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Biomedical subjects

Y Imai

Publications and source records attributed to Y Imai.

At least 271 records · Page 15Linked to original sources

67Ga planar imaging with a low-energy collimator and scatter correction using the triple energy window method.

To improve the spatial resolution and contrast of 67Ga planar imaging, we used a low-energy collimator and two lower-energy windows with a triple-energy-window (TEW) scatter compensation method. The spatial resolution is better than with a medium-energy collimator, and the TEW method can correct for scattered photons and reduce the background counts. In a phantom study and a clinical study involving 44 patients, the images obtained by the proposed method were compared with the images obtained with a medium-energy collimator and three energy windows without scatter compensation (the conventional method). The spatial resolution and the counts were measured. Two nuclear medicine physicians interpreted the images and clinical usefulness was evaluated. The spatial resolution and contrast were improved by our proposed method. It enabled the detection of lesions in five locations in the clinical study. The counts were reduced but misreadings were not seen. We conclude that our proposed method shows a clinical advantage over the conventional method. It can be used easily and quickly with commercially available equipment and is useful in clinical practice.

Adult↗

Immunohistochemical and molecular analysis of giant cell carcinoma of the pancreas: a report of three cases.

We performed molecular biological studies as well as immunohistochemical analysis of three cases of giant cell carcinoma of the pancreas. Histologically, one case was a pleomorphic giant cell carcinoma consisting of pleomorphic giant/ small cells and spindle cells, one an osteoclast-like giant cell tumor composed of osteoclastoid giant cells and pleomorphic small cells, and one a pleomorphic giant cell carcinoma with osteoclastoid giant cells. Immunohistochemically, pleomorphic giant cells and small pleomorphic cells were positive for epithelial and mesenchymal markers throughout the cases. Osteoclastoid cells were strongly positive for PG-M1 (CD68), but negative for lysozyme and epithelial markers. Pleomorphic spindle cells showed the same immunoreactivity as pleomorphic giant/small cells. Genetically, all cases contained a mutation in the K-ras (codons 12, 13) oncogene, but neither p53 (exons 5-8) nor p16INK4 (exons 1, 2) gene mutations were found in any case. Furthermore, Loss of heterozygosity (LOH) of the p53, p161NK4. APC, and DPC4 gene loci was not found in any of the cases. Immunohistochemical study demonstrated this tumor to be of epithelial origin with mesenchymal differentiation. Genetically, initiation of the tumor is similar to that of usual ductal adenocarcinoma, but progression might be rather different. The peculiar histologic and biologic features of this tumor would be the result of changes in other functional genes.

Aged↗

Task force II: Ambulatory blood pressure monitoring in population studies.

Ambulatory blood pressure (ABP) has only rarely been employed in population studies because of the difficulty posed by the greater complexity of this technique. The cross-sectional studies that have been published, however, have allowed a number of conclusions to be drawn. One, 24h average blood pressure of populations is significantly but not closely related to office blood pressure, which thus can not predict accurately daily-life values of blood pressure. Two, 24h average blood pressure is usually less than office blood pressure, the discrepancy increasing with the increase in office values and being of magnitude several mmHg at the office blood pressure of 140/90 mmHg (systolic/diastolic) Three, ABP in women is somewhat less than that in men and ABP for both sexes increases less with aging than does office blood pressure. Four, a circadian profile of blood pressure consisting in values that are much lower at night than are those during daytime characterizes both sexes and all ages with the possible exception of individuals aged 75 years and more, in whom the nocturnal hypotension appears to be attenuated. A similar attenuation has been found for blacks in comparison with whites. The upper limit of normality of ABP has not yet been defined conclusively, although 24h average values </=125/80 mmHg are almost invariably regarded as normal. Normality of ABP should be defined, however, by longitudinal population studies in which ambulatory values are related to prognosis. One of these studies has already been published and others will be completed in the near future.

Blood Pressure Monitoring, Ambulatory↗

Task force VI: Self-monitoring of the blood pressure.

