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ObjectiveTo study the short-term exposure to ambient particulate matter less than 10 μm in aerodynamic diameter (PM10) on daily mortality in residents of six typical cities in central and western Inner Mongolia Autonomous Region (Inner Mongolia) to provide evidence for the development of air pollution control policies. MethodsData on daily mortality of permanent residents in six typical cities in central and western Inner Mongolia during 2017 – 2021 were collected from the Death Registration and Reporting Information System of municipal disease prevention and control centers, and data on daily meteorological conditions were collected from the municipal meteorological bureaus of the six cities, including Hohhot, Baotou, Ordos, Bayannur, Wuhai, and Alxa League. The daily average atmospheric PM10, sulfur dioxide (SO2), nitrogen dioxide (NO2) and ozone (O3) during the same period were calculated from the detection records of 24 national air pollutant monitoring stations in the six cities. A generalized linear model was used to quantitatively assess the relationship between PM10 exposure and daily mortality among residents of these cities, with stratified analysis by gender, age, education, and marital status. ResultsFor the six cities during the 5-year period, the daily mean PM10 concentration was 89.17 ± 84.71 μg/m3; the daily mean number of total non-accidental deaths, deaths from respiratory diseases, and deaths from circulatory diseases were 71 ± 15, 10 ± 4, and 34 ± 10, respectively. Single-day lag effect analysis showed that a 10 μg/m3 increase in daily mean PM10 concentration was associated with increased total non-accidental mortality (excess risk [ER] = 0.11%, 95% confidence interval [95%CI]: 0.03% – 0.20%) and circulatory disease mortality (ER = 0.12%, 95%CI: 0.03% – 0.20%) at lag day 0 in all residents and increased non-accidental mortality in female residents (ER = 0.17%, 95%CI: 0.05% – 0.30%), older residents ≥ 65 years (ER = 0.15%, 95%CI: 0.05% – 0.25%), residents with a junior high school education or less (ER = 0.12%, 95%CI: 0.02% – 0.22%), and unmarried residents (ER = 0.25%, 95%CI: 0.11% – 0.39%). Cumulative lag effect analysis showed that a 10 μg/m3 increase in daily mean PM10 concentration was associated with increased total non-accidental mortality (ER = 0.25%, 95%CI: 0.08% – 0.42%) and circulatory disease mortality (ER = 0.26%, 95%CI: 0.03% – 0.50%) at lag day 7 in all residents and increased non-accidental mortality in female residents (ER = 0.47%, 95%CI: 0.22% – 0.72%), older residents ≥ 65 years (ER = 0.33%, 95%CI: 0.13% – 0.52%), residents with a junior high school education or less (ER = 0.25%, 95%CI: 0.06% – 0.45%), and married residents (ER = 0.32%, 95%CI: 0.03% – 0.61%); a 10 μg/m3 increase in daily mean PM10 concentration was also associated with increased total non-accidental mortality among married residents (ER = 0.34%, 95%CI : 0.07% – 0.61%) on lag day 6. ConclusionExposure to PM10 is associated with increased total non-accidental mortality and circulatory disease mortality among all residents and the increased total non-accidental mortality and circulatory disease mortality are much more significant among female residents, older residents ≥ 65 years, residents with a junior high school education or less, and unmarried residents in six typical cities in central and western Inner Mongolia.

Enterovirus 71 (EV71) is a significant causative agent of hand, foot and mouth disease (HFMD). However, the precise mechanism by which EV71 infection leads to alterations in the immune response remain elusive. To address this knowledge gap, we conducted a study where we introduced the Inner Mongolia EV71 C33λ strain into Vero cells, derived from African green monkey kidney cells. Subsequently, we performed RNA sequencing (RNA-Seq) to investigate the changes in the transcriptome of these infected Vero cells. Our primary objective was to establish a foundational understanding that could inform future research on EV71-associated immune factors. In our study, we identified a total of 942 differentially expressed genes (DEGs) in Vero cells infected with Enterovirus 71 (EV71), with 568 gene exhibiting increased expression and 374 gene showing decreased expression. To elucidate the functional implications of these DEGs, we conducted a comprehensive functional enrichment analysis using Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathways. This analysis revealed three genes that were significantly upregulated, which we subsequently validated using reverse transcription polymerase chain reaction technology (RT-qPCR). The RT-qPCR results were in strong agreement with our RNA-Seq data, confirming the reliability of our findings. This study represents the pioneering RNA-Seq analysis that delves into the cellular response of Vero cells to EV71 infection. Our results not only provide a foundational understanding of the molecular changes induced by EV71 but also offer crucial insights into the mechanisms by which EV71 modulates the host immune system. These insights are pivotal for future research endeavors aimed at developing effective therapeutic strategies against EV71 and related pathogens, as well as for understanding the broader implications of viral infections on host immunity.

