Structural Changes in Titin and Nebulin Filaments Specific to Calcium Ions at 0.1 mM: Factors of Meat Tenderization During Postmortem Aging

ABSTRACT Postmortem structural changes in titin and nebulin filaments were investigated by incubating isolated myofibrils in a solution containing 0.1 mM calcium ions and various concentrations of a protease inhibitor. The inhibition curves showed 2 abnormal steps with increases in the concentration of leupeptin or calpastatin domain I. While the amounts of unchanged titin and nebulin were constant in the 1st step, the 2nd occurred at higher protease inhibitor concentrations. These facts indicated that excess amounts of leupeptin and calpastatin domain I caused deterioration in titin and nebulin properties, thus interfering with the binding of calcium ions. We concluded that the severance of titin and nebulin filaments in the 1st step were induced by calcium ions at 0.1 mM.     

Catalytic decomposition of HCFC22 (CHClF2)

The catalytic decomposition of CHClF₂ was studied over various acidic metal oxides in a fixed-bed reactor. The Cr₂O₃ZrO₂ exhibited the highest activity. The presence of water vapor in the reaction system suppresses the transformation of oxides to fluorides, progresses the formation of CO₂, and it improves the catalysts life.     

A 0.1-μm delta-doped MOSFET fabricated with post-low-energyimplanting selective epitaxy

A simple fabrication technology for delta-doped MOSFETs, named post-low-energy implanting selective epitaxy (PLISE) is presented. The PLISE technology needs no additional photo-lithography mask, deposition step or etching step even for CMOS devices. The only additional step is growing undoped epitaxial channel layers by UHV-CVD after the channel implantation. With this technology, delta-doped NMOSFETs with 0.1-μm gate length were successfully fabricated. By optimizing the epi-layer thickness and the channel doping level, short-channel effects are suppressed enough to achieve 0.1-μm gate length. Moreover, the junction capacitance at zero bias is reduced by 50%     

A new non-random chromosomal translocation t(3;6)(q27;p21.3) associated with BCL6 rearrangement in two patients with non-Hodgkin's lymphoma

We describe two cases of non-Hodgkin's lymphoma associated with t(3;6)(q27;p21.3) and BCL6 rearrangement. The first case was in a 78-year old woman, whose performance status (PS) was 1, the serum lactate dehydrogenase (LDH) level was elevated, and the Ann Arbor stage was IIIA with no extra nodal lymphomatous site. The pathological diagnosis from a biopsy of the inguinal lymph node was 'malignant lymphoma (ML), follicular, small cleaved' according to the Working Formulation. Complete remission was achieved. Although she had relapse in 1992, remission was obtained again. The second case was in a 62-year old man, whose PS was 1, the serum LDH was normal, and Ann Arbor stage was IVA with the involvement of the small intestine. Histological diagnosis of the cervical lymph node was 'ML, diffuse, large cell'. Complete remission was obtained without relapse. The 3q27 translocations, found in 20-30% of non-Hodgkin's lymphoma, are unique in having multiple chromosomal translocation partners. Chromosome band 6p21.3 is one of these partner sites that may be the site of a novel gene. The two cases presented here show that this translocation is a non-random chromosomal change involving 3q27 and BCL6. Since t(3;6) was the sole karyotypic abnormality in one case, this translocation may play a role in lymphomagenesis.     

Deterioration of connectin/titin and nebulin filaments by an excess of protease inhibitors

