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Recently, the amount of scientific data has been increasing because of technological advancement in measurement and high-performance computing. As the result, visualization technologies are becoming increasingly important to analyze the scientific data. Among visualization technologies, SAGE is gathering attention of scientists in these days. It not only enables the visualization of tens of million pixel-class high-resolution image but also has the potential to realize the collaboration environment where scientists can work together for their common research purpose. However, there remain still technical issues in SAGE, since it is still in the process of development. A problem of application operability, which prevents SAGE users from efficiently operating various applications on SAGE, is targeted in this paper. This problem is caused from the architectural design that SAGE users have to manage window-related operation and application-related operation from different interfaces. For solving the problem, we have developed a built-in application control module for SAGE. Our built-in application control module unifies the separate interfaces for window management and application operation. As a result, users can control application from a unified user interface, SAGE UI.

Coeur d'Alene Lake in northern Idaho is fed by two major rivers: the Coeur d'Alene River from the east and the St. Joe River from the south, with the Spokane River as its outlet to the north. This phosphorus-limited lake has been subjected to decades of mining (primarily for zinc and silver) and other anthropogenic inputs. A 32 full-factorial experimental design was used to examine the interactive effects of free (uncomplexed) zinc ion and dissolved-orthophosphate concentrations on phytoplankton that were isolated from two sites along a longitudinal zinc-concentration gradient in Coeur d'Alene Lake. The two sites displayed different dominanttaxa. Chlorella minutissima, a dominant species near the southern St. Joe River inlet, exhibited greater sensitivity to free Zn ions than Asterionella formosa, collected nearer the Coeur d'Alene River mouth with elevated dissolved-zinc concentrations. Empirical phytoplankton-response models were generated to describe phytoplankton growth in response to remediation strategies in the surrounding watershed. If dissolved Zn can be reduced in the water column from500 nM (i.e., current concentrations near and down stream of the Coeur d'Alene River plume) to3 nM (i.e., concentrations near the southern St. Joe River inlet) such that the lake is truly phosphorus limited, management of phosphorus inputs by surrounding communities will ultimately determine the limnologic state of the lake.

Beneficial treatment has not been established for chronic sensory ataxic neuropathy associated with Sjögren's syndrome (CSAN-SS). We describe two patients with CSAN-SS who clinically improved in response to D-penicillamine treatment. Their neuropathic symptoms were lessened after D-penicillamine, and the results of electrophysiologic studies support the clinical improvement. D-Penicillamine can be considered a potentially beneficial agent in the treatment of CSAN-SS.

Concentrations of many anthropogenic contaminants in the San Francisco Estuary exist at levels that have been associated with biological effects elsewhere, so there is a potential for them to cause biological effects in the Estuary. The purpose of this paper is to summarize information about biological effects on the Estuary's plankton, benthos, fish, birds, and mammals, gathered since the early 1990s, focusing on key accomplishments. These studies have been conducted at all levels of biological organization (sub-cellular through communities), but have included only a small fraction of the organisms and contaminants of concern in the region. The studies summarized provide a body of evidence that some contaminants are causing biological impacts in some biological resources in the Estuary. However, no general patterns of effects were apparent in space and time, and no single contaminant was consistently related to effects among the biota considered. These conclusions reflect the difficulty in demonstrating biological effects due specifically to contamination because there is a wide range of sensitivity to contaminants among the Estuary's many organisms. Additionally, the spatial and temporal distribution of contamination in the Estuary is highly variable, and levels of contamination covary with other environmental factors, such as freshwater inflow or sediment-type. Federal and State regulatory agencies desire to develop biological criteria to protect the Estuary's biological resources. Future studies of biological effects in San Francisco Estuary should focus on the development of meaningful indicators of biological effects, and on key organism and contaminants of concern in long-term, multifaceted studies that include laboratory and field experiments to determine cause and effect to adequately inform management and regulatory decisions.

