Regulation of Two-Dimensional Platelet Micelles with Tunable Core Composition Distribution via Coassembly Seeded Growth Approach.

Seeded growth termed "living" crystallization-driven self-assembly (CDSA) has been identified as a powerful method to create one- or two-dimensional nanoparticles. Epitaxial crystallization is usually regarded as the growth mechanism for the formation of uniform micelles. From this perspective, the unimer depositing rate is largely related to the crystallization temperature, which is a key factor to determine the crystallization rate and regulate the core composition distribution among nanoparticles. In the present work, the coassembly of two distinct crystallizable polymers is explored in detail in a one-pot seeded growth protocol. Results have shown that polylactone containing a larger number of methylene groups (-CH2-) in their repeating units such as poly(η-octalactone) (POL) has a faster crystallization rate compared to poly(ε-caprolactone) (PCL) with a smaller number of -CH2- at ambient temperature (25 °C), thus a block or blocky platelet structure with heterogeneous composition distribution is formed. In contrast, when the crystallization temperature decreases to 4 °C, the difference of crystallization rate between both cores become negligible. Consequently, a completely random component distribution within 2D platelets is observed. Moreover, we also reveal that the core component of seed micelles is also paramount for the coassembly seeded growth, and a unique structure of flower-like platelet micelle is created from the coassembly of PCL/POL using POL core-forming seeds. This study on the formation of platelet micelles by one-pot seeded growth using two crystallizable components offers a considerable scope for the design of 2D polymer nanomaterials with a controlled core component distribution.

Histone lactylation bridges metabolic reprogramming and epigenetic rewiring in driving carcinogenesis: Oncometabolite fuels oncogenic transcription.

Heightened lactate production in cancer cells has been linked to various cellular mechanisms such as angiogenesis, hypoxia, macrophage polarisation and T-cell dysfunction. The lactate-induced lactylation of histone lysine residues is noteworthy, as it functions as an epigenetic modification that directly augments gene transcription from chromatin. This epigenetic modification originating from lactate effectively fosters a reliance on transcription, thereby expediting tumour progression and development. Herein, this review explores the correlation between histone lactylation and cancer characteristics, revealing histone lactylation as an innovative epigenetic process that enhances the vulnerability of cells to malignancy. Moreover, it is imperative to acknowledge the paramount importance of acknowledging innovative therapeutic methodologies for proficiently managing cancer by precisely targeting lactate signalling. This comprehensive review illuminates a crucial yet inadequately investigated aspect of histone lactylation, providing valuable insights into its clinical ramifications and prospective therapeutic interventions centred on lactylation.

The role of long-lived plasma cells in viral clearance.

The adaptive immune system has two types of plasma cells (PC), long-lived plasma cells (LLPC) and short-lived plasma cells (SLPC), that differ in their lifespan. In this paper, we propose that LLPC is crucial to the clearance of viral particles in addition to reducing the viral basic reproduction number in secondary infections. We use a sequence of within-host mathematical models to show that, CD8 T cells, SLPC and memory B cells cannot achieve full viral clearance, and the viral load will reach a low positive equilibrium level because of a continuous replenishment of target cells. However, the presence of LLPC is crucial for viral clearance.

Genome-Wide Identification of the GhANN Gene Family and Functional Validation of GhANN11 and GhANN4 under Abiotic Stress.

Annexins (ANNs) are a structurally conserved protein family present in almost all plants. In the present study, 27 GhANNs were identified in cotton and were unevenly distributed across 14 chromosomes. Transcriptome data and RT-qPCR results revealed that multiple GhANNs respond to at least two abiotic stresses. Similarly, the expression levels of GhANN4 and GhANN11 were significantly upregulated under heat, cold, and drought stress. Using virus-induced gene silencing (VIGS), functional characterization of GhANN4 and GhANN11 revealed that, compared with those of the controls, the leaf wilting of GhANN4-silenced plants was more obvious, and the activities of catalase (CAT), peroxidase (POD), and superoxide dismutase (SOD) were lower under NaCl and PEG stress. Moreover, the expression of stress marker genes (GhCBL3, GhDREB2A, GhDREB2C, GhPP2C, GhRD20-2, GhCIPK6, GhNHX1, GhRD20-1, GhSOS1, GhSOS2 and GhSnRK2.6) was significantly downregulated in GhANN4-silenced plants after stress. Under cold stress, the growth of the GHANN11-silenced plants was significantly weaker than that of the control plants, and the activities of POD, SOD, and CAT were also lower. However, compared with those of the control, the elasticity and orthostatic activity of the GhANN11-silenced plants were greater; the POD, SOD, and CAT activities were higher; and the GhDREB2C, GhHSP, and GhSOS2 expression levels were greater under heat stress. These results suggest that different GhANN family members respond differently to different types of abiotic stress.