Summary: Hyperfunction of the dopamine system has been implicated in manic episodes in bipolar disorders. How dopaminergic neuronal function is regulated in the pathogenesis of mania remains unclear. Histaminergic neurons project dense efferents into the midbrain dopaminergic nuclei. Here, we present mice lacking dopaminergic histamine H2 receptor (H2R) in the ventral tegmental area (VTA) that exhibit a behavioral phenotype mirroring some of the symptoms of mania, including increased locomotor activity and reduced anxiety- and depression-like behavior. These behavioral deficits can be reversed by the mood stabilizers lithium and valproate. H2R deletion in dopaminergic neurons significantly enhances neuronal activity, concurrent with a decrease in the γ-aminobutyric acid (GABA) type A receptor (GABAAR) membrane presence and inhibitory transmission. Conversely, either overexpression of H2R in VTA dopaminergic neurons or treatment of H2R agonist amthamine within the VTA counteracts amphetamine-induced hyperactivity. Together, our results demonstrate the engagement of H2R in reducing VTA dopaminergic activity, shedding light on the role of H2R as a potential target for mania therapy.

Objective: Browning of white adipocytes is considered an efficient approach to combat obesity. Rosiglitazone induces the thermogenetic program of white adipocytes, but the underlying mechanisms remain elusive.Methods: Expression levels of browning and autophagy flux markers were detected by real-time PCR and immunoblotting. H&E and Oil Red O staining were performed to evaluate the lipid droplets area. Nuclear protein extraction and immunoprecipitation were used to detect the proteins interaction.Results: In this study, we reported that rosiglitazone promoted adipocyte browning and inhibited autophagy. Rapamycin, an autophagy inducer, reversed adipocyte browning induced by rosiglitazone. Autophagy inhibition by rosiglitazone does not prevent mitochondrial clearance, which was considered to promote adipose whitening. Instead, autophagy inhibition increased p62 nuclear translocation and stabilized the PPARγ–RXRα heterodimer, which is an essential transcription factor for adipocyte browning. We found that rosiglitazone activated NRF2 in mature adipocytes. Inhibition of NRF2 by ML385 reversed autophagy inhibition and the pro-browning effect of rosiglitazone.Conclusion: Our study linked autophagy inhibition with rosiglitazone-promoted browning of adipocytes and provided a mechanistic insight into the pharmacological effects of rosiglitazone.

Summary: Previous studies have focused on the impact of individual RNA modifications on tumor development. This study comprehensively investigated the effects of multiple RNA modifications, including m6A, alternative polyadenylation, pseudouridine, adenosine-to-inosine editing, and uridylation, on gastric cancer (GC). By analyzing 1,946 GC samples from eleven independent cohorts, we identified distinct clusters of RNA modification genes with varying survival rates and immunological characteristics. We assessed the chromatin activity of these RNA modification clusters through regulon enrichment analysis. A prognostic model was developed using Stepwise Regression and Random Survival Forest algorithms and validated in ten independent datasets. Notably, the low-risk group showed a more favorable prognosis and positive response to immune checkpoint blockade therapy. Single-cell RNA sequencing confirmed the abundant expression of signature genes in B cells and plasma cells. Overall, our findings shed light on the potential significance of multiple RNA modifications in GC prognosis, stemness development, and chemotherapy resistance.