A field study at Coeur d'Alene Lake, Idaho, USA, was conducted between October 1998 and August 2001 to examine the potential importance of sediment-water interactions on contaminant transport and to provide the first direct measurements of the benthic flux of dissolved solutes of environmental concern in this lake. Because of potential ecological effects, dissolved zinc and orthophosphate were the solutes of primary interest. Results from deployments of an in situ flux chamber indicated that benthic fluxes of dissolved Zn and orthophosphate were comparable in magnitude to riverine inputs. Tracer analyses and benthic-community metrics provided evidence that solute benthic flux were diffusion-controlled at the flux-chamber deployment sites. That is, effects of biomixing (or bioturbation) and ground-water interactions did not strongly influence benthic flux. Remediation efforts in the river might not produce desired water-quality effects in the lake because imposed shifts in concentration gradients near the sediment-water interface would generate a benthic feedback response. Therefore, development of water-quality models to justify remediation strategies requires consideration of contaminant flux between the water column and underlying sediment in basins that have been affected by long-term (decadal) anthropogenic activities.

Technologies that enable traceability for fishery products are increasing their demands. Recently proposed technologies are mainly based on disposal RF(IC) tags which are able to record information directly onto them. However, the current systems based on RF tags have problems of expensive price of tags, and weakness of reading information if applied onto surface of products containing much water, which prevents to construct practically feasible systems using the RF tags. To provide a traceability system that uses much inexpensive media and that assures as high security as the RF tags, we propose a system based on a combination of printed 2D codes and internet connection, with security control similar to on-line electronic transactions. The proposed system identifies a fishery product by giving it a unique serial ID, which is issued by a database server, and printed in 2D code onto a paper or a plastic plate, which is directly put on the product. All the trace information sent from client (producer, transporters, and retailer) via internet is associated to the ID and stored to the server. Since 2D code is able to be read by such as mobile phones with built-in camera, a consumer is able to get history of the product with a single scanning operation. For the weakness of printed codes against duplication by copying, we propose a method to identify its validity by digital encryption, along with identification by weight information. The system is assured its usability by a series of experiments conducted for the distribution of cultured flounder in Hakodate, Japan

Aqueous concentrations of nickel in the southern component of San Francisco Bay (South Bay) have periodically exceeded the water-quality criteria (8.2 ppb Ni) established in accordance with the EPA’s Clean Water Act. Nickel-rich serpentinite formations around the San Francisco Bay-estuary, particularly South Bay, are eroded, transported and accumulated in estuarine sediments, providing a natural source of nickel (Fig. 1). Although the areal coverage of these formations is not pronounced, their potential importance is suggested by the spatial distribution of serpentinite throughout nearly all watersheds surrounding South Bay. This non-anthropogenic source, as well as the intermittent exceedances in South Bay nickel concentrations, has motivated a reexamination of potential nickel-transport processes and regulatory strategies.

A 72-year-old male underwent coronary artery bypass grafting for 3 vessels disease. After the operation, the peak C-reactive protein (CRP) level was 0.85 mg/dl and CRP levels stayed very low. Forty days after the operation the patient developed a progressive median chest wound dehiscence but the bacterial cultures were negative. In spite of conventional therapies such as debridement of necrotic tissue or irrigation, the wound granulation was underdeveloped. After 6 months an epidermis had developed to cover the wound.

To investigate whether or not the pattern and extent of autonomic involvement differ between the two subtypes of Guillain-Barré syndrome (GBS), namely acute inflammatory demyelinating polyneuropathy (AIDP) and acute motor axonal neuropathy (AMAN).Head-up tilt test, R-R interval variation, plasma noradrenaline concentration, skin vasomotor reflex (SVR) and sympathetic sweat response (SSwR) were used to estimate autonomic function in seven AIDP and eight AMAN patients.Heart rate and plasma noradrenaline concentration were significantly high in the AIDP group but not in the AMAN group. Skin vasomotor reflexes were generally preserved and SSwRs were impaired in patients with severe neurological deficits for both AIDP and AMAN groups.The patterns of autonomic involvement are qualitatively different between AIDP and AMAN. Acute inflammatory demyelinating polyneuropathy is characterized by cardio-sympathetic hyperactivity, excessive or reduced sudomotor function and preserved skin vasomotor function, while AMAN is not necessarily generally associated with marked autonomic dysfunction except for the sudomotor hypofunction seen in patients with severe neurological deficits.