Quantitative analysis of microglia morphological changes in the hypothalamus of chronically stressed rats.

Based on the successful establishment of a rat model of chronic restraint stress, we used multiple algorithms to quantify the morphological changes of rat hypothalamic microglia from various perspectives, providing a pathomorphological basis for the subsequent study of molecular mechanisms of hypothalamic stress injury, such as neuroinflammation. To verify the successful establishment of the chronic stress model, an enzyme-linked immunosorbent assay was performed to detect serum glucocorticoid levels. Microglia labeled with Iba1 in frozen sections of rat hypothalamus were scanned and photographed at multiple levels using confocal microscopy. Subsequently, images were processed for external contouring and skeletonization, and morphological indices of microglia were calculated and analyzed using fractal, skeleton, and Sholl analysis. In addition, the co-expression of CD68 (a marker that can reflect phagocytic activity) and Iba1 was observed by immunofluorescence technique. Compared with the control group, microglia in the chronic stress group displayed reduced fractal dimension and lacunarity, increased density and circularity, enlarged soma areas, and shortened and reduced branches. Sholl analysis confirmed the reduced complexity of microglia following chronic stress. Meanwhile, microglia CD68 increased significantly, indicating that the microglia in the chronic stress group have greater phagocytosis activity. In summary, chronic restraint stress promoted the conversion of microglia in the rat hypothalamus to a less complex form, manifested as larger soma, shorter and fewer branches, more uniform and dense texture, and increased circularity; indeed, the shape of these microglia resembled that of amoeba and they displayed strong phagocytosis activity.

The effects of disease control measures on the reproduction number of COVID-19 in British Columbia, Canada.

We propose a new method to estimate the change of the effective reproduction number with time, due to either disease control measures or seasonally varying transmission rate. We validate our method using a simulated epidemic curve and show that our method can effectively estimate both sudden changes and gradual changes in the reproduction number. We apply our method to the COVID-19 case counts in British Columbia, Canada in 2020, and we show that strengthening control measures had a significant effect on the reproduction number, while relaxations in May (business reopening) and September (school reopening) had significantly increased the reproduction number from around 1 to around 1.7 at its peak value. Our method can be applied to other infectious diseases, such as pandemics and seasonal influenza.

The dynamics of the risk perception on a social network and its effect on disease dynamics.

The perceived infection risk changes individual behaviors, which further affects the disease dynamics. This perception is influenced by social communication, including surveying their social network neighbors about the fraction of infected neighbors and averaging their neighbors' perception of the risk. We model the interaction of disease dynamics and risk perception on a two-layer random network that combines a social network layer with a contact network layer. We found that if information spreads much faster than disease, then all individuals converge on the true prevalence of the disease. On the other hand, if the two dynamics have comparable speeds, the risk perception still converges to a value uniformly on the network. However, the perception lags behind the true prevalence and has a lower peak value. We also study the behavior change caused by the perception of infection risk. This behavior change may affect the disease dynamics by reducing the transmission rate along the edges of the contact network or by breaking edges and isolating the infectious individuals. The effects on the basic reproduction number, the peak size, and the final size are studied. We found that these two effects give the same basic reproduction number. We find edge-breaking has a larger effect on reducing the final size, while reducing the transmission rate has a larger effect on reducing the peak size, which is true for both scale-free and Poisson networks.

FTO alleviates cerebral ischemia/reperfusion-induced neuroinflammation by decreasing cGAS mRNA stability in an m6A-dependent manner.

