Structural Design and Parameter Optimization of Magnetic Gradient Tensor Measurement System.

Magnetic anomaly detection (MAD) technology based on the magnetic gradient tensor (MGT) has broad application prospects in fields such as unexploded ordnance detection and mineral exploration. The difference approximation method currently employed in the MGT measurement system introduces measurement errors. Designing reasonable geometric structures and configuring optimal structural parameters can effectively reduce measurement errors. Based on research into differential MGT measurement, this paper proposes three simplified planar MGT measurement structures and provides the differential measurement matrix. The factors that affect the design of the baseline distance of the MGT measurement system are also theoretically analyzed. Then, using the magnetic dipole model, the error analysis of the MGT measurement structures is carried out. The results demonstrate that the planar cross-shaped structure is optimal, with the smallest measurement error, only 3.15 × 10-10 T/m. Furthermore, employing the control variable method, the impact of sensor resolution constraints, noise level, target magnetic moment, and detection distance on the design of the optimal baseline distance of the MGT measurement system is simulated and verified. The results indicate that the smaller the target magnetic moment, the farther the detection distance, the lower the magnetometer resolution, the greater the noise, and the greater the baseline distance required. These conclusions provide reference and guidance for the construction of the MGT measurement system based on triaxial magnetometers.

A Remote Two-Point Magnetic Localization Method Based on SQUID Magnetometers and Magnetic Gradient Tensor Invariants.

In practical application, existing two-point magnetic gradient tensor (MGT) localization methods have a maximum detection distance of only 2.5 m, and the magnetic moment vectors of measured targets are all unknown. In order to realize remote, real-time localization, a new two-point magnetic localization method based on self-developed, ultra-sensitive superconducting quantum interference device (SQUID) magnetometers and MGT invariants is proposed. Both the magnetic moment vector and the relative position vector can be directly calculated based on the linear positioning model, and a quasi-Newton optimization algorithm is adopted to further improve the interference suppression capability. The simulation results show that the detection distance of the proposed method can reach 500 m when the superconducting MGT measurement system is used. Compared with Nara's single-point tensor (NSPT) method and Xu's two-point tensor (XTPT) method, the proposed method produces the smallest relative localization error (i.e., significantly less than 1% in the non-positioning blind area) without sacrificing real-time characteristics. The causes of and solutions to the positioning blind area are also analyzed. The equivalent experiments, which were conducted with a detection distance of 10 m, validate the effectiveness of the localization method, yielding a minimum relative localization error of 4.5229%.

Differences in the Determination of Volatile Organic Compounds between Chrysanthemum morifolium Ramat. and Chrysanthemum indicum L. (Wild Chrysanthemum) by HS-GC-IMS.

Chrysanthemums and wild chrysanthemums are herbs with high application value. As edible plants of the Asteraceae family, they have good antioxidant, anti-inflammatory and hepatoprotective properties. Chrysanthemums and wild chrysanthemums contain a wide variety of volatile organic compounds, and these volatile components are the main factors contributing to the flavor differences. Therefore, in this study, we investigated the volatile components of holland chrysanthemum from Bozhou, Anhui Province, Chu-chrysanthemum from Chuzhou, Anhui Province, Gong-chrysanthemums from Huangshan, Anhui Province, Huai-chrysanthemums from Jiaozuo, Henan Province, Hang-chrysanthemum from Hangzhou, Zhejiang Province, and wild chrysanthemum from Dabie Mountain by headspace-gas chromatography-ion mobility spectrometry (HS-GC-IMS) coupled with principal component analysis (PCA). The results showed that Chrysanthemum and wild chrysanthemum contain alcohols, esters, hydrocarbons, ketones, aldehydes, acids, camphor, pyrazines and furans. Among them, alcohols, esters and hydrocarbons accounted for more than 15%. It was hypothesized that 2-methyl-1-propanol, 2-methylbutanol, 1-hexanol in alcohols and hexyl acetate, 3-methylbutyl acetate and ethyl 2-methylpropanoate in esters might be the main reasons for the alcoholic and sweet flavors of chrysanthemum and chrysanthemum officinale. Based on the principal component analysis, cluster analysis with the Euclidean distance and similarity analysis of fingerprints, it was found that there were significant differences in the volatile components in chrysanthemums from different origins, among which the differences between Chu-chrysanthemum and Hang-chrysanthemum were the most significant. In addition, as a genus of wild chrysanthemum with the same species, it contains a richer variety of volatile organic compounds, and the content of hydrocarbons and alcohols is significantly higher than that of chrysanthemum.

