High molecular mass type IV collagen-specific metalloprotease from human carcinoma tissue

AbstractA protease degrading type IV collagen was purified more than 8000-fold from human stomach carcinoma tissue. This protease degraded type IV collagen, while type I, II, III and V collagen, laminin, fibronectin, casein, albumin and hemoglobin were not affected. This enzyme had a pH optimum of pH 7.0–8.0 and was inhibited completely by EDTA and o-phenanthroline, but not by seryl, thiol and carboxyl protease inhibitors. Furthermore, the molecular mas of this enzyme was estimated to be 1 MDa by Sepharose 6B column and HPLC-gel filtration. The molecular mass and substrate specificity of this metalloprotease from human carcinoma tissue indicate it to be a new protease

SEX DIFFERENCES IN RACE PROFILE AND STROKE VARIABLES DURING 200-M SPRINT IN JUNIOR KAYAKERS

The purpose of present study was to examine sex differences in race profile and stroke variables during 200-m sprint in junior kayakers. 200-m race time of the male kayakers showed 11% shorter than the female kayakers. In both groups, significant positive correlations were found between kayak velocity and stroke rate. In the three part of duration (Initial: 0-25m, Middle: 100-125m, Finish: 175-Zoom), male kayakers were faster than female kayakers. Kayak velocity of male kayakers significantly decreased in the finish part from the middle part, while the kayak velocity of female kayakers showed a most constant. In conclusion, these different raw profiles might be explained by physiological differences in the upper body power or anaerobic capacities between males and females

Takotsubo cardiomyopathy with marked ST-segment elevation and electrical alternans complicated with hyperglycemic hyperosmolar state

金沢大学医薬保健研究域医学系This is the first report of a case of Takotsubo cardiomyopathy with a hyperglycemic hyperosmolar state (HHS). This case presented with marked ST-segment elevation and electrical alternans, uncommon findings in Takotsubo cardiomyopathy. We believe that hyperosmolarity-induced myocardial dehydration and consequent increase in intracellular calcium concentration may be the mechanism of Takotsubo cardiomyopathy and electrical alternans in HH

Polar Patrol Balloon experiment in Antarctica during 2002-2003

The first scientific campaign of the Polar Patrol Balloon (PPB) experiment (1st-PPB) was performed at Syowa Station in Antarctica during 1990-1991 and 1992-1993. Based on the fruitful results of the 1st-PPB experiment, the next campaign (2nd-PPB) will be carried out in the austral summer of 2002-2003. This paper summarizes the 2nd-PPB experiment. Four balloons in total will be launched to make astrophysics observations (1 balloon) and upper atmosphere physics observations (3 balloons). The first payload will carry a very sophisticated instrument that will observe primary cosmic-ray electrons in the energy range of 10 GeV - 1 TeV. The payloads of the latter 3 flights are identical to each other. They will be launched in as rapid a succession as weather conditions permit to form a cluster of balloons during their flights. Such a "Balloon Cluster" is suitable for observing the temporal evolution and spatial distribution of various phenomena in the various magnetospheric and ionospheric regions and their boundaries that the balloons will traverse during their circumpolar trajectory. The expected flight duration of each balloon is 20 days. Observation data will be obtained mainly by a satellite communication system with a much higher temporal resolution than that used in the 1st-PPB experiment

Decreased ADP-Ribosyl Cyclase Activity in Peripheral Blood Mononuclear Cells from Diabetic Patients with Nephropathy

