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Biomedical subjects

T Araki

Publications and source records attributed to T Araki.

At least 325 records · Page 18Linked to original sources

Fetal plasma hypoxanthine level in growth-retarded fetuses before labor.

Hypoxanthine is one of the purine nucleotides and is presumed to accumulate during hypoxia and acidemia. It remains uncertain, however, whether plasma hypoxanthine concentration is a useful indicator of fetal asphyxia; and its relationship to other markers of fetal physiologic state is not clearly defined. The aim of this study was to evaluate whether the level of fetal plasma hypoxanthine is correlated with fetal hypoxia and acidosis in growth-retarded fetuses before the onset of labor. Cordocentesis was performed in 34 growth-retarded fetuses at 31-35 weeks' gestation for the measurement of umbilical venous plasma concentrations of hypoxanthine, hemoglobin and lactate concentrations, blood gases, and base deficit. Umbilical venous plasma hypoxanthine concentration was found to be increased significantly, in parallel with the degree of acidosis (r = -0.74, P < 0.05) and base deficit (r = -0.41, P < 0.05), but not to bear a significant relationship to the degree of hypoxemia or other measured variables. We conclude that increases in the plasma concentration of hypoxanthine may reflect an impaired physiological state in growth-retarded fetuses before labor.

Acid-Base Equilibrium↗

Effects of maternal infection on prostaglandin production and uterine contraction in late-gestation pregnant goats.

The main objective of this study was to evaluate the relationship between maternal infection induced by pyrogen administration and the changes in maternal and fetal plasma levels of prostaglandin E2 (PGE2) and F 2 alpha (PGF 2 alpha) and uterine contraction. We administered one mg of pyrogen (E. coli endotoxin) into the maternal femoral vein; then then the changes in maternal and fetal core temperatures, plasma levels of PGE2, [PGE2] and PGF 2 alpha, [PGF 2 alpha]. pO2, pCO2, pH and maternal uterine contractions were measured in late-gestation pregnant goats (n = 8). Maternal and fetal core temperatures were elevated significantly 30 min after pyrogen administration (p < 0.05), reached their peak levels after 3 hours, and after 5 hours mean core temperatures returned to levels indistinguishable from initial control. Maternal plasma [PGE2] and [PGF 2 alpha] increased to 4318 +/- 321 pg/ml after 1 hour and to 670.8 +/- 58.4 pg/ml after 3 hours respectively (p < 0.05). Fetal plasma [PGF 2 alpha] increased significantly (p < 0.05) to 811.0 +/- 64.0 pg/ml after 1 hour; however, plasma [PGE2] did not change throughout the study. Periodic uterine contractions appeared after 3 hours and disappeared after 5 hours. These results suggest that pyrogen induces the elevation of maternal and fetal core temperatures and prostaglandin production, and that eventually causes uterine contractions.

Animals↗

Thermographic demonstration of nonshivering thermogenesis in human newborns after birth: its relation to umbilical gases.

This study was undertaken to measure the extent of nonshivering thermogensis (NST) in brown adipose tissue of human newborns receiving routine thermal care and to examine the influence of oxygen levels at birth on the initiation of NST. Fifteen human neonates were studied in an incubator set at 31-31 degrees C. Thermographic measurements were made every 5 seconds for 5 minutes at 10 and 30 minutes, 1, 3, 6 and 24 hours, and 3 days after birth. The skin temperature and rate of heat dissipation from the interscapular area (location of subcutaneous brown adipose tissue), whole back area, and head area were measured. A heat dissipation ratio (HDR) was calculated as (A-B)/B, where A and B, expressed in Cal/cm2/h, represent rates of heat dissipation from the interscapular area and the whole back area, respectively. Umbilical arterial blood gases were measured immediately after birth. The skin temperature of the interscapular, whole back, and head areas increased significantly during the interval from 10 minutes to 1 hour after birth (p < 0.05). The skin temperature of the interscapular area was highest among the sampled sites during the first hour after birth (p < 0.05). The HDR was highest 10 minutes after birth (p < 0.05). By 1 hour after birth the temperature had reached constant values with low HDR. There was a negative correlation between the HDR and the temperature of the whole back area (p < 0.001). A positive correlation was found between the HDR within 30 minutes after birth and the PO2 of the umbilical arterial blood (p < 0.001). The data support the conclusion that nonshivering thermogenesis is initiated within minutes of birth and contributes to the elevation of body temperature. Furthermore, nonshivering thermogenesis after birth is reduced by low arterial PO2 at the time of birth.

