Social, Behavioral, and Metabolic Risk Factors and Racial Disparities in Cardiovascular Disease Mortality in U.S. Adults : An Observational Study.

BACKGROUND: Cardiovascular disease (CVD) mortality is persistently higher in the Black population than in other racial and ethnic groups in the United States. OBJECTIVE: To examine the degree to which social, behavioral, and metabolic risk factors are associated with CVD mortality and the extent to which racial differences in CVD mortality persist after these factors are accounted for. DESIGN: Prospective cohort study. SETTING: NHANES (National Health and Nutrition Examination Survey) 1999 to 2018. PARTICIPANTS: A nationally representative sample of 50 808 persons aged 20 years or older. MEASUREMENTS: Data on social, behavioral, and metabolic factors were collected in each NHANES survey using standard methods. Deaths from CVD were ascertained from linkage to the National Death Index with follow-up through 2019. RESULTS: Over an average of 9.4 years of follow-up, 2589 CVD deaths were confirmed. The age- and sex-standardized rates of CVD mortality were 484.7 deaths per 100 000 person-years in Black participants, 384.5 deaths per 100 000 person-years in White participants, 292.4 deaths per 100 000 person-years in Hispanic participants, and 255.1 deaths per 100 000 person-years in other race groups. In a multiple Cox regression analysis adjusted for all measured risk factors simultaneously, several social (unemployment, low family income, food insecurity, lack of home ownership, and unpartnered status), behavioral (current smoking, lack of leisure-time physical activity, and sleep <6 or >8 h/d), and metabolic (obesity, hypertension, and diabetes) risk factors were associated with a significantly higher risk for CVD death. After adjustment for these metabolic, behavioral, and social risk factors separately, hazard ratios of CVD mortality for Black compared with White participants were attenuated from 1.54 (95% CI, 1.34 to 1.77) to 1.34 (CI, 1.16 to 1.55), 1.31 (CI, 1.15 to 1.50), and 1.04 (CI, 0.90 to 1.21), respectively. LIMITATION: Causal contributions of social, behavioral, and metabolic risk factors to racial and ethnic disparities in CVD mortality could not be established. CONCLUSION: The Black-White difference in CVD mortality diminished after adjustment for behavioral and metabolic risk factors and completely dissipated with adjustment for social determinants of health in the U.S. population. PRIMARY FUNDING SOURCE: National Institutes of Health.

USP14 regulates autophagy by suppressing K63 ubiquitination of Beclin 1.

The ubiquitin-proteasome system (UPS) and autophagy are two major intracellular degradative mechanisms that mediate the turnover of complementary repertoires of intracellular proteomes. Simultaneously activating both UPS and autophagy might provide a powerful strategy for the clearance of misfolded proteins. However, it is not clear whether UPS and autophagy can be controlled by a common regulatory mechanism. K48 deubiquitination by USP14 is known to inhibit UPS. Here we show that USP14 regulates autophagy by negatively controlling K63 ubiquitination of Beclin 1. Furthermore, we show that activation of USP14 by Akt-mediated phosphorylation provides a mechanism for Akt to negatively regulate autophagy by promoting K63 deubiquitination. Our study suggests that Akt-regulated USP14 activity modulates both proteasomal degradation and autophagy through controlling K48 and K63 ubiquitination, respectively. Therefore, regulation of USP14 provides a mechanism for Akt to control both proteasomal and autophagic degradation. We propose that inhibition of USP14 may provide a strategy to promote both UPS and autophagy for developing novel therapeutics targeting neurodegenerative diseases.

The Wnt gene family in Tenebrio molitor and other coleopterans.