Aims/hypothesis. ADP-ribosyl-cyclase activity (ADPRCA) of CD38 and other ectoenzymes mainly generate cyclic adenosine 5’diphosphate-(ADP-) ribose (cADPR) as a second messenger in various mammalian cells, including pancreatic beta cells and peripheral blood mononuclear cells (PBMCs). Since PBMCs contribute to the pathogenesis of diabetic nephropathy, ADPRCA of PBMCs could serve as a clinical prognostic marker for diabetic nephropathy. This study aimed to investigate the connection between ADPRCA in PBMCs and diabetic complications. Methods. PBMCs from 60 diabetic patients (10 for type 1 and 50 for type 2) and 15 nondiabetic controls were fluorometrically measured for ADPRCA based on the conversion of nicotinamide guanine dinucleotide (NGD+) into cyclic GDP-ribose. Results. ADPRCA negatively correlated with the level of HbA1c (P = .040, R2 = .073), although ADPRCA showed no significant correlation with gender, age, BMI, blood pressure, level of fasting plasma glucose and lipid levels, as well as type, duration, or medication of diabetes. Interestingly, patients with nephropathy, but not other complications, presented significantly lower ADPRCA than those without nephropathy (P = .0198) and diabetes (P = .0332). ANCOVA analysis adjusted for HbA1c showed no significant correlation between ADPRCA and nephropathy. However, logistic regression analyses revealed that determinants for nephropathy were systolic blood pressure and ADPRCA, not HbA1c. Conclusion/interpretation. Decreased ADPRCA significantly correlated with diabetic nephropathy. ADPRCA in PBMCs would be an important marker associated with diabetic nephropathy

Observations of hard X-rays of auroral origin with Polar Patrol Balloons No. 8 and 10

In the Polar Patrol Balloon (PPB) project, two balloons named PPB-8 and -10 were launched in rapid succession to form a cluster of balloons during their flight on January 13, 2003, from Syowa Station, Antarctica. In order to make the two-dimensional images for auroral X-rays and to obtain the energy spectra of auroras with energy range from 30 keV to 778 keV, the same instruments for hard X-rays were installed on PPB-8 and -10, respectively. These detection systems observed several auroral X-ray events during the flight. In particularly on January 25, 2003, strong auroral events were detected at about 0919 UT by PPB-10 and at 0927 UT by PPB-8. The aurora observed by PPB-10 was observed after about 8 min by PPB-8 located a 650 km west of PPB-10. The energy spectra of the bright aurora at 0919 UT and 0927 UT for PPB-10 and -8 is obtained as E0 = (78+-5) keV and (70+-5) keV, respectively

A case report of crystalline light chain inclusion-associated kidney disease affecting podocytes but without Fanconi syndrome

RATIONALE:Crystalline light chain inclusion-associated kidney disease affects mainly tubular epithelial cells and is often clinically manifested as Fanconi syndrome. However, only very few case reports about the crystalline deposits within the podocytes are available, and the nature of the pathogenic monoclonal light chain implicated in these cases is still unknown. We report a case of crystalline inclusion-associated kidney disease manifested as crystalline podocytopathy in which we identified the complete structure of the pathogenic monoclonal light chain as belonging to the germ-line gene of Vκ1-39.PATIENT CONCERNS:We describe a 65-year-old woman with crystalline light chain inclusion-associated kidney disease showing mild proteinuria and renal insufficiency with monoclonal gammopathy of undetermined significance without Fanconi syndrome. She had crystalline inclusions mainly within podocytes, tubular epithelial cells and histiocytes in the kidney. Light microscopy showed vacuolation of podocytes and tubular epithelial cells, while eosin negative pale needle-like crystals were present within these cells. Electron microscopy showed accumulation of club-like crystals with high electron density in podocytes, proximal tubular epithelial cells and interstitial histiocytes. Clonal analysis revealed that a pathogenic monoclonal light chain was derived from germline gene, Vκ1-39.DIAGNOSES:The diagnosis of crystalline light chain inclusion-associated kidney disease was made.INTERVENTIONS AND OUTCOMES:Bortezomib and dexamethasone were started and her renal function improved to eGFR 36 mL/min/1.73 m after 9 courses of therapy.LESSONS:Patients with light chain crystalline podocytopathy may have a similar pathogenic monoclonal light chain derived from the same germline gene, Vκ1-39, to that of patients with light chain proximal tubulopathy