Improved Alkaline Hydrogen Evolution Performance of Dealloying Fe75-xCoxSi12.5B12.5 Electrocatalyst.

The electrocatalytic performance of a Fe65Co10Si12.5B12.5 Fe-based compounds toward alkaline hydrogen evolution reaction (HER) is enhanced by dealloying. The dealloying process produced a large number of nanosheets on the surface of NS-Fe65Co10Si12.5B12.5, which greatly increased the specific surface area of the electrode. When the dealloying time is 3 h, the overpotential of NS-Fe65Co10Si12.5B12.5 is only 175.1 mV at 1.0 M KOH and 10 mA cm-2, while under the same conditions, the overpotential of Fe65Co10Si12.5B12.5 is 215 mV, which is reduced. In addition, dealloying treated electrodes also show better HER performance than un-dealloying treated electrodes. With the increase in Co doping amount, the overpotential of the hydrogen evolution reaction decreases, and the hydrogen evolution activity is the best when the addition amount of Co is 10%. This work not only provides a basic understanding of the relationship between surface activity and the dealloying of HER catalysts, but also paves a new way for doping transition metal elements in Fe-based electrocatalysts working in alkaline media.

HACE1 exerts a neuroprotective role against oxidative stress in cerebral ischemia-reperfusion injury by activating the PI3K/AKT/Nrf2 pathway.

HECT domain and Ankyrin repeat-containing E3 ubiquitin protein ligase 1 (HACE1) is an E3 ubiquitin ligase involving oxidative stress, an important contributor in cerebral ischemia-reperfusion injury (CIRI). It was proposed to be associated with the PI3K/AKT pathway and Nrf2 nuclear translocation, which are important players of oxidative stress. Therefore, we supposed that HACE1 might affect CIRI by regulating the PI3K/AKT/Nrf2 pathway. Here, we used the transient middle cerebral artery occlusion-reperfusion (tMCAO/R) model to induce CIRI in rats and found lower HACE1 expression in ischemic rats compared with the control. To explore the exact role of HACE1, the lentivirus vector carrying the HACE1 sequence was administrated to rats by intracerebroventricular injection (1 × 109 TU/mL, 9 µL) one week before tMCAO/R operation. HACE1 overexpression alleviated tMCAO/R-induced brain damage in rats. Further studies revealed that it reduced oxidative stress via activating the PI3K/AKT/Nrf2 pathway, thereby inhibiting neuronal apoptosis in the ischemic penumbra of rats with CIRI. Then, differentiated PC12 cells were cultured in oxygen-glucose deprivation-reoxygenation (OGD/R) conditions (OGD: 1 % O2, 94 % N2, and 5 % CO2; R: normal atmosphere) to simulate CIRI in vitro. Similarly, HACE1 overexpression inhibited neuronal apoptosis caused by OGD/R treatment. The PI3K inhibitor LY294002 reversed the inhibitory effects of HACE1 overexpression on oxidative stress in OGD/R-injured cells, accompanied by the inactivated AKT/Nrf2 pathway. Altogether, our results suggest that HACE1 protects against oxidative stress-induced neuronal apoptosis in CIRI by activating the PI3K/AKT/Nrf2 pathway, providing a new insight into the CIRI treatment.

Development of a diagnostic model for detecting mild cognitive impairment in young and middle-aged patients with obstructive sleep apnea: a prospective observational study.

Objectives: Obstructive sleep apnea (OSA) is a common sleep-disordered breathing condition linked to the accelerated onset of mild cognitive impairment (MCI). However, the prevalence of undiagnosed MCI among OSA patients is high and attributable to the complexity and specialized nature of MCI diagnosis. Timely identification and intervention for MCI can potentially prevent or delay the onset of dementia. This study aimed to develop screening models for MCI in OSA patients that will be suitable for healthcare professionals in diverse settings and can be effectively utilized without specialized neurological training. Methods: A prospective observational study was conducted at a specialized sleep medicine center from April 2021 to September 2022. Three hundred and fifty consecutive patients (age: 18-60 years) suspected OSA, underwent the Montreal Cognitive Assessment (MoCA) and polysomnography overnight. Demographic and clinical data, including polysomnographic sleep parameters and additional cognitive function assessments were collected from OSA patients. The data were divided into training (70%) and validation (30%) sets, and predictors of MCI were identified using univariate and multivariate logistic regression analyses. Models were evaluated for predictive accuracy and calibration, with nomograms for application. Results: Two hundred and thirty-three patients with newly diagnosed OSA were enrolled. The proportion of patients with MCI was 38.2%. Three diagnostic models, each with an accompanying nomogram, were developed. Model 1 utilized body mass index (BMI) and years of education as predictors. Model 2 incorporated N1 and the score of backward task of the digital span test (DST_B) into the base of Model 1. Model 3 expanded upon Model 1 by including the total score of digital span test (DST). Each of these models exhibited robust discriminatory power and calibration. The C-statistics for Model 1, 2, and 3 were 0.803 [95% confidence interval (CI): 0.735-0.872], 0.849 (95% CI: 0.788-0.910), and 0.83 (95% CI: 0.763-0.896), respectively. Conclusion: Three straightforward diagnostic models, each requiring only two to four easily accessible parameters, were developed that demonstrated high efficacy. These models offer a convenient diagnostic tool for healthcare professionals in diverse healthcare settings, facilitating timely and necessary further evaluation and intervention for OSA patients at an increased risk of MCI.

