USP9X regulates the proliferation, survival, migration and invasion of gastric cancer cells by stabilizing MTH1.

BACKGROUND: MutT homolog 1 (MTH1) sanitizes oxidized dNTP pools to promote the survival of cancer cells and its expression is frequently upregulated in cancers. Polyubiquitination stabilizes MTH1 to facilitate the proliferation of melanoma cells, suggesting the ubiquitin system controls the stability and function of MTH1. However, whether ubiquitination regulates MTH1 in gastric cancers has not been well defined. This study aims to investigate the interaction between MTH1 and a deubiquitinase, USP9X, in regulating the proliferation, survival, migration, and invasion of gastric cancer cells. METHODS: The interaction between USP9X and MTH1 was evaluated by co-immunoprecipitation (co-IP) in HGC-27 gastric cancer cells. siRNAs were used to interfere with USP9X expression in gastric cancer cell lines HGC-27 and MKN-45. MTT assays were carried out to examine the proliferation, propidium iodide (PI) and 7-AAD staining assays were performed to assess the cell cycle, Annexin V/PI staining assays were conducted to examine the apoptosis, and transwell assays were used to determine the migration and invasion of control, USP9X-deficient, and USP9X-deficient plus MTH1-overexpressing HGC-27 and MKN-45 gastric cancer cells. RESULTS: Co-IP data show that USP9X interacts with and deubiquitinates MTH1. Overexpression of USP9X elevates MTH1 protein level by downregulating its ubiquitination, while knockdown of USP9X has the opposite effect on MTH1. USP9X deficiency in HGC-27 and MKN-45 cells causes decreased proliferation, cell cycle arrest, extra apoptosis, and defective migration and invasion, which could be rescued by excessive MTH1. CONCLUSION: USP9X interacts with and stabilizes MTH1 to promote the proliferation, survival, migration and invasion of gastric cancer cells.

Brain structural correlates of postoperative axial pain in degenerative cervical myelopathy patients following posterior cervical decompression surgery: a voxel-based morphometry study.

OBJECTIVE: To investigate the brain structural correlates of postoperative axial pain (PAP) in degenerative cervical myelopathy (DCM) following posterior cervical decompression surgery. METHODS: Structural images with high-resolution T1 weighting were collected from 62 patients with DCM and analyzed, in addition to 42 age/gender matched subjects who were healthy. Voxel-based morphometry (VBM) was analyzed, grey matter volume (GMV) was computed. One-way ANOVA was performed to reveal the GMV differences among DCM patients with PAP, patients without PAP and healthy controls (HC). Post-hoc analyses were conducted to identify the pair-wise GMV differences among these three groups. Analyses of correlations were conducted to uncover the link between clinical measurements and GMV variations. Last, support vector machine (SVM) was conducted to test the utility of GMV for classifying PAP and nPAP DCM patients. RESULTS: Three main findings were observed: [1] Compared to healthy controls, DCM patients showed a significantly lower GMV in the precuneus preoperatively. DCM patients with PAP also exhibited a lower GMV within precuneus than those without; [2] In DCM patients with PAP, the precuneus GMV was inversely related to the postoperative pain intensity; [3] Moreover, successful classification between PAP and nPAP were observed via SVM based on precuneus GMV as features. CONCLUSION: In summary, our results indicate that precuneus GMV may be linked to PAP in DCM, and could be employed to forecast the emergence of PAP in DCM patients.

Application effect of head-mounted mixed reality device combined with 3D printing model in neurosurgery ventricular and hematoma puncture training.

BACKGROUND: The purpose of this study was to explore the applicability of application effect of head-mounted mixed reality (MR) equipment combined with a three-dimensional (3D) printed model in neurosurgical ventricular and haematoma puncture training. METHODS: Digital Imaging and Communications in Medicine (DICOM) format image data of two patients with common neurosurgical diseases (hydrocephalus and basal ganglia haemorrhage) were imported into 3D Slicer software for 3D reconstruction, saved, and printed using 3D printing to produce a 1:1-sized head model with real person characteristics. The required model (brain ventricle, haematoma, puncture path, etc.) was constructed and imported into the head-mounted MR device, HoloLens, and a risk-free, visual, and repeatable system was designed for the training of junior physicians. A total of 16 junior physicians who studied under this specialty from September 2020 to March 2022 were selected as the research participants, and the applicability of the equipment and model during training was evaluated with assessment score sheets and questionnaires after training. RESULTS: According to results of the assessment and questionnaire, the doctors trained by this system are more familiar with the localization of the lateral anterior ventricle horn puncture and the common endoscopic surgery for basal ganglia haemorrhage, as well as more confident in the mastery of these two operations than the traditional training methods. CONCLUSIONS: The use of head-mounted MR equipment combined with 3D printing models can provide an ideal platform for the operation training of young doctors. Through holographic images created from the combination of virtual and real images, operators can be better immersed in the operation process and deepen their understanding of the operation and related anatomical structures. The 3D printed model can be repeatedly reproduced so that doctors can master the technology, learn from mistakes, better achieve the purpose of teaching and training, and improve the effect of training.

