Optimization of HS-SPME for GC-MS Analysis and Its Application in Characterization of Volatile Compounds in Sweet Potato.

Volatile compounds are the main chemical species determining the characteristic aroma of food. A procedure based on headspace solid-phase microextraction (HP-SPME) coupled to gas chromatography-mass spectrometry (GC-MS) was developed to investigate the volatile compounds of sweet potato. The experimental conditions (fiber coating, incubation temperature and time, extraction time) were optimized for the extraction of volatile compounds from sweet potato. The samples incubated at 80 °C for 30 min and extracted at 80 °C by the fiber with a divinylbenzene/carboxen/polydimethylsiloxane (DVB/CAR/PDMS) coating for 30 min gave the most effective extraction of the analytes. The optimized method was applied to study the volatile profile of four sweet potato cultivars (Anna, Jieshu95-16, Ayamursaki, and Shuangzai) with different aroma. In total, 68 compounds were identified and the dominants were aldehydes, followed by alcohols, ketones, and terpenes. Significant differences were observed among the volatile profile of four cultivars. Furthermore, each cultivar was characterized by different compounds with typical flavor. The results substantiated that the optimized HS-SPME GC-MS method could provide an efficient and convenient approach to study the flavor characteristics of sweet potato. This is the basis for studying the key aroma-active compounds and selecting odor-rich accessions, which will help in the targeted improvement of sweet potato flavor in breeding.

FAK activates AKT-mTOR signaling to promote the growth and progression of MMTV-Wnt1-driven basal-like mammary tumors.

BACKGROUND: Breast cancer is a heterogeneous disease. Hence, stratification of patients based on the subtype of breast cancer is key to its successful treatment. Among all the breast cancer subtypes, basal-like breast cancer is the most aggressive subtype with limited treatment options. Interestingly, we found focal adhesion kinase (FAK), a cytoplasmic tyrosine kinase, is highly overexpressed and activated in basal-like breast cancer. METHODS: To understand the role of FAK in this subtype, we generated mice with conditional deletion of FAK and a knock-in mutation in its kinase domain in MMTV-Wnt1-driven basal-like mammary tumors. Tumor initiation, growth, and metastasis were characterized for these mice cohorts. Immunohistochemical and transcriptomic analysis of Wnt1-driven tumors were also performed to elucidate the mechanisms underlying FAK-dependent phenotypes. Pharmacological inhibition of FAK and mTOR in human basal-like breast cancer cell lines was also tested. RESULTS: We found that in the absence of FAK or its kinase function, growth and metastasis of the tumors were significantly suppressed. Furthermore, immunohistochemical analyses of cleaved caspase 3 revealed that loss of FAK results in increased tumor cell apoptosis. To further investigate the mechanism by which FAK regulates survival of the Wnt1-driven tumor cells, we prepared an isogenic pair of mammary tumor cells with and without FAK and found that FAK ablation increased their sensitivity to ER stress-induced cell death, as well as reduced tumor cell migration and tumor sphere formation. Comparative transcriptomic profiling of the pair of tumor cells and gene set enrichment analysis suggested mTOR pathway to be downregulated upon loss of FAK. Immunoblot analyses further confirmed that absence of FAK results in reduction of AKT and downstream mTOR pathways. We also found that inhibition of FAK and mTOR pathways both induces apoptosis, indicating the importance of these pathways in regulating cell survival. CONCLUSIONS: In summary, our studies show that in a basal-like tumor model, FAK is required for survival of the tumor cells and can serve as a potential therapeutic target.

Correction to: FAK activates AKT-mTOR signaling to promote the growth and progression of MMTV-Wnt1-driven basal-like mammary tumors.

An amendment to this paper has been published and can be accessed via the original article.

Comparison of the CASA and InVEST models' effects for estimating spatiotemporal differences in carbon storage of green spaces in megacities.

Urban green space is a direct way to improve the carbon sink capacity of urban ecosystems. The carbon storage assessment of megacity green spaces is of great significance to the service function of urban ecosystems and the management of urban carbon zoning in the future. Based on multi-period remote sensing image data, this paper used the CASA model and the InVEST model to analyze the spatio-temporal variation and driving mechanism of carbon storage in Shenzhen green space and discussed the applicability of the two models to the estimation of carbon storage in urban green space. The research results showed that, from 2008 to 2022, in addition to the rapid expansion of construction land, the area of green space and other land types in Shenzhen showed a significant decrease trend. The estimation results of the carbon storage model showed that the carbon storage of green space shows a significant trend of reduction from 2008 to 2022, and the reduction amounts are 0.8 × 106 t (CASA model) and 0.64 × 106 t (InVEST model), respectively. The evaluation results of the model show that, in megacities, the spatial applicability of InVEST model is lower than that of CASA model, and the CASA model is more accurate in estimating the carbon storage of urban green space. The research results can provide a scientific basis for the assessment of the carbon sink capacity of megacity ecosystems with the goal of "dual carbon".

