is a potent vasodilator peptide. We investigated whether inhalation of aerosolized AM ameliorates monocrotaline (MCT)-induced pulmonary hypertension in rats. Male Wistar rats given MCT (MCT rats) were assigned to receive repeated inhalation of AM (n = 8) or 0.9% saline (n = 8). AM (5 mug/kg) or saline was inhaled as an aerosol using an ultrasonic nebulizer for 30 min four times a day. After 3 wk of inhalation therapy, mean pulmonary arterial pressure and total pulmonary resistance were markedly lower in rats treated with AM than in those given saline [mean pulmonary arterial pressure: 22 +/- 2 vs. 35 +/- 1 mmHg (-37%); total pulmonary resistance: 0.048 +/- 0.004 vs. 0.104 +/- 0.006 mmHg.ml(-1).min(-1).kg(-1) (-54%), both P < 0.01]. Neither systemic arterial pressure nor heart rate was altered. Inhalation of AM significantly attenuated the increase in medial wall thickness of peripheral pulmonary arteries in MCT rats. Kaplan-Meier survival curves demonstrated that MCT rats treated with aerosolized AM had a significantly higher survival rate than those given saline (70% vs. 10% 6-wk survival, log-rank test, P < 0.01). In conclusion, repeated inhalation of AM inhibited MCT-induced pulmonary hypertension without systemic hypotension and thereby improved survival in MCT rats.

A novel migrative addition reaction of hydrazines to the diketone derivative of C60.

A novel addition reaction of an aromatic hydrazine to the diketone derivative of C60 occurs highly regioselectively with an unusual migration of two hydrogen atoms from the hydrazine to the fullerene and affords a fluorescent product having a methylene carbon along the orifice.

Hemodynamic and hormonal effects of beraprost sodium, an orally active prostacyclin analogue, in patients with secondary precapillary pulmonary hypertension.

Earlier studies have shown that administration of beraprost sodium (BPS), an orally active prostacyclin analogue, improves hemodynamics in patients with primary pulmonary hypertension (PH), but it is not known whether BPS has beneficial effects in secondary precapillary PH. The present study investigated the hemodynamic and hormonal parameters of 18 patients with secondary precapillary PH (8 patients with chronic thromboembolic PH, 7 with collagen vascular disease, and 3 with residual PH after surgery for atrial septal defect). Hemodynamics were repeatedly measured by right heart catheterization. Treatment with BPS improved New York Heart Association (NYHA) functional class in 10 of the 18 patients and significantly decreased pulmonary vascular resistance by 17% (12.9+/-1.1 to 10.7+/-1.2 Wood units, p<0.01). Circulating brain natriuretic peptide and uric acid significantly decreased from 246+/-61 to 215+/-65 pg/ml and from 6.5+/-0.6 to 5.3+/-0.3 mg/dl, respectively. In summary, BPS therapy improved NYHA functional class, hemodynamics, and hormonal parameters in patients with secondary precapillary PH. Thus, oral administration of BPS may be a new therapeutic strategy for the treatment of secondary precapillary PH.

Effect of orally active prostacyclin analogue on survival in patients with chronic thromboembolic pulmonary hypertension without major vessel obstruction.