[Influence of Tis108 on GA content and expression of key enzyme GeCYP714A1 involved in GA deactivation of Gastrodia elata].

To investigate the influence of the strigolactone inhibitor Tis108 on the growth of Gastrodia elata, this study treated G. elata tuber with Tis108 solution of 10 µmol·L~(-1) and measured the content of endogenous hormone gibberellin(GA) in the tuber. By using reverse transcription-polymerase chain reaction(RT-PCR) technology, the key enzyme GeCYP714A1 gene involved in GA deactivation was cloned. Bioinformatics analysis on the GeCYP714A1 gene was carried out by using ExPASy, SWISS-MODEL, MEGA, etc., and its expression levels in different parts of G. elata were determined. The results showed that after Tis108 treatment, GA content in G. elata tuber was significantly increased, and the transcription level of the GeCYP714A1 gene was significantly decreased. The full length of the coding region of the GeCYP714A1 gene is 1 173 bp, encoding 390 amino acids. The protein has a molecular weight of 44.85 kDa, a theoretical isoelectric point of 9.83, an instability index of 49.20, an aliphatic index of 89.03, and a grand average of hydropathicity of-0.235, classifying it as an unstable, basic, hydrophilic protein, and the GeCYP714A1 protein was localized in the mitochondria, lacking a signal peptide and a transmembrane structure. Phylogenetic tree analysis revealed that GeCYP714A1 was most closely related to the DcCYP714C2(PKU78454.1) protein from Dendrobium candidum, with a sequence identity of 67.25%. The qRT-PCR analysis of the expression patterns of the GeCYP714A1 gene indicated that GeCYP714A1 had the highest transcription level in G. elata tuber, followed by stem and inflorescence. The study represented that Tis108 inhibited the transcription level of GeCYP714A1 involved in GA deactivation in G. elata tuber, thereby increasing the accumulation of GA and affecting the growth of G. elata tuber. These results provided a basis for further studies of strigolactone regulation of GA signal and tuber development in G. elata.

[Establishment and optimization of Agrobacterium tumefaciens-mediated genetic transformation system for Polyporus umbellatus].

The unstable quality of Polyporus umbellatus sclerotia during cultivation is the key factor affecting the quality and yield of P. umbellatus sclerotia. In order to provide technical support for obtaining superior P. umbellatus by molecular breeding, the genetic transformation system mediated by Agrobacterium tumefaciens was studied in this paper. A. tumefaciens-mediated method was used to investigate the effects of antibiotic concentration, strain type, A. tumefaciens concentration, receptor material, infection time, co-culture time, and screening conditions on the genetic transformation efficiency of P. umbellatus. The transformants were screened and detected by hygromycin resistance marker genes, polymerase chain reaction(PCR) of specific primers, and fluorescence detection methods. The results showed that the A. tumefaciens GV3101 strain could genetically transfer P. umbellatus mycelium cells, and the optimal conditions for infection were as follows: the A. tumefaciens concentration A_(600 nm)= 0.6, P. umbellatus mycelium cells as receptor material, infection time of 30 min, and co-culture time of 3 days. The two-step screening method involving hygromycin of 9 and 13 µg·mL~(-1 )was the best screening condition. The results of hygromycin resistance screening, PCR detection of specific primers, and fluorescence detection showed that the exogenous gene eGFP had been transferred into the P. umbellatus mycelium cells, integrated into the genome, and successfully expressed. Under optimal conditions, the conversion efficiency could be increased to 2.3%, and the genetic transformation period was shortened from more than 90 days to less than 60 days. This study established and optimized the genetic transformation system of P. umbellatus mycelium cells mediated by A. tumefaciens, laying a foundation for the analysis of the molecular mechanism of P. umbellatus during growth and molecular breeding.

