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Biomedical subjects

J Adachi

Publications and source records attributed to J Adachi.

At least 19 recordsLinked to original sources
PubMed2004

Calcium supplementation on bone loss in postmenopausal women.

BACKGROUND: Although calcium is one the simplest and least expensive strategies for preventing osteoporotic fractures calcium supplementation is nevertheless not without controversy (Kanis 1989; Nordin 1990). The Food and Drug Administration in the US has permitted a bone health claim for calcium-rich foods, and the NIH in its Consensus Development Process approved a statement that high calcium intake reduces the risk of osteoporosis. OBJECTIVES: To assess the effects of calcium on bone density and fractures in postmenopausal women. SEARCH STRATEGY: We searched Cochrane Controlled Register, MEDLINE and EMBASE up to 2001, and examined citations of relevant articles and proceedings of international meetings. SELECTION CRITERIA: Trials that randomized postmenopausal women to calcium supplementation or usual calcium intake in the diet and reported bone mineral density of the total body, vertebral spine, hip, or forearm or recorded the number of fractures, and followed patients for at least one year were considered for inclusion. DATA COLLECTION AND ANALYSIS: Three independent reviewers assessed the methodologic quality and extracted data for each trial. For each bone density site (lumbar spine, total body, combined hip and combined forearm), we calculated the weighted mean difference in bone density between treatment and control groups using the percentage change from baseline. We constructed regression models in which the independent variables were year and dose, and the dependent variable was the effect size. This regression was used to determine the years across which pooling was appropriate. Heterogeneity was assessed. For each fracture analysis we calculated a risk ratio. MAIN RESULTS: Fifteen trials, representing 1806 participants, were included. Calcium was more effective than placebo in reducing rates of bone loss after two or more years of treatment. The pooled difference in percentage change from baseline was 2.05% (95% CI 0.24 to 3.86) for total body bone density, 1.66% (95% CI 0.92 to 2.39) for the lumbar spine at 2 years, 1.60% (95% CI 0.78 to 2.41) for the hip, and 1.91% (95% CI 0.33 to 3.50) for the distal radius. The relative risk of fractures of the vertebrae was 0.79 (95% CI 0.54 to 1.09); the relative risk for non-vertebral fractures was 0.86 (95% CI 0.43 to 1.72). REVIEWER'S CONCLUSIONS: Calcium supplementation alone has a small positive effect on bone density. The data show a trend toward reduction in vertebral fractures, but it is unclear if calcium reduces the incidence of non vertebral fractures.

Bone Density↗
PubMed2003

Shape-resonance-enhanced vibrational effects in the angular distributions of C 1s photoelectrons from fixed-in-space CO molecules.

Angular distributions of C 1s photoelectrons from fixed-in-space CO molecules have been measured with vibrational resolution. A strong dependence of the angular distributions on the vibrational states of the residual molecular ion has been found for the first time in the region of the shape resonance. Calculations in the relaxed core Hartree-Fock approximation have reproduced the angular distributions fairly well in the general shapes of the angular distributions due to the correct description of nuclear motion as an average of the internuclear-distance-dependent dipole amplitudes.

Journal Article↗
PubMed2003

Calcium supplementation on bone loss in postmenopausal women.

BACKGROUND: Although calcium is one the simplest and least expensive strategies for preventing osteoporotic fractures calcium supplementation is nevertheless not without controversy (Kanis 1989; Nordin 1990). The Food and Drug Administration in the US has permitted a bone health claim for calcium-rich foods, and the NIH in its Consensus Development Process approved a statement that high calcium intake reduces the risk of osteoporosis. OBJECTIVES: To assess the effects of calcium on bone density and fractures in postmenopausal women. SEARCH STRATEGY: We searched Cochrane Controlled Register, MEDLINE and EMBASE up to 2001, and examined citations of relevant articles and proceedings of international meetings. SELECTION CRITERIA: Trials that randomized postmenopausal women to calcium supplementation or usual calcium intake in the diet and reported bone mineral density of the total body, vertebral spine, hip, or forearm or recorded the number of fractures, and followed patients for at least one year were considered for inclusion. DATA COLLECTION AND ANALYSIS: Three independent reviewers assessed the methodologic quality and extracted data for each trial. For each bone density site (lumbar spine, total body, combined hip and combined forearm), we calculated the weighted mean difference in bone density between treatment and control groups using the percentage change from baseline. We constructed regression models in which the independent variables were year and dose, and the dependent variable was the effect size. This regression was used to determine the years across which pooling was appropriate. Heterogeneity was assessed. For each fracture analysis we calculated a risk ratio. MAIN RESULTS: Fifteen trials, representing 1806 participants, were included. Calcium was more effective than placebo in reducing rates of bone loss after two or more years of treatment. The pooled difference in percentage change from baseline was 2.05% (95% CI 0.24 to 3.86) for total body bone density, 1.66% (95% CI 0.92 to 2.39) for the lumbar spine at 2 years, 1.60% (95% CI 0.78 to 2.41) for the hip, and 1.91% (95% CI 0.33 to 3.50) for the distal radius. The relative risk of fractures of the vertebrae was 0.79 (95% CI 0.54 to 1.09); the relative risk for non-vertebral fractures was 0.86 (95% CI 0.43 to 1.72). REVIEWER'S CONCLUSIONS: Calcium supplementation alone has a small positive effect on bone density. The data show a trend toward reduction in vertebral fractures, but it is unclear if calcium reduces the incidence of non vertebral fractures.