Landscape of B Cell Receptor Repertoires in COVID-19 Patients Revealed Through CDR3 Sequencing of Immunoglobulin Heavy and Light Chains.

The outbreak and persistence of coronavirus disease 2019 (COVID-19) threaten human health. B cells play a vital role in fighting the infections caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Despite many studies on the immune responses in COVID-19 patients, it is still unclear how B cell receptor (BCR) constituents, including immunoglobulin heavy (IGHs) and light chains (IGLs), respond to SARS-CoV-2 in patients with varying symptoms. In this study, we conducted complementarity-determining region 3 (CDR3) sequencing of BCR IGHs and IGLs from the peripheral blood of COVID-19 patients and healthy donors. The results showed significantly reduced clonal diversity, more expanded clones, and longer CDR3 lengths of IGH and IGL in COVID-19 patients than those in healthy individuals. The IGLs had a much higher percentage of VJ skew usage (47.83% IGLV and 42.86% IGLJ were significantly regulated) than the IGHs (12.09% IGHV and 0% IGHJ) between the healthy individuals and patients, which indicated the importance of BCR light chains. Furthermore, we found a largely expanded IGLV3-25 gene cluster mostly pairing with IGLJ1 and ILGJ2 in COVID-19 patients and a newly identified upregulated IGLJ1 gene and IGLJ2+IGLV13-21 recombination, both of which are potential sources of SARS-CoV-2-targeting antibodies. Our findings on specific immune B-cell signatures associated with COVID-19 have clinical implications for vaccine and biomarker development for disease diagnosis.

The qualitative accuracy of clinical dermatophytes via matrix-assisted laser desorption ionization-time of flight mass spectrometry: A meta-analysis.

Dermatophytes are an important part of superficial fungal infections, and accurate diagnosis is paramount for successful treatment. Recently, matrix-assisted laser desorption ionization-time of flight mass spectrometry (MALDI-TOF MS) has emerged as a powerful tool to identify clinical pathogens; its advantages are cost-effectiveness, rapid detection, and high accuracy. However, as the accurate identification of clinical dermatophytes via MALDI-TOF MS has still not been fully evaluated, we performed a meta-analysis for its systematic evaluation. Fifteen eligible studies were involved and showed high accuracy with an identification ratio of 0.96 (95% CI = 0.92─1.01) and 0.91 (95% CI = 0.86─0.96) at the genus and species levels, respectively. The results showed higher accuracy ratio of Vitek MS (91%) than MALDI Biotyper (85%). Dermatophytes such as Trichophyton interdigitale (0.99, 95% CI = 0.97─1.02), T. mentagrophytes var interdigitale (1.00, 95% CI = 0.98─1.02), and Microsporum canis (0.97, 95% CI = 0.89─1.04) showed high accuracy in detected clinical dermatophytes. Moreover, a library with self-built database set up by laboratories showed higher accuracy than commercial database, and 15-day cultivation for dermatophytes showed highest accuracy considering culture time. High heterogeneity was observed and decreased only with the subgroup analysis of species. The subgroup analysis of mass spectrometry, library database, and culture time also exhibited high heterogeneity. In summary, our results showed that MALDI-TOF MS could be used for highly accurate detection of clinically pathogenic dermatophytes, which could be an alternative diagnostic method in addition to morphological and molecular methods.

This meta-analysis comprehensively investigated the qualitative accuracy of clinical dermatophytes through MALDI-TOF MS. Owing to the high accuracy observed at both genus and species levels, this approach could be an alternative diagnostic method in addition to morphological and molecular methods.

DNA Methylation in Pulmonary Fibrosis.

