Increased LDL susceptibility to oxidation accelerates future carotid artery atherosclerosis

<p>Abstract</p> <p>Background</p> <p>We analyzed the causal relationship between LDL susceptibility to oxidation and the development of new carotid artery atherosclerosis over a period of 5 years. We previously described the determinants related to a risk of cardiovascular changes determined in a Japanese population participating in the Niigata Study, which is an ongoing epidemiological investigation of the prevention of cardiovascular diseases.</p> <p>Methods</p> <p>We selected 394 individuals (169 males and 225 females) who underwent a second carotid artery ultrasonographic examination in 2001 - 2002 for the present study. The susceptibility of LDL to oxidation was determined as the photometric absorbance and electrophoretic mobility of samples that had been collected in 1996 - 1997. The measurements were compared with ultrasonographic findings obtained in 2001 - 2002.</p> <p>Results</p> <p>The multivariate-adjusted model showed that age (odds ratio (OR), 1.034; 95% confidence interval (95%CI), 1.010 - 1.059), HbA1c (OR, 1.477; 95%CI, 0.980 - 2.225), and photometric O/N (OR, 2.012; 95%CI, 1.000 - 4.051) were significant variables that could independently predict the risk of new carotid artery atherosclerosis.</p> <p>Conclusion</p> <p>The susceptibility of LDL to oxidation was a significant parameter that could predict new carotid artery atherosclerosis over a 5-year period, and higher susceptibility was associated with a higher incidence of new carotid artery atherosclerosis.</p

Helicobacter suis-Associated Gastritis Mimicking Conventional H. pylori-Associated Atrophic Gastritis

A 45-year-old Japanese man underwent esophagogastroduodenoscopy, which revealed spotty redness at the gastric fornix, mucosal swelling, diffuse redness in the corpus, and mucosal atrophy in the gastric angle and antrum. Histological examination showed rod-shaped bacteria that appeared larger than Helicobacter pylori. The patient tested positive for rapid urease test, and serum anti-H. pylori IgG antibody test results were negative. Further examination of the bacteria revealed that H. suis antibody test was positive, and the presence of H. suis was confirmed using H. suis-specific real-time PCR. H. suis was successfully eradicated after triple therapy with vonoprazan, amoxicillin, and clarithromycin. This case reinforces the notion that non-H. pylori Helicobacter species such as H. suis and H. heilmannii may be involved in the pathogenesis of active gastritis in patients who test negative for H. pylori antibodies

Anderson's disease/chylomicron retention disease in a Japanese patient with uniparental disomy 7 and a normal SAR1B gene protein coding sequence

<p>Abstract</p> <p>Background</p> <p>Anderson's Disease (AD)/Chylomicron Retention Disease (CMRD) is a rare hereditary hypocholesterolemic disorder characterized by a malabsorption syndrome with steatorrhea, failure to thrive and the absence of chylomicrons and apolipoprotein B48 post-prandially. All patients studied to date exhibit a mutation in the <it>SAR1B </it>gene, which codes for an essential component of the vesicular coat protein complex II (COPII) necessary for endoplasmic reticulum to Golgi transport. We describe here a patient with AD/CMRD, a normal <it>SAR1B </it>gene protein coding sequence and maternal uniparental disomy of chromosome 7 (matUPD7).</p> <p>Methods and Results</p> <p>The patient, one of two siblings of a Japanese family, had diarrhea and steatorrhea beginning at five months of age. There was a white duodenal mucosa upon endoscopy. Light and electron microscopy showed that the intestinal villi were normal but that they had lipid laden enterocytes containing accumulations of lipid droplets in the cytoplasm and lipoprotein-size particles in membrane bound structures. Although there were decreased amounts in plasma of total- and low-density lipoprotein cholesterol, apolipoproteins AI and B and vitamin E levels, the triglycerides were normal, typical of AD/CMRD. The presence of low density lipoproteins and apolipoprotein B in the plasma, although in decreased amounts, ruled out abetalipoproteinemia. The parents were asymptomatic with normal plasma cholesterol levels suggesting a recessive disorder and ruling out familial hypobetalipoproteinemia. Sequencing of genomic DNA showed that the 8 exons of the <it>SAR1B </it>gene were normal. Whole genome SNP analysis and karyotyping revealed matUPD7 with a normal karyotype. In contrast to other cases of AD/CMRD which have shown catch-up growth following vitamin supplementation and a fat restricted diet, our patient exhibits continued growth delay and other aspects of the matUPD7 and Silver-Russell Syndrome phenotypes.</p> <p>Conclusions</p> <p>This patient with AD/CMRD has a normal <it>SAR1B </it>gene protein coding sequence which suggests that factors other than the SAR1B protein may be crucial for chylomicron secretion. Further, this patient exhibits matUPD7 with regions of homozygosity which might be useful for elucidating the molecular basis of the defect(s) in this individual. The results provide novel insights into the relation between phenotype and genotype in these diseases and for the mechanisms of secretion in the intestine.</p

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ABSTRACT This paper describes the effect of renitriding for hot work die steel. We noticed a decrease of compressive residual stress on the nitrided die surface during thermal fatigue process. X-ray stress measurement was used to detect the decomposition of nitride layer on hot work die steel (H13). As a result, compressive residual stress decreased gradually during the thermal fatigue test, almost restoring to the pre-test level by renitriding. The number of cracks decreased with the frequency of test by surface removal effect of shot peening while renitriding. Comparing the renitrided specimen with non renitrided specimen (single nitride), the number of cracks had decreased. 1.INTRODUCTION On the surface of hot work die, such as die-casting die, heat cycles are applied during the operation. Then, the cracks occurred due to thermal stresses caused by thermal cycles. To extend die-casting die life, nitriding is often applied to the die surface 1) . Even with nitriding, the nitride layer is damaged by heat during the die-casting operation. Thus, if renitriding will be available with the detecting damaged layer quantitatively, extension of die life can be expected. On the other hand, high compressive residual stress about -900MPa is caused on the surface of hot work die steel (AISI-H13) by nitriding. And the reheating decreases the residual stress 2) . We noticed the compressive residual stress, and tried to detect decomposition of nitride layer in thermal fatigue process by X-ray stress measurement. And repair effect of nitride layer by renitriding with shot peening was investigated. During the thermal fatigue test, renitriding was applied several times and changes of residual stress and half-value breadth were measured. After the test, distribution of residual stress, maximum crack length and number of cracks were measured