OBJECTIVE: To investigate HLA class II allele associations with autoantibody responses to Ro/SS-A and La/SS-B among Japanese subjects. METHODS: Haplotype and allele distributions, along with molecular polymorphisms, of HLA class II genes were analyzed by polymerase chain reaction-restriction fragment length polymorphism in 41 Japanese women with precipitating autoantibodies to Ro/SS-A and/or La/SS-B. RESULTS: Among women with both Ro/SS-A and La/SS-B antibodies, the HLA class II haplotype DRB1*08032/DQA1*0103/DQB1*0601 and DRB1*08032 allele showed significantly increased frequencies compared with patients with anti-Ro/SS-A alone or with normal controls. All women with both anti-Ro/SS-A and anti-La/SS-B, but not those with anti-Ro/SS-A alone, carried DRB1 alleles that shared the same amino acid residues at positions 14-31 and 71 of the hypervariable regions of the DRB1 chain. All anti-Ro/SS-A positive women carried 1 or 2 alleles of DQB1*06 and DQB1*03 subtypes that shared the same amino acid residues at positions 71-77 of the DQB1 chain. HLA class II allele distributions did not differ among 3 anti-Ro/SS-A positive groups with different disease expressions, i.e., patients with systemic lupus erythematosus, patients with primary Sj?gren's syndrome, and women with no apparent symptoms of rheumatic disease. CONCLUSION: HLA class II allele distributions differ among anti-Ro/SS-A positive subjects according to the presence or absence of coexisting anti-La/SS-B antibodies, but not according to disease expression. Our findings suggest that different HLA class II molecules might control the development of anti-Ro/SS-A and/or anti-La/SS-B antibodies in the autoimmune response to the Ro/SS-A-La/SS-B complex.     

Mechanisms responsible for resistance of sublines derived from leukemia cell lines to an antitumor agent 9-beta-D-arabinofuranosyl-2-fluoroadenine

An agent 9-beta-D-arabinofuranosyl-2-fluoroadenine (2-F-Ara-A) is a main metabolite of fludarabine, a fluorinated purine analogue with antitumor activity in lymphoproliferative malignancies. In this study, the mechanism responsible for the resistance of cancer cells to fludarabine was examined using the 2-F-Ara-A-resistant sublines JOK-1/F-Ara-A and L1210/F-Ara-A from a human hairy leukemic cell line (JOK-1) and a mouse leukemic cell line (L1210) respectively, which were established by continuous treatment of the parental cell lines with 2-F-AraA. JOK-1/F-Ara-A and L1210/F-Ara-A cells were more than 55 and 29 times more resistant to 2-F-Ara-A than were their parent cell lines, and showed a high cross-resistance to 1-beta-D-arabinofuranosylcytosine but not to doxorubicin or vincristine. These resistant sublines intracellularly accumulated almost the same amount of 2-F-Ara-A as did their parent cell lines. However, the amount of 2-F-Ara-ATP, a cytotoxic metabolite of 2-F-Ara-A, decreased by 2.6% (JOK-1/F-Ara-A C3), 6% (L1210/F-Ara-A C1) and 3.7% (L1210/F-Ara-A C7) relative to the levels in the parent cell lines. Enzymatically, these resistant cells hardly activated deoxycytidine (dCyd) and 2-F-Ara-A. In addition, the abilities to phosphorylate deoxyadenosine and deoxyguanosine were also decreased in the resistant cells in comparison with the parent cells. These findings suggest that the deficiency in activity of dCyd kinase may contribute to the resistance of 2-F-Ara-A.     

Sialon formation by Si+ and N2 + ion implantation into sapphire

Single-crystal alumina was implanted firstly with 400 keV Si⁺ and subsequently with N₂ ⁺ ions and then annealed at 1673 K in an No atmosphre. The implanted layers were characterized by means of X-ray diffraction, Rutherford backscattering-channelling of 2 MeV He⁺ ions, and the resonance nuclear reaction¹⁵N(p,)¹²C. The annealing of sapphire implanted at ambient temperature resulted in the formation of-sialon, a solid solution of-silicon nitride and alumina in the subsurface layer, while implantation at 100 K resulted in the formation of aluminium oxynitride in the surface layer. In the latter case, the implanted silicon atoms were believed not to react vxi1h the implanted nitrogen atoms but with the substrate oxygen atoms. These crystalline precipitates were found to have epitaxial relations with the sapphire substrate.