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The genus Impatiens comprises more than 1000 species and displays enormous morphological diversity. As a taxon that is notoriously difficult to classify morphologically, the taxonomic significance of pollen morphology has been discussed in previous studies. However, there was only limited study on the evolution of palynological and macroscopic character in this genus before. In this paper, we observed pollen of 143 species of Impatiens, including all representatives of infrageneric groups and discussed their taxonomic value. Meanwhile, based on the reconstructed phylogenetic framework, we selected five pollen traits, and nine macroscopic traits including both vegetative and reproductive organs for evolutionary analysis. The character reconstruction showed that the morphology and number of aperture, granules in lumina, seed number of per capsule, number of sepals, lateral united petals connate, spur length, and phyllotaxy could be identified as unambiguous, while other characters were ambiguous in the last common ancestor of Impatiens. The results of comprehensively macroscopic characters and palynological evidence suggest that these traits experienced a complicated evolution, exhibit high levels of instability and variability and occur character multiple reversals in the evolutionary processes of Impatiens due to different selection pressures. In addition, we found that there is an evident mosaic evolution in this genus. Pollen and macroscopic character are conserved with a slower evolutionary rate in the I. subgen. Clavicarpa, however, these characters showed higher diversity with a rapid rate of evolution in the I. subgen. Impatiens. Furthermore, the relationship between floral morphology and pollinators was discussed. [ABSTRACT FROM AUTHOR]

Impatiens spiralis, a new species of Balsaminaceae from Hekou County, Yunnan, China, is described and illustrated. This new species is similar to I. hongkongensis, but differs in its obovate‐lanceolate or oblong lamina, without glands at base, spirally curved spur and dorsal petal suborbicular or oblate. Moreover, a phylogenetic analysis based on nuclear ITS and plastid atpB‐rbcL suggests that the new species should be placed in I. subg. Clavicarpa. [ABSTRACT FROM AUTHOR]

In situ growing transition metals on N‐doped carbon by atomic doping produces a class of promising alternatives to replace Pt‐based catalysts for redox reactions, yet still suffer from unsatisfactory activity and durability in acidic and basic media. Herein, a simple synthetic strategy to fabricate an MnO modifying Co‐Nx/C catalyst with high activity and robust durability is presented. The interphase engineering well controls the Co and N species in the carbon matrix, affording the material with more pyridine N and graphite N; the interaction between Co‐Nx and MnO phase is also well discussed. Accordingly, the obtained Co‐Nx/C‐MnO catalyst exhibits excellent electrocatalytic properties towards oxygen reduction reaction, achieving a half‐wave potential of 0.87 and 0.66 V versus reversible hydrogen electrode in 0.1 m KOH and 0.1 m HClO4 solutions, as well as excellent durability with only −16.9 and −12.2 mV shift after 1000 cycles, respectively. This study provides insights into the design of noble‐metal‐free electrocatalysts from the perspective of active sites and catalyst carriers. [ABSTRACT FROM AUTHOR]

Metal‐organic frameworks (MOFs) with abundant active sites, a class of materials composed of metal nodes and organic ligands, is widely used for photocatalytic degradation of pollutants. However, the rapid recombination of photoinduced carriers of MOFs limits its photocatalytic degradation performance. Herein, Ti3C2Tx nanosheets‐based NH2‐MIL‐101(Fe) hybrids with Schottky‐heterojunctions were fabricated by in situ hydrothermal assembly for improved photocatalytic activity. The photodegradation efficiencies of the NH2‐MIL‐101(Fe)/Ti3C2Tx (N‐M/T) hybrids for phenol and chlorophenol were 96.36 % and 99.83 % within 60 minutes, respectively. The N‐M/T Schottky‐heterojunction duly transferred electrons to the Ti3C2Tx nanosheets surface via built‐in electric fields, effectively suppressing the recombination of photogenerated carriers, thereby improving the photocatalytic performance of NH2‐MIL‐101(Fe). Moreover, the Fe‐mixed‐valence in the N‐M/T led to improvement in the efficiency of the in situ generated photo‐Fenton reactions, further enhancing the photocatalytic activity with more generated reactive oxygen species (ROS). The study proposes a highly effective removal of phenolic pollutants in wastewater. [ABSTRACT FROM AUTHOR]

