Correlation of foetal body weight by coronet width measurement using ultrasonography in prepartum cows: a pilot study.

This study aimed to clarify the effectiveness of foetal body weight estimation by measuring foetal coronet width using transrectal ultrasonography in beef cows during near-term pregnancy. A characteristic 'gull wing' pattern was obtained from the foetal coronet cross-section from the dewclaw side using ultrasonography. This pattern was matched to the bone surface of the distal part of the middle phalanx. Then, the relationship between coronet width and body weight at birth of 22 Japanese Brown calves was analysed and a high correlation coefficient of 0.8965 (P < 0.001) was obtained. In conclusion, the coronet width of the fetus is depicted as a 'gull wing' hyperechoic structure and can be measured by ultrasonography per rectum during near-term pregnancy. This technique may be a useful tool to identify high-risk cows with dystocia before calving. High foetal coronet values may predispose cattle to dystocia.

Contribution of testosterone to the clock system in rat prostate mesenchyme cells.

Circadian rhythms are modulated in a variety of peripheral tissues including the prostate, in which the mesenchyme and epithelium cells are controlled under androgens. Here, we investigated the testosterone regulation of core clock genes such as Bmal1, Clock, Per2 and Nr1d1 under a deficient state of testosterone. In vivo studies showed that the Bmal1 mRNA expression in the prostates displayed a peak at ZT 20 and a trough at ZT 12. Both Bmal1 and Clock transcripts decreased after castration. Conversely, the expression of Per2 that is promoted by binding of Bmal1 and Clock heterodimers to the E-box, enhanced or did not decease at least within 1 week after castration. The clock gene transcripts were recovered to the intact levels, when 1 mg testosterone was administered daily for 5 days. Fluorescent immunohistochemical studies revealed the increased staining of caspase 3 in the epithelium and Per2 in both the mesenchyme and epithelium after 1-week castration. In the mesenchyme cells prepared from castrated rats, the Per2 oscillation was generated in response to dexamethasone. The circadian rhythms of Bmal1 and Nr1d1 transcripts were obviously antiphase in the cells. However, the mesenchyme cells displayed the different profiles in the presence or absence of testosterone; the amplitude of the first phase was significantly decreased by testosterone. Addition of testosterone significantly increased the transcripts of Bmal1, Clock and Casp3 in cultured cells, whereas the Per2 and Nr1d1 transcripts were significantly inhibited. Collectively, the present results demonstrated that Bmal1 and Clock, but not Per2 and Nr1d1, are down-regulated in mesenchyme cells by testosterone deficiency. In addition to the conservative interlocked transcriptional-translational feedback loop, it is strongly suggested that the prostate clock system is controlled under androgen.

Salting-out taste-masking system generates lag time with subsequent immediate release.

Salting-out effects were utilized for developing a multiparticulate system balancing numbness masking and high bioavailability. A "salting-out taste-masking system" consisting of a drug core containing acetaminophen as a model drug, a salting-out layer containing sodium carbonate (Na(2)CO(3)) and hydroxypropylmethylcellulose (HPMC), and a water-penetration-control layer consisting of cetanol was designed and prepared. The system successfully generated a long lag time while achieving immediate drug release. In the system, the Na(2)CO(3) release rate was slower and the lag time was longer than when the water-penetration-control layer was not present. During the release of Na(2)CO(3) from the system, the release of HPMC and drug was suppressed. These results indicated that the water-penetration-control layer maintained a high concentration of Na(2)CO(3), prevented HPMC's dissolution, and generated a long lag time of drug release. The system generated longer lag time and released drug more immediately than formulation containing the water-penetration-control layer of same thickness without the salting-out layers. These results indicated the salting-out layers were necessary for obtain a long lag time and subsequent immediate drug release. This novel taste-masking system has the potential to be a useful multiparticulate dosage form for effective, safe, and user-friendly drug therapy.

Acute-phase proteins and Chlamydia pneumoniae infection: which one is more important in acute coronary syndrome?