DNA methylations, including global methylation pattern and specific gene methylation, are associated with pathogenesis and progress of pulmonary fibrosis. This chapter illustrates alteration of DNA methylation in pulmonary fibrosis as a predictive or prognostic factor. Treatment with the DNA methylation inhibitors will be an emerging anti-fibrosis therapy, although we are still in the pre-clinical stage of using epigenetic markers as potential targets for biomarkers and therapeutic interventions.

Methylation of Inflammatory Cells in Lung Diseases.

This chapter overviews roles of DNA methylation in inflammatory cell biology with the focuses on lymphocytes and macrophages/monocytes in lung diseases, although the molecular mechanisms by which target genes are methylated and regulated in lung diseases remain unclear. Most of epigenetic studies on DNA methylation of target genes in lung diseases mainly demonstrated the correlation of DNA methylation of target genes with the levels of other corresponding factors, with the specificity of clinical phenomes, and with the severity of lung diseases. There is an urgent need to identify and validate the specificity and regulatory mechanisms of inflammatory cell epigenetics in depth. The epigenetic heterogeneity among different subsets of T cells and among promoters or non-promoters of target genes should be furthermore clarified in acute or chronic lung diseases and cancers. The hyper/hypo-methylation and modifications of chromosol and extrachromosomal DNA may result in alternations in proteins within inflammatory cells, which can be identified as disease-specific biomarkers and therapeutic targets.

ALDOLASE A regulates invasion of bladder cancer cells via E-cadherin-EGFR signaling.

Glycolysis and glycogenesis are known to be tightly associated with cancer cell migration. However, their roles in bladder cancer have not been reported. In this study, ALDOLASE A (ALDOA) was identified in a coexpression network generated using glycolysis- and glycogenesis-related genes in Kyoto Encyclopedia of Genes and Genomes. ALDOA was located in the central region in the network, and the cancer genome atlas (TCGA) data suggest that ALDOA expression levels are associated with viability in patients with cancer at the middle and late stages. Bladder cancer cell lines, T24 and RT4, were used to knockdown (sh) or overexpress (OE) ALODA to analyze its role. The sh-ALDOA reduced cell viability, colony formation rate, and invasion cell number; while OE had an opposite effect compared with sh-ALDOA. Further, the sh-ALDOA expression induced E-cadherin level while reduced N-cadherin and vimentin levels. The OE cells reduced E-cadherin and induced N-cadherin and vimentin levels. In addition, epidermal growth factor receptor (EGFR), mitogen-activated protein kinase (MAPK), and AKT serine/threonine kinase (AKT) phosphorylation levels are all reduced in sh-ALODA while activated in OE cells compared with the control group. But either sh-ALODA or OE did not change total protein levels of EGFR, MAPK, and AKT. To further analyze E-cadherin function in ALDOA regulation on bladder cancer cells, sh-ALDOA and sh-E-cadherin were cotransfected in T24 and RT4 cells. The results indicated that sh-ALDOA and sh-E-cadherin expressions eliminated sh-ALDOA function, resulting similar cell viability, colony formation rate, and invasion cell number with control group. Also, sh-ALDOA and shE-cadherin expressions increased EGFR, MAPK, and AKT phosphorylation levels; and the levels were similar to the control group. But, sh-ALDOA and sh-E-cadherin expressions did not change N-cadherin and vimentin levels, which maintain similar levels with sh-ALDOA-expressing cells. Taken together, these results suggest that ALDOA might play an important function in bladder cancer and its action may be though E-cadherin-EGFR signaling.

Citrullinemia type I is associated with a novel splicing variant, c.773 + 4A > C, in ASS1: a case report and literature review.

BACKGROUND: Citrullinemia type I (CTLN1) is a rare autosomal recessive disorder of the urea cycle caused by a deficiency in the argininosuccinate synthetase (ASS1) enzyme due to mutations in the ASS1 gene. Only a few Chinese patients with CTLN1 have been reported, and ASS1 gene mutations have been identified sporadically in China. CASE PRESENTATION: A Chinese family with one member affected with mild CTLN1 was enrolled. Targeted exome sequencing was performed on the proband, and Sanger sequencing was used to validate the detected mutation. We also reviewed the genetic and clinical characteristics of CTLN1 in Chinese patients that have been published to date. Newborn screening showed remarkably increased concentrations of citrulline with elevated ratios of citrulline/arginine and citrulline/phenylalanine, and the patient presented with a speech delay at age three. The urinary organic acid profiles were normal. A novel homozygous splicing variant c.773 + 4A > C in the ASS1 gene was identified in the proband, and it was predicted to affect splicing by in silico analysis. To date, only nine Chinese patients with CTLN1 have been reported, with a total of 15 ASS1 mutations identified and no high frequency or hot spot mutations found; the mutation spectrum of Chinese patients with CTLN1 was heterogeneous. CONCLUSIONS: We described a mild Chinese CTLN1 case with a novel homozygous splicing variant c.773 + 4A > C and reviewed previous genotypes and phenotypes in Chinese patients with CTLN1. Thus, our findings contribute to understanding the molecular genetic background and clinical phenotype of CTLN1 in this population.

