High-power laser experiment forming a supercritical collisionless shock in a magnetized uniform plasma at rest.

We present an experimental method to generate quasiperpendicular supercritical magnetized collisionless shocks. In our experiment, ambient nitrogen (N) plasma is at rest and well magnetized, and it has uniform mass density. The plasma is pushed by laser-driven ablation aluminum (Al) plasma. Streaked optical pyrometry and spatially resolved laser collective Thomson scattering clarify structures of plasma density and temperatures, which are compared with one-dimensional particle-in-cell simulations. It is indicated that just after the laser irradiation, the Al plasma is magnetized by a self-generated Biermann battery field, and the plasma slaps the incident N plasma. The compressed external field in the N plasma reflects N ions, leading to counterstreaming magnetized N flows. Namely, we identify the edge of the reflected N ions. Such interacting plasmas form a magnetized collisionless shock.

Bradykinin directly triggers GLUT4 translocation via an insulin-independent pathway.

Physical exercise induces translocation of GLUT4 from an intracellular pool to the cell surface in skeletal muscles and increases glucose uptake via an insulin-independent pathway. However, the molecular mechanism remains to be identified. Some studies have suggested that bradykinin is locally released from contracting muscles and may be responsible for GLUT4 translocation and the increase of glucose transport in skeletal muscles. To determine whether bradykinin directly triggers GLUT4 translocation, we established L6 myotubes, 3T3-L1 adipocytes, and Chinese hamster ovary cells stably expressing c-myc epitope-tagged GLUT4 (GLUT4myc) and bradykinin B2 receptors. We found that bradykinin directly triggered GLUT4myc translocation and increased the rate of glucose uptake in a dose-dependent manner in these cells. The translocation with bradykinin occurred even after pretreatment with an islet-activating protein, wortmannin, and phorbol 12,13-dibutyrate. The signaling pathway does not seem to be mediated by Gi, phosphatidylinositol 3-kinase, or protein kinase C. It is insulin-independent and via trimeric G-protein Gq. Bradykinin is probably one of the factors responsible for exercise-stimulated glucose uptake in skeletal muscles.

Intracellular signaling in rat cultured vascular smooth muscle cells: roles of nuclear factor-kappaB and p38 mitogen-activated protein kinase on tumor necrosis factor-alpha production.

Lipopolysaccharide (LPS) is responsible for initiating host responses leading to septic shock, and tumor necrosis factor-alpha (TNF alpha) is thought to be its primary mediator. In addition, TNF alpha is one of the major components of the pathogenesis of insulin resistance in various conditions. It has been shown that LPS induced TNF alpha production in rat vascular smooth muscle cells (VSMC). However, little is known about the signaling pathway by which VSMC in culture produce TNF alpha. We investigated the possible signaling components involved in this pathway. LPS elicited phosphorylation of p42/44 mitogen-activated protein kinase (MAPK) and p38 MAPK, degradation of inhibitor of kappaB (IkappaB), and an increase in nuclear binding activity of activating protein-1 and nuclear factor-kappaB (NF-kappaB). Different types of NF-kappaB inhibitors, pyrrolidine dithiocarbamate and MG132, which specifically abolished IkappaB degradation and subsequent NF-kappaB activation by LPS, suppressed TNF alpha secretion from VSMC. Although PD98059, a specific MAPK kinase inhibitor and SB203580, a specific p38 MAPK inhibitor, had no effect on NF-kappaB activity, SB203580 suppressed TNF alpha secretion; however, PD98059 did not. A cotransfection assay showed that transfection of dominant negative IkappaB or pretreatment with SB203580 suppressed the TNF alpha gene promotor-dependent transcription. TNF alpha messenger RNA expression induced by LPS was inhibited by pyrrolidine dithiocarbamate, MG132, and SB203580, but not by PD98059. These observations indicate that TNF alpha production in VSMC is stimulated by LPS, and its transcription and translation are dependent on NF-kappaB activation through proteasome-mediated IkappaB degradation. It is likely that p38 MAPK may play a critical role in regulating transcription of the TNF alpha gene in VSMC, unlike in other cell lines.