Elevated levels of acute-phase proteins, a systemic marker for inflammation, predict coronary events; Chlamydia pneumoniae (C. pneumoniae) infection is associated with coronary atherosclerosis. The present study investigated whether inflammation or infection is involved in the pathogenesis of acute coronary syndrome (ACS) and which one has the more important role. The study group comprised 49 patients with angiographically diagnosed ACS, 48 cases of chronic coronary heart disease (CCHD), and 44 subjects with a normal coronary profile. The levels of serum C-reactive protein (CRP), fibrinogen and anti-C. pneumoniae IgG antibody were measured. The IgG antibody against C. pneumoniae was higher in the ACS and CCHD groups compared with the control group after adjusting for age and gender. The levels of CRP and fibrinogen were significantly increased in patients with ACS compared with controls and CCHD patients. Multiple stepwise logistic regression analysis revealed that C. pneumoniae IgG antibody is an independent risk factor for both ACS and CCHD (odds ratio 2.3 and 2.1, respectively), but the CRP level is a risk factor only for ACS (odds ratio 6.9). The inflammatory response, as indicated by acute-phase proteins, especially CRP, rather than C. pneumoniae infection, may contribute more to the clinical course of ACS.

Overexpression of EC-SOD suppresses endothelial-cell-mediated LDL oxidation.

Reactive oxygen species have been proposed to play important roles in atherosclerosis. To investigate the protective role of extracellular superoxide dismutase (EC-SOD), its inhibition of endothelial-cell-mediated LDL oxidation was examined. We constructed the recombinant adenovirus AxCAEC-SOD expressing human EC-SOD by CAG promoter. Infection of endothelial cells with AxCAEC-SOD resulted in EC-SOD protein secretion in a dose-dependent manner and a decrease of endothelial-cell-derived superoxide production. Moreover, it was proven to coexist with heparan sulfate by immunohistochemical staining. Endothelial-cell-mediated LDL oxidation enhanced by ferric-sodium EDTA was inhibited by 47% in TBARS formation by AxCAEC-SOD infection. In agarose gel electrophoresis, AxCAEC-SOD decreased the negative charge of oxidized LDL by 50% and suppressed fragmentation of apolipoprotein B. These results suggested that human EC-SOD localized in the extracellular space and reduced endothelial-cell-mediated LDL oxidation. In subendothelial space, EC-SOD bound on heparan sulfate might suppress LDL oxidation through reduction of superoxide anion.

Homocysteine inhibits angiogenesis in vitro and in vivo.

Homocysteine has been reported to inhibit endothelial cell proliferation, which is closely related to angiogenesis. However, the relationship between homocysteine and angiogenesis is unknown. To clarify whether homocysteine would inhibit angiogenesis in vitro and in vivo, we examined the effect of homocysteine on tube formation by bovine aortic endothelial cells (BAECs) and by human microvessel endothelial cell-1 (HMEC-1) in vitro, and on angiogenesis in vivo using the chorioallantoic membrane (CAM) assay, as well as on BAEC proliferation and migration. Homocysteine, but not cysteine, inhibited BAEC proliferation, migration, and tube formation in a dose-dependent manner at concentrations from 0 to 10 mM. Homocysteine also inhibited tube formation by HMEC-1s. In these assay, 50% inhibition was induced by about 1 mM homocysteine. In the in vivo CAM assay, 0, 10, 100, 500, and 1000 microgram homocysteine induced an avascular zone by 0, 0, 16.7, 53.3 and 76.5%, respectively, also showing a dose-dependent effect. It was suggested that homocysteine inhibited angiogenesis by preventing proliferation and migration of endothelial cells.

Chlamydia pneumoniae infection and accelerated development of coronary artery disease in patients with chronic renal failure.

