Regular graphs with a complete bipartite graph as a star complement

Let $G$ be a graph of order $n$ and $\mu$ be an adjacency eigenvalue of $G$ with multiplicity $k\geq 1$. A star complement $H$ for $\mu$ in $G$ is an induced subgraph of $G$ of order $n-k$ with no eigenvalue $\mu$, and the vertex subset $X=V(G-H)$ is called a star set for $\mu$ in $G$. The study of star complements and star sets provides a strong link between graph structure and linear algebra. In this paper, we study the regular graphs with $K_{t,s}\ (s\geq t\geq 2)$as a star complement for an eigenvalue$\mu$, especially, characterize the case of$t=3$completely, obtain some properties when$t=s$, and propose some problems for further study

Fast growth of monolayer organic 2D crystals and their application in organic transistors

Growth of monolayer 2D organic crystal has been an interesting topic in recent years owing to their promising properties. However, it is still a tough challenge to obtain the 2D organic crystal with precise thickness control and uniform morphology. Herein, we reported the fabrication of 2D crystals of alkane molecules C44H90 with only monolayer thickness and tunable size through the simple dip-coating process. Benefitted from the low solubility of the C44H90 and the isotropic Van der Waals interaction, quadrilateral-shape monolayer 2D crystals with size from several micrometers to nearly hundreds of micrometers can be achieved in the dip-coating process. Utilized the X-ray diffraction and high resolution atomic force microscopy, we obtained the clear packing mode of these monolayer crystals. In addition, these smooth 2D crystals show promising application in the thin film transistors by acting as a molecular template layer. It leads to an increment of about one magnitude on the charge mobility owing to the decreasing of both morphology defects and interface traps.</p

Volume-regulated Cl- current: contributions of distinct Cl- channel and localized Ca2+ signals.

The swelling-activated chloride current (ICl,swell) is induced when a cell swells and plays a central role in maintaining cell volume in response to osmotic stress. The major contributor of ICl,swell is the volume regulated anion channel (VRAC). LRRC8A (SWELL1) was recently identified as an essential component of VRAC but the mechanisms of VRAC activation are still largely unknown; moreover, other Cl- channels, such as anoctamin 1 (ANO1) were also suggested to contribute to ICl,swell. In this present study, we investigated the roles of LRRC8A and ANO1 in activation of ICl,swell; we also explored the role of intracellular Ca2+ in ICl,swell activation. We used CRISPR/Cas9 gene editing approach, electrophysiology, live fluorescent imaging, selective pharmacology and other approaches to show that both LRRC8A and ANO1 can be activated by cell swelling in HEK293 cells. Yet, both channels contribute biophysically and pharmacologically distinct components to ICl,swell, with LRRC8A being the major component. Cell swelling induced oscillatory Ca2+ transients and these Ca2+ signals were required to activate both, the LRRC8A- and ANO1-dependent components of ICl,swell. Both ICl,swell components required localized rather than global Ca2+ for activation. Interestingly, while intracellular Ca2+ was necessary and sufficient to activate ANO1, it was necessary but not sufficient to activate LRRC8A-mediated currents. Finally, Ca2+ transients linked to the ICl,swell activation were mediated by the GPCR-independent PLC isoforms

YY1 Positively Regulates Transcription by Targeting Promoters and Super-Enhancers through the BAF Complex in Embryonic Stem Cells

Yin Yang 1 (YY1) regulates early embryogenesis and adult tissue formation. However, the role of YY1 in stem cell regulation remains unclear. YY1 has a Polycomb group (PcG) protein-dependent role in mammalian cells. The PcG-independent functions of YY1 are also reported, although their underlying mechanism is still undefined. This paper reports the role of YY1 and BAF complex in the OCT4-mediated pluripotency network in mouse embryonic stem cells (mESCs). The interaction between YY1 and BAF complex promotes mESC proliferation and pluripotency. Knockdown of Yy1 or Smarca4, the core component of the BAF complex, downregulates pluripotency markers and upregulates several differentiation markers. Moreover, YY1 enriches at both promoter and super-enhancer regions to stimulate transcription. Thus, this study elucidates the role of YY1 in regulating pluripotency through its interaction with OCT4 and the BAF complex and the role of BAF complex in integrating YY1 into the core pluripotency networkThis research was funded by grants from the National Key Research and Development Program (2016YFA [0101700] and 2017YFA0102800), the National Natural Science Foundation of China (31771639), the Guangdong Innovative and Entrepreneurial Research Team Program 2016ZT06S029, the Fundamental Research Funds for the Central Universities (17ykzd04), and Thousand Youth Talents Plan to J.D., the National Natural Science Foundation of China (81703086) to J.W. and the NIH (1R01-GM095942 and 1R21HD087722) and the Empire State Stem Cell funded through the New York State Department of Health (NYSTEM; C028103 and C028121) to J.W.S