Highly efficient Ni(II) adsorption by industrial lignin-based biochar: a pivotal role of dissolved substances within biochar.

In the context of carbon neutrality, promoting resource utilization of industrial alkali lignin addressing heavy metal pollution is crucial for China's pollution alleviation and carbon reduction. Microwave pyrolysis produced functionalized biochar from industrial alkali lignin for Ni(II) adsorption. LB400 achieved 343.15 mg g-1 saturated adsorption capacity in 30 min. Pseudo-second-order kinetic and Temkin isotherm models accurately described the adsorption, which was endothermic and spontaneous (ΔGÏ´ < 0, ΔHÏ´ > 0). Quantitative analysis revealed that both dissolved substances and carbon skeleton from biochar contributed to adsorption, with the former predominates (93.76%), including mineral precipitation NiCO3 (Qp) and adsorption of dissolved organic matter (QDOM). Surface complexation (Qc) and ion exchange (Qi) on the carbon skeleton accounted for 6.3%. Higher biochar preparation temperature reduced Ni(II) adsorption by dissolved substances. Overall, biochar which comes from the advantageous disposal of industrial lignin effectively removes Ni(II) contamination, encouraging ecologically sound treatment of heavy metal pollution and sustainable resource utilization.

High-throughput phenotyping of nutritional quality components in sweet potato roots by near-infrared spectroscopy and chemometrics methods.

The lack of an efficient approach for quality evaluation of sweet potatoes significantly hinders progress in quality breeding. Therefore, this study aimed to establish a near-infrared spectroscopy (NIRS) assay for high-throughput analysis of sweet potato root quality, including total starch, amylose, amylopectin, the ratio of amylopectin to amylose, soluble sugar, crude protein, total flavonoid content, and total phenolic content. A total of 125 representative samples were utilized and a dual-optimized strategy (optimization of sample subset partitioning and variable selection) was applied to NIRS modeling. Eight optimal equations were developed with an excellent coefficient of determination for the calibration (R2C) at 0.95-0.99, cross-validation (R2CV) at 0.93-0.98, external validation (R2V) at 0.89-0.96, and the ratio of prediction to deviation (RPD) at 6.33-11.35. Overall, these NIRS models provide a feasible approach for high-throughput analysis of root quality and permit large-scale screening of elite germplasm in future sweet potato breeding.

Combining Metabolomics and Transcriptomics to Reveal the Mechanism of Coloration in Purple and Cream Mutant of Sweet Potato (Ipomoea batatas L.).

Purple sweet potato is considered as a healthy food because of its high anthocyanins. To understand the coloring mechanism and quality change between purple-fleshed sweet potato (cv. Xuzi201) and its cream fleshed mutant (M1001), a combined metabolomic and transcriptomic analysis was performed. The metabolome data showed that 4 anthocyanins, 19 flavones, 6 flavanones, and 4 flavonols dramatically decreased in M1001, while the contents of 3 isoflavones, 3 flavonols, 4 catechins, and 2 proanthocyanins increased. Transcriptomic analyses indicated that the expression of 49 structural genes in the flavonoid pathway and transcription factors (TFs) (e.g., bHLH2, R2R3-MYB, MYB1) inducting anthocyanin biosynthesis were downregulated, but the repressor MYB44 was upregulated. The IbMYB1-2 gene was detected as a mutation gene in M1001, which is responsible for anthocyanin accumulation in the storage roots. Thus, the deficiency of purple color in the mutant is due to the lack of anthocyanin accumulation which was regulated by IbMYB1. Moreover, the accumulation of starch and aromatic volatiles was significantly different between Xuzi201 and M1001. These results not only revealed the mechanism of color mutation but also uncovered certain health-promoting compounds in sweet potato.

Integrated Systems Analysis Explores Dysfunctional Molecular Modules and Regulatory Factors in Children with Autism Spectrum Disorder.