The Wnt gene family is involved in a wide range of developmental processes. Despite its significance, the evolution and function of Wnt genes remain largely unclear. Here, an exhaustive survey of Wnt genes was conducted in Tenebrio molitor and 17 other beetle genomes. A total of 146 Wnt genes were identified, creating a comprehensive coleopteran Wnt gene catalog. Comparative genomics indicates that dynamic evolutionary patterns of Wnt gene loss and duplication occurred in Coleoptera, leading to the diverse Wnt gene repertoire in various beetles. A striking loss of particular Wnt gene subfamilies occurs in Coleoptera. Remarkably, Wnt gene duplication was discovered for the first time in insects. Further analysis of Wnt gene expression in T. molitor indicates that each Wnt gene, including the duplicated ones, has a unique spatial or temporal expression pattern. The current study provides valuable insight into the evolution and functional validation of Wnt genes in Coleoptera.

Lifestyle behaviors and cardiovascular risk profiles among parous women by gestational diabetes status, 2007-2018.

BACKGROUND AND AIMS: Women with prior gestational diabetes mellitus (GDM) are at elevated risk of type 2 diabetes mellitus and cardiovascular disease. We compared cardiometabolic risk factors among parous U.S. women ages 20-44 by history of GDM. METHODS AND RESULTS: Using data from the National Health and Nutrition Examination Survey (NHANES) from 2007 to 2018, 3537 parous women were classified by self-reported GDM history. We compared anthropometric measures, glycemia, blood pressure, lipids, lifestyle factors, cardiovascular health, and cardiometabolic disease prevalence by GDM status. NHANES survey design was taken into account. Women without history of GDM were younger and, after adjusting for age, race/ethnicity, and education, had more favorable cardiometabolic risk factor profiles for measures of anthropometry, glycemia, diabetes, many lipids, physical activity, diet, and overall cardiovascular health than women with history of GDM. Many patterns persisted after further adjustment for lifestyle factors. In analyses stratified by race/ethnicity, many patterns persisted, though there were key differences. Hypertension prevalence differed by GDM history only among Hispanic women. In women of other race/ethnicity, there was no difference in healthy eating or body mass index by GDM history. In non-Hispanic Black women, there was no difference in healthy eating by GDM history. CONCLUSION: Among parous U.S. women ages 20-44, those with history of GDM had less favorable cardiometabolic risk factor profiles than those without history of GDM. This highlights the importance of continued efforts to develop and test multilevel interventions to improve cardiometabolic risk factors among reproductive-age women with a history of GDM.

Antifungal mechanisms of lavender essential oil in the inhibition of rot disease caused by Monilinia fructicola in postharvest flat peaches.

Lavender essential oil (LEO), a natural antimicrobial agent, is generally recognized as safe and effective in the inhibition of phytopathogenic fungi. Direct contact and fumigation (in vivo and in vitro) were used to study the fungistatic effect of LEO on Monilinia fructicola. Additionally, the effect on the ultrastructure of cells and the degree of destruction of the cell membrane of M. fructicola were revealed. In addition, the effects of LEO on the expression levels of apoptosis-related genes in M. fructicola cells were detected, and GC-MS was used to analyze the main components of LEO. LEO had a good inhibitory efficacy against M. fructicola in flat peaches, with almost complete growth inhibition at 800 µL/L. These effects were associated with the leakage of cytoplasmic contents, hyphal distortion, and spore disruption. Moreover, the expression of apoptosis RTG1 and RLM1 genes increased with LEO treatment. These results demonstrate that LEO can inhibit M. fructicola by inducing cytoplasmic membrane damage and cell apoptosis in fungi, and that the major ingredients of LEO are monoterpenes and sesquiterpenes, which are presumed to contribute to the inhibitory effects.

Death-domain dimerization-mediated activation of RIPK1 controls necroptosis and RIPK1-dependent apoptosis.

