Modification of urinary bladder function after spinal cord injury.
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Biomedical subjects
Publications and source records attributed to I Araki.
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The B-line presumptive muscle cells of ascidian embryos have extensive potential for self-differentiation dependent on determinants prelocalized in the myoplasm of fertilized eggs. Ascidian larval muscle cells therefore provide an experimental system with which to explore an intrinsic genetic program for autonomous specification of embryonic cells. Experiments with egg fragments suggested that maternal mRNAs are one of the components of muscle determinants. Expression of larval muscle actin genes begins as early as the 32-cell stage, prior to the developmental fate restriction of the cells. The timing of initiation of the actin gene expression proceeds the expression of an ascidian homologue of vertebrate MyoD by a few hours. Mutations in the proximal E-box of the 5' flanking region of the actin genes did not alter the promoter activity for muscle-specific expression of reporter gene. These results, together with results of deletion constructs of fusion genes, suggest that muscle determinants regulate directly, or indirectly via regulatory factors other than MyoD, the transcription of muscle-specific structural genes leading to the terminal differentiation.
Gene duplication is thought to be a major genetic change that may have permitted the evolution of vertebrates from invertebrates. The myogenic genes encode basic helix-loop-helix (bHLH) transcriptional factors essential for the formation of skeletal muscle. The invertebrate genome contains only a single myogenic bHLH gene, whereas the vertebrate genome contains four (MyoD, Myf-5, myogenin and MRF4). Since the tunicate genome contains a single myogenic bHLH gene, its duplication might have occurred some time during chordate evolution. To determine whether the duplication of the myogenic bHLH gene occurred prior to, or after the divergence of vertebrates from the cephalochordate lineage, we amplified target fragments from the amphioxus, Branchiostoma floridae, by means of PCR. Sequence analysis and genomic Southern analysis revealed that the amphioxus genome contains two myogenic bHLH genes (BMD1 and BMD2). A comparison of the amino acid sequences in the bHLH domain between BMD1, BMD2 and four vertebrate myogenic bHLH gene products, however, showed that neither BMD1 nor BMD2 resembled any of the four genes. These results suggested that the duplication of amphioxus myogenic bHLH gene occurred independently of that leading to the four myogenic bHLH genes in vertebrates.
OBJECTIVE: To assess the influence of continuous hemodiafiltration (CHDF) on cortisol and catecholamine kinetics in multiple organ dysfunction syndrome. DESIGN: Consecutive clinical study. SETTING: General intensive care unit of a university hospital. PATIENTS: Ten adult patients with multiple organ dysfunction syndrome requiring CHDF. MEASUREMENTS AND RESULTS: A total of 40 samples were collected during CHDF for cortisol and catecholamine assays. The clearances for cortisol, epinephrine, norepinephrine and dopamine were 2.5 +/- 1.7 ml/min, 26.3 +/- 2.7 ml/min, 16.7 +/- 4.2 ml/min and 26.3 +/- 2.6 ml/min (Mean +/_ SE), and their daily extractions were 1.8 +/- 0.2 mg/day, 11.4 +/- 4.8 micrograms/day, 1.0 +/- 0.1 micrograms and 2.3 +/- 0.3 micrograms/day, respectively. There were no significant changes in blood cortisol and catecholamine levels during CHDF conducted for 48 h. CONCLUSIONS: The cortisol and catecholamine losses during CHDF were small and unlikely to lead to hemodynamic disturbances.
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1. Excitatory postsynaptic currents (EPSCs) in parasympathetic preganglionic neurons (PGNs) were examined by the use of the whole cell patch-clamp recording technique in slice preparations of the neonatal rat lumbosacral spinal cord. Synaptic responses were evoked in PGNs by extracellular stimulation of a neighboring interneuron. 2. Stimulation of interneurons medial to the sacral parasympathetic nucleus (SPN) elicited EPSCs or inhibitory postsynaptic currents in 58 and 11%, respectively, of PGNs. Stimulation of interneurons dorsal to the SPN evoked EPSCs in 70% of PGNs. 3. EPSCs occurred at short latency (2.1 ms) and were usually elicited in an all-or-none manner, indicating that they were monosynaptic and mediated by a single interneuron (i.e., unitary). 4. EPSCs were mediated by both non-N-methyl-D-aspartate (non-NMDA) and NMDA receptors. 5. Unitary excitatory postsynaptic potentials evoked by single stimuli did not induce action potentials in PGNs, but repetitive stimulation (> 20 Hz) of the single interneurons could evoke firing of PGNs. 2-Amino-5-phosphonovalerate, an NMDA receptor antagonist, reduced the synaptic depolarization induced in PGNs by high-frequency interneuronal impulses. 6. EPSCs mediated by dorsal interneurons were smaller in amplitude (36.3 +/- 15.7 pA, mean +/- SD) than EPSCs mediated by medial interneurons (88.4 +/- 45.7 pA). 7. Paired-pulse facilitation of EPSCs was observed in PGNs (147.2 +/- 26.2%). The degree of facilitation was higher in dorsal (174.6 +/- 10.3%) than in medial interneuronal pathways (120.9 +/- 3.6%). Within each of interneuronal pathways the degree of facilitation was independent of the magnitude of the unitary EPSC. 8. The results show that PGNs receive monosynaptic glutamatergic excitatory inputs from two distinct populations of interneurons in the dorsal and medial regions of the SPN. These two populations of interneurons are likely to have different functions in the regulation of the preganglionic outflow to the pelvic organs.
