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Additional file 1: Figure S1. Morphology of malaria parasite during synchronization. (a���c) Plasmodium knowlesi culture, (d���f) P. falciparum culture. (a and b) mixed stages of parasites, (b and e) synchronized schizont stage, and (d and f) newly invaded ring stage. Plasmodium knowlesi synchronized schizont requires 10 h to reach the ring stage, while P. falciparum needs approximately 18 h.

Additional file 2: Figure S2. Schematic illustrations of injection cannula placements in mice used for behavior experiments. Related to Fig. 3, 4 and 5.

Additional file 1: Figure S1. Schematic illustrations of injection cannula placements in mice used for behavior experiments. Related to Figs. 1, 2.

Purpose Benign prostatic hyperplasia (BPH) impacts quality of life in men by causing lower urinary tract symptoms. α1-Adrenoceptor (α1-AR) blockers improve lower urinary tract symptoms. We investigated the efficacy of add-on therapy with α1-AR blockers on BPH rats. Methods Rats in the drug-treated groups were orally administered each drug once a day for 30 days after orchiectomy. To induce BPH, rats were castrated and testosterone (20 mg/kg) was injected subcutaneously once per day for 30 days. Cystometry was conducted to measure voiding contraction pressure and the interval contraction time, immunohistochemistry was performed to measure c-Fos and nerve growth factor (NGF) expression in the neuronal voiding centers, and nicotinamide adenine dinucleotide phosphate-diaphorase histochemistry was used to measure nitric oxide synthase (NOS) expression. Results Orchiectomy and testosterone injection decreased voiding contraction pressure and the interval contraction time, suggesting BPH symptoms. Voiding contraction pressure and the interval contraction time were greater in the group that received the combination treatment (tamsulosin with naftopidil) than in the tamsulosin monotherapy or naftopidil monotherapy groups. c-Fos, NGF, and NOS expression in the neuronal voiding centers was enhanced by BPH induction. c-Fos, NGF, and NOS expression was suppressed by the combination treatment (tamsulosin with naftopidil) to a greater extent than was the case for tamsulosin monotherapy or naftopidil monotherapy. Conclusions Combination therapy of tamsulosin and naftopidil showed greater efficacy for the treatment of BPH than tamsulosin monotherapy or naftopidil monotherapy; therefore, combination therapy can be considered as a novel therapeutic method for BPH.

Purpose Rocuronium bromide is a nondepolarizing neuromuscular blocking drug and has been used as an adjunct for relaxation or paralysis of the skeletal muscles, facilitation of endotracheal intubation, and improving surgical conditions during general anesthesia. However, intravenous injection of rocuronium bromide induces injection pain or withdrawal movement. The exact mechanism of rocuronium bromide-induced injection pain or withdrawal movement is not yet understood. We investigated whether rocuronium bromide treatment is involved in the induction of inflammation and pain in vascular endothelial cells. Methods For this study, calf pulmonary artery endothelial (CPAE) cells were used, and 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay, Western blot, nitric oxide detection, and prostaglandin E2 immunoassay were conducted. Results Rocuronium bromide treatment inhibited endothelial nitric oxide synthase and suppressed nitric oxide production in CPAE cells. Rocuronium bromide activated cyclooxygenase-2, inducible nitric oxide synthase and increased prostaglandin E2 synthesis in CPAE cells. Conclusions Rocuronium bromide induced inflammation and pain in CPAE cells. Suppressing nitric oxide production and enhancing prostaglandin E2 synthesis might be associated with rocuronium bromide-induced injection pain or withdrawal movement.

Figure S1. Uncropped western blot images for hippocampus samples related with Fig. 3a. (PDF 126 kb)

Additional file 1: Figure S1. Pv50 amino acid sequence alignment with orthologues.

Additional file 2: Figure S1. Molecular phylogenetic analysis by the maximum likelihood method.

Additional file 1. FACS analysis of invasion inhibition assay. P1, total cells of being counted; P2, single cells of being counted; P3, early rings; P4, late trophozoites and schizonts; P5, infected erythrocytes (P3â +â P4).

Additional file 1: Table S1. Origin of pv32 gene sequences from worldwide isolates.

Additional file 2. Microscopic analysis after 10Â h post-invasion. Arrows, newly rings; NI, non-immunized IgG.

Additional file 1. Pvmsa180 sequence information.

Additional file 1: Figure S1. Cytokine levels in supernatant of 72 hr splenocyte cultures of rPbMSP8-immunized BABL/C mice stimulated with PvMSP8 in vitro. (A) The levels (O.D. 450 nm) of splenocytes from mice immunized with rPvMSP8 after stimulation with 2.5 Îźg/mL of rPvMSP8. The asterisks indicate significant differences on the graph. (B) The levels of IFN-g, TNF-a, IL-2, IL-4, IL-10 cytokines from rPvMSP8-immunized mouse splenocytes stimulated with PvMSP8. Table S1. Peptide sequence information of overlapped 18-mer from the C terminus of PvMSP8. Table S2. Prevalence (% positive), 95% confidence intervals, and mean fluorescence intensity of IgG responses to rPvMSP8 in patient and healthy individual serum samples. Table S3. Prevalence, 95% confidence intervals, and normalized mean fluorescence intensity of IgG responses to rPvMSP8 in 1-month follow-up and archival sera samples.

Additional file 1. Paris of primers used to amplified the target genes.

Figure S1. A representative Western blot (left) and quantification (right) of ApCPEB4 in Aplysia pleural ganglia extracts prepared from animals exposed to 5-HT in vivo for 2Â h. Total extracts were prepared at indicated times and 20Â Îźg of proteins were blotted with anti-ApCPEB4 antibodies (left, top panel). The same extracts were also stained with Coomassie blue as loading controls (left, bottom panel). (PDF 49 kb)

In this study, a ventilation model was developed to determine a ventilation rate for the balance of heat, moisture and in a mushroom house. Internal and external temperature, relative humidity and concentration were measured and used to validate the ventilation model. The effects of various environmental factors on physiological responses of mushroom were also investigated. The verified model was simulated under the observed ventilation rates with a difference of (relative error of ) when external temperature varied 22.5 to and average ventilation rates was . The optimal conditions for mushroom growth (internal temperature , relative humidity , concentration 1,000 ppm) were used for the model application with external temperature, relative humidity and concentration of , , and 355 ppm, respectively. Thermal balance was a important factor for an optimum ventilation up to the external temperature of , while concentration balance was more important over . This suggests that humidification for moisture balance is required to maintain temperature and concentration at an optimal level by ventilation in a mushroom house.