Biomedical subjects
Publications and source records attributed to H Abe.
Remote cerebral hypoperfusion associated with pontine lesions is rare. We describe a patient who showed transient ipsilateral hypoperfusion in the thalamus and cerebral cortex after a pontine infarct. This resolved within 8 days after onset. Anatomical considerations strongly suggested involvement of the cerebellothalamocortical pathway in this case.
The facial electromyographic response was monitored intraoperatively in 40 patients with hemifacial spasm who were operated on by microvascular decompression of the facial nerve. All 40 patients showed an abnormal facial electromyographic response (lateral spread response) with a latency of about 10 msec after stimulation. The abnormal response resolved before decompression in 22, resolved immediately with decompression in 16, and failed to resolve in two. Of the 38 patients in whom the abnormal response disappeared during surgery, 36 were postoperatively free from hemifacial spasm and two had mild hemifacial spasm. The two patients in whom the lateral spread response did not disappear during surgery showed persistent hemifacial spasm. In conclusion. Disappearance of the lateral spread response during surgery correlated with the absence of hemifacial spasm in the early postoperative period. The prognosis of hemifacial spasm was good in cases in whom the lateral spread response disappeared. Therefore, the authors think that intra-operative facial electromyography is very useful in assessing the efficacy of microvascular decompression and in predicting the prognosis of hemifacial spasm.
Mucus secretion is increased by various causative agents of inflammation in the mucosa. Although mucus production of the choledochal epithelial cells (except goblet cells) has never been noted in the rat in normal physiological conditions, it is seen as an inflammatory reaction in animals with choledochoenterostomy, which brings bacteria and active digestive enzymes into the common bile duct through regurgitation of intestinal contents. It is known that stagnant bile alone can cause inflammation in the mucosa of the gallbladder in patients with aseptic acalculous cholecystitis. In this study, aseptic bile stagnation was caused by choledochal dilation made by detaching the common bile duct from the hepatoduodenal ligament in five rats, and histological changes of the choledochal epithelium were observed by light and transmission electron microscopy 17 months after the operative procedure to determine whether stagnant bile could cause mucus production in choledochal epithelial cells. Mucus production was noted in two rats by light microscopy and in all the rats by transmission electron microscopy, and so it was demonstrated that stagnant bile could give rise to this phenomenon in the rat choledochal epithelium.
Hyperinsulinaemia may play a role in the development of atherosclerosis; however, the direct effect of endogenous insulin on the atherosclerotic process is not well understood. To clarify this situation we performed pancreas transplantation with systemic venous drainage in Wistar Shionogi (WS) and Spontaneous Hypertensive (SHR) rats. Both rats received syngeneic pancreaticoduodenal transplants from donor rats. SHR rats were used to observe the additive effects of both hypertension and hyperinsulinaemia on the atherosclerotic process. Peak blood insulin levels after a glucose load were approximately two times higher in transplanted rats than in non-transplanted WS and SHR rats. By contrast, there was no difference in plasma glucose responses between transplanted and non-transplanted rats. Hyperinsulinaemia was not related to dyslipidaemia and hypertension in transplanted rats. Nine months after transplantation, the cholesterol ester contents of the aortas of both WS and SHR transplanted rats were significantly higher than in the control rats (WS: 1.9 +/- 1.0 vs 3.8 +/- 2.1 mg/g dry tissue, p < 0.01; SHR: 1.7 +/- 1.3 vs 3.7 +/- 1.4 mg/g dry tissue, p < 0.05). No differences were demonstrated in the thickness of the intima or in the histology of the aortas of transplanted and control rats. To study the mechanism for cholesterol ester accumulation in the arterial wall, we measured neutral cholesterol ester hydrolase activities in vascular medial smooth muscle cells. Insulin significantly suppressed neutral cholesterol ester hydrolase activities in medial smooth muscle cells. Our results indicate that endogenous hyperinsulinaemia contributes to the development of atherosclerosis by accelerating cholesterol ester accumulation in the arterial wall.
