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J Yamakita

Publications and source records attributed to J Yamakita.

At least 19 recordsLinked to original sources
PubMed2003

Antimicrobial resistance in respiratory pathogens isolated in Brazil during 1999-2000.

The in vitro antimicrobial susceptibility of the respiratory pathogens Streptococcus Pneumoniae, Hemophilus influenzae, and Moraxella catarrhalis to commonly tested and prescribed agents was investigated during 1999-2000 and compared with results obtained during a previous 1997-1998 study. Of 448 isolates of S. Pneumoniae collected and tested in 1999-2000, 77.2% were susceptible, 19.9% were intermediate, and 2.9% were resistant to penicillin, demonstrating that there were no major changes in susceptibility to penicillin from 1997-1998 (77.1% susceptible, 18.7% intermediate, 4.2% resistant). All S. Pneumoniae isolates from 1999-2000 were susceptible to levofloxacin and vancomycin and >90% were susceptible to the B-lactams (amoxicillin-clavulanate, ceftriaxone, and cefuroxime) and macrolides (axithyromycin and clarithromycin), showing that susceptibility to these agents also remained unchanged since 1997-1998. The most notable increase in resistance between the two studies was demonstrated by trimethoprim-sulfamethoxazole, which increased from 23.4% to 38.6%. Penicillin resistance correlated with resistance to B-lactams, macrolides, and trimethoprim-sulfamethoxazole in both studies. In H. influenzae, the prevalence of B-lactamase-producing isolates remained unchanged (10.6% in 1999-2000; 11.0% in 1997-1998). All H. influenzae isolates were susceptible to levofloxacine, ceftriaxone, cefuroxime, and azithromycin, and showed no change between the two studies. Trimethoprim-sulfamethoxazole resistance was present in 40.1% of isolates in 1999-2000, and in 45.2% in 1997-1998. In M. catarrhalis, the prevalence of B-lactamase-producing isolates was unchanged (97.9% in 1999-2000;98.0% in 1997-1998). The most active agents against M. catarrhalis were azithromycin (MIC(90),< or = 0.03 microg/ml) and levofloxacin (MIC(90),< or = 0.03 microg/ml). Overall, these results suggest that, in Brazil, between 1999-2000 and 1997-1998, there have been no significant changes in the susceptibility of respiratory pathogens to any of the commonly tested and prescribed agents with the exception of trimethoprim-sulfamethoxazole for S. Pneumoniae.

Anti-Bacterial Agents↗
PubMed2002

Antimicrobial resistance among respiratory pathogens collected in Thailand during 1999-2000.

A multi-center surveillance study was conducted in Thailand during 1999-2000 to determine antimicrobial susceptibilities among the respiratory pathogens Streptococcus pneumoniae (n = 206), Haemophilus influenzae (n = 305), and Moraxella catarrhalis (n = 39). Of the S. pneumoniae isolates collected, 33.5% were penicillin-susceptible, 27.2% intermediate and 39.3% resistant. Expectedly, resistance rates to beta-lactams were higher among penicillin-resistant (ceftriaxone, 14.8%; amoxicillin-clavulanate, 42.0%; cefuroxime, 100%) than penicillin-susceptible (ceftriaxone, 0%; amoxicillin-clavulanate, 0%; cefuroxime, 0%) isolates. Likewise, azithromycin and clarithromycin resistances were 4.3% and 5.8% among penicillin-susceptible isolates, and 77.8% and 95.1% among penicillin-resistant isolates. All S. pneumoniae remained susceptible to vancomycin and 99.5% were susceptible to levofloxacin. Multidrug resistance (resistance to >3 antimicrobial classes) was present in 25.2% of pneumococcal isolates (n = 52), with resistance to azithromycin, penicillin and trimethoprim-sulfamethoxazole the most common phenotype (40/52 isolates; 77.0%). Among the isolates of H. influenzae, the prevalence of beta-lactamase production was 45.2%. All isolates of H. influenzae were susceptible to amoxicillin-clavulanate, azithromycin, ceftriaxone, cefuroxime and levofloxacin while 49.5% were resistant to trimethoprim-sulfamethoxazole. All 39 isolates of M. catarrhalis produced beta-lactamase. Azithromycin (MIC90, < or = 0.03 microg/ml) and levofloxacin (MIC90, 0.03 microg/ml) were the most active agents tested against M. catarrhalis. The results of this study may serve as a baseline for future studies to monitor antimicrobial susceptibilities among respiratory pathogens in Thailand.

