Selective Lattice Doping Enables a Low-Cost, High-Capacity and Long-Lasting Potassium Layered Oxide Cathode for Potassium and Sodium Storage.

Layered transition metal oxides are highly promising host materials for K ions, owing to their high theoretical capacities and appropriate operational potentials. To address the intrinsic issues of KxMnO2 cathodes and optimize their electrochemical properties, a novel P3-type oxide doped with carefully chosen cost-effective, electrochemically active and multi-functional elements is proposed, namely K0.57Cu0.1Fe0.1Mn0.8O2. Compared to the pristine K0.56MnO2, its reversible specific is increased from 104 to 135 mAh g-1. In addition, the Cu and Fe co-doping triples the capacity under high current densities, and contributes to long-term stability over 500 cycles with a capacity retention of 68 %. Such endeavor holds the potential to make potassium-ion batteries particularly competitive for application in sustainable, low-cost, and large-scale energy storage devices. In addition, the cathode is also extended for sodium storage. Facilitated by the interlayer K ions that protect the layered structure from collapsing and expand the diffusion pathway for sodium ions, the cathode shows a high reversible capacity of 144 mAh g-1, fast kinetics and a long lifespan over 1000 cycles. The findings offer a novel pathway for the development of high-performance and cost-effective sodium-ion batteries.

Residue quality drives SOC sequestration by altering microbial taxonomic composition and ecophysiological function in desert ecosystem.

Plant residues are important sources of soil organic carbon in terrestrial ecosystems. The degradation of plant residue by microbes can influence the soil carbon cycle and sequestration. However, little is known about the microbial composition and function, as well as the accumulation of soil organic carbon (SOC) in response to the inputs of different quality plant residues in the desert environment. The present study evaluated the effects of plant residue addition from Pinus sylvestris var. mongolica (Pi), Artemisia desertorum (Ar) and Amorpha fruticosa (Am) on desert soil microbial community composition and function in a field experiment in the Mu Us Desert. The results showed that the addition of the three plant residues with different C/N ratios induced significant variation in soil microbial communities. The Am treatment (low C/N ratio) improved microbial diversity compared with the Ar and Pi treatments (medium and high C/N ratios). The variations in the taxonomic and functional compositions of the dominant phyla Actinobacteria and Proteobacteria were higher than those of the other phyla among the different treatments. Moreover, the network links between Proteobacteria and other phyla and the CAZyme genes abundances from Proteobacteria increased with increasing residue C/N, whereas those decreased for Actinobacteria. The SOC content of the Am, Ar and Pi treatments increased by 45.73%, 66.54% and 107.99%, respectively, as compared to the original soil. The net SOC accumulation was positively correlated with Proteobacteria abundance and negatively correlated with Actinobacteria abundance. These findings showed that changing the initial quality of plant residue from low C/N to high C/N can result in shifts in taxonomic and functional composition from Actinobacteria to Proteobacteria, which favors SOC accumulation. This study elucidates the ecophysiological roles of Actinobacteria and Proteobacteria in the desert carbon cycle, expands our understanding of the potential microbial-mediated mechanisms by which plant residue inputs affect SOC sequestration in desert soils, and provides valuable guidance for species selection in desert vegetation reconstruction.

Arecoline induces neurotoxicity in HT22 cells via the promotion of endoplasmic reticulum stress and downregulation of the Nrf2/HO-1 pathway.