Background and Purpose: Tacrolimus a first‐line medication used after transplantation can induce β‐cell dysfunction, causing new‐onset diabetes mellitus (NODM). Regenerating islet‐derived protein 3 gamma (Reg3g), a member of the pancreatic regenerative gene family, has been reported to improve type 1 diabetes by promoting β‐cell regeneration. We aim to investigate the role of Reg3g in reversing tacrolimus‐induced β‐cell dysfunction and NODM in mice. Experimental Approach Circulating REG3A (the human homologue of mouse Reg3g) in heart transplantation patients treated with tacrolimus was detected. The glucose‐stimulated insulin secretion and mitochondrial functions, including mitochondria membrane potential (MMP), mitochondria calcium, ATP production, oxygen consumption rate and mitochondrial morphology were investigated in β‐cells. Additionally, effects of Reg3g on tacrolimus‐induced NODM in mice were analysed. Key Results: Circulating REG3A level in heart transplantation patients with NODM significantly decreased compared with those without diabetes. Tacrolimus down‐regulated Reg3g via inhibiting STAT3‐mediated transcription activation. Moreover, Reg3g restored glucose‐stimulated insulin secretion suppressed by tacrolimus in β‐cells by improving mitochondrial functions, including increased MMP, mitochondria calcium uptake, ATP production, oxygen consumption rate and contributing to an intact mitochondrial morphology. Mechanistically, Reg3g increased accumulation of pSTAT3(Ser727) in mitochondria by activating ERK1/2‐STAT3 signalling pathway, leading to restoration of tacrolimus‐induced mitochondrial impairment. Reg3g overexpression also effectively mitigated tacrolimus‐induced NODM in mice. Conclusion and Implications: Reg3g can significantly ameliorate tacrolimus‐induced β‐cell dysfunction by restoring mitochondrial function in a pSTAT3(Ser727)‐dependent manner. Our observations identify a novel Reg3g‐mediated mechanism that is involved in tacrolimus‐induced NODM and establish the novel role of Reg3g in reversing tacrolimus‐induced β‐cell dysfunction. [ABSTRACT FROM AUTHOR]

Impatiens rapiformis (Balsaminaceae), a new species from Malipo County, Yunnan, China, is described and illustrated. The new species is superficially similar to I. apalophylla, I. malipoensis and I. guizhouensis, but differs by having cylindric or subfusiform root tuber, elliptic or obovate‐oblong leaf blades and falcate outer lateral sepals. The characters of its seed micromorphology and pollen morphology under SEM are given. A preliminary molecular phylogenetic study suggests that I. rapiformis should be placed in I. subg. Clavicarpa. [ABSTRACT FROM AUTHOR]

Background: The aim of this study was to investigate differences in clinical features and HLA genotypes between adult‐onset and childhood‐onset patients with type 1 diabetes in a Chinese population. Materials and Methods: This study enrolled 716 Han Chinese patients with type 1 diabetes from Guangdong (258 childhood‐onset and 458 adult‐onset) to compare their clinical features. Of them 214 patients with classical type 1 diabetes (100 childhood‐onset and 114 adult‐onset) were selected for HLA DR and DQ genotyping by next‐generation sequencing. Results: Adult‐onset patients were characterized by longer duration of symptoms before diagnosis, lower frequency of DKA at disease onset, less frequent autoantibody positivity, higher serum C‐peptide concentrations, and better glycemic control. These findings were replicated in the restricted cohort of 214 patients with classical type 1 diabetes. Compared with childhood‐onset patients, adult‐onset patients had a lower frequency of the DR9 haplotype, as well as lower frequency of high‐risk DR3/DR4 and DR3/DR9 genotypes, but higher frequency of DR3/DR3 genotype and DR3/X, DR4/X or DR9/X (X, non‐risk) genotypes. Conclusions: Adult‐onset type 1 diabetic patients with susceptible haplotypes (DR3, DR4 or DR9) were more likely to carry protective DR‐DQ haplotypes than childhood‐onset patients, which suggested the association between less risk DR‐DQ genotypes and the less severe clinical manifestation in adult‐onset patients. [ABSTRACT FROM AUTHOR]