To explore the possible histogenesis of superficially spreading carcinoma of the esophagus, the clinicopathological features of these tumors (n = 44) were compared with those of ordinary superficial carcinoma (n = 163). Tumors of a heterogeneous histological type and having in situ carcinoma components were significantly more common (P.05), and the number of residual squamous islands was significantly greater (P0.05) in the former group than the latter. Furthermore, the tumor size was not different among in situ, intramucosal, and submucosal carcinomas of the former, whereas the tumors became larger according to the depth of invasion in the latter group. These results indicate that the collision of multiple simultaneously developing superficial tumors is a plausible histogenesis of superficially spreading carcinoma of the esophagus.

To clarify the relations of the axonal form of Guillain-Barré syndrome (GBS) to anti-ganglioside antibodies and Campylobacter jejuni infection, 86 consecutive Japanese GBS patients were studied. Electrodiagnostic criteria showed acute inflammatory demyelinating polyneuropathy in 36% of the patients and acute motor axonal neuropathy (AMAN) in 38%. Frequent anti-ganglioside antibodies were of the IgG class and against GM1 (40%), GD1a (30%), GalNAc-GD1a (17%), and GD1b (21%). Identified infections were C. jejuni (23%), cytomegalovirus (10%), Mycoplasma pneumoniae (6%), and Epstein-Barr virus (3%). There was a strong association between AMAN and IgG antibodies against GM1, GD1a, GalNAc-GD1a, or GD1b. Almost all the patients with at least one of these antibodies had the AMAN pattern or rapid resolution of conduction slowing/block possibly because of early-reversible changes on the axolemma. C. jejuni infection was frequently associated with AMAN or anti-ganglioside antibodies, but more than half of the patients with AMAN or anti-ganglioside antibodies were C. jejuni-negative. These findings suggest that the three phenomena "axonal dysfunctions (AMAN or early-reversible conduction failure)," "IgG antibodies against GM1, GD1a, GalNAc-GD1a, or GD1b," and "C. jejuni infection" are closely associated but that microorganisms other than C. jejuni frequently trigger an anti-ganglioside response and elicit axonal GBS.

Using the previously reported method of experimental localized brainstem infarct in dogs, we designed this study to elucidate sequential changes of regional cerebral blood flow (rCBF) in three separate regions of the central nervous system: the cerebral cortex, thalamus, and midbrain. The data obtained were referred to in subsequent investigations of cerebrovascular autoregulation and vasomotor reactivity to CO2. Localized brainstem infarct was produced by permanently occluding the perforators of the posterior cerebral arteries between the bilateral origins of the posterior communicating arteries. The hydrogen clearance method was applied to measure rCBF. Cerebrovascular autoregulation and CO2 reactivity were assessed in three regions 1, 3, and 5 h after vascular occlusion, respectively. Vascular occlusion resulted in a decrease of rCBF that was 65% in the midbrain and close to 30%-40% in the thalamus. However, no significant change was seen in the cerebral cortex even 5 h after vascular occlusion. Induced hypertension impaired autoregulation in the thalamus, while it was preserved in the cerebral cortex. Induced hypotension did not alter autoregulation in any of the three regions. A marked loss of CO2 reactivity was observed in the ischemic brainstem, although it was well preserved in the cerebral cortex. The results suggest that noradrenergic fibers originating from the cervical sympathetic ganglia play a main role in the cerebrovascular autoregulation in the cerebral cortex, while noradrenergic fibers possibly originating from the autonomic centers in the brainstem are responsible in the thalamus; that the noradrenergic neuron probably is not involved in the maintenance of cerebral blood flow during hypotension; and that the effect of CO2 is mediated by its direct effect on the arteriolar wall in the central nervous system.