Functional disomy for Xq26.3-qter in a boy with an unbalanced t(X;21)(q26.3;p11.2) translocation.

A nine-month-old boy, with functional disomy for Xq26-qter and multiple congenital abnormalities, is reported. The boy had severe pre- and postnatal growth retardation, profound developmental delay, hypotonia, microcephaly, agenesis of the corpus callosum, dysmorphic facial features, cryptorchidism, and left multidysplastic kidney. He developed feeding difficulties and infantile spasms. G-banding analysis of his chromosomes showed additional material on the short arm of chromosome 21. His parents refused to submit to chromosome analysis. Analysis with chromosome microdissection followed by reverse and forward chromosome painting indicated his karyotype as 46,XY,der(21)t(X;21)(q26;p11.2). This is the first description of pure functional disomy for Xq26-qter due to an unbalanced X-autosome translocation.

Recyclable characteristics of hyaluronate-polyhydroxyethyl acrylate blend hydrogel for controlled releases.

Hyaluronate-hydroxyethyl acrylate blend hydrogels which have a wide range of composition and characteristics were investigated. Glycidyl methacrylate derivatized hyaluronate (GMA-HA) were synthesized by coupling GMA to hyaluronate (HA) in the presence of a photoinduced initiator for polymerization. By copolymerizing radically GMA-HA and hydroxyethyl acrylate (HEA) under various compositions (weight ratios of HEA and GMA-HA: 1-20), GMA-HA hydrogels could be prepared in wide ranges of characteristics. These HA-PHEA gels possessed the feature that the dried ones recovered completely to the original swelling states on repeated runs, i.e. recyclable gels. The water contents of these hydrogels in equilibrium swellings in water (W(w)) were 0.99-0.86, and their viscoelastic properties were measured by a creep. The spontaneous elastic moduli were 1.05x10(5)-1.94x10(5) N m(-2), and they were mechanically tough. Their effective charge densities were estimated from the partition coefficients of sodium benzoate (NaBA) and decreased from -0.033 to -0.044 mol dm(-3) with increasing contents of HEA. Release of NaBA was studied, and the diffusion coefficients were found to be from 6.95x10(-10) to 0.12x10(-10) m(2) s(-1) with increasing the ratio of HEA. Their diffusion coefficients were found to be much less than the values estimated from the lattice model.

Overexpression of wild-type Akt1 promoted insulin-stimulated p70S6 kinase (p70S6K) activity and affected GSK3 beta regulation, but did not promote insulin-stimulated GLUT4 translocation or glucose transport in L6 myotubes.

We have developed a simple, direct and sensitive method to detect GLUT4 on the cell surface. Using this system, we found that PI3-kinase plays a key role in the signaling pathway of insulin-stimulated GLUT4 translocation. One of the down stream effectors of PI3-kinase is serine-threonine kinase Akt (protein kinase B, RAK-PK), but the involvement of Akt in insulin-stimulated GLUT4 translocation is controversial. To investigate whether Akt1 regulates insulin-stimulated GLUT4 translocation and glucose uptake in L6 myotubes, we established L6 myotubes stably expressing c-myc epitope-tagged GLUT4 (GLUT4myc) and mouse wild type (WT) Akt1. We found that overexpression of WT Akt1 promoted insulin-stimulated p70S6 kinase (p70S6K) activity and increased the basal activity of GSK3 beta, but did not promote insulin-stimulated GLUT4 translocation or glucose uptake. These data supported the result that Akt is not a main signaling molecule to transmit the signal of insulin-stimulated GLUT4 translocation or glucose uptake from insulin-activated PI3-kinase.

Peduncular hallucinosis associated with ruptured basilar-superior cerebellar artery aneurysm--case report.

A 65-year-old female developed peduncular hallucinosis 3 days after rupture of a basilar-superior cerebellar artery aneurysm. There were no neurological deficits except slight anisocoria when she first complained of hallucinations. Vasospasm of the perforating arteries to the upper brainstem, rather than direct brainstem damage caused by the bleeding, was probably the cause. Peduncular hallucinosis is possibly the only localizing sign of ruptured upper posterior circulation aneurysm.