Summary: Overly strong fear memories can cause pathological conditions. Histamine H3 receptor (H3R) has been viewed as an optimal drug target for CNS disorders, but its role in fear memory remains elusive. We find that a selective deficit of H3R in cholinergic neurons, but not in glutamatergic neurons, enhances freezing level during contextual fear memory retrieval without affecting cued memory. Consistently, genetically knocking down H3R or chemogenetically activating cholinergic neurons in the ventral basal forebrain (vBF) mimics this enhanced fear memory, whereas the freezing augmentation is rescued by re-expressing H3R or chemogenetic inhibition of vBF cholinergic neurons. Spatiotemporal regulation of H3R by a light-sensitive rhodopsin-H3R fusion protein suggests that postsynaptic H3Rs in vBF cholinergic neurons, but not presynaptic H3Rs of cholinergic projections in the dorsal hippocampus, are responsible for modulating contextual fear memory. Therefore, precise modulation of H3R in a cell-type- and subcellular-location-specific manner should be explored for pathological fear memory.

Abstract Background The occurrence of nonunion after tibial fracture surgery is mainly related to insufficient blood supply. Therefore, anatomical study of the internal and external tibial artery is very important, but there is no good method for displaying the intraosseous artery clearly and intuitively. This hinders the protection and reconstruction of it by surgeons, as well as the development of new instruments and techniques by researchers. Objective To develop a transparent specimen that could clearly display the intraosseous artery of the tibia. Methods In 10 isolated pig calves with popliteal vessels, the popliteal artery was exposed and a tube was placed. A casting agent was then injected at constant pressure, and the tissue around the blood vessel was preliminarily removed after solidification. The perivascular tissue and periosteum were further removed via alkali corrosion, and the tibia was fixed with an external fixator to protect the non-corrosive areas at both ends. Alternate acid corrosion and flushing were then applied until the intraosseous artery was completely exposed. The distribution and branches of intraosseous nutrient arteries were observed with the naked eye and via microscopy. Three-dimensional (3D) scanning and 3D printing filling techniques were used to make transparent tibia specimens with preservation of intraosseous arteries. Results A cast specimen of the intraosseous artery of porcine tibia was successfully generated via epoxy resin perfusion combined with acid–alkali etching, and the intraosseous artery was clearly visible. The 3D printing and filling technique successfully produced a transparent tibia specimen with preservation of internal bone arteries, and accurately restored the external shape of the tibia. The foramen of the nutrient artery appeared near the middle upper third of the lateral edge of the tibia. After entering the tibia, the nutrient artery proceeded forward, medial, and downward for a certain distance, twisted and turned near the midpoint of the medullary cavity, and divided into the ascending and descending branches. After going in the opposite direction for a distance, the ascending trunk sent out 2–3 branches, and the descending trunk sent out 2–3 branches. Conclusion The cast specimen of pig intraosseous artery generated via the above-described perfusion corrosion method provides methodological guidance for the study of anatomical characteristics of the intraosseous artery, and a theoretical basis for the study of new methods of internal fixation and reconstruction of the blood supply of the lower tibia.

Objective To describe a method to display the three‐dimensional distribution of intraosseous arteries in the femoral head by vascular corrosion casting. Methods An experimental study was done to expose the intraosseous arteries of the femoral head by a microperfusion corrosion method between January 2021 and May 2021. Specimens were 23 swine femoral heads (12 female specimens and 11 male specimens, where age of swine ranged from 8 to 12 months, and the weight was approximately 150 kg). The femoral heads were microperfused with the vascular casting resin through retinacular arteries, and the bone of the femoral head was dissolved with 50% sodium hydroxide and 10% hydrochloric acid and rinsed under the microscope until the vessel casts were completely exposed. The distribution and anastomosis of the arteries in the femoral head were observed under direct vision and microscopy. The diameter of the artery in the femoral head was measured at 0.5 cm after its entry into the bone of the femoral head with a microscale under the microscope. The number of internal arteries with diameter ≥0.05 mm was counted. The number and diameter of the main trunk of the epiphyseal arteries in the femoral head between male and female swine were compared. Results The vascular casting specimen of the swine femoral head was successfully produced by using epoxy resin as a casting agent, and the three‐dimensional intraosseous vascular structures were clearly visible. The number of epiphyseal arteries in male and female swine was 8.55 ± 2.15 and 8.83 ± 2.15 (t = −0.31, p = 0.38), respectively. The diameters of the superior epiphyseal arteries in male and female swine were 0.35 ± 0.09 and 0.31 ± 0.08 mm (t = 1.03, p = 0.16), the diameters of the inferior epiphyseal arteries were 0.47 ± 0.05 and 0.49 ± 0.09 mm (t = −0.57, p = 0.29), and the diameters of the anterior epiphyseal arteries were 0.34 ± 0.08 and 0.33 ± 0.13 mm (t = 0.32, p = 0.37). There was no significant difference in the number and diameter of the main trunk of intraosseous arteries between male and female swine (p > 0.05). The main trunk of intraosseous arteries formed an anastomosis in the center of the femoral head. Among 23 swine femoral head samples, three types of intraosseous anastomosis were observed, including 13 (57%) posterior superior‐posterior inferior, seven (30%) posterior inferior‐anterior, and three (13%) uniform intraosseous anastomosis. Conclusion The microperfusion corrosion method can produce the vascular casting specimen of swine femoral head revealing the three‐dimensional structure of the intraosseous artery, which clearly shows the origin, course and branches, and diameter, as well as the anastomosis, of nutrient arteries in the femoral head. This method provides a simple and rapid technique for quantifying and visualizing intraosseous arteries.