To examine the validity of electrodiagnostic tests to help diagnosis and to evaluate disease activity of juvenile atrophy of unilateral upper limb (Hirayama's disease), we reviewed the results of nerve conduction studies, motor unit number estimates, electromyography, and somatosensory evoked potentials in consecutive 38 patients. There was selective involvement of the C8-T1 myotomes, in which motor unit loss was more prominent in the abductor digiti minimi than in the abductor pollicis brevis muscles, and F wave persistency was decreased out of proportion to the motor unit loss. These findings may help diagnosis. With respect to the disease activity and treatment, denervation potentials in the flexor carpi radialis muscle were more frequent in patients with shorter disease duration than those with longer duration. Median F wave persistency was greater in patients treated with neck brace than in patients without the treatment. These parameters can monitor the disease activity and efficacy of treatment.

The ferrite plating with applying power ultrasound waves of 19.5 kHz and 600 W enabled us to encapsulate entirely MnZn ferrite cores for transformers with Ni/sub x/Zn/sub y/Fe/sub 3-x-y/O/sub 4/ coating. Supplying a NH/sub 4/OH solution during the plating broke the limit of the solubility of Ni ions to ferrite-plated films. The electrical resistance of the NiZn ferrite increased with increasing the Ni and Zn content, reaching 2.3/spl times/10/sup 5/ /spl Omega/ cm at the composition of Ni/sub 0.24/Zn/sub 0.30/Fe/sub 2.46/O/sub 4/. The saturation magnetization was 540 emu/cm/sup 3/. The MnZn ferrite cores were successfully encapsulated with NiZn ferrite coating, resulting in the increase of their surface resistance to over 100 k/spl Omega/.

To investigate the pathophysiological role of anti-GM1 antibody in Guillain-Barré syndrome (GBS), we reviewed sequential nerve conduction studies of 345 nerves in 34 GBS patients. Statistically significant correlation between IgG anti-GM1 antibodies and electrodiagnoses was found. Sixteen IgG anti-GM1-positive patients were classified as having acute motor or acute motor sensory axonal neuropathy (AMAN or AMSAN) (12 patients), as having acute inflammatory demyelinating polyneuropathy (AIDP) (3 patients), or as undetermined (1 patient) by electrodiagnostic criteria. Besides axonal features, there was rapid resolution of conduction slowing and block. In 3 patients initially diagnosed as having AIDP, conduction slowing was resolved within days, and 1 of them and 3 AMAN patients showed markedly rapid increases in amplitudes of distal compound muscle action potentials that were not accompanied by prolonged duration and polyphasia. The time courses of conduction abnormalities were distinct from those in IgG anti-GM1-negative AIDP patients. Rapid resolution of conduction slowing and block, and the absence of remyelinating slow components, suggest that conduction failure may be caused by impaired physiological conduction at the nodes of Ranvier. Reversible conduction failure as well as axonal degeneration constitutes the pathophysiological mechanisms in IgG anti-GM1-positive GBS. In both cases, immune-mediated attack probably occurs on the axolemma of motor fibers.

