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Biomedical subjects

Y Watahiki

Publications and source records attributed to Y Watahiki.

35 records · Page 2Linked to original sources
PubMed1992

Age-related decline of cerebral oxygen metabolism in normal population detected with positron emission tomography.

Using positron emission tomography (PET), cerebral blood flow (CBF) and cerebral metabolic rate of oxygen (CMRO2) were measured in 32 healthy volunteers aged from 27 to 67 years. In bilateral putamen, left supratemporal, left infrafrontal and left parietal cortices, CMRO2 showed a significant decline during aging. The age-related decline of CBF was seen only at the left superior temporal cortex. The mean CMRO2 was significantly lower in the elder group (over 51 years old) than in the younger group (under 50 years old), whereas no significant difference in mean CBF between the two groups. The poor correlation of CBF to the age could be explained partly by the fact that CBF is easily influenced by the physiological, psychological and/or environmental factors. The age-related changes of CMRO2 were more marked in the association cortices of the left hemisphere than in that of the right hemisphere.

Adult↗
PubMed1989

Potentiation by Lys-plasminogen of clot lysis by single or two chain urokinase-type plasminogen activator or tissue-type plasminogen activator.

Study has been made of the influence of addition of human NH2 terminal glutamic acid plasminogen (Glu-Plg) or human NH2 terminal lysine plasminogen (Lys-Plg) to normal citrated plasma upon the rate of lysis of fully crosslinked plasma clots in the presence of single or two chain urokinase type plasminogen activator (scu-PA/tcu-PA) or tissue plasminogen activator (t-PA). The specificity of any thrombolytic property was evaluated by measurement of plasma fibrinogen levels. Lys-Plg added to a concentration of 20% of normal plasma plasminogen caused 5 to 6 fold increase in the extent of lysis observed at 6 hours by 100 units/ml of scu-PA and with a small increase in fibrinogenolysis. Glu-Plg added at 20% of normal level had no influence on thrombolysis but at 50% of normal caused increased thrombolysis with rapid depletion of plasma fibrinogen. An apparently synergistic effect of addition of tcu-PA on scu-PA activity was increased by addition of plasminogen (e.g. addition of 20% Lys-Plg increased the lysis rate 4 to 5 fold over the first hour equivalent to an increase of potency of approximately three to four fold). Addition of plasminogen up to double the normal plasma concentration was observed to have no influence on clot lysis in the presence of t-PA. Plasminogen potentiated the rate of lysis by scu-PA/t-PA synergic mixtures with an approximately 1.5 to 1.9 fold increase in potency. Potentiation occurred without increase in the depletion of plasma fibrinogen.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Coagulation Tests↗
PubMed1989

Activation of pro-urokinase by plasmin: non-Michaelian kinetics indicates a mechanism of negative cooperativity.

Enzyme kinetic plots relating the initial rate of activation of pro-urokinase to urokinase by plasmin, according to the concentration of substrate, were smooth downward curves and indicated that an apparent decrease in binding affinity occurred with increase in the concentration of pro-urokinase. Such nonlinear plots were obtained with plasmin 1 and also plasmin 2. Over sections of each curve it was possible to estimate apparent kinetic constants. At the uppermost concentrations of substrate tested, these were Km 2.9 microM and kcat 35.5 min-1 for plasmin 1, and at the lowermost concentrations, Km 9.5 nM and kcat 2.0 min-1. Linear plots were obtained when the single proteolytic cleavage was made by K5-plasmin or undegraded plasmin in the presence of 1.0 mM 6-aminohexanoic acid (6-AHa). Constants were estimated for catalysis of this reaction by K5 plasmin to be Km 6.0 microM and kcat 38 min-1 (r = 0.987). The catalytic efficiency of plasmin, at the lowermost concentrations of pro-urokinase tested, was therefore 33-fold higher than that of K5-plasmin. Plotting of data for the cleavage of pro-urokinase by plasmin 1 (in the absence of 6-AHa) according to the model of Hill, gave a slope of 0.5 at the lowermost concentrations of pro-urokinase increasing to 1.0 at higher concentrations (greater than 0.3 microM); such a profile is characteristic of negative cooperativity. The rates of formation of plasmin and urokinase in a mixture containing a low concentration of plasminogen and pro-urokinase were measured and compared to those predicted by a computer program designed to calculate theoretical rates using available kinetic data. The observed rates of generation of both plasmin and urokinase coincided to those predicted from the negative cooperativity model. The mechanism of the negative cooperativity may reside in a conformational change induced by binding of pro-urokinase to the kringle structure of plasmin. This property may be of significance in controlling the fibrinolytic properties of the urokinase-type plasminogen activator system.

