Dimerization and polymerization of butadiene with zero-valent nickel and protonic acids

The behavior of hydridonickel coordination compounds as catalysts for the oligomerization and polymerization of butadiene in various solvents was studied. In the presence of alcohol bis(tricyclohexylphosphine)chlorohydridonickel ( 4 , X = Cl) (HNiCl[P(C₆H₁₁)₃]₂) catalyzes the linear dimerization. With hydridotetrakis(phosphite)nickel(1+) ( 2 ) ([HNi{P(OR)₃}₄]⁺), which is prepared from tetrakis(phosphite)nickel ( 1 ) (Ni[P(OR)₃]₄) and trifluoroacetic acid, dimerization occurs in sec-alcohol but there is no reaction in tert-alcohol. The main product is 2-methylenevinylcyclopentane ( 8 ). The other products are 4-vinylcyclohexene ( 10 ), 1,5-cyclooctadiene ( 5 ), 1,3,7-octatriene ( 7 ) and 1,3,6-octatriene ( 9 ). The hydridonickel coordination compound, prepared with inorganic acids, does not afford the dimers but the 1,4-trans polymer.     

Small vessel vasculitis limited to pleuropulmonary manifestations,possibly induced by endotoxin

AIMS: We investigated a rare case of small vessel vasculitis (SVV) limited to pleuropulmonary manifestations, possibly induced by endotoxin, to determine the activation of immuno-mediated cells and endothelia in the pleuropulmonary circulation. METHODS AND RESULTS: A 44-year-old man with a high fever was X-rayed, revealing bilateral pleural effusion and atelectasis in the chest. His laboratory data were within normal limits except for a high white blood cell count and a high C-reactive protein level. Autoantibodies including anti-neutrophil cytoplasmic antibody were negative. Endotoxin was detected in his sera, but repeated cultures of sputa, urine, blood and the pleural effusion were negative for bacteria. Video-assisted thoracic surgery was performed and lung and parietal pleura specimens were obtained. Histology showed arterioles or small arteries infiltrated by monocytes or neutrophils with fibrinoid necrosis and acute or chronic venulitis. A diagnosis of SVV in the lung and pleura was made. Immunohistochemistry revealed that interleukin (IL)-1beta was expressed in monocytes and vascular cell adhesion molecule (VCAM)-1 on endothelial cells in the vasculitic lesions in the lung. CONCLUSIONS: Endotoxin possibly induced the inflammation in this apparently unique case of pleuropulmonary small vessel vasculitis. Immunohistochemistry revealed the expression of IL-1beta and VCAM-1 which may have caused activation of monocytes and endothelial cells within the vasculitic lesions.     

Strain difference in transgene-induced tumorigenesis and suppressive effect of ionizing radiation

Transgenic expression in medaka of the Xiphophorus oncogene xmrk, under a pigment cell specific mitf promoter, induces hyperpigmentation and pigment cell tumors. In this study, we crossed the Hd-rR and HNI inbred strains because complete genome information is readily available for molecular and genetic analysis. We prepared an Hd-rR (p53^+/−, p53^−/−) and Hd-rR HNI hybrid (p53^+/−) fish-based xmrk model system to study the progression of pigment cells from hyperpigmentation to malignant tumors on different genetic backgrounds. In all strains examined, most of the initial hyperpigmentation occurred in the posterior region. On the Hd-rR background, mitf:xmrk-induced tumorigenesis was less frequent in p53^+/− fish than in p53^−/− fish. The incidence of hyperpigmentation was more frequent in Hd-rR/HNI hybrids than in Hd-rR homozygotes; however, the frequency of malignant tumors was low, which suggested the presence of a tumor suppressor in HNI genetic background fish. The effects on tumorigenesis in xmrk-transgenic immature medaka of a single 1.3 Gy irradiation was assessed by quantifying tumor progression over 4 consecutive months. The results demonstrate that irradiation has a different level of suppressive effect on the frequency of hyperpigmentation in purebred Hd-rR compared with hybrids.     

