Why chronically ill children face challenges in regular classrooms: perspectives from nursing teachers in Japan.

BACKGROUND: Chronically ill children are increasingly expected to join their peers in regular classrooms. However, sometimes schools do not provide adequate assistance. This study explores nursing teachers' thoughts and experiences on integrating such students into regular classrooms in Japan. METHODS: We analysed 79 essays written by nursing teachers collectively titled 'The challenges of having chronically ill children in regular classrooms'. We conducted a qualitative study using Kinoshita's Modified Grounded Theory Approach. RESULTS: Nursing teachers identified three main obstacles: insufficient resources to support chronically ill students, parents not playing a supporting role in aiding them at school and a regular classroom not being suitable for them. However, collaborating with the children's medical staff proved successful at integrating them into regular classrooms. CONCLUSIONS: Given these obstacles, it seems very difficult for nursing teachers to lead the way toward establishing cooperative support systems for the children. Instructions from medical staff could empower teachers to set up such systems.

Disclosing haemophilia at school: strategies employed by mothers of children with haemophilia in Japan.

INTRODUCTION: Most children with haemophilia in Japan study in mainstream schools. However, many mothers have difficulty deciding whether to inform teachers of their child's haemophilia because of the accompanying potential discrimination and prejudice, particularly after the press coverage on the HIV scandal in the 1980s. AIMS: We therefore aim to explore and describe disclosure strategies of mothers of children with haemophilia. METHODS: A qualitative study was conducted using the modified grounded theory approach to explore disclosure strategies of mothers of children with haemophilia. Semi-structured interviews were conducted with 19 selected mothers (12 children were HIV positive and 7 were HIV-negative). RESULTS: In the pre-HIV/AIDS crisis period, the kind of strategy employed - full disclosure, conditional full disclosure and partial disclosure - depended on the extent of mothers' fears about mainstream schools refusing admission because of their child's haemophilia. After the HIV/AIDS crisis in the 1980s in Japan, the three categories of strategies employed by mothers of children with haemophilia were limited disclosure, non-disclosure and full disclosure. These depended on mothers' expectations of discrimination towards their child because of the social stigma around haemophilia and being HIV-positive. CONCLUSION: For children with haemophilia to feel safe attending school, public schools must establish care management and anti-discrimination systems for children with chronic diseases, thus assuring parents of their children's welfare at school.

Three-dimensional SAFT imaging for anisotropic materials using photoacoustic microscopy.

A pulsed laser illuminates a target zone that causes rapid thermoelastic expansion, generating broadband high-frequency ultrasonic wave (photoacoustic wave, PA wave). We developed a PA microscopy (PAM) with a confocal area of laser and ultrasonic wave for applications in nondestructive testing (NDT). The synthetic aperture focusing technique (SAFT) is applied in the PAM for the three-dimensional (3D) imaging of interior flaws. Here, we report proof-of-concept experiments for the NDT of a subsurface flaw in a thin laminar material. Graphical abstract (a) shows a specimen of carbon-fiber-reinforced plastic (CFRP) with an artificial delamination. Here, it should be noted that the group velocity varies directionally due to the strong anisotropy of the CFRP specimen (see Graphical abstract (b)). By considering the group velocity distribution in the SAFT, the shape and location of the subsurface delamination were accurately estimated as shown in Graphical abstract (c). Coating the surface of the CFRP specimen with a light-absorbent material improved the amplitude of the PA wave. This finding showed that the signal-to-noise ratio of the waves scattered from the flaws can be improved.

Preferential action of mexiletine on central common pathway of reentrant ventricular tachycardia.