Microglia-mediated inflammation is a major contributor to the brain damage in cerebral ischemia and reperfusion (I/R) injury, and N6-Methyladenosine (m6A) has been implicated in cerebral I/R injury. Here, we explored whether m6A modification is associated with microglia-mediated inflammation in cerebral I/R injury and its underlying regulatory mechanism using an in vivo mice model of intraluminal middle cerebral artery occlusion/reperfusion (MCAO/R) and in vitro models of primary isolated microglia and BV2 microglial cells subjected to oxygen-glucose deprivation and reoxygenation (OGD/R) were used. We found microglial m6A modification increased and microglial fat mass and obesity-associated protein (FTO) expression decreased in cerebral I/R injury in vivo and in vitro. Inhibition of m6A modification by intraperitoneal injection of Cycloleucine (Cyc) in vivo or transfection of FTO plasmid in vitro significantly alleviated brain injury and microglia-mediated inflammatory response. Through Methylated RNA immunoprecipitation sequencing (MeRIP-Seq), RNA sequencing (RNA-Seq) and western blotting, we found that m6A modification promoted cerebral I/R-induced microglial inflammation via increasing cGAS mRNA stability to aggravate Sting/NF-κB signaling. In conclusion, this study deepens our understanding on the relationship of m6A modification and microglia-mediated inflammation in cerebral I/R injury, and insights a novel m6A-based therapeutic for inhibiting inflammatory response against ischemic stroke.

The effectiveness of control measures during the 2022 COVID-19 outbreak in Shanghai, China.

BACKGROUND: In March 2022, the Omicron variant of SARS-CoV-2 spread rapidly in Shanghai, China. The city adopted strict non-pharmacological intervention (NPI) measures, including lockdown (implemented on March 28 in Pudong and April 1 in Puxi) and blanket PCR testing (April 4). This study aims to understand the effect of these measures. METHODS: We tabulated daily case counts from official reports and fitted a two-patch stochastic SEIR model to the data for the period of March 19 to April 21. This model considered two regions in Shanghai, namely Pudong and Puxi, as the implementation of control measures in Shanghai was carried out on different dates in these regions. We verified our fitting results using the data from April 22 to June 26. Finally, we applied the point estimate of parameter values to simulate our model while varying the dates of control measure implementation, and studied the effectiveness of the control measures. RESULTS: Our point estimate for the parameter values yields expected case counts that agree well the data for both the periods from March 19 to April 21 and from April 22 to June 26. Lockdown did not significantly reduce the intra-region transmission rates. Only about 21% cases were reported. The underlying basic reproduction number R0 was 1.7, and the control reproduction number with both lockdown and blanket PCR testing was 1.3. If both measures were implemented on March 19, only about 5.9% infections would be prevented. CONCLUSIONS: Through our analysis, we found that NPI measures implemented in Shanghai were not sufficient to reduce the reproduction number to below unity. Thus, earlier intervention only has limited effect on reducing cases. The outbreak dies out because of only 27% of the population were active in disease transmission, possibly due to a combination of vaccination and lockdown.

Bioinformatics Analysis of Molecular Interactions between Endoplasmic Reticulum Stress and Ferroptosis under Stress Exposure.