Stachyose is a well-known gut microbiota-oriented prebiotic that could directly reach colon and influence the intestinal microenvironment. Through an in vitro fermentation on fecal microbiota from a drug-naive new-onset and a perennial patient, we for the first time revealed a novel function of stachyose on promoting the microbial transformation from tryptophan to indole catabolites (i.e., indole-3-propionic acid, indole-3-lactic acid and indole-3-carboxaldehyde), which has shown to improve intestinal functions and glucose metabolism. Stachyose increased Bifidobacterium and Lactobacillus genera, while reducing Lactococcus and Streptococcus. Similar regulatory effects on microbial transformation of tryptophan and its related microbiota were confirmed in C57BL/6 mice with high-fat-diet induced impaired fasting glucose and gut dysbacteria. Additionally, stachyose up-regulated microbiota related metabolites with ameliorative effects on type 2 diabetes, i.e., hyocholic acid and conjugated linoleic acid in vitro. Our study proves benefits of stachyose for management of type 2 diabetes via regulating microbial metabolism of tryptophan.

Background: Baicalein is an active ingredient extracted from the root of S. baicalensis Georgi, which exhibits cardiovascular protection, anti-inflammatory, and anti-microbial properties. Our previous study showed that chronic treatment of Baicalein ameliorated cognitive dysfunction in a mouse model of Alzheimer's disease (AD). However, it remains unknown whether Baicalein ameliorates cognitive deficits in AD mouse models by altering gut microbiota and its metabolites.Methods: Behavioral tests, metagenomic and untargeted metabolomics analyses were used to evaluate the effects of Baicalein on the APP/PS1 mice.Results: Our research showed that treatment of Baicalein for 2 weeks ameliorated cognition and memory in a dose-dependent manner, as indicated by the significant increases in the Discrimination index and Number of crossings and decrease in latency to the previous platform location in 8-month of age APP/PS1 mice in novel object recognition and water maze tests. The metagenomic analysis showed the abundance of the dominant phyla in all groups, including Bacteroidetes (14.59%–67.02%) and Firmicutes (20.19%–61.39%). LEfSe analysis of metagenomics identified three species such as s__Roseburia_sp_1XD42_69, s__Muribaculaceae_bacterium_Isolate_104_HZI, s__Muribaculaceae_bacterium_Isolate_110_HZI as Baicalein-treated potential biomarkers. Metabolite analysis revealed the increment of metabolites, including glutamate, thymine and hexanoyl-CoA.Conclusion: The effects of Baicalein on memory and cognition may relate to the metabolism of nucleotides, lipids and glucose.

