An improved method of embedding data into pictures by modulomasking

An improved scheme using vertical block allocation to embed data in industrial-quality monochrome analog pictures by modulo masking is investigated. The video signal on each scan line is sampled, and a data bit is inserted into a block of three pels by a scrambling of the luminance level of only one pel in the block. The performance of the system is compared to that of a conventional system. The number of data bits embedded in an image for the proposed system is about 1.3 times as large as that of the conventional system. In addition, the SNR (signal-to-noise ratio) of the recovered image in the proposed system is increased by about 3-4 dB     

The efficiency of helical strakes for the suppression of vortex-excited oscillation of steel stacks

Helical strikes are well known as a device to suppress the vortex-excited oscillation of stacks and have been applied to some stacks to prevent the oscillation. Wind tunnel experiments on two-dimensional models were performed to reconsider the optimum configuration of the strakes. Based on the model experimental results, the effectiveness of the strakes was confirmed by experiments on an actual stack. Finally, the stack with strakes was shown to be more economical than the plain stack without strakes.     

Different effects of carboxy-terminal deletion in the adrenodoxin molecule on cytochrome c and acetylated cytochrome c reductions

In immunoblotting analysis using a rabbit antibody to bovine adrenodoxin, the total proteins of the bovine adrenal cortex gave two bands, suggesting the presence of two forms of adrenodoxin in vivo: full-length and carboxy-terminal deleted adrenodoxins. To examine the effect of the carboxy-terminal deletion of adrenodoxin on its activity, cDNAs for Arg115stop mutant adrenodoxin and for Asp113stop mutant adrenodoxin were constructed. The wild type [Ad(2-128)] and carboxy-terminal deleted [Ad(2-114) and Ad(2-112)] recombinant adrenodoxins expressed in Escherichia coli were purified to give a single band on SDS-PAGE. They showed an A414/A276 value of 0.92. In an NADPH-cytochrome c reduction assay, the Km values for cytochrome c in the reconstituted system with AD(2-128), Ad(2-114) and Ad(2-112) were 39, 235 and 618 mM, respectively. The Vmax values were 638, 700 and 898 mol/min/mol flavin, respectively. In an NADPH-acetylated cytochrome c reduction assay, the maximum activity of Ad(2-128) was obtained at 50 mM NaCl, while the maximum activities of Ad(2-114) and Ad(2-112) were obtained at 100 mM NaCl; the latter values were 4-times higher than that of Ad(2-128). In the presence of 100 mM NaCl, the Km values for acetylated cytochrome c in the system reconstituted with Ad(2-128), Ad(2-114) and Ad(2-112) were 220, 33 and 22 microM, respectively. The Vmax values were 352, 305 and 382 mol/min/mol flavin, respectively. These results indicate that the effects of the carboxy-terminal deletion of adrenodoxin on NADPH-cytochrome c and acetylated cytochrome c reductions are different; the carboxy-terminal region (residues 113-128) of adrenodoxin largely contributes to the binding with cytochrome c but disturbs the binding with acetylated cytochrome c.     

Donor resting B cells induce indefinite prolongation of fully allogeneic cardiac grafts when delivered with anti-immunoglobulin-D monoclonal antibody: evidence for tolerogenicity of donor resting B cells in vivo

BACKGROUND: Resting B (rB) cells have been shown to induce T-cell anergy in vitro and to prolong the survival of skin and cardiac grafts mismatched for minor histocompatibility antigens. However, rB cells were unable to modulate the rejection response when grafts mismatched for major histocompatibility complex antigens were transplanted. We reasoned that donor antigens, which presented via the indirect pathway by recipient antigen-presenting cells, in particular B cells, might influence the ability of rB cells to induce unresponsiveness. To explore this hypothesis, we used an anti-immunoglobulin (Ig)-D monoclonal antibody (mAb) specific for recipient B cells to deplete these cells, thereby decreasing the potential for indirect presentation in vivo. METHODS: CBA mice were pretreated with 1 x 10(7) donor rB or activated B (aB) cells 7 days before transplantation of a C57BL/10 cardiac graft in the absence or presence of anti-IgD mAb. RESULTS: Naive CBA mice rejected C57BL/10 grafts acutely (median survival time [MST]=8 days). Pretreatment with rB cells alone resulted in a modest prolongation of graft survival (MST=11.5 days). In marked contrast, when rB cells were delivered with anti-IgD mAb, indefinite graft prolongation (MST>100 days) was observed in all recipients. Interestingly, aB cells produced only a small prolongation of graft survival when delivered with anti-IgD mAb (MST=15 days). Recipients treated with anti-IgD mAb alone rejected C57BL/10 cardiac allografts acutely (MST=8 days). CONCLUSION: These data suggest that depletion of recipient B cells in vivo can augment the ability of donor rB cells to induce indefinite prolongation of fully allogeneic cardiac grafts. Thus, IgD+ B cells in the recipient may influence the development of unresponsiveness in vivo.     