Bone Density↗
PubMed2003

Novel mutations in GJB2 encoding connexin-26 in Japanese patients with keratitis-ichthyosis-deafness syndrome.

BACKGROUND: Germline missense mutations in the GJB2 gene that encodes connexin-26 (Cx26) have recently been found to be the cause of the keratitis-ichthyosis-deafness (KID) syndrome. OBJECTIVES: To define the GJB2 mutations in three Japanese patients with KID syndrome. METHODS: Genomic DNA was extracted from peripheral blood and used to amplify the GJB2 gene. Direct sequencing and endonuclease digestion were used for mutation analysis and DNA-based diagnosis. RESULTS: We identified two heterozygous mis-sense mutations (D50Y, D50N) in the GJB2 gene in three Japanese patients with KID syndrome. All mutations were located on the first extracellular domain of Cx26. CONCLUSIONS: These data expand the GJB2 mutation database and show that a dominant mutation of Cx26 can cause KID syndrome in Japanese patients.

Adult↗
PubMed2002

Analysis of the mouse transcriptome based on functional annotation of 60,770 full-length cDNAs.

Only a small proportion of the mouse genome is transcribed into mature messenger RNA transcripts. There is an international collaborative effort to identify all full-length mRNA transcripts from the mouse, and to ensure that each is represented in a physical collection of clones. Here we report the manual annotation of 60,770 full-length mouse complementary DNA sequences. These are clustered into 33,409 'transcriptional units', contributing 90.1% of a newly established mouse transcriptome database. Of these transcriptional units, 4,258 are new protein-coding and 11,665 are new non-coding messages, indicating that non-coding RNA is a major component of the transcriptome. 41% of all transcriptional units showed evidence of alternative splicing. In protein-coding transcripts, 79% of splice variations altered the protein product. Whole-transcriptome analyses resulted in the identification of 2,431 sense-antisense pairs. The present work, completely supported by physical clones, provides the most comprehensive survey of a mammalian transcriptome so far, and is a valuable resource for functional genomics.

Alternative Splicing↗
PubMed2002

Direct probe of the shape resonance mechanism in 2sigma(g)-shell photoionization of the N2 molecule.

Angular distributions of photoelectrons from a 2sigma(g) shell of fixed-in-space N2 molecules have been measured for left- and right-elliptically polarized and for linearly polarized light at several photon energies in the region of sigma(*) shape resonance. That allowed the determination of a set of dipole matrix elements and phase shift differences characterizing the process. These data clearly show the enhancement of the fsigma(u) partial cross section in the resonance simultaneously with an abrupt increase of the corresponding phase shift by pi, which is the first experimental demonstration of the nature of the sigma(*) shape resonance in homonuclear diatomic molecules.

Journal Article↗
PubMed2001

Lipid peroxidation in the rat brain after CO inhalation is temperature dependent.

We reported previously that 7-hydroperoxycholesterols, 7 alpha- and 7 beta-hydroperoxycholest-5-en-3 beta-ol (7 alpha-OOH and 7 beta-OOH), indicated lipid peroxidation. In the present study, we measured not only 7-hydroperoxycholesterols but also oxysterols (7 alpha- and 7 beta-hydroxycholesterol, 7 alpha-OH, and 7 beta-OH) and 3 beta-hydroxycholest-5-en-7-one (7-keto) in the brains of rats that underwent either a sham operation (control), hypoxia, or CO inhalation (1005 ppm) at 37 degrees C for 90 min followed by 48 h of recovery. The levels of 7-hydroperoxycholesterols, 7 beta-OH, and 7-keto were low in the hypoxia group, while the levels were unaltered in the CO group compared with the controls. Among the three groups of CO inhalation, these levels were high in the hyperthermia group (39 degrees C), and the 7-hydroperoxycholesterols were low in the hypothermia group (32 degrees C), compared with the control group. The blood O(2) saturation was almost normal in the hypothermia group, while it was similarly low in the hyperthermia and normothermia groups. The temperature-dependent lipid peroxidation in the brain after CO inhalation and recovery can not be explained by hypoxia due to CO-hemoglobin formation, but may contribute to the delayed neuronal death following CO inhalation. Hypothermia may be applicable to treat patients after CO inhalation.