Background New York City Emergency Medical Services implemented a prehospital triage protocol using a modified Speech–Los Angeles Motor Scale to identify patients with large‐vessel occlusion. Patients with Speech–Los Angeles Motor Scale ≥4 and last known well within 5 hours were routed to the nearest thrombectomy‐capable stroke center. Our aim was to describe the Speech–Los Angeles Motor Scale Triage Positive (STP) cohort and compare to a cohort that ultimately underwent endovascular thrombectomy (EVT) but were missed by the protocol (not triaged as Speech–Los Angeles Motor Scale positive [NSTP]). Methods A prospectively collected database identified patients arriving within 5 hours from last known well between April 2019 and March 2020. STP patients (N=145) were assessed for medical history, acute stroke time metrics, and clinical accuracy. NSTP (N=65) was subdivided into those who arrived directly to a thrombectomy‐capable stroke center (direct NSTP, N=30), and those transferred to a thrombectomy‐capable stroke center (transferred NSTP, N=35). Comparisons were made between the cohorts that underwent EVT. Results In the STP cohort, stroke was diagnosed in 110 of 145 (75.9%) patients: 31 hemorrhagic, 79 ischemic. There were 45 patients (31.0%) with large vessel occlusion and 34 (23.4%) underwent EVT. STP and NSTP subgroups had no difference in first medical contact‐to‐intravenous thrombolysis (≈90 minutes) despite STP patients taking 5 minutes longer to arrive. Ambulance travel times were similar (11 minutes). First medical contact‐to‐arterial access was similar in STP (137.9 minutes) and direct NSTP (137.9 minutes) groups but significantly shorter against transferred NSTP (252.1 minutes; P

Abstract Mitophagy is a highly conserved cellular process that maintains the mitochondrial quantity by eliminating dysfunctional or superfluous mitochondria through autophagy machinery. The mitochondrial outer membrane protein BNIP3L/Nix serves as a mitophagy receptor by recognizing autophagosomes. BNIP3L is initially known to clear the mitochondria during the development of reticulocytes. Recent studies indicated it also engages in a variety of physiological and pathological processes. In this review, we provide an overview of how BNIP3L induces mitophagy and discuss the biological functions of BNIP3L and its regulation at the molecular level. We further discuss current evidence indicating the involvement of BNIP3L-mediated mitophagy in human disease, particularly in cancer and neurological disorders.

Cerebral ischemia is one of the leading causes of human mortality and disability worldwide. The treatment of cerebral ischemia is refractory due to its short therapeutic window and lack of effective clinical drugs. Mitophagy, the autophagic elimination of damaged mitochondria, attenuates neuronal injury in cerebral ischemia, indicating the potential of mitophagy inducers as therapies for cerebral ischemia. We previously determined that, by enhancing autophagy flux, the steroidal alkaloid tomatidine can function as a neuroprotective agent against ischemic injury. However, its effects on mitophagy remain unknown. For this purpose, neuroblastoma cell lines Neuro‐2a and SH‐SY5Y were subjected to ischemic injury induced by oxygen–glucose deprivation/reperfusion (OGD/R) and then treated with tomatidine. OGD/R induced a general decrease of cellular contents, and this study revealed that tomatidine had no impact on mitophagy. In addition, tomatidine did not affect mitochondrial contents, including translocase of outer mitochondrial membrane 20 and voltage‐dependent anion channel 1, in either OGD/R‐treated or intact SH‐SY5H cells. Our results indicate that tomatidine exhibits its neuroprotective effects by enhancing autophagy, but in a potentially mitophagy‐independent manner, and provide insights for further investigation into its mechanism(s) and potential therapeutic use against cerebral ischemia.

Stroke is considered a leading cause of mortality and neurological disability, which puts a huge burden on individuals and the community. To date, effective therapy for stroke has been limited by its complex pathological mechanisms. Autophagy refers to an intracellular degrading process with the involvement of lysosomes. Autophagy plays a critical role in maintaining the homeostasis and survival of cells by eliminating damaged or non-essential cellular constituents. Increasing evidence support that autophagy protects neuronal cells from ischemic injury. However, under certain circumstances, autophagy activation induces cell death and aggravates ischemic brain injury. Diverse naturally derived compounds have been found to modulate autophagy and exert neuroprotection against stroke. In the present work, we have reviewed recent advances in naturally derived compounds that regulate autophagy and discussed their potential application in stroke treatment.