Leak Detection and Localization in Multi-Grid Space Using Improved Gaussian Plume Model.

Leak detection and localization of liquid or gas is of great significance to avoid potential danger and reduce the waste of resources. Leak detection and localization methods are varied and uniquely suited to specific application scenarios. The existing methods are primarily applied to conventional pressurized pipelines and open areas, and there are few methods suitable for multi-grid spaces. In this paper, a gas diffusion model applied to multi-grid space is constructed, and a method for leak detection and localization using the concentration gradient of characteristic gas is proposed according to the prediction behavior. The Gaussian plume model is selected due to its advantages of simplicity and the interpretation of gas diffusion behavior is closer to reality; the expression of the improved model is also obtained. To verify the correctness of the model and the applicability of the localization method, taking the coolant leakage in the circuit system as an example, three experiments with different source strengths were repeated. The fitting correlation coefficients between the gas concentration data of the three experiments and the model are 0.995, 0.997 and 0.997, respectively. The experimental results show that the model has a strong correlation with the real plume behavior, and it is reasonable to use the gas concentration gradient for the localization of the leak source. This study provides a reference for future research on the leak detection and localization of gas- or liquid-containing volatile substances in a complex multi-grid space.

Icaritin inhibits neuroinflammation in a rat cerebral ischemia model by regulating microglial polarization through the GPER-ERK-NF-κB signaling pathway.

BACKGROUND: Activated microglia play a key role in initiating the inflammatory cascade following ischemic stroke and exert proinflammatory or anti-inflammatory effects, depending on whether they are polarized toward the M1 or M2 phenotype. The present study investigated the regulatory effect of icaritin (ICT) on microglial polarization in rats after cerebral ischemia/reperfusion injury (CI/RI) and explored the possible anti-inflammatory mechanisms of ICT. METHODS: A rat model of transient middle cerebral artery occlusion (tMCAO) was established. Following treatment with ICT, a G protein-coupled estrogen receptor (GPER) inhibitor or an extracellular signal-regulated kinase (ERK) inhibitor, the Garcia scale and rotarod test were used to assess neurological and locomotor function. 2,3,5-Triphenyltetrazolium chloride (TTC) and Fluoro-Jade C (FJC) staining were used to evaluate the infarct volume and neuronal death. The levels of inflammatory factors in the ischemic penumbra were evaluated using enzyme-linked immunosorbent assays (ELISAs). In addition, western blotting, immunofluorescence staining and quantitative PCR (qPCR) were performed to measure the expression levels of markers of different microglial phenotypes and proteins related to the GPER-ERK-nuclear factor kappa B (NF-κB) signaling pathway. RESULTS: ICT treatment significantly decreased the cerebral infarct volume, brain water content and fluorescence intensity of FJC; improved the Garcia score; increased the latency to fall and rotation speed in the rotarod test; decreased the levels of interleukin-1 beta (IL-1ß), tumor necrosis factor-alpha (TNF-α), Iba1, CD40, CD68 and p-P65-NF-κB; and increased the levels of CD206 and p-ERK. U0126 (an inhibitor of ERK) and G15 (a selective antagonist of GPER) antagonized these effects. CONCLUSIONS: These findings indicate that ICT plays roles in inhibiting the inflammatory response and achieving neuroprotection by regulating GPER-ERK-NF-κB signaling and then inhibiting microglial activation and M1 polarization while promoting M2 polarization, which provides a new therapeutic for against cerebral ischemic stroke.