Summary: Hydrogen sulphide (H2S) is the latest identified small gaseous mediator enabled by its lipophilic nature to freely permeate the biological membranes. Initially, H2S was recognized by its roles in neuronal activity and vascular relaxation, which makes it an important molecule involved in paracrine signalling pathways. Recently, the immune regulatory function of gasotransmitters, H2S in particular, is increasingly being appreciated. Endogenous H2S level has been linked to macrophage activation, polarization and inflammasome formation. Mechanistically, H2S‐induced protein S‐sulphydration suppresses several inflammatory pathways including NF‐κB and JNK signalling. Moreover, H2S serves as a potent cellular redox regulator to modulate epigenetic alterations and to promote mitochondrial biogenesis in macrophages. Here in this review, we intend to summarize the recent advancements of H2S studies in macrophages, and to discuss with focus on the therapeutic potential of H2S donors by targeting macrophages. The feasibility of H2S signalling component as a macrophage biomarker under disease conditions would be also discussed. [ABSTRACT FROM AUTHOR]

Background: Since the outbreak of 2019 novel coronavirus (severe acute respiratory syndrome coronavirus 2 [SARS‐CoV‐2]) pneumonia, thousands of patients with fever or cough were flocked into fever clinic of designated hospitals in Wuhan, China. To date, no data have ever been reported to reflect the prevalence of coronavirus disease 2019 (COVID‐19) among these outpatients. Moreover, it is almost unknown to discriminate COVID‐19 and nucleic acid negative patients based on clinical features in the fever clinics. Methods: The infectious status of SARS‐CoV‐2 was estimated among the outpatients. The epidemiological and clinical characteristics were compared between COVID‐19 and nucleic acid negative patients. Results: The nucleic acid positive rate for SARS‐CoV‐2 in the outpatients from our fever clinic was 67·1%, while the majority of patients with COVID‐19 were mild cases. The predominant initial symptom in those patients with COVID‐19 was fever (78.2%), followed by cough (15.6%). Very significantly lower number of eosinophils was characterized in patients with COVID‐19 as compared with that of nucleic acid negative patients. More importantly, the proportion of subjects with eosinophil counts lower than normal levels in patients with COVID‐19 was much higher than that of nucleic acid negative patients. Fever combined with bilateral ground‐glass opacities in computed tomography imaging and eosinophil count below the normal level are probably a valuable indicator of COVID‐19 infection in those outpatients. Conclusions: Those findings may provide critical information for the regions, such as Europe and United States that are facing the same situation as Wuhan experienced, and could be valuable to prevent those nucleic acid negative patients from misdiagnosis before antibody testing. Highlights: This article may provide critical information for the regions that are facing epidemic, and could be valuable to prevent those nucleic acid negative patients from misdiagnosis before antibody testing. [ABSTRACT FROM AUTHOR]

Although emerging data demonstrated mortality of young COVID‐19 patients, no data have reported the risk factors of mortality for these young patients, and whether obesity is a risk for young COVID‐19 patients remains unknown. We conducted a retrospective study including 13 young patients who died of COVID‐19 and 40 matched survivors. Logistic regression was employed to characterize the risk factors of mortality in young obese COVID‐19 patients. Most of the young deceased COVID‐19 patients were mild cases at the time of admission, but the disease progressed rapidly featured by a higher severity of patchy shadows (100.00% vs 48.70%; P =.006), pleural thickening (61.50% vs 12.80%; P =.012), and mild pericardial effusion (76.90% vs 0.00%; P <.001). Most importantly, the deceased patients manifested higher body mass index (odds ratio [OR] = 1.354; 95% confidence interval [CI] = 1.075‐1.704; P =.010), inflammation‐related index C‐reactive protein (OR = 1.014; 95% CI = 1.003‐1.025; P =.014), cardiac injury biomarker hs‐cTnI (OR = 1.420; 95% CI = 1.112‐1.814; P =.005), and increased coagulation activity biomarker D‐dimer (OR = 418.7; P =.047), as compared with that of survivors. Our data support that obesity could be a risk factor associated with high mortality in young COVID‐19 patients, whereas aggravated inflammatory response, enhanced cardiac injury, and increased coagulation activity are likely to be the mechanisms contributing to the high mortality. [ABSTRACT FROM AUTHOR]