We conducted a retrospective study on 711 patients with early gastric cancer. Twenty-two patients (4.0%) developed recurrent disease and 21 died of recurrence during this study. One hundred and sixty-three patients died of unrelated or unknown causes. The recurrence patterns of 22 patients were as follows: hematogeneous metastasis to the liver in 11 patients, peritoneal dissemination in 3, recurrence in the remnant stomach in 3, and in the distant lymphonodes in 1. The mean survival period of patients with recurrent disease was 50.4 months, and 7 of these patients (31.8%) died more than 5 years after surgery. A retrospective clinicopathologic evaluation of the 22 patients and 526 patients without recurrence revealed significant differences between the two groups with respect to mean age at the time of surgery (62.5 years in the recurrent group vs 57.3 years in the nonrecurrent group), tumor size (41.2 vs 30.6 mm), depth of invasion (submucosal cancer: 19 vs 256), lymphnode metastasis (11 vs 48), lymphatic (11 vs 89) and venous (7 vs 18) invasion, and operative curability (curability B: 8 vs 48). Three patients with intramucosal cancer who died of hematogenous and/or peritoneal recurrence within 7 years after surgery had neither lymphnode metastasis nor lymphatic or venous invasion, suggesting that new techniques are needed for prediction of recurrent disease in patient with early gastric cancer.

We described a-44-year old male patient with Isaacs' syndrome occurring 8 months before the recurrence of malignant thymoma. Electrophysiological examination suggested that spontaneous muscle activities were generated at the distal terminals of the motor nerves. Double filtration plasmapheresis alleviated the symptoms of neuromyotonia for a short term. Administration of valproic acid had more prolonged effects lasting for 2 months until his death from relapsed thymoma. Our results support that autoimmune mechanisms, especially humoral factors, are playing an important role in the pathogenesis of Isaacs' syndrome and that anti-convulsants therapy is important.

The aim of this study was to determine whether latent viral infection is associated with idiopathic pulmonary fibrosis (IPF), an interstitial lung disease whose aetiology remains to be elucidated. Cytomegalovirus (CMV) immunoglobulin G (IgG) and complement fixation (CF), Epstein-Barr (EB) viral capsid antigen (VCA) IgG, herpes simplex virus (HSV) IgG, adenovirus CF, and parainfluenza 3 virus haemagglutinin inhibition (HI) titres were measured in the serum from patients with pulmonary diseases. The study included five subject groups: 35 normal controls (aged (mean +/- SD) 38 +/- 17 yrs); 43 IPF (63 +/- 10 yrs), seven collagen vascular disease-related interstitial pneumonitis (CVD-IP) (62 +/- 12 yrs); 22 sarcoidosis (36 +/- 14 yrs); and 17 emphysema (66 +/- 11 yrs). Levels of CMV IgG in IPF (87.6 +/- 51.7) and CVD-IP (101.2 +/- 69.9) were significantly elevated compared to those in the control (30.9 +/- 24.1), sarcoidosis (34.4 +/- 38.3) and emphysema groups (40.3 +/- 24.6), whereas CMV immunoglobulin M (IgM) was generally below the limit of detection. Similarly, CMV CF titres in IPF and CVD-IP were elevated compared to those in other diseases. EB VCA IgG titres in IPF, CVD-IP and emphysema and HSV IgG in IPF were also elevated. In contrast, adenovirus CF and parainfluenza 3 HI titres demonstrated no significant difference among all of the groups investigated. Increases in cytomegalovirus immunoglobulin G and complement fixation titres with negative cytomegalovirus immunoglobulin M suggest that latent cytomegalovirus infection may be more prominent in idiopathic pulmonary fibrosis or collagen vascular disease-related interstitial pneumonitis. Together with the elevation of Epstein-Barr virus viral capsid antigen and herpes simplex virus immunoglobulin G in idiopathic pulmonary fibrosis and/or collagen vascular disease-related interstitial pneumonitis, it is rational to assume that these viruses may be implicated in the development of pulmonary fibrosis. Further study is necessary to investigate the relationship between latent viral infection and pulmonary fibrosis.