CRISPR/Cas9 with single guide RNA expression driven by small tRNA promoters showed reduced editing efficiency compared to a U6 promoter.

Multiplex genome engineering in vivo with CRISPR/Cas9 shows great promise as a potential therapeutic approach. The ability to incorporate multiple single guide RNA (sgRNA) cassettes together with Cas9 gene expression in one AAV vector could greatly enhance the efficiency. In a recent Method article, Mefferd and coworkers indicated that small tRNA promoters could be used to drive sgRNA expression to facilitate the construction of a more effective AAV vector. In contrast, we found that when targeting endogenous genomic loci, CRISPR/Cas9 with tRNA promoter-driven sgRNA expression showed much reduced genome editing activity, compared with significant cleavage with U6 promoter-driven sgRNA expression. Though the underlying mechanisms are still under investigation, our study suggests that the CRISPR/Cas9 system with tRNA promoter-driven sgRNA expression needs to be reevaluated before it can be used for therapeutic genome editing.

PAQR3 modulates H3K4 trimethylation by spatial modulation of the regulatory subunits of COMPASS-like complexes in mammalian cells.

Histone modification plays important roles in many biological processes such as development and carcinogenesis. Methylation of histone H3 lysine 4 (H3K4) is commonly associated with transcriptional activation of genes. H3K4 methylation in mammalian cells is carried out by COMPASS (complex of proteins associated with Set1)-like complexes that are composed of catalytic subunits such as MLL1 (mixed-lineage leukaemia 1) and multiple regulatory subunits in which WDR5 (WD40 repeat-containing protein 5), RBBP5 (retinoblastoma-binding protein 5), ASH2 (absent, small or homoeotic discs 2) and DPY30 [constituting the WRAD sub-complex (WDR5-ASH2-RBBP5-DPY30 complex)] are the major ones shared from yeast to metazoans. We report, in the present paper, a new mode of spatial regulation of H3K4 methyltransferase complexes. PAQR3 (progestin and adipoQ receptors member 3), a tumour suppressor specifically localized in the Golgi apparatus, negatively regulates H3K4 trimethylation (H3K4me3) in mammalian cells. Consistently, HOXC8 and HOXA9 gene expression was negatively regulated by PAQR3 expression levels. Hypoxia-induced H3K4me3 was augmented by PAQR3 knockdown and suppressed by PAQR3 overexpression in AGS gastric cancer cells. PAQR3 was able to interact directly or indirectly with the four members of the WRAD sub-complex and tether them to the Golgi apparatus, accompanied by reduction in histone methyltransferase activity in the nucleus. PAQR3 also interfered with the interaction of WDR5 with the C-terminus of MLL1 (C-ter). Collectively, our study indicates that PAQR3 negatively modulates H3K4 methylation via altering the subcellular compartmentalization of the core regulatory subunits of the COMPASS-like complexes in mammalian cells.

Use of genome editing tools in human stem cell-based disease modeling and precision medicine.

Precision medicine emerges as a new approach that takes into account individual variability. The successful conduct of precision medicine requires the use of precise disease models. Human pluripotent stem cells (hPSCs), as well as adult stem cells, can be differentiated into a variety of human somatic cell types that can be used for research and drug screening. The development of genome editing technology over the past few years, especially the CRISPR/Cas system, has made it feasible to precisely and efficiently edit the genetic background. Therefore, disease modeling by using a combination of human stem cells and genome editing technology has offered a new platform to generate " personalized " disease models, which allow the study of the contribution of individual genetic variabilities to disease progression and the development of precise treatments. In this review, recent advances in the use of genome editing in human stem cells and the generation of stem cell models for rare diseases and cancers are discussed.