Anti-Bacterial Agents↗
PubMed2001

Increased visceral fat accumulation further aggravates the risks of insulin resistance in gout.

We performed the present study to determine the degree of visceral fat accumulation and incidence of visceral fat obesity in 138 gout patients who were classified as overexcretion type (n = 53) and underexcretion type (n = 85) by their levels of uric acid clearance and urinary uric acid excretion. We also investigated the relationship between visceral fat accumulation and insulin resistance expressed by the homeostasis model assessment (HOMA) index. Visceral fat area (VFA)/surface body area (SBA) was significantly increased in patients with gout as compared with control subjects (79.7 +/- 30.8 cm(2)/m(2) v 65.1 +/- 24.1 cm(2)/m(2), P <.001). It was also shown that VFA/SBA in the gout overexcretion group was significantly increased as compared with the gout underexcretion group (88.3 +/- 32.8 cm(2)/m(2) v 74.3 +/- 28.3 cm(2)/m(2), P <.01). Although the incidence of visceral fat obesity (VFO) was not different between gout patients and control subjects, the incidence of VFO was significantly higher in the gout overexcretion type than the gout underexcretion type (19 of 53 v 11 of 85, P <.01). Further, there was a significant relationship between visceral fat area and HOMA index. Gout patients possess some factors that are included in the insulin resistance syndrome, irrespective of the presence of VFO, and the insulin resistance risk factors observed in gout become more prominent when it is complicated with VFO. Our results suggest that gout patients, especially the overexcretion type who have greater levels of visceral fat accumulation, may be more vulnerable to atherosclerotic diseases.

Adult↗
PubMed2001

Spot urine uric acid to creatinine ratio used in the estimation of uric acid excretion in primary gout.

OBJECTIVE: Uric acid overexcretion in patients with gout is frequently assessed by the measurement of 24 hour urinary uric acid excretion, which is cumbersome with ambulatory patients, and requires accurate timing and complete collection of the specimen. We assessed whether uric acid to creatinine ratio (Uua/Ucr) in spot urine is useful for the estimation of uric acid overexcretion in patients with gout. METHODS: One hundred thirty male patients with gout and 33 non-gout male control subjects were studied. Early morning urine and/or a portion of 24 h collected urine (24 h urine) were used as spot urine samples. Uric acid overexcreters were defined as those with a 24 h urinary uric acid excretion > or = 1000 mg/day, while uric acid underexcreters were defined as those with uric acid clearance < 6 ml/min. RESULTS: There was a significant relationship between 24 h urinary uric acid excretion and early morning urine Uua/Ucr in patients with gout, while no such relationship was observed in controls. No significant difference in Uua/Ucr was observed between patients with gout and controls, or in Uua/Ucr between gout uric acid overexcreters and underexcreters in early morning urine. A significant difference in this value was observed between the 2 groups in the 24 h urine specimens. Although the diagnostic accuracy of gout uric acid overexcretion was 87.2% using early morning urine and 89.6% using 24 h urine, the sensitivity of gout uric acid overexcretion was only 25.0% when using early morning urine and 25.0% when using 24 h urine, when the cutoff value of Uua/Ucr was 0.63 and 0.64, respectively. CONCLUSION: Uua/Ucr using spot urine, especially early morning urine, is not an accurate indicator of uric acid overexcretion in patients with gout.

Chemistry, Clinical↗
PubMed2000

Effect of branched-chain amino acids on the plasma concentration of uridine does not occur via the action of glucagon or insulin.

