BackgroundDespite being a relatively small genus, the taxonomy of the paper mulberry genus Broussonetia remains problematic. Much of the controversy is related to the identity and taxonomic status of Broussonetia kaempferi var. australis, a name treated as a synonym in the floras of Taiwan and yet accepted in the floras of China. At the generic level, the monophyly of Corner (Gard Bull Singap 19:187–252, 1962)’s concept of Broussonetia has not been tested. In recent studies of Broussonetia of Japan, lectotypes of the genus were designated and three species (B. kaempferi, Broussonetia monoica, and Broussonetia papyrifera) and a hybrid (B. ×kazinoki) were recognized. Based on the revision and molecular phylogenetic analyses, this article aims to clarify these issues.ResultsHerbarium studies, field work, and molecular phylogenetic analyses indicate that all Taiwanese materials identifiable to B. kaempferi var. australis are conspecific with B. monoica of Japan and China. Molecular phylogenetic analyses showed that Broussonetia sensu Corner (Gard Bull Singap 19:187–252, 1962) contains two clades corresponding to sect. Broussonetia and sect. Allaeanthus, with Malaisia scandens sister to sect. Broussonetia.ConclusionsBased on our analyses, B. kaempferi var. australis is treated as a synonym of B. monoica and that B. kaempferi is not distributed in Taiwan. To correct the non-monophyly of Broussonetia sensu Corner (Gard Bull Singap 19:187–252, 1962), Broussonetia is recircumscribed to contain only sect. Broussonetia and the generic status of Allaeanthus is reinstated.Electronic supplementary materialThe online version of this article (doi:10.1186/s40529-017-0165-y) contains supplementary material, which is available to authorized users.

Oropharyngeal swallowing and its coordination with respiration are affected in patients with early-stage Parkinson's disease, and safety compensation mechanisms were used more than efficiency during swallowing. The results of this study may serve as a baseline for further research into new treatment regimens and to improve the management of swallowing in patients with Parkinson's disease.

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Inflammasomes are intracellular multiple protein complexes that mount innate immune responses to tissue damage and invading pathogens. Their excessive activation is crucial in the development and pathogenesis of inflammatory disorders. Microtubules have been reported to provide the platform for mediating the assembly and activation of NLRP3 inflammasome. Recently, we have identified the microtubule-associated immune molecule guanine nucleotide exchange factor-H1 (GEF-H1) that is crucial in coupling microtubule dynamics to the initiation of microtubule-mediated immune responses. However, whether GEF-H1 also controls the activation of other immune receptors that require microtubules is still undefined. Here we employed GEF-H1-deficient mouse bone marrow-derived macrophages (BMDMs) to interrogate the impact of GEF-H1 on the activation of NLRP3 inflammasome. NLRP3 but not NLRC4 or AIM2 inflammasome-mediated IL-1β production was dependent on dynamic microtubule network in wild-type (WT) BMDMs. However, GEF-H1 deficiency did not affect NLRP3-driven IL-1β maturation and secretion in macrophages. Moreover, α-tubulin acetylation and mitochondria aggregations were comparable between WT and GEF-H1-deficient BMDMs in response to NLRP3 inducers. Further, GEF-H1 was not required for NLRP3-mediated immune defense against Salmonella typhimurium infection. Collectively, these findings suggest that the microtubule-associated immune modulator GEF-H1 is dispensable for microtubule-mediated NLRP3 activation and host defense in mouse macrophages.

Aberrant neutrophil extracellular trap (NET) formation and the loss of barrier integrity in inflamed intestinal tissues have long been associated with inflammatory bowel disease (IBD). However, whether NETs alter intestinal epithelium permeability during colitis remains elusive. Here, we demonstrated that NETs promote the breakdown in intestinal barrier function for the pathogenesis of intestinal inflammation in mouse models of colitis. NETs were abundant in the colon of mice with colitis experimentally induced by dextran sulfate sodium (DSS) or 2,4,6-trinitrobenzene sulfonic acid (TNBS). Analysis of the intestinal barrier integrity revealed that NETs impaired gut permeability, enabling the initiation of luminal bacterial translocation and inflammation. Furthermore, NETs induced the apoptosis of epithelial cells and disrupted the integrity of tight junctions and adherens junctions. Intravenous administration of DNase I, an enzyme that dissolves the web-like DNA filaments of NETs, during colitis restored the mucosal barrier integrity which reduced the dissemination of luminal bacteria, and attenuated intestinal inflammation in both DSS and TNBS models. We conclude that NETs serve a detrimental factor in the gut epithelial barrier function leading to the pathogenesis of mucosal inflammation during acute colitis.

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A method to perform exercise testing for patients with hemiplegia is unavailable though over half of them have cardio-pulmonary disorders. We aimed to assess the reliability and validity of using a stepper in cardiopulmonary exercise testing (CPET) in this population. 14 stroke patients with hemiplegia who failed to ride the stationary bike were included. Exclusion criteria included manual muscle strength ≦1 in the lower extremity, and conventional contraindications of CPET. They underwent CPET twice by using a stepper to evaluate test–retest reliability and validity. Additionally, 10 healthy participants underwent CPET twice on the cycle ergometer and stepper respectively. In the test–retest, the ratio of two-time difference to mean was 5.0, 3, 11.3 and 12.0% on average for peak oxygen consumption, peak heart rate (HR), anaerobic threshold and minute ventilation - carbonic dioxide production slope respectively. Cronbach's alpha coefficient of peak oxygen consumption and anaerobic threshold were 0.992 and 0.919. In the stepper exercise testing of the hemiplegic participants, the ratio of peak HR to age-predicted maximal HR was 75% on average. Peak respiratory exchange ratio (mean ± standard deviation = 1.17 ± 0.08) was not different from that of healthy controls (1.21 ± 0.09). Notably, VO 2 trajectory in relation to work rate is nonlinear and different in the rest-retest. This is the first research to study CPET variables in detail using stepper in patients with hemiplegia. CPET variables associated with peak are valid and reliable; nonetheless, those with sub-maximum are not. The study provides a method to do exercise testing for the patients with hemiplegia and its notice in application.