BACKGROUND: Self-monitoring of the blood pressure by patients at home or in other nonclinical settings has become increasingly common in recent years. This phenomenon has been fueled in part by the increase in availability of automatic sphygmomanometers, which are now both affordable and easy for patients to use. BENEFITS OF SELF-MONITORING: Self-monitoring of the blood pressure can be an important adjunct to management of hypertension. The technique allows patients to participate more in their care. Self-measured values of blood pressure are more likely to be representative of the average daily blood pressure than is a clinic measurement and may be better related to hypertensive involvement of target organs and cardiovascular morbidity than is the clinic blood pressure. Finally, the self-monitoring of blood pressure has the potential to reduce the costs of hypertension-related care. LIMITATIONS OF SELF-MONITORING: There are several issues that prevent the more widespread use of self-monitoring of the blood pressure in clinical practice. First, devices marketed for use by patients have advanced technically during the 1990s, but many have not been subjected to rigorous clinical validation for precision and reliability (e.g. in terms of Association for the Advancement of Medical Instrumentation and British Hypertension Society guidelines). It is recommended that devices for measuring blood pressure used by patients at home be subjected to the same validation processes as those that are applied to ambulatory recordings. Second, although the upper limits of normal for self-monitored blood pressure of a general population can be defined statistically (it is approximately 135/85 mmHg), it is not yet possible to determine the normal self-monitored blood pressure because these values must be linked to classical clinical cardiovascular endpoints or outcomes. Third, the relationships among self-monitored, clinic, and ambulatory blood pressures are defined for some populations but their behaviors according to age, sex, ethnicity, and treatment status require further study. Fourth, several different schedules for self-monitoring of the blood pressure by patients have been used in clinical research and practice. It will be necessary to determine the optimal schedule and number of recordings required when patients perform self-monitoring of the blood pressure. Fifth, self-monitoring of the blood pressure in clinical trials of antihypertensive therapies is certainly feasible but has typically not been included in their design, either by investigators or by the pharmaceutical sponsors. Sixth, there have been data suggesting that self-monitoring of the blood pressure reduces the comprehensive costs associated with hypertension care on an annual basis. However, since most work on the economic impact of self-monitoring of the blood pressure has been performed in managed-care environments in the USA, it is not known whether this reduction in health-care costs would be applicable to other types of practice environments on a worldwide basis. CONCLUSIONS: Self-monitoring of the blood pressure is at present useful as an adjunct measurement for the management of hypertensive patients and might provide benefits in clinical trials of antihypertensive therapy. Nevertheless, the available data on self-monitoring of the blood pressure are inadequate as grounds for clinicians to make primary diagnostic or therapeutic decisions and should not override the blood pressure obtained by clinical measurement or via ambulatory monitoring.

Blood Pressure↗

Determination of members of a Borrelia afzelii-related group isolated from Ixodes nipponensis in Korea as Borrelia valaisiana.

The 16S rRNA sequences of the Korean Borrelia strains 5MT and 9MT, isolated from Ixodes nipponensis, showed identities of 99.0-99.1% to that of B. afzelii. The strains were tentatively classified as belonging to the B. afzelii-related group. In this study, Korean isolates, including these strains, were characterized further and compared with recently described new species. These strains generated a RFLP pattern that has not been found previously in RFLP analysis of the 5S-23S rRNA intergenic spacer and the flagellin gene. When phylogenetic trees were constructed, based on the 5S-23S rRNA intergenic spacer, flagellin gene and 16S rRNA sequences, these Korean isolates formed a cluster with the Borrelia strain Am501 isolated from Ixodes columnae in Japan and Borrelia valaisiana strains VS116T and UK isolated from Ixodes ricinus in Europe and were distinguishable from the other species. However, these three groups of strains were divergent from each other in the molecular masses of the putative outer surface protein A (OspA) and in the sequences of the ospA gene. These findings suggest that these Korean isolates and one Japanese isolate are members of B. valaisiana and that OspA of this species is divergent, as is that of Borrelia garinii. This led to the speculation that B. valaisiana strains are adapted to the vector ticks found in each locality.

Animals↗

Mutational inactivation of mitotic checkpoint genes, hsMAD2 and hBUB1, is rare in sporadic digestive tract cancers.

Genetic instability is a key mechanism of tumorigenesis, and the instability exists at two distinct levels, the nucleotide and the chromosome levels. Disruption of the mitotic spindle checkpoint is one of the underlying mechanisms leading to aneuploidy and alterations of hsMAD2 and hBUB1, assumed to take part in the spindle checkpoint in human cells, have been found to be associated with chromosomal instability in some tumor cell lines. Therefore, we investigated the mutational status of the hsMAD2 and hBUB1 genes in 32 sporadic digestive tract cancers by reverse transcription-polymerase chain reaction-single strand conformation polymorphism analysis. The entire coding sequence of the hsMAD2 gene, and conserved regions (codons 21-152 and codons 732-1043) presumed to be functionally important in the hBUB1 gene were analyzed. Mutation of the hsMAD2 gene was not observed at all and missense mutation of the hBUB1 gene was noted in one rectal cancer case. Sequencing analysis revealed an AGT-to-GGT missense mutation, substituting glycine for serine, at codon 950, which is conserved between budding yeast and human. These results indicate that mutations of the hsMAD2 and hBUB1 genes are very rare and presumably play a very restricted role in tumor development of sporadic cancers.