To examine whether branched-chain amino acids affect the plasma concentration of uridine, we administered branched-chain amino acids (L-isoleucine, 2.85 g, L-leucine 5.71 g, and L-valine, 3.43 g) orally to 6 healthy subjects. Plasma uridine and glucose decreased by 44% and 12%, respectively, together with an increase in plasma isoleucine, leucine, and valine 90 minutes after administration. However, branched-chain amino acids did not affect the plasma concentration and urinary excretion of purine bases (hypoxanthine, xanthine, and uric acid) and uridine or the plasma concentration of insulin, glucagon, and cyclic adenosine monophosphate (cAMP). Since small amounts of regular insulin, which were found to decrease plasma glucose more than the amino acids, did not decrease the plasma concentration of uridine, these results suggest that plasma uridine was decreased by a direct effect of the branched-chain amino acids on the cellular uptake and/or release of uridine.

Adult↗
PubMed2000

Effect of urine storage on urinary uric acid concentrations.

Accurate determination of serum and urinary uric acid concentrations is essential for the diagnosis and classification of gout according to uric acid metabolism derangement. Urine and/or serum samples are often kept at either 4 degrees C or -20 degrees C until assayed, when a large number of samples are handled simultaneously. Our preliminary study indicated a significant decrease in urinary uric acid concentration after preservation, regardless of the storage temperature. Uric acid crystals were often observed in these cases which showed a marked decrease in urinary uric acid concentration after storage. In the present study, we sought the factor(s) that might cause this decrease in urinary uric acid concentration, as well as measures to overcome the problem. High urinary uric acid concentration and low pH proved to play major roles in the decrease in urinary uric acid concentration after storage. In contrast, dilution of the urine samples before storage resulted in no significant change in urinary uric acid concentration. Based on these results, we recommend diluting urine before storage for determination of uric acid concentration and avoiding underestimation.

Gout↗
PubMed1999

Effect of interferon-gamma on purine catabolic and salvage enzyme activities in rats.

To determine whether interferon-gamma affects rat purine catabolic and salvage enzyme activities, rats were injected with interferon-gamma (600000 U/kg, i.p.) and, similarly to a vehicle-injected control group, killed before or after injection at 6, 12, and 24 h. Organ homogenates were prepared and enzymatic reactions with substrates were carried out, after which the products were measured either chromatographically or spectrophotometrically. Western and Northern blotting also were performed. In contrast to the vehicle-injected rats, interferon-gamma-injected rats showed a significant rise in xanthine oxidoreductase activity in the liver, while enzyme activity was unchanged in the spleen, kidney, and lung. Western analysis of hepatic xanthine oxidoreductase showed an increased concentration of this protein 12 and 24 h after interferon-gamma injection. Northern analysis disclosed an enhanced mRNA expression coding for this enzyme, peaking 12 h after injection. Contrastingly, the activities of adenosine deaminase, purine nucleoside phosphorylase, hypoxanthine guanine phosphoribosyltransferase, and adenine phosphoribosyltransferase were not affected by interferon-gamma in any organ tested. While interferon-gamma causes an increased hepatic biosynthesis of xanthine oxidoreductase, the physiologic role of this enzyme induction remains undetermined.

Adenine Phosphoribosyltransferase↗
PubMed1999

Effect of glucose on the plasma concentration and urinary excretion of uridine and purine bases.

To examine whether glucose increases the plasma concentration of purine bases and uridine, 75 g glucose was administered orally to eight healthy subjects and two patients with hyperuricemia. The plasma concentration of uridine increased by 21%, 25%, and 20% 30, 60, and 90 minutes after administration of glucose, respectively. However, urinary excretion of uridine was not affected, nor were the plasma concentrations and urinary excretion of purine bases (hypoxanthine, xanthine, and uric acid). These results suggest that the glucose-induced increase in plasma uridine was not concomitant with adenosine triphosphate (ATP) consumption-induced purine degradation, but instead was ascribable to a uridine diphosphate (UDP)-glucose consumption-induced pyrimidine degradation (UDP-glucose-->UDP-->uridine monophosphate [UMP]-->uridine).

Adult↗
PubMed1999

Effects of fructose and xylitol on the urinary excretion of adenosine, uridine, and purine bases.