Stress has become a universal biological phenomenon in the body, which leads to pathophysiological changes. However, the molecular network interactions between endoplasmic reticulum (ER) stress and ferroptosis under stressful conditions are not clear. For this purpose, we screened the gene expression profile of GSE173795 for intersection with ferroptosis genes and screened 68 differentially expressed genes (DEGs) (63 up-regulated, 5 down-regulated), mainly related to lipid and atherosclerosis, autophagy-animal, mitophagy-animal, focal adhesion, DNA replication, proteasome, oocyte meiosis, toll-like receptor signaling pathway, cell cycle, etc. Immune infiltration analysis revealed that stress resulted in decreased B cells memory, T cells CD8 and T cells CD4 memory resting, monocytes, macrophages M2, and increased B cells naive, T cells follicular helper, and macrophages M1. 19 core-DEGs (ASNS, TRIB3, ATF4, EIF2S1, CEBPG, RELA, HSPA5, DDIT3, STAT3, MAP3K5, HIF1A, HNF4A, MAPK14, HMOX1, CDKN1A, KRAS, SP1, SIRT1, EGFR) were screened, all of which were up-regulated DEGs. These biological processes and pathways were mainly involved in responding to ER stress, lipid and atherosclerosis, cellular response to stress, cellular response to chemical stress, and regulation of DNA-templated transcription in response to stress, etc. Spearman analysis did not find MAPK14 to be significantly associated with immune cells. Other core-DEGs were associated with immune cells, including B cells naive, T cells follicular helper, and monocytes. Based on core-DEGs, 283 miRNAs were predicted. Among the 22 miRNAs with highly cross-linked DEGs, 11 had upstream lncRNA, mainly targeting STAT3, SP1, CDKN1A, and SIRT1, and a total of 39 lncRNA were obtained. 85 potential drugs targeting 11 core-DEGs were identified and were expected to be potential immunotherapeutic agents for stress injury. Our experiments also confirmed that Liproxstatin-1 alleviates common cross-linked proteins between ER stress and ferroptosis. In conclusion, our study explored the molecular mechanisms and network interactions among stress-ER stress-ferroptosis from a novel perspective, which provides new research ideas for studying stressful injury.

Epstein-Barr Virus Envelope Glycoprotein gp110 Inhibits IKKi-Mediated Activation of NF-κB and Promotes the Degradation of ß-Catenin.

Epstein-Barr virus (EBV) infects host cells and establishes a latent infection that requires evasion of host innate immunity. A variety of EBV-encoded proteins that manipulate the innate immune system have been reported, but whether other EBV proteins participate in this process is unclear. EBV-encoded envelope glycoprotein gp110 is a late protein involved in virus entry into target cells and enhancement of infectivity. Here, we reported that gp110 inhibits RIG-I-like receptor pathway-mediated promoter activity of interferon-ß (IFN-ß) as well as the transcription of downstream antiviral genes to promote viral proliferation. Mechanistically, gp110 interacts with the inhibitor of NF-κB kinase (IKKi) and restrains its K63-linked polyubiquitination, leading to attenuation of IKKi-mediated activation of NF-κB and repression of the phosphorylation and nuclear translocation of p65. Additionally, gp110 interacts with an important regulator of the Wnt signaling pathway, ß-catenin, and induces its K48-linked polyubiquitination degradation via the proteasome system, resulting in the suppression of ß-catenin-mediated IFN-ß production. Taken together, these results suggest that gp110 is a negative regulator of antiviral immunity, revealing a novel mechanism of EBV immune evasion during lytic infection. IMPORTANCE Epstein-Barr virus (EBV) is a ubiquitous pathogen that infects almost all human beings, and the persistence of EBV in the host is largely due to immune escape mediated by its encoded products. Thus, elucidation of EBV's immune escape mechanisms will provide a new direction for the design of novel antiviral strategies and vaccine development. Here, we report that EBV-encoded gp110 serves as a novel viral immune evasion factor, which inhibits RIG-I-like receptor pathway-mediated interferon-ß (IFN-ß) production. Furthermore, we found that gp110 targeted two key proteins, inhibitor of NF-κB kinase (IKKi) and ß-catenin, which mediate antiviral activity and the production of IFN-ß. gp110 inhibited K63-linked polyubiquitination of IKKi and induced ß-catenin degradation via the proteasome, resulting in decreased IFN-ß production. In summary, our data provide new insights into the EBV-mediated immune evasion surveillance strategy.

Systematic characterization of chromodomain proteins reveals an H3K9me1/2 reader regulating aging in C. elegans.