AIMS: This study examined the relationship between Chlamydia pneumoniae (C. pneumoniae) infection and the accelerated development of coronary artery disease (CAD) in patients with chronic renal failure (CRF). METHODS: Two-hundred and fourteen patients undergoing coronary angiography, including 67 controls and 147 patients with CAD (97 without CRF and 50 with CRF), were enrolled in this study. Anti-C. pneumoniae specific IgG and IgA antibodies were measured using an enzyme-linked immunosorbent assay (ELISA). RESULTS: Coronary artery disease (expressed as CAD score) was more severe in patients with than without CRF (14.9 +/- 6.0 vs. 11.3 +/- 6.0, p < 0.01). Seropositive rates of IgG and IgA antibodies against C. pneumoniae were higher in all CAD patients than in the controls (76.2% vs. 44.8%, p < 0.001 for IgG; 59.9% vs. 40.3%, p < 0.01 for IgA). In both CAD subgroups, IgG seropositive rates were similarly elevated (82.0% and 73.2% vs. 44.8% for control, p < 0.001, respectively), whereas those of IgA were significantly elevated only in CAD with CRF (68.0% vs. 55.7% for control, p < 0.01). The mean antibody index of IgG was elevated in all CAD patients compared with the controls (1.9 +/- 1.0 vs. 1.3 +/- 0.9, p < 0.0001), but that of IgA was not (1.5 +/- 1.0 vs. 1.2 +/- 0.9). Levels of IgG were elevated in all patients with CAD compared with the control (2.4 +/- 1.1 and 1.8 +/- 1.0 vs. 1.3 +/- 0.9, p < 0.001 and p < 0.001, respectively), whereas those of IgA were elevated only in CAD with CRF (1.8 +/- 1.1 vs. 1.2 +/- 0.9, p < 0.05). Stepwise logistic regression analysis revealed that the elevated IgG antibody index was an independent risk factor for CAD regardless of CRF (odds ratios 1.9, 1.8, and 2.3), whereas the IgA index was a risk factor only in CAD with CRF (odds ratio 1.7). CONCLUSIONS: Chlamydia pneumoniae infection may be related to the accelerated CAD in patients with CRF, which was specifically suggested by an elevated IgA level. In other words, the prevalence of active C. pneumoniae infection is higher in patients with CAD and CRF than that in those with CAD without CRF.

A 15-year longitudinal follow-up study of heart rate and heart rate variability in healthy elderly persons.

BACKGROUND: Few researchers have conducted heart rate (HR) studies in healthy very elderly subjects aged 70 years or older, and there are no longitudinal follow-up studies in this population. The objective of this study was to evaluate long-term changes in HR and heart rate variability (HRV) with aging in healthy elderly persons by means of comparison between two Holter monitor recordings obtained at an interval of 15 years. METHODS: The study population consisted of 15 healthy elderly persons (10 women and 5 men) aged 64 to 80 years (mean 70 +/- 4.1) at the first recording, and 79 to 95 years old (mean 85 +/- 4.1 years) at the second recording 15 years later. Nighttime (midnight to 5 AM) and daytime (noon to 5 PM) HR and HRV were obtained, and paired t tests were performed to assess the differences in each parameter of nighttime and daytime HR and HRV between the two (15-year interval) Holter monitor recordings. RESULTS: The results of the t-test comparisons were as follows: there was a significant increase in minimal, maximal, and average HRs (nighttime, p < .01; daytime, p < .05, respectively). On the other hand, with regard to HRV, there was a significant nighttime decrease in the SDNN index (mean of standard deviations of normal RR intervals between adjacent QRS complexes resulting from sinus node depolarizations for all 5-minute segments) (p = .0086), and a significant daytime increase in the NN50 (number of adjacent normal RR intervals >50 milliseconds) per hour (p = .0425). Moreover, there was a significant decrease in the low-frequency (LF) component (nighttime, p = .0151; daytime, p = .0032), and a significant decrease in the LF/HF ratio (nighttime, p = .0270; daytime, p = .0371), but there was no significant change in the nighttime or daytime high-frequency (HF) component. CONCLUSIONS: HR increased with age over the 15-year period in the healthy elderly persons. As for concurrent changes in HRV, however, the parameters of sympathetic modulation decreased, and the parameters of parasympathetic modulation were unchanged or slightly increased.

Ulinastatin, an elastase inhibitor, inhibits the increased mRNA expression of prostaglandin H2 synthase-type 2 in Kawasaki disease.

Kawasaki disease is an inflammatory disease of unknown cause that causes panvasculitis, including coronary arteritis. Polymorphonucleocytosis in the early stage of the illness suggests the implication of neutrophils in the pathogenesis of the disease. In the acute phase of Kawasaki disease, mRNA expression of prostaglandin H2 synthase (PHS)-2, as determined by reverse transcription-polymerase chain reaction, was markedly enhanced, and thromboxane A2 (TXA2)-synthesizing activity was increased in polymorphonuclear leukocytes (PMNL). This up-regulation of PHS-2 was suppressed by ulinastatin (a neutrophil-elastase inhibitor) treatment. Lipopolysaccharide-induced enhancement of PHS-2 mRNA was also inhibited by therapeutic doses of ulinastatin in vitro by use of PMNL from healthy volunteers. Thus, ulinastatin inhibits arachidonate PHS metabolism by inhibiting new induction of PHS-2 at the mRNA level, which is a novel pharmacologic action of this substance. Ulinastatin treatment is possibly an additional therapeutic approach to Kawasaki disease.