H2 sensors using Fe2O3-based thin film

This paper describes the fabrication procedure as well as the sensing properties of new hydrogen sensors using Fe₂O₃-based thin film. The film is deposited by the r.f. sputtering technique; its composition is Fe₂O₃, TiO₂(5 mol%) and MgO(0–12 mol%). The conductance change of the film is examined in various test gases. The sensitivity to hydrogen gas is enhanced by treating the film in vacuum at 550 °C for 4 h and then in air at 700 °C for 2 h. The sputtered film is identified to be polycrystalline -Fe₂O₃ based on X-ray diffraction patterns. However, the surface layer is considered to be changed to Fe₃O₄ after heating in vacuum and then to γ-Fe₂O₃ after heating in air. The film is thus a multilayer one with a thin γ-Fe₂O₃ layer on a -Fe₂O₃ layer. The sensing mechanism is discussed based on measurements of the physical properties of the film, such as the temperature dependence of the sensor conductance, X-ray diffraction pattern, surface morphology, RBS (Rutherford back-scattering) spectrum and optical absorption spectrum.     

Corneal endothelial cell loss caused by detached opacified anterior lens capsule in the anterior chamber

From 1984 to 1986, we performed cataract surgery through a 1.5 mm anterior capsule hole in 77 eyes. The hole was enlarged to 6.0 mm by a slit incision, and an intraocular lens was implanted into an almost completely intact capsular bag. Twelve (16%) eyes developed severe postoperative anterior capsule opacification. The opacified central anterior capsule, approximately 5 mm in diameter, was detached by can-opener anterior capsulotomy using a neodymium:YAG laser and fell into the inferior anterior chamber. Inferior corneal endothelial cell loss occurred in nine of the 12 eyes within 20 months after detachment; in six of the nine, inferior corneal endothelial cell density decreased 50% more than central cornea cell density. This method will be unsuitable for treating the extensive anterior capsule opacification that will occur when endocapsular cataract surgery that retains most of the lens capsule is widely performed in the future.     

Life-threatening reperfusion injury in skeletal muscle: a simple technique to control critical hyperkalemia

A 55-year-old male suffering from acute abdominal aortic occlusion due to iatrogenic aortic dissection was urgently admitted to hospital. An axillo-bifemoral bypass was constructed 6 hours from the onset of dissection. Before and after revascularization, blood samples were repeatedly obtained from a systemic artery and femoral vein. The arterial potassium concentration gradually increased, reaching 7.3 mM/L. Oliguria and arrhythmias occurred, and the left lower limb became rigid 3 hours after reperfusion. The femoral artery and vein were clamped and within 30 minutes, the arterial potassium concentration fell to 4.8 mM/L. The urine output increased. The left lower limb was amputated, and the patient survived. Immediately following revascularization, hyperkalemia may occur. Clamping of the afferent and efferent vessels is recommended as a simple and practical technique to quickly control life-threatening hyperkalemia.     

A case of malignant rheumatoid arthritis complicated by secondary amyloidosis and membranous nephropathy

A 30-year-old man had been treated for malignant rheumatoid arthritis from 1989 with a non-steroidal anti-inflammatory drug, then bucillamine for six months and prednisolone. Mild proteinuria appeared in May 1994, 4 years after bucillamine therapy was conducted. The patient was admitted to our hospital for a renal biopsy in July 1994. The specimen revealed secondary amyloidosis and membranous nephropathy (MGN). These findings suggest that MGN unrelated to bucillamine therapy might have occurred with secondary amyloidosis in rheumatoid arthritis.     

Mutations in the hepatocyte nuclear factor-1alpha/MODY3 gene in Japanese subjects with early- and late-onset NIDDM

Recent studies have shown that mutations in the hepatocyte nuclear factor (HNF)-1alpha gene are the cause of maturity-onset diabetes of the young type 3 (MODY3). We have screened 193 unrelated Japanese subjects with NIDDM for mutations in this gene: 83 with early-onset NIDDM (diagnosis at <30 years of age) and 110 with late-onset NIDDM (diagnosis > or = 30 years of age). All of the members of the latter group also had at least one sibling with NIDDM. The 10 exons, flanking introns, and promoter region were amplified using polymerase chain reaction and were sequenced directly. Mutations were found in 7 of the 83 (8%) unrelated subjects with early-onset NIDDM. The mutations were each different and included four missense mutations (L12H, R131Q, K205Q, and R263C) and three frameshift mutations (P379fsdelCT, T392fsdelA, and L584S585fsinsTC). One of the 110 subjects with late-onset NIDDM was heterozygous for the missense mutation G191D. This subject, who was diagnosed with NIDDM at 64 years of age, also had a brother with NIDDM (age at diagnosis, 54 years) who carried the same mutation, suggesting that this mutation contributed to the development of NIDDM in these two siblings. None of these mutations were present in 50 unrelated subjects with normal glucose tolerance (100 normal chromosomes). Mutations in the HNF-1alpha gene occur in Japanese subjects with NIDDM and appear to be an important cause of early-onset NIDDM in this population. In addition, they are present in about 1% of subjects with late-onset NIDDM.