Polyether toxin analysis of the top minnow (Poecilia vitatta)

A detailed toxicity analysis was performed on the top minnow utilizing the stick‐enzyme immunoassay (S‐EIA), the mouse bioassay, the guinea pig atrium assay and fluorometric HPLC. The S‐EIA test indicated 96% of the samples tested contained polyether toxins. Mice injected with acetone extractions from top minnow displayed symptoms of toxicity while the guinea pig atrium assay demonstrated the presence of a polar, Na⁺ channel inhibitor.     

Cell type-specific involvement of RIG-I in antiviral response

Toll-like receptors (TLRs) play an important role in antiviral response by recognizing viral components. Recently, a RNA helicase, RIG-I, was also suggested to recognize viral double-stranded RNA. However, how these molecules contribute to viral recognition in vivo is poorly understood. We show by gene targeting that RIG-I is essential for induction of type I interferons (IFNs) after infection with RNA viruses in fibroblasts and conventional dendritic cells (DCs). RIG-I induces type I IFNs by activating IRF3 via IkappaB kinase-related kinases. In contrast, plasmacytoid DCs, which produce large amounts of IFN-alpha, use the TLR system rather than RIG-I for viral detection. Taken together, RIG-I and the TLR system exert antiviral responses in a cell type-specific manner.     

Sesaminol from sesame seed induces apoptosis in human lymphoid leukemia Molt 4B cells

The exposure of human lymphoid leukemia Molt 4B cells to sesaminol, a component of sesame oil led to both growth inhibition and the induction of apoptosis. Morphological change showing apoptotic bodies was observed in the cells treated with sesaminol. The fragmentation of DNA by sesaminol to oligonucleosomal-sized fragments that are characteristics of apoptosis was observed to be concentration- and time-dependent. These findings suggest that growth inhibition of Molt 4B cells by sesaminol results from the induction of apoptosis in the cells.     

Effects of short-term pulmonary rehabilitation on exercise capacity and quality of life in patients with chronic obstructive pulmonary disease

Although the rehabilitation of patients with chronic obstructive pulmonary disease (COPD) improves both exercise capacity and quality of life, a standard protocol for COPD patients has not been established. To clarify whether physiologic and quality-of-life improvements can be achieved by an inpatient pulmonary rehabilitation program 5 days per week for 3 weeks, 18 patients with COPD were enrolled in a rehabilitation program. The physical exercise training regimen consisted of respiratory muscle stretch gymnastics and cycle ergometer exercise training. Pulmonary function tests, an incremental ergometer exercise test, a 6-min walking test, and a quality of life assessment by the Chronic Respiratory Questionnaire were administered before and after the program. The peak VO2, an indicator of maximal exercise capacity, did not increase, although the 6-min walking distance, an indicator of functional exercise capacity, increased significantly after rehabilitation. There was a significant improvement in the quality of life in terms of dyspnea, fatigue, and emotional state. These findings suggest that even a 3-week program may be beneficial for COPD patients. Increases in functional exercise capacity, even without an increase in maximal exercise capacity, are helpful for reducing dyspnea and improving quality of life parameters in patients with COPD.     

Interleukin-1 receptor antagonist attenuates airway hyperresponsiveness following exposure to ozone

The role of an interleukin (IL)-1 receptor antagonist (IL-1Ra) on the development of airway hyperresponsiveness (AHR) and airway inflammation following acute O(3) exposure in mice was investigated. Exposure of C57/BL6 mice to O(3) at a concentration of 2.0 ppm or filtered air for 3 h resulted in increases in airway responsiveness to inhaled methacholine (MCh) 8 and 16 h after the exposure, and an increase in neutrophils in the bronchoalveolar lavage (BAL) fluid. IL-1beta expression, assessed by gene microarray, was increased 2-fold 4 h after O(3) exposure, and returned to baseline levels by 24 h. Levels of IL-1beta in lung homogenates were also increased 8 h after O(3) exposure. Administration of (human) IL-1Ra before and after O(3) exposure prevented development of AHR and decreased BAL fluid neutrophilia. Increases in chemokine levels in lung homogenates, tumor necrosis factor-alpha, MIP-2, and keratinocyte chemoattractant following O(3) exposure were prevented by IL-1Ra. Inhalation of dexamethasone, an inhibitor of IL-1 production, blocked the development of AHR, BAL fluid neutrophilia, and decreased levels of IL-1 following O(3) exposure. In summary, acute exposure to O(3) induces AHR, neutrophilic inflammation, epithelial damage, and IL-1. An IL-1Ra effectively prevents the development of altered airway function, inflammation, and structural damage.     