Lipocalin-2 induced LDHA expression promotes vascular remodelling in pulmonary hypertension.

Aerobic glycolysis is involved in the pathogenesis of pulmonary hypertension (PH). The mechanisms by which glycolysis is increased and how it contributes to pulmonary vascular remodelling are not yet fully understood. In this study, we demonstrated that elevated lipocalin-2 (LCN2) in PH significantly enhances aerobic glycolysis in human pulmonary artery smooth muscle cells (PASMCs) by up-regulating LDHA expression. Knockout of Lcn2 or having heterozygous LDHA deficiency in mice significantly inhibits the progression of hypoxic PH. Our study reveals that LCN2 stimulates LDHA expression by activating Akt-HIF-1α signalling pathway. Inhibition of Akt or HIF-1α reduces LDHA expression and proliferation of PASMCs. Both Akt and HIF-1α play critical roles in the development of PH and are suppressed in the pulmonary vessels of hypoxic PH mice lacking LCN2. These findings shed light on the LCN2-Akt-HIF1α-LDHA axis in aerobic glycolysis in PH.

Dynamic responses of systemic immunity and splenic inflammation to long-term cyclic high-temperature exposure in growing pullets and laying hens.

Two trials were conducted to draw the phase-response curve of productive and immunological variables in heat-exposed layer chickens at different ages (71 to 130 d, and 211 to 270 d). Birds were acclimated to the following conditions for 60 d: constant optimal ambient temperature at 24°C and high ambient temperature at 34°C for 8 h/d (10:00-18:00). Data collection and biochemical measurements were performed every 10 d. In both age ranges, high temperature favored the innate immunity (P < 0.01) at the cost of performance (P < 0.05) during a given period, including the relative abundance of B and T-helper lymphocytes, lymphocyte proliferation ratio (B and T lymphocytes), and serum immunoglobulin contents (IgG and IgM) in the peripheral blood, as well as splenic expression of inflammation-related genes (iNOS, TLR-4, TNF-α, IL-6, and INF-γ). Compared with laying hens, growing pullets showed a time-delayed activation of immune response following heat challenge, and had no immunosuppression up to the end of exposure. Overall, the immune system of layer birds has a trade-off with production tissues in a hot environment, and exhibits distinct age-range-specific responses of acclimatization.

Spinocerebellar ataxia type 4 is caused by a GGC expansion in the ZFHX3 gene and is associated with prominent dysautonomia and motor neuron signs.

BACKGROUND: Spinocerebellar ataxia 4 (SCA4), characterized in 1996, features adult-onset ataxia, polyneuropathy, and linkage to chromosome 16q22.1; its underlying mutation has remained elusive. OBJECTIVE: To explore the radiological and neuropathological abnormalities in the entire neuroaxis in SCA4 and search for its mutation. METHODS: Three Swedish families with undiagnosed ataxia went through clinical, neurophysiological, and neuroimaging tests, including PET studies and genetic investigations. In four cases, neuropathological assessments of the neuroaxis were performed. Genetic testing included short read whole genome sequencing, short tandem repeat analysis with ExpansionHunter de novo, and long read sequencing. RESULTS: Novel features for SCA4 include dysautonomia, motor neuron affection, and abnormal eye movements. We found evidence of anticipation; neuroimaging demonstrated atrophy in the cerebellum, brainstem, and spinal cord. [18F]FDG-PET demonstrated brain hypometabolism and [11C]Flumazenil-PET reduced binding in several brain lobes, insula, thalamus, hypothalamus, and cerebellum. Moderate to severe loss of Purkinje cells in the cerebellum and of motor neurons in the anterior horns of the spinal cord along with pronounced degeneration of posterior tracts was also found. Intranuclear, mainly neuronal, inclusions positive for p62 and ubiquitin were sparse but widespread in the CNS. This finding prompted assessment for nucleotide expansions. A polyglycine stretch encoding GGC expansions in the last exon of the zink finger homeobox 3 gene was identified segregating with disease and not found in 1000 controls. CONCLUSIONS: SCA4 is a neurodegenerative disease caused by a novel GGC expansion in the coding region of ZFHX3, and its spectrum is expanded to include dysautonomia and neuromuscular manifestations.

Explanatory Cognitive Diagnosis Models Incorporating Item Features.