To assess the prevalences and neurological symptoms of destructive spondyloarthropathy (DSA) and other cervical spinal diseases in long-term hemodialysis, a questionnaire survey of the medical histories and subjective sensory-motor symptoms was taken on 191 patients undergoing dialysis for 0.2-23 years (mean 8.6 +/- 6.3) with a mean age of 56.6 +/- 11.8 years (range 23-86). Furthermore, plain radiographic examinations of the cervical spine were carried out in 90% of the patients, and neurologic examinations were also performed on 29 patients. DSA was diagnosed in 18 cases (10%): moderate narrowing of the intervertebral space (NIS-I) in 8, severe narrowing (NIS-II) in 18, ossification of posterior longitudinal ligaments (OPLL) in 6, cervical spondylosis (CS) in 12 and other abnormalities in 6; 104 cases were normal. NIS-I was considered to reflect an early stage of DSA. The age of patients with DSA (mean 61.5 +/- 10.2 years), as well as with CS, was significantly higher than the normal group (52.2 +/- 10.6; p0.001), but younger than CS (68.5 +/- 10.0). The duration of dialysis in DSA patients (mean 12.1 +/- 6.0 years) was the longest and significantly longer than normal (7.7 +/- 6.5; p0.01) and (:S patients (3.8 +/- 3.0; p0.001). Through comparative evaluations of prior histories of the diseases, such as diabetes mellitus, carpal tunnel syndrome, amyloid osteoarthropathy (AOA) and parathyroidectomy, along with large calcification of the nuchal soft tissues on plain films, it was found that DSA, in conjunction with NIS-I, correlated with only AOA (p0.05). Subjective sensory symptoms, which consisted chiefly of arthralgic type followed by polyneuritic type, were noted in 60% of all patients and 56% of DSA patients. No significant differences were evident between any two particular groups. The score of subjective motor symptoms of the lower extremities in 5 patients with myelopathy was significantly higher than that in 5 other patients without neurological disorders (p0.05). Thirty-eight percent of DSA patients showed myelopathy; the frequency was higher than those of previous similar studies (0 = 5%). In conclusion, this study demonstrated that 1) DSA occurred in 10% of dialysis patients, which was also evident in previous reports (9 = 10%); this prevalence was higher than those of CS or OPLL, 2) DSA correlated with the duration of dialysis and AOA, 3) subjective motor symptoms of the lower extremities could indicate presence of myelopathy whereas subjective sensory symptoms contributed little to differential diagnosis, and 4) a careful neurologic examination can more frequently disclose myelopathy in patients with DSA than so far believed.

We report a 23-year-old woman, who had a relapsing-remitting multiple mononeuropathy with multifocal nerve enlargement. The patient was characterized by asymmetrical, marked enlargement of multiple nerves in the arms (median and ulnar nerves) and neck (accessory nerve) bilaterally. Sequential nerve conduction studies revealed persistent demyelinative abnormalities, especially across the segment of nerve thickening. The MRI of the proximal arm confirmed the markedly enlarged median and ulnar nerves which showed high signal intensity on T2-weighted images and partial enhancement after administration of gadolinium. We consider that the patient had the clinical features of "multifocal pseudohypertrophic neuropathy" described by Adams et al, and that chronic demyelination and inflammation associated with impairment of the blood-nerve barrier might be underlying mechanisms.

A 56-year-old man was admitted to our hospital in November, 1991 because of hyperproteinemia and anemia. Total protein showed 12 g/dl and serum immunoglobulins were as follows; IgG 974 mg/dl, IgA 142 mg/dl, IgM 9270 mg/dl. M-component was identified as IgM-kappa with immunoelectrophoresis and serum viscosity indicated 6.9. Although the patient had no history of severe streptococcal infection, his serum showed very high activity of ASLO (6890 IU/ml). Bence Jones protein was detected in the urine and determined to be of kappa-type. Plasma cells occupied 43% of bone marrow nucleated cells and their cytoplasms were stained with FITC-labeled anti-IgM and anti-kappa antibodies. X-ray examination disclosed punched out lesions in the skull. Consequently, the patient was diagnosed as having IgM-myeloma. At first, VCAP regimens were given after plasmapheresis, but had no effect. Therefore, the patient was treated with CHOP protocol and the serum IgM decreased in amount and the proportion of bone marrow myeloma cells got down to 17%. ASLO titer also decreased in parallel with IgM. These findings suggest that IgM in this case had ASLO activity.