The chromatin organization modifier domain (chromodomain) is an evolutionally conserved motif across eukaryotic species. The chromodomain mainly functions as a histone methyl-lysine reader to modulate gene expression, chromatin spatial conformation and genome stability. Mutations or aberrant expression of chromodomain proteins can result in cancer and other human diseases. Here, we systematically tag chromodomain proteins with green fluorescent protein (GFP) using CRISPR/Cas9 technology in C. elegans. By combining ChIP-seq analysis and imaging, we delineate a comprehensive expression and functional map of chromodomain proteins. We then conduct a candidate-based RNAi screening and identify factors that regulate the expression and subcellular localization of the chromodomain proteins. Specifically, we reveal an H3K9me1/2 reader, CEC-5, both by in vitro biochemistry and in vivo ChIP assays. MET-2, an H3K9me1/2 writer, is required for CEC-5 association with heterochromatin. Both MET-2 and CEC-5 are required for the normal lifespan of C. elegans. Furthermore, a forward genetic screening identifies a conserved Arginine124 of CEC-5's chromodomain, which is essential for CEC-5's association with chromatin and life span regulation. Thus, our work will serve as a reference to explore chromodomain functions and regulation in C. elegans and allow potential applications in aging-related human diseases.

3D Visualization System-Assisted Vitrectomy for Rhegmatogenous Retinal Detachment: Leave Out the Perfluorocarbon Liquid.

INTRODUCTION: Pars plana vitrectomy (PPV) is a primary strategy to restore vision for patients who have rhegmatogenous retinal detachment (RRD). Perfluorocarbon liquid (PFCL) is frequently used during PPV surgery. However, the unintended intraocular retention of PFCL may cause retina toxicity and thus lead to possible postoperative complications. In this paper, the experiences and surgical outcomes of a NGENUITY 3D Visualization System-assisted PPV are shown to evaluate the possibility of excluding the application of PFCL. METHODS: A consecutive series of 60 cases with RRD were presented, all of whom had undergone 23-gauge PPV with the assistance of a three-dimensional (3D) visualization system. Among them, 30 cases used PFCL to assist the drainage of subretinal fluid (SRF), while the other 30 cases did not. Parameters including retinal reattachment rate (RRR), best-corrected visual acuity (BCVA), operation time, and SRF residual were compared between the two groups. RESULTS: Baseline data showed no statistical significance between the two groups. At the last postoperative follow-up, the RRR of all the 60 cases reached 100% and best-corrected visual acuity (BCVA) gained significant improvement. The BCVA (logMAR) increased from 1.293 ± 0.881 to 0.479 ± 0.316 in the PFCL-excluded group, exhibiting better results than the PFCL included group, whose final BCVA was 0.650 ± 0.371. More importantly, excluding PFCL greatly reduced the operation time (decrease of 20%), therefore, avoiding possible complications caused by both the use of PFCL and the operation process. CONCLUSION: With the assistance of the 3D visualization system, it is feasible to treat RRD and perform PPV without using PFCL. The 3D visualization system is highly recommendable, as not only can it achieve the same surgical effect without the assistance of PFCL, but also simplify the operation procedure, shorten the operation time, save costs, and avoid complications related to PFCL.

[Determination of 14 paralytic shellfish toxins in plasma and urine by ultra-high performance liquid chromatography-tandem mass spectrometry].

The detection of paralytic shellfish toxins in human biological matrices is important for the diagnosis and treatment of food poisoning caused by them. An ultra-high performance liquid chromatography-tandem mass spectrometry (UHPLC-MS/MS) method was established for the determination of 14 paralytic shellfish toxins in plasma and urine. The effect of solid phase extraction (SPE) cartridges was also investigated and the pretreatment and chromatographic conditions were optimized. Under these optimal conditions, 0.2 mL water, 0.4 mL methanol, and 0.6 mL acetonitrile were successively added to plasma and urine samples for extraction. The supernatants from plasma extraction were subjected to an UHPLC-MS/MS analysis, whereas the supernatants from urine extraction were further purified using polyamide (PA) SPE cartridges and then analyzed by UHPLC-MS/MS. Chromatographic separation was conducted on a Poroshell 120 HILIC-Z column (100 mm×2.1 mm, 2.7 µm) with a flow rate of 0.5 mL/min. The mobile phase was 0.1% (v/v) formic acid aqueous solution containing 5 mmoL/L ammonium formate and acetonitrile containing 0.1% (v/v) formic acid. The analytes were detected in the multiple reaction monitoring (MRM) mode after being ionized by an electrospray ion (ESI) in positive and negative modes. Quantitation of the target compounds was performed using the external standard method. Under the optimal conditions, the method showed good linearity in the range of 0.24-84.06 µg/L, with correlation coefficients greater than 0.995. The limits of quantification (LOQs) for the plasma and urine samples were 1.68-12.04 ng/mL and 4.80-34.4 ng/mL, respectively. The average recoveries for all the compounds were 70.4%-123.4% at spiked levels of 1, 2, and 10 times the LOQs, the intra-day precisions were 2.3%-19.1% and the inter-day precisions were 5.0%-16.0%. The established method was used to determine the target compounds in the plasma and urine from mice intraperitoneally injected with 14 shellfish toxins. All 14 toxins were detected in the 20 urine and 20 plasma samples, with contents of 19.40-55.60 µg/L and 8.75-13.86 µg/L, respectively. The method is simple, sensitive, and only requires a small amount of sample. Therefore, it is highly suitable for the rapid detection of paralytic shellfish toxins in plasma and urine.