Crystallization and preliminary x-ray analysis of beta-amylase from Bacillus polymyxa.

A truncated beta-amylase (E.C. 3.2.1.2) from Bacillus polymyxa has been crystallized using the hanging-drop vapour-diffusion method at 277 K. The crystals belong to the orthorhombic space group P212121 with cell dimensions a = 64.6, b = 141.9, c = 155.1 A and diffract to 2.5 A resolution. The asymmetric unit containing three protein molecules was derived from an electron-density map calculated at 4 A resolution using MIR phases. This gives a Vm value of 2.36 A3 Da-1.

Changes in the heparin affinity of extracellular-superoxide dismutase in patients with coronary artery atherosclerosis.

Extracellular-superoxide dismutase [EC 1.15.1.1] (EC-SOD) is a secretory glycoprotein with high affinity for heparin. This enzyme locates in blood vessel walls at a high enough level to suppress oxidative stress under normal conditions. EC-SOD is the major SOD isozyme in plasma, anchored to heparan sulfate proteoglycans in the glycocalyx of endothelial cell surfaces. Plasma EC-SOD is heterogeneous in heparin affinity and can be divided into five fractions, I to V, by heparin-HPLC. It has been suggested that EC-SOD form V is the primary form synthesized in the body and that EC-SOD forms with reduced heparin affinity are the result of proteolytic truncation of the C-terminal end of EC-SOD form V which is responsible for the binding with heparin. Recently, we reported that only plasma EC-SOD form V, with the highest heparin affinity, was increased by intravenous injection of heparin. The heparin affinity of plasma EC-SOD in patients with coronary atherosclerosis (CA+ patients) was compared in this study. The increase of plasma EC-SOD form V after heparin injection in CA+ patients was significantly less than that in subjects without evidence of stenosis in their major coronary arteries (CA- subjects). On the other hand, in CA+ patients, EC-SOD forms I to III, with low heparin affinity, were significantly increased compared to those in CA- subjects. EC-SOD in plasma apparently forms an equilibrium between the plasma phase and endothelial cell surface, and EC-SOD on the endothelial cell surface contributes to protecting the vessel wall against oxidative stress. These findings suggest that the quantitative and qualitative changes of EC-SOD, i.e., the decrease of bound EC-SOD on the endothelial cell surface, might suppress the defense systems against oxidative stress, which causes in part the development of coronary artery atherosclerosis.

Atherogenic lipoproteins inhibit catecholamine secretion in cultured bovine adrenal medullary cells.

The effects of lipoproteins on ion channel-mediated catecholamine secretion were investigated in cultured bovine adrenal medullary cells. Low density lipoprotein (LDL: 20-80 mg/dl) and lipoprotein(a) [Lp(a); 10-80 mg/dl] inhibited catecholamine secretion induced by carbachol, an activator of nicotinic acetylcholine receptor-ion channels. LDL and Lp(a) suppressed carbachol-induced 22Na+ influx as well as 45Ca2+ influx in a concentration-dependent manner similar to that of catecholamine secretion. The inhibition of catecholamine secretion by Lp(a) was not overcome by increasing the concentration of carbachol. On the other hand, high density lipoprotein (HDL; < 150 mg/dl) had no effect on 22Na+ influx, 45Ca2+ influx, and catecholamine secretion. Like LDL and Lp(a), a synthetic peptide homologous to human plasma apolipoprotein B (apoB), apoB fragment(3358-3372)-amide (3-60 microM), attenuated 22Na+ influx, 45Ca2+ influx, and catecholamine secretion caused by carbachol. The apoB fragment also suppressed 22Na+ influx induced by veratridine (an activator of voltage-dependent Na+ channels) and 45Ca2+ influx induced by 56 mM K+ (an indirect activator of voltage-dependent Ca2+ channels). These findings suggest that atherogenic lipoproteins such as LDL and Lp(a) suppress catecholamine secretion by interfering with Na+ influx through nicotinic acetylcholine receptor-ion channels, in which apoB, a structural component common to both LDL and Lp(a), plays an important role. The inhibition by atherogenic lipoproteins of catecholamine secretion may influence the progression of atherosclerosis induced by these lipoproteins.

Effects of carbamazepine on hippocampal serotonergic system.