RIPK1 is a critical mediator of cell death and inflammation downstream of TNFR1 upon stimulation by TNFα, a potent proinflammatory cytokine involved in a multitude of human inflammatory and degenerative diseases. RIPK1 contains an N-terminal kinase domain, an intermediate domain, and a C-terminal death domain (DD). The kinase activity of RIPK1 promotes cell death and inflammation. Here, we investigated the involvement of RIPK1-DD in the regulation of RIPK1 kinase activity. We show that a charge-conserved mutation of a lysine located on the surface of DD (K599R in human RIPK1 or K584R in murine RIPK1) blocks RIPK1 activation in necroptosis and RIPK1-dependent apoptosis and the formation of complex II. Ripk1K584R/K584R knockin mutant cells are resistant to RIPK1 kinase-dependent apoptosis and necroptosis. The resistance of K584R cells, however, can be overcome by forced dimerization of RIPK1. Finally, we show that the K584R RIPK1 knockin mutation protects mice against TNFα-induced systematic inflammatory response syndrome. Our study demonstrates the role of RIPK1-DD in mediating RIPK1 dimerization and activation of its kinase activity during necroptosis and RIPK1-dependent apoptosis.

Based on RNA-Seq analysis identification and expression analysis of Trans-scripusinA synthesize-related genes of UV-treatment in postharvest grape fruit.

Stilbenes, an active substances closely related to resistance and quality of grapes, are rarely found in natural resources. However its cumulative amount is affected by ultraviolet radiation (UV). The purpose of this study is to screen key genes in biosynthesis of stilbenes Trans-scripusin A and explore its synthetic pathway. We tested content of stilbenes with UHPLC-QQQ-MS2, results revealed that stilbenes accumulation is positively correlated with UV-B exposure time. Then, we performed transcriptome high-throughput sequencing of grapes under treatments. Results shown that 13,906 differentially expressed genes were obtained, which were mainly enriched in three major regions (ribosome, plant-pathogen interaction and biosynthesis of flavonoid). Three genes of trans-scripusin A synthesis pathway key got by combining KEGG annotation and reference gene HsCYP1B1. Phylogenetic analysis showed that SAH genes had high homology with other hydroxylase genes, and distributed in two subgroups. Gene structure analysis showed that SAH genes contained four exons, indicating that gene has low genetic diversity. Chromosome localization revealed that SAH genes were distributed on different chromosomes, in addition, the number of gene pairs between Vitis vinifera and other species was not related to genome size of other species. The expression profiles of SAH genes in different parts of Vitis vinifera L. were analyzed using qRT-PCR analysis, results indicated that expression of SAH genes be specific to fruit part. These paper provide theoretical basis for further study of polyphenols biosynthesis pathway in grape fruits. The study provides novel insights for further understanding quality of grapes response to UV radiation.

PELI1 functions as a dual modulator of necroptosis and apoptosis by regulating ubiquitination of RIPK1 and mRNA levels of c-FLIP.

Apoptosis and necroptosis are two distinct cell death mechanisms that may be activated in cells on stimulation by TNFα. It is still unclear, however, how apoptosis and necroptosis may be differentially regulated. Here we screened for E3 ubiquitin ligases that could mediate necroptosis. We found that deficiency of Pellino 1 (PELI1), an E3 ubiquitin ligase, blocked necroptosis. We show that PELI1 mediates K63 ubiquitination on K115 of RIPK1 in a kinase-dependent manner during necroptosis. Ubiquitination of RIPK1 by PELI1 promotes the formation of necrosome and execution of necroptosis. Although PELI1 is not directly involved in mediating the activation of RIPK1, it is indispensable for promoting the binding of activated RIPK1 with its downstream mediator RIPK3 to promote the activation of RIPK3 and MLKL. Inhibition of RIPK1 kinase activity blocks PELI1-mediated ubiquitination of RIPK1 in necroptosis. However, we show that PELI1 deficiency sensitizes cells to both RIPK1-dependent and RIPK1-independent apoptosis as a result of down-regulated expression of c-FLIP, an inhibitor of caspase-8. Finally, we show that Peli1-/- mice are sensitized to TNFα-induced apoptosis. Thus, PELI1 is a key modulator of RIPK1 that differentially controls the activation of necroptosis and apoptosis.

Modeling abnormal early development with induced pluripotent stem cells from aneuploid syndromes.

