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Abstract To determine the optimal temperature in rearing of fry stream groupers, Acrossocheilus fasciatus, a total of 540 fry fish with an initial body weight of (0.57 ± 0.16) g, and body length of (4.08 ± 0.40) cm were randomly distributed to 18 15‐L tanks and reared at six different temperatures (12, 16, 20, 24, 26, and 28°C) for a period of 60 days. Fish were hand‐fed to satiation under all six different temperature treatments. At the end of the experiment, almost all the growth, feeding, and gonadal development parameters were higher in the 26°C group than in the rest of the groups. As temperature increased from 12 to 26°C, the specific growth rate and feeding efficiency of fry significantly increased (p 0.05). In conclusion, increases in temperature significantly improved the growth rate, feeding performance, and gonadal development rate of fry A. fasciatus. Regression analysis based on growth and feeding performance showed that the optimal temperature of rearing fry A. fasciatus was 23.81–26.57°C.

Abstract Glioblastoma (GBM) is an aggressive intracranial tumour, and current chemotherapy regimens have limited efficacy. Aloperine (ALO), a natural alkaline compound, has shown potential as an antitumor agent. However, the effect of ALO against GBM remains unclear. This study aimed to investigate the function of ALO in treating GBM. U87, A172, and GL261 cell lines were used for in vitro experiments, and GL261 was also used to establish in vivo models. The results showed that ALO inhibited the proliferation of GBM cells by cell cycle arrest and apoptosis. Furthermore, autophagy was found to play a critical role, suggested by observation of autophagosomes under the transmission electron microscopy. It was discovered for the first time that ALO targeted lysosomes directly in glioma cells, tested by fluo-rescence-labelled ALO and organelle-localizing probes. In addition, ALO inhibited late autophagy and induced paraptosis in GBM, verified by classical gene expression changes in qPCR and western blotting. Also, ALO inhibited tumour growth and acted synergistically with temozolomide in intracranial glioma mice models in vivo. Our findings suggest that ALO targets lysosomes to inhibit late autophagy in GBM, inducing cell cycle arrest, paraptosis, and apoptosis. ALO may therefore be a promising therapeutic agent for the treatment of GBM.

Introduction: The majority of individuals diagnosed with advanced colorectal cancer (CRC) will ultimately acquire resistance to 5-FU treatment. An increasing amount of evidence indicates that aerobic glycolysis performs a significant function in the progression and resistance of CRC. Nevertheless, the fundamental mechanisms remain to be fully understood.Methods: Proteomic analysis of 5-FU resistant CRC cells was implemented to identify and determine potential difference expression protein.Results: These proteins may exhibit resistance mechanisms that are potentially linked to the process of aerobic glycolysis. Herein, we found that nucleolar protein 58 (NOP58) has been overexpressed within two 5-FU resistant CRC cells, 116-5FuR and Lovo-5FuR. Meanwhile, the glycolysis rate of drug-resistant cancer cells has increased. NOP58 knockdown decreased glycolysis and enhanced the sensitivity of 116-5FuR and Lovo-5FuR cells to 5FU.Conclusion: The proteomic analysis of chemoresistance identifies a new target involved in the cellular adaption to 5-FU and therefore highlights a possible new therapeutic strategy to overcome this resistance.

Nkx2.3, a transcription factor, plays important roles in various developmental processes. However, the mechanisms underlying nkx2.3's regulation of pouch and pharyngeal arch development in zebrafish remain unclear. In this study, we demonstrated that knockdown or knockout of nkx2.3 resulted in the absence of posterior ceratobranchial cartilages in zebrafish. The absence of posterior pharyngeal cartilages is a consequence of the compromised proliferation and differentiation and survival of cranial neural crest cells (CNCCs). Notably, we found that nkx2.3 was not involved in endoderm pouch formation. Additionally, our findings suggested that nkx2.3 negatively regulated Fibroblast growth factor (Fgf) signaling, as overexpression of fgf8 could mimic the phenotype observed in nkx2.3 morphants, suppressing CNCC differentiation. Moreover, inhibiting Fgf signaling restored the abnormalities in posterior cartilages induced by nkx2.3 knockdown. These findings establish the essential role of nkx2.3 in the development of posterior ceratobranchial cartilages through the inhibition of fgf8.