Autism spectrum disorder (ASD) is a genetic neurodevelopmental disorder involving multiple genes that occurs in early childhood, and a number of risk genes have been reported in previous studies. However, the molecular mechanism of the polygenic regulation leading to pathological changes in ASD remains unclear. First, we identified 8 dysregulated gene coexpression modules by analyzing blood transcriptome data from 96 children with ASD and 42 controls. These modules are rich in ASD risk genes and function related to metabolism, immunity, neurodevelopment, and signaling. The regulatory factors of each module including microRNA (miRNA) and transcription factors (TFs) were subsequently predicted based on transcriptional and posttranscriptional regulation. We identified a set of miRNAs that regulate metabolic and immune modules, as well as transcription factors that cause dysregulation of the modules, and we constructed a coregulatory network between the regulatory factors and modules. Our work reveals dysfunctional modules in children with ASD, elucidates the role of miRNA and transcription factor dysregulation in the pathophysiology of ASD, and helps us to further understand the underlying molecular mechanism of ASD.

Drug repositioning based on network-specific core genes identifies potential drugs for the treatment of autism spectrum disorder in children.

Identification of exact causative genes is important for in silico drug repositioning based on drug-gene-disease relationships. However, the complex polygenic etiology of the autism spectrum disorder (ASD) is a challenge in the identification of etiological genes. The network-based core gene identification method can effectively use the interactions between genes and accurately identify the pathogenic genes of ASD. We developed a novel network-based drug repositioning framework that contains three steps: network-specific core gene (NCG) identification, potential therapeutic drug repositioning, and candidate drug validation. First, through the analysis of transcriptome data for 178 brain tissues, gene network analysis identified 365 NCGs in 18 coexpression modules that were significantly correlated with ASD. Second, we evaluated two proposed drug repositioning methods. In one novel approach (dtGSEA), we used the NCGs to probe drug-gene interaction data and identified 35 candidate drugs. In another approach, we compared NCG expression patterns with drug-induced transcriptome data from the Connectivity Map database and found 46 candidate drugs. Third, we validated the candidate drugs using an in-house mental diseases and compounds knowledge graph (MCKG) that contained 7509 compounds, 505 mental diseases, and 123,890 edges. We found a total of 42 candidate drugs that were associated with mental illness, among which 10 drugs (baclofen, sulpiride, estradiol, entinostat, everolimus, fluvoxamine, curcumin, calcitriol, metronidazole, and zinc) were postulated to be associated with ASD. This study proposes a powerful network-based drug repositioning framework and also provides candidate drugs as well as potential drug targets for the subsequent development of ASD therapeutic drugs.

Non-invasive remote limb ischemic postconditioning protects rats against focal cerebral ischemia by upregulating STAT3 and reducing apoptosis.

The signal transducer and activator of transcription 3 (STAT3) signaling pathway has been implicated in cell apoptosis and inflammatory processes. Ischemic preconditioning (IPC) and ischemic postconditioning (IPTC) inhibit both of these processes. In the present study, we investigated the role of phosphorylated STAT3 (p-STAT3)-mediated apoptosis and inflammation following non-invasive remote limb IPTC (NRIPoC) using a classic rat model of focal cerebral ischemia. Forty-five adult male Sprague-Dawley rats were divided randomly into 3 groups (n=15 per group): the sham-operated, ischemia/reperfusion (I/R) and NRIPoC groups. NRIPoC was implemented at the beginning of reperfusion. At 24 h after cerebral reperfusion, we evaluated the neurological deficit score (NDS), assessed the cerebral infarct size and tissue morphology, and evaluated neuronal apoptosis. The protein expression levels of Bcl-2, Bax, nuclear factor-κB (NF-κB), tumor necrosis factor-α (TNF-α) and p-STAT3 in the penumbra region were assessed by western blot analysis. The cerebral infarct volume, the number of apoptotic cells and the protein expression levels of Bcl-2, Bax, NF-κB and TNF-α were all found to be increased in the I/R group compared with the sham-operated group. However, these levels were decreased in the NRIPoC group compared with the I/R group. The number of apoptotic cells in the penumbra in the I/R group was increased compared with that in the NRIPoC and sham-operated groups. The protein expression of p-STAT3 was increased in the NRIPoC group compared with the sham-operated and I/R groups. These results indicate that the protective effects of NRIPoC against cerebral I/R injury may be related to the attenuation of neuronal apoptosis and inflammation through the activation of STAT3.