We studied the effect of double filtration and immunoadsorption plasmapheresis in Guillain-Barré syndrome retrospectively in 70 patients. Thirty three patients had plasmapheresis, of whom 23 had double filtration and 10 immunoadsorption. The rest of 37 patients consisted of a control group. Clinical disability was evaluated using the functional grading scale by Hughes. In patients having a maximum disability of grade 4 and 5, the double filtration plasmapheresis group showed statistically significant improvement at 3 months after the treatment. There was no significant difference in prognoses between the immunoadsorption plasmapheresis and control groups. In mildly-illed patients having grade 2 and 3, the prognoses were not different between the three groups. In Guillain-Barré syndrome, double filtration plasmapheresis, as well as well-established plasma exchange, had benefit for severely-illed patients.

In order to evaluate the significance of motor evoked potentials (MEPs) in central nervous system monitoring, the authors conducted two sets of experiments using feline ischemic models. Twenty-three adult mongrel cats were divided into two groups: global (n = 9) and focal ischemic (n = 14) groups. In the case of global ischemia, which was induced by hypovolemic hypotension due to blood letting, deterioration of the D wave began when the mean arterial blood pressure (MABP) approached 45 mmHg, and regional cerebral blood flow (rCBF) dropped to 40% of control. Complete disappearance of the D wave was observed below 30 mmHg in MABP and 20% of control in rCBF. In the case of focal ischemia, which was induced by transorbital occlusion of the middle cerebral artery, the percentages of rCBF at which the D wave disappeared ranged from 9 to 20%. Changes in the amplitude of the D wave--an increase and following decrease--preceded the prolongation of its latency. In contrast with the D wave I waves were too easily affected by ischemia. Moreover, rCBF at the point of disappearance of the I wave varied greatly. In conclusion, the D wave is stable in mild ischemia and is a reliable indicator of critically profound ischemia (%rCBF40%). Monitoring the D wave of MEPs seems to be a useful method for avoiding the deterioration of motor function by ischemic insult.

Several attempts have been made to detect and retrieve fetal nucleated cells including nucleated erythrocytes (NRBCs), leukocytes, and trophoblasts in maternal blood. We have recently developed a new method for non-invasive fetal DNA diagnosis from maternal blood. Peripheral blood granulocytes including NRBCs were isolated by a discontinuous density gradient method using Percoll (Pharmasia). NRBCs were found and retrieved at a single cell level using a micromanipulator under a microscope. To determine whether the origin of the NRBCs was maternal or fetal, the NRBCs were analysed by polymerase chain reaction (PCR) amplification to determine the presence of a Y-chromosome-specific repeat sequence in mothers carrying male fetuses. We were successful in predicting fetal sex accurately in 10 out of 11 samples taken from maternal blood. This new technique opens up fetal DNA diagnosis from maternal blood during the first trimester of pregnancy to the whole population because there is no risk to the fetus or the mother.