OBJECTIVES: The action of mexiletine on diseased myocardium was assessed in reentrant ventricular tachycardia (VT). BACKGROUND: Whether class Ib antiarrhythmic agents exert a preferential action on the central common pathway of reentrant ventricular tachycardia has not yet been studied in humans. METHODS: In 10 consecutive patients (7 with a previous myocardial infarction, 3 with nonischemic disease), VT was induced and entrained with rapid pacing. The orthodromic conduction time was measured from stimulus to the entrained electrogram at the exit from the presumed central common pathway (i.e., the earliest site of activation). Mexiletine at 125 to 250 mg was administered intravenously, and when VT with the same configuration was induced, the study was repeated. The action of mexiletine on the central common pathway was assessed from the changes in VT cycle length and orthodromic conduction time. The effects on QRS complex duration, local conduction time between the exit and the pacing site and duration of the local electrogram were compared between normal and diseased myocardium. RESULTS: Mexiletine prolonged the VT cycle length in all patients, from (mean +/- SD) 316 +/- 30 to 360 +/- 64 ms (mean change 20 +/- 7%, p < 0.001); during entrainment of VT, the orthodromic conduction time was prolonged, from 306 +/- 58 to 367 +/- 89 ms (mean change 18 +/- 9%, p < 0.001). These changes were highly correlated (r = 0.95, p < 0.001). QRS duration changed little (4 +/- 3%), and local conduction time showed no change. The duration of the fragmented electrogram width was prolonged by mexiletine: from 146 +/- 50 to 176 +/- 56 ms (mean change 23 +/- 8% during VT, p < 0.001). Only a slight change occurred in the effective refractory period, both at the pacing site and at the exit. CONCLUSIONS: Mexiletine caused little change in conduction time in normal myocardium but prolonged VT cycle length, orthodromic conduction time and duration of the local electrogram at the earliest site of activation of VT. From these findings, a preferential action of mexiletine on diseased myocardium was suggested but seemed to occur only at higher frequencies during tachycardia.

Tetraethylammonium, a K+ channel blocker, inhibits interferon-gamma-induced major histocompatibility class II antigen (Ia) expression and DNA synthesis in rat astrocytes.

Astrocytes play an important role in antigen presentation to T lymphocytes by their ability to express major histocompatibility class II (Ia) antigen upon exposure to a number of agents, including interferon-gamma (IFN-gamma). Astrocytes have been shown to express a variety of voltage-sensitive ion channels including voltage-sensitive K+ channels. The function(s) of these channels in astrocyte functions is not clearly understood. In this investigation, we examined: (1) the comparative effects of mouse, rat, and human recombinant IFN-gamma (rIFN-gamma) on the induction of Ia antigen and DNA synthesis in rat astrocytes; (2) the effect of tetraethylammonium (TEA), a K+ channel blocker, on rat IFN-gamma-induced Ia expression and DNA synthesis in rat astrocytes. Our data show that all INF-gamma induce DNA synthesis in rat astrocytes but only rat and mouse and not the human IFN-gamma will induce Ia expression. TEA in a dose-dependent manner inhibited both Ia expression and DNA synthesis in rat astrocytes. The concentration kinetics of TEA with regard to maximum inhibition of Ia and DNA synthesis were different. Furthermore, these inhibitory effects were not a result of toxic or nonspecific effect of TEA on astrocytes as demonstrated by viability data and lack of any effect of tetramethylammonium, an analogue of TEA, that does not block K+ ion channels. These data suggest a role of K+ channels in Ia expression and DNA synthesis, therefore in immunological functions of astrocytes.

Absence of TrkB and insulin receptor beta in the Triton insoluble low-density fraction (raft).

Cholesterol- and glycolipid-enriched microdomains within the plasma membrane of animal cells, including neurons, have been purified and used as a low-density membrane domain after extraction with Triton X-100 (raft), or after subcellular fractionation without detergent (LDM). In this study, we compared the protein compositions in the raft and the LDM. Membrane receptors, acylated- and glycosylphosphatidylinositol (GPI)- anchored proteins were enriched in the LDM. Further treatment of the LDM with Triton X-100 excluded the membrane receptors, TrkBs and insulin receptor beta. In the presence of calcium ions, the endogenous tyrosine kinase activities in the LDM and the raft were enhanced, suggesting an important role of calcium ions in the signal transduction via the LDM and the raft.