Motor dysfunction is frequently noted in human immunodeficiency virus type 1 (HIV-1)-infected patients. Until recently, neuropathological changes found in the basal ganglia were advanced as pathogenetic mechanisms. In the present study, further brain structures involved in motor control were analyzed morphometrically. The volume density, numerical density, and the size of neurons in the cerebellar dentate nucleus and in both inferior olivary nuclei were determined. In both regions of HIV-1-infected brains, a significant reduction in the volume density, the numerical density of neurons and neuronal size was apparent. The morphometric data from the present study disclose involvement of both types of nuclei investigated during the course of HIV-1 infection, and might constitute a possible morphological substrate for the motor dysfunction seen in HIV-1-infected patients.
Carnitine palmitoyltransferase II (CPT II) deficiency has two different clinical forms, one with "hepatic" and the other with "muscular" symptoms. We studied the molecular basis of the "hepatic" form in two Japanese siblings. Their CPT II activity in lymphoblasts was reduced to 3% of the level observed in normal controls. cDNA analysis showed that the proband was a compound heterozygote. One allele carried a new mutation, G621-->A (Glu174-->Lys). The other carried three single-base substitutions; a new mutation, T1249-->A (Phe383-->Tyr), and two previously reported polymorphisms. The brother had the same four substitutions. Neither of the two new mutations in this study was detected in the 60 alleles of 30 Japanese control subjects. Secondary structure prediction analysis of the mutated CPT II protein was different from that of the normal protein. We concluded that these mutations caused the "hepatic" form of CPT II deficiency in the probands.
BACKGROUND: Recent studies have indicated that near-infrared spectroscopy (NIRS) could continuously and noninvasively observe the changes in cerebral oxygenation state during hypoxia and ischemia, using their optical properties. Its validity and usefulness during cerebrovascular surgery, however, still remain to be clarified. METHODS: Using NIRS, we continuously monitored the changes in the concentration of oxyhemoglobin, deoxyhemoglobin, and total hemoglobin ([oxy-HB], [deoxy-Hb], and [total Hb], respectively) and redox state of cytochrome oxidase (cyt ox) during carotid endarterectomy for 22 patients, and we compared the NIRS responses with those of intraoperative somatosensory evoked potentials (SEP) and regional cerebral blood flow (rCBF). RESULTS: In 9 of 22 patients, cross-clamping of the carotid artery caused a continuous decrease [oxy-Hb] and [total Hb], and an increase in [deoxy-Hb]. Cyt ox was partially reduced during the clamping. These NIRS responses demonstrated the occurrence of severe hypoxia in the ipsilateral cerebral tissue. These patients showed a marked decrease in the N20 amplitude of SEP and rCBF. In contrast, the other 13 patients did not show a significant decrease in the cerebral oxygenation state, which showed no remarkable changes in either SEP or in rCBF. CONCLUSIONS: NIRS could successfully jude the cerebral oxygenation state noninvasively during carotid surgery and was more sensitive to ischemic crisis than other indirect methods.
To investigate the effect of different etiologies of hypertension on left ventricular structure and function, we compared echocardiographic findings in 10 patients with renovascular hypertension (35 +/- 9 years), 10 patients with primary aldosteronism (42 +/- 9 years), and 14 patients with essential hypertension (41 +/- 6 years). There were no significant differences among the three groups in age, sex, body surface area, blood pressure, interventricular septal thickness, posterior wall thickness, left ventricular end-diastolic dimension or end-systolic dimension, relative wall thickness, left ventricular mass index, or spectrum of left ventricular adaptation (concentric remodeling, concentric hypertrophy, or eccentric hypertrophy). There were no differences in systolic function or diastolic function, which was assessed in terms of the peak rate of increase in dimension normalized for left ventricular end-diastolic dimension (dD/dt/D), the relaxation time, and the relaxation time to peak velocity of lengthening among groups. Multiple regression analysis showed that the systolic blood pressure was the most important determinant of left ventricular mass index (r = 0.56, P < .01), and that left ventricular mass index was the most important determinant of relaxation time and the relaxation time to peak velocity of lengthening (r = 0.48, P < .01 and r = 0.59, P < .01, respectively). The dD/dt/D was correlated only with left ventricular end-systolic dimension (r = 0.59, P < .01). Our results suggest that blood pressure may be a strong determinant of left ventricular hypertrophy, irrespective of the etiology of hypertension, and that the degree of hypertrophy may be related to left ventricular diastolic dysfunction in hypertensive patients with normal systolic function.