IntroductionThe excessive use of chemical fertilizer causes increasing environmental and food security crisis. Organic fertilizer improves physical and biological activities of soil. Rhizosphere microbiota, which consist of highly diverse microorganisms, play an important role in soil quality. However, there is limited information about the effects of different fertilization conditions on the growth of Qingke plants and composition of the rhizosphere microbiota of the plants.MethodsIn this study, we characterized the rhizosphere microbiota of Qingke plants grown in three main Qingke-producing areas (Tibet, Qinghai, and Gansu). In each of the three areas, seven different fertilization conditions (m1–m7, m1: Unfertilized; m2: Farmer Practice; m3: 75% Farmer Practice; m4: 75% Farmer Practice +25% Organic manure; m5: 50% Farmer Practice; m6: 50% Farmer Practice +50% Organic manure; m7: 100% Organic manure) were applied. The growth and yields of the Qingke plants were also compared under the seven fertilization conditions.ResultsThere were significant differences in alpha diversity indices among the three areas. In each area, differences in fertilization conditions and differences in the growth stages of Qingke plants resulted in differences in the beta diversity of the rhizosphere microbiota. Meanwhile, in each area, fertilization conditions, soil depths, and the growth stages of Qingke plants significantly affected the relative abundance of the top 10 phyla and the top 20 bacterial genera. For most of microbial pairs established through network analysis, the significance of their correlations in each of the microbial co-occurrence networks of the three experimental sites was different. Moreover, in each of the three networks, there were significant differences in relative abundance and genera among most nodes (i.e., the genera Pseudonocardia, Skermanella, Pseudonocardia, Skermanella, Aridibacter, and Illumatobacter). The soil chemical properties (i.e., TN, TP, SOM, AN, AK, CEC, Ca, and K) were positively or negatively correlated with the relative abundance of the top 30 genera derived from the three main Qingke-producing areas (p

IntroductionOat (Avena sativa L.) is an important cereal crop grown worldwide for grain and forage, owing to its high adaptability to diverse environments. However, the genetic and genomics research of oat is lagging behind that of other staple cereal crops. MethodsIn this study, a collection of 288 oat lines originating worldwide was evaluated using 2,213 single nucleotide polymorphism (SNP) markers obtained from an oat iSelect 6K-beadchip array to study its genetic diversity, population structure, and linkage disequilibrium (LD) as well as the genotype–phenotype association for hullessness and lemma color.ResultsThe average gene diversity and polymorphic information content (PIC) were 0.324 and 0.262, respectively. The first three principal components (PCs) accounted for 30.33% of the genetic variation, indicating that the population structure of this panel of oat lines was stronger than that reported in most previous studies. In addition, accessions could be classified into two subpopulations using a Bayesian clustering approach, and the clustering pattern of accessions was closely associated with their region of origin. Additionally, evaluation of LD decay using 2,143 mapped markers revealed that the intrachromosomal whole-genome LD decayed rapidly to a critical r2 value of 0.156 for marker pairs separated by a genetic distance of 1.41 cM. Genome-wide association study (GWAS) detected six significant associations with the hullessness trait. Four of these six markers were located on the Mrg21 linkage group between 194.0 and 205.7 cM, while the other two significant markers mapped to Mrg05 and Mrg09. Three significant SNPs, showing strong association with lemma color, were located on linkage groups Mrg17, Mrg18, and Mrg20.DiscussionOur results discerned relevant patterns of genetic diversity, population structure, and LD among members of a worldwide collection of oat landraces and cultivars proposed to be ‘typical’ of the Qinghai-Tibetan Plateau. These results have important implications for further studies on association mapping and practical breeding in high-altitude oat.

Abstract Background To investigate the effect of superficial temporal artery-middle cerebral artery (STA-MCA) bypass in the treatment of MCA stenosis or occlusion. Methods The clinical and imaging data of 31 MCA stenosis or occlusion patients with STA-MCA bypass were analyzed retrospectively. The operation was performed by STA-MCA M4 segment bypass via the frontotemporal approach. Modified Rankin Scale (mRS) was used to evaluate the neurological function of patients. Results After operation, head computed tomography (CT) showed that there was no new infarction or hemorrhage in the operation area. CTA and CTP showed that the bypass vessel was unobstructed in 29 cases and the cerebral perfusion was improved in 31 cases. Among the 31 patients, 7 patients had postoperative complications and 13 patients had improvement of clinical symptoms. The other patients had no complications and the clinical symptoms remained unchanged. The mRs score of 31 patients after operation indicated that the neurological function was significantly improved than pre-operation. Of the 31 patients, 23 cases were followed up. The mRs score showed that the neurological function of these 23 patients was further improved than that at discharge. In addition, DSA (or CTA) and CTP showed that the bypass vessel was unobstructed and the cerebral perfusion was further improved. Conclusion STA-MCA bypass was an effective method for the treatment of MCA stenosis or occlusion. However, the results should be further verified by large sample, multi-center and long-term follow-up.