Allosteric Regulation↗
PubMed1989

Sympathetic skin response in diabetic neuropathy.

Sympathetic function test was undertaken using the sympathetic skin response (SSR), a technique for assessment of sudomotor activity, in 67 diabetics, and the results were compared with those from 45 age-matched normal subjects. The SSR was readily elicitable in normal subjects, but absent in six patients with diabetes. In 28 patients, the SSR was preserved, but their amplitude was below the normal range. The decrease in the SSR amplitude correlated well with a fall in motor and sensory conduction velocity. The SSR magnitude correlated well to the impaired R-R interval variation during deep breathing and the heart rate increase and the blood pressure change on standing, indicating a close correlation between the disturbance of sudomotor function and that of other sympathetic and parasympathetic functions. Most of the patients with clinical evidence of dysautonomia and with insulin treatment revealed diminished or absent SSR.

Adolescent↗
PubMed1989

[Chronic demyelinating polyradiculoneuropathy associated with malignant histiocytosis].

A case of malignant histiocytosis (MH) presenting with peripheral nerve involvement is described. A 67-year-old man initially noted left facial weakness on July 20, 1986. The symptom was improved within a week, however, two weeks later he noticed numbness in his fingers and a burning pain in his legs, which was followed by double vision and progressive weakness in all four limbs. On examination, he was found to have total ophthalmoparesis of the right eye and a trace of the left facial palsy. There was severe weakness of the leg muscles, as well as mild weakness of the arms. This was accompanied by wasting of his limbs. All tendon reflexes were absent. Planter responses were flexor. Although cutaneous sensation was intact, vibratory sense was markedly impaired in the legs below the knees. The sphincter function was mildly disturbed. The sedimentation rate was 32 mm/hr. The hemoglobin was 11.9 g/dl and the leukocyte count was 5,700/mm3. The platelet count fell to 60,000/mm3. Results of routine biochemical and radiological studies were unremarkable. The cerebrospinal fluid protein level was 129 mg/dl with a normal cell count. Motor nerve conduction study revealed marked reduction in amplitude of the compound muscle action potential, slow motor nerve conduction velocities and multifocal conduction blocks along the nerve trunks (the left ulnar nerve in the forearm, the bilateral tibial nerve in the lower leg). F-wave was absent or elicited with prolonged latency and with increased chrono-dispersion. Sensory nerve had normal or nearly normal conduction. EMG sampling showed an impaired interference pattern during voluntary contraction and a few denervation potentials at rest.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗
PubMed1987

Kinetic analyses of the activation of Glu-plasminogen by urokinase in the presence of fibrin, fibrinogen or its degradation products.

The kinetics of the activation of Glu-plasminogen (Glu-plg) and Lys-plasminogen (Lys-plg) by urokinase (UK) were studied in purified systems. The activation of plasminogen by UK in the purified systems followed Michaelis-Menten kinetics with a Michaelis constant (Km) of 1.45 microM and a catalytic rate constant (kcat) of 0.93/sec for Glu-plg as compared to 0.25 microM (Km) and 0.82/sec (kcat) for Lys-plg. In the presence of fibrin and fibrinogen or its plasmin degradation products (fragment D and fragment E), Km for Glu-plg hardly changed, whereas kcat for Glu-plg increased. Effect on increase in kcat was in the order of fibrin greater than fibrinogen greater than D greater than E. Fibrin, fibrinogen, D and E did not influence the activation of Lys-plg by UK. These results indicate that Glu-plg bound to fibrin, fibrinogen, D or E becomes easily activatable by UK. The activation of Lys-plg, however, is not influenced in the presence of fibrin, fibrinogen, D or E.

Enzyme Activation↗
PubMed1987

[Akinetic mutism from recurrent hydrocephalus: successful treatment with levodopa, bromocriptine and trihexyphenidyl].

A case of akinetic mutism was reported with reference to a marked improvement by levodopa, bromocriptine and trihexyphenidyl. A 39-year-old male, first seen on February 2, 1981, had an occipitalgia, accompanied by nausea and vomiting. For several months before this consultation, the patient had suffered from asthenopia. Brain CT scan and cerebral angiogram demonstrated internal hydrocephalus due to aqueduct stenosis of unknown etiology. After a ventriculoperitoneal shunt operation on February 20, 1981, he completely recovered. Two years and a half after the shunt insertion he had no difficulty in his daily life. He reentered the hospital on December 21, 1983, because of personality change, mental deterioration and bradykinesia. Brain CT scan showed recurrent hydrocephalus resulting from shunt blockage. Following the shunt revision, hydrocephalus was resolved. Nevertheless, the patient did not return to his previous state. And he became bed-ridden, incontinent of urine, and unable to take fluids or foods, following which he went into a state of akinetic mutism. Other neurological findings were as follows: upward gaze palsy, impaired convergence, convergence nystagmus, plastic rigidity of neck and all four limbs, and diffuse hyperreflexia with right Babinski's sign. Abnormal involuntary movement was not seen. On March 27, 1984, levodopa therapy was instituted and on April 2, trihexyphenidyl was combined with levodopa. Shortly after administration of levodopa and trihexyphenidyl, akinetic mutism began to improve, but upward gaze palsy was not affected. He began to speak and could walk unassisted by the end of July.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Release of N-terminal peptides from Glu-plasminogen by plasmin in the presence of fibrin.