PURPOSE: We performed functional magnetic resonance imaging associated with brain activity to evaluate the abnormality of the visual pathway in hemianoptic patients. METHODS: We studied five patients with homonymous hemianopsia caused by retrochiasmal lesions and five control subjects. On the basis of a blood oxygenation level-dependent contrast mechanism, magnetic resonance imaging was performed with a standard clinical 1.5-tesla system. We evaluated the asymmetrically increased signal intensities in the calcarine cortex during visual stimulation and compared them with the findings of Goldmann perimetry. RESULTS: Cortical activations with a marked interhemispheric contrast of the primary visual cortex consistent with the visual field defects were observed in three of the five patients. In two of the patients without macular field preservation in the defective hemifield, functional magnetic resonance imaging showed an absence of response in the primary visual cortex of the affected side. In the patient with superior quadrantanopsia, we could detect clear laterality by selecting the imaging plane inferior to the calcarine fissure. The other two hemianoptic patients with macular sparing showed symmetric responses. CONCLUSIONS: These findings suggest that functional magnetic resonance imaging is valuable in assessing local brain function in patients with visual deficits; therefore, it is a promising method for the objective detection of abnormalities in the afferent visual system.
PURPOSE: To evaluate functional magnetic resonance imaging as an objective method for detecting visual dysfunction in various ophthalmologic disorders involving the optic nerve and the chiasm. METHODS: We performed functional magnetic resonance imaging during monocular visual stimulation on seven patients with visual field loss caused by lesions of the optic nerve and the chiasm and on three normal control subjects with no visual field loss. We correlated static threshold perimetry in the seven patients with the results of functional magnetic resonance imaging. RESULTS: In the three normal control subjects, we found good intrasubject similarity in areas of bilateral occipital lobe activation between monocular stimulation of the right and left eyes. In the patients with unilateral optic neuropathy, including glaucoma, stimulation of the affected eye induced no activation of the primary visual cortex in the portion corresponding to the central visual field defects and reduced activity of the associated visual cortex. In the patients with chiasmal compression, monocular stimulation resulted in a marked asymmetry of activation in the primary visual cortex, which corresponded to the visual field abnormality. CONCLUSIONS: Functional magnetic resonance imaging appears to be useful in confirming the clinical diagnosis of optic atrophy because it can objectively disclose visual field loss, even a small defect such as central scotoma.
Twenty-one dogs (group 1) had retrograde brain perfusion for 90 minutes through the sagittal sinus and superior vena cava with pressure-regulated cardiopulmonary bypass, and 10 dogs (group 2) had 60 minutes of circulatory arrest with an additional 30-minute evaluation of brain slices, both at 20 degrees C. In group 1, cerebral blood flow determined by laser flowmetry was 8.98 +/- 2.02 ml/100 gm/min with a driving pressure of 29.69 +/- 9.92 mm Hg during the retrograde perfusion, whereas it was 0.85 ml/100 gm/min during solitary perfusion through the superior vena cava. Retrograde cerebral vascular resistance was slightly higher than the antegrade resistance. Neutral red stain was given intraperitoneally as an intracellular pH indicator. Regional intracellular pH was calculated from photoabsorption at 440 and 535 nm with the use of color transparency photographs of the brain and spinal cord slices taken after retrograde cerebral perfusion in group 1 and after circulatory arrest in group 2. The pH mapping showed that the retrograde brain perfusion maintained the pH within 6.77 to 7.14, whereas the cerebral pH decreased to 6.24 to 6.43 at 60 minutes of circulatory arrest and further decreased to 5.81 to 6.22 at 90 minutes. The pH after the retrograde brain perfusion was significantly higher than the pH after circulatory arrest in the entire brain and the spinal cord. We conclude that the brain is protected when perfused retrogradely beyond the venous valves with a driving pressure above 20 mm Hg.