Epstein-Barr virus envelope glycoprotein 110 inhibits NF-κB activation by interacting with NF-κB subunit p65.

Epstein-Barr virus (EBV) is a member of the lymphotropic virus family and is highly correlated with some human malignant tumors. It has been reported that envelope glycoprotein 110 (gp110) plays an essential role in viral fusion, DNA replication, and nucleocapsid assembly of EBV. However, it has not been established whether gp110 is involved in regulating the host's innate immunity. In this study, we found that gp110 inhibits tumor necrosis factor α-mediated NF- κB promoter activity and the downstream production of NF- κB-regulated cytokines under physiological conditions. Using dual-luciferase reporter assays, we showed that gp110 might impede the NF-κB promoter activation downstream of NF-κB transactivational subunit p65. Subsequently, we used coimmunoprecipitation assays to demonstrate that gp110 interacts with p65 during EBV lytic infection, and that the C-terminal cytoplasmic region of gp110 is the key interaction domain with p65. Furthermore, we determined that gp110 can bind to the N-terminal Rel homologous and C-terminal domains of p65. Alternatively, gp110 might not disturb the association of p65 with nontransactivational subunit p50, but we showed it restrains activational phosphorylation (at Ser536) and nuclear translocation of p65, which we also found to be executed by the C-terminal cytoplasmic region of gp110. Altogether, these data suggest that the surface protein gp110 may be a vital component for EBV to antagonize the host's innate immune response, which is also helpful for revealing the infectivity and pathogenesis of EBV.

Development of an In Vitro Test Method to Replace an Animal-Based Potency Test for Pertactin Antigen in Multivalent Vaccines.

There is increasing interest to replace animal-based potency assays used routinely to test vaccines, since they are highly variable, are costly, and present ethical concerns. The development of relevant in vitro assays is part of the solution. Using pertactin (PRN) antigen as an example in DTaP-IPV (diphtheria, tetanus, acellular pertussis, and inactivated poliovirus) vaccines, a PRN antigenicity ELISA was developed using two monoclonal antibodies with a high affinity to unique PRN epitopes, relevance to human immune responses, and evidence of functionality. The ELISA measured consistent PRN antigenicity between the vaccine lots and was validated to demonstrate its accuracy, precision, linearity, and specificity. Notably, the PRN antigenicity ELISA was more sensitive than the mouse-based potency test and could more effectively differentiate between degraded and intact vaccine lots compared to the in vivo test. From these studies, the PRN antigenicity ELISA is proposed as an in vitro replacement for the in vivo potency test for PRN in DTaP-IPV-based formulations. Important considerations in this study included comprehensive antibody characterization, testing of multiple vaccine lots, method validation, and comparison to animal-based potency. Together, these factors form part of an overall strategy that ensures reliable and relevant in vitro assays are developed to replace animal tests.

Structural insights into the recognition of telomeric variant repeat TTGGGG by broad-complex, tramtrack and bric-à-brac - zinc finger protein ZBTB10.

