Properties of Heavy Higgs Bosons and Dark Matter under Current Experimental Limits in the μ\muNMSSM

Searches for new particles beyond the Standard Model (SM) are an important task for the Large Hadron Collider (LHC). In this paper, we investigate the properties of the heavy non-SM Higgs bosons in the $\mu$-term extended Next-to-Minimal Supersymmetric Standard Model ($\mu$NMSSM). We scan the parameter space of the $\mu$NMSSM considering the basic constraints from Higgs data, dark matter (DM) relic density, and LHC searches for sparticles. And we also consider the constraints from the LZ2022 experiment and the muon anomaly constraint at 2$\sigma$ level. We find that the LZ2022 experiment has a strict constraint on the parameter space of the $\mu$NMSSM, and the limits from the DM-nucleon spin-independent (SI) and spin-dependent (SD) cross-sections are complementary. Then we discuss the exotic decay modes of heavy Higgs bosons decaying into SM-like Higgs boson. We find that for doublet-dominated Higgs $h_3$ and $A_2$, the main exotic decay channels are $h_3\rightarrow Z A_1$, $h_3\rightarrow h_1 h_2$, $A_2\rightarrow A_1 h_1$ and $A_2\rightarrow Z h_2$, and the branching ratio can reach to about 23$\%$, 10$\%$, 35$\%$ and 10$\%$ respectively. At the 13 TeV LHC, the production cross-section of $ggF\rightarrow h_3\rightarrow h_1 h_2$ and $ggF\rightarrow A_2\rightarrow A_1 h_1$ can reach to about $10^{-11}$pb and $10^{-10}$pb, respectively

The Phenomenological Research on Higgs and dark matter in the Next-to-Minimal Supersymmetric Standard Model

The $Z_3$-invariant next-to-minimal supersymmetric standard model (NMSSM) can provide a candidate for dark matter (DM). It can also be used to explain the hypothesis that the Higgs signal observed on the Large Hadron Collider (LHC) comes from the contribution of the two lightest CP-even Higgs bosons, whose masses are near 125 GeV. At present, XENON1T, LUX, and PandaX experiments have imposed very strict restrictions on direct collision cross sections of {dark matter}. In this paper, we consider a scenario that the observed Higgs signal is the superposition of two mass-degenerate Higgs in the $Z_3$-invariant NMSSM and scan the seven-dimension parameter space composing of $\lambda, \kappa, \tan\beta, \mu, A_k, A_t, M_1$ via the Markov chain Monte Carlo (MCMC) method. We find that the DM relic density, as well as the LHC searches for sparticles, especially the DM direct detections, has provided a strong limit on the parameter space. %Please check intended meaning has been retained. The allowed parameter space is featured by a relatively small $\mu \le 300$ GeV and about $\tan\beta\in(10,20)$. In addition, the DM is Higgsino-dominated because of $|\frac{2\kappa}{\lambda}|>1$. Moreover, the co-annihilation between $\tilde{\chi}_1^0$ and $\tilde{\chi}_1^\pm$ must be taken into account to obtain the reasonable DM relic density

Novel Roles for Kv7 Channels in Shaping Histamine-Induced Contractions and Bradykinin-Dependent Relaxations in Pig Coronary Arteries.

Voltage-gated Kv7 channels are inhibited by agonists of Gq-protein-coupled receptors, such as histamine. Recent works have provided evidence that inhibition of vascular Kv7 channels may trigger vessel contractions. In this study, we investigated how Kv7 activity modulates the histamine-induced contractions in “healthy” and metabolic syndrome (MetS) pig right coronary arteries (CAs). We performed isometric tension and immunohistochemical studies with domestic, lean Ossabaw, and MetS Ossabaw pig CAs. We found that neither the Kv7.2/Kv7.4/Kv7.5 activator ML213 nor the general Kv7 inhibitor XE991 altered the tension of CA rings under preload, indicating that vascular Kv7 channels are likely inactive in the preloaded rings. Conversely, ML213 potently dilated histamine-pre-contracted CAs, suggesting that Kv7 channels are activated during histamine applications and yet partially inhibited by histamine. Immunohistochemistry analysis revealed strong Kv7.4 immunostaining in the medial and intimal layers of the CA wall, whereas Kv7.5 immunostaining intensity was strong in the intimal but weak in the medial layers. The medial Kv7 immunostaining was significantly weaker in MetS Ossabaw CAs as compared to lean Ossabaw or domestic CAs. Consistently, histamine-pre-contracted MetS Ossabaw CAs exhibited attenuated ML213-dependent dilations. In domestic pig CAs, where medial Kv7 immunostaining intensity was stronger, histamine-induced contractions spontaneously decayed to ~31% of the peak amplitude within 4 minutes. Oppositely, in Ossabaw CAs, where Kv7 immunostaining intensity was weaker, the histamine-induced contractions were more sustained. XE991 pretreatment significantly slowed the decay rate of histamine-induced contractions in domestic CAs, supporting the hypothesis that increased Kv7 activity correlates with a faster rate of histamine-induced contraction decay. Alternatively, XE991 significantly decreased the amplitude of bradykinin-dependent dilations in pre-contracted CAs. We propose that in CAs, a decreased expression or a loss of function of Kv7 channels may lead to sustained histamine-induced contractions and reduced endothelium-dependent relaxation, both risk factors for coronary spasm

