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Notes: We describe some attempts to observe magnetic structure in various actinide (5f-electron) materials. Our experimental technique is neutron powder diffraction as practiced at a spallation (pulsed) neutron source. We will discuss our investigations of α-Pu, δ-Pu, α-UD3, and β-UD3. β-UD3 is a simple ferromagnet: Surprisingly, the moments on the two nonequivalent uranium atoms are the same within experimental error. α-UD3, α-Pu, and δ-Pu are nonmagnetic, within the limits of our observations. Our work with pulsed neutron diffraction shows that it is a useful technique for research on magnetic materials.

Notes: The replacement of Cu by Mn in UCu2Si2 causes surprisingly large increases in both the Curie temperature and the coercivity of this ferromagnetic material. We have performed neutron powder diffraction experiments on a series of U(Cu,Mn)2Si2 alloys and found that UCu2Si2 is a simple ferromagnet with a magnetic moment of 2.0(1)μB on the U atoms pointing along the crystallographic c axis of the tetragonal unit cell. The alloy U(Cu0.75Mn0.25)2Si2 is also a ferromagnet with moments on both U and Mn pointing in the c direction. The moment on the U atoms is 1.7(1)μB, and the average moment on the (Cu,Mn) site is 0.16(5)μB. No indication of chemical ordering on the (Cu,Mn) site was detected.

Notes: The compound UCu2Si2 has been found to be ferromagnetic at low temperatures with a Curie temperature (TC) of 101 K. The magnetization follows a Curie–Weiss law in the paramagnetic region with an effective magneton number of 2.12 μB per uranium atom. Partial substitution of Th atoms for the U atoms results in an expansion of the lattice, a rapid drop in TC, and a sizable increase in the coercive field. Magnetization measurements have been conducted on various compositions of U1−xThxCu2Si2 over the range of 0〈x〈1.0 and the variation of the lattice parameters and the magnetic properties determined. A correlation between the change in the magnetic properties and the U−U separation due to the lattice expansion and the statistical distribution separation effects will be presented.

Notes: The neurotrophin responsive gene vgf is widely expressed in central and peripheral neurones, and in certain neuroendocrine cell populations. Its encoded VGF precursor protein (proVGF1: 617 amino acids in rat, 615 in man, 〉 85% homology) gives rise to several low molecular weight species. We studied a range of neuroendocrine and neuronal cells, in which VGF-processing products were prominent with an apparent molecular weight of 20 and 10 kDa (VGF20 and VGF10, respectively). Such peptides were recognized by antibodies specific for the C-terminal rat VGF nonapeptide, thus indicating that they included the C-terminus of proVGF. Ectopic expression of the neuroendocrine-specific prohormone convertases PC1/3 or PC2 in GH3 cells showed that both could generate VGF20, while VGF10 was preferentially produced by PC1/3. Site-directed mutagenesis was used to identify the KRKRKK488 motif as the target within VGF sequence which leads to the production of VGF20. Molecular characterization of rat VGF10, on the other hand, revealed that this peptide is produced by cleavage at the RPR555 site. By the combined use of high-resolution separation techniques, matrix-assisted laser desorption/ionization time of flight (MALDI-ToF) mass spectrometry and manual Edman degradation we identified in rat brain a VGF fragment analogous to bovine peptide V and two novel peptides also derived from the C-terminal region of proVGF.

Notes: Spontaneous occurrence of an acquired inhibitor to factor VIII (FVIII) is a rare event. About 50% of cases are idiopathic. Among younger people, inhibitors are often found in the postpartum period. Treatment must be administered either to overcome haemorrhagic symptoms or to eradicate the inhibitor. Several approaches have been proposed for inhibitor eradication, based on immunosuppressive drugs such as corticosteroids, cyclophosphamide and azathioprine, with varying results. High-dose immunoglobulin (HDIg) has been recently proposed as first-line therapy. We report on four cases with acquired inhibitor to FVIII occurring 4–8 months after delivery. At diagnosis, inhibitor titre was 〈 5 Bethesda units mL–1 (BU mL–1) in three cases and 〉 5 BU mL–1 in one. Factor VIII coagulant activity (FVIII:C) was 〈 1 U dL–1〉 in three cases and 12 U dL–1 in one. We treated the patients with HDIg (400 mg kg–1 day–1 for 5 consecutive days) and dexamethasone (24 mg day–1 for 5–7 consecutive days), administered at the same time. In three women, the inhibitor was suppressed in 2–50 weeks. After an off-therapy period ranging from 20 to 104 weeks, the FVIII:C was persistently normal and the inhibitor undetectable. The fourth woman remained unresponsive. In two cases, recombinant activated factor VII administration stopped the bleeding. Thus, intermediate- to high-dose dexamethasone and HDIg given at the same time could be a successful and safe therapeutic approach for a rapid and complete remission from the development of FVIII inhibitors.