Arecoline, the predominant bioactive substance extracted from areca nut (AN), is the world's fourth most frequently used psychoactive material. Research has revealed that chewing AN can affect the central nervous system (CNS) and may lead to neurocognitive deficits that are possibly linked to the action of arecoline. However, the mechanism behind the neurotoxicity caused by arecoline remains unclear. This study aimed to investigate the neurotoxic effects of arecoline and its underlying mechanism. The results showed that arecoline caused cytotoxicity against HT22 cells in a dose-dependent manner and induced apoptosis by upregulating the expression of pro-apoptotic caspase and Bcl-2 family proteins. Furthermore, arecoline escalated intracellular reactive oxygen species (ROS) levels and Ca2+ concentration with increasing doses, thereby motivating endoplasmic reticulum stress (ERS) and ERS-associated apoptotic protein expression. Additionally, the study found that arecoline attenuates intracellular antioxidant defense by inhibiting the translocation of NF-E2-related factor-2 (Nrf2) into the nucleus and decreasing downstream Heme oxygenase-1 (HO-1) levels. The specific inhibitor Sodium 4-phenylbutyrate (4-PBA) can dramatically attenuate arecoline-mediated cell apoptosis and ERS-associated apoptotic pathway expression by blocking ERS. The antioxidant N-Acetylcysteine (NAC) also effectively reverses the arecoline-mediated increase of ERS-related apoptotic pathway protein levels by scavenging intracellular ROS accumulation. In conclusion, this study suggests that arecoline induces neurotoxicity in HT22 cells via ERS mediated by oxidative stress- and Ca2+ disturbance, as well as by downregulation of the Nrf2/HO-1 pathway.

Discharge preparation experiences and needs of intergenerational caregivers of neonatal intensive care unit preterm: A qualitative study.

PURPOSE: This study aimed to explore the real experiences and needs of neonatal intensive care unit (NICU) preterm intergenerational caregivers for discharge preparation and provide a basis for nursing staff to formulate systemic and personalized health education plans and continuous nursing plans for preterm discharge. DESIGN AND METHODS: This was a descriptive qualitative study. An objective sampling method was used to select 16 intergenerational caregivers of preterm infants admitted to the NICU of tertiary obstetrics and gynecology hospitals in Zhejiang and Jilin provinces from December 2023 to February 2024. Semi-structured interviews were conducted on the day of discharge of the preterm infants and six weeks after discharge. Colaizzi's seven-step analysis method was used to analyze the interview data. RESULTS: Based on the existence, relatedness, and growth (ERG) theory, the discharge preparation experiences and needs of neonatal intergenerational caregivers in the NICU were summarized into three themes: psychological condition, care capacity condition, and multi-party support needs. CONCLUSIONS: In the process of hospital discharge preparation, intergenerational caregivers of premature infants in NICU have multiple needs, including enhancing nursing ability and obtaining psychological and multi-party support. It is helpful to take effective interventions to improve their readiness for discharge. PRACTICE IMPLICATIONS: The nursing staff should develop personalized discharge health education plans and continuous nursing plans to improve the level of discharge preparation. PATIENT OR PUBLIC CONTRIBUTIONS: There were no patient or public contributions.

The Stylo Cysteine-Rich Peptide SgSnakin1 Is Involved in Aluminum Tolerance through Enhancing Reactive Oxygen Species Scavenging.

Stylo (Stylosanthes spp.) is an important pasture legume with strong aluminum (Al) resistance. However, the molecular mechanisms underlying its Al tolerance remain fragmentary. Due to the incomplete genome sequence information of stylo, we first conducted full-length transcriptome sequencing for stylo root tips treated with and without Al and identified three Snakin/GASA genes, namely, SgSnakin1, SgSnakin2, and SgSnakin3. Through quantitative RT-PCR, we found that only SgSnakin1 was significantly upregulated by Al treatments in stylo root tips. Histochemical localization assays further verified the Al-enhanced expression of SgSnakin1 in stylo root tips. Subcellular localization in both tobacco and onion epidermis cells showed that SgSnakin1 localized to the cell wall. Overexpression of SgSnakin1 conferred Al tolerance in transgenic Arabidopsis, as reflected by higher relative root growth and cell vitality, as well as lower Al concentration in the roots of transgenic plants. Additionally, overexpression of SgSnakin1 increased the activities of SOD and POD and decreased the levels of O2·- and H2O2 in transgenic Arabidopsis in response to Al stress. These findings indicate that SgSnakin1 may function in Al resistance by enhancing the scavenging of reactive oxygen species through the regulation of antioxidant enzyme activities.