To examine whether fructose and xylitol increase the plasma concentration and urinary excretion of adenosine, as well as uridine and purine bases (hypoxanthine, xanthine, and uric acid), we intravenously administered xylitol and, 2 weeks later, fructose, to five healthy subjects. Analyses of blood and urine samples obtained during these infusion studies demonstrated that fructose increased the urinary excretion of adenosine and uridine 11.9- and 105.5-fold, respectively, and caused only a small increase in the plasma concentrations of uridine and purine bases. It was further demonstrated that xylitol increased the urinary excretion of uridine 58.4-fold, with a marked increase in the plasma concentrations of purine bases and uridine but without an increase in the urinary excretion of adenosine. However, neither infusion increased the plasma concentration of adenosine. These results suggest that in addition to many organs, including the liver, fructose is significantly metabolized by an abrupt adenosine triphosphate (ATP) consumption in the kidney, leading to an increase in the urinary excretion of adenosine and uridine. They also suggest that xylitol is not significantly metabolized in the kidney.

Adenosine↗
PubMed1999

Effect of amino acids on the plasma concentration and urinary excretion of uric acid and uridine.

To determine the effect of amino acids on the plasma level and urinary excretion of uric acid and uridine, 200 mL 12% amino acid solution, and 2 weeks later, 100 mL physiological saline solution containing glucagon (1.2 microg/kg weight), was infused into five healthy men. Both increased the urinary excretion of uric acid and the concentration of glucagon, insulin, and glucose in plasma and pyruvic acid in blood, whereas they decreased the concentration of uridine and inorganic phosphate in plasma. However, neither the amino acid infusion nor glucagon infusion affected the concentration of purine bases (hypoxanthine, xanthine, and uric acid), cyclic adenosine monophosphate (cAMP) in plasma, or lactic acid in blood or the urinary excretion of oxypurines (hypoxanthine and xanthine), uridine, or sodium. These results suggest that glucagon may have an important role in the amino acid-induced increase in urinary excretion of uric acid and decrease in plasma uridine.

Adult↗
PubMed1999

'Pseudohypouricosuria' in alcaptonuria: homogentisic acid interference in the measurement of urinary uric acid with the uricase-peroxidase reaction.

Urinary excretion of uric acid was found to be extremely low in a 58-year-old female patient with alcaptonuria. This was due to interference with the uricase-peroxidase method used, because analysis using high-performance liquid chromatography (HPLC) showed a normal urinary concentration of uric acid. In vitro experiments demonstrated that a high concentration of homogentisic acid in the patient's urine inhibited the peroxidase reaction, possibly due to inhibition of the colour development of 3-methyl-N-ethyl-N-(beta-hydroxyethyl)aniline (MEHA) and 4-aminoantipyrine, via the peroxidase reaction. A homogentisic acid concentration equivalent to that in plasma did not affect the uricase-peroxidase reaction. This result suggests that any assay based on a peroxidase method is affected by a high urinary concentration of homogentisic acid in patients with alcaptonuria.

Alkaptonuria↗
PubMed1998

Determination of adenosine and deoxyadenosine in urine by high-performance liquid chromatography with column switching.

The means of measurement of adenosine and deoxyadenosine in urine was developed by separating adenosine and deoxyadenosine from other compounds using high-performance liquid chromatography with column switchings. This method is simple and convenient since no pretreatment of the urine is needed. Using this method, it could be demonstrated that urinary adenosine was higher in an adenosine deaminase (ADA) deficient patient who had a bone marrow transplant treatment (1.97 micromol/mmol creatinine) and in a heterozygote who had a markedly low erythrocyte ADA activity (1% of control ADA activity) (1.33 micromol/mmol creatinine) as compared to normal subjects (0.22+/-0.09 micromol/mmol creatinine, n=11). It was also noted that urinary deoxyadenosine was below the detection limits in the ADA-deficient bone marrow transplant patient, but it was detected in the heterozygote (3.7 micromol/mmol creatinine). Furthermore, it was also demonstrated that a fructose infusion increased the urinary concentration of adenosine from 0.21+/-0.03 to 2.66+/-1.21 micromol/mmol creatinine in five normal subjects.

