Influences of Soaking Temperature and Storage Conditions on Hardening of Soybeans (Glycine max) and Red Kidney Beans (Phaseolus vulgaris).

The influences of soaking treatment and storage conditions on the softening of cooked beans, namely, soybeans and red kidney beans, were investigated. It was revealed that the softening of fresh soybeans and fresh red kidney beans was suppressed during subsequent boiling after soaking treatment at 50 and 60 °C. Furthermore, in treated aged soybeans and red kidney beans that were subjected to storage at 30 °C/75% relative humidity for 6 mo and soaking treatment at 50 to 60 °C, the hardness during cooking was further amplified. This suggested that the mechanism of softening suppression differs depending on the influences of soaking and storage. Analysis of the pectin fraction in alcohol insoluble solid showed insolubilization of metal ions upon storage at high temperature and high humidity in both soybeans and red kidney beans, which suggests interaction between Ca ions and hemicellulose or cellulose as cell wall polysaccharides. The results of differential scanning calorimetry (DSC) showed that aged soybeans exhibited a shift in the thermal transition temperature of glycinin-based protein to a higher temperature compared with fresh soybeans. From the results of DSC and scanning electron microscopy for aged red kidney beans, damaged starch is not conspicuous in the raw state after storage but is abundant upon soaking treatment. As for the influence of soaking at 60 °C, it can be suggested that its influence on cell wall crosslinking was large in soybeans and red kidney beans in both a fresh state and an aged state.

[A study of children with special needs in mainstream schools and the role of nursing teachers].

OBJECTIVE: Principals of elementary schools and classroom teachers of classes for children with special needs were surveyed by questionnaire to identify the features of children with special needs in mainstream schools and the role of nursing teachers. METHODS: Subjects in Y prefecture were asked to consider several items including the following: 1) presence in class of children with special needs; 2) presence of a child with special needs who was a target of a class or a school for children with special needs; 3) presence of education for special needs experience; 4) obstacles that such children face; 5) the relation with a nursing teacher from June to August in 1998. RESULTS: 1. There was no class for children with special needs in 87 among 135 schools. Children with special needs were present in 27 out of 87 schools, and the frequency of children with special needs was about 0.3% in mainsteam classes. 2. The total number of children in classes for special needs was 177 including 142 (79.8%) with intellectual disabilities, 77 (43.3%) with complex disabilities and 61 (34.3%) requiring medical care. 3. Ninety percent of teachers of special needs classes asked a school nurse about health care for special needs and how to cope with matters relating to disabilities. 4. Ninety percent of teachers of special needs classes were concerned about matters such as the method of teaching and coping with matters relating to disabilities. CONCLUSION: The survey found that there are children with special needs in mainstream classes. The situation with the disabilities is an appreciable number of complex, so teachers of special needs classes had many concerns. Those teachers are inclined to be isolated in school. To achieve good educational outcomes for children with special needs it is important to develop a systematic network between school and experts such as medical doctors and educational professionals. Nursing teachers could play an important role in their relation, with medical specialists.

Mepenzolate bromide displays beneficial effects in a mouse model of chronic obstructive pulmonary disease.

The clinical treatment of chronic obstructive pulmonary disease (COPD) requires not only an improvement of airflow by bronchodilation but also the suppression of emphysema by controlling inflammation. Here we screen a compound library consisting of clinically used drugs for their ability to prevent elastase-induced airspace enlargement in mice. We show that intratracheal administration or inhalation of mepenzolate bromide, a muscarinic antagonist used to treat gastrointestinal disorders, decreases the severity of elastase-induced airspace enlargement and respiratory dysfunction. Although mepenzolate bromide shows bronchodilatory activity, most other muscarinic antagonists do not improve elastase-induced pulmonary disorders. Apart from suppressing elastase-induced pulmonary inflammatory responses and the production of superoxide anions, mepenzolate bromide reduces the level of cigarette smoke-induced airspace enlargement and respiratory dysfunction. Based on these results, we propose that mepenzolate bromide may be an effective therapeutic for the treatment of COPD due to its anti-inflammatory and bronchodilatory activities.

Loss of Keap1 function activates Nrf2 and provides advantages for lung cancer cell growth.

Oxidative and electrophilic stresses are sensed by Keap1, which activates Nrf2 to achieve cytoprotection by regulating the expression of drug-metabolizing and antioxidative stress enzymes/proteins. Because oxidative and electrophilic stresses cause many diseases, including cancer, we hypothesized that an abnormality in the Nrf2-Keap1 system may facilitate the growth of cancer cells. We sequenced the KEAP1 gene of 65 Japanese patients with lung cancer and identified five nonsynonymous somatic mutations at a frequency of 8%. We also identified two nonsynonymous somatic KEAP1 gene mutations and two lung cancer cell lines expressing KEAP1 at reduced levels. In lung cancer cells, low Keap1 activity (due to mutations or low-level expression) led to nuclear localization and constitutive activation of Nrf2. The latter resulted in constitutive expression of cytoprotective genes encoding multidrug resistance pumps, phase II detoxifying enzymes, and antioxidative stress enzymes/proteins. Up-regulation of these target genes in lung cancer cells led to cisplatin resistance. Nrf2 activation also stimulated growth of lung cancer-derived cell lines expressing KEAP1 at low levels and in mutant cell lines and in Keap1-null mouse embryonic fibroblasts under homeostatic conditions. Thus, inhibition of NRF2 may provide new therapeutic approaches in lung cancers with activation of Nrf2.