Pediatric cerebellar infarction caused by atlantoaxial subluxation--case report.

An 11-year-old girl developed cerebellar infarction presenting as a posterior fossa mass lesion after stretching and flexing her neck. Cerebral angiography demonstrated irregular narrowing of the right vertebral artery at the C2 level and x-rays of the upper cervical spine showed atlantoaxial subluxation with os odontoideum. She underwent surgical decompression with removal of infarcted tissue. The cerebellar infarction probably resulted from occlusion of the vertebral artery, followed by brain swelling due to recanalization.

[Effect of external decompression on the development of delayed ischemic neurological deficits after subarachnoid hemorrhage].

The protective effect of a large decompressive craniectomy against delayed ischemic neurological deficits (DIND) was evaluated in patients operated on after subarachnoid hemorrhage due to a ruptured aneurysm. In 54 cases, a large decompressive craniectomy was performed (Group D), and 41 patients underwent conventional craniotomy (Group ND). Transient DIND appeared in three (17%) of the 18 Group D patients of Hunt and Kosnik grade I or II, but permanent deficits were not observed in this group. In Group ND, permanent DIND developed in seven (21%) of the 33 grade I or II patients, despite their having received the same medical care. This difference was statistically significant. However, there were no differences in outcome among patients of grades III, IV, and V. These results suggest that, at least in patients of grade I or II, a large decompressive craniectomy, performed early, will prevent DIND after subarachnoid hemorrhage. The procedure may prevent the increase in intracranial pressure and decrease in perfusion pressure brought on by vasospasm and the development of brain edema.

[Diffuse hemispheric low density on CT scan following acute interhemispheric subdural hematoma in an infant. Case report].

A 17-month-old boy was admitted to our hospital in a semicomatose state after a minor head injury. Computed tomography (CT) scans revealed a posterior interhemispheric and a thin convexity subdural hematoma. Two and a half hours later, repeated CT scans disclosed a development of the right hemispheric diffuse low density and an enlargement of the interhemispheric subdural hematoma. Decompressive craniectomy and removal of the hematoma was performed immediately. On the second postoperative day, the diffuse low density areas developed in the contralateral frontal and temporal lobes. On the 14th postoperative day, the gyri which had been low in density were markedly enhanced with contrast enhancement. On the 16th postoperative day, CT scans showed a diffuse hemispheric gyral high density with bleeding in the right parieto-occipital lobe. A right occipital lobectomy and removal of the hematoma was performed. Histological examination suggested cerebral infarction probably due to venous congestion. It is also suggested that the diffuse hemispheric gyral high density observed on the 16th postoperative day was the hemorrhagic cerebral infarction.

[Atypical computed tomographic features of meningioma: a case report].

Diagnosis of intracranial meningiomas with computed tomography (CT) is usually easy. However, some authors have reported cases preoperatively misdiagnosed because of atypical computed tomographic features. We report a case of non-cystic meningioma presenting a ring enhanced mass lesion, with CT scan. A 48-year-old male was admitted to our hospital on January 5, 1987, because of progressive monoparesis of his left lower limb. This had continued for 1 1/2 years. Neurological examination revealed monoparesis, hypesthesia and decreased deep sensation of the left lower limb. X-ray films of the skull appeared normal. A CT scan demonstrated a ring-like high density mass attached to the falx in the right frontoparietal area with perifocal low density. The ring-like high density was irregularly increased with contrast enhancement. Right carotid angiograms showed a doughnut like tumor stain without meningeal blood supply. Brain scintigrams revealed a dense round hot lesion in the frontoparietal area at 5 minutes, and the hot lesion was still visualized after 90 minutes. We diagnosed a cystic parasagittal meningioma. A right frontoparietal craniotomy was performed, and total removal of the parasagittal tumor was made. The center of the tumor was very soft but it could not be said that it was not cystic. Histologically the tumor was a meningotheliomatous meningioma. The center of the tumor, which was very soft, was necrotic with arteriolar hyalinization. The meningioma cells survived around the patent vessels. These intact meningioma cells were scattered like islands in extensive necrosis. This is so called "oasis phenomenon" indicating that the necrosis of the tumor was caused by intratumoral ischemia.(ABSTRACT TRUNCATED AT 250 WORDS)

[Anterior decompression of the thoracic spine through the posterior approach: its usefulness, indications, technique, and the preservation of postoperative spinal stability].