Impatiens bomiensis, a new species of Balsaminaceae from Bomi County, Xizang, China, is described and illustrated. This new species is similar to Impatiens fragicolor based on morphological characters and molecular data, but differs in the shape of the lower sepal, the dorsal petal and the number of globose glands at petiole base. [ABSTRACT FROM AUTHOR]

Objectives: Hypoxia is an important risk factor for pulmonary arterial remodelling in pulmonary arterial hypertension (PAH), and the Janus kinase 2 (JAK2) is believed to be involved in this process. In the present report, we aimed to investigate the role of JAK2 in vascular smooth muscle cells during the course of PAH. Methods: Smooth muscle cell (SMC)‐specific Jak2 deficient mice and their littermate controls were subjected to normobaric normoxic or hypoxic (10% O2) challenges for 28 days to monitor the development of PAH, respectively. To further elucidate the potential mechanisms whereby JAK2 influences pulmonary vascular remodelling, a selective JAK2 inhibitor was applied to pre‐treat human pulmonary arterial smooth muscle cells (HPASMCs) for 1 hour followed by 24‐hour hypoxic exposure. Results: Mice with hypoxia‐induced PAH were characterized by the altered JAK2/STAT3 activity in pulmonary artery smooth muscle cells. Therefore, induction of Jak2 deficiency in SMCs protected mice from hypoxia‐induced increase of right ventricular systolic pressure (RVSP), right ventricular hypertrophy and pulmonary vascular remodelling. Particularly, loss of Jak2 significantly attenuated chronic hypoxia‐induced PASMC proliferation in the lungs. Similarly, blockade of JAK2 by its inhibitor, TG‐101348, suppressed hypoxia‐induced human PASMC proliferation. Upon hypoxia‐induced activation, JAK2 phosphorylated signal transducer and activator of transcription 3 (STAT3), which then bound to the CCNA2 promoter to transcribe cyclin A2 expression, thereby promoting PASMC proliferation. Conclusions: Our studies support that JAK2 could be a culprit contributing to the pulmonary vascular remodelling, and therefore, it could be a viable target for prevention and treatment of PAH in clinical settings. [ABSTRACT FROM AUTHOR]

Polycyclic aromatic hydrocarbons (PAHs), a class of ubiquitous pollutants in marine environments, exhibit moderate to high adverse effects on aquatic organisms and humans. However, the lack of PAH toxicity data for aquatic organism has limited evaluation of their ecological risks. In the present study, aquatic predicted no-effect concentrations (PNECs) of 16 priority PAHs were derived based on species sensitivity distribution models, and their probabilistic ecological risks in seawater of Liaodong Bay, Bohai Sea, China, were assessed. A quantitative structure-activity relationship method was adopted to achieve the predicted chronic toxicity data for the PNEC derivation. Good agreement for aquatic PNECs of 8 PAHs based on predicted and experimental chronic toxicity data was observed ( R2 = 0.746), and the calculated PNECs ranged from 0.011 µg/L to 205.3 µg/L. A significant log-linear relationship also existed between the octanol-water partition coefficient and PNECs derived from experimental toxicity data ( R2 = 0.757). A similar order of ecological risks for the 16 PAH species in seawater of Liaodong Bay was found by probabilistic risk quotient and joint probability curve methods. The individual high ecological risk of benzo[ a]pyrene, benzo[ b]fluoranthene, and benz[ a]anthracene needs to be determined. The combined ecological risk of PAHs in seawater of Liaodong Bay calculated by the joint probability curve method was 13.9%, indicating a high risk as a result of co-exposure to PAHs. Environ Toxicol Chem 2016;35:1587-1593. © 2015 SETAC [ABSTRACT FROM AUTHOR]

Impatiens liboensis K. M. Liu. R. P. Kuang,. new species collected from Xiaoqikong Scenic Area in southern Guizhou, China, is described and illustrated, including its seed and pollen micro-morphology. Impatiens liboensis is similar to I. chishuiensis Y. X. Xiong and I. tubulosa Hemsl., but differs by having obviously irregular underground tubers, white or pink-white flowers, lower sepal with. 1.2-1.5 cm long spur, obovate dorsal petal, and obovate-oblong or obliquely obovate lower lobes of the lateral petals with retuse apex. [ABSTRACT FROM AUTHOR]