[Efficient genome editing in human pluripotent stem cells through CRISPR/Cas9].

The RNA-guided CRISPR (clustered regularly interspaced short palindromic repeat)-associated Cas9 nuclease has offered a new platform for genome editing with high efficiency. Here, we report the use of CRISPR/Cas9 technology to target a specific genomic region in human pluripotent stem cells. We show that CRISPR/Cas9 can be used to disrupt a gene by introducing frameshift mutations to gene coding region; to knock in specific sequences (e.g. FLAG tag DNA sequence) to targeted genomic locus via homology directed repair; to induce large genomic deletion through dual-guide multiplex. Our results demonstrate the versatile application of CRISPR/Cas9 in stem cell genome editing, which can be widely utilized for functional studies of genes or genome loci in human pluripotent stem cells.

Luteolin alleviates alcoholic liver disease induced by chronic and binge ethanol feeding in mice.

Ethanol consumption can lead to hepatic steatosis that contributes to late-stage liver diseases such as cirrhosis and hepatocellular carcinoma. In this study, we investigated the potential protective effect of a flavonoid, luteolin, on ethanol-induced fatty liver development and liver injury. Six-wk-old male C57BL/6 mice were divided into 3 groups: a control group; a group exposed to alcohol by using a chronic and binge ethanol feeding protocol (EtOH); and a group that was administered daily 50 mg/kg of luteolin in addition to ethanol exposure (EtOH + Lut). A chronic and binge ethanol feeding protocol was used, including chronic ethanol consumption (1%, 2%, and 4% for 3 d, and 5% for 9 d) and a binge (30% ethanol) on the last day. Compared with the control group, the EtOH group had a significant elevation in serum concentrations of alanine aminotransferase (ALT) (561%), triglyceride (TG) (47%), and LDL cholesterol (95%), together with lipid accumulation in the liver. Compared with the EtOH group, the EtOH + Lut group had significant reductions in serum concentrations of ALT (43%), TG (22%), LDL cholesterol (52%), and lipid accumulation in the liver. Ethanol elevated liver expression of lipogenic genes including sterol regulatory element-binding protein 1c (Srebp1c) (560%), fatty acid synthase (Fasn) (190%), acetyl-CoA carboxylase (Acc) (48%), and stearoyl-CoA desaturase 1 (Scd1) (286%). Luteolin reduced ethanol-induced expression of these genes in the liver: Srebp1c (79%), Fasn (80%), Acc (60%), and Scd1 (89%). In cultured hepatocytes, luteolin prevented alcohol-induced lipid accumulation and increase in the expression of lipogenic genes. The transcriptional activity of the master regulator of lipid synthesis, sterol regulatory element-binding protein (SREBP), was enhanced by ethanol treatment (160%) and reduced by luteolin administration (67%). In addition, ethanol-induced reduction of AMP-activated protein kinase and SREBP-1c phosphorylation was abrogated by luteolin. Collectively, our study indicates that luteolin is effective in ameliorating ethanol-induced hepatic steatosis and injury.

Research Progress on New Functions of Animal and Plant Proteins.

Protein is composed of peptides, essential nutrients for human survival and health, and the easy absorption of peptides further promotes human health. According to the source of the protein, it can be divided into plants, animals, and micro-organisms, which have important physiological effects on the health of the body, especially in enhancing immunity. The most widely used raw materials are animal protein and plant protein, and the protein composition formed by the two in a certain proportion is called "double protein". In recent years, China's State Administration for Market Regulation has issued an announcement on the "Implementation Rules for the Technical Evaluation of New Functions and Products of Health Foods (Trial)", which provides application conditions and listing protection for the research and development of new functions of health foods. At present, some researchers and enterprises have begun to pay attention to the potential of animal and plant proteins to be used in new functions. In this article, the research progress of animal and plant proteins in the new functions of Chinese health food is reviewed in detail, and suggestions for future research on animal and plant proteins are put forward.