TP53-induced glycolysis and apoptosis regulator (TIGAR) alleviates oxidative stress and protects against ischemic neuronal injury by shifting glucose metabolism into the pentose phosphate pathway (PPP). However, the brain alters glucose metabolism from PPP to glycolysis during prolonged ischemia. It is still unknown whether and how TIGAR exerts the antioxidant activity and neuroprotection in prolonged ischemic brains. Here, we determined the significant upregulation of TIGAR that was proportional to the duration of ischemia. However, TIGAR failed to upregulate the NADPH level but still alleviated oxidative stress in neuronal cells with prolonged oxygen glucose-deprivation (OGD). Furthermore, inhibiting PPP activity, either by the expression of mutant TIGAR (which lacks enzymatic activity) or by silencing Glucose 6-phosphate dehydrogenase, still retained antioxidant effects and neuroprotection of TIGAR with prolonged OGD. Intriguingly, TIGAR-induced autophagy alleviated oxidative stress, contributing to neuron survival. Further experiments indicated that TIGAR-induced autophagy neutralized oxidative stress by activating Nrf2, which was cancelled by ML385 or Nrf2 knockdown. Remarkably, either Atg7 deletion or Nrf2 silencing abolished the neuroprotection of TIGAR in mice with prolonged ischemia. Taken together, we found a PPP-independent pathway in which TIGAR alleviates oxidative stress. TIGAR induces autophagy and, thus, activates Nrf2, offering sustainable antioxidant defense in brains with extended ischemia. This previously unexplored mechanism of TIGAR may serve as a critical compensation for antioxidant activity caused by the lack of glucose in ischemic stroke.

Social impairment and anhedonia are common negative symptoms in patients with schizophrenia. Here, the authors show that the histamine H1 receptor in cholinergic neurons in the basal forebrain has a critical role in sensorimotor gating, social behaviour, and anhedonia-like behaviour in mice.

Abstract The identification and tracking for model pigs, as a vital research content for studying the habits of model pigs, drawed more and more considerable attention. To fulfill people requirements for the effectiveness of the non-significant model pig tracking in breeding environment, a Camshift tracking approach based on correlation probability graph, i.e., C a m T r a c o r −P G , is proposed in this paper, in which the correlation probability graph is introduced to achieve target positioning and tracking. Technically, acquiring images through a vision sensor, according to the circular arrangement of pixels in the inverse probability projection graph, and multiplying the inverse projection probability value of a pixel by its surrounding pixels could obtain the weighted sum. Then, the target projection grayscale graph is established by utilizing the correlation probability value for positioning, identification, and tracking of model pigs. Finally, extensive experiments are conducted to validate reliability and efficiency of our approach.

Inhibition of phosphodiesterase 2 and 4 (PDE2A and PDE4) increases the intracellular cAMP and/or cGMP levels, which may prevent Amyloid β 42 oligomers (Aβ) related cognitive impairment and dementias. Baicalein, one of natural flavones found in the root of Scutellaria baicalensis Georgi, has a wide range of pharmacological activities including antioxidant and anti-inflammatory effects. However, no studies suggest whether baicalein mediated anti-Alzheimer’s disease (AD) events involve PDEs subtypes-mediated neuroprotective pathways. The present study examined whether memory enhancing effects of baicalein on Aβ- induced cognitive impairment are related to regulating neuroplasticity via PDE2 and PDE4 subtypes dependent cAMP/cGMP neuroprotective pathway. The results suggested that microinjected of Aβ into CA1 of hippocampus induced cognitive and memory impairment in mice, as evidenced by decreased recognition index in the novel object recognition (NOR) task, impaired memory acquisition, retention and retrieval in the Morris water maze (MWM) and shuttle box tests. These effects were reversed by treatment with baicalein for 14 days. Moreover, Aβ-induced neuronal atrophy and decreased expression of two synaptic proteins, synaptophysin and PSD 95, were prevented by baicalein. The increased expression of PDE2A and PDE4 subtypes (PDE4A, PDE4B and PDE4D), and decreased levels of cAMP/cGMP, pCREB/CREB and BDNF induced by Aβ were also blocked by chronic treatment of baicalein for 14 days. These findings suggest that baicalein’s reversal of Aβ-induced memory and cognitive disorder may involve the regulation of neuronal remodeling via regulation of PDE2/PDE4 subtypes related cAMP/cGMP -pCREB-BDNF pathway.