Notes: Auto-immune mechanisms, mostly cell mediated, have been described as the basic abnormality in polymyositis and dermatomyositis. We report here the case of a patient affected with dermatopolymyositis, resistant to therapy, who was treated with corticosteroids and cyclosporin. She presented with in infiltrative, erythematous rash on the neck, eyelids and cheeks and weakness of the proximal limb and cervical muscles.The dramatic and persistant response to cyclosporin obtained in this case represents a clear demonstration of the action of this drug in cases of dermatomyositis.

Notes: Background:  Hepatitis C virus infection is more common in patients with inflammatory bowel disease than in general population. Limited data are available as to the safety and efficacy of α-interferon therapy for chronic active hepatitis C in patients with concomitant inflammatory bowel disease.Aim:  To evaluate the efficacy and safety of α-interferon monotherapy in patients with chronic active hepatitis C and inactive or mildly active inflammatory bowel disease.Methods:  A total of 513 consecutive inflammatory bowel disease patients at a single centre were tested for antibodies to hepatitis C virus (anti-hepatitis C virus) between 1995 and 2000. Twenty-one patients had detectable anti-hepatitis C virus Ab and were hepatitis C virus-RNA positive with histologically proved chronic active hepatitis. Each of these patients, whose inflammatory bowel disease was in clinical remission or mildly active, was sex- and age-matched to three controls with similar histological grade and stage of chronic hepatitis C virus but without inflammatory bowel disease; and all were treated with human leucocyte α-interferon 6 million units given thrice weekly for 12 months. Responses to treatment were classified as follows: complete response – persistently normal alanine aminotransferase and viral clearance (hepatitis C virus-RNA–ve) at the end-of-treatment, incomplete response – alanine aminotransferase normalization without viral clearance (hepatitis C virus-RNA+ve), and sustained response – alanine aminotransferase normalization and hepatitis C virus clearance 12 months after the end-of-treatment.Results:  Twenty-one patients with chronic active hepatitis C and inflammatory bowel disease (10 with Crohn's disease and 11 with ulcerative colitis) and 63 sex- and age-matched controls with chronic hepatitis C virus alone received α-interferon monotherapy. Response rates to interferon were similar for inflammatory bowel disease patients compared with controls [CR 42% vs. 35% and SR 24% vs. 18% (P, not significant), respectively]. None of the 21 inflammatory bowel disease patients had severe adverse effects and the mild ones observed were comparable with those seen in the control group. No patients developed an inflammatory bowel disease relapse during the interferon treatment period or in the 12 months thereafter.Conclusions:  The biochemical and virological response to a 12-month human leucocyte α-interferon treatment in patients with chronic active hepatitis C are similar to that observed in matched controls with chronic hepatitis C virus without inflammatory bowel disease. Adverse effects are similar in both groups of patients and unrelated to the underlying inflammatory bowel condition. This provides hepatologists with evidence that α-interferon can be safely administered to patients with chronic hepatitis C virus and inflammatory bowel disease provided that the inflammatory bowel condition is in clinical remission.

Notes: X-ray and electron diffraction studies were made on the two phases of 11-aminoundecanoic acid, C11H21NO2. Phase I: dihydrate, monoclinic, C2/c, z = 8, a = 15.96±0.03, b = 4.71±0.01, c = 35.48±0.08 Å, β = 82.1±0.3°. Phase II: anhydrate, orthorhombic, P212121, z = 4, a = 7.526±0.003, b = 4.623±0.003, c = 32.42±0.01 Å.