Adenocarcinoma↗

Intratracheal anti-tumor necrosis factor-alpha antibody attenuates ventilator-induced lung injury in rabbits.

To evaluate the role of tumor necrosis factor (TNF)-alpha in the pathogenesis of ventilator-induced lung injury, we 1) measured TNF-alpha production in the lung caused by conventional mechanical ventilation (CMV) and 2) evaluated the protective effect of anti-TNF-alpha antibody (Ab) in saline-lavaged rabbit lungs. After they received saline lung lavage, rabbits were intratracheally instilled with 1 mg/kg of polyclonal anti-TNF-alpha Ab in the high-dose group (n = 6), 0.2 mg/kg of anti-TNF-alpha Ab in the low-dose group (n = 6), serum IgG fraction in the Ab control group (n = 6), and saline in the saline control group (n = 7). Animals then underwent CMV for 4 h. Levels of TNF-alpha in lung lavage fluid were significantly higher after CMV than before in both control groups. Pretreatment with intratracheal instillation of high and low doses of anti-TNF-alpha Ab improved oxygenation and respiratory compliance, reduced the infiltration of leukocytes, and ameliorated pathological findings. CMV led to TNF-alpha production in the lungs, and intratracheal instillation of anti-TNF-alpha Ab attenuated CMV-induced lung injury in this model.

Acute-Phase Reaction↗

Degradation of composite materials composed of tricalcium phosphate and a new type of block polyester containing a poly(L-lactic acid) segment.

Degradation of a new type of poly(L-lactic acid)/poly(ethylene; hexamethylene/ sebacate) block polyester and its composite containing 10 and 30 wt% tricalcium phosphate (TCP) were studied in vitro. Film specimens of thickness 100 and 250 microm for each of the three materials were immersed in phosphate buffered saline (pH 7.4) at 37 degrees C for up to 24 weeks. At appropriate intervals, water absorption, dry and wet tensile strength, molecular weight, and thermal properties of the specimens were measured by weighing, tensile strength testing, size exclusion chromatography, and differential scanning calorimetry, respectively. The decrease in tensile strength was greater in the unblended and thicker polymer film than in the other five films. The retention of tensile strength after 24 weeks increased with increasing TCP content. This trend was also noticed in the retention of molecular weight. The tensile strength of the materials having molecular weights below 5 x 10(4)-6 x 10(4) Mw or 2 x 10(4)-3 x 10(4) Mn dropped substantially and the materials became fragile. Blending of TCP to the PLLA block polyester retarded degradation, suggesting that TCP neutralized the carboxyl end groups formed by hydrolysis of ester bonds.

Absorption↗

Effect of blending tricalcium phosphate on hydrolytic degradation of a block polyester containing poly(L-lactic acid) segment.

The effect of blending tricalcium phosphate (TCP) on hydrolytic degradation of a new type of poly(L-lactic acid)/poly(ethylene:hexamethylene/sebacate) block polyester (60: 40 wt%) was studied. 100- and 250-microm film specimens blended with 0, 10, and 30 wt% TCP were immersed in phosphate buffered saline (pH 7.4) at 37 degrees C for up to 80-104 weeks. At appropriate intervals, water absorption, dry and wet tensile strength, molecular weight, and thermal properties of the specimens were measured by weighing, tensile strength testing, size exclusion chromatography, and differential scanning calorimetry, respectively. Some samples were characterized by 1H NMR spectroscopy. Blending of TCP with the block polyester was effective in retarding degradation. The blended TCP was thought to retard degradation for the most part by neutralizing the lactic acid oligomers produced by hydrolysis of the poly(lactic acid) part during the initial stage of degradation.

Calcium Phosphates↗

Roles of phosphatidylinositol 3-kinase and mitogen-activated protein kinase pathways in stimulation of vascular smooth muscle cell migration and deoxyriboncleic acid synthesis by insulin-like growth factor-I.