Illegal Intrusion Detection of Internet of Things Based on Deep Mining Algorithm

In this study, to reduce the influence of The Internet of Things (IoT) illegal intrusion on the transmission effect, and ensure IoT safe operation, an illegal intrusion detection method of the Internet of Things (IoT) based on deep mining algorithm was designed to accurately detect IoT illegal intrusion. Moreover, this study collected the data in the IoT through data packets and carries out data attribute mapping on the collected data, transformed the character information into numerical information, implemented standardization and normalization processing on the numerical information, and optimized the processed data by using a regional adaptive oversampling algorithm to obtain an IoT data training set. The IoT data training set was taken as the input data of the improved sparse auto-encoder neural network. The hierarchical greedy training strategy was used to extract the feature vector of the sparse IoT illegal intrusion data that were used as the inputs of the extreme learning machine classifier to realize the classification and detection of the IoT illegal intrusion features. The experimental results indicate that the feature extraction of the illegal intrusion data of the IoT can effectively reduce the feature dimension of the illegal intrusion data of the IoT to less than 30 and the dimension of the original data. The recall rate, precision, and F1 value of the IoT intrusion detection are 98.3%, 98.7%, and 98.6%, respectively, which can accurately detect IoT intrusion attacks. The conclusion demonstrates that the intrusion detection of IoT based on deep mining algorithm can achieve accurate detection of IoT illegal intrusion and reduce the influence of IoT illegal intrusion on the transmission effect

Population Structure and Genetic Diversity in a Rice Core Collection (Oryza sativa L.) Investigated with SSR Markers

The assessment of genetic diversity and population structure of a core collection would benefit to make use of these germplasm as well as applying them in association mapping. The objective of this study were to (1) examine the population structure of a rice core collection; (2) investigate the genetic diversity within and among subgroups of the rice core collection; (3) identify the extent of linkage disequilibrium (LD) of the rice core collection. A rice core collection consisting of 150 varieties which was established from 2260 varieties of Ting's collection of rice germplasm were genotyped with 274 SSR markers and used in this study. Two distinct subgroups (i.e. SG 1 and SG 2) were detected within the entire population by different statistical methods, which is in accordance with the differentiation of indica and japonica rice. MCLUST analysis might be an alternative method to STRUCTURE for population structure analysis. A percentage of 26% of the total markers could detect the population structure as the whole SSR marker set did with similar precision. Gene diversity and MRD between the two subspecies varied considerably across the genome, which might be used to identify candidate genes for the traits under domestication and artificial selection of indica and japonica rice. The percentage of SSR loci pairs in significant (P<0.05) LD is 46.8% in the entire population and the ratio of linked to unlinked loci pairs in LD is 1.06. Across the entire population as well as the subgroups and sub-subgroups, LD decays with genetic distance, indicating that linkage is one main cause of LD. The results of this study would provide valuable information for association mapping using the rice core collection in future

Molecular Determinants of the Sensitivity to Gq/11-Phospholipase C-dependent Gating, Gd3+ Potentiation, and Ca2+ Permeability in the Transient Receptor Potential Canonical Type 5 (TRPC5) Channel