Many human diseases share a developmental origin that manifests during childhood or maturity. Aneuploid syndromes are caused by supernumerary or reduced number of chromosomes and represent an extreme example of developmental disease, as they have devastating consequences before and after birth. Investigating how alterations in gene dosage drive these conditions is relevant because it might help treat some clinical aspects. It may also provide explanations as to how quantitative differences in gene expression determine phenotypic diversity and disease susceptibility among natural populations. Here, we aimed to produce induced pluripotent stem cell (iPSC) lines that can be used to improve our understanding of aneuploid syndromes. We have generated iPSCs from monosomy X [Turner syndrome (TS)], trisomy 8 (Warkany syndrome 2), trisomy 13 (Patau syndrome) and partial trisomy 11;22 (Emanuel syndrome), using either skin fibroblasts from affected individuals or amniocytes from antenatal diagnostic tests. These cell lines stably maintain the karyotype of the donors and behave like embryonic stem cells in all tested assays. TS iPSCs were used for further studies including global gene expression analysis and tissue-specific directed differentiation. Multiple clones displayed lower levels of the pseudoautosomal genes ASMTL and PPP2R3B than the controls. Moreover, they could be transformed into neural-like, hepatocyte-like and heart-like cells, but displayed insufficient up-regulation of the pseudoautosomal placental gene CSF2RA during embryoid body formation. These data support that abnormal organogenesis and early lethality in TS are not caused by a tissue-specific differentiation blockade, but rather involves other abnormalities including impaired placentation.

Artificial neural network and genetic algorithm coupled fermentation kinetics to regulate L-lysine fermentation.

Fermentation plays a pivotal role in the industrialization of bioproducts, yet there is a substantial lag in the fermentation process regulation. Here, an artificial neural network (ANN) and genetic algorithm (GA) coupled with fermentation kinetics were employed to establish an innovative lysine fermentation control. Firstly, the strategy of coupling GA with ANN was established. Secondly, specific lysine formation rate (qp), specific substrate consumption rate (qs), and specific cell growth rate (µ) were predicted and optimized by ANN-GA. The optimal ANN model adopts a three-layer feed-forward back-propagation structure (4:10:1). The optimal fermentation control parameters are obtained through GA. Finally, when the carbon to nitrogen ratio, residual sugar concentration, ammonia nitrogen concentration, and dissolved oxygen were [2.5, 4.5], [6.5, 9.5] g·L-1, [1.0, 2.0] g·L-1 and [20, 30] %, respectively, the lysine concentration reaches its peak at 213.0 ± 5.10 g·L-1. The novel control strategy holds significant potential for optimizing the fermentation of other bioproducts.

ß-Lapachone, an NQO1 bioactivatable drug, prevents lung tumorigenesis in mice.

Lung cancer is one of the most lethal cancers with high incidence worldwide. The prevention of lung cancer is of great significance to reducing the social harm caused by this disease. An in-depth understanding of the molecular changes underlying precancerous lesions is essential for the targeted chemoprevention against lung cancer. Here, we discovered an increased NQO1 level over time within pulmonary premalignant lesions in both the KrasG12D-driven and nicotine-derived nitrosamine ketone (NNK)-induced mouse models of lung cancer, as well as in KrasG12D-driven and NNK-induced malignant transformed human bronchial epithelial cells (BEAS-2B and 16HBE). This suggests a potential correlation between the NQO1 expression and lung carcinogenesis. Based on this finding, we utilized ß-Lapachone (ß-Lap), an NQO1 bioactivatable drug, to suppress lung tumorigenesis. In this study, the efficacy and safety of low-dose ß-Lap were demonstrated in preventing lung tumorigenesis in vivo. In conclusion, our study suggests that long-term consumption of low-dose ß-Lap could potentially be an effective therapeutic strategy for the prevention of lung premalignant lesions. However, further studies and clinical trials are necessary to validate our findings, determine the safety of long-term ß-Lap usage in humans, and promote the use of ß-Lap in high-risk populations.