Administration, Inhalation↗
PubMed2001

Indirubin and indigo are potent aryl hydrocarbon receptor ligands present in human urine.

Aryl hydrocarbon receptor (AhR) is a ligand-activated transcription factor that regulates genes involved in xenobiotic metabolism, cellular proliferation, and differentiation. Numerous xenobiotic and biological compounds are known to interact with AhR, but it remains an orphan receptor, because its physiological ligand is unknown. We identified AhR ligands in human urine using a yeast AhR signaling assay and then characterized their properties. Two ligands, indirubin and indigo, were both present at average concentrations of approximately 0.2 nm in the urine of normal donors. Indirubin was also detected in fetal bovine serum and contributed half of the total AhR ligand activity. The activities of indirubin and indigo were comparable with or more potent than that of the archetypal ligand, 2,3,7,8-tetrachlorodibenzo-p-dioxin, in yeast AhR activation assays. We suggest that the endogenous levels and potencies of indirubin and indigo are such that they activate AhR-mediated signaling mechanisms in vivo.

Genes, Reporter↗
PubMed2001

Functional annotation of a full-length mouse cDNA collection.

The RIKEN Mouse Gene Encyclopaedia Project, a systematic approach to determining the full coding potential of the mouse genome, involves collection and sequencing of full-length complementary DNAs and physical mapping of the corresponding genes to the mouse genome. We organized an international functional annotation meeting (FANTOM) to annotate the first 21,076 cDNAs to be analysed in this project. Here we describe the first RIKEN clone collection, which is one of the largest described for any organism. Analysis of these cDNAs extends known gene families and identifies new ones.

Animals↗
PubMed2001

Acute effect of ethanol on 7-hydroperoxycholesterol in muscle and liver.

We tested the hypotheses that ethanol sensitivities of muscle and liver can be discerned in the initial periods of ethanol exposure, especially when acetaldehyde levels are markedly raised with cyanamide, an aldehyde dehydrogenase inhibitor. To test this, we measured cholesterol hydroperoxides in soleus (Type I) and plantaris (Type II) muscle in four groups of rats acutely (i.e., 2.5 h) exposed to: [S] saline (control), [Cy] cyanamide, [EtOH] ethanol, or [Cy + EtOH] cyanamide + ethanol. Comparative reference was also made to the response of the liver. After 2.5 h, ethanol alone significantly increased 7 alpha-hydroperoxycholest-5-en-3 beta-ol (7 alpha-OOH) and 7 beta-hydroperoxycholest-5-en-3 beta-ol (7 beta-OOH) levels in plantaris muscle. Identical qualitative effects were seen in rats treated with cyanamide + ethanol, but there was no discernible difference between groups [EtOH] and [Cy + EtOH]. In both the soleus muscle and liver, none of the treatments with either ethanol or cyanamide + ethanol had any effect on any of the measured parameters. This is the first report of a differential response of 7 alpha-OOH and 7 beta-OOH in Type II, compared to Type I predominant muscles, and the first time that muscle has been shown to be more sensitive than the liver in terms of its lipid marker response to oxidative stress. Perturbations in the muscle membrane lipid domain may contribute to impairment of muscle in alcoholism.

Acetaldehyde↗
PubMed2001

Alcoholic skeletal muscle myopathy: definitions, features, contribution of neuropathy, impact and diagnosis.