ZmASY1 interacts with ZmPRD3 and is crucial for meiotic double-strand break formation in maize.

During meiosis, recombination-mediated pairing and synapsis of homologous chromosomes begin with programmed DNA double-strand breaks (DSBs). In yeast and mice, DSBs form in a tethered loop-axis complex, in which DSB sites are located within chromatin loops and tethered to the proteinaceous axial element (AE) by DSB-forming factors. In plants, the molecular connection between DSB sites and chromosome axes is poorly understood. By integrating genetic analysis, immunostaining technology, and protein-protein interaction studies, the putative factors linking DSB formation to chromosome axis were explored in maize meiosis. Here, we report that the AE protein ZmASY1 directly interacts with the DSB-forming protein ZmPRD3 in maize (Zea mays) and mediates DSB formation, synaptonemal complex assembly, and homologous recombination. ZmPRD3 also interacts with ZmPRD1, which plays a central role in organizing the DSB-forming complex. These results suggest that ZmASY1 and ZmPRD3 may work as a key module linking DSB sites to chromosome axes during DSB formation in maize. This mechanism is similar to that described in yeast and recently Arabidopsis involving the homologs Mer2/ZmPRD3 and HOP1/ZmASY1, thus indicating that the process of tethering DSBs in chromatin loops to the chromosome axes may be evolutionarily conserved in diverse taxa.

Proteomic Analysis of Protective Effects of Dl-3-n-Butylphthalide against mpp + -Induced Toxicity via downregulating P53 pathway in N2A Cells.

BACKGROUND: Dl-3-n-butylphthalide (NBP) is an important medial therapy for acute ischemic stroke in China. Recent studied have revealed that NBP not only rescued the loss of dopaminergic neurons in cellular and animal models of Parkinson's disease (PD), but also could improve motor symptoms in PD patients. However, the protective mechanism is not fully understood. P53 is a multifunctional protein implicated in numerous cellular processes, including apoptosis, DNA repair, mitochondrial functions, redox homeostasis, autophagy and protein aggregations. In PD, p53 integrated with various neurodegeneration-related signals inducing neuronal loss, indicating the suppression of P53 might be a promising target for PD treatment. Therefore, the purpose of the current study was to systemically screen new therapeutic targets of NBP in PD. METHOD: In our study, we constructed mpp + induced N2A cells to investigate the benefit effect of NBP in PD. MTT assay was performed to evaluate the cell viability; TMT-based LC-MS/MS was applied to determine the different expressed proteins (DEPs) of NBP pretreatment; online bioinformatics databases such as DAVID, STRING, and KEGG was used to construe the proteomic data. After further analyzed and visualized the protein-protein interactions (PPI) by Cytoscape, DEPs were verified by western blot. RESULT: A total of 5828 proteins were quantified in the comparative proteomics experiments and 417 proteins were considered as DEPs (fold change > 1.5 and p < 0.05). Among the 417 DEPs, 140 were upregulated and 277 were downregulated in mpp + -induced N2A cells with NBP pretreatment. KEGG pathway analysis indicated that lysosome, phagosome, apoptosis, endocytosis and ferroptosis are the mainly enriched pathways. By using MCL clustering in PPI analysis, 48 clusters were generated and the subsequent KEGG analysis of the top 3 clusters revealed that P53 signaling pathway was recognized as the dominant pathway for NBP treatment. CONCLUSION: NBP significantly relived mpp + -induced cell toxicity. The neuroprotective role of NBP was implicated with P53 signaling pathway in some extent. These findings will reinforce the understanding of the mechanism of NBP in PD and identify novel therapeutic targets.

Verification of a loss of heterozygosity at the D8S1179 locus in a paternity case by the MiSeq FGx system.