Introduction: Fibroblast growth factor homologous factors (FHFs), among other fibroblast growth factors, are increasingly found to be important regulators of ion channel functions. Although FHFs have been link to several neuronal diseases and arrhythmia, its role in inflammatory pain still remains unclear. Objectives: This study aimed to investigate the role and mechanism of FGF13 in inflammatory pain. Methods: Fgf13 conditional knockout mice were generated and CFA-induced chronic inflammatory pain model was established to measure the pain threshold. Immunostaining, western blot and quantitative real-time reverse transcription PCR (qRT-PCR) were performed to detect the expression of FGF13 in CFA-induced inflammatory pain. Whole-cell patch clamp recording was used to record the action potential firing properties and sodium currents of DRG neurons. Results: Conditional knockout of Fgf13 in dorsal root ganglion (DRG) neurons (Fgf13-/Y) led to attenuated pain responses induced by complete Freund's adjuvant (CFA). FGF13 was expressed predominantly in small-diameter DRG neurons. CFA treatment resulted in an increased expression of FGF13 proteins as well as an increased excitability in nociceptive DRG neurons which was inhibited when FGF13 was absent. The role of FGF13 in neuronal excitability of DRG was linked to its modulation of voltage-gated Na+ channels mediated by microtubules. Overexpression of FGF13, but not FGF13 mutant which lacks the ability to bind and stabilize microtubules, rescued the decreased neuronal excitability and Na+ current density in DRG neurons of Fgf13-/Y mice. Conclusion: This study revealed that FGF13 could stabilize microtubules to modulate sodium channel function in DRG neurons and modulate inflammatory pain. This study provides a novel mechanism for FGF13 modulation of sodium channel function and suggests that FGF13 might be a novel target for inflammatory pain treatment.

Avena chinensis is recognized as one of the cereals with high nutritional value in the world. In this study, the complete chloroplast (cp) genome sequence of A. chinensis was reported. The complete cp genome of A. chinensis was 135,899 bp in length with a GC content of 38.51%, including a large single copy (LSC) region of 80,117 bp, a small single copy (SSC) region of 12,576 bp, and a pair of inverted repeated regions of 21,603 bp. The A. chinensis cp genome encoded 128 functional genes, including 82 protein-coding genes, 38 tRNAs, and eight rRNAs. The phylogenetic analysis showed that A. chinensis was closely related to Avena hybrid and Avena occidentalis.

Acute central nervous system (CNS) injuries, including ischemic stroke, traumatic brain injury (TBI), spinal cord injury (SCI) and subarachnoid hemorrhage (SAH), are the most common cause of death and disability around the world. As a kind of non-coding ribonucleic acids (RNAs) with endogenous and conserve, circular RNAs (circRNAs) have recently attracted great attentions due to their functions in diagnosis and treatment of many diseases. A large number of studies have suggested that circRNAs played an important role in brain development and involved in many neurological disorders, particularly in acute CNS injuries. It has been proposed that regulation of circRNAs could improve cognition function, promote angiogenesis, inhibit apoptosis, suppress inflammation, regulate autophagy and protect blood brain barrier (BBB) in acute CNS injuries via different molecules and pathways including microRNA (miRNA), nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), ph1osphatidylinositol-4,5-bisphosphate 3-kinase/protein kinase B (PI3K/AKT), Notch1 and ten-eleven translocation (TET). Therefore, circRNAs showed great promise as potential targets in acute CNS injuries. In this article, we present a review highlighting the roles of circRNAs in acute CNS injuries. Hence, on the basis of these properties and effects, circRNAs may be developed as therapeutic agents for acute CNS injury patients.

In this work, we propose a new crack image detection and segmentation method for addressing the issues regarding the poor detection of crack structures in certain complex background conditions, such as the light and shadow, and the easy-to-lose details in segmentation. This method can be categorized into two phases, where the first one is the coding phase. In this phase, the channel attention mechanism and crack characteristics, using the correlation channel with different scales increasing the network robustness and ability of feature extraction, have been introduced to decouple the channel dimension and space dimension. It also avoids underfitting caused by information redundancy during the jumping connection. In the second stage, i.e., the decoding stage, the spatial attention mechanism has been introduced to capture the crack edge information through the global maximum pooling and global average pooling of the high-dimensional features. Then, the correlation between the space and channel has been recovered through multiscale image information fusion to achieve accurate crack positioning. Furthermore, the Dice loss function has been employed to solve the problem of pixel imbalance between the categories. Finally, the proposed method has been tested and compared with existing methods. The experimental results illustrate that our method has a higher crack segmentation accuracy than existing methods. Furthermore, the mean intersection over the union ratio reaches 87.2% on the public dataset and 83.9% on the self-built dataset, and it has a better segmentation effect and richer details. It can solve the problem of crack image detection and segmentation under a complex background.