Investigation on epidermal structure and water migration of postharvest passion fruit during storage.

Passion fruit is a tropical fruit that has plenty of fruit fragrance. During storage, passion fruit quickly loses water, resulting in its poor quality. Researching the mechanism of water loss contributes to prolonging the storage time. In this study, passion fruit was stored at 7 or 25°C to analyze the relationship between epidermal structure and water migration. The epidermal wax and structure of passion fruit began to show signs of destruction from the middle stage (day 8) during storage. The mobility of free water was decreased at 7°C and increased at 25°C in passion fruit from the middle stage of storage (day 8). The migration rate of free water in passion fruit stored at 7°C was lower than that at 25°C. The mobility of immobile water was weaker in the late storage period but that of bound water changed barely. These results showed that the migration of free, immobile, and bound water had a connection with the epidermal structure. Incomplete epidermal structure promoted water loss in passion fruit, with the most pronounced loss of free water. PRACTICAL APPLICATION: Maintaining the epidermal structure of passion fruit well can decrease the water loss ratio. Passion fruit stored at low temperatures could better sustain the integrity of epidermal wax and structure; it was able to change the water migration rate in the epidermis of passion fruit, which was conducive to maintaining the water content.

In vivo analyses reveal hippocampal subfield volume reductions in adolescents with schizophrenia, but not with major depressive disorder.

BACKGROUND: Adult studies have reported atypicalities in the hippocampus and subfields in patients with schizophrenia (SCZ) and major depressive disorder (MDD). Both affective and psychotic disorders typically onset in adolescence, when human brain develops rapidly and shows increased susceptibility to adverse environments. However, few in vivo studies have investigated whether hippocampus subfield abnormalities occur in adolescence and whether they differ between SCZ and MDD cases. METHODS: We recruited 150 adolescents (49 SCZ patients, 67 MDD patients, and 34 healthy controls) and obtained their structural images. We used FreeSurfer to automatically segment hippocampus into 12 subfields and analyzed subfield volumetric differences between groups by analysis of covariance, covarying for age, sex, and intracranial volume. Composite measures by summing subfield volumes were further compared across groups and analyzed in relation to clinical characteristic. RESULTS: SCZ adolescents showed significant volume reductions in subfields of CA1, molecular layer, subiculum, parasubiculum, dentate gyrus and CA4 than healthy controls, and almost significant reductions, as compared to the MDD group, in left molecular layer, dentate gyrus, CA2/3 and CA4. Composite analyses showed smaller volumes in SCZ group than in healthy controls in all bilateral composite measures, and reduced volumes in comparison to MDD group in all left composite measures only. CONCLUSIONS: SCZ adolescents exhibited both hippocampal subfield and composite volumes reduction, and also showed greater magnitude of deviance than those diagnosed with MDD, particularly in core CA regions. These results indicate a hippocampal disease process, suggesting a potential intervention marker of early psychotic patients and risk youths.

Kaempferol modulates IFN-γ induced JAK-STAT signaling pathway and ameliorates imiquimod-induced psoriasis-like skin lesions.

Immune-mediated inflammation contributes to the development of psoriasis. However, long-term treatment with global immunosuppressive agents may cause a variety of side effects including recurrent infections. Kaempferol (KP), a natural flavonol, present in various plants is proposed to be useful for the treatment of psoriasis patients. Nevertheless, an explicit understanding of KP induced mechanisms is a prerequisite for its use in clinics. Therefore, we investigated the therapeutic effects and potential mode of action of KP using IFN-γ induced HaCaT cells and imiquimod-induced psoriasis-like skin lesions in mice. In this study, we found KP reduced intracellular ROS production, inhibited rhIFN-γ-induced IFN-γR1 expression, and up-regulated SOCS1 levels in HaCaT cells. In addition, KP inhibited rhIFN-γ-induced phosphorylation of JAK-STAT signaling molecules in HaCaT cells. Most importantly, KP alleviated imiquimod-induced psoriasis-like skin lesions in mice, histopathology and proportion of DCs in the skin. Besides, it reduced the population of γδT17 cells in the lymph nodes of the psoriatic mice and also decreased the gene expression of many proinflammatory cytokines, including interleukin IL-23, IL-17A, TNF-α, IL-6, and IL-1ß in addition to down-regulation of the proinflammatory JAK-STAT signaling pathway. Thus, KP modulated IFN-γ induced JAK-STAT signaling pathway by inducing IFN-γR1 expression and up-regulating SOCS1 expression. In addition, KP also ameliorated imiquimod-induced psoriasis by reducing the dendritic cell numbers, and γδT17 cell population, along with down- modulation of the JAK-STAT pathway.