Insulin-like growth factor-I (IGF-I) is a potent stimulator of vascular smooth muscle cell (SMC) migration, a process that contributes to the accumulation of SMC within atherosclerotic lesions. Our previous studies have shown that IGF-I increases the affinity of the alphaVbeta3 integrin toward ligands and that occupancy of this integrin is indispensable for IGF-I to stimulate cell migration. In this study, the role of phosphatidylinositol 3-kinase (PI 3-kinase) and mitogen-activated protein kinase (MAPK) pathways in IGF-I induced cell motility and integrin activation was studied using porcine aortic smooth muscle cells (pSMC). Two structurally different inhibitors of PI 3-kinase decreased IGF-I-stimulated pSMC migration in a dose-dependent manner. The IC50 of wortmannin for inhibiting migration was 10 nM, and that of LY294002 was 0.3 microM. These inhibitors also suppressed IGF-I-induced phosphorylation of protein kinase B PKB/Akt at Ser437 using concentrations that also inhibited cell motility. PD98059, an inhibitor of the MAPK pathway, was somewhat less potent than PI 3-kinase inhibitors in blocking cell migration that had been stimulated by IGF-I. When IGF-I increased migration of pSMC 2.1-fold above control, 100 nM wortmannin inhibited this response by 79%, 1 microM LY294002 inhibited it by 58%, and 50 microM PD98059 caused a 34% reduction. In comparison, 100 nM wortmannin inhibited IGF-I stimulated DNA synthesis by 57%, 1 microM LY294002 inhibited it by 59%, whereas 50 microM PD98059 suppressed it completely. Thus, activation of PI 3-kinase plays the major role in IGF-I-stimulated migration and proliferation of pSMC. While the activation of the MAPK pathway seems to be necessary for stimulation of mitogenesis by IGF-I, the contribution of this pathway in IGF-I-induced cell migration is limited in pSMC. Interestingly, neither PI 3-kinase inhibitors nor PD98059 blocked the increase in alphaVbeta3 integrin affinity that followed IGF-I treatment. Therefore, although both the PI 3-kinase and MAPK pathways were used by IGF-I to increase migration of pSMC, alphaVbeta3 integrin activation did not depend on either PI 3-kinase or MAPK activation, suggesting the possible importance of some other signal transduction pathway to account for its full actions on pSMC.

Androstadienes↗

Relationships among blood pressures obtained using different measurement methods in the general population of Ohasama, Japan.

To examine the relationships between casual, ambulatory and home blood pressure measurements in the general population, these measurements were obtained in 1,695 of 3,744 subjects aged 20 yr or older in Ohasama, Japan. Of these 1,695 subjects, 1,207 measured their home blood pressure more than 14 times in each of the morning and evening (881 untreated subjects including normotensives and untreated hypertensives, 56.4 +/- 11.5 yr of age; 326 treated subjects, 66.0 +/- 9.2 yr of age). We analyzed data in these 1,207 subjects, examining the distribution of each measurement, the relationships among measurements, and the factors affecting the blood pressure differences among the measurements. For systolic pressure, the casual measurement was the highest among the methods examined. The daytime ambulatory measurement was significantly higher than morning and evening home measurements. Morning home measurements were significantly higher than those in the evening. For diastolic pressure, however, the morning home measurement was the highest among the methods examined. Short-term pressure variability (standard deviation and variation coefficient of ambulatory measurements) was greater than long-term pressure variability (standard deviation and variation coefficient of home measurements). The pressure variability in treated subjects was greater than that in untreated subjects. The correlation between casual pressure and the other pressures was not as strong (r<0.567). Among the relationships between ambulatory and home measurements, the strongest correlation was observed between the 24-h ambulatory measurement and the morning home measurement (r=0.738) in untreated subjects. The morning home measurement was highly correlated with the evening home measurement (r>0.814). The differences among the methods examined were affected by blood pressure level and age. It should be noted that in elderly and treated subjects, blood pressure measurement using one method does not necessarily correlate with that obtained using the other methods. This information is useful for the estimation of the value of one type of blood pressure measurement from values obtained with other methods.

Adult↗

Development of follicular dendritic cells: a study using short-term bone marrow cell grafting in SCID mice.

