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Biomedical subjects

Y Masana

Publications and source records attributed to Y Masana.

16 recordsLinked to original sources
PubMed1999

[Use of Ommaya CSF reservoir for refractory chronic subdural hematoma].

Ten patients with refractory chronic subdural hematoma were the subjects of this paper. All patients had severe diseases influencing the clinical course of chronic subdural hematoma, such as cerebral infarction, liver cirrhosis, thrombocytopenia, severe parkinsonism, severe heart disease, and spino-cerebellar degeneration. They were first treated in a usual manner; irrigation and drainage of the hematoma cavity. After recurrence of the hematoma, an Ommaya CSF reservoir was put into place and whenever the volume of the hematoma increased the reservoir was punctured. Postoperatively, 7 patients returned to the same conditions as they had before the onset. However, one patient died of myocardial infarction and 2 patients with parkinsonism could not maintain the condition they had before the onset of their disease, resulting in their partially dependent state. Complications were minor bleeding in one patient and an occlusion of the reservoir in another patient. By using this method reoperation was unnecessary, and the patients were able to move early in the post-operative period. This method was suitable for refractory chronic subdural hematoma with severe disease influencing its clinical course.

Aged↗
PubMed1995

Increase in plasma nitric oxide end products following rat cortical injury.

The changes in plasma nitric oxide (NO) end products, nitrite (NO2-) and nitrate (NO3-), were studied following cortical injury in rats. At 3 days after stereotactic cortical injury (day 3), plasma NO end products were significantly increased (P < 0.01), and decreased by day 7. This increase on day 3 was inhibited by a selective inhibitor of inducible NO synthase (NOS), aminoguanidine (100 mg/kg, i.p. on days 1 and 2, P < 0.001). The present study first demonstrated the temporary increase in plasma NO end products, which is attributable to the inducible NOS activation after cerebral injury.

Animals↗
PubMed1995

Reaction of microglial cells and macrophages after cortical incision in rats: effect of a synthesized free radical scavenger, (+/-)-N,N'-propylenedinicotinamide (AVS)

Reactive microglial cells and macrophages appear after trauma to the brain. To investigate the accumulation patterns of reactive microglial cells and macrophages after cortical incision, these cells were stained immunohistochemically with anti-ED1 antibody in the brain sections before and 1, 3, 5, and 7 days after incision. And to ascertain the participation of oxygen free radicals in these cellular reactions, a synthesized free radical scavenger, (+/-)-N,N'-propylenedinicotinamide (AVS) was administered in this model. Rats were administered AVS (300 mg/kg, i.p.) 30 min before, 2.5 h and every 24 h after incision (AVS group), while only saline was administered in the same manner as a control (saline group). In the saline group, both reactive microglial cells and macrophages had already appeared on day 1 post-incision. The former continued to increase in number during the following days, whereas the latter increased in number up to day 3 and thereafter decreased. Both the numbers of reactive microglial cells and macrophages were significantly decreased (P < 0.05) in the AVS group on days 5 and 7. The results suggest the participation of oxygen free radicals in the reaction of microglial cells and macrophages in traumatic brain injury.

Animals↗
PubMed1993

Localization of trkB mRNA in postnatal brain development.

We investigated the localization of trkB mRNA, which encodes a putative component of high-affinity brain-derived neurotrophic factor (BDNF) or the neurotrophin-3 (NT-3) receptor, in the postnatal rat brain by in situ hybridization histochemistry. At birth, trkB mRNA was strongly expressed in various regions with the thalamus and cerebral cortex showing the strongest expression. As the rat grows, expression generally persisted or declined in most regions with the exception of the hippocampus where trkB mRNA expression increased during postnatal development. In the adult brain, trkB mRNA was detected in the olfactory system, cerebral cortex, hippocampal formation, amygdala, and cerebellar cortex. These findings, together with the developmental profiles of BDNF and NT-3 mRNA expressions, suggest that trkB product (gp145trkB) mainly transduces NT-3 signals early in the postnatal period, and BDNF signals later in the period.