To understand the molecular mechanism controlling the size of barley grains, a number of traits were analyzed and RNA-seq was conducted on grains of two barley materials with a significant difference in thousand-grain weight (TGW) after flowering. The trait dataset delineates the dynamic changes in grain size after flowering, and it provides an understanding of the source of the difference in TGW. By comparing the transcripts of barley grains at several stages after flowering, we identified the gene expression characteristics and significantly enriched pathways in each stage. At the early stage of grain development, genes involved in fatty acid metabolism, plant hormone signal transduction, and pathways involved in cytoskeleton formation were significantly upregulated. At the later stage of grain development, genes involved in starch synthesis, glucose metabolism, and other pathways were significantly upregulated. Further, we used weighted gene coexpression network analysis (WGCNA) and correlation analysis of trait datasets to identify the coexpressed gene modules significantly associated with traits, such as grain length (GL), grain width (GW), and dry weight (DW). After comparing the modules with the differentially expressed gene (DEG) set, 12 candidate genes were selected, and among these, four genes were homologous to genes that regulate grain size in rice and other plants. The combined analysis identified many potential key regulatory factors that may control barley grain size and yield potential, thus providing new insights into the molecular mechanism of barley grain size.

CNS injuries, such as traumatic brain injury (TBI), subarachnoid hemorrhage (SAH), intracerebral hemorrhage (ICH), and cerebral ischemic stroke, are important causes of death and long-term disability worldwide. As an important class of pervasive genes involved in many pathophysiological processes, long non-coding RNAs (lncRNAs) have received attention in the past decades. Multiple studies indicate that lncRNAs are abundant in the CNS and have a key role in brain function as well as many neurological disorders, especially in CNS injuries. Several investigations have deciphered that regulation of lncRNAs exert pro-angiogenesis, anti-apoptosis, and anti-inflammation effects in CNS injury via different molecules and pathways, including microRNA (miRNA), nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB), phosphatidylinositol-4,5-bisphosphate 3-kinase/protein kinase B (PI3K/AKT), Notch, and p53. Thus, lncRNAs show great promise as molecular targets in CNS injuries. In this article, we provide an updated review of the current state of our knowledge about the relationship between lncRNAs and CNS injuries, highlighting the specific roles of lncRNAs in CNS injuries. Keywords: CNS injuries, long non-coding RNAs, MALAT1, MEG3, downstream molecules

The EARLY MATURITY 8 (EAM8) gene of barley is homologous to the EARLY FLOWERING 3 (ELF3) gene in Arabidopsis, as loss-of-function mutations in this circadian clock gene promote rapid flowering. A previous study demonstrated that the early flowering phenotype of a hulless barley, Lalu, was due to allele eam8.l carrying an alternative splicing mutation in intron 3 that led to intron retention. In the present study, we verified that eam8.l encoded a truncated protein. Although EAM8 was expressed at a higher level in Lalu than in other barley lines with a longer growth period, it did not negatively regulate flowering time. This result further proved that the eam8.l protein was nonfunctional in regulating flowering in barley. The early flowering phenotype of Lalu plants was strongly dependent on the biosynthesis of gibberellin (GA). The eam8.l mutation stopped the suppression of GA biosynthesis, and Lalu accumulated excessive GA, especially in leaves. This was achieved through the upregulated expression of genes in the GA pathway, including GA20ox2, LFY1, SOC1, PAP2, and FPF3. The mutation of the EAM8 gene also abolished the inhibition of FLOWERING LOCUS T-like (FT1) gene expression at night. During the night, expression levels of the FT1 gene were higher than those during the day in Lalu. However, the GA-dependent pathway and FT1 gene mechanism are two independent pathways that promote flowering in Lalu. Alleles of EAM8, therefore, demonstrated an important breeding value in barley, which is probably effective in many other day-length-sensitive crop plants as well; thus, they could be used to tune adaptation in different geographic regions and climatic conditions, a critical issue in times of global warming.

In this study, we determined the complete mitochondrial genome of Geoemyda spengleri. The genome was 17,448bp in length and contained 13 protein-coding genes, 22 transfer RNA genes, 2 ribosomal RNA genes, and 1 main non-coding regions. The overall base composition of G. spengleri is A 33.67%, T 27.64%, C 25.56%, and G 13.14%, with a highly A + T bias of 61.31%. Here, we describe a phylogenetic analysis of 16 species of Tesudines based on the complete mitochondrial genome, the result showed that G. japonica is most closely related to G. spengleri. This mitogenome sequence data would play an important role in the investigation of phylogenetic relationship, taxonomic resolution and phylogeography of the Tesudines.