Changes in BDNF-immunoreactive structures in the hippocampal formation of the aged macaque monkey.

We investigated the changes of brain-derived neurotrophic factor (BDNF)-immunoreactive structures in the hippocampal formation of aged macaques (Macaca fuscata fuscata). At adult stages (10 and 12 years), BDNF immunoreactivity occurred in the neurons of the dentate gyrus, the pyramidal neurons in the CA1, CA2, CA3 subfields and the subiculum, and the neurons in the CA4 subfield and the entorhinal cortex. The apical dendrites were also BDNF immunopositive. In aged monkeys (26, 30 and 32 years), the intensity of the BDNF-immunoreactivity declined significantly in cell bodies and dendrites of the neurons in the hippocampal formation except the CA2 pyramidal neurons. These findings indicate that BDNF is one of the vulnerable signal molecules during the aging process of the primate hippocampal formation.

Change of expression of full-length and truncated TrkBs in the developing monkey central nervous system.

We examined the expression of full-length TrkB (TrkBTK+) and truncated TrkB (TrkBTK-) in the central nervous system (CNS) of the macaque monkey (Macaca fascicularis) using a western blot analysis. At the adult stage, the levels of TrkBTK+ in cerebral cortices were higher than those in other structures of CNS and the expressions of TrkBTK+ in the association cortices (except area PE) were relatively lower than those in the primary cortices. In contrast, TrkBTK- in the hippocampus and the cerebellum was significantly higher than in other structures. In various developing cerebral cortices, TrkBTK+ was detected at the same levels from embryonic day 120 (E120) to the adult period. In contrast, the expression of TrkBTK- increased remarkably after the newborn stage (NB), reached the maximum level at postnatal day 60 (P60) and maintained the same level into adulthood. The peaks of TrkBTK- in the association cortices were more delayed than in the primary cortices. The expression of TrkBTK- occurred at a time that correlates with the elimination of axons and the down-regulation of neuropeptides. The present study suggests that TrkBTK- plays an important role in the axonal remodelling and that it may act as a negative effector of TrkBTK+ in the primate CNS, reducing responsiveness to BDNF and/or NT-4/5.

Development of full-length Trk B-immunoreactive structures in the hippocampal formation of the macaque monkey.

Distribution and morphological changes of cells containing the signal transducing neurotrophin receptor, full-length Trk B (fl-Trk B), were investigated in the hippocampal formation of the macaque monkey between embryonic day 140 and the adult stage. Western blot analysis showed that one main protein band, which migrated at 141 kDa, was detected in both the embryonic and adult hippocampal formation. In the pyramidal cells in CA1 and CA3 subfields, the subiculum, and the entorhinal cortex, fl-Trk B-immunoreactive dendrites were observable in the embryonic stage. In contrast, in the granule cells of the dentate gyrus, few dendrites were immunoreactive during embryonic and early developmental stages. This difference may be due to the later growth of the granule cells of the dentate gyrus. The existence of fl-Trk B immunoreactivity in the cell body and dendrites in the embryonic hippocampal neurons, suggests that BDNF and/or NT4/5 act on the hippocampal cells by autocrine/paracrine mechanisms. In the entorhinal cortex, fl-Trk B immunoreactivity became localized in the stellate cells in layer II and the pyramidal cells in layers III, V and VI in adulthood. This indicates that BDNF and/or NT4/5 are important for the maintenance of the projection neurons in the entorhinal cortex at the adult stage. The strongest fl-Trk B immunoreactivity in the hippocampal neurons occurred at postnatal month 4, corresponding to the period of greatest synapse production in the monkey hippocampus, suggesting that BDNF and/or NT4/5 with fl-Trk B may play a role in synapse formation in the monkey hippocampus.