To establish the mechanism of action of the antiepileptic and psychotropic effects of carbamazepine (CBZ), its effects on serotonin (5-HT) transmission, metabolism and re-uptake activity in the rat hippocampus were studied. After acute and chronic administrations of 25 mg/kg CBZ, the plasma concentration of CBZ was found to be within the therapeutic range, whereas both acute and chronic administrations of 50 and 100 mg/kg CBZ resulted in a supratherapeutic plasma concentration. Acute administration of the therapeutic dose of CBZ resulted in an increase in the hippocampal extracellular and total level of 5-HT, its metabolite, 5-hydroxydoleacetic acid (5-HIAA) and its precursor, 5-hydroxytryptophan (5-HTP). The acute administration of 50 mg/kg CBZ resulted in an increase in the hippocampal levels of extracellular 5-HT and 5-HIAA as well as in the total levels of 5-HTP, whereas hippocampal levels of extracellular 5-HTP, total 5-HT and 5-HIAA remained unaffected. CBZ at a dose of 100 mg/kg decreased the levels of all of these substances. After chronic administration, 25 mg/kg/day CBZ increased hippocampal total levels of 5-HT, 5-HTP and 5-HIAA, whereas 100 mg/kg/day CBZ decreased all of these total levels. CBZ at a dose of 50 mg/kg/day decreased total levels of 5-HT, however neither total levels of 5-HIAA nor 5-HTP were affected. Both therapeutic and supratherapeutic plasma concentrations of CBZ inhibited 5-HTP accumulation, and did not affect 5-HT re-uptake activity in vitro. These results suggest that a therapeutic concentration of CBZ enhances 5-HT turnover and transmission, whereas a supratherapeutic concentration of CBZ inhibits 5-HT turnover and transmission without affecting 5-HT re-uptake activity. These effects of CBZ on serotonergic systems may be, at least partially, involved in the mechanisms of action of CBZ.

Enhanced macrophage uptake of lipoprotein(a) after Ca2+-induced aggregate-formation.

We tested the hypothesis that aggregated lipoprotein(a) [Lp(a)] is avidly taken up by macrophages. Lp(a) was isolated by sequential centrifugations and gel chromatography from a patient with high plasma levels of Lp(a) who was being treated with low density lipoprotein (LDL)-apheresis. Aggregated Lp(a) was prepared by mixing native Lp(a) with 2.5 mmol/L CaCl2, and 54% of the 125I-Lp(a) aggregated after interacting with CaCl2. The binding and degradation of aggregated Lp(a) in macrophages were 4.6- and 4.7-fold higher than those of native Lp(a), respectively. An excess amount of LDL did not inhibit either increase. Cholesterol esterification in macrophages was markedly stimulated by aggregated Lp(a), and macrophages were transformed into foam cells. Cytochalasin B, a phagocytosis inhibitor, strongly inhibited the degradation and cholesterol esterification (78 and 83%, respectively). These findings suggested that aggregation may be partially involved in Lp(a) accumulation, thereby contributing to the acceleration of atherosclerosis.

Effects of Ca2+ channel antagonists on striatal dopamine and DOPA release, studied by in vivo microdialysis.

1. To elucidate the mechanisms regulating the release of striatal dopamine and its precursor, 3,4-dihydroxyphenylalanine (DOPA), we determined the effects of various Ca2+ channel antagonists, an N-type Ca2+ channel antagonist, omega-conotoxin GVIA, a P-type Ca2+ channel antagonist, omega-agatoxin IVA, and a Q-type Ca2+ channel antagonist, omega-conotoxin MVIIC, on the basal and Ca2+- and K+-evoked release of striatal dopamine and DOPA, by use of in vivo microdialysis. 2. Omega-conotoxin GVIA strongly inhibited striatal basal dopamine release (IC50 = 0.48 nM), whereas this toxin only weakly modulated basal striatal DOPA release (IC50 = 9.55 nM). Neither omega-agatoxin IVA nor omega-conotoxin MVIIC affected the basal striatal release of dopamine and DOPA. 3. Omega-conotoxin GVIA strongly inhibited Ca2+-evoked striatal dopamine release (IC50 = 0.40 nM), whereas Ca2+-evoked striatal DOPA release only was weakly modulated (IC50 = 10.51 nM). Neither omega-agatoxin IVA nor omega-conotoxin MVIIC affected the Ca2+-evoked release of striatal dopamine and DOPA. 4. Both omega-agatoxin IVA and omega-conotoxin MVIIC inhibited the K+-evoked release of striatal dopamine (IC50 of omega-agatoxin IVA = 2.65 nM; IC50 of omega-conotoxin MVIIC = 12.54 nM) and DOPA (IC50 of omega-agatoxin IVA = 0.15 nM; IC50 of omega-conotoxin MVIIC = 3.05 nM), whereas omega-conotoxin GVIA had no effect on the K+-evoked release of striatal dopamine and DOPA. 5. An increase in the extracellular Ca2+ and K+ concentrations (Ca2+- and K+-evoked stimulation) did not affect tyrosine hydroxylase activity in vivo. 6. These findings suggest that striatal DOPA release is neurotransmitter-like and that, unlike the mechanisms of striatal dopaminergic transmission, this striatal DOPA transmission is at least partly regulated by voltage-sensitive Ca2+ channels.