To evaluate the cellular origin of follicular dendritic cells (FDC) in lymphoid follicles (LFs), severe combined immunodeficient (SCID) mice (H-2d) were grafted with 5-bromo-2'-deoxyuridine (BrdU)-incorporated bone marrow cells from CB-17 mice (H-2d) and with non-BrdU-incorporated bone marrow cells from C3H mice (H-2k) and Wistar rats (RT1u). This procedure was followed by antigenic stimulation with horseradish peroxidase and related immune complex (mouse peroxidase anti-peroxidase) administration. Secondary LFs in the lymph nodes and spleen of the reconstructed SCID mice were examined morphologically and immunocytochemically. LFs reconstructed with CB-17 mouse bone marrow cells contained FDCs capable of trapping and/or retaining mouse peroxidase anti-peroxidase as immune complexes. Secondary LFs contained BrdU-incorporated germinal center lymphocytes but not non-lymphoid stromal cells. A cell grafting study in SCID mice using bone marrow cells from C3H mice and Wistar rats demonstrated that FDCs in reconstructed LFs exhibited a marker specific for the recipient but not for the donor. These data indicate that functionally active FDCs occur de novo in reconstructed LFs in SCID mice, and do not support the view that FDCs originate from bone marrow cells in short-term reconstructed LFs.

Animals↗

Effect of streptozotocin-induced diabetes mellitus on type 1 deiodinase (D1) in inherited D1-deficient mice.

We investigated the effects of streptozotocin (STZ)-induced diabetes on thyroid hormone levels, type 1 deiodinase (D1) activity and messenger RNA (mRNA) levels in inherited D1 deficient C3H mice in a comparative manner with control C57 mice. The apparent maximum velocity (Vmax) D1 values in C3H mice were 3% (liver) and 26% (kidney) of those in C57 mice. In C3H mice, similar serum T3, slightly higher T4, and 2.6-fold higher rT3 levels were observed compared with C57 mice. In STZ-induced diabetes, serum T4 level markedly decreased in both C3H and C57 mice. Serum T3 levels in STZ-C3H mice similarly decreased as in STZ-C57 mice. On the other hand, serum rT3 levels increased to 3.3-fold higher in STZ-C3H than in STZ-C57 mice. The Vmax values were decreased to 12% (STZ-C3H) and to 30% (STZ-C57) in liver, and decreased to 33% (both STZ-C3H and STZ-C57) in kidney. The changes in D1 mRNA levels in diabetes versus control were comparable to those of D1 activities in both strains. In summary, similar mechanism(s) to those which decrease the D1 expression and the serum T3 level in diabetes, function in D1 deficient C3H mice as in C57 mice. It appears that hepatic and renal D1 activity alone can not explain the similar reduction in T3 level in STZ-C3H mice and STZ-C57 mice.

Animals↗

Type 1 iodothyronine deiodinase in heart --effects of triiodothyronine and angiotensin II on its activity and mRNA in cultured rat myocytes.

We previously demonstrated that iodothyronine 5'-deiodination (5'D) activity is present and increased by triiodothyronine (T3) and angiotensin II (Ang II) in cultured rat cardiac myocytes. To further elucidate the stimulatory mechanism of Ang II, we investigated the effect of intracellular Ca2+ and protein kinase C on myocardial 5'D activity. Moreover, to elucidate the molecular mechanism of the stimulatory effect of T3 and Ang II, we detected the mRNA levels by means of a reverse-transcriptase polymerase chain reaction (RT-PCR). 5'D activity was increased by adding Bay-k 8644, Ca2+ channel agonist and the effect of Bay-k 8644 was completely blocked by nifedipine, a Ca2+ channel antagonist. 12-O-tetradecanoylphorbol-13-acetate, a protein kinase C activator, similarly stimulated 5'D activity. The addition of a high concentration (20-40 mM) of K+, which caused the depolarization of the membrane had significant stimulatory effects on 5'D activity. Type 1 deiodinase (D1) mRNA was evident in myocardial cells by RT-PCR in a single 758 bp band similar to that in the liver. Cardiac fibroblasts did not express the D1 mRNA. A significant increase in D1 mRNA was also evident after adding T3 and Ang II. These findings indicate that 5'D activity in myocardial cells is increased by activating the voltage sensitive Ca2+ channel, protein kinase C, and membrane depolarization, and that the D1 mRNA is present in cardiac myocytes and is increased by T3 and Ang II. This study therefore suggests that Ang II could affect the action of thyroid hormone on the heart by increasing the D1 gene expression.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗

Simulation of spike-burst generation and Ca(2+) oscillation in pancreatic beta-cells.