Adult↗

Perfusion-weighted MR imaging in the upper abdomen: preliminary clinical experience in 61 patients.

OBJECTIVE: We quantitatively analyzed the potential usefulness of perfusion-weighted (PW) MR imaging of the upper abdomen performed with a single-shot gradient-recalled echo echoplanar (GRE EP) sequence. SUBJECTS AND METHODS: PW imaging of the upper abdomen with a GRE EP sequence was performed in 61 patients who had suspected liver or pancreatic disease. PW imaging was started at the time of administration of 0.1 mmol/kg of gadopentetate dimeglumine, and images were obtained every 2 sec for 88 sec. Time-intensity curves for the liver, pancreas, spleen, and kidney, and for subgroups of patients with various pathologic conditions, were constructed for quantitative analysis. RESULTS: The signal-intensity changes seen throughout the PW imaging process differed for each abdominal organ and pathologic condition. In the spleen, pancreas, and renal cortex, a transient signal-intensity decrease was seen in the perfusion phase (42%, 39%, and 78%, respectively). In the liver and renal medulla, the maximum signal-intensity decrease occurred in the later phase rather than in the perfusion phase. Signal-intensity recovery in the spleen and pancreas occurred soon after the maximum signal-intensity decrease, whereas such recovery was delayed in the liver and renal cortex. In cirrhotic livers, the signal-intensity change seen throughout the examination was minimal. CONCLUSION: Unlike conventional MR imaging, PW imaging with a GRE EP sequence can provide detailed hemodynamic information about upper abdomen organs and about disorders of these organs because of its excellent temporal resolution and susceptibility to contrast enhancement.

Abdomen↗

Improvement of estradiol-17 beta-D-glucuronide-induced cholestasis by sodium tauroursodeoxycholate therapy in rats.

BACKGROUND: Estradiol-17 beta-D-glucuronide (E-17G), a metabolite of natural estrogen, is well known to cause intrahepatic cholestasis in humans. We therefore investigated the effect of sodium tauroursodeoxycholate (T-UDCA), on E-17G-induced cholestasis in female rats. METHODS: For the evaluation of the drug, animals given E-17G (10 mumol/kg) were divided into three groups, and T-UDCA was administered intravenously at various doses after E-17G treatment. RESULTS: T-UDCA significantly prevented a marked reduction of bile flow in E-17G-treated rats in all experimental schedules. Furthermore, T-UDCA significantly increased in the biliary E-17G excretion rate at an early stage after E-17G treatment in rats. However, this drug caused no significant change in the biliary excretion rate of estradiol-3-sulfate-17 beta-D-glucuronide (E-3S-17G), which is identified as the major biliary metabolite with E-17G throughout the recovery periods. CONCLUSION: These results suggest that T-UDCA can improve E-17G induced acute cholestasis by rapidly increasing the biliary E-17G excretion rate. Thus our finding may provide a useful approach for attempts to prevent drug-induced acute cholestasis in humans.

Animals↗

MR of the endolymphatic duct and sac: findings in Menière disease.

PURPOSE: To compare the visibility of the endolymphatic duct and sac on high-resolution MR images with the symptoms and clinical course in patients with Menière disease. METHODS: Twenty-two patients with unilateral Menière disease were sorted into two groups on the basis of the clinical stage of their disease at the time of imaging. Group 1 included patients in the acute phase, who presented with vertigo. Group 2 comprised patients in the nonacute phase of the disease, who were studied 9 days or more after an episode of vertigo. RESULTS: During acute attacks, the endolymphatic duct and sac were not adequately visible in the affected ear but were visible in the unaffected ear. During remission, the endolymphatic duct and sac were not observed in clinically advanced patients, but they were seen in patients in the early and intermediate stages. CONCLUSION: High-resolution MR imaging can be used to evaluate the endolymphatic duct and sac: visible abnormalities and lack of a visible endolymphatic duct and sac correlate with the clinical course of Menière disease.

Acute Disease↗

[Effect of daily administration of oral etoposide for non-small cell lung cancer treated with concurrent radiation therapy].

