Spermatophyta (Plantae) and invasive alien plants of Wanda Mountains in China: a first checklist.

Background: China is one of the most biodiverse countries in the world and has given birth to unique ecosystems, abundant species and rich genetic variety. More and more attention has been paid to biodiversity research in China. The Wanda Mountains, located in the east of Heilongjiang Province in northeast Chia, is a northern extension of the Changbai Mountains, one of the main mountains ranges in the region. In this study, we present the first checklist of spermatophyte and invasive alien plant species in the Wanda Mountains, which was compiled using published materials, specimen records and field surveys conducted from 2018 to 2020. This checklist, which has been published in the Global Biodiversity Information Facility (GBIF), provides a comprehensive overview of the plant species richness of the Wanda Mountains. New information: This data paper presents the first checklist of spermatophytes and invasive alien plants in the Wanda Mountains, comprising a total of 704 species and infraspecific taxa. Amongst these, there are 656 native plants belonging to 328 genera and 94 families and 48 invasive alien plants belonging to 39 genera and 20 families. The checklist includes 251 new records of native plants and 39 new records of invasive plants. This is the first widely shared data on an independent floristic unit in northeast China and can serve as a valuable resource for future biodiversity research in this region and, moreover, trigger more biodiversity data papers in this data-valued country.

Changes in Pregnancy-Associated Deaths in the US During the COVID-19 Pandemic in 2020.

This cross-sectional study assesses changes in pregnancy-associated mortality from drug overdose, homicide, suicide, and other causes in the US from 2018 through 2020.

Fetal reduction, moral permissibility and the all or nothing problem.

There is an ongoing debate about whether multifetal pregnancy reduction from twins to singletons (2-to-1 MFPR) is morally permissible. By applying the all or nothing problem to the cases of reducing twin pregnancies to singletons, Räsänen argues that an implausible conclusion seems to follow from two plausible claims: (1) it is permissible to have an abortion and (2) it is wrong to abort only one fetus in a twin pregnancy. The implausible conclusion is that women considering 2-to-1 MFPR for social reasons ought to abort both fetuses rather than just one. To avoid the conclusion, Räsänen suggests that it is best to carry both fetuses to term and give one for adoption. In this article, I argue that Räsänen's argument fails for two reasons: the inference from (1) and (2) to the conclusion rests on a bridge principle that does not work in certain circumstances, and there is good reason to reject the claim that it is wrong to abort only one fetus.

One-step microwave synthesis of red-emissive carbon dots for cell imaging in extreme acidity and light emitting diodes.

Red emissive carbon dots (R-CDs) have received great attention in biological fields due to their deep tissue penetrability, great bioimaging capability, low interference from auto-fluorescence, and potential for optoelectronic applications. Herein, excitation-independent, highly acid-sensitive R-CDs were successfully obtained via one-step microwave treatment of o-phenylenediamine (o-PD) and phosphoric acid and carefully purified by column chromatography. The relationship between the fluorescence emission and surface groups of the R-CDs was studied in detail using XPS, NMR, and fluorescence spectroscopy, and the different mechanisms of action of the R-CDs and acid in H2O and ethanol were determined. The excellent anti-interference ability and biocompatibility of the R-CDs were confirmed, and the probes were successfully used for imaging A549 and Escherichia coli (E. coli) cells in extreme acidity. Finally, based on their relatively high quantum yield and long wavelength emission, the application potential of the R-CDs in the fabrication of red light-emitting diodes (LEDs) was investigated.

The fairness of ventilator allocation during the COVID-19 pandemic.

There is ongoing debate on how to fairly allocate scarce critical care resources to patients with COVID-19. The debate revolves around two views: those who believe that priority for scarce resources should primarily aim at saving the most lives (SML) or at saving the most life-years, and those who believe that public health should focus on health equity to address health disparities and social determinants of health. I argue that maximizing medical outcomes by saving the greatest number of patients is not a plausible strategy for combating COVID-19. There are reasons of fairness to give each patient who can meet general eligibility requirements a chance of being saved. Rather than focusing on outcome maximization, a better solution would be the individualist lottery that takes account of probability of survival and duration of treatment. Although the individualist lottery allocates scarce resources in a fair way that is responsive to health equity concerns, it still gives considerable weight to the concern of SML. Thus, this procedure can be reasonably accepted by all key stakeholders.

