We aimed to elucidate the molecular changes in intervertebral discs (IVDs) caused by passive smoking. Rats were subjected to 8 weeks of passive smoking; thereafter, their lumbar vertebrae were harvested. The annulus fibrosus and cartilage endplate (AF/CEP) were harvested together, and the nucleus pulposus (NP) was isolated separately. The expression of 27,342 rat genes was analyzed. In 3 "nonsmoking" rats, 96 of 112 genes whose expression varied !10-fold between the AF/CEP and NP were more highly expressed in the AF/CEP. With these differentially expressed genes, we uncovered novel AF/CEP and NP marker genes and indicated their possible novel functions. Although passive smoking induced less marked alteration in the gene expression profiles of both the AF/CEP and NP, multiple clock-related genes showed altered expression. These genes were expressed with a circadian rhythm in IVD cells, and most genes showed a phase shift of À6 to À9 h induced by passive smoking. Some clock-related genes showed abolished oscillation in the NP. Passive smoking also changed the expression levels of proteases and protease inhibitors and reduced the expression of NP marker genes. Thus, passive smoking induces changes in the circadian rhythm of a peripheral clock (IVD clock) that might be involved in molecular events related to IVD degeneration. Keywords: cigarette smoking; intervertebral disc; circadian rhythm; phase shift; microarray Lower back pain is a very common complaint among adults, and is caused, to some extent, by intervertebral disc (IVD) degeneration. The etiologic factors of IVD degeneration include age, sex, occupation, and smoking status.1 There have been many studies on the relation between lower back pain or IVD degeneration and tobacco smoking.2-5 However, there are also conflicting reports stating no association between smoking and lower back pain or IVD degeneration.6-9 Thus, it is not yet clear whether smoking causes IVD degeneration. However, the causal relationship can be examined by using animal models. We have previously generated passive smoking rats and investigated IVD degeneration. The changes in the IVD tissue of the passive smoking rat model have been verified. 10 For example, the alterations in gene expression levels that lead to or prevent degeneration have been observed simultaneously. 11Furthermore, differential expression of stress responserelated genes was observed.12 Recently, Wang et al. 13designed a chronic human tobacco-smoker model using mice and observed more significant degeneration than we observed with our passive smoking rat model. Akmal et al. 14 also reported that nicotine reduces the synthesis of glycosaminoglycans and collagen and causes a change in cellular metabolism, directly inducing IVD degeneration. On the other hand, since human IVD degeneration is well known to be age-associated, aged rats were used, which showed changes in the molecular phenotype of nucleus pulposus (NP) cells of IVD. 15Recently, accelerated aging animal models were also used to propose a cell senes...
The prevalence and risk factors for renal artery stenosis (RAS) and chronic kidney disease (CKD) are unclear in Japanese patients with peripheral arterial disease (PAD). To examine these issues, we performed renal angiography in 410 patients with PAD. Renal function and damage were assessed using the estimated glomerular filtration rate (eGFR) and urinary level of microalbumin (MA). Multiple logistic and multiple regression analyses were used to examine the relationships of potential risk factors with RAS and CKD. In all, 94 subjects (22.9%) had RAS 450% and 45 subjects (11.0%) had RAS 475%. The incidences of an abnormal level of MA and renal insufficiency (eGFR o60 ml min -1 per 1.73 m 2 ) were 37.0 and 60.7%, respectively. RAS X50% was associated with critical limb ischemia (CLI; hazard ratio (HR) 2.519; 95% confidence interval (CI) 1.203-5.276, P¼0.014), coronary heart disease (CHD; HR 2.143; 95% CI 1.129-4.069; P¼0.020) and hypertension (HR 1.907; 95% CI 1.009-3.628; P¼0.045). RAS X75% had a relationship with hypertension (HR 3.093; 95% CI 1.002-9.548; P¼0.048). eGFR was negatively correlated with age, uric acid and CHD (P¼0.013), and MA had a significant positive correlation with low-density lipoprotein cholesterol, CLI, age, CHD and diabetes (Po0.001). These results show that the prevalences of RAS and CKD are very high in Japanese patients with PAD; that CLI and CHD are major risk factors for RAS; and that hyperuricemia, hypercholesterolemia and diabetes are risk factors for CKD in PAD. We also found that MA is a simple and noninvasive marker of renal dysfunction and general vascular damage.
In order to evaluate sensory compatibility of alcoholic beverages with food, beverages and dried squid, namely, "surume", a common Japanese accompaniment, were consumed together. White wine and dried squid pairings had a more undesirable taste and more fishy off-odor than sake and dried squid pairings. The undesirable taste and fishy off-odor appeared to be caused by degradation of unsaturated fatty acids (e.g., docosahexaenoic acid (DHA)), which are found in fish and squid. Upon addition of DHA to the beverage, bitterness intensity, measured by instrumental taste sensor analysis, and the concentration of certain aldehydes reported to contribute to fishy flavors, increased in white wines, whereas they remained largely the same in sake. Among the major chemical constituents that distinguish wine from sake, only wine-specific sulfite markedly increased bitterness intensity and aldehyde levels upon addition of DHA. These results suggest that sulfur dioxide in wine participated in degradation of unsaturated fatty acids, causing an increase in undesirable taste and fishy off-odor in wine and seafood pairings.
Pleural involvement of systemic amyloidosis has been rarely reported. We report a case with multiple myeloma presenting an intractable right pleural effusion, in which pleural amyloidosis was diagnosed through pleural biopsy using a Cope needle. The diagnosis of pleural amyloidosis is important, because its refractory pleural effusion should be treated with pleurodesis. Since closed pleural biopsy using a Cope needle is much less invasive than thoracoscopy, the former should be attempted first whenever pleural amyloidosis is suspected.
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