Long noncoding RNAs (lncRNAs) participate extensively in biological processes of various cancers. The majority of these transcripts are uniquely expressed in differentiated tissues or specific cancer types. lncRNAs are aberrantly expressed in gliomas and exert diverse functions. In this article, we provided an overview of how lncRNAs regulate cellular processes in glioma, enumerated the lncRNAs that may act as glioma biomarkers, and showed their potential clinical implications. Keywords: long noncoding RNA, glioma, biomarker

Cathepsin S (CTSS), a lysosomal cysteine protease, is overexpressed in various cancers, including glioblastoma (GB). A high level of CTSS is associated with tumor progression and poor outcome in GB. However, the underlying mechanisms of its role in the biological characteristics of G5B remain to be elucidated. Here, we uncovered a potential role of CTSS in the lysosomes and mitochondria of GB cells (GBCs). Downregulation of CTSS in GBCs could increase the expression of autophagy-related proteins; however, there was no significant change in p62, suggesting autophagy blockade. Moreover, inhibition of CTSS increased the expression of mitochondrial calcium uniporter (MCU) and enhanced mitochondrial Ca2+ uptake ability, causing mitochondrial Ca2+ overload, the generation of copious reactive oxygen species (ROS) and eventual mitochondrial apoptosis. Additionally, elevated damage to mitochondria exacerbated the burden of autophagy. Finally, we found that silence of MCU could alleviate the inhibition of CTSS-induced autophagosome accumulation and mitochondrial stress. Collectively, these results demonstrate that CTSS plays an important role in the process of autophagic flux and mitochondrial functions in GBCs.

Emergent evidences revealed that long noncoding RNAs (lncRNAs) participate in neoplastic progression. HMMR is an oncogene that is highly expressed in glioblastoma (GBM) and supports GBM growth. Whether lncRNAs regulate HMMR in GBM remains unknown. Herein, we identify that an HMMR antisense lncRNA, HMMR-AS1, is hyperexpressed in GBM cell lines and stabilizes HMMR mRNA. Knockdown of HMMR-AS1 reduces HMMR expression; inhibits cell migration, invasion, and mesenchymal phenotypes; and suppresses GBM cell growth both in vitro and in vivo. Moreover, knockdown of HMMR-AS1 radiosensitizes GBM by reducing DNA repair proteins ATM, RAD51, and BMI1. Our data demonstrate a mechanism of sense-antisense interference between HMMR and HMMR-AS1 in GBM and suggest that targeting HMMR-AS1 is a potential strategy for GBM treatment.

Autophagy is associated with secondary injury following traumatic brain injury (TBI) and is expected to be a therapeutic target. Baicalin, a neuroprotective agent, has been proven to exert multi-functional bioactive effects in brain injury diseases. However, it is unknown if Baicalin influences autophagy after TBI. In the present study, we aimed to explore the effects that Baicalin had on TBI in a mice model, focusing on autophagy as a potential mechanism. We found that Baicalin administration significantly improved motor function, reduced cerebral edema, and alleviated disruption of the blood-brain barrier (BBB) after TBI in mice. Besides, TBI-induced apoptosis was reversed by Baicalin evidenced by Nissl staining, terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay, and the level of cleaved caspase-3. More importantly, Baicalin enhanced autophagy by detecting the autophagy markers (LC3, Beclin 1, and p62) using western blot and LC3 immunofluorescence staining, ameliorating mitochondrial apoptotic pathway evidenced by restoration of the TBI-induced translocation of Bax and cytochrome C. However, simultaneous treatment with 3-MA inhibited Baicalin-induced autophagy and abolished its protective effects on mitochondrial apoptotic pathway. In conclusion, we demonstrated that Baicalin enhanced autophagy, ameliorated mitochondrial apoptosis and protected mice brain in TBI mice model.

Chiari 0 malformation (CM-0) with syringomyelia syringobulbia and syrinx cavity in pons simultaneously is rare. We present a case of 31-year-old man, review the available literature, and discuss the experience of therapy from the neurosurgical perspective.

Traumatic brain injury (TBI) is one of the most devastating forms of brain injury. Many pathological mechanisms such as oxidative stress, apoptosis and inflammation all contribute to the secondary brain damage and poor outcomes of TBI. Current therapies are often ineffective and poorly tolerated, which drive the explore of new therapeutic targets for TBI. Autophagy is a highly conserved intracellular mechanism during evolution. It plays an important role in elimination abnormal intracellular proteins or organelles to maintain cell stability. Besides, autophagy has been researched in various models including TBI. Previous studies have deciphered that regulation of autophagy by different molecules and pathways could exhibit anti-oxidative stress, anti-apoptosis and anti-inflammation effects in TBI. Hence, autophagy is a promising target for further therapeutic development in TBI. The present review provides an overview of current knowledge about the mechanism of autophagy, the frequently used methods to monitor autophagy, the functions of autophagy in TBI as well as its potential molecular mechanisms based on the pharmacological regulation of autophagy.