The effect of preoperative oral fluid intake on the volume and pH of gastric fluid was examined in 45 elective surgical patients ranged in ages from 18 to 70 years. Two hours preoperatively they all received oral roxatidine 75 mg with 10 ml water, immediately followed by 150 ml oral water or 150 ml refreshing drink or no fluid as control. Just after the induction of anesthesia, a Salem-sump tube was put down to the stomach to collect gastric fluid in each patient. The volume and pH of gastric fluid taken were 10.9 +/- 7.9 ml, 16.3 +/- 2.3 in control group, 8.0 +/- 6.0 ml, 6.2 +/- 2.4 in the water group and 6.3 +/- 6.0 ml, 7.1 +/- 1.7 in the refreshing drink group. As there were no significant differences in gastric pH values in the three groups, the highest value was found in the refreshing drink group. No significant difference in VAS of hungry and thirsty feeling was found among the three groups. We conclude that preoperative oral water or refreshing drink with roxatidine 75 mg 2 hours before the start of anesthesia may not increase the risk of aspiration during the induction of anesthesia.
This study was undertaken to evaluate the effect of isoflurane anaesthesia on the hypothalamic contents of both prostaglandin D2 and E2 which affect the sleep-wakefulness cycle. Sixty-three Wistar rats were divided into three equal groups, control, isoflurane and recovery groups. Twenty-one rats of the control did not receive isoflurane. In the other groups 21 rats received isoflurane 2% for 30 min and 21 received isoflurane 2% for 30 min and were allowed to recover their usual behaviours, including righting reflex, spontaneously. The hypothalamus was removed and the contents of PGD2 and PGE2 were measured by enzyme immunoassay. The PGD2 content in the hypothalamus was 397.9 +/- 226.0 pg.g-1 for the control group, 134.2 +/- 41.2 pg.g-1 for the isoflurane group and 269.1 +/- 124.6 pg.g-1 for the recovery group, respectively. The hypothalamic PGE2 contents were 381.4 +/- 139.0 pg.g-1 for the control group, 183.3 +/- 26.4 pg.g-1 for the isoflurane group and 312.2 +/- 96.0 pg.g-1 for the recovery group, respectively. The hypothalamic PGD2 and PGE2 contents in the isoflurane group were lower (P < 0.05) than those in the control and recovery groups, while both the PGD2 and PGE2 contents of the control and the recovery groups were similar. We conclude that decreased hypothalamic PGD2 and PGE2 contents may be related to some manifestations of general anaesthesia with isoflurane.
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A 70-year-old woman with poorly controlled diabetes mellitus was admitted because of persistent remittent fever. Soon a liver abscess was detected as the cause of the fever by ultrasonography, and antibiotic therapy was started. However, suddenly serious dyspnea with chest and back pain developed. The morbid condition was definitely diagnosed as septic pulmonary emboli (SPE) with pulmonary perfusion scan. It should be recognized that liver abscess can be a latent focus of systemic metastatic complications such as SPE, and not only early detection but also prompt appropriate drainage of liver abscesses is essential.