Aging↗
PubMed1993

Differential expression of two members of FGF receptor gene family, FGFR-1 and FGFR-2 mRNA, in the adult rat central nervous system.

The fibroblast growth factor (FGF) receptor gene family now contains four members that encode homologous receptor-tyrosine kinases (RTKs) to each other. We have demonstrated that one of the members, FGFR-1 (also termed as flg), is expressed in the widespread but specific neuronal populations in the adult rat central nervous system (CNS). In the present study, we examined the expression pattern of another member, FGFR-2 (also termed as bek) and compared it with that of FGFR-1. In contrast with FGFR-1, we detected FGFR-2 expression primarily in the fiber tracts of the adult rat CNS, suggesting that the oligodendrocytes are the main sites of the FGFR-2 expression. These findings indicate that FGF may regulate neurons and glial cells through different subtypes of its cognate receptor.

Animals↗
PubMed1992

Direct approach to a traumatic giant internal carotid artery aneurysm associated with a carotid-cavernous fistula. Case report.

The case is reported of a giant intracranial internal carotid artery aneurysm associated with a carotid-cavernous fistula following a closed head injury. The aneurysm and the fistula disappeared after only the neck of the aneurysm was clipped. This is the first case in which a direct surgical approach was successful in sparing the internal carotid flow. Reports of similar cases are reviewed.

Adult↗
PubMed1991

Purine catabolites in cerebral interstitial fluid during progression of and recovery from ischemia.

The concentrations of purine catabolites in the cerebral interstitial fluid during progression of and recovery from ischemia were studied using brain microdialysis and high-performance liquid chromatography. Sealed 0.5-mm hollow dialysis fibers were stereotactically implanted into either the cerebral cortex or hippocampus of ketamine anesthetized gerbils and perfused with artificial cerebrospinal fluid at 2 microliters/min. Cerebral ischemia was induced by occlusion of the bilateral common carotid arteries. The reflectance spectra of oxy- and deoxyhemoglobin at the brain surface were monitored over the scalp to assess ischemia and confirm recirculation. Ischemia caused a rapid, 4.8-fold increase in the extracellular concentration of adenosine. The progressive increase in the concentration of adenosine, inosine, and hypoxanthine soon after recirculation is particularly interesting. The subsequent decrease in purine compound concentration was rapid for adenosine but more gradual for inosine and hypoxanthine. Calculated K values for adenosine deaminase and purine nucleoside phosphorylase were 0.045/min and 0.016/min, respectively. However, no xanthine, uric acid, or purine nucleotides were found in the perfusate. These observations indicated the presence of purine catabolites in the cerebral interstitial space as well as consecutive degradation and recycling involving the interconversion of purine compounds by biochemical metabolic pathways.

Animals↗
PubMed1990

[Lymphocytic adenohypophysitis. Case report].

The patients was a 27-year-old female, gravida 0, para 0, with complaint of headache and visual disturbance for about 1 month. Ophthalmological examination showed impaired visual acuity and enlargement of Mariotte's spot on the left. A computed tomography scan disclosed an enhanced mass in the sellar and suprasellar region. Endocrinological examination revealed slight elevation of thyroxin, growth hormone, and prolactin. A trans-sphenoidal hypophysectomy was carried out with a preoperative diagnosis of nonfunctioning pituitary adenoma. Histological examination showed a marked infiltration of lymphocytes and interstitial fibrosis, diagnosed as lymphocytic adenohypophysitis. She received hormone-replacement therapy owing to postoperative hypopituitarism. Twenty-eight cases of lymphocytic adenohypophysitis including the author's are classified clinically into two types; fulminant type and chronic type. The former type occurs frequently with disturbance of consciousness because of the end organ insufficiency and proceeds to death in a fulminant course. The latter type occurs frequently with headache and visual disturbances, closely related to pregnancy and the postpartum period and survival occurs with hormone replacement therapy. This disease should be kept in mind in the diagnosis of sellar and suprasellar mass lesions.