Closure of Bronchopleural Fistula with Mesenchymal Stem Cells: Case Report and Brief Literature Review.

Closure of bronchopleural fistula remains a difficult challenge for clinicians. Although several therapeutic approaches have been proposed, the clinical results are commonly unsatisfactory. Previous reports have indicated that autologous mesenchymal stem cells (MSCs) are useful for aiding treatment of bronchopleural fistula. We report here the use of umbilical cord MSCs to effect the successful closure of a bronchopleural fistula (5 mm) in a 33-year-old woman 6 months after a lobectomy. A review of the relevant literature is included. The use of MSCs may be a promising therapeutic method for the closure of bronchopleural fistula. Randomized controlled trials with larger samples are required.

Effects of huoxin formula on the arterial functions of patients with coronary heart disease.

Context: Huoxin formula is a Traditional Chinese Medicine for coronary heart disease (CHD) treatment. Objective: To explore the therapeutic mechanism of the Huoxin formula on arterial functions in CHD patients. Materials and methods: Fifty-eight CHD patients receiving cardiovascular drugs including ß-receptor blocker, statins, and antiplatelet medications or others were randomized into intervention [additionally 13.5 g Huoxin formula granules dissolved in 150 mL warm water per time, twice a day (n = 30)] and control [only cardiovascular drugs (n = 28)] groups. Serum biomarkers (hs-CRP, IL-18, IL-17, TNF-α, MMP-9), and cardiovascular indicators of the common and internal carotid arteries (ICAs) were monitored before and after the treatments. Results: After 3 months of treatment, the increases of intima-media thicknesses (IMT) of the left and right common carotid arteries (CCAs) as well as of the left and right ICAs and the increases of the left and right cardio-ankle vascular index were all significantly (all p < 0.001) less in the intervention than in control group (all p < 0.001). Serum concentrations reductions of hs-CRP, IL-18, IL-17 and MMP9 (all p < 0.001) levels were higher in the intervention compared to the control group, which correlated with the changes of left ICA (hs-CRP: r = 0.581, p = 0.009; IL-18: r = 0.594, p = 0.007; IL-17: r = 0.575, p = 0.006). Discussion and conclusion: Since the Huoxin formula improved arterial functions and reduced inflammatory factor activities in CHD patients, a large-scale clinical trial is warranted.

Omega-3 polyunsaturated fatty acid attenuates traumatic brain injury-induced neuronal apoptosis by inducing autophagy through the upregulation of SIRT1-mediated deacetylation of Beclin-1.

BACKGROUND: Enhancing autophagy after traumatic brain injury (TBI) may decrease the expression of neuronal apoptosis-related molecules. Autophagy-mediated neuronal survival is regulated by the sirtuin family of proteins (SIRT). Omega-3 polyunsaturated fatty acids (ω-3 PUFA) are known to have antioxidative and anti-inflammatory effects. We previously demonstrated that ω-3 PUFA supplementation attenuated neuronal apoptosis by modulating the neuroinflammatory response through SIRT1-mediated deacetylation of the HMGB1/NF-κB pathway, leading to neuroprotective effects following experimental traumatic brain injury (TBI). However, no studies have elucidated if the neuroprotective effects of ω-3 PUFAs against TBI-induced neuronal apoptosis are modulated by SIRT1-mediated deacetylation of the autophagy pathway. METHODS: The Feeney DM TBI model was adopted to induce TBI rats. Modified neurological severity scores, the rotarod test, brain water content, and Nissl staining were employed to determine the neuroprotective effects of ω-3 PUFA supplementation. Immunofluorescent staining and western blot analysis were used to detect Beclin-1 nuclear translocation and autophagy pathway activation. The impact of SIRT1 deacetylase activity on Beclin-1 acetylation and the interaction between cytoplasmic Beclin-1 and Bcl-2 were assessed to evaluate the neuroprotective effects of ω-3 PUFAs and to determine if these effects were dependent on SIRT1-mediated deacetylation of the autophagy pathway in order to gain further insight into the mechanisms underlying the development of neuroprotection after TBI. RESULTS: ω-3 PUFA supplementation protected neurons against TBI-induced neuronal apoptosis via enhancement of the autophagy pathway. We also found that treatment with ω-3 PUFA significantly increased the NAD+/NADH ratio and SIRT1 activity following TBI. In addition, ω-3 PUFA supplementation increased Beclin-1 deacetylation and its nuclear export and induced direct interactions between cytoplasmic Beclin-1 and Bcl-2 by increasing SIRT1 activity following TBI. These events led to the inhibition of neuronal apoptosis and to neuroprotective effects through enhancing autophagy after TBI, possibly due to elevated SIRT1. CONCLUSIONS: ω-3 PUFA supplementation attenuated TBI-induced neuronal apoptosis by inducing the autophagy pathway through the upregulation of SIRT1-mediated deacetylation of Beclin-1.