Microglial activation and the inflammatory response in the central nervous system (CNS) play important roles in secondary damage after traumatic brain injury (TBI). Transcriptional activation of genes that limit secondary damage to the CNS are mediated by a cis-acting element called the antioxidant responsive element (ARE). ARE is known to associate with the transcription factor NF-E2-related factor 2 (Nrf2), a transcription factor that is associated with histone deacetylases (HDACs). This pathway, known as the Nrf2/ARE pathway, is a critical antioxidative factor pathway that regulates the balance of oxygen free radicals and the inflammatory response, and is also related to autophagic activities. Although valproic acid (VPA) is known to inhibit HDACs, it is unclear whether VPA plays a role in the microglia-mediated neuroinflammatory response after TBI via regulating oxidative stress and autophagy induced by the Nrf2/ARE signaling pathway. In this study, we demonstrate that microglial activation, oxidative stress, autophagy, and the Nrf2/ARE signaling pathway play essential roles in secondary injury following TBI. Treatment with VPA alleviated TBI-induced secondary brain injury, including neurological deficits, cerebral edema, and neuronal apoptosis. Moreover, VPA treatment upregulated the occurrence of autophagy and Nrf2/ARE pathway activity after TBI, and there was an increase in H3, H4 histone acetylation levels, accompanied by decreased transcriptional activity of the HDAC3 promoter in cortical lesions. These results suggest that VPA-mediated up-regulation of autophagy and antioxidative responses are likely due to increased activation of Nrf2/ARE pathway, through direct inhibition of HDAC3. This inhibition further reduces TBI-induced microglial activation and the subsequent inflammatory response, ultimately leading to neuroprotection.

Objective: To investigate the clinical application value of intraoperative magnetic resonance imaging (iMRI) in large invasive pituitary adenoma surgery. Methods: A total of 30 patients with large pituitary adenoma underwent microscopic tumor resection under the assistance of an iMRI system; 26 cases received surgery through the nasal–transsphenoidal approach, and the remaining four cases received surgery through the pterion approach. iMRI was performed one or two times depending on the need of the surgeon. If a residual tumor was found, further resection was conducted under iMRI guidance. Results: iMRI revealed residual tumors in 12 cases, among which nine cases received further resection. Of these nine cases, iMRI rescanning confirmed complete resection in six cases, and subtotal resection in the remaining three. Overall, 24 cases of tumor were totally resected, and six cases were subtotally resected. The total resection rate of tumors increased from 60% to 80%. Conclusion: iMRI can effectively determine the resection extent of pituitary adenomas. In addition, it provides an objective basis for real-time judgment of surgical outcome, subsequently improving surgical accuracy and safety, and increasing the total tumor resection rate.

Astaxanthin (ATX) is a xanthophyll carotenoid which has been approved by the United States Food and Drug Administration (USFDA) as food colorant in animal and fish feed. It is widely found in algae and aquatic animals and has powerful anti-oxidative activity. Previous studies have revealed that ATX, with its anti-oxidative property, is beneficial as a therapeutic agent for various diseases without any side effects or toxicity. In addition, ATX also shows preclinical anti-tumor efficacy both in vivo and in vitro in various cancer models. Several researches have deciphered that ATX exerts its anti-proliferative, anti-apoptosis and anti-invasion influence via different molecules and pathways including signal transducer and activator of transcription 3 (STAT3), nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB) and peroxisome proliferator-activated receptor gamma (PPARγ). Hence, ATX shows great promise as chemotherapeutic agents in cancer. Here, we review the rapidly advancing field of ATX in cancer therapy as well as some molecular targets of ATX.

Aplastic anemia (AA) is a common malignant blood disease, and chronic intermittent hypobaric hypoxia (CIHH) has a beneficial effect against different diseases. The aim of the present study was to investigate the protective effect of CIHH against AA and underlying mechanisms. 5-Fluorouracil and busulfan treatment induced AA model in rats with reduction of hematological parameters and bone marrow tissue injury and decrease of the colony numbers of progenitor cells. CIHH pretreatment significantly reduced the incidence rate of AA and alleviated above symptoms in AA model. The adhesive molecules of bone marrow mesenchymal stem cells (BMMSCs) in AA model, VLA-4, VCAM-1, and ICAM-1 were upregulated, and those of CD162 and CD164 were downregulated by CIHH pretreatment. The expressions of HIF-1α and NF-κB in BMMSCs were also decreased through CIHH pretreatment. Overall, the results demonstrated for the first time that CIHH has an anti-AA effect through improving the adhesiveness and stress of mesenchymal stem cells in rats. CIHH could be a promising and effective therapy for AA.