Item quality is crucial to psychometric analyses for cognitive diagnosis. In cognitive diagnosis models (CDMs), item quality is often quantified in terms of item parameters (e.g., guessing and slipping parameters). Calibrating the item parameters with only item response data, as a common practice, could result in challenges in identifying the cause of low-quality items (e.g., the correct answer is easy to be guessed) or devising an effective plan to improve the item quality. To resolve these challenges, we propose the item explanatory CDMs where the CDM item parameters are explained with item features such that item features can serve as an additional source of information for item parameters. The utility of the proposed models is demonstrated with the Trends in International Mathematics and Science Study (TIMSS)-released items and response data: around 20 item linguistic features were extracted from the item stem with natural language processing techniques, and the item feature engineering process is elaborated in the paper. The proposed models are used to examine the relationships between the guessing/slipping item parameters of the higher-order DINA model and eight of the item features. The findings from a follow-up simulation study are presented, which corroborate the validity of the inferences drawn from the empirical data analysis. Finally, future research directions are discussed.

APC mutations disrupt ß-catenin destruction complex condensates organized by Axin phase separation.

The Wnt/ß-catenin pathway is critical to maintaining cell fate decisions. Recent study showed that liquid-liquid-phase separation (LLPS) of Axin organized the ß-catenin destruction complex condensates in a normal cellular state. Mutations inactivating the APC gene are found in approximately 80% of all human colorectal cancer (CRC). However, the molecular mechanism of the formation of ß-catenin destruction complex condensates organized by Axin phase separation and how APC mutations impact the condensates are still unclear. Here, we report that the ß-catenin destruction complex, which is constructed by Axin, was assembled condensates via a phase separation process in CRC cells. The key role of wild-type APC is to stabilize destruction complex condensates. Surprisingly, truncated APC did not affect the formation of condensates, and GSK 3ß and CK1α were unsuccessfully recruited, preventing ß-catenin phosphorylation and resulting in accumulation in the cytoplasm of CRCs. Besides, we propose that the phase separation ability of Axin participates in the nucleus translocation of ß-catenin and be incorporated and concentrated into transcriptional condensates, affecting the transcriptional activity of Wnt signaling pathway.

Association of LOX gene G473A polymorphism with the occurrence of allergic rhinitis and efficacy of montelukast sodium in children.

Allergic rhinitis (AR) is very common in adolescents, and current treatment options are complex and unsatisfactory. The objective of this study was to analyze the association of lysyl oxidase (LOX) gene G473A polymorphism with susceptibility to AR in children. In addition, we analyzed the therapeutic effect of montelukast sodium on AR. Forty-five children with AR (research group, 8.16±2.88 years old) and 51 healthy children (control group, 8.22±3.87 years old) during the same period were selected. The LOX gene G473A polymorphism was detected with polymerase chain reaction (PCR)-restriction fragment length polymorphism method. The effect of G473A polymorphism in the occurrence of AR was assessed by logistic regression analysis. In addition, the levels of C-reactive protein (CRP), Interleukin (IL-6), and IL-8 were measured to observe the relationship between G473A polymorphism and inflammatory factors. Finally, montelukast sodium was given to children with AR to investigate the effect of G473A polymorphism on clinical outcomes. The number of G473A polymorphisms in the research group was not significantly different from the control group for GA-type (P = 0.521). However, the number of GG-type polymorphisms was less while the number of type AA was more than the control group (P = 0.044 and 0.046). Children carrying the AA gene had an approximately 4-fold increased risk of AR, while those carrying the GG gene had a decreased risk (P < 0.001). Moreover, children carrying the GG gene had lower levels of CRP, IL-6, and IL-8 and better clinical outcomes, while those carrying the AA gene had higher levels of inflammatory factors and worse outcomes (P<0.05). LOX gene G473A polymorphism is closely associated with AR pathogenesis and may have an important research value in antagonizing the therapeutic effect of montelukast sodium.

IGF2BP3 promotes the progression of colorectal cancer and mediates cetuximab resistance by stabilizing EGFR mRNA in an m6A-dependent manner.