Capillary electrophoresis is widely used to study short tandem repeats (STRs) in forensic genetics. However, next-generation sequencing platforms have become a new strategy for forensic DNA typing. In this study, we report a false four-step STR mutation between an alleged father (AF) and child in a paternity case. A total of 23 autosomal STR loci were evaluated using the Huaxia™ Platinum and Goldeneye™ 20A kits, revealing a single mismatch in D8S1179 between the AF (10/10) and the male child (14/14). Additional Y-STR typing of the AF and child was performed, and the results were consistent with those based on 27 Y-STR loci. To further confirm the experimental results, we sequenced the individuals using the MiSeq FGx system and detected 10/15 unbalanced alleles in the D8S1179 locus of the AF and 14/15 unbalanced alleles in the D8S1179 locus of the child. Sanger sequencing revealed that both the AF and child had the C→G point mutation in the primer binding region of D8S1179 resulting in allelic dropout. Therefore, the verification of STR typing by different sequencing systems is helpful for the interpretation of results in cases of multistep STR mutations.

ZmSPO11-2 is critical for meiotic recombination in maize.

Most plant species have three or more SPO11/TOPOVIA homologs and two TOPOVIB homologs, which associate to trigger meiotic double-strand break (DSB) formation and subsequent meiotic recombination. In Zea mays L. (maize), ZmSPO11-1 and ZmMTOPVIB have been reported to be indispensable for the initiation of meiotic recombination, yet the function of ZmSPO11-2 remains unclear. In this study, we characterized meiotic functions of ZmSPO11-2 during male meiosis in maize. Two independent Zmspo11-1 knock-out mutants exhibited normal vegetative growth but both male and female sterility. The formation of meiotic DSBs of DNA molecules was fully abolished in the Zmspo11-2 plants, leading to the defective homologous chromosome paring, synapsis, recombination, and segregation. However, the bipolar spindle assembly was not noticeably affected in Zmspo11-2 meiocytes. Overall, our results demonstrate that as its partner ZmSPO11-1 and ZmMTOPVIB, ZmSPO11-2 plays essential roles in DSB formation and homologous recombination in maize meiosis.

Quantitative Proteomics Reveals Neuroprotective Mechanism of Ginkgolide B in Aß1-42-induced N2a Neuroblastoma Cells.

OBJECTIVE: Ginkgolide B (GB) possesses anti-inflammatory, antioxidant, and anti-apoptotic properties against neurotoxicity induced by amyloid beta (Aß), but the potential neuroprotective effects of GB in Alzheimer's therapies remain elusive. We aimed to conduct proteomic analysis of Aß1-42 induced cell injury with GB pretreatment to uncover the underlying pharmacological mechanisms of GB. METHODS: Tandem mass tag (TMT) labeled liquid chromatography-tandem mass spectrometry (LC-MS/MS) method was applied to analyze protein expression in Aß1-42 induced mouse neuroblastoma N2a cells with or without GB pretreatment. Proteins with fold change >1.5 and p < 0.1 from two independent experiments were regarded as differentially expressed proteins (DEPs). Gene ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analyses were performed to analyze the functional annotation information of DEPs. Two key proteins osteopontin (SPP1) and ferritin heavy chain 1 (FTH1) were validated in another three samples using western blot and quantitative real-time PCR. RESULTS: We identified a total of 61 DEPs in GB treated N2a cells, including 42 upregulated and 19 downregulated proteins. Bioinformatic analysis showed that DEPs mainly participated in the regulation of cell death and ferroptosis by down-regulating SPP1 protein and up-regulating FTH1 protein. CONCLUSIONS: Our findings demonstrate that GB treatment provides neuroprotective effects on Aß1-42 induced cell injury, which may be related to the regulation of cell death and ferroptosis. The research puts forward new insights into the potential protein targets of GB in the treatment of Alzheimer's disease (AD).

Genetic polymorphism and forensic efficiency of 21 autosomal STR loci from Shandong Han population in Northern China.