OBJECTIVES: This study investigated whether treatment with beraprost sodium (BPS), an orally active prostacyclin analog, improves hemodynamics and survival in patients with peripheral-vessel chronic thromboembolic pulmonary hypertension (CTEPH), for which there is no surgical option. BACKGROUND: Oral administration of BPS has been shown to improve the hemodynamics and prognosis in patients with primary pulmonary hypertension; however, whether BPS has beneficial effects in CTEPH remains unknown. METHODS: Forty-three patients with peripheral-vessel CTEPH were classified into two groups: patients treated with BPS (BPS group, n = 20) and those without BPS (conventional group, n = 23). Baseline demographic and hemodynamic data did not significantly differ between the two groups. RESULTS: BPS therapy improved New York Heart Association functional class in 10 patients (50%) and significantly decreased total pulmonary resistance from 18 +/- 6 to 15 +/- 8 Wood units (p < 0.05) [mean +/- SD]. Sixteen patients died of cardiopulmonary causes in the conventional group during a mean follow-up period of 58 +/- 45 months. In contrast, only three patients died of cardiopulmonary causes in the BPS group during a mean follow-up period of 44 +/- 30 months. The absence of BPS therapy, elevated total pulmonary resistance, heart rate, and age were independently related to the mortality by Cox proportional hazard analysis. The 1-year, 3-year, and 5-year survival rates for the BPS group were 100%, 85%, and 76%, respectively, compared to 87%, 60%, and 46% in the conventional group. CONCLUSIONS: This preliminary study suggests that oral administration of BPS may improve hemodynamics and survival in patients with peripheral-vessel CTEPH, for which there is no surgical option.

Cardiovascular and hormonal effects of subcutaneous administration of ghrelin, a novel growth hormone-releasing peptide, in healthy humans.

Ghrelin is a novel GH (growth hormone)-releasing peptide isolated from the stomach. The cardiovascular and hormonal effects of the subcutaneous administration of ghrelin in humans remain unknown. Six healthy volunteers each received subcutaneous administration of three doses of ghrelin (1, 5 or 10 microg/kg) and placebo; the order of administration was randomized, and separate doses were given at least 24 h apart. The serum GH level dose-dependently increased from 0.5 +/- 0.4 to 3.6 +/- 2.1 ng/ml (1 microg/kg ghrelin; P=0.99 compared with baseline), 27.1 +/- 12.0 ng/ml (5 microg/kg; P<0.01 compared with baseline) and 45.4 +/- 12.8 ng/ml (10 microg/kg; P<0.01 compared with baseline) 30 min after ghrelin administration. Subcutaneous administration of ghrelin did not significantly alter circulating levels of corticotropin, cortisol, insulin-like growth factor-1, noradrenaline or adrenaline, although 10 microg/kg ghrelin slightly increased the prolactin level. No significant changes in heart rate or mean arterial pressure were observed. In contrast, the left ventricular ejection fraction, as assessed by echocardiography, increased dose-dependently from 63.5 +/- 0.6% to 65.1 +/- 0.9% (1 microg/kg ghrelin; P=0.97 compared with baseline), 69.6 +/- 1.3% (5 microg/kg; P<0.01 compared with baseline) and 71.5 +/- 0.9% (10 microg/kg; P<0.01 compared with baseline) 30 min after ghrelin administration. These haemodynamic and hormonal changes were still apparent 60 min after ghrelin injection. In conclusion, subcutaneous administration of ghrelin dose-dependently induced relatively specific GH release and enhanced cardiac performance in humans.

Hyperglycaemia suppresses the secretion of ghrelin, a novel growth-hormone-releasing peptide: responses to the intravenous and oral administration of glucose.

Ghrelin is a novel growth hormone (GH)-releasing peptide, isolated from the stomach, which may also cause a positive energy balance by stimulating food intake and reducing fat utilization. However, whether glucose influences the release of ghrelin remains unknown. Accordingly, we examined circulating levels of ghrelin and GH in response to the intravenous or oral administration of 50 g of glucose in eight healthy humans. After the administration of intravenous glucose (50 g), the plasma ghrelin level decreased significantly from 127+/-9 to 98+/-9 fmol/ml (P<0.01), associated with an increase in plasma glucose from 85+/-3 to 357+/-19 mg/dl (P<0.01). Ingestion of 50 g of glucose decreased the plasma ghrelin level significantly from 134+/-12 to 97+/-15 fmol/ml (P<0.01), associated with an increase in plasma glucose from 93+/-3 to 166+/-10 mg/dl (P<0.01). The decrease in the plasma ghrelin level lasted for more than 30 min after recovery of the plasma glucose level. In conclusion, ghrelin secretion may be suppressed, at least in part, by an increased plasma glucose level in healthy humans.