The purpose of this study was to explore the effect of daily administration of oral etoposide (25 mg) for patients with non-small cell lung cancer treated with concurrent radiation therapy. Planned endpoints were response, survival and toxicity. Forty-one patients with non-small cell lung cancer were divided into 25 patients given daily oral etoposide (25 mg) with concurrent radiation therapy (ERT group) and 16 patients given radiation therapy alone (RT group). Etoposide was administrated in the morning throughout radiation therapy. The median total irradiated dose was 63.1 Gy in the ERT group and 64.0 Gy in the RT group. Twenty-four patients completed therapy in the ERT group and 16 in the RT group. Three (15%) ERT patients achieved complete response (CR) and 9 (45%) achieved partial response (PR). In the RT group, no patients achieved CR and 9 (69%) achieved PR. One-year survival was 22.6% with ERT and 23.0% with RT. The prognosis of stage III patients in the ERT group was worse than that in the RT group because radiation pneumonitis and radiation esophagitis were more severe with ERT. In conclusion, the ERT group had better local response but worse in survival than the RT group. Complications of ERT were severe enough to cause death in some patients. ERT had no clear advantage over RT.

Administration, Oral↗

[Clinical results of left ventricular free wall rupture following acute myocardial infarction].

We studied 19 cases of Left Ventricular Free Wall Rupture (LVFWR) following acute myocardial infarction, admitted to our CCU between 1987 and 1996. We were able to treat 15 patients and diagnosed 4 cases as LVFWR at postmortem after sudden deaths. Of the treated 15 patients, 11 survived: 1 out of 2 repaired under cardiopulmonary bypass (CPB), 5 out of 7 repaired without CPB, and 5 out of 6 non-surgically treated. Although the survival rate for those able to be treated was 73%, overall rate was 58%. There were 7 cases of blow-out type: 4 of which were sudden deaths, and 3 were operated. Thoracotomy and direct closure of rupture without CPB was done at bed-side in 2 cases. Even though hemostasis was successful, they did not survive. The 3rd case survived with the patch closure under CPB. In this case, the circulation was maintained pre-operatively with the pericardial-central venous bypass drainage method. This method seems to be extremely effective in saving blow-out cases. There were 12 subacute patients. Although 2 cases were lost, total of 10 patients were saved, including 2 direct suture closures of rupture without CPB, 3 median sternotomy and fibrin-glue fixations, 1 where only pericardial drainage was done, and 4 in whom percutaneous intrapericardial fibrin-glue fixation therapy was utilized. Since the risk of secondary damage to the fragile infarcted are from direct suturing of ruptured myocardium exists in LVFWR, we changed to the Infarction Exclusion Technique under CPB during surgical repair, based on our experiences with ruptured intraventricular septum. In general, the only treatment believed to be available for LVFWR has been surgical. However, our experiences suggest that other treatments may also be effective. If the best suitable method could be chosen from various therapies, it may contribute to improving outcome statistics. The reduction of left ventricular pressure in the treatment is extremely important, being the key to improving survival rate.

Aged↗

[Active MR tracking system at 0.2T MR, a preliminary report: real time position tracking on interventional MR].

An active MR tracking system was installed in a 0.2 T open-type MRI. Interventional devices with a receive-only microcoil at their tips were newly developed for tracking at 0.2T. The low signal-to-noise ratio at 0.2T required the microcoils to have a diameter of about 2 mm and 20 turns for stable tracking. Simulation of MR-guided biopsy using biplane images with tracking in the gelatin phantom was performed. MR tracking in the aorta and IVC of a dog by a catheter with a microcoil at its tip was successful.

Animals↗

Execution mechanisms of programmed cell death by caspase (ICE/CED-3) family proteases.

Molecular genetic study of Caenorhabditis elegans revealed the cell death-executing gene ced-3. Structural and functional similarities between CED-3 and mammalian ICE family (caspase) gene products provide the evidence that mammalian caspases are common mediators in executing programmed cell death. These findings suggest that the execution mechanisms of cell death by caspase family protease may be evolutionarily conserved from worms to mammals. This report summarizes the unique properties of caspases in apoptosis.