1. The actions of gamma-aminobutyric acid (GABA) on sacral parasympathetic preganglionic (SPP) neurons were examined in slice preparations using the whole cell patch-clamp technique. 2. Inhibitory postsynaptic currents (IPSCs), which were evoked by focal electrical stimulation, were recorded from SPP neurons in the presence of 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX), a glutamate receptor antagonist. The IPSCs were substantially reduced by strychnine (1 microM), a glycine receptor antagonist. The remaining IPSCs were completely blocked by bicuculline (20 microM), a GABAA receptor antagonist. The mean peak amplitude of bicuculline-sensitive, GABAergic currents recorded at -60 mV was 53.6 +/- 10.9%, mean +/- SD (n = 8), of that of the total IPSCs. The GABAergic currents were reversed in polarity at about -30 mV, near the Cl- equilibrium potential. 3. GABA (5-50 microM) induced inward currents in SPP neurons with symmetrical internal and external Cl- concentrations. This response was completely blocked by 100 microM bicuculline. Muscimol (2-8 microM), a GABAA agonist, mimicked the GABA-induced responses, whereas a GABAB receptor agonist, baclofen (20-200 microM), produced responses in only a few cells. The GABA-induced currents reversed their polarity at approximately 0 mV, near the Cl- equilibrium potential. When the internal Cl- concentration was reduced, the reversal potential was shifted according to the Nernst equation for Cl-. 4. GABA-induced currents exhibited an outward "hump" between -35 and 15 mV. This voltage range coincided with that at which a depolarization-induced inward whole cell current was elicited.(ABSTRACT TRUNCATED AT 250 WORDS)
We report a case of pneumonitis induced by PL granules. A 45-year-old man took PL granules and other drugs for fever and headache. Because he subsequently developed high grade fever, cough and diarrhea, he was admitted to our hospital. His chest X-ray film revealed multiple patchy shadows in both lung fields. Analysis of bronchoalveolar lavage fluid (BALF) disclosed a high number of cells (total), lymphocytes, and a high CD4/CD8 ratio. Microscopic examination of transbronchial lung biopsy (TBLB) specimens showed infiltration of mononuclear cells and thickening of the alveolar wall. After discontinuation of drugs, his condition (symptoms, laboratory data, and chest X-ray findings) promptly improved. Lymphocyte stimulation tests (LST) for PL granules and acetaminophen were positive and an oral challenge test with PL granules was also positive. Based on these findings, we diagnosed this as a case of pneumonitis and enteritis due to PL granules. To our knowledge, this is the first reported case of pneumonitis due to PL granules.
1. Rat facial motoneurones axotomized on the day after birth were examined morphologically, and their electrical properties were characterized using the whole-cell recording technique in thin slices of the brainstem. 2. About 40% of facial motoneurones were lost within 4 days of axotomy, and only about 20% of the neurones survived 9 days after axotomy. 3. The surviving facial motoneurones examined 4 or 6 days after axotomy were reduced in size, and this was associated with a decrease in their input capacitance. 4. Both the resting potential and the amplitude of action potentials remained unchanged in axotomized facial motoneurones. 5. Facial motoneurones examined 4 or 6 days after axotomy showed an increase in the spike duration. When the preparation was superfused with a Ca(2+)-free solution, the spike duration of axotomized facial motoneurones was shortened, whereas the spike duration of control facial motoneurones was prolonged. 6. The voltage-gated transient K+ current (IA) density was significantly reduced in axotomized motoneurones, whereas the Ca(2+)-dependent transient K+ current (IK, Ca) density was not affected. 7. Voltage-gated Ca2+ currents in facial motoneurones showed inactivation, displaying an initial transient phase followed by a sustained phase. The rate of inactivation of Ca2+ currents was significantly faster in axotomized neurones than in control neurones. 8. A small subpopulation of facial motoneurones examined 4 or 6 days after axotomy had a disproportionately high input resistance and a significantly longer after-hyperpolarization. The probability of this occurring was correlated with the time course of cell death induced by axotomy. 9. It is concluded that facial motoneurones axotomized in neonatal rats comprise two subpopulations. The subpopulation characterized by a markedly high input resistance is suggested to represent the neurones which are at the 'prelethal' stage or in the process of cell death.
We evaluated EEG pattern during total intravenous anesthesia with droperidol, fentanyl and ketamine (DFK). Four surgical patients, ranged in age from 35 to 43, were the subjects of this study. Two male underwent oral or orthopedic surgery and the other two female patients underwent gynecological surgery. They were all free from hepato-renal dysfunction and central nervous system disorders. For the induction of anesthesia, droperidol 0.06-0.1 ml.kg-1, fentanyl 2-4 micrograms.kg-1, and ketamine 1.0-1.5 mg.kg-1 were slowly administered intravenously. A total dose of 5-15 micrograms.kg-1 of fentanyl was given intravenously with continuous infusion of ketamine 2 mg.kg-1.h-1 during the surgical procedure. The total amounts of fentanyl and ketamine administered were 4.9-22.2 micrograms.kg-1 and 240-340 mg.kg-1, respectively. We used HZI'Brain Function Monitoring system to evaluate their EEG patterns. When adequate depth of anesthesia was obtained as clinically evaluated by vital signs, theta wave pattern was dominant on the EEG tracings in any of these patients. DFK anesthesia would provide a stable anesthetic course, if those drugs are administered adequately considering vital signs including systemic blood pressure, heart rate, lacrimation and involuntary muscle movements of the face and extremities.