Angular spectral approach to reflection of focused beams with oblique incidence in spherical-planar-pair lenses.

The characteristics of the output signal from spherical-planar-pair (SPP) lenses in the ultrasonic microspectrometer (UMSM) are described. The angular spectral approach is used to obtain the mathematical formula of the output signal. Although isotropic specimens are assumed, anisotropic materials can be treated as well with a small modification. A 2-D approximation is introduced to analyze the specular reflection, the Rayleigh critical angular phenomenon, and V (z) of the specular reflection. Numerical calculations are also performed for specimens with copper substrate, steel substrate, and layered structures, by numerically integrating the 2-D formulas of the output signal. It is found that a ray optical treatment is a good approximation of the wave propagation in the SPP lenses. The incident angular dependence of a reflection coefficient can be estimated by tilting the sensor unit.

[Changes of 24-h Holter monitor recordings in association with interferon alpha therapy for chronic hepatitis C].

We examined cardiovascular complication of interferon (IFN) therapy in 23 patients with chronic hepatitis C who did not have cardiac disease prospectively. Twenty four-h Holter monitor recordings were performed before and during IFN therapy. Seven of these patients (30%) showed abnormalities on their 24-h Holter monitoring recordings. Premature ventricular contraction (PVC) occurred in two patients, intermittent WPW syndrome in one, and ST-T change in four. Only one patient with PVC complained of palpitation. These complications were not severe and immediately after IFN therapy was stopped. There was no correlation between Holter ECG abnormalities and sex, age, quantity of HCV, or 2-5 oligoadenylate synthetase activity. It was suggested that cardiovascular complications caused by IFN therapy occurred more frequently than expected. However, diagnosis of these complications is difficult because most patients have no subjective symptoms and there is scarcely any change in laboratory test results. Careful observation of patients may be required during IFN therapy regardless of cardiovascular symptoms.

[Helicobacter pylori infection and eradication].

H. pylori infection is associated with various gastroduodenal diseases such as gastritis, peptic ulcer, gastric cancer, gastric MALT lymphoma. H. pylori infection is suggested that it plays a role as protective factor not promoting factor for reflux esophagitis and GERD. Epidemiological studies showed lower prevalence of H. pylori infection in reflux esophagitis and Barrett's esophagus comparing the control. Increased occurrence of reflux esophagitis after curing of H. pylori infection was reported. However, the relationship between H. pylori infection and reflux esophagitis has not been actually made clear. Also the mechanism of reflux esophagitis occurrence after H. pylori eradication is not obscure.

A new aspect of the TrkB signaling pathway in neural plasticity.

In the central nervous system (CNS), the expression of molecules is strictly regulated during development. Control of the spatiotemporal expression of molecules is a mechanism not only to construct the functional neuronal network but also to adjust the network in response to new information from outside of the individual, i.e., through learning and memory. Among the functional molecules in the CNS, one of the best-studied groups is the neurotrophins, which are nerve growth factor (NGF)-related gene family molecules. Neurotrophins include NGF, brain-derived neurotrophic factor (BDNF), neurotrophin 3 (NT-3), and NT-4/5 in the mammal. Among neurotrophins and their receptors, BDNF and tropomyosin-related kinases B (TrkB) are enriched in the CNS. In the CNS, the BDNF-TrkB signaling pathway fulfills a wide variety of functions throughout life, such as cell survival, migration, outgrowth of axons and dendrites, synaptogenesis, synaptic transmission, and remodeling of synapses. Although the same ligand and receptor, BDNF and TrkB, act in these various developmental events, we do not yet understand what kind of mechanism provokes the functional multiplicity of the BDNF-TrkB signaling pathway. In this review, we discuss the mechanism that elicits the variety of functions performed by the BDNF-TrkB signaling pathway in the CNS as a tool of pharmacological therapy.