Can aggressive lipid lowering using low-density lipoprotein apheresis prevent restenosis after percutaneous transluminal coronary angioplasty in patients with normocholesterolemia?

We examined whether aggressive lipid lowering using low-density lipoprotein (LDL) apheresis could prevent restenosis after percutaneous transluminal coronary angioplasty (PTCA). Fifteen patients with 17 lesions underwent LDL apheresis once within a week before and after PTCA and thereafter every 2 or 3 weeks (apheresis group) for about 4 months. The control group consisted of 17 patients with 17 lesions. No patients received additional lipid lowering drugs after PTCA. In the apheresis group, the time interval means of the total and LDL cholesterol levels were significantly lower than those in the control group whereas no significant differences were found between the 2 groups regarding the mean percent diameter stenosis or minimal lumen diameter before and after PTCA and at follow-up. The restenosis rate was 29.4% in the apheresis group and 47.1% in the control group. The restenosis rate tended to be slightly lower in the apheresis group. The overall results, however, indicated that aggressive lipid lowering does not prevent restenosis.

Effects of adenosine receptor subtypes on hippocampal extracellular serotonin level and serotonin reuptake activity.

To clarify the effects of adenosine receptor subtypes (A1, A2, and A3) on hippocampal serotoninergic function, hippocampal extracellular serotonin (5-HT) levels were determined by in vivo microdialysis in freely moving rats under various conditions. Both adenosine and an adenosine A1 receptor agonist, 2-chloro-N6-cyclopentyladenosine, decreased extracellular 5-HT levels, whereas an adenosine A1 receptor antagonist, 8-cyclopentyl-1,3-dimethylxanthine (CPT), and caffeine increased these levels. A selective A2A receptor agonist (CGS-21680), an adenosine A2 receptor agonist (PD-125944), an adenosine A2 receptor antagonist, 3,7-dimethyl-1-propargylxanthine (DMPX), and an adenosine A3 receptor agonist, N6-2-(4-aminophenyl)ethyladenosine (APNEA), did not affect extracellular 5-HT levels. When the adenosine A1 receptor was blocked by CPT, the hippocampal extracellular 5-HT level was increased by adenosine, CGS-21680, and PD-125944, and decreased by caffeine, DMPX, and APNEA. When both adenosine A1 and A2 receptors were blocked by CPT and DMPX, the extracellular 5-HT level was decreased by adenosine, caffeine, and APNEA. The hippocampal extracellular 5-HT level was not affected by administration of APNEA alone, but was decreased by this agent when the adenosine A1 receptor was blocked, irrespective of whether the adenosine A2 receptor was functional. These inhibitory effects of adenosine, caffeine, and APNEA on extracellular 5-HT levels, during both adenosine A1 and A2 receptor blockade, were inhibited by selective 5-HT reuptake inhibitors. These results indicate that the stimulatory effects of the adenosine A2 receptor and the inhibitory effects of the A3 receptor on hippocampal extracellular 5-HT levels are masked by the inhibitory effects of the adenosine A1 receptor.

A case of X-linked alpha-thalassemia/mental retardation syndrome: analysis of hemoglobin by an automated glycated hemoglobin analyzer.

A 5-year-old male patient with X-linked alpha-thalassemia/mental retardation syndrome is reported. He showed multiple minor anomalies including characteristic facial abnormalities, alpha-thalassemia, severe mental retardation, and hypogonadism. Analysis of his hemoglobin by high performance liquid chromatography using an automated glycated hemoglobin analyzer revealed an abnormal peak. Identification of an abnormal peak by an automated glycated hemoglobin analyzer will aid in the diagnosis of patients with X-linked alpha-thalassemia/mental retardation syndrome.