In this paper, we propose to boost the cross-modal retrieval through mutually aligning images and captions on the aspects of both features and relationships. First, we propose a multi-feature based visual-semantic embedding (MVSE++) space to retrieve the candidates in another modality, which provides a more comprehensive representation of the visual content of objects and scene context in images. Thus, we have more potential to find a more accurate and detailed caption for the image. However, captioning concentrates the image contents by semantic description. The cross-modal neighboring relationships start from the visual and semantic sides are asymmetric. To retrieve a better cross-modal neighbor, we propose to re-rank the initially retrieved candidates according to the ${k}$ nearest reciprocal neighbors in MVSE++ space. The method is evaluated on the benchmark datasets of MSCOCO and Flickr30K with standard metrics. We achieve highe accuracy in caption retrieval and image retrieval at both R@1 and R@10.

The present study was conducted to clarify the differences in the multi-element, volatile organic compound, fatty acid, and metabolite fingerprints between black and white sesame seeds. A total of 53 chemical elements, 32 volatile flavor compounds, 40 fatty acids, and 283 metabolites were identified and evaluated in the two groups of sesame seeds. Univariate and multivariate statistics indicated a distinct separation between the two groups of sesame seeds. A panel of 16 chemical elements, 3 volatile compounds, 8 individual fatty acids, and 54 metabolites with p value < 0.05 and variable importance in projection score > 1 were selected as the most important discriminants for the two types of sesame seeds. Overall, these data reveal the influence of genotype on the chemical composition of sesame seeds. Our findings also demonstrate that the hybrid model of instrumental analysis and chemometrics is feasible for the discrimination of black and white sesame seeds.

Summary: The neurological recovery following traumatic brain injury (TBI) is limited, largely due to a deficiency in neurogenesis. The present study explores the effects of histamine H3 receptor (H3R) antagonism on TBI and mechanisms related to neurogenesis. H3R antagonism or H3R gene knockout alleviated neurological injury in the late phase of TBI, and also promoted neuroblast differentiation to enhance neurogenesis through activation of the histaminergic system. Histamine H1 receptor, but not H2 receptor, in neural stem cells is shown to be essential for this promotion by using Hrh1fl/fl;NestinCreERT2 and Hrh2fl/fl;NestinCreERT2 mice. Moreover, increase in mature and functional neurons at the penumbra area conferred by H3R antagonism was abrogated in Hrh1fl/fl;NestinCreERT2 mice. Taken together, H3R antagonism provides neuroprotection against TBI in the late phase through the promotion of neurogenesis, and the H1 receptor in neural stem cells is required for this action. H3R may serve as a new target for clinical treatment of TBI. : Hu and colleagues show that histamine H3R antagonism provides neuroprotection against traumatic brain injury in the late phase through the promotion of neurogenesis. Through specific deletion histamine receptors in neural stem cells, they found that the H1 receptor in neural stem cells is required for this action. H3R antagonists can be the potential candidate drugs for the therapy. Keywords: differentiation, histamine H3 receptor, histamine H1 receptor, neurogenesis, neuroprotection, traumatic brain injury

Leaf is an important organ for photosynthesis and transpiration associated with the plants’ growth. Through the study of leaf phenotype, it the physiological characteristics produced by the interaction of the morphological parameters with the environment can be understood. In order to realize the assessment of the spatial morphology of leaves, a method based on three-dimensional stereo vision was introduced to extract the shape information, including the length and width of the leaves. Firstly, a depth sensor was used to collect the point cloud of plant leaves. Then, the leaf coordinate system was adjusted by principal component analysis to extract the region of interest; and compared with a cross-sectional method, the geodesic distance method, we proposed a method based on the cutting plane to obtain the intersecting line of the three-dimensional leaf model. Eggplant leaves were used to compare the accuracy of these methods in the measurement of a single leaf.