This study was undertaken to find a relationship between cardiac function indices and endocrine functions during prostaglandin E1 induced hypotension in surgical patients. Thirteen patients who underwent either orthopedic or gynecologic surgery were the subjects of the study. Systolic blood pressure decreased to 80 torr with prostaglandin E1 infusion (0.5-2 micrograms.kg-1 x min-1) under enflurane-N2O anesthesia. The cardiac function were judged by transesophageal echo-cardiography. Plasma ANP and ADH levels were measured by radioimmunoassay. Significant reductions in the left atrial diameter and A/R and significant increases in cardiac output were observed, but there were no significant changes in fractional shortening and pulmonary vein flow. Plasma ANP concentrations decreased significantly from 45.3 +/- 5.1 pg.ml-1 (mean +/- SE) of pre-hypotension to 32.6 +/- 2.2 pg.ml-1 of control, but plasma ADH levels increased significantly during hypotension (P < 0.05). We could not find any significant correlation between the cardiac function indices and plasma hormone levels. Transesophageal echocardiography is an excellent monitor during induced hypotension. It is difficult to predict the ANP and ADH levels by measuring cardiac function as judged by TEE.
Nineteen patients with ischemic heart disease were studied to determine plasma levels of isosorbide dinitrate (ISDN) and its metabolites, isosorbide-2-mononitrate (2-ISMN) and isosorbide-5-mononitrate (5-ISMN) for 6 hrs during intravenous administration of ISDN, using gas chromatography. Differences in plasma levels of these substances were also evaluated in patients with or without preanesthetic medication of ISDN. These patients ranging in ages from 42 to 80 years were administered ISDN intravenously at a rate of 1 micrograms.kg-1 x min-1 during anesthesia and surgery. Preanesthetic administration of ISDN consisted of transdermal application of 40 mg dose. Surgery included gastrectomy, pneumonectomy, extended cholecystectomy, radical mastectomy and so on under either enflurane anesthesia or neuroleptanesthesia. Plasma ISDN levels increased and reached a plateau 3 hrs after the start of intravenous infusion of ISDN in patients of both groups. Plasma 2-ISMN levels increased gradually and reached a plateau 5 hrs after the commencement of intravenous administration of ISDN in patients of both groups. Plasma 5-ISMN levels increased gradually reaching the peak 6 hrs after the start of intravenous infusion of ISDN in both groups. Plasma ISDN, 2-ISMN and 5-ISMN levels were slightly higher in patients who received preanesthetic ISDN than in those who did not receive preanesthetic ISDN. However, there were no statistical differences in plasma ISDN or 2-ISMN levels between the groups except prior to the infusion. On the contrary, plasma 5-ISMN levels were significantly higher in patients who received preanesthetic ISDN than in those who did not receive preanesthetic ISDN for 3 hrs after the start of the infusion.
Effect of pirenzepine, famotidine or a combination of both agents on gastric secretion during anesthesia and surgery was evaluated in 42 surgical patients ranged in age from 17 y to 70 y. They underwent orthopedic, ophthalmic, ENT, plastic, oral or non-abdominal surgery under either neuroleptanesthesia or enflurane anesthesia. They received either pirenzepine 10 mg, famotidine 20 mg or the combination of both agents intravenously just before the induction of anesthesia. Volume and acidity of gastric juice were measured during 3 hours after the administration of these agents. A continued decrease in volume and acidity of gastric juice was observed 3 hrs after the administration of the agents both in the pirenzepine group and in the famotidine group. Efficacy of the combination of pirenzepine and famotidine on gastric secretion tended to be more prominent than that of either pirenzepine or famotidine alone.
In the chicken genome, downstream from the delta 1 gene, encoding delta-crystallin, a highly homologous gene called delta 2 is found, but neither its expression nor its function has been clarified. Close similarity of the delta 2 gene to mammalian argininosuccinate lyase (ASL)-encoding genes in organization and deduced amino acid sequence of the encoded protein suggested that this gene may encode chicken ASL. To test this possibility, we cloned the delta 2 gene on a plasmid, introduced it into mouse cells, and assessed expression and ASL activity in comparison with delta 1. We found that delta 2 was expressed well in fibroblastic L cells, which resulted in synthesis of a protein with a size (50 kDa) and antigenicity very close to delta-crystallin, but it was repressed in lens cells in which expression of delta 1 was activated. Transfectant L cell lines expressing delta 2 exhibited significantly higher ASL activity than those without. We conclude that the delta 2 gene codes for chicken ASL, but has a tissue specificity distinct from delta 1 in its expression.