Transient receptor potential canonical type 5 (TRPC5) is a Ca2+-permeable cation channel that is highly expressed in the brain and is implicated in motor coordination, innate fear behavior, and seizure genesis. The channel is activated by a signal downstream of the G-protein-coupled receptor (GPCR)-Gq/11-phospholipase C (PLC) pathway. In this study we aimed to identify the molecular mechanisms involved in regulating TRPC5 activity. We report that Arg-593, a residue located in the E4 loop near the TRPC5 extracellular Gd3+ binding site, is critical for conferring the sensitivity to GPCR-Gq/11-PLC-dependent gating on TRPC5. Indeed, guanosine 5'-O-(thiotriphosphate) and GPCR agonists only weakly activate the TRPC5R593A mutant, whereas the addition of Gd3+ rescues the mutant's sensitivity to GPCR-Gq/11-PLC-dependent gating. Computer modeling suggests that Arg-593 may cross-bridge the E3 and E4 loops, forming the "molecular fulcrum." While validating the model using site-directed mutagenesis, we found that the Tyr-542 residue is critical for establishing a functional Gd3+ binding site, the Tyr-541 residue participates in fine-tuning Gd3+-sensitivity, and that the Asn-584 residue determines Ca2+ permeability of the TRPC5 channel. This is the first report providing molecular insights into the molecular mechanisms regulating the sensitivity to GPCR-Gq/11-PLC-dependent gating of a receptor-operated channel

R125H, W240S, C386R, and V507I SLC4A11 mutations associated with corneal endothelial dystrophy affect the transporter function but not trafficking in PS120 cells

SLC4A11 mutations are associated with Fuchs’ endothelial corneal dystrophy (FECD), congenital hereditary endothelial dystrophy (CHED) and Harboyan syndrome (endothelial dystrophy with auditory deficiency). Mice with genetically ablated Slc4a11 recapitulate CHED, exhibiting significant corneal edema and altered endothelial morphology. We recently demonstrated that SLC4A11 functions as an NH3 sensitive, electrogenic H+ transporter. Here, we investigated the properties of five clinically relevant SLC4A11 mutants: R125H, W240S, C386R, V507I and N693A, relative to wild type, expressed in a PS120 fibroblast cell line. The effect of these mutations on the NH4Cl-dependent transporter activity was investigated by intracellular pH and electrophysiology measurements. Relative to plasma membrane expression of NaK ATPase, there were no significant differences in plasma membrane SLC4A11 expression among each mutant and wild type. All mutants revealed a marked decrease in acidification in response to NH4Cl when compared to wild type, indicating a decreased H+ permeability in mutants. All mutants exhibited significantly reduced H+ currents at negative holding potentials as compared to wild type. Uniquely, the C386R and W240S mutants exhibited a different inward current profile upon NH4Cl challenges, suggesting an altered transport mode. Thus, our data suggest that these SLC4A11 mutants, rather than having impaired protein trafficking, show altered H+ flux properties

Egy 14. századi új Salamon: V. (Bölcs) Károly francia király

The result of in-hospital all mortality (P < 0.001; RR 3.23; 95% CI 2.28–4.57). (DOCX 54 kb

PKC-dependent Phosphorylation of the H1 Histamine Receptor Modulates TRPC6 Activity

Transient receptor potential canonical 6 (TRPC6) is a cation selective, DAG-regulated, Ca2+-permeable channel activated by the agonists of Gq-protein-coupled heptahelical receptors. Dysfunctions of TRPC6 are implicated in the pathogenesis of various cardiovascular and kidney conditions such as vasospasm and glomerulosclerosis. When stimulated by agonists of the histamine H1 receptor (H1R), TRPC6 activity decays to the baseline despite the continuous presence of the agonist. In this study, we examined whether H1R desensitization contributes to regulating the decay rate of TRPC6 activity upon receptor stimulation. We employed the HEK expression system and a biosensor allowing us to simultaneously detect the changes in intracellular diacylglycerol (DAG) and Ca2+ concentrations. We found that the histamine-induced DAG response was biphasic, in which a transient peak was followed by maintained elevated plateau, suggesting that desensitization of H1R takes place in the presence of histamine. The application of PKC inhibitor Gö6983 slowed the decay rate of intracellular DAG concentration. Activation of the mouse H1R mutant lacking a putative PKC phosphorylation site, Ser399, responsible for the receptor desensitization, resulted in a prolonged intracellular DAG increase and greater Mn2+ influx through the TRPC6 channel. Thus, our data support the hypothesis that PKC-dependent H1R phosphorylation leads to a reduced production of intracellular DAG that contributes to TRPC6 activity regulation