Adenosine↗
PubMed1998

Decreased serum concentrations of 1,25(OH)2-vitamin D3 in patients with gout.

We measured the serum concentrations of 1,25(OH)2-vitamin D3, 25(OH)-vitamin D3, parathyroid hormone (PTH) in 82 male patients with primary gout whose serum uric acid was significantly higher than that of 41 normal control male subjects (8.8 +/- 0.2 vs 5.6 +/- 0.2 mg/dL, p < 0.001). The serum 1,25(OH)2-vitamin D3 concentration was significantly lower in the patients with gout compared with the control subjects (39.6 +/- 1.4 vs 44.8 +/- 1.7 pg/mL, p < 0.05), while no differences were observed between the two groups in either the serum concentration of 25(OH)-vitamin D3 or PTH. The administration of uric acid lowering agent to the patients for 1 year caused a significant increase in their serum 1,25(OH)2-vitamin D3 concentration which was associated with a significant decrease in their serum uric acid concentration. In contrast, the serum concentrations of 25(OH)-vitamin D3 and PTH were not affected by these drugs. These results suggest that uric acid per se may directly decrease the serum concentration of 1,25(OH)2-vitamin D3 in patients with gout by inhibiting 1-hydroxylase activity.

Allopurinol↗
PubMed1998

Effect of Tofu (bean curd) ingestion and on uric acid metabolism in healthy and gouty subjects.

The effect of Tofu (bean curd) ingestion on uric acid metabolism was examined in 8 healthy and 10 gout subjects. Ingestion of Tofu increased plasma concentration of uric acid, together with increases in uric acid clearance and urinary excretion of uric acid. However, the increase in plasma concentration of uric acid was fairy small. Interestingly, no significant rise in the plasma, urinary and clearance of uric acid was observed in gout patients with uric acid clearance > 6.0 mL/min (lower normal limit). The results suggest that tofu is a preferable source of protein, especially in gout patients with uric acid clearance > 6.0 mL/min.

Adult↗
PubMed1998

Zonal distribution of allopurinol-oxidizing enzymes in rat liver.

We describe an enzymatic histochemical localization of two allopurinol-oxidizing enzymes, xanthine oxidase and aldehyde oxidase in rat hepatic tissues. This method is based on the tetrazolium salt procedures by use of a tissue protectant, polyvinyl alcohol, with tetra-nitro BT as the final electron acceptor. The present study demonstrated that both oxidases are present in the cytoplasm of hepatic cells. However, the distribution of the enzymes was uneven, being seen mainly in the pericentral rather than the periportal area. When allopurinol was used as a substrate, the specific staining by xanthine oxidase was more prominent than that of aldehyde oxidase. The results suggested that xanthine oxidase is more effective in oxidizing allopurinol than aldehyde oxidase.

Aldehyde Oxidase↗
PubMed1998

Effect of glucagon on the plasma concentration of uridine.

To determine whether glucagon affects the plasma concentration of uridine, we administered 100 mL physiological saline containing 1 mg glucagon or 100 mL physiological saline alone intravenously over 1 hour to healthy subjects. Glucagon decreased the plasma concentration of uridine from 5.72 +/- 1.05 to 4.80 +/- 0.60 micromol/L but increased the concentrations of cyclic adenosine monophosphate (cAMP) in plasma and pyruvic acid and lactic acid in blood 59-, 1.4-, and 1.3-fold, respectively. Although glucagon increased urinary excretion of uric acid, it did not affect the plasma concentration of purine bases (hypoxanthine, xanthine, and uric acid) or urinary excretion of oxypurines and uridine, indicating that glucagon does not affect purine degradation and suggesting that glucagon does not affect adenosine triphosphate (ATP) consumption-induced pyrimidine degradation. In contrast, physiological saline did not affect any of the measured variables. These results suggest that glucagon enhanced Na+-dependent uridine uptake from the blood into the cells, since glucagon stimulates Na+-dependent uridine uptake into cells in vitro.

Adult↗