Genistein-3'-sodium sulfonate enhances neurological function in neonatal rats with hypoxia-ischemia during the recovery period.

Hypoxic-ischemic (HI) can cause neonatal brain damage leading to disability. Patients with HI experience long-term neurological issues impacting quality of life. Limited clinical treatments are available despite extensive research on HI's molecular mechanisms. Genistein-3'-sodium sulfonate (GSS), a phytoestrogen, has been found to improve acute brain injury in neonatal rats caused by hypoxic-ischemia, but its potential for chronic stage neurological recovery in HI is unknown. HI neonatal rats were treated with 1 mg/kg GSS once a day for 21 days. Then, a series of behavioral experiments was performed to evaluate the learning, memory, cognition, anxiety level and depression-like behaviors of the rats. GSS treatment reduced neuronal loss, enhanced learning, memory and cognitive function while also alleviated anxiety and depression-like behaviors in HI rats during the recovery period. These findings indicated that GSS exerted enhance neurological function in HI rats during the chronic stage, prompting further research on how it works to potentially develop new therapies.

Therapeutic Effects of Natural Products on Liver Cancer and Their Potential Mechanisms.

Liver cancer ranks third globally among causes of cancer-related deaths, posing a significant public health challenge. However, current treatments are inadequate, prompting a growing demand for novel, safe, and effective therapies. Natural products (NPs) have emerged as promising candidates in drug development due to their diverse biological activities, low toxicity, and minimal side effects. This paper begins by reviewing existing treatment methods and drugs for liver cancer. It then summarizes the therapeutic effects of NPs sourced from various origins on liver cancer. Finally, we analyze the potential mechanisms of NPs in treating liver cancer, including inhibition of angiogenesis, migration, and invasion; regulation of the cell cycle; induction of apoptosis, autophagy, pyroptosis, and ferroptosis; influence on tumor metabolism; immune regulation; regulation of intestinal function; and regulation of key signaling pathways. This systematic review aims to provide a comprehensive overview of NPs research in liver cancer treatment, offering a foundation for further development and application in pharmaceuticals and functional foods.

AD16 attenuates neuroinflammation induced by cerebral ischemia through down-regulating astrocytes A1 polarization.

A1 polarization of astrocytes mediated prolonged inflammation contributing to brain injury in ischemic stroke. We have previously shown that AD16 protects against neonatal hypoxic-ischemic brain damage in vivo and oxygen-glucose deprivation in vitro. More recently, AD16 has demonstrated safety, tolerability, and favorable pharmacokinetics in a randomized controlled phase I trial. In this study, we utilized a rat model of transient middle cerebral artery occlusion (tMCAO) to explore whether the anti-inflammatory compound AD16 protects against ischemic brain injury by regulating A1 polarization and its underlying mechanisms. Our results showed that AD16 treatment significantly reduced the brain infarcted volume and improved neurological function in tMCAO rats. GO analysis results show that differential genes among the Sham, tMCAO and AD16 treatment groups are involved in the regulation of cytokine and inflammatory response. KEGG enrichment pathways analysis mainly enriched in cytokine-cytokine receptor interaction, viral protein interaction with cytokine-cytokine receptor, TNF, chemokine, NF-κB and IL-17 signaling pathway. Furthermore, AD16 treatment decreased the permeability of the blood-brain barrier and suppressed neuroinflammation. AD16 treatment also significantly reduced the polarization of A1 and inhibited NF-κB and JAK2/STAT3 signaling pathways. This study demonstrates that AD16 protects against brain injury in ischemic stroke by reducing A1 polarization to suppress neuroinflammation through downregulating NF-κB and JAK2/STAT3 signaling. Our findings uncover a potential molecular mechanism for AD16 and suggest that AD16 holds promising therapeutic potential against cerebral ischemia.