Previous studies have consistently demonstrated that dopamine D1-like receptor ( D1-like- R) signalling is implicated in the pathogenesis of experimental autoimmune encephalomyelitis and type I diabetes. Given that allergic asthma shares certain disease aetiology similarities with autoimmune diseases, we conducted studies in OVA-induced mice aiming to address the impact of D1-like- R signalling on the pathogenesis of allergic asthma. It was noted that blockade of D1-like- R signalling provided protection for mice against OVA-induced acute asthma. Particularly, treatment of OVA-induced mice with SCH23390, a D1-like- R antagonist, significantly attenuated inflammatory infiltration in the airways along with repressed goblet cell hyperplasia and mucus production, as well as airway resistance. By contrast, administration of SKF83959, a D1-like- R agonist, displayed the opposite effect. Blockade of D1-like- R signalling impaired Th17 function, as manifested by a significant reduction of Th17 cells in the spleen and bronchoalveolar lavage fluid. Mechanistic studies revealed that D1-like- R signalling enhances B-cell activating transcription factor activity, which then transcribes the expression of RORγt, a Th17 transcription factor; accordingly, D1-like- R signalling regulates Th17 differentiation to promote the development of allergic asthma. Taken together, the data obtained in the present suggest that blockade of D1-like- R signalling could be an effective therapeutic strategy for the prevention and treatment of allergic asthma in clinical practice. [ABSTRACT FROM AUTHOR]

Although alloxan-resistant (ALR) mice share 70% of the NOD genome, ALR islets are remarkably resistant to oxidative stress and autoimmunity. Using 2D PAGE comparative analysis, we have characterized 55 proteins that are differentially expressed between the NOD and ALR islet proteome. Ten proteins were found to be highly expressed in the NOD islets. Typically, proteins associated with pancreatic inflammation and autoimmunity, such as amylase and carboxypeptidase, are highly expressed in the NOD islets. Forty-five proteins showed significantly higher expression in the ALR islets. Among these, 30 are proteins implicated in the regulation of intracellular stress including heat-shock proteins, disulfide isomerase–associated proteins, ROS detoxification enzymes, and apoptotic regulators. Our results clearly demonstrate that the 30% unique ALR genome encodes protective determinants expressed at islet levels, which render the islets of this strain of mice resistant to oxidative stress and autoimmunity. [ABSTRACT FROM AUTHOR]

The article discusses the role of high-mobility group box 1 (HMGB1) in the regulation of osteoclastogenesis that is induced by receptor activator of NF-B ligand (RANKL) in association with the receptor for advanced glycation endproducts (RAGE). The study suggests that signaling in HMGB1, a nonhistone nuclear protein, and RAGE immunoglobins appears to regulate actin cytoskeleton reorganization and have some association with inflammatory mechanisms and bone resorption.

Background We investigated the hypothesis that overexpression of indoleamine 2,3-dioxygenase (IDO) by a cardiac allograft may result in a survival advantage of the allograft by creating a tolerogenic microenvironment. Methods An adenoviral vector encoding for murine IDO cDNA (AdIDO) was transfected into murine allogeneic cardiac allografts, and transplantation was performed for evaluation of the effects of local AdIDO transfection on allograft survival. Intragraft IDO expression and lymphocytes infiltration were measured by immunohistochemical and histological analysis. Quantitative polymerase chain reaction assays, mixed lymphocyte reaction and flow cytometric analysis were employed to determine the expression of mRNA for Foxp3, IDO, pro-inflammatory cytokines, allogeneic T-cell proliferation and the proportion of CD4+CD25+Foxp3+ regulatory T cells (Tregs) from graft-infiltrating lymphocytes and splenocytes of recipients, respectively. Results Cardiac allografts transfected with AdIDO showed a significant prolonged survival compared to the control groups. Hearts treated with AdIDO exhibited considerable up-regulation of IDO expression, whereas contained significantly reduced transcript levels for interleukin (IL)-2, interferon-γ and IL-17. These T cells isolated from allografts pre-treated with AdIDO displayed a dramatic reduction of proliferation capacity to alloantigen stimuli and had a significant higher proportion of Tregs compared to the control, as demonstrated by an increase of Foxp3 expression in allografts pre-treated with AdIDO compared to control groups. Conclusions Overexpression of IDO significantly delays cardiac allograft acute rejection by shaping the types of T-cell responses elicited by alloantigen stimuli. Copyright © 2008 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