BACKGROUND: Highly polymorphic autosomal STR loci are useful for understanding population structure better and for forensic application, however the non-CODIS STR loci in the Han population of Shandong, located in Northern China, are not well-characterised. AIM: To investigate population genetic polymorphism and forensic efficiency of 21 autosomal STR loci from the Shandong Han population in Northern China and reveal the genetic relationships with other populations both at home and abroad. SUBJECTS AND METHODS: In this study, population genetic data of 21 autosomal STR loci included in the Goldeneye DNA ID 22NC Kit that includes four CODIS loci and 17 non-CODIS loci were determined for 523 unrelated Han individuals in Shandong. RESULTS: Significant deviations from Hardy-Weinberg equilibrium were not observed. A total of 233 alleles were detected with allele frequencies ranging from 0.0010 to 0.3728. The combined power of discrimination was 0.99999999999999999999999990011134, and the combined power of exclusion was 0.99999999788131. Furthermore, in an analysis of population differentiation Nei's standard genetic distance and multidimensional scaling analysis, which were conducted based on the overlapping 15 STR loci, revealed that the Shandong Han population was most closely related to populations in close geographic proximity. CONCLUSIONS: This study demonstrated that the 21 autosomal STR loci included in the GoldeneyeTM DNA ID 22NC system are highly polymorphic and suitable for forensic identification and paternity testing in the Shandong Han population. Additionally, the present results enrich the population genetic database.

Development of a test strip for rapid detection of Gymnodinium catenatum.

Harmful algal blooms (HABs) are major ecological and environmental problems in China's coastal waters and seriously threaten the stability of the marine ecosystem and human health. Gymnodinium catenatum is a toxic red tide dinoflagellate. It can produce paralytic shellfish toxins (PSP), which cause serious hazards to marine organisms, public health, and safety. In this paper, a test strip based on colloidal gold immunochromatography (GICG) was developed for the rapid detection of Gymnodinium catenatum. The experimental results showed that the test strip has good specificity and sensitivity. It not only detects the different components of Gymnodinium catenatum but also may detect algal toxins. The lowest density of Gymnodinium catenatum that can be detected by this test strip is approximately 120 cells/mL. Cross-reaction indicated that the test strip had a high specificity for Gymnodinium catenatum. This test strip provides a rapid method for in situ detection of Gymnodinium catenatum and a reference method for the monitoring of other harmful algae to serve as an early warning of upcoming red tides. It also provides a new way to prepare more detection methods for toxic algal toxins.

Cattle Encephalon Glycoside and Ignotin Protects Neurons Against Microglia-Induced Neuroinflammation via Elevating BDNF Expression and Inhibiting TLR4/NF-κB Pathway.

Neuroinflammation is involved in the pathology and progression of Alzheimer's disease (AD) and is closely related to microglial activation. We have previously reported that cattle encephalon glycoside and ignotin (CEGI) could inhibit the activation of microglia in APP/PS1 mice, a mouse model of familial AD. However, the anti-neuroinflammatory mechanisms of CEGI have not yet been fully elucidated. Here, we aimed to investigate the role of CEGI in microglia-mediated neuroinflammation in AD. APP/PS1 mice were treated with CEGI intraperitoneally for 30 days, and then their cognition was assessed. We showed that CEGI alleviated cognitive damage with higher nesting scores, preferential indices, and spontaneous alternation rates in APP/PS1 mice. Moreover, CEGI treatment effectively reduced microglial activation and Iba-1 levels in the cortex of APP/PS1 mice. Additionally, CEGI decreased pro-inflammatory factors production and neuroinflammation-mediated neuronal damage in vivo and in vitro. Finally, CEGI upregulated BDNF levels and downregulated TLR4 and p-NF-κB p65 levels in vivo and in vitro. Taken together, these findings indicated that CEGI could attenuate cognitive deficits in APP/PS1 mice and suppress microglia-induced neuroinflammation via increasing BDNF expression and inhibiting the TLR4/NF-κB pathway.