Animals↗

Adenosine A1-receptor agonist attenuates the light-induced phase shifts and fos expression in vivo and optic nerve stimulation-evoked field potentials in the suprachiasmatic nucleus in vitro.

Adenosine is widely accepted to act as an inhibitory neuromodulator in the mammalian central nervous system. In the present study, we examined whether adenosine receptor agonist modifies the photic entraining responses in the rat suprachiasmatic nucleus both in vivo and in vitro. Light (200 lux, 15 min)-induced phase shifts of hamster wheel-running rhythms was attenuated by a systemic administration of A1-adenosine receptor agonist N6-cyclohexyladenosine (N-CHA) in a dose-dependent manner; 0.5 mg/kg N-CHA caused 60% inhibition of light-induced phase shifts. On the other hand, A2-adenosine receptor agonist N6-[2-(3,5-dimethoxyphenyl)-2-(2-methylphenyl)-ethyl]adenosine (DPMA) failed to inhibit light-induced phase shifts. Systemic administration of N-CHA but not of DPMA inhibited light (300 lux, 1 h)-induced Fos expression in the suprachiasmatic nucleus in a dose-dependent manner; 1 mg/kg N-CHA caused 73% inhibition of light-induced Fos expression. Bath application of N-CHA but not of DPMA inhibited optic nerve stimulation-evoked field potentials in rat suprachiasmatic nucleus slices. The present results suggest that activation of adenosine A1-receptor attenuates the photic input through the inhibition of retinohypotalamic pathway to the SCN.

Adenosine↗

Positions of disulfide bonds in yam (Dioscorea japonica) acidic class IL (class IV) chitinase.

Yam acidic class I chitinase belongs to a low molecular weight subclass of class I (class IL; corresponds to class IV) chitinase. The positions of disulfide bonds in this chitinase were examined. Chitinase protein was digested with acid protease and thermolysin, and the resulting disulfide bond containing peptides were separated by reversed-phase HPLC and detected using the SBD-F (7-fluorobenzo-2-oxa-1,3-diazole-4-sulfonic acid ammonium salt) method. Four intradisulfide bonds containing peptides were purified and three disulfide bonds in the catalytic domain were identified as Cys-66 and Cys-115, Cys-128 and Cys-136, and Cys-218 and Cys-250. Location of disulfide bonds in the catalytic domain was identical to that of barley class II chitinase but different from rye class II chitinase at the C-terminal. Conservation of S-S bonds at the N-terminal half of the catalytic domain between class I and class II chitinases strongly suggests that this region is important for formation of the active site.

Amino Acid Sequence↗

Microglial activation by epileptic activities through the propagation pathway of kainic acid-induced hippocampal seizures in the rat.

We studied the distribution of activated microglia in the brain during kainic acid-induced acute hippocampal seizures in rats. Although no microglial activation was observed 4 h after seizure induction, activation was detected in the primary focus and also in other selected structures in the limbic and non-limbic structures after 8 and 24 h, in the absence of any obvious morphological changes in the neurons. The structures with activated microglia were highly consistent with those included in the propagation pathways of the hippocampal seizures. These findings thus suggest that the microglial cells are activated through the propagation pathways by the seizure activities that propagate transynaptically from the primary focus, even without any apparent neuronal injury.

Animals↗

Progressive expression of immunomolecules on activated microglia and invading leukocytes following focal cerebral ischemia in the rat.

In order to evaluate the involvement of inflammatory reactions following focal cerebral ischemia in the rat, we immunohistochemically visualized microglial cells and blood-borne leukocytes (neutrophils and monocytes) using various antibodies directed against immunomolecules expressed on these cells. Focal cerebral ischemia was produced by intraluminal occlusion of the right middle cerebral artery for 1 h. The brains were perfusion-fixed at 4 h, 1 day, 3 days, 7 days and 14 days after ischemia. Frozen brain sections were prepared and stained with monoclonal antibodies to complement receptor type 3 (OX42), major histocompatibility complex (MHC) class I and class II antigens (OX18 and OX6, respectively), a pan-macrophage/monocyte marker (ED1), intercellular adhesion molecule-1 (ICAM-1), LFA-1 alpha chain (CD11a) and beta chain (CD18), and T cells (CD5). In ischemic areas where infarction developed later, microglial cells were destroyed (beginning at 4 h), neutrophils migrated (1-3 days), and then monocytes/macrophages infiltrated and covered the entire lesions (3-14 days). The invading leukocytes expressed CD11 and CD18 adhesion molecules on their cell surface while ICAM-1 was expressed on endothelial cells. In surrounding areas, in contrast, there was a rapid activation of microglia showing morphological changes and upregulation of OX42 immunoreactivity (4 h-7 days), especially in the transitional rim of the infarct (7 days). ED1 and MHC antigens were expressed on both activated microglia and invading leukocytes. Thus, developing infarction was accompanied by accumulation of inflammatory cells of both intrinsic (microglia) and extrinsic (leukocytes) origins. Thus, results suggest that the relative importance of each source is determined by the time after ischemia and the site within the lesion, and that the expression of immunological molecules plays an important role in eliciting such inflammatory reactions.