The present investigation was carried out to elucidate a possible molecular mechanism related to the protective effect of quercetin administration against oxidative stress on various mitochondrial respiratory complex subunits with special emphasis on the role of nuclear factor erythroid 2-related factor 2 (Nrf2) in mitochondrial biogenesis. Recently, quercetin has been proved to have a protective effect against mitochondria damage after traumatic brain injury (TBI). However, its precise role and underlying mechanisms in traumatic brain injury are not yet fully understood. The aim of the present study was to investigate the effect of quercetin on the potential mechanism of these effects in a weight-drop model of TBI in male mice that were treated with quercetin or vehicle via intraperitoneal injection administrated 30 min after TBI. In this experiment, ICR mice were divided into four groups: A sham group, TBI group, TBI + vehicle group, and TBI + quercetin group. Brain samples were collected 24 h later for analysis. Quercetin treatment resulted in an upregulation of Nrf2 expression and cytochrome c, malondialdehyde (MDA) and superoxide dismutase (SOD) levels were restored by quercetin treatment. Quercetin markedly promoted the translocation of Nrf2 protein from the cytoplasm to the nucleus. These observations suggest that quercetin improves mitochondrial function in TBI models, possibly by activating the Nrf2 pathway.

In order to improve the efficiency of solar thermal power (STP) system, a novel modular system combining cooling, heating, and power generation (CCHP) is proposed and introduced in this work. This modular CCHP system can simultaneously provide 10 kW electricity, −15~5°C coolant, and 60°C hot water to meet the requirements of cooling, heating, and electricity in a general family or other fields. The flow chart and working process of the modular system are introduced, based on which the energy and exergy efficiencies at the CCHP and STP operation modes are primarily evaluated and discussed. The results show that when the output electricity is constant, the overall efficiencies of energy and exergy of the system operating at the CCHP mode are 9.37 times and 2.62 times as big as those of the system operating at the STP mode, respectively. Thus, the modular solar thermal CCHP system can improve the energy and exergy efficiencies. Furthermore, calculation shows that both the overall energy and exergy efficiencies decrease with increase of inlet vapor temperature at given inlet vapor pressure, but both the efficiencies increase with increase of inlet vapor pressure at given inlet temperature.

Cathepsin S (CatS) is a cysteine protease normally present in lysosomes. It has long been regarded as an enzyme that is primarily involved in general protein degradation. More recently, mounting evidence has shown that it is involved in Alzheimer disease, seizures, age-related inflammatory processes, and neuropathic pain. In this study, we investigated the time course of CatS protein and mRNA expression and the cellular distribution of CatS in a mouse model of traumatic brain injury (TBI). To clarify the roles of CatS in TBI, we injected the mice intraventricularly with LHVS, a nonbrain penetrant, irreversible CatS inhibitor, and examined the effect on inflammation and neurobehavioral function. We found that expression of CatS was increased as early as 1 h after TBI at both protein and mRNA levels. The increased expression was detected in microglia and neurons. Inhibition of CatS significantly reduced the level of TBI-induced inflammatory factors in brain tissue and alleviated brain edema. Additionally, administration of LHVS led to a decrease in neuronal degeneration and improved neurobehavioral function. These results imply that CatS is involved in the secondary injury after TBI and provide a new perspective for preventing secondary injury after TBI.

It has been proved that Nrf2 depletion enhances inflammatory process through activation of NF-κB in the brain after TBI, but little is known about the relationship between Nrf2 and NF-κB in astrocytes after TBI. Hence, we used primary cultured astrocytes from either Nrf2 wildtype or knockout mice to study the influence of Nrf2 on the activation of NF-κB and expression of proinflammatory cytokines in a model of TBI in vitro. Primary cultured astrocytes were scratched to mimic the traumatic injury in vitro. Then the DNA-binding activity of NF-κB was evaluated by EMSA. The mRNA and protein levels of TNF-α, IL-1β, IL-6, and MMP9 were also evaluated. Gelatin zymography was performed to detect the activity of MMP9. The activity of NF-κB and expression of proinflammatory cytokines mentioned above were upregulated at 24 h after scratch. The expression and activity of MMP9 were also elevated. And such tendency was much more prominent in Nrf2 KO astrocytes than that in WT astrocytes. These results suggest that the absence of Nrf2 may induce more aggressive inflammation through activation of NF-κB and downstream proinflammatory cytokines in astrocytes.