Insight into the Neuroprotective Effect of Genistein-3'-Sodium Sulfonate Against Neonatal Hypoxic-Ischaemic Brain Injury in Rats by Bioinformatics.

Therapeutic hypothermia (TH) is the only intervention approved for the treatment of neonatal hypoxic-ischaemic encephalopathy (HIE), but its treatment window is narrow (within 6 h after birth), and its efficacy is not ideal. Thus, alternative treatments are urgently needed. Our previous studies showed that genistein-3'-sodium sulfonate (GSS), a derivative of genistein (Gen), has a strong neuroprotective effect in rats with ischaemic stroke, but its role in HIE is unclear. A hypoxia-ischaemia (HI) brain injury model was established in neonatal male Sprague‒Dawley (SD) rats. Twenty-four hours after reperfusion, rats treated with GSS were assessed for cerebral infarction, neurological function, and neuronal damage. RNA-Seq and bioinformatics analysis were used to explore differentially expressed genes (DEGs) and regulated signalling pathways, which were subsequently validated by Western blotting and immunofluorescence. In this study, we found that GSS not only significantly reduced the size of brain infarcts and alleviated nerve damage in rats with HIE but also inhibited neuronal loss and degeneration in neonatal rats with HIE. A total of 2170 DEGs, of which 1102 were upregulated and 1068 were downregulated, were identified in the GSS group compared with the HI group. In an analysis based on Kyoto Encyclopedia of Genes and Genomes (KEGG) categories, the downregulated DEGs were significantly enriched in the pathways "Phagosome", "NF-κB signalling", and "Complement and coagulation cascades", amongst others. Meanwhile, the upregulated DEGs were significantly enriched in the pathways "Neurodegeneration", "Glutamatergic synapse", and "Calcium signalling pathway", amongst others. These results indicate that GSS intervenes in the process of HIE-induced brain injury by participating in multiple pathways, which suggests potential candidate drugs for the treatment of HIE.

Icaritin alleviates cerebral ischemia‒reperfusion injury by regulating NMDA receptors through ERK signaling.

N-methyl-D-aspartate (NMDA) receptors are key signaling molecules that mediate excitotoxicity during cerebral ischemia. GluN2A-containing NMDA receptors, which are mostly located in the intrasynaptic region, mediate normal physiological processes and promote neuronal survival. GluN2B-containing NMDA receptors, which are mostly located in the extrasynaptic region, mediate excitotoxicity injury and promote neuronal death during ischemia. This study investigated the ability of icaritin (ICT) to protect against cerebral ischemia‒reperfusion injury (CI/RI) by regulating GluN2B-containing NMDA receptors through extracellular signaling regulatory kinases/death associated protein kinase 1 (ERK/DAPK1) signaling. A rat CI/RI model was established by transient middle cerebral artery occlusion (tMCAO). Following treatment with ICT and the ERK-specific inhibitor U0126, cerebral infarction, neurological function, and excitotoxicity-related molecule expression were assessed 24 h after reperfusion. ICT treatment significantly decreased cerebral infarct volume, improved neurological function, and regulated NMDA receptor subtype expression and ERK/DAPK1 signaling activation. The ability of ICT to increase GluN2A and postsynaptic density protein 95 (PSD95) mRNA and protein expression, inhibit GluN2B expression, and regulate DAPK1 activation was reversed after administration of the ERK-specific inhibitor U0126. These data indicated that ICT inhibited excitotoxicity injury and exerted a protective effect against CI/RI that was likely mediated by increased ERK signaling pathway activation and regulation of extrasynaptic and intrasynaptic NMDA receptor function, providing a new therapeutic target for ischemic encephalopathy.

Citrus ichangensis Peel Extract Exhibits Anti-Metabolic Disorder Effects by the Inhibition of PPARγ and LXR Signaling in High-Fat Diet-Induced C57BL/6 Mouse.