Three patients with thoracic myelopathy were operated on using a modified surgical approach, anterior decompression of the thoracic cord through the posterior approach. The usefulness of and indication for this approach were discussed. Operative technique is as follows. In the prone position, laminae are removed widely enough to include the medial half of the facets and pedicles. This creates cavities lateral to the dural sac as deep as the diameter of the spinal canal. Through these cavities the anterior wall of the spinal canal and the posterior portion of the intervertebral disc are drilled out to make a space into which lesions are pulled away from the dural sac. The lesions can be removed under direct vision with minimum retraction to the dural sac. Our technique preserves the integrity of the spinous processes and supra/inter spinal ligaments, which do not restrict access to the cord and have the potential to be one of the supports of the spine. Postoperative course was uneventful in all of the patients. This approach has several advantages. It can be applied to any levels of the thoracic spine and can be used for decompression all around the thoracic cord. The procedure is minimumly invasive. The indications for this operation are considered to be 1) lesions at the level of T3, 2) anterior lesions associated with OYL at the same or adjacent level, 3) multilevel lesions which need staged operations, 4) laterally protruded discs and 5) lesions in elderly or high risk patients.

[Opsoclonus-polymyoclonia syndrome suppressed with reserpine].

A 38-year-old man was admitted to Iwakuni National Hospital on July 6, 1978, with the complaints of difficulty seeing and walking. Two weeks before admission, he first experienced dizziness and it slowly progressed to uncontrollable tremor-like movements of the whole body. On admission, he was alert, oriented and afebrile. He had not experienced nausea, vomiting nor headache. He showed irregular horizontal oscillations of the eyes. Electronystagmographic study showed that this jerky eye movement appeared especially with changes of fixation of the eyes. It was also recorded during conjugate eye movement, and while he closed his eyes. He was ataxic, unable to walk, but no other abnormalities in cerebellar functions were observed. Spinal tap was performed and yielded watery clear cerebrospinal fluid containing 9/mm3 mononuclear cells. Clonazepam was given, 1.5 mg per day, for three days followed by doses of 3 mg per day. Improvement in walking was observed one week after starting the medication, when reserpine was started at a dose of 1 mg per day and increased to a dose of 1.5 mg per day in three days. One week after starting reserpine, opsoclonus improved markedly and he became able to read again. He was discharged home on September 3, 1978. Six months after admission, reserpine was decreased to 0.5 mg per day. Difficulty in reading developed within a month. Reserpine was given 1.0 mg per day and the doses was continuously given for next three months. One year after admission, he is back to his former occupation without medication. He complains of slight difficulty in reading for more than an hour, and in watching TV.(ABSTRACT TRUNCATED AT 250 WORDS)

Cloning and characterization of a short variant of the corticotropin-releasing factor receptor subtype from rat amygdala.

We have identified and characterized a cDNA encoding a novel isoform of the corticotropin-releasing factor (CRF) receptor, referred to as CRF2alpha-tr, from the rat amygdala cDNA library. The nucleotide sequence of the cloned cDNA has a structure of an alternatively spliced form of the CRF2alpha receptor, which contains unspliced introns 6 and 7 in the message, and encodes a 236-amino-acid truncated protein that comprises three unique transmembrane domains. Northern blot analysis shows that the CRF2alpha-tr receptor is more strongly expressed in the rat amygdala, thalamus, and hypothalamus than the intact CRF2alpha receptor. Western blot analysis also reveals that the CRF2alpha-tr protein can be expressed in transfected COS-7 cells as well as CRF2alpha. Furthermore, this receptor binds rat/human CRF with almost the same low affinity (Kd = 12.7 nM) as the CRF2alpha and without accumulation of intracellular cAMP. Interestingly, it does not bind sauvagine or rat urocortin. These findings suggest that this truncated CRF receptor is the major isoform of CRF2alpha receptor mRNA transcripts in the amygdala and would mediate some functions of CRF pathways in the central nervous system.