Susceptibility to type 1 diabetes (T1D) is determined by interactions of multiple genes with unknown environmental factors. Despite the characterization of over 20 susceptibility regions for T1D, identification of specific genes in these regions is still a formidable challenge. In 2004, we first reported the cloning of a novel, small ubiquitin-like modifier ( SUMO) gene, SUMO4, in the IDDM5 interval on chromosome 6q25, and presented strong genetic and functional evidence suggesting that SUMO4 is a T1D susceptibility gene. Subsequent studies have consistently confirmed this association in multiple Asian populations despite controversial observations in Caucasians. In this review, we will update the genetic evidence supporting SUMO4 as a T1D susceptibility gene and discuss the possible explanations for the discrepant associations observed in Caucasians. We will then discuss the mechanisms through which SUMO4 contributes to the pathogenesis of T1D. Copyright © 2007 John Wiley & Sons, Ltd. [ABSTRACT FROM AUTHOR]

Genomewide linkage analyses since the early 1990s suggested over 20 genomic intervals that may contain susceptibility genes for type 1 diabetes. However, the identification of the specific genes in these intervals presents a formidable challenge due to a number of difficulties associated with genetic mapping and cloning of genes implicated in complex diseases. One of the difficulties is due to the presence of many weak and different susceptibility genes in different patients and populations, a phenomenon known as genetic heterogeneity. In 2004, we reported the cloning of a novel small ubiquitin-like modifier ( SUMO) gene, SUMO4, in the IDDM5 interval on chromosome 6q25, and presented strong genetic and functional evidence suggesting that SUMO4 is a susceptibility gene for type 1 diabetes mellitus (T1DM). In this article, we will summarize genetic association data suggesting that SUMO4 is consistently associated with T1DM in the Asian populations while the association is more heterogeneous in the Caucasian populations. We will also discuss the possible molecular pathways through which sumoylation may regulate T1DM and autoimmunity. [ABSTRACT FROM AUTHOR]

The article discusses the importance of accurate characterization of nanoparticles (NP) in biological systems and environmental media to ensure reproducible toxicity tests. It says that nanotoxicity experiments without characterization limit the value due to unknown experimental variability in the conditions of the NP. It also mentions the NP characteristics which are considered to deserve quantification before the toxicity tests including size, state of dispersion, and surface area.

The prevalence of juvenile-onset Huntington's disease (HD) is about ten times lower than adult HD. Here we report a Chinese HD family showing both intergeneration CAG expansion and contraction. The expansion resulted from a paternal transmission which leads to juvenile-onset HD for a 17-year-old Chinese boy (III-5). More interestingly, a contraction was noticed in a maternal transmission (III-3), which changed the CAG repeat from an expanded, disease-causing allele (48 repeats) to a normal or intermediate allele (34 repeats). Of note, the contraction resulted in a deletion of 14 CAG repeats, which is much larger than previously reported contractions. Our results are consistent with previous observations in Western Caucasians that juvenile-onset HD is more likely inherited through the male germline., (Copyright 2006 Wiley-Liss, Inc.)

The urofacial (Ochoa) syndrome (UFS) characterized by congenital obstructive uropathy and abnormal facial expression is a rare disorder caused by a single recessive disease gene. Our previous studies using homozygosity mapping have located the UFS gene to a genomic interval of approximately 360 kb on chromosome 10q23-10q24. In this study, we have constructed a genomic sequence map covering the entire UFS interval and narrowed the disease interval to a genomic region of 220 kb that harbor the newly identified ACDP1 gene in addition to part of the GOT1 gene which has already been excluded as a candidate for UFS. Extensive search for mutations in the coding region, the 5' and 3' untranslated regions, the promoter region, and the exon/intron junctions failed to identify a pathogenic mutation in UFS patients. Furthermore, our analyses indicated that the same gene on chromosome 10q is responsible for all UFS patients from multiple ethnic groups., (Copyright 2003 Wiley-Liss, Inc.)