Dietary Modification Trial in Community-Dwelling Japanese Elderly: A Pilot Study.

BACKGROUND: This study examined the effects of 6-month nutrition education programs for community-dwelling elderly. METHODS: This study enrolled 50 community-dwelling elderly who regularly visit outpatient clinics. The programs had three goals: salt reduction, increase in dietary fiber, and adequate protein intake. Since it would be difficult for elderly to achieve all goals concurrently, a single goal was chosen by participants themselves. Anthropometric measurements, blood sampling, and assessment of dietary intake were performed at baseline, 3 months, and 6 months. RESULTS: The nutrition education program for salt reduction was well accepted by the participants and the amount of daily salt intake showed median value of 9.6 g at baseline, 8.0 g at 3 months and 8.1 g at 6 months (P = 0.005). The amount of dietary fiber intake only slightly increased after taking the nutrition program (median value of 13.4 g at baseline, 15.3 g at 3 months and 15.5 g at 6 months; P = 0.695), because of difficulties in introducing new food options to the diet. After taking the adequate protein intake program, participants showed small decreases in protein (a modification from 1.24 g/kg IBW to 1.20 g/kg IBW) and salt intake (8.2 to 7.3 g) at 3 months, but the effects were not sustained at 6 months. CONCLUSION: This nutrition education program focusing on a single nutrient may serve as a strategy to successfully reduce salt intake and improve systolic blood pressure control in community-dwelling elderly individuals who regularly visit outpatient clinics. In our view, dietary and lifestyle habits should be taken into account as much as possible in nutrition education for elderly individuals.

Impact of passive smoking on the bones of rats.

Many epidemiological surveys have identified smoking as a risk factor for osteoporosis, but it is unclear whether smoking has a direct effect on bone metabolism and if such an effect could cause osteoporosis. Therefore, we examined whether smoking causes osteoporosis based on the impact of smoke exposure on the bones of rats. A rat model of passive cigarette smoking was prepared by breeding rats in a cigarette-smoking box for 4 or 8 weeks. Histological changes, micro-computed tomographic (CT) analysis, mechanical bone strength, and bone mineral density of the femur and lumbar vertebrae were examined in these rats and in control rats that were not exposed to smoke. Lower mechanical bone strength was observed in smoke-exposed rats, but these differences were not significant. Significantly lower bone mineral density was found in the femur (P<.01) and lumbar bones (P<.001) of 8-week smoke-exposed rats compared to controls. In a micro-CT scan of lumbar vertebrae, the bone volume, trabecular thickness, trabecular number, and trabecular separation differed significantly between smoke-exposed rats and controls. Histologically, the osteocytes in the smoke-exposed rats were small (approximately 25% of the size in controls), and decreased numbers of marrow cells and osteoblasts (P<.01), as well as a black carbon dust-like substance, were found in the bone of smoke-exposed rats. These results indicate that smoking significantly decreases bone mineral density, which causes osteoporosis, and the organizational changes in the bone suggest a direct effect of smoking on bone structure. Fewer marrow cells were present in the smoke-exposed rats, and a black carbon dust-like substance was observed.

Gene expression changes in an early stage of intervertebral disc degeneration induced by passive cigarette smoking.

STUDY DESIGN: This study attempts to determine the molecular changes in intervertebral disc degeneration of rats induced by passive cigarette smoking. OBJECTIVES: To quantitate and compare the gene expression levels in intervertebral discs from passively cigarette smoking rats and nonsmoking rats. SUMMARY OF BACKGROUND DATA: The molecular mechanism of intervertebral disc degeneration has been investigated mainly in vitro but little in vivo, and gene expression analysis has been performed in a few studies. The cigarette smoking is a risk factor of low back pain. We developed a smoking box to create a rat model of intervertebral disc degeneration induced by passive cigarette smoking. METHODS: Total RNA was extracted from intervertebral discs of rats that were raised in a cigarette-smoking box for 2 to 7 weeks. After synthesis of cDNA, the quantitative analysis of gene expression was performed by the real-time PCR. The remaining spines were subjected to the histologic examination. RESULTS: Histologic changes of the nucleus pulposus and the anulus fibrosus were detected after 2 weeks of smoking and were frequently found after 7 weeks. Collagen genes were downregulated remarkably after 7 weeks of smoking. No significant increase was observed in the expressions of matrix metalloproteinase-3, but the expression of tissue inhibitor of metalloproteinases-1 started to increase at 4 weeks of smoking. Aggrecan also started to be up-regulated at 4 weeks. CONCLUSIONS: Changes in gene expression by passive cigarette smoking precede the histologic changes in the intervertebral discs. Reactions to suppress the destruction of tissue matrix and to regenerate the intervertebral discs are occurring at the same time as the degenerative histologic changes.

Alteration of gene expression in intervertebral disc degeneration of passive cigarette- smoking rats: separate quantitation in separated nucleus pulposus and annulus fibrosus.

OBJECTIVE: We constructed a passive cigarette-smoking model with rats to investigate the molecular mechanism of intervertebral disc degeneration, and found by gene expression analysis that passive cigarette smoking stimulated the stress-responsive signal pathway and inhibited the apoptotic pathway. In this study, to clarify that these changes were derived from either nucleus pulposus (NP) or annulus fibrosus (AF), we separately collected NP and AF and quantitatively analyzed gene expression. METHODS: Total RNA was extracted from NP and AF of the lumbar intervertebral discs from rats which were kept in a smoking box for 4 and 8 weeks. Gene expression was measured by real-time PCR of cDNA synthesized from the total RNA. RESULTS: Stress-responsive protein, heat shock protein 70, was expressed similarly in NP and AF, and was upregulated to the same degree after 8 weeks of passive cigarette smoking. The protein tyrosine phosphatase gene was expressed more strongly in AF than in NP, and was upregulated after 8 weeks of smoking in both tissue parts. The type II collagen and aggrecan genes were predominantly expressed in AF and NP, respectively. CONCLUSION: These results indicate that passive cigarette smoking stimulates both NP and AF, and induces the stress-responsible genes such as heat shock protein 70 and protein tyrosine phosphatase in both.

Hippocampal lesion delays the acquisition of egocentric spatial memory in chicks.

Effects of bilateral chemical lesion of the hippocampus was examined in 1- to 2-week-old domestic chicks. Chicks were trained and tested in an egocentric spatial task, in which subject chicks should memorize location of a rewarding object in reference to the subject's viewpoint. Two beads were simultaneously presented on a wall, and chicks pecked at one of them based on relative location (left-right or above-below) to gain a reward. Comparison of training curves revealed that the lesion significantly delayed, but did not impair, the acquisition. Recall of the spatial cue, as well as conditioning with color cues, was not impaired. Hippocampus could thus be involved in memory formation of spatial relationships between nearby objects.