Saving Lives: For the Best Outcome?

In this article, I critique a moral argument developed in Frances Kamm's Intricate Ethics: Rights, Responsibilities, and Permissible Harm. The argument, which I label the Best Outcome Argument, aims to criticize the Taurekian idea that it is not worse if more people die than if fewer do in conflict situations, where it is hard to distinguish individuals from one another solely by reference to the relative strength of their claims. I argue that the Best Outcome Argument is flawed for three reasons: (1) the symmetry feature defined by the impartiality principle holds only in a limited class of conflict situations; (2) individuals should be treated in a consistent way throughout the whole process of reasoning; (3) comparative evaluations gained in different contexts, at least in some cases, cannot be used in one and the same argument.

T4 and waist:hip ratio as biomarkers of antipsychotic-induced weight gain in Han Chinese inpatients with schizophrenia.

Second-generation antipsychotic agents (SGAs) cause serious metabolic side effects, including weight gain, dyslipidemia, and glucose metabolism abnormalities, which occur by unknown mechanisms. Therefore, the search for prospective markers for antipsychotic-induced weight gain (AIWG) has been of major interest. So far, predictive factors predisposing patients to the develop obesity and related metabolic disturbances induced by SGAs have been relatively less studied among large samples of Chinese schizophrenic patients. In this study, 264 Han Chinese inpatients diagnosed with schizophrenia or schizoaffective disorder initiated treatment with olanzapine (n=131) or risperidone (n=133) and were followed for 12weeks. Anthropometric measurements and laboratory analyses of thyroid hormone, fasting plasma glucose (FPG), and lipid levels were conducted as part of routine medical care. The results showed baseline thyroxine (T4) and waist:hip ratio (WHR)were negatively correlated to AIWG (T4: rs=-0.154, P=0.014; WHR: rs=-0.199, P=0.008). Correlations remained significant after multiple regression analyses. The two treatment groups statistically differed for changes in body mass index, WHR, LDL cholesterol, and FPG; in both groups FPG decreased at first and then increased. Our findings suggest basal T4 and WHR may serve as early biomarkers for weight gain as a side effect of single-SGA treatment.

TOX and ADIPOQ Gene Polymorphisms Are Associated with Antipsychotic-Induced Weight Gain in Han Chinese.

To find the genetic markers related to the antipsychotic-induced weight gain (AIWG), we analyzed associations among candidate gene single-nucleotide polymorphisms (SNPs) and quantitative traits of weight changes and lipid profiles in a Chinese Han population. A total of 339 schizophrenic patients, including 86 first-episode patients (FEPs), meeting the entry criteria were collected. All patients received atypical antipsychotic drug monotherapy and hospitalization and were followed for 12 weeks. Forty-three SNPs in 23 candidate genes were calculated for quantitative genetic association with AIWG, performed by PLINK. The TOX gene SNP rs11777927 (P = 0.009) and the ADIPOQ gene SNP rs182052 (P = 0.019) were associated with AIWG (in body mass index, BMI). In addition, the BDNF SNP rs6265 (P = 0.002), BDAF SNP rs11030104 SNP (P = 0.001), and ADIPOQ SNPs rs822396 (P = 0.003) were significantly associated with the change of waist-to-hip ratio (WHR) induced by atypical antipsychotics. These results were still significant after age and gender adjustments. These findings provide preliminary evidence supporting the role of TOX, ADIPOQ and BDNF in weight and WHR gain induced by atypical antipsychotics.

Astragalin-induced cell death is caspase-dependent and enhances the susceptibility of lung cancer cells to tumor necrosis factor by inhibiting the NF-кB pathway.

Flavonoids are naturally occurring polyphenolic compounds and are among the most promising anticancer agents. Here, we demonstrate that the flavonoid astragalin (AG), also known as kaempferol-3-O-ß-D-glucoside, induces cell death. This was prevented by the caspase inhibitors z-DEVD-FMK and z-LEHD-FMK. AG-induced cell death was associated with an increase in the Bax:Bcl-2 ratio and amplified by the inhibition of extracellular signal-regulated kinase (ERK)-1/2 and Akt signaling. Meanwhile, AG suppressed LPS-induced NF-κB activation. Additional studies revealed that AG inhibited tumor necrosis factor-alpha (TNFα)-induced NF-κB activity. AG also potentiated TNFα-induced apoptosis in A549 cells. Furthermore, using a mouse xenograft model, we demonstrated that AG suppressed tumor growth and induced cancer cell apoptosis in vivo. Taken together, these results suggest that AG may be a promising cancer therapeutic drug that warrants further investigation into its potential clinical applications.