High-density proteoglycan induces specific suppression of adjuvant-induced arthritis in rats.

We compared the levels of serum antibodies in male and female C57Bl/6 mice during the primary and after challenge infection with Giardia muris. Male mice began passing cysts in their faeces earlier than females, and were shedding cysts for over 60 days, while females stopped shedding cysts by day 20 after infection. In both males and females there were significant increases in parasite-specific IgM 10 and 20 days after infection. No differences in parasite-specific serum IgA were observed until 40 days after infection. Parasite-specific IgG (whole) levels were elevated on days 20 and 40 in females, while males showed no significant increases. In addition, females had a much stronger IgG2b and IgG3 response than males. After challenge with either cysts or soluble parasite protein only the females had significant increases in specific anti-parasite IgG2b. Our data show differential ability of males and females to control the infection with G. muris is paralleled by a difference in the anti-parasite serum IgG response of the mice.     

Long-term enhancement of synaptic transmission induced by veratridine in rat CA3 hippocampal neurons

Veratridine is a neurotoxin that induces persistent activation of sodium channels in excitable cells. We investigated the effects of this toxin on excitatory synaptic transmission in CA3 neurons of juvenile rat hippocampus using whole-cell patch-clamp and field-potential recordings. The population spikes evoked by electrical stimulation of the mossy fiber were gradually enhanced after washout of veratridine (0.3 microM), but they were not enhanced by the co-application of veratridine and an N-methyl-D-aspartate (NMDA) receptor antagonist (D-APV, 30 microM). When a pipette solution contained QX-314 that antagonized the effect of veratridine in the recorded neuron, oscillatory membrane depolarization appeared in the early stage during bath-application of veratridine and gradually decreased in the late stage. After washout of veratridine, however, the oscillatory depolarization was gradually restored and maintained for at least 3 h. This oscillatory depolarization was also abolished by D-APV. We suggest that the activation of NMDA receptors is involved in the veratridine-induced long-lasting enhancement in the excitatory synaptic transmission in rat CA3 hippocampal neurons.     

Comparative study of effects of cyclosporins A and G on collagen arthritis in mice

The effects of the immunosuppressive agents cyclosporin G (CsG) and cyclosporin A (CsA) on collagen arthritis were compared in mice. When administered subcutaneously daily on days 0–13 after immunization with type II collagen, CsG and CsA were both capable of suppressing the development of collagen arthritis in mice as well as the immunological response to native type II collagen in a dose-dependent manner. Histopathologically, no marked inflammatory lesions were observed in diarthroidal joints from mice treated with 100 mg/kg per day of CsA or 800 mg/kg per day of CsG. However, an analysis of dose response showed CsG to be 8 times less potent than CsA in inhibiting the development of arthritis.     

Modulation of H reflex of pretibial muscles and reciprocal Ia inhibition of soleus muscle during voluntary teeth clenching in humans

A previous study has demonstrated that the soleus H reflex is facilitated in association with voluntary teeth clenching in proportion with biting force in humans. The present study tried to elucidate the functional significance of this facilitation of the soleus H reflex, by examining 1) whether the facilitation of the H reflex is reciprocal or nonreciprocal between the ankle extensors and flexors and 2) whether the reciprocal Ia inhibition of crural muscles is facilitated or depressed in association with voluntary teeth clenching. The H reflex of the pretibial muscles was evoked by stimulation of the common peroneal nerve in seven healthy subjects with no oral dysfunction. The pretibial H reflex was facilitated in association with voluntary teeth clenching in a force-dependent manner. The facilitation started preceding the onset of electromyographic activity of the masseter muscle. Stimulation of the common peroneal nerve at low intensities subthreshold for evoking the M wave of the pretibial muscles inhibited the soleus H reflex after a short latency corresponding with a disynaptic inhibition, indicating that the reciprocal Ia inhibition was depressed in association with voluntary teeth clenching. Thus, the present study has shown that voluntary teeth clenching evokes a nonreciprocal facilitation of ankle extensor and flexor muscles and attenuated reciprocal Ia inhibition from the pretibial muscles to the soleus muscle. It is concluded that voluntary teeth clenching contributes to improve stability of stance rather than smoothness of movements.