The hallmark features of rho-independent transcription terminators are a G(+)C-rich dyad symmetry sequence followed by a run of T residues on a sense strand. Both of these structural elements are required for efficient transcription termination. Besides its primary function, rho-independent terminators are also known to enhance expression of an upstream gene by stabilizing RNA in a few cases. The Escherichia coli crp gene encoding cAMP receptor protein (CRP) contains a typical rho-independent terminator. To gain further insight into the roles of the G(+)C-rich dyad symmetry sequence and the poly(T) tract both in transcription termination and mRNA stabilization, we constructed a series of variant crp terminators and analyzed their abilities regarding these two functions. Disruption of the G(+)C-rich dyad symmetry sequence almost completely eliminated terminator activity while disruption of the poly(T) tract reduced terminator activity significantly but not completely. Thus, the contribution of the G(+)C-rich dyad symmetry sequence to transcription termination is larger than that of the poly(T) tract. Disruption of the G(+)C-rich dyad symmetry region reduced expression of the upstream crp gene by accelerating the rate of mRNA degradation. However, disruption of the poly(T) sequence had no effect on the stability of the crp mRNA, indicating that the poly(T) tract plays no role in mRNA stabilization. When the crp terminator was replaced by terminators derived from other genes, the fusion genes expressed the crp mRNA at the same level as did the native crp gene, suggesting that the mRNA stabilization effect is probably a general nature of rho-independent terminators.
The synthetic hexapeptide GH-releasing peptide (His-D-Trp-Ala-Trp-D-Phe-Lys-NH2; GHRP-6) and GH releasing hormone (GHRH) are both potent stimulators of GH release in rats. Using reverse hemolytic plaque assay (RHPA), we have compared the effects of human GHRH and GHRP-6 on GH release from the dispersed individual cells of rat anterior pituitary. In a single RHPA, we quantified the percentage of plaque forming cells (% PFC) and their mean plaque area (MPA) after 30 min-incubation, and calculated a total secretion index (TSI) by multiplying % PFC and MPA. 10 nM GHRH and 100 nM GHRP-6 each caused a significant increase in % PFC (%) (GHRH 39.15, GHRP-6 29.4, vs vehicle 24.3, P < 0.01), MPA (x 10(-2) microns2) (GHRH 124.04, GHRP-6 94.80, vs vehicle 44.57, P < 0.01) and TSI (x 10(-2)) (GHRP-6 32.87, vs vehicle 10.84, P < 0.01). Simultaneous addition of both secretagogues caused a further increase in GH release (%PFC 46.4, MPA 142.55, TSI 69.82, P < 0.01 vs vehicle), although the effect was additive but not synergistic. Somatostatin analog, SMS201-995 (SMS) partially suppressed all parameters in GH secretion after stimulation by GHRH and/or GHRP-6. A double RHPA was then performed to test whether all somatotrophs respond equally to GHRH and GHRP-6 or some cells formed plaques only be either GHRH or GHRP-6. There were somatotrophs responsive to only GHRH (23.3% vs control 6.2%, P < 0.01), those responsive to only GHRP-6 (11.9% vs control 6.1%, P < 0.01), and those responsive to both GHRH and GHRP-6 (7.8% vs control 0.2%, P < 0.01). These results confirmed the previous findings that GHRP-6 and GHRH directly but independently stimulate GH release from the pituitary cells, and further suggest that presence of at least three functionally distinct somatotroph subpopulations concerning the responsiveness to GHRP-6 and GHRH in rats.
The first committed step in the formation of diterpenoids leading to gibberellin (GA) biosynthesis is the conversion of geranylgeranyl diphosphate (GGDP) to ent-kaurene. ent-Kaurene synthase A (KSA) catalyzes the conversion of GGDP to copalyl diphosphate (CDP), which is subsequently converted to ent-kaurene by ent-kaurene synthase B (KSB). A full-length KSB cDNA was isolated from developing cotyledons in immature seeds of pumpkin (Cucurbita maxima L.). Degenerate oligonucleotide primers were designed from the amino acid sequences obtained from the purified protein to amplify a cDNA fragment, which was used for library screening. The isolated full-length cDNA was expressed in Escherichia coli as a fusion protein, which demonstrated the KSB activity to cyclize [3H]CDP to [3H]ent-kaurene. The KSB transcript was most abundant in growing tissues, but was detected in every organ in pumpkin seedlings. The deduced amino acid sequence shares significant homology with other terpene cyclases, including the conserved DDXXD motif, a putative divalent metal ion-diphosphate complex binding site. A putative transit peptide sequence that may target the translated product into the plastids is present in the N-terminal region.