Multiple proteins bind to telomeric DNA and are important for the role of telomeres in genome stability. A recent study established a broad-complex, tramtrack and bric-à-brac - zinc finger (BTB-ZF) protein, ZBTB10 (zinc finger and BTB domain-containing protein 10), as a telomeric variant repeat-binding protein at telomeres that use an alternative method for lengthening telomeres). ZBTB10 specifically interacts with the double-stranded telomeric variant repeat sequence TTGGGG by employing its tandem C2H2 zinc fingers (ZF1-2). Here, we solved the crystal structure of human ZBTB10 ZF1-2 in complex with a double-stranded DNA duplex containing the sequence TTGGGG to assess the molecular details of this interaction. Combined with calorimetric analysis, we identified the vital residues in TTGGGG recognition and determined the specific recognition mechanisms that are different from those of TZAP (telomere zinc finger-associated protein), a recently defined telomeric DNA-binding protein. Following these studies, we further identified a single amino-acid mutant (Arg767Gln) of ZBTB10 ZF1-2 that shows a preference for the telomeric DNA repeat TTAGGG sequence. We solved the cocrystal structure, providing a structural basis for telomeric DNA recognition by C2H2 ZF proteins.

Buyang Huanwu decoction improves neural recovery after spinal cord injury in rats through the mTOR signaling pathway and autophagy.

BACKGROUND: Spinal cord injury (SCI) refers to the interruption of the tracts inside the spinal cord caused by various factors. The repair of damaged axons has always been a difficult point in clinical treatment and neuroscience research. The treatment of SCI with Buyang huanwu decoction (BYHWD), a well-known recipe for invigorating Qi (a vital force forming part of any living entity in traditional Chinese culture) and promoting blood circulation, shows a good effect. METHODS: The rubrospinal tract (RST) transection model in rats was established in this study and rats were administrated with low (BL), medium (BM), or high (BH) doses of BYHWD. RESULTS: Compared with the SCI group, BL, BM moderately, and BH significantly improved the motor function of forelimbs and increased the number of red nucleus neurons in SCI rats. As for the possible molecular mechanism, BL, BM moderately, and BH significantly increased mTOR whereas decreased Beclin-1 and LC3 in the red nucleus. CONCLUSION: In conclusion, low, medium, and high doses of BYHWD could promote neural recovery in SCI rats through improving motor function and neuron survival in the red nucleus. The neuroprotective effects of BYHWD might be associated with affecting the mTOR signaling pathway and autophagy.

Frequency modulation of terahertz microcavity via strong coupling with plasmonic resonators.

Tunable terahertz (THz) microcavities are crucial for the compact on-chip THz devices, aiming to future cloud-based computing, and artificial-intelligence technologies. However, the solutions to effectively modulate THz microcavities remain elusive. Strong coupling has been widely demonstrated in many configurations at different ambient conditions to date and may serve as a promising tool to modulate THz microcavities. Here, we schematically design a microcavity-plasmon hybrid system, and propose an effective approach to modulating the resonant frequencies of THz microcavities by the microcavity-resonator strong coupling. In this case, we observed the strongly coupling states, where the resultant two-polariton branches exhibit an anti-crossing splitting in the frequency domain, experimentally exhibiting a ∼6.2% frequency modulation to the microcavity compared to the uncoupled case. This work provides an efficient approach to modulating chip-scale THz microcavities, thereby facilitating the development and application of compact THz integrated devices, further empowering the evolution of future information processing and intelligent computing system.

ERH Gene and Its Role in Cancer Cells.

Cancer is a major public health problem worldwide. Studies on oncogenes and tumor-targeted therapies have become an important part of cancer treatment development. In this review, we summarize and systematically introduce the gene enhancer of rudimentary homolog (ERH), which encodes a highly conserved small molecule protein. ERH mainly exists as a protein partner in human cells. It is involved in pyrimidine metabolism and protein complexes, acts as a transcriptional repressor, and participates in cell cycle regulation. Moreover, it is involved in DNA damage repair, mRNA splicing, the process of microRNA hairpins as well as erythroid differentiation. There are many related studies on the role of ERH in cancer cells; however, there are none on tumor-targeted therapeutic drugs or related therapies based on the expression of ERH. This study will provide possible directions for oncologists to further their research studies in this field.