Roles of airway smooth muscle dysfunction in chronic obstructive pulmonary disease.

The airway smooth muscle (ASM) plays an indispensable role in airway structure and function. Dysfunction in ASM plays a central role in the pathogenesis of chronic obstructive pulmonary disease (COPD) and contributes to alterations of contractility, inflammatory response, immunoreaction, phenotype, quantity, and size of airways. ASM makes a key contribution in COPD by various mechanisms including altered contractility and relaxation induce by [Ca2+]i, cell proliferation and hypertrophy, production and modulation of extracellular cytokines, and release of pro-and-anti-inflammatory mediators. Multiple dysfunctions of ASM contribute to modulating airway responses to stimuli, remodeling, and fibrosis, as well as influence the compliance of lungs. The present review highlights regulatory roles of multiple factors in the development of ASM dysfunction in COPD, aims to understand the regulatory mechanism by which ASM dysfunctions are initiated, and explores the clinical significance of ASM on alterations of airway structure and function in COPD and development of novel therapeutic strategies for COPD.

Genomic analysis of the multi-drug-resistant clinical isolate Myroides odoratimimus PR63039.

Myroides odoratimimus (M. odoratimimus) has been gradually implicated as an important nosocomial pathogen that poses a serious health threat to immunocompromised patients owing to its multi-drug resistance. However, the resistance mechanism is currently unclear. To clarify the antibiotic resistance and infectivity mechanisms of M. odoratimimus, whole genome sequencing was performed on the multi-drug-resistant M. odoratimimus strain PR63039. The genome sequence was completed with single molecule real-time (SMRT) technologies. Then, annotation was performed using RAST and IMG-ER. A number of databases and software programs were used to analyze the genomic characteristics, including GC-Profile, ISfinder, CG viewer, ARDB, CARD, ResFinder, the VFDB database, PHAST and Progressive Mauve. The M. odoratimimus PR63039 genome consisted of a chromosome and a plasmid. The genome contained a large number of resistance genes and virulence factors. The distribution of the resistance genes was distinctive, and a resistance region named MY63039-RR was found. The subsystem features generated by RAST indicated that the annotated genome had 108 genes that were potentially involved in virulence, disease and defense, all of which had strong associations with resistance and pathogenicity. The prophage analysis showed two incomplete prophages in the genome. The genomic analysis of M. odoratimimus PR63039 partially clarified its antibiotic resistance mechanisms and virulence factors. Obtaining a clear understanding of its genomic characteristics will be conducive to the management of multidrug-resistant M. odoratimimus.

[Design of Noninvasive Blood Constituent Spectrum Data Acquisition System Based on FPGA].