Liver Targeting of Interferon Through Pullulan Conjugation

Purpose. The purpose of this study was to actively target interferon (IFN) to the liver through its chemical conjugation with pullulan, a water-soluble polysaccharide with a high affinity for the liver. Methods. Chemical conjugation of IFN with pullulan was achieved by a cyanuric chloride method. Following intravenous injection of the conjugates to mice, their body distribution and the activity of an IFN-induced enzyme, 2,5-oligoadenylate (2-5A) synthetase in the liver and other organs, were evaluated. Results. The cyanuric chloride method enabled us to prepare an IFN-pullulan conjugate that retained approximately 7–9 % of the biological activity of IFN. Pullulan conjugation enhanced the liver accumulation of IFN and the retention period with the results being reproducible. When injected intravenously to mice, the IFN-pullulan conjugate enhanced the activity of 2-5A synthetase in the liver. The activity could be induced at IFN doses much lower than those of free IFN injection. In addition, the liver 2-5A synthetase induced by conjugate injection was retained for 3 days, whereas it was lost within the first day for the free IFN-injected mice. Conclusions. IFN-pullulan conjugation was promising for IFN targeting to the liver with efficient exertion of its antiviral activity therein.     

An infant with Costelio syndrome complicated with fatal hypertrophic obstructive cardiomyopathy

We report a 3-month-old girl with Costelio syndrome complicating fatal hypertrophic obstructive cardio-myopathy. She had typical findings of this syndrome, slight dyspnea and persistent wheezing. Doppler echocardiography revealed asymmetric septal hypertrophy and systolic anterior movement of the anterior mitral leaflet. There was grade 1 mitral regurgitation. Although once her heart failure had been controlled medically, she died suddenly following deterioration of her heart condition. Costelio syndrome can complicate fatal hypertrophic obstructive cardiomyopathy.     

Mutation Analysis of the WT1 Gene in Myelodysplastic Syndromes

The WT1 tumor suppressor gene was examined for mutations in a panel of 44 patients with myelo-dysplastic syndromes (MDS) including acute myelogenous leukemias (AML) secondary to MDS, using polymerase chain reaction single-strand conformation polymorphism (PCR-SSCP) analysis and sequencing analysis. A WT1 mutation was detected in one out of 17 cases of AML secondary to MDS. This mutation exists upstream of the zinc finger region and is predicted to produce a truncated WT1 protein lacking the zinc finger region. No mutations were detected in 27 MDS patients who had not progressed to AML. This is the first report of analysis for WT1 mutations in a large number of MDS patients, suggesting that WT1 mutations are uncommon in MDS. Abnormalities in this gene may, however, contribute to a small proportion of cases showing progression from MDS into AML.     

Age-specific effects of noradrenergic alpha-2 agonist clonidine on the development of amygdaloid kindling in developing rats

The effects of clonidine on the development of amygdaloid kindling were studied in rats of various ages (14, 21, 28 and 70 postnatal days). Administration of clonidine (0.2, 0.5 mg/kg i.p.) caused a significant retardation of kindling development in the 28-day-old rats as well as in the adult rats, whereas, in the 14-day-old rats, the development of kindling was significantly facilitated by clonidine. No significant effect of clonidine was observed in the 21-day-old rats. These results indicate that in rats the effects of clonidine on the development of amygdaloid kindling vary during development.     

Necrotizing Bacillus cereus infection of the meninges without inflammatory reaction in a patient with acute myelogenous leukemia: a case report

A 64-year-old man in a severely immunocompromised state due to acute myelogenous leukemia died, respirator-unaided, about 10 h after the abrupt onset of coma. An earlier blood culture had yielded Bacillus cereus. The autopsy, performed 2 h after death, demonstrated diffuse subarachnoid hemorrhage without berry aneurysms, and the formalin-fixed brain was tinged with gray-brownish discoloration. The sections of the brain presented a whitish tint of the surface layer of all portion of the cerebral cortices, even those in the sulci. Histological examination of the brain revealed leptomeningeal B. cereus dissemination, and widespread necrosis of the leptomeninges and arachnoid vessels without inflammatory cell reaction. The grossly recognizable whitish surface layer of the cerebral cortex showed overt hyperchromatism, and contained neurons more degenerative than those located in the deeper cortical layer. The total absence of inflammatory reaction may be explained by a combination of the immunocompromised state of the patient and the character of B. cereus infection, which in itself induces little inflammatory reaction. The prominent lesions were confined to the cerebral surface layer and leptomeningeal tissue including the arachnoid vessels, which were all bathed in the cerebrospinal fluid, suggesting that some necrotizing toxins had been secreted into the fluid by the B. cereus. The necrosis of arachnoid vessels is thought to have in turn caused diffuse subarachnoid hemorrhage and marked disturbance of the cerebral blood flow, resulting in the terminal coma. Received: 4 April 1996 / Revised, accepted: 8 September 1996