Based on the experimental evidence that Na(+)-Ca(2+) exchange participates in the regulation of intracellular Ca(2+) concentration in pancreatic beta-cells, we construct a mathematical model for the cyclic spike-bursts and oscillations of intracellular Ca(2+) concentration. In our model, an increase in ATP concentration by the stimulation of glucose metabolism leads to the closure of ATP-sensitive K(+) channels (K(ATP) channels) and gradual depolarization to the threshold of voltage-gated Ca(2+) channels. Spikes are generated by the alternate activation of voltage-gated Ca(2+) and K(+) channels, causing Ca(2+) entry. The accumulated Ca(2+) ions are extruded by Na(+)-Ca(2+) exchange and Ca(2+) active transport. An increase in Na(+) influx through Na(+)-Ca(2+) exchangers results in a rise in intracellular Na(+) concentration and the activation of Na(+)-K(+) active transport. The consumption of ATP during the process of Ca(2+) extrusion leads to the opening of K(ATP) channels and repolarization. The present model could reproduce the main experimental features of the spike-burst activity and Ca(2+) oscillations following changes in the extracellular glucose concentration. As the rate of ATP production increases, the spike-burst pattern changes from bursts with long silent phases to continuous spiking. Changes in the pattern of electrical activity produced by the alteration of extracellular Na(+) and K(+) concentrations and the addition of ouabain could be reproduced in the present model.

Action Potentials↗

Inhibition of Ca(2+) entry caused by depolarization in acetylcholine-stimulated antral mucous cells of guinea pig: G protein regulation of Ca(2+) permeable channels.

The effects of depolarizing conditions resulting from increasing extracellular K(+) concentration or nystatin treatment on intracellular Ca(2+) concentration ([Ca(2+)](i)) were studied in guinea pig antral mucous cells following acetylcholine (ACh) stimulation. ACh stimulation evoked a biphasic increase in [Ca(2+)](i), that is, an initial transient increase followed by a plateau. Depolarizing conditions reduced the [Ca(2+)](i) in the plateau phase during ACh stimulation. However, pertussis toxin (PTX, a G protein inhibitor) treatment caused [Ca(2+)](i) in the ACh-evoked plateau phase to increase under depolarizing conditions, while it had no effect on [Ca(2+)](i) under hyperpolarized conditions. Based on these observations, Ca(2+) permeable channels are regulated by a G protein which is activated by depolarized conditions and inhibited by hyperpolarized conditions and PTX; activation of the G protein (depolarization) causes Ca(2+) permeable channels to inhibit, and in turn, inhibition of the G protein (hyperpolarization) causes them to activate.

Acetylcholine↗

The effect of pravastatin on renal function and lipid metabolism in patients with renal dysfunction with hypertension and hyperlipidemia. Pravastatin and Renal Function Research Group.

The effect of pravastatin on renal function in hypertensive patients with mild renal dysfunction and hyperlipidemia was examined. A total of 57 subjects given dihydropyridine calcium blockers were randomly assigned to placebo (n = 25) and pravastatin groups (n = 32). The period of study was 6 months. In the placebo group, lipid metabolism did not change throughout the study period, but the serum creatinine concentration (Scr) increased from a baseline of 1.6+/-0.07 mg/dl to 2.1+/-0.2 mg/dl in the 6th month of study and blood urea nitrogen (BUN) increased from 26.2+/-1.1 mg/dl to 32.4+/-30.1 mg/dl. In the pravastatin group, the serum total cholesterol decreased from a baseline of 251.4+/-7.3 mg/dl to 218.2+/-6.5 mg/dl in the 6th month of study, while Scr (1.3+/-0.07 mg/dl vs. 1.3 +/-0.09 mg/dl) and BNU (20.5+/-1.2 mg/dl vs. 21.0+/-1.4 mg/dl) did not change. The change in Scr in the placebo group was significantly different from that in the pravastatin group (F = 3.75, p = 0.05). The slope of the change in 1/Scr was 0.02+/-0.07 dl x mg(-1) x month(-1) in placebo group and -0.01+/-0.03 dl x mg(-1) month(-1) in pravastatin group (P<0.05). The results indicate that pravastatin attenuates the deterioration of renal function in patients with mild renal dysfunction, together with an improvement of lipid metabolism.

Blood Urea Nitrogen↗