Insulin-like growth factor 2 mRNA-binding protein 3 (IGF2BP3), an RNA-binding protein, is associated with tumorigenesis and progression. However, the exact molecular mechanisms of IGF2BP3 in colorectal cancer (CRC) oncogenesis, progression, and drug resistance remain unclear. This study found that IGF2BP3 was upregulated in CRC tissues. Clinically, the elevated IGF2BP3 level is predictive of a poor prognosis. Functionally, IGF2BP3 enhances CRC tumorigenesis and progression both in vitro and in vivo. Mechanistically, IGF2BP3 promotes epidermal growth factor receptor (EGFR) mRNA stability and translation and further activates the EGFR pathway by serving as a reader in an N6-methyladenosine (m6A)-dependent manner by cooperating with METTL14. Furthermore, IGF2BP3 increases the drug resistance of CRC cells to the EGFR-targeted antibody cetuximab. Taken together, our results demonstrated that IGF2BP3 was a functional and clinical oncogene of CRC. Targeting IGF2BP3 and m6A modification may therefore offer rational therapeutic targets for patients with CRC.

ASCL2 induces an immune excluded microenvironment by activating cancer-associated fibroblasts in microsatellite stable colorectal cancer.

Proficient mismatch repair or microsatellite stable (pMMR/MSS) colorectal cancers (CRCs) are vastly outnumbered by deficient mismatch repair or microsatellite instability-high (dMMR/MSI-H) tumors and lack a response to immune checkpoint inhibitors (ICIs). In this study, we reported two distinct expression patterns of ASCL2 in pMMR/MSS and dMMR/MSI-H CRCs. ASCL2 is overexpressed in pMMR/MSS CRCs and maintains a stemness phenotype, accompanied by a lower density of tumor-infiltrating lymphocytes (TILs) than those in dMMR/MSI CRCs. In addition, coadministration of anti-PD-L1 antibodies facilitated T cell infiltration and provoked strong antitumor immunity and tumor regression in the MC38/shASCL2 mouse CRC model. Furthermore, overexpression of ASCL2 was associated with increased TGFB levels, which stimulate local Cancer-associated fibroblasts (CAFs) activation, inducing an immune-excluded microenvironment. Consistently, mice with deletion of Ascl2 specifically in the intestine (Villin-Cre+, Ascl2 flox/flox, named Ascl2 CKO) revealed fewer activated CAFs and higher proportions of infiltrating CD8+ T cells; We further intercrossed Ascl2 CKO with ApcMin/+ model suggesting that Ascl2-deficient expression in intestinal represented an immune infiltrating environment associated with a good prognosis. Together, our findings indicated ASCL2 induces an immune excluded microenvironment by activating CAFs through transcriptionally activating TGFB, and targeting ASCL2 combined with ICIs could present a therapeutic opportunity for MSS CRCs.

Exploration of the Stacking Ensemble Machine Learning Algorithm for Cheating Detection in Large-Scale Assessment.

Cheating detection in large-scale assessment received considerable attention in the extant literature. However, none of the previous studies in this line of research investigated the stacking ensemble machine learning algorithm for cheating detection. Furthermore, no study addressed the issue of class imbalance using resampling. This study explored the application of the stacking ensemble machine learning algorithm to analyze the item response, response time, and augmented data of test-takers to detect cheating behaviors. The performance of the stacking method was compared with that of two other ensemble methods (bagging and boosting) as well as six base non-ensemble machine learning algorithms. Issues related to class imbalance and input features were addressed. The study results indicated that stacking, resampling, and feature sets including augmented summary data generally performed better than its counterparts in cheating detection. Compared with other competing machine learning algorithms investigated in this study, the meta-model from stacking using discriminant analysis based on the top two base models-Gradient Boosting and Random Forest-generally performed the best when item responses and the augmented summary statistics were used as the input features with an under-sampling ratio of 10:1 among all the study conditions.

Joint modeling of action sequences and action time in computer-based interactive tasks.

Process data refers to data recorded in computer-based assessments that reflect the problem-solving processes of participants and provide greater insight into how they solve problems. Action time, namely the amount of time required to complete a state transition, is also included in such data along with actions. In this study, an action-level joint model of action sequences and action time is proposed, in which the sequential response model (SRM) is used as the measurement model for action sequences, and a new log-normal action time model is proposed as the measurement model for action time. The proposed model can be regarded as an extension of the SRM by incorporating action time within the joint-hierarchical modeling framework and as an extension of the conventional item-level joint models in process data analysis. Results of the empirical and simulation studies demonstrated that the model setup was justified, model parameters could be interpreted, parameter estimates were accurate, and taking into account participants' action time further was beneficial for obtaining a deep understanding of participants' behavioral patterns. Overall, the proposed action-level joint model provides an innovative modeling framework for analyzing process data in computer-based assessments from the latent variable modeling perspective.

Differential expressions of hypothalamic thermosensitive TRP ion channels may underlie the posthatching ontogeny of brain cooling capacity in broiler chickens.