The rate of plasmin-catalyzed Glu-plasminogen to Lys-plasminogen conversion was faster in the presence of fibrin than in its absence when assayed by SDS-polyacrylamide gel electrophoresis followed by quantification of stained bands by densitometer. Experiments with the isozymes Glu-plasminogen I and Glu-plasminogen II showed that plasmin-catalyzed formation of Lys-plasminogen II was especially facilitated in the presence of fibrin.

Electrophoresis, Polyacrylamide Gel↗
PubMed1986

Effects of fibrin on the enhanced activation of plasminogen by urokinase and tissue plasminogen activator: role of cross-link.

When human plasma was activated by urokinase (UK) in the presence of thrombin, thrombin plus Ca++, Ca++ or in their absence and the plasmin activity was measured by the hydrolysis of S-2251, plasmin activity was higher in the presence of cross-linked or non cross-linked plasma clot. The results of similar experiments utilizing plasma after severe exercise indicated that the hydrolysis of S-2251 by plasma containing tissue plasminogen activator (t-PA) was also higher in cross-linked or non cross-linked plasma clot. Fibrinolysis was faster in thrombin-induced plasma clot, but was later shown significantly in plasma clot induced by thrombin and Ca++, whereas practically no fibrinogenolysis was shown in plasma. When Glu-plasminogen (Glu-plg) was activated by UK in the presence of cross-linked or non cross-linked fibrin and alpha 2 antiplasmin (alpha 2AP), fibrinolysis was faster in cross-linked fibrin than non cross-linked fibrin in the presence of alpha 2AP. No fibrinogenolysis was shown either. Plasmin activity measured by the hydrolysis of S-2251 was also higher in cross-linked or non cross-linked fibrin than in fibrinogen in the presence of alpha 2AP. These results indicate that enhanced activation of Glu-plg by UK or t-PA in the presence of fibrin was a more significant event than the inactivation of plasmin in the plasma clot or purified clot by alpha 2AP cross-linked to fibrin.

Calcium↗
PubMedDate not supplied

Vascular and metabolic reserve in Alzheimer's disease.

Vascular and metabolic reserve were analyzed in probable Alzheimer's disease (AD) and vascular dementia (VaD). Cerebral blood flow (CBF), cerebral blood volume (CBV), cerebral metabolic rate of oxygen (CMRO(2)), and oxygen extraction fraction (OEF) were measured quantitatively with positron emission tomography (PET). Vascular reactivity (VR) was also calculated by comparing the CBF during 5% CO(2) inhalation with the CBF during normal breathing. Vascular transit time (VTT) that was calculated as a ratio of CBV/CBF and VR reflect vasodilating capacity of the small resistance vessels, whereas OEF designates metabolic (oxygen-extraction) reserve in threatening brain ischemia. Significant increase in OEF was seen in the parieto-temporal cortex and both VTT and VR were preserved in AD patients. By constrast, there was no significant increase in OEF whereas VTT was prolonged and VR was markedly depressed in VaD patients. The increase of OEF and preserved VTT and VR seen in AD patients indicate the possible participation of vascular factors in the pathogenesis of AD perhaps at the capillary level.

Aged↗
PubMedDate not supplied

Dramatic recovery from neurological deficits in a patient with central pontine myelinolysis following severe hyponatremia.

A 28-year-old woman developed central pontine myelinolysis (CPM) following severe hyponatremia. Radiological examinations demonstrated a characteristic pontine lesion of CPM. Her neurological symptoms (drowsiness, emotional lability, dysarthria, dysphagia, and quadriparesis) were improved dramatically by treatment with thyrotropin-releasing hormone (TRH) and rehabilitation. However, results of repeat computed tomographic (CT) scans of the brain remained unchanged. This case therefore suggests that TRH may be beneficial for the treatment of CPM, and that CT findings appear to be a limited prognostic indicator for CPM.

Abortion, Induced↗