Two cDNAs, isolated from a Xenopus laevis embryonic library, encode proteins of 168 amino acids, both of which are 77% identical to chick cofilin and 66% identical to chick actin-depolymerizing factor (ADF), two structurally and functionally related proteins. These Xenopus ADF/cofilins (XADs) differ from each other in 12 residues spread throughout the sequence but do not differ in charge. Purified GST-fusion proteins have pH-dependent actin-depolymerizing and F-actin-binding activities similar to chick ADF and cofilin. Similarities in the developmental and tissue specific expression, embryonic localization, and in the cDNA sequence of the noncoding regions, suggest that the two XACs arise from allelic variants of the pseudotetraploid X. laevis. Immunofluorescence localization of XAC in oocyte sections with an XAC-specific monoclonal antibody shows it to be diffuse in the cortical cytoplasm. After fertilization, increased immunostaining is observed in two regions: along the membrane, particularly that of the vegetal hemisphere, and at the interface between the cortical and animal hemisphere cytoplasm. The cleavage furrow and the mid-body structure are stained at the end of first cleavage. Neuroectoderm derived tissues, notochord, somites, and epidermis stain heavily either continuously or transiently from stages 18-34. A phosphorylated form of XAC (pXAC) was identified by 2D Western blotting, and it is the only species found in oocytes. Dephosphorylation of >60% of the pXAC occurs within 30 min after fertilization. Injection of one blastomere at the 2 cell stage, either with constitutively active XAC or with an XAC inhibitory antibody, blocked cleavage of only the injected blastomere in a concentration-dependent manner without inhibiting nuclear division. The cleavage furrow of eggs injected with constitutively active XAC completely regressed. Blastomeres injected with neutralized antibody developed normally. These results suggest that XAC is necessary for cytokinesis and that its activity must be properly regulated for cleavage to occur.
Asparagus officinalis seedlings treated with either thiocarbamates or carbamates are induced to flower within 2-3 weeks of application. SDS-PAGE and 2-D PAGE resolutions of total soluble proteins of treated seedlings showed the accumulation of an acidic 17 kDa polypeptide. Partial amino acid sequence of the acidic protein showed homology to the wound-responsive A. officinalis PR 1, AoPR1. We named this protein EFP, early flowering protein, owing to its advanced appearance during the early transition from vegetative to floral phase. Carbamates and thiocarbamates that induced more than 80% flowering rates corresponded with increased level of EFP while compounds that are weak flower inducers showed reduced amount of EFP. The observation thus defined the correlationship of EFP to variable flowering rates.
Cellular schwannoma, a variant of benign schwannomas characterized by a high pseudosarcomatous cellularity, rarely involves the cranial nerves. In this report, we present the case of a 74-year-old woman with a cellular schwannoma of the VIIIth cranial nerve, which recurred from an ordinary schwannoma resected 9 years before. The tumor has been controlled for 35 months by a simple re-excision, indicating the benign nature of this tumor, although the tumor showed bone destruction and a high MiB-1 labeling ratio.
BACKGROUND: Cardiopulmonary bypass (CPB) causes a systemic inflammatory response. TNF alpha, which is a major inflammatory mediator, has been found in the circulation during and after CPB. Although previous studies have shown that heparin coating of the extracorporeal circuits reduces complement and granulocyte activation, and the inflammatory response, the possible effect of heparin coating on TNF alpha formation and the inflammatory response has not been fully investigated. METHODS: Eighteen patients scheduled for coronary artery bypass grafting were divided randomly into two groups. One group of patients had extracorporeal perfusion using heparin coated circuits (HC group, n = 9). The other group had extra-corporeal perfusion using an identical circuit that was not coated (UC group, n = 9). Blood samples were drawn before, during, and after CPB for measurement of plasma TNF alpha, plasma IL-8, neutrophil count, and neutrophil elastase. RESULTS: Plasma levels of TNF alpha increased during CPB in the UC group but not in the HC group. Plasma concentrations of IL-8 increased similarly during and after CPB in both groups. Coating the circuits with heparin did not affect the levels of IL-8. In both groups, the neutrophil count increased after the release of the aortic cross clamp and remained elevated for three days. In the HC group, however, the increase of neutrophil count was significantly lower compared with the UC group. Plasma concentrations of neutrophil elastase were significantly increased during and after CPB in both groups. However, the levels of elastase were significantly lower at certain time points in the HC group. CONCLUSION: From these observations, we conclude that heparin coating of the extracorporeal circuits reduces the TNF alpha formation during CPB, which may reduce neutrophil activation.