Adenoma↗
PubMed1989

[Extracellular purine catabolites and tissue nucleotides and purine catabolites during progression and recovery of ischemia].

During progression and recovery of ischemia, extracellular purine catabolites were measured and compared with purine catabolites and adenine nucleotide levels in the tissue. Ischemia was induced by bilateral occlusion of the common carotid arteries in gerbil. Extracellular purine catabolites were sampled by in vivo brain microdialysis technique, and tissue adenine nucleotides and purine catabolites were extracted from in situ frozen and lypholized brain tissue. These metabolites were measured with simple method of isoclatic condition by HPLC system. Ischemia depleted tissue ATP and ADP, whereas AMP and purine catabolites accumulated strikingly. In parallel, extracellular purine catabolites increased as consecutive degradation on the biochemical metabolic pathway in the same animal. Levels of tissue ATP and adenosine normalized in the recovery phase of ischemia immediately. However, extracellular purine catabolites during the recovery are much higher than those during the progression of ischemia. These data indicated extracellular high levels of purine catabolites during the ischemic insult, and especially adenosine as neuromodulator which may turn off spontaneous neuronal activity and exert antiepileptic effects during the recovery rather than the progression of ischemia.

Adenine Nucleotides↗
PubMed1988

[S-adenosyl-L-methionine concentration in cerebral interstitial fluid monitored by intracerebral microdialysis].

Ketamine-anesthetized gerbils were implanted with 0.5 mm diameter microdialysis tubing through the cortex, hippocampus and thalamus with a stereotaxic instrument. The cannula was perfused with artificial cerebrospinal fluid at a flow rate of 2 microliters/min. Samples of the perfusate representing the cerebral interstitial fluid were collected and subsequently analyzed for their content of S-adenosyl-L-methionine (SAM) with high performance liquid chromatography (HPLC). In vitro tests using the dialysis cannula gave SAM recovery which varied from 3.44 +/- 0.31% (n = 3) at a perfusion flow rate of 8 microliters/min to 43.8 +/- 3.81% (n = 3) at 0.5 microliters/min (mean +/- SEM). The in vivo SAM content of the perfusate was studied and the endogenous SAM level in cerebral interstitial fluid of gerbil was 3.49 +/- 1.52 nmol per ml (n = 3). Intraperitoneal injection of SAM (250 mg/kg) produced 10-fold increases in the perfusate SAM concentration. After the experiment the brains were checked by immunopathological study using anti-albumin antibody to examine the degree of damage to the blood-brain barrier permeability. These results show that intracerebral microdialysis offers several potential advantages for studies of extracellular neurochemistry.

Animals↗
PubMed1987

[Cerebrospinal fluid concentrations of creatinine and purine metabolites determined by high performance liquid chromatography: preliminary report on head injury and stroke patients].

A prospective high performance liquid chromatography (HPLC) study was performed in eighteen patients with head injury and stroke and four control volunteers to evaluate creatinine and purine metabolites concentration (adenosine, inosine, hypoxanthine, uric acid) in cerebrospinal fluid (CSF). The present HPLC method is rapid, accurate and sensitive in the same isocratic run and no specimen pretreatment of 0.02 ml CSF is necessary. The creatinine level in CSF was increased from 122 to 169 mumol/l in some patients, and was found unrelated to that of serum. The uric acid levels varied between 5.8 and 121 mumol/l and were associated with decrease in Glasgow Coma Scale score and had a critical point of 30 mumol/l. We present initial results in application of HPLC method to measure the creatinine and purine metabolites in CSF. This preliminary report presents that these high levels in CSF of head injury and stroke patients probably reflect tissue damage and an increased tissue catabolism.

Adenosine↗