The optical transmission properties of the metallic film with an array of compound rectangular nanoholes are numerically investigated by the finite-difference time-domain (FDTD) method. The compound rectangular nanohole (unit cell) in such a structure consists of a large square hole with two small rectangular holes symmetrically distributed at its both sides. Extraordinary optical transmission (EOT) of more than 85% is obtained in this structure, which is larger than that found in the metal film perforated only with the large hole array (55%) or the small hole array (18%). The EOT in the optical regime mainly results from the excitation and coupling of localized surface plasmon resonances and surface plasmon polaritons. The EOT properties can be efficiently tailored in both wavelength and transmission intensity by varying the size and shape of nanoholes. Our structure also shows the sensitivity to environmental dielectric constant. These results indicate that our structure has potential applications in plasmonic filters and sensors.

It has been demonstrated that cerebral ischemia induces astrocyte reactivity, and subsequent glial scar formation inhibits axonal regeneration during the recovery phase. Investigating the mechanism of glial scar formation will facilitate the development of strategies to improve axonal regeneration. However, an in vitro model of ischemia-induced glial scar has not yet been systematically established.In the present study, we at the first time found that oxygen-glucose deprivation (OGD) in vitro can induce rat cortical astrocytes to present characteristics of glial scar. After OGD for 6 h, astrocytes showed a remarkable proliferation following 24 h reperfusion, evaluated by 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide assay and BrdU immunocytochemistry. Meanwhile, the expression of glial fibrillary acidic protein significantly increased, so did the expression of neurocan, which is a hallmark of the glial scar. In further experiments, neurons were co-cultured with astrocytes, which had been exposed to OGD, and then the immunostaining of class III β-tubulin was carried out to assess the neurite growth. When the co-culture was performed at 48 h reperfusion of astrocytes, the neurite growth was obviously inhibited, and this inhibition could be reversed by chondroitinase ABC, which digests glycosaminoglycan chains on CSPGs, including neurocan. However, the processes of neurons were elongated, when the co-culture was performed immediately after OGD.Our results indicated that after conditioned OGD the astrocytes presented the characteristics of the glial scar, which are also comparable to the astrocytes in acute and chronic phases after cerebral ischemia in vivo. Therefore, the present system may be used as an in vitro model to explore the mechanisms underlying glial scar formation and the treatments to improve axonal regeneration after cerebral ischemia.

Background Ischaemic stroke triggers neuronal mitophagy, while the involvement of mitophagy receptors in ischaemia/reperfusion (I/R) injury-induced neuronal mitophagy remain not fully elucidated. Here, we aimed to investigate the involvement of mitophagy receptor FUN14 domain-containing 1 (FUNDC1) and its modulation in neuronal mitophagy induced by I/R injury.Methods Wild-type and FUNDC1 knockout mice were generated to establish models of neuronal I/R injury, including transient middle cerebral artery occlusion (tMCAO) in vivo and oxygen glucose deprivation/reperfusion in vitro. Stroke outcomes of mice with two genotypes were assessed. Neuronal mitophagy was analysed both in vivo and in vitro. Activities of FUNDC1 and its regulator Src were evaluated. The impact of Src on FUNDC1-mediated mitophagy was assessed through administration of Src antagonist PP1.Results To our surprise, FUNDC1 knockout mice subjected to tMCAO showed stroke outcomes comparable to those of their wild-type littermates. Although neuronal mitophagy could be activated by I/R injury, FUNDC1 deletion did not disrupt neuronal mitophagy. Transient activation of FUNDC1, represented by dephosphorylation of Tyr18, was detected in the early stages (within 3 hours) of neuronal I/R injury; however, phosphorylated Tyr18 reappeared and even surpassed baseline levels in later stages (after 6 hours), accompanied by a decrease in FUNDC1-light chain 3 interactions. Spontaneous inactivation of FUNDC1 was associated with Src activation, represented by phosphorylation of Tyr416, which changed in parallel with the level of phosphorylated FUNDC1 (Tyr18) during neuronal I/R injury. Finally, FUNDC1-mediated mitophagy in neurons under I/R conditions can be rescued by pharmacological inhibition of Src.Conclusions FUNDC1 is inactivated by Src during the later stage (after 6 hours) of neuronal I/R injury, and rescue of FUNDC1-mediated mitophagy may serve as a potential therapeutic strategy for treating ischaemic stroke.