Obesity is a common nutritional disorder associated with type 2 diabetes, cardiovascular diseases, dyslipidemia, and certain cancers. In this study, we investigated the effects of Citrus ichangensis peel extract (CIE) in high-fat (HF) diet-induced obesity mice. Female C57BL/6 mice were fed a chow diet or an HF diet alone or supplemented with 1% w/w CIE for 8 weeks. We found that CIE treatment could lower blood glucose level and improve glucose tolerance. In the HF+CIE group, body weight gain, serum total cholesterol (TC) and low-density lipoprotein cholesterol (LDL-c) levels, and liver triglyceride (TG) and TC concentrations were significantly (P < 0.05) decreased relative to those in the HF group. To elucidate the mechanism of CIE on the metabolism of glucose and lipid, related genes expression in liver were examined. In liver tissue, CIE significantly decreased the mRNA expression levels of peroxisome proliferator-activated receptor γ (PPARγ) and its target genes, such as fatty acid synthase (FAS) and acyl-CoA oxidase (ACO). Moreover, CIE also decreased the expression of liver X receptor (LXR) α and ß which are involved in lipid and glucose metabolism. These results suggest that CIE administration could alleviate obesity and related metabolic disorders in HF diet-induced obesity mice through the inhibition of PPARγ and LXR signaling.

Does HIV-Related Stigma Depress Social Well-Being of Youths Affected by Parental HIV/AIDS?

Parental illness or death due to HIV/AIDS has long-term impacts on children's social well-being, potentially challenging the children's basic developmental needs and future. Based on the theoretical model of social well-being, the present study tested a moderated mediation model that HIV-related stigma moderated the mediating role of social trust on the relationship between perceived social support (PSS) and social well-being. A sample of 297 youths aged 20-30 years affected by parental HIV/AIDS (57.2% male), including 129 (43.40%) AIDS orphans and 168 vulnerable youths (56.60%) completed questionnaires of perceived social support, social well-being, social trust, and HIV-related stigma. IBM SPSS 25.0 was used to conduct descriptive statistics and multiple regressions. Results showed that the mean score of PSS was 61.34 (SD = 13.99), social well-being was 57.33 (SD = 10.15), social trust was 56.21 (SD = 11.55), perceived stigma was 64.44 (SD = 16.72), and enacted stigma was 21.91 (SD = 9.73) among youths affected by parental HIV/AIDS and the PSS could predict increasing social well-being via increasing social trust. Moreover, the positive influence of PSS on social trust was moderated by the enacted stigma (p = 0.03), in which the positive influence was stronger among youths affected by parental HIV/AIDS who perceived or experienced low enacted stigma than those who perceived or experienced high enacted stigma. The positive impact of social trust on social well-being was moderated by perceived stigma (p = 0.04), in which the positive impact was more significant among youths affected by parental HIV/AIDS who perceived or experienced high perceived stigma than those who perceived or experienced low perceived stigma. These findings explained how and when the PSS affected social well-being and contributed toward an understanding of the experiences and perceptions of HIV-related stigma among youths affected by parental HIV/AIDS. This understanding may inform future research and policies toward improving the social well-being of youths affected by parental HIV/AIDS. The study also highlighted the importance of strengthening interventions on social relations and reducing HIV-related stigma for them.

Isolation of a new monoterpenoid glycoside from Anhua dark tea based on an NMR-guided method and its cytotoxic activity against MDA-MB-231 and SH-SY5Y cell lines.

Based on an NMR-guided method, one new monoterpenoid glycoside (1) was isolated from Anhua dark tea, together with five known compounds (2-6). The structure of the new compound was determined as 3-(5,5-dimethyltetrahydrofuranyl)-1-buten-3-ol primeveroside, and trivially named anhuaterpenoside A (1), on the basis of detailed spectroscopic analyses, and acidic hydrolysis. Compound 1 exhibits cytotoxic activity against MDA-MB-231 and SH-SY5Y cell lines with IC50 value of 23.26 µM and 18.57 µM, respectively.