Evaluation of atrial anatomical remodeling in atrial fibrillation with machine-learned morphological features.

PURPOSE: To elucidate the role of atrial anatomical remodeling in atrial fibrillation (AF), we proposed an automatic method to extract and analyze morphological characteristics in left atrium (LA), left atrial appendage (LAA) and pulmonary veins (PVs) and constructed classifiers to evaluate the importance of identified features. METHODS: The LA, LAA and PVs were segmented from contrast computed tomography images using either a commercial software or a self-adaptive algorithm proposed by us. From these segments, geometric and fractal features were calculated automatically. To reduce the model complexity, a feature selection procedure is adopted, with the important features identified via univariable analysis and ensemble feature selection. The effectiveness of this approach is well illustrated by the high accuracy of our models. RESULTS: Morphological features, such as LAA ostium dimensions and LA volume and surface area, statistically distinguished ([Formula: see text]) AF patients or AF with LAA filling defects (AF(def+)) patients among all patients. On the test set, the best model to predict AF among all patients had an area under the receiver operating characteristic curve (AUC) of 0.91 (95% CI, 0.8-1) and the best model to predict AF(def+) among all patients had an AUC of 0.92 (95% CI, 0.81-1). CONCLUSION: This study automatically extracted and analyzed atrial morphology in AF and identified atrial anatomical remodeling that statistically distinguished AF or AF(def+). The importance of identified atrial morphological features in characterizing AF or AF(def+) was validated by corresponding classifiers. This work provides a good foundation for a complete computer-assisted diagnostic workflow of predicting the occurrence of AF or AF(def+).

A carrier-free nano-drug assembled via π-π stacking interaction for the treatment of osteoarthritis.

Osteoarthritis (OA) is considered to be the most common joint disorder. Exogenous drug intervention is one of the effective means for OA treatment. Clinical applications of numerous drugs are restricted owing to the short retention as well as rapid clearance in the joint cavity. A wide variety of carrier-based nanodrugs have been developed, but additional carriers may bring unexpected side effects or even toxicity. Herein, by exploiting the spontaneous fluorescence of Curcumin, we designed a new carrier-free self-assembly nanomedicine Curcumin (Cur)/icariin (ICA) nanoparticles with adjustable particle size, which is composed of two small-molecule natural drugs assembled via π-π stacking interaction. Experimental results revealed that Cur/ICA NPs endowed with little cytotoxicity, high cellular uptake and sustained drug release, could inhibit secretion of inflammatory cytokines and reduce cartilage degeneration. Moreover, both the in vitro and in vivo experiments showed the NPs exerted superior synergism effects in anti-inflammatory and cartilage protection than either Cur or ICA alone, and self-monitored its retention by autofluorescence. Thus, the new self-assembly nano-drug combining Cur and ICA represents a new strategy for the treatment of osteoarthritis.

Self-inducing Reactors for Bioengineering.