Alcohol misusers frequently have difficulties in gait, and various muscle symptoms such as cramps, local pain and reduced muscle mass. These symptoms are common in alcoholic patients and have previously been ascribed as neuropathological in origin. However, biochemical lesions and/or the presence of a defined myopathy occur in alcoholics as a direct consequence of alcohol misuse. The myopathy occurs independently of peripheral neuropathy, malnutrition and overt liver disease. Chronic alcoholic myopathy is characterized by selective atrophy of Type II fibres and the entire muscle mass may be reduced by up to 30%. This myopathy is arguably the most prevalent skeletal muscle disorder in the Western Hemisphere and occurs in approximately 50% of alcohol misusers. Alcohol and acetaldehyde are potent inhibitors of muscle protein synthesis, and both contractile and non-contractile proteins are affected by acute and chronic alcohol dosage. Muscle RNA is also reduced by mechanisms involving increased RNase activities. In general, muscle protease activities are either reduced or unaltered, although markers of muscle membrane damage are increased which may be related to injury by reactive oxygen species. This supposition is supported by the observation that in the UK, alpha-tocopherol status is poor in myopathic alcoholics. Reduced alpha-tocopherol may pre-dispose the muscle to metabolic injury. However, experimental alpha-tocopherol supplementation is ineffective in preventing ethanol-induced lesions in muscle as defined by reduced rates of protein synthesis and in Spanish alcoholics with myopathy, there is no evidence of impaired alpha-tocopherol status. In conclusion, by a complex series of mechanisms, alcohol adversely affects skeletal muscle. In addition to the mechanical changes to muscle, there are important metabolic consequences, by virtue of the fact that skeletal muscle is 40% of body mass and an important contributor to whole-body protein turnover.

Alcoholic Neuropathy↗
PubMed2001

Emergence of trimethoprim-resistant Escherichia coli in healthy persons in the absence of prophylactic or therapeutic antibiotics during travel to Guadalajara, Mexico.

Thirty-nine healthy US students without diarrheal disease and who had not received prophylactic or therapeutic antibiotics were monitored for emergence of trimethoprim-resistant gram-negative fecal flora for a 3-week period after arrival in Guadalajara, Mexico. During this time period, most students showed no change in total fecal gram-negative bacteria (p > 0.05) but showed an increasing level of trimethoprim (TMP) resistance (p < 0.01) among fecal coliforms. Escherichia coli was the TMP-resistant organism isolated in 18 of 39 (46%) healthy students. These 18 TMP-resistant E. coli were also resistant to ampicillin (44%), azithromycin (11%), chloramphenicol (39%), ciprofloxacin (11%), doxycycline (89%), erythromycin (100%), furazolidone (72%), levofloxacin (17%), trimethoprim-sulfamethoxazole (89%) and trovafloxacin (17%). In the absence of prophylactic and therapeutic antibiotics, increased acquisition of TMP-resistant gram-negative fecal flora in this developing country is probably due to poor sanitary conditions and the recurrent and heavy exposure to antimicrobial-resistant indigenous flora as a result of contaminated food and drink.

Adolescent↗
PubMed2001

Heart 7-hydroperoxycholesterol and oxysterols are elevated in chronically ethanol-fed rats.

Recently, cholesterol hydroperoxides have been shown to be sensitive pathogenic markers of reactive oxygen species (ROS)-mediated damage though they have never been measured in heart tissue. We hypothesized that cholesterol hydroperoxides and oxysterols, putative cardiotoxic products of cholesterol oxidation, are elevated in the hearts of alcoholics as a consequence of ROS-mediated reactions. To test this, we measured 7alpha- and 7beta-hydroperoxycholest-5-en-3beta-ol (7alpha-OOH and 7beta-OOH) by HPLC with postcolumn chemiluminescence as well as 7alpha- and 7beta-hydroxycholesterol (7alpha-OH and 7beta-OH) and 3beta-hydroxycholest-5-en-7-one (also termed 7-ketocholesterol; 7-keto) by HPLC-UV in cardiac muscle of alcohol-fed rats. Alcohol feeding was carried out using a pair-feeding protocol with 35% of total dietary energy as ethanol; controls were pair-fed isocaloric glucose. After 6-7 wk treatment with alcohol, heart 7alpha-OOH, 7beta-OOH and 7beta-OH were significantly greater than in controls. Levels of heart phospholipid 16:0 and 18:1 were lower than in controls, while 18:0 and 18:2 were greater. This is the first report of the presence of 7alpha-OOH, 7beta-OOH and 7alpha-OH in cardiac tissue. The elevations in 7alpha-OOH and 7beta-OOH as well as 7beta-OH are evidence of increased oxidative stress and possible membrane changes. Alterations in the proportions of 16:0, 18:1, 18:2 and 18:0 in heart phospholipids provide further evidence of an altered membrane domain.

Administration, Oral↗
PubMed2001

Increased oxysterols associated with iron accumulation in the brains and visceral organs of acaeruloplasminaemia patients.