Ethyl pyruvate (EP) has demonstrated neuroprotective effects against acute brain injury through its anti-inflammatory action. The nuclear protein high-mobility group box 1 (HMGB1) can activate inflammatory pathways when released from dying cells. This study was designed to investigate the protective effects of EP against secondary brain injury in rats after Traumatic Brain Injury (TBI). Adult male rats were randomly divided into three groups: (1) Sham + vehicle group, (2) TBI + vehicle group, and (3) TBI + EP group (n=30 per group). Right parietal cortical contusion was made by using a weight-dropping TBI method. In TBI + EP group, EP was administered intraperitoneally at a dosage of 75 mg/kg at 5 min, 1 and 6 h after TBI. Brain samples were harvested at 24 h after TBI. We found that EP treatment markedly inhibited the expressions of HMGB1 and TLR4, NF-κB DNA binding activity and inflammatory mediators, such as IL-1β, TNF-α and IL-6. Also, EP treatment significantly ameliorated beam walking performance, brain edema, and cortical apoptotic cell death. These results suggest that the protective effects of EP may be mediated by the reduction of HMGB1/TLR4/NF-κB-mediated inflammatory response in the injured rat brain.

Traumatic brain injury (TBI) can induce intestinal inflammatory response and mucosal injury. Antioxidant transcription factor nuclear factor erythroid 2-related factor 2 (Nrf2) has been shown in our previous studies to prevent oxidative stress and inflammatory response in gut after TBI. The objective of this study was to test whether tert-butylhydroquinone (tBHQ), an Nrf2 inducer, can protect against TBI-induced intestinal inflammatory response and mucosal injury in mice. Adult male ICR mice were randomly divided into three groups: (1) sham + vehicle group, (2) TBI + vehicle group, and (3) TBI + tBHQ group (n=12 per group). Closed head injury was adopted using Hall's weight-dropping method. Intestinal mucosa apoptosis and inflammatory-related factors, such as nuclear factor kappa B (NF-κB), tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), interleukin-6 (IL-6) and intercellular adhesion molecule-1 (ICAM-1), were investigated at 24 h after TBI. As a result, we found that oral treatment with 1% tBHQ prior to TBI for one week markedly decreased NF-κB activation, inflammatory cytokines production, and ICAM-1 expression in the gut. Administration of tBHQ also significantly attenuated TBI-induced intestinal mucosal apoptosis. The results of the present study suggest that tBHQ administration could suppress the intestinal inflammation and reduce the mucosal damage following TBI.

Matrix metalloproteinase-9 (MMP-9) plays an important role in the acute periods of spinal cord injury (SCI), and its expression is related to the inflammation which could cause the disruption of the blood-spinal barrier (BBB). Nuclear factor erythroid 2-related factor 2 (Nrf2) is a key transcription factor that plays a crucial role in cytoprotection against inflammation. The present study investigated the role of Nrf2 in upregulating of nuclear factor kappa B (NF-κB) activity, tumor necrosis factor-α (TNF-α), and MMP-9 after SCI. Wild-type Nrf2 (+/+) and Nrf2-deficient (Nrf (−/−)) mice were subjected to an SCI model induced by the application of vascular clips (force of 10 g) to the dura after a three-level T8-T10 laminectomy. We detected the wet/dry weight ratio of impaired spinal cord tissue, the activation of NF-κB, the mRNA and protein levels of TNF-α and MMP-9, and the enzyme activity of MMP-9. Nrf2 (−/−) mice were demonstrated to have more spinal cord edema, NF-κB activation, TNF-α production, and MMP-9 expression after SCI compared with the wild-type controls. The results suggest that Nrf2 may play an important role in limiting the upregulation of NF-κB activity, TNF-α, and MMP-9 in spinal cord after SCI.

Inflammatory response plays an important role in the pathogenesis of secondary brain injury after traumatic brain injury (TBI). Nuclear factor erythroid 2-related factor 2 (Nrf2) is a key transcription factor that plays a crucial role in cytoprotection against inflammation. The present study investigated the role of Nrf2 in the cerebral upregulation of NF-κB activity, proinflammatory cytokine, and ICAM-1 after TBI. Wild-type Nrf2 (+/+) and Nrf2 (−/−)-deficient mice were subjected to a moderately severe weight-drop impact head injury. Electrophoretic mobility shift assays (EMSAs) were performed to analyze the activation of nuclear factor kappa B (NF-κB). Enzyme-linked immunosorbent assays were performed to quantify the production of tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and interleukin-6 (IL-6). Immunohistochemistry staining experiments were performed to detect the expression of intercellular adhesion molecule-1 (ICAM-1). Nrf2 (−/−) mice were shown to have more NF-κB activation, inflammatory cytokines TNF-α, IL-1β and IL-6 production, and ICAM-1 expression in brain after TBI compared with their wild-type Nrf2 (+/+) counterparts. The results suggest that Nrf2 plays an important protective role in limiting the cerebral upregulation of NF-κB activity, proinflammatory cytokine, and ICAM-1 after TBI.