Role of STAT3 in cancer cell epithelial­mesenchymal transition (Review).

Since its discovery, the role of the transcription factor, signal transducer and activator of transcription 3 (STAT3), in both normal physiology and the pathology of numerous diseases, including cancer, has been extensively studied. STAT3 is aberrantly activated in different types of cancer, fulfilling a critical role in cancer progression. The biological process, epithelial­mesenchymal transition (EMT), is indispensable for embryonic morphogenesis. During the development of cancer, EMT is hijacked to confer motility, tumor cell stemness, drug resistance and adaptation to changes in the microenvironment. The aim of the present review was to outline recent advances in knowledge of the role of STAT3 in EMT, which may contribute to the understanding of the function of STAT3 in EMT in various types of cancer. Delineating the underlying mechanisms associated with the STAT3­EMT signaling axis may generate novel diagnostic and therapeutic options for cancer treatment.

A water-soluble arabinoxylan from Chinese liquor distillers' grains: Structural characterization and anti-colitic properties.

Chinese liquor distillers' grain (CLDG) is a valuable and abundant by-product from traditional Chinese baijiu production, containing a diverse array of bioactive components that have attracted significant interest. Herein, a water-soluble polysaccharide, DGPS-2B, with a weight-average molecular weight of 37.3 kDa, was isolated from the alkali-extract fraction of CLDG. Methylation and NMR analysis identified that the primary constituents of DGPS-2B are arabinoxylans, with an arabinose-to-xylose ratio of 0.66. In an animal model of colitis, DGPS-2B treatment significantly altered the gut microbiota composition by increasing the SCFA-producing bacteria (e.g., Butyricicoccus) and reducing the mucin-degrading bacteria such as Muribaculaceae. This microbial shift resulted in elevated production of butyrate, acetate, and propionate, which subsequently suppressed NF-κB signaling, decreased the levels of IL-1ß, IL-6, and TNFα, and potentially inactivated Notch signaling. These multifaceted effects stimulated mucin 2 production, reduced inflammation and apoptosis in the gut epithelium, and ultimately alleviated colitis symptoms. Collectively, this study not only elucidates the purification and characterization of DGPS-2B from CLDG but also illuminates its anti-colitic properties and the underlying molecular mechanisms. These findings underscore the potential of DGPS-2B as a therapeutic intervention for managing inflammatory bowel disease and emphasize CLDG as a promising source for developing value-added products.

GPR55 activation improves anxiety- and depression-like behaviors of mice during methamphetamine withdrawal.

Methamphetamine is a potent and highly addictive neurotoxic psychostimulant that triggers a spectrum of adverse emotional responses during withdrawal. G-protein coupled receptor 55 (GPR55), a novel endocannabinoid receptor, is closely associated with mood regulation. Herein, we developed a murine model of methamphetamine-induced anxiety- and depressive-like behavior during abstinence which showed a decreased GPR55 expression in the hippocampus. Activation of GPR55 mitigated these behavioral symptoms, concomitantly ameliorating impairments in hippocampal neurogenesis and reducing neuroinflammation. These findings underscore the pivotal role of GPR55 in mediating the neuropsychological consequences of methamphetamine withdrawal, potentially via mechanisms involving the modulation of hippocampal neurogenesis and inflammation.

IL-37 possesses both anti-inflammatory and antiviral effects against Middle East respiratory syndrome coronavirus infection.

