No abstract

Abstract. In the present study, we investigated the effects of angiotensin AT 1 -receptor blockers, KT3-671 and losartan, on the cardiac vagal neurotransmission in pithed rats. The bradycardia induced by vagal nerve stimulation (VNS, at 5 Hz) was potentiated significantly and dose-dependently by KT3-671 and also losartan. This enhancement effect of KT3-671 (10 mg/kg) was slightly potent than that of losartan (10 mg/kg). On the other hand, an angiotensin AT 2 -receptor blocker, PD123319 (10 mg/kg), did not affect VNS-induced bradycardia. KT3-671 and losartan did not affect the exogenous acetylcholine-evoked bradycardia. Intravenous infusion of AngII (100 ng/kg per min) attenuated the VNS-induced bradycardia. This inhibitory effect of AngII on bradycardia was restored by both KT3-671 and losartan. These results suggest that endogenous AngII can have a tonic inhibitory effect on cardiac vagal transmission by stimulating the presynaptic AT 1 receptors not AT 2 receptors. Suppression of this mechanism by the AT 1 -receptor blockers causes the facilitation of acetylcholine release from vagal nerve endings. This acceleratory effect of AT 1 -receptor blockers on cardiac vagal neurotransmission may contribute to the lack of reflex tachycardia following hypotension.

A novel marine bacterium, designated strain 4k5 T , was isolated from a sediment sample of the Pacific Ocean. The strain was Gram-stain-negative, strictly aerobic, non-motile, oxidase-positive and catalase-positive and required Na + for growth. Its major isoprenoid quinone was ubiquinone

A 68-year-old man was admitted to our hospital for cough and dyspnea. Laboratory data showed positive human T-lymphotropic virus type 1 (HTLV-1) antibody and elevated level of soluble interleukin-2 receptor (4225 U/ml). Thoracic computed tomography showed emphysema, reticular shadow, ground-glass attenuation, and subpleural consolidation (Figure 1). Bronchofiberscopy was carried out and cytologic examination of bronchoalveolar lavage fluid revealed atypical lymphocytes. These cells showed positive reaction for CD2, CD3, CD4, CD5, and CD25 and negative for CD8 in flow cytometry. Specimens of transbronchial lung biopsy showed massive infiltration of malignant lymphocytes, which were

A prospective study was made to seek for a convenient biomarker to predict progression of bone destruction (PBD) in early stages of rheumatoid arthritis (ERA). All participated patients had definite RA and their radiographic stages were mild less than stage II of the Steinbrocker classification, naïve for treatment of any DMARDs or corticosteroids. After the entry, they were treated according to the 2002 ACR management guideline for RA. The candidate biomarkers (RF-IgM, RF-IgG, CARF, ACPA, CRP, ESR, NTx, MMP-3, IL-6 and osteopontin) were measured at the entry. PBD was assessed radiographically by interval changes in the modified Sharp scores (ΔSHS) for 24 months. The associations between ΔSHS and baseline biomarkers were assessed statistically by multivariate regression analyses. Both the baseline ACPA and IL-6 levels correlated with PBD, suggesting that they could predict PBD in ERA.