Bioinformatics study of the potential therapeutic effects of ginsenoside Rh3 in reversing insulin resistance

BackgroundIn recent years, the incidence of insulin resistance is increasing, and it can cause a variety of Metabolic syndrome. Ginsenosides have been clinically proven to improve fat metabolism and reduce insulin resistance, but their components and mechanism of action are still unclear.ObjectiveGinsenoside, a bioactive compound derived from ginseng, exhibits significant potential in treating obesity, diabetes, and metabolic disorders. Despite evidence supporting its efficacy in ameliorating insulin resistance (IR) in obesity, the specific bioactive components and underlying mechanisms remain obscure. In this study, we endeavored to elucidate the potential molecular targets and pathways influenced by ginsenoside Rh3 (GRh3) to ameliorate IR in liver tissue. We employed a comprehensive approach that integrates system pharmacology and bioinformatics analysis.Materials and methodsOur methodology involved the identification of candidate targets for GRh3 and the profiling of differentially expressed genes (DEGs) related to IR in individuals with insulin resistance. The coalescence of candidate targets and DEGs facilitated the construction of a “GRh3-targets-disease” network for each tissue type, ultimately yielding 38 shared target genes. Subsequently, we conducted pathway enrichment analysis, established protein-protein interaction (PPI) networks, and identified hub targets among the GRh3 targets and IR-related DEGs. Additionally, we conducted animal experiments to corroborate the role of these hub targets in the context of GRh3.ResultsOur investigation identified a total of 38 overlapping targets as potential candidates. Notably, our analysis revealed crucial hub targets such as EGFR, SRC, ESR1, MAPK1, and CASP3, alongside implicated signaling pathways, including those related to insulin resistance, the FoxO signaling pathway, the PPAR signaling pathway, and the IL-17 signaling pathway. This study establishes a robust foundation for the mechanisms underlying GRh3’s efficacy in mitigating IR. Furthermore, these results suggest that GRh3 may serve as a representative compound within the ginsenoside family.ConclusionThis study elucidates the potential molecular targets and associated pathways through which GRh3 ameliorates IR, showcasing its multifaceted nature, spanning multiple targets, pathways, and mechanisms. These findings establish a robust foundation for subsequent experimental inquiries and clinical applications

Neuroimaging anomalies in asymptomatic middle cerebral artery steno-occlusive disease with normal-appearing white matter

BackgroundAsymptomatic chronic cerebrovascular steno-occlusive disease is common, but the cognitive function and alterations in the brain’s structural and functional profiles have not been well studied. This study aimed to reveal whether and how patients with asymptomatic middle cerebral artery (MCA) steno-occlusive disease and normal-appearing white matter differ in brain structural and functional profiles from normal controls and their correlations with cognitive function.MethodsIn all, 26 patients with asymptomatic MCA steno-occlusive disease and 22 healthy controls were compared for neurobehavioral assessments, brain volume, cortical thickness, fiber connectivity density (FiCD) value, and resting-state functional connectivity (FC) using multimodal MRI. We also investigated the associations between abnormal cortical thicknesses, FiCD values, and functional connectivities with the neurobehavioral assessments.ResultsPatients performed worse on memory tasks (Auditory Verbal Learning Test-Huashan version) compared with healthy controls. Patients were divided into two groups: the right group (patients with right MCA steno-occlusive disease) and the left group (patients with left MCA steno-occlusive disease). The left group showed significant cortical thinning in the left superior parietal lobule, while the right group showed significant cortical thinning in the right superior parietal lobule and caudal portion of the right middle frontal gyrus. Increased FiCD values in the superior frontal region of the left hemisphere were observed in the left group. In addition, a set of interhemispheric and intrahemispheric FC showed a significant decrease or increase in both the left and right groups. Many functional connectivity profiles were positively correlated with cognitive scores. No correlation was found between cortical thickness, FiCD values, and cognitive scores.ConclusionEven if the patients with MCA steno-occlusive disease were asymptomatic and had normal-appearing white matter, their cognitive function and structural and functional profiles had changed, especially the FC. Alterations in FC may be an important mechanism underlying the neurodegenerative process in patients with asymptomatic MCA steno-occlusive disease before structural changes occur, so FC assessment may promote the detection of network alterations, which may be used as a biomarker of disease progression and therapeutic efficacy evaluation in these patients

Relaxation of the one child policy and trends in caesarean section rates and birth outcomes in China between 2012 and 2016: observational study of nearly seven million health facility births.