BACKGROUND: The aim was to elucidate the function of IL-37 in middle east respiratory syndrome coronavirus (MERS-CoV) infection, thereby providing a novel therapeutic strategy for managing the clinical treatment of inflammatory response caused by respiratory virus infection. METHODS: We investigated the development of MERS by infecting hDPP4 mice with hCoV-EMC (107 TCID50 [50% tissue culture infectious dose]) intranasally. We infected A549 cells with MERS-CoV, which concurrently interfered with IL-37, detecting the viral titer, viral load, and cytokine expression at certain points postinfection. Meanwhile, we administered IL-37 (12.5 µg/kg) intravenously to hDPP4 mice 2 h after MERS-CoV-2 infection and collected the serum and lungs 5 days after infection to investigate the efficacy of IL-37 in MERS-CoV infection. RESULTS: The viral titer of MERS-CoV-infected A549 cells interfering with IL-37 was significantly reduced by 4.7-fold, and the viral load of MERS-CoV-infected hDPP4 mice was decreased by 59-fold in lung tissue. Furthermore, the administration of IL-37 suppressed inflammatory cytokine and chemokine (monocyte chemoattractant protein 1, interferon-γ, and IL-17A) expression and ameliorated the infiltration of inflammatory cells in hDPP4 mice. CONCLUSION: IL-37 exhibits protective properties in severe pneumonia induced by MERS-CoV infection. This effect is achieved through attenuation of lung viral load, suppression of inflammatory cytokine secretion, reduction in inflammatory cell infiltration, and mitigation of pulmonary injury.

HPIP is upregulated in liver cancer and promotes hepatoma cell proliferation via activation of G2/M transition.

Hematopoietic pre-B-cell leukemia transcription factor (PBX)-interacting protein (HPIP) has been shown to play a role in cancer development and progression. However, the detailed role of HPIP in cancer cell growth and the exact mechanism by which HPIP regulates cancer cell proliferation remains unclear. Here, we report that HPIP is overexpressed in most of 328 liver cancer patients and regulates hepatoma cell proliferation through G2/M checkpoint activation. HPIP increased anchorage-dependent and -independent growth of human liver cancer cell lines. The amino acid region 531-631 of HPIP was important for its modulation of liver cancer cell growth. The increased effects of HPIP on liver cancer cell proliferation were associated with activation of the G2/M cell-cycle concomitant with a marked increase of cyclin B1 and the inhibition of the negative G2/M phase regulator GADD45α. HPIP knockdown dramatically suppressed the growth of HepG2 liver cancer cells in nude mice. These data highlight the important role of HPIP in liver cancer cell growth and suggest that HPIP may be a good target for liver cancer therapy.

The role of antenatal corticosteroids in twin pregnancy.

Twin pregnancy was associated with significantly higher rates of adverse neonatal and perinatal outcomes. One of the underlying causes is that twins are prone to preterm birth. Antenatal corticosteroids are widely used for reducing the incidence of neonatal respiratory distress syndrome initially and other neonatal mortality and morbidities subsequently. As it is widely used as a prophylactic treatment for potential premature births, there remain controversies of issues relating to twin gestations, including window for opportunity, timing of use, repeat course, optimal administration-to-delivery intervals, dosage, and type of corticosteroid. Thus, we present a thorough review of antenatal corticosteroids usage in twin gestation, emphasizing the aforementioned issues and attempting to offer direction for future investigation and clinical practice.

rAAV2-Mediated Restoration of GALC in Neural Stem Cells from Krabbe Patient-Derived iPSCs.

Krabbe disease is a rare neurodegenerative fatal disease. It is caused by deficiency of the lysosomal enzyme galactocerebrosidase (GALC), which results in progressive accumulation of galactolipid substrates in myelin-forming cells. However, there is still a lack of appropriate neural models and effective approaches for Krabbe disease. We generated induced pluripotent stem cells (iPSCs) from a Krabbe patient previously. Here, Krabbe patient-derived neural stem cells (K-NSCs) were induced from these iPSCs. By using nine kinds of recombinant adeno-associated virus (rAAV) vectors to infect K-NSCs, we found that the rAAV2 vector has high transduction efficiency for K-NSCs. Most importantly, rAAV2-GALC rescued GALC enzymatic activity in K-NSCs. Our findings not only establish a novel patient NSC model for Krabbe disease, but also firstly indicate the potential of rAAV2-mediated gene therapy for this devastating disease.