Background TH-302 is a hypoxia targeted prodrug with a hypoxia-triggered 2-nitroimidazole component designed to release the DNA alkylator, bromo-isophosphoramide mustard (Br-IPM), when reduced in severe hypoxia. A randomized Phase 2B study (NCT01144455) was conducted to assess the benefit of G + T to standard dose G as first-line therapy of PAC. Materials and methods An open-label multi-center study of two dose levels of TH-302 (240 mg/m2 or 340 mg/m2) in combination with G versus G alone (randomized 1:1:1). G (1000 mg/m2) and T were administered IV over 30-60 minutes on Days 1, 8 and 15 of a 28-day cycle. Patients on the G could crossover after progression and be randomized to a G + T arm. The primary efficacy endpoint was a comparison of progression-free survival (PFS) between the combination arms and G alone (80% power to detect 50% improvement in PFS with one-sided alpha of 10%). Summary PFS outcome has previously been reported; more detailed PFS as well as the initial overall survival (OS) data are presented. Results 214 pts were treated; 164 (77%) Stage IV and 50 (23%) Stage IIIB. Median age 65 (range 29-86); 126 M/88 F; 40% ECOG 0/60% ECOG 1. Receiving 6 or more cycles: 32% G; 45% G + T240; 55% G + T340. Median PFS was 3.6 mo in G vs 5.5 mo in G + T240 (p = 0.031) and 6.0 mo in G + T340 (p = 0.008). Poorer prognostic factors (older age, poorer performance status, reduced albumin) were associated with larger treatment effect. Median OS was 7.0 mo in G vs 9.0 in G + T240 and 9.5 mo in G + T340. RECIST best response was 12% in G vs 17% in G + T240 and 27% in G + T340. CA19-9 decreases were significantly greater G + T340. A >50% CA19-9 decrease was 52% with G vs 50% with G + T240 and 70% with G + T340. AEs leading to discontinuation were: 16% G, 15% G + T240 and 11% G + T340. Rash (45% in G + T340) and stomatitis (36% in G + T340) were greater in combination, 4 pts Grade 3 rash. Grd 3/4 thrombocytopenia were 11% G, 39% G + T240 and 59% G + T340 and Grd 3/4 neutropenia were 28% G, 56% G + T240 and 59% G + T340. Conclusions The combination of G plus TH-302 improved the efficacy of G. A TH-302 dose of 340 mg2 was identified for future studies. Skin and mucosal toxicity and myelosuppression were the most common TH-302 related AEs with no increase in treatment discontinuation. Disclosure All authors have declared no conflicts of interest.

We investigated excitability of cervical lower motoneurons in 18 patients with juvenile muscular atrophy of the distal upper limb (Hirayama's disease), by F wave analysis and electrophysiological estimation of the number of motor units in the abductor pollicis brevis muscles of the affected side. In all the 18 patients, F wave persistencies and numbers of motor units were decreased, whereas amplitudes of single motor unit potentials were increased, compared to those of age-matched normal controls. Patients in a progressive phase showed markedly decreased F wave persistencies, overwhelming the degree of decreases in numbers of motor units. In half of them, F waves were significantly increased in number during neck flexion. On the other hand, patients treated with neck brace and patients having stabilized symptoms with longer duration showed F wave persistence reduction corresponded to the degree of the motor unit loss, and no changes in F wave persistencies in a posture of neck flexion. These results suggest that the disorder is characterized by decreased excitabilities of survived cervical anterior horn cells, as well as denervation and reinnervation, presumably resulting from local compression or circulatory failure by anterior shift of the posterior dural wall during neck flexion.

We found an electromyographical proof of reconstruction of the motor nerve terminals following hyperbaric oxygen therapy. A 38-year-old man who had been partially recovered for thirty four months from acute onset paraplegia following a gastrointestinal infection developed progressive muscular atrophy and weakness of the lower limbs, and was first admitted to our hospital. Cerebrospinal fluid examination was normal and nerve conduction studies showed small compound muscle action potentials without an evidence of segmental demyelination. There were ample fibrillation potentials on electromyography. Single fiber electromyography (SFEMG) showed increased fiber density, abnormal jitter and blockings without neurogenic jitter, which were similar to findings in post-poliomyelitis syndrome. He was treated by hyperbaric oxygen consisting of two hour exposures to pressures of two atmospheres breathing 100% oxygen. These exposures continued for a month daily, and thereafter once a week for one year. Clinical improvement of the weakness and a decrease in amount of fibrillation potentials occurred on and after a month after treatment. We found significant changes on SFEMG a year later. There were increased fiber densities and decreased mean values of consecutive differences. These changes indicate diminished degeneration and enhanced regeneration of the terminal axons. We think that hyperbaric oxygen has a beneficial effect on oxygen metabolism of remaining motoneurons which may not be able to maintain excessive metabolic demands of all their sprouting axons.