OBJECTIVE: To examine how the relaxation of the one child policy and policies to reduce caesarean section rates might have affected trends over time in caesarean section rates and perinatal and pregnancy related mortality in China. DESIGN: Observational study. SETTING: China's National Maternal Near Miss Surveillance System (NMNMSS). PARTICIPANTS: 6 838 582 births at 28 completed weeks or more of gestation or birth weight ≥1000 g in 438 hospitals in the NMNMSS between 2012 and 2016. MAIN OUTCOME MEASURES: Obstetric risk was defined using a modified Robson classification. The main outcome measures were changes in parity and age distributions and relative frequency of each Robson group, crude and adjusted trends over time in caesarean section rates within each risk category (using Poisson regression with a robust variance estimator), and trends in perinatal and pregnancy related mortality over time. RESULTS: Caesarean section rates declined steadily between 2012 and 2016 (crude relative risk 0.91, 95% confidence interval 0.89 to 0.93), reaching an overall hospital based rate of 41.1% in 2016. The relaxation of the one child policy was associated with an increase in the proportion of multiparous births (from 34.1% in 2012 to 46.7% in 2016), and births in women with a uterine scar nearly doubled (from 9.8% to 17.7% of all births). Taking account of these changes, the decline in caesarean sections was amplified over time (adjusted relative risk 0.82, 95% confidence interval 0.81 to 0.84). Caesarean sections declined noticeably in nulliparous women (0.75, 0.73 to 0.77) but also declined in multiparous women without a uterine scar (0.65, 0.62 to 0.77). The decrease in caesarean section rates was most pronounced in hospitals with the highest rates in 2012, consistent with the government's policy of targeting hospitals with the highest rates. Perinatal mortality declined from 10.1 to 7.2 per 1000 births over the same period (0.87, 0.83 to 0.91), and there was no change in pregnancy related mortality over time. CONCLUSIONS: China is the only country that has succeeded in reverting the rising trends in caesarean sections. China's success is remarkable given that the changes in obstetric risk associated with the relaxation of the one child policy would have led to an increase in the need for caesarean sections. China's experience suggests that change is possible when strategies are comprehensive and deal with the system level factors that underpin overuse as well as the various incentives at work during a clinical encounter

Inflammatory mediator bradykinin increases population of sensory neurons expressing functional T-type Ca2+ channels

T-type Ca2+ channels are important regulators of peripheral sensory neuron excitability. Accordingly, T-type Ca2+ currents are often increased in various pathological pain conditions, such as inflammation or nerve injury. Here we investigated effects of inflammation on functional expression of T-type Ca2+ channels in small-diameter cultured dorsal root ganglion (DRG) neurons. We found that overnight treatment of DRG cultures with a cocktail of inflammatory mediators bradykinin (BK), adenosine triphosphate (ATP), norepinephrine (NE) and prostaglandin E2 (PGE2) strongly increased the population size of the small-diameter neurons displaying low-voltage activated (LVA, T-type) Ca2+ currents while having no effect on the peak LVA current amplitude. When applied individually, BK and ATP also increased the population size of LVA-positive neurons while NE and PGE2 had no effect. The PLC inhibitor U-73122 and B2 receptor antagonist, Hoe-140, both abolished the increase of the population of LVA-positive DRG neurons. Inflammatory treatment did not affect CaV3.2 mRNA or protein levels in DRG cultures. Furthermore, an ubiquitination inhibitor, MG132, did not increase the population of LVA-positive neurons. Our data suggest that inflammatory mediators BK and ATP increase the abundance of LVA-positive DRG neurons in total neuronal population by stimulating the recruitment of a 'reserve pool' of CaV3.2 channels, particularly in neurons that do not display measurable LVA currents under control conditions