Packed tower reactors, mechanically stirred reactors, airlift reactors, and gas-self-inducing reactors are frequently utilized among the various types of reactors. Self-inducing reactors exhibit notable advantages owing to their simple structure, effective gas-liquid intermixing, and low energy requirements, rendering them highly suitable for bioengineering endeavors. The purpose of this analysis is to shed light on the use of self-inducing reactors in bioengineering by examining the following five parameters: critical speed, suction rate, volumetric mass transfer coefficient, power characteristics, and gas hold-up. Through a comprehensive analysis of the advancements achieved in these domains, it is possible to determine the challenges and opportunities that lie ahead in the realm of bioengineering.

Discovery of potential biomarkers for osteoporosis using LC/GC-MS metabolomic methods.

Purpose: For early diagnosis of osteoporosis (OP), plasma metabolomics of OP was studied by untargeted LC/GC-MS in a Chinese elderly population to find possible diagnostic biomarkers. Methods: A total of 379 Chinese community-dwelling older adults aged ≥65 years were recruited for this study. The BMD of the calcaneus was measured using quantitative ultrasound (QUS), and a T value ≤-2.5 was defined as OP. Twenty-nine men and 47 women with OP were screened, and 29 men and 36 women were matched according to age and BMI as normal controls using propensity matching. Plasma from these participants was first analyzed by untargeted LC/GC-MS, followed by FC and P values to screen for differential metabolites and heatmaps and box plots to differentiate metabolites between groups. Finally, metabolic pathway enrichment analysis of differential metabolites was performed based on KEGG, and pathways with P ≤ 0.05 were selected as enrichment pathways. Results: We screened metabolites with FC>1.2 or FC<1/1.2 and P<0.05 and found 33 differential metabolites in elderly men and 30 differential metabolites in elderly women that could be potential biomarkers for OP. 2-Aminomuconic acid semialdehyde (AUC=0.72, 95% CI 0.582-0.857, P=0.004) is highly likely to be a biomarker for screening OP in older men. Tetradecanedioic acid (AUC=0.70, 95% CI 0.575-0.818, P=0.004) is highly likely to be a biomarker for screening OP in older women. Conclusion: These findings can be applied to clinical work through further validation studies. This study also shows that metabolomic analysis has great potential for application in the early diagnosis and recurrence monitoring of OP in elderly individuals.

Generation of induced pluripotent stem cells from urine.

Forced expression of selected transcription factors can transform somatic cells into embryonic stem cell (ESC)-like cells, termed induced pluripotent stem cells (iPSCs). There is no consensus regarding the preferred tissue from which to harvest donor cells for reprogramming into iPSCs, and some donor cell types may be more prone than others to accumulation of epigenetic imprints and somatic cell mutations. Here, we present a simple, reproducible, noninvasive method for generating human iPSCs from renal tubular cells present in urine. This procedure eliminates many problems associated with other protocols, and the resulting iPSCs display an excellent ability to differentiate. These data suggest that urine may be a preferred source for generating iPSCs.

Structure, thermostability and magnetic properties of cubic Ce2-x Ti2O7 pyrochlore obtained via sol-gel preparation.

Lanthanum-based titanates have been attracting considerable interest by virtue of their structural operability and hence diverse physical properties. The preparation of lanthanum-based titanates with novel crystal structure is a fascinating task. In this work, we report the preparation of a cubic Ce2-x Ti2O7 pyrochlore using the sol-gel method. The crystal structure, thermostability and magnetism were studied via the temperature dependence of X-ray powder diffraction, X-ray photoelectron spectroscopy and magnetization measurements. It has been revealed that the as-prepared Ce2-x Ti2O7 pyrochlore possesses a cubic symmetry (space group: Fd3̄m), however there is an 18(1)% vacancy of Ce ions in the as-prepared samples. No distinct phase transition and thermal expansion anomaly were observed in the investigated temperature range from 300 K to 700 K. Intriguingly, lattice defects may favor the transformation of Ce valence from +3 to +4 and an unusual weak magnetic ordering state emerged up to 400 K. The persistence of magnetism at such high temperatures is rare and mysterious for cerium titanates. Our findings provide the possibility of adjusting the crystal structure and magnetic properties of cerium titanates, anticipated to the development of lanthanum-based oxides.