Animals↗

Regional age-related alterations in cholinergic and GABAergic receptors in the rat brain.

The age-related changes of cholinergic and gamma-aminobutyric acid (GABA)ergic receptors were studied in 3-week- and 6-, 12-, 18- and 24-month-old Fisher 344 male rat brains using receptor autoradiography. [3H]Quinuclidinyl benzilate (QNB), [3H]hemicholinium-3 (HC) and [3H]muscimol were used to label acetylcholine receptors, acetylcholine reuptake sites and GABAA receptors, respectively. In immature rats (3-week-old), [3H]QNB and [3H]muscimol binding showed a significant increase in most brain areas, compared to adult young animals (6-month-old), whereas [3H]HC binding exhibited a significant increase only in the dentate gyrus, substantia nigra and cerebellum. In contrast, [3H]QNB and [3H]HC binding showed no significant changes in all brain areas during aging. On the other hands, [3H]muscimol binding showed a significant reduction in the substantia nigra and cerebellum of adult mature rats (12-month-old). Thereafter, the age-related reduction in [3H]muscimol binding was observed in all brain areas of aged rats (24-month-old). Our results demonstrate that the GABAergic system is susceptible to aging processes in the central nervous system, whereas the cholinergic system is unaltered by aging. Furthermore, our results suggest significant regional changes in both GABAergic and cholinergic systems in the brain even 3 weeks after birth. These findings suggest that the disturbance in GABAergic-cholinergic interactions may play a key role in age-related neurological deficits and cognitive dysfunction.

Aging↗

N (epsilon)-(carboxymethyl)lysine protein adduct is a major immunological epitope in proteins modified with advanced glycation end products of the Maillard reaction.

Long-term incubation of proteins with glucose leads to the formation of advanced glycation end products (AGE). Recent immunological studies have suggested the potential role of AGE in atherosclerosis, aging, and diabetic complications. We previously prepared a monoclonal (6D12) as well as a polyclonal anti-AGE antibody and proposed the presence of a common AGE structure(s) that may act as a major immunochemical epitope [Horiuchi, S., Araki, N., & Morino, Y. (1991) J. Biol. Chem. 266, 7329-7332]. The purpose of the present study was to determine the major epitope. Amino acid analysis of AGE-proteins indicated that N(epsilon)-(carboxymethyl)lysine (CML) was a major modified lysine residue. Immunologic studies demonstrated the positive reaction of 6D12 not only to all CML-modified proteins tested, but also to BSA modified with several aldehydes known to generate a CML-protein adduct, and a linear correlation between the CML contents of CML-BSA and their immunoreactivity to 6D12 up to approximately 8 mol/mol of protein. Further experiments with CML analogs revealed that the epitope of 6D12 is a CML-protein adduct with an important carbonyl group. In contrast to 6D12, our polyclonal anti-AGE antibody showed a significant but much weaker immunoreactivity to CML-BSA, suggesting that the polyclonal antibody contains two populations, one reactive to CML (CML-PA) and the other unreactive to CML (Non-CML-PA). Non-CML-PA separated from CML-PA by CML-BSA affinity chromatography did not react with all CML-modified preparations, but retained its property to react commonly with AGE preparations obtained from proteins, lysine derivatives, and monoaminocarboxylic acids. Therefore, it is clear that a CML-protein adduct is a major immunological epitope in AGE structures, but there still exist other major epitope(s) expressed commonly in AGE-proteins.

Animals↗