Apigenin potentiates TRAIL therapy of non-small cell lung cancer via upregulating DR4/DR5 expression in a p53-dependent manner.

Apigenin (APG) is an edible plant-derived flavonoid that shows modest antitumor activities in vitro and in vivo. APG treatment results in cell growth arrest and apoptosis in various types of tumors by modulating several signaling pathways. In the present study, we evaluated interactions between APG and TRAIL in non-small cell lung cancer (NSCLC) cells. We observed a synergistic effect between APG and TRAIL on apoptosis of NSCLC cells. A549 cells and H1299 cells were resistant to TRAIL treatment alone. The presence of APG sensitized NSCLC cells to TRAIL-induced apoptosis by upregulating the levels of death receptor 4 (DR4) and death receptor 5 (DR5) in a p53-dependent manner. Consistently, the pro-apoptotic proteins Bad and Bax were upregulated, while the anti-apoptotic proteins Bcl-xl and Bcl-2 were downregulated. Meanwhile, APG suppressed NF-κB, AKT and ERK activation. Treatment with specific small-molecule inhibitors of these pathways enhanced TRAIL-induced cell death, mirroring the effect of APG. Furthermore, using a mouse xenograft model, we demonstrated that the combined treatment completely suppressed tumor growth as compared with APG or TRAIL treatment alone. Our results demonstrate a novel strategy to enhance TRAIL-induced antitumor activity in NSCLC cells by APG via inhibition of the NF-κB, AKT and ERK prosurvival regulators.

FADD is a key regulator of lipid metabolism.

FADD, a classical apoptotic signaling adaptor, was recently reported to have non-apoptotic functions. Here, we report the discovery that FADD regulates lipid metabolism. PPAR-α is a dietary lipid sensor, whose activation results in hypolipidemic effects. We show that FADD interacts with RIP140, which is a corepressor for PPAR-α, and FADD phosphorylation-mimic mutation (FADD-D) or FADD deficiency abolishes RIP140-mediated transcriptional repression, leading to the activation of PPAR-α. FADD-D-mutant mice exhibit significantly decreased adipose tissue mass and triglyceride accumulation. Also, they exhibit increased energy expenditure with enhanced fatty acid oxidation in adipocytes due to the activation of PPAR-α. Similar metabolic phenotypes, such as reduced fat formation, insulin resistance, and resistance to HFD-induced obesity, are shown in adipose-specific FADD knockout mice. Additionally, FADD-D mutation can reverse the severe genetic obesity phenotype of ob/ob mice, with elevated fatty acid oxidation and oxygen consumption in adipose tissue, improved insulin resistance, and decreased triglyceride storage. We conclude that FADD is a master regulator of glucose and fat metabolism with potential applications for treatment of insulin resistance and obesity.

Identification of sequence polymorphisms in the D-loop region of mitochondrial DNA as risk biomarkers for malignant fibrous histiocytoma.

Single nucleotide polymorphisms (SNPs) in the mitochondrial DNA Displacement-loop (D-loop) region particularly in a highly polymorphic homopolymeric C stretch named D310 have been reported to be associated with cancer risk in several types of cancer. In order to evaluate the frequency of D-loop SNPs in a large series of malignant fibrous histiocytoma (MFH) and establish correlations with cancer risk, we sequenced the D-loop of 92 MFH patients and analyzed their use as predictive biomarkers for MFH risk. The minor alleles of nucleotides 73G, 151T were associated with an increased risk for MFH patients, whereas the alleles of nucleotides 16,298C, 152C, and insertion of C at the site 315 (located within the D310) were associated with a decreased risk for MFH patients. These results suggest that SNPs in the mitochondrial D-loop should be considered as a biomarker which may be useful for the early detection of MFH in individuals at risk of this cancer.