Two trials were performed to evaluate the association of hypothalamic abundances of thermosensitive transient receptor potential (TRP) ion channels with thermoregulation in broiler chickens. In trial 1, temporal changes in body temperatures, and hypothalamic expression patterns of TRP channels and thermoregulatory neurotransmitter concentrations were assessed from 3 to 42 d of age. In trial 2, the same variables were compared at 2 age stages between 2 distinct types of birds with high or low rectal temperatures (HRT or LRT). The core-to-brain temperature difference exhibited a rapid increase after hatching, arriving at a steady state in the fourth week (P < 0.01). The hypothalamus saw a progressive decrease of TRPV4 protein expression through 28 d (P < 0.01), followed by a great increase in the abundance of other channels right up to the end (P < 0.05). Compared to LRT birds, a decline in hypothalamic content of TRPV4 (P < 0.05), together with a bigger core-to-brain temperature difference (P < 0.01), was evident in the HRT counterpart at 33 d. In both trials, the core-to-brain and core-to-surface temperature differences were controlled in a synchronous and coordinated manner. These results allow concluding that developmental changes in the thermal sensitivity of hypothalamic neurons, determined by brain cooling capacity, involve a neuro-genomic mechanism, which regulates the ratio between thermosensitive TRP ion channels to attain a lower proportion of TRPV4 in comparison with other channels.

[Excellent appearance of Dao-di Ginseng Radix et Rhizoma and interaction mechanism between genetic and environmental factors: a review].

Dao-di medicinal materials produced in a specific environment always present excellent appearance and high quality. Because of the unique appearance, Ginseng Radix et Rhizoma is regarded as a paradigm in the research on excellent appearance. This paper systematically summarized the research progress in the genetic and environmental factors influencing the formation of the excellent appearance of Ginseng Radix et Rhizoma, aiming to provide reference for the quality improvement of Ginseng Radix et Rhizoma and the scientific connotation of Dao-di Chinese medicinal materials. The Ginseng Radix et Rhizoma with high quality generally has a robust and long rhizome, a large angle between branch roots, and the simultaneous presence of a robust basal part of rhizome, adventitious roots, rhizome bark with circular wrinkles, and fibrous roots with pearl points. The cultivated and wild Ginseng Radix et Rhizoma have significant differences in the appearance and no significant difference in the population genetic diversity. The differences in the appearance are associated with cell wall modification, transcriptional regulation of genes involved in plant hormone transduction, DNA methylation, and miRNA regulation. The rhizosphere soil microorganisms including Fusarium and Alternaria, as well as the endophytes Trichoderma hamatum and Nectria haematococca, may be the key microorganisms affecting the growth and development of Panax ginseng. Cultivation mode, variety, and root exudates may be the main factors influencing the stability of rhizosphere microbial community. Ginsenosides may be involved in the formation of the excellent appearance. However, most of the available studies focus on the partial or single factors in the formation of Dao-di medicinal materials, ignoring the relationship within the complex ecosystems, which limits the research on the formation mechanism of Dao-di medicinal materials. In the future, the experimental models for the research involving genetic and environmental factors should be established and mutant materials should be developed to clarify the internal relationship between factors and provide scientific support for the research on Dao-di medicinal materials.

[Effect of BBM gene on callus growth and ginsenoside content in Panax quinquefolius].

Baby Boom(BBM) gene is a key regulatory factor in embryonic development and regeneration, cell proliferation, callus growth, and differentiation promotion. Since the genetic transformation system of Panax quinquefolius is unstable with low efficiency and long period, this study attempted to transfer BBM gene of Zea mays to P. quinquefolius callus by gene gunship to investigate its effect on the callus growth and ginsenoside content, laying a foundation for establishing efficient genetic transformation system of P. quinquefolius. Four transgenic callus of P. quinquefolius with different transformation events were obtained by screening for glufosinate ammonium resistance and molecular identification by PCR. The growth state and growth rate of wild-type and transgenic callus were compared in the same growth period. The content of ginsenoside in transgenic callus was determined by ultra-high performance liquid chromatography-triple quadrupole mass spectrometry(UPLC-MS/MS). The results showed that transgenic callus growth rate was significantly higher than that of wild-type callus. In addition, the content of ginsenoside Rb_1, Rg_1, Ro, and Re was significantly higher than that in wild-type callus. The paper preliminarily proved the function of BBM gene in promoting growth rate and increasing ginsenoside content, which provided a scientific basis to establish a stable and efficient genetic transformation system for Panax plants in the future.