Acaeruloplasminaemia is characterized by excessive neurovisceral iron accumulation due to mutation of the caeruloplasmin gene. Excess iron functions as a potent catalyst of biological oxidation, and increased iron concentration is associated with the products of lipid peroxidation in the serum and cerebrospinal fluid. We investigated whether the amount of iron accumulated paralleled lipid peroxidation levels in acaeruloplasminaemia tissues, examining brains and visceral organs of two affected patients at autopsy for iron and copper content, and oxysterols, including 7-hydroxycholesterol and 7-ketocholesterol, which are directly produced from cholesterol by active oxygen species. The amount of iron accumulated in various tissues was correlated with the levels of the oxysterols. These findings suggest that lipid peroxidation produced by the intracellular accumulation of iron is involved in the pathogenesis of acaeruloplasminaemia.

Aged↗
PubMed2001

Recent advances in the pathology of alcoholic myopathy.

This article represents the proceedings of a symposium at the 2000 ISBRA Meeting in Yokohama, Japan. The chairs were Victor R. Preedy and Junko Adachi. The presentations were (1) Alcoholic myopathy: Past, present and future, by Timothy J. Peters and Victor R. Preedy; (2) Protein adducts in the type I and II fiber-predominant muscles of the ethanol-fed rat, by Simon Worrall, Seppo Parkkila, and Onni Niemela; (3) Hydroperoxides and changes in alcoholic myopathy, by Junko Adachi, Migiwa Asamo, and Yasuhino Ueno; and (4) A close association between testicular atrophy, muscle atrophy, and the increase in protein catabolism after chronic ethanol administration, by Kunihiko Takeda, Masayoshi Yamauchi, Kazuhiko Sakamoto, Masaru Takagi, Hisato Nakajima, and Gotaro Toda.

Alcoholism↗
PubMed2001

Discrimination of changes in osteoporosis outcomes.

The purpose of this paper was to identify existing work related to discrimination, responsiveness, and minimal clinically important differences (MCID) for 4 key clinical outcomes in osteoporosis, to serve as a background to discussions about how to define MCID for both individuals and groups. The outcomes assessed were bone density, fractures, quality of life, and function. We conducted a systematic literature search in MEDLINE, EMBASE, and Current Contents for articles that discussed responsiveness, detectable difference, improvement criteria, and clinical importance. We used the Beaton cube to classify the studies depending on whether they compared differences between or changes within individuals or groups. Although a number of studies were identified that presented data on detectable differences beyond error and observed differences, few studies presented data on how to define clinically important differences. A key priority for future research is to define minimally clinical important differences for clinically important osteoporosis outcomes using a consensus based approach that will be accepted by the osteoporosis community at large. Furthermore, these MCID will likely be different for individual patients seen in clinical practice than for individuals in a clinical trial.

Clinical Trials as Topic↗
PubMed2000

Photoelectron angular distributions from O K shell of oriented CO molecules: A critical comparison between theory and experiment

The dynamical information (ten dipole matrix elements and eight phase differences) has been deduced from the measured angular distributions of photoelectrons from O K shell of oriented CO molecules near the ionization threshold in the region of a sigma(*) shape resonance. Light polarization parallel and perpendicular to the molecular axis has been used. An important contribution of six lsigma partial waves with 0</=l</=5 to the sigma(*) shape resonance is demonstrated. A comparison with our calculations in the relaxed core Hartree-Fock approximation reveals only a qualitative agreement, therefore a more advanced theory is needed.

Journal Article↗
PubMed2000

Tetrahydro-beta-carboline-3-carboxylic acids and contaminants of L-tryptophan.

Methods for the separation, identification, and quantitative assay of contaminants of L-tryptophan implicated in eosinophilia-myalgia syndrome (EMS) are described. Propylsulfonic acid (PRS), benzenesulfonic acid (SCX), and octyl-derivatized silica (C8) bonded-phase cartridges were used for the separation; LC-MS and GC-MS for identification; and HPLC-UV-fluorescence detection for quantitative analyses of norharman, harman, tetrahydro-beta-carboline-3-carboxylic acid (TCCA), 1-methyltetrahydro-beta-carboline-3-carboxylic acid (MTCA), 1,1'-ethylidenbis(tryptophan) (EBT), and 3-(phenylamino)alanine (PAA). The tissue distribution, excretion, and metabolism of these contaminants of L-tryptophan associated with EMS after acute and chronic dosage regimens are described. Considerable amounts of EBT were observed in the large intestine of rats administered EBT, showing a transfer without decomposition in gastric fluid. In addition, MTCA was detected in the blood and urine as well as the organs of rats treated with EBT, suggesting MTCA as a major metabolite of EBT. PAA accumulated markedly in the brain, among the organs of rats, after both acute and chronic administration of PAA, while MTCA accumulated in the kidneys of rats after chronic dosage of MTCA. Ethanol and/or acetaldehyde-induced formation of MTCA, as well as tryptophan-induced formation of TCCA, occurred endogenously in man and animals.

Animals↗