Blood constituent examination is an important means of health diagnosis. For blood constituent examination, we usually adopt the method of drawing blood, which bring pain and the risk of cross infection to the patient. Near infrared spectrum spectroscopy (NIRS) is a research hotspot in noninvasive blood constituent examination. The spectral data acquisition system of existing instruments is using a Single Chip Microcomputer (SCM) as its microcontroller. The spectral data acquisition system cannot realize the high speed multi-channel acquisition and storage of large amounts of data because of the SCM itself has certain deficiency. So a high speed multi-channel spectral data acquisition system based on Field Programmable Gate Array (FPGA) was designed in this paper in order to realize the system of high speed, multi-channel and high signal-to-noise ratio (SNR) in the area of noninvasive blood constituent examination by near infrared spectroscopy. An Altera Cyclone IV series FPGA was used as the microcontroller in this spectral data acquisition system, which simultaneously controlled two pieces of eight channels AD conversion chip acquiring 16 channels blood pulse wave signal parallel. Under the control of FPGA, the data was cached in FPGA internal ping-pong RAM first, after that it was transferred to an SRAM chip, finally it was sent to the computer via the USB port. Experiment result shows that the spectral data acquisition system can collect 16 channels signal parallel and fast under the sampling frequency of 19 531 Hz and the repetitive signal-to-noise ratio is over 40 000∶1. The system can collect 305 spectrograms per second, more over it can get high SNR human body blood pulse wave signal under the same circumstances. The spectral data acquisition system satisfies the basic requirements of the noninvasive blood constituent examination instrument by NIRS and it can make the instrument collect the human body blood pulse wave data at a high speed. The main innovation point of this article is applying FPGA to the spectral data acquisition system of near infrared noninvasive blood constituent examination instrument. FPGA is able to simultaneously control two pieces of eight channels AD conversion chip acquiring 16 channels blood pulse wave signal parallel. By using FPGA as the microcontroller of the spectral data acquisition system, we solve the problem that SCM as the microcontroller can't realize multi-channel high speed data acquisition and storage of large amounts of data. The acquisition speed is greatly faster than the system before. The second innovation point of this article is we use FPGA internal resources establish a ping-pong RAM buffer. The spectral data from the AD chip is 24 bit, however, the SRAM chip has only 16 bit data bus. Via the ping-pang RAM buffer, the spectral data can transfer from AD chip to SRAM chip. The ping-pong RAM can realize different digits data seamless transfer from AD chip to SRAM chip.

Dihydroartemisinin suppresses glioma proliferation and invasion via inhibition of the ADAM17 pathway.

Dihydroartemisinin (DHA) is a semi-synthetic derivative of artemisinin, a well-tolerated and effective drug for malaria treatment, and has recently been shown to have antitumorigenic activity. However, the mechanistic basis of these activities in gliomas is unknown. The objective of this study was to evaluate whether DHA inhibits cell proliferation and invasion in glioma cells, and to elucidate the underlying mechanisms. The results demonstrate that DHA treatment significantly inhibited cell proliferation, migration and invasion, as determined using viability, transwell migration, and matrix penetration assays, respectively. Western blot analysis revealed that protein expression levels of a disintegrin and metalloproteinase 17 (ADAM17), and phosphorylated epidermal growth factor receptor and AKT (p-EGFR and p-AKT, respectively), were suppressed by DHA. EGFR and AKT phosphorylation was enhanced by stimulation with the ADAM17 agonist chemokine phorbol myristate acetate. These data suggest that DHA inhibits glioma proliferation and invasion through suppression of ADAM17 and downregulation of EGFR-PI3 K-AKT signaling.

Downregulation of SCAI enhances glioma cell invasion and stem cell like phenotype by activating Wnt/ß-catenin signaling.

SCAI (suppressor of cancer cell invasion), has been recently characterized as a novel tumor suppressor that inhibits the invasive migration of several human tumor cells. However, the expression pattern, biological role and molecular mechanism of SCAI in human glioma remain unknown. In this study, we found that levels of SCAI protein and mRNA expression were significantly down-regulated in glioma tissues and cell lines. Overexpression of SCAI inhibited, but silencing of SCAI robustly promoted the invasive and cancer stem cell-like phenotypes of glioma cells. Furthermore, we demonstrated that SCAI downregualtion activated the Wnt/ß-catenin signaling, and blockade of the Wnt/ß-catenin pathway abrogated the effects of SCAI downregulation on glioma cell aggressiveness. Taken together, our results provide the first demonstration of SCAI downregulation in glioma, and its downregulation contributes to increased glioma cell invasion and self-renewal by activating the Wnt/ß-catenin pathway.

[The effect of MSC spectral pretreatment regions on near infrared spectroscopy calibration results].

In the present paper, 60 whole wheat flour samples were prepared and corresponding NIR spectra were collected. After the determinations of calibration range, several spectral sub-regions containing calibration range and prepared for the correction using multiple scattering correction (MSC) were obtained in the whole spectral region firstly, and MSC correction based on different spectral sub-region followed subsequently. Corresponding spectral data were obtained from the fixed calibration range of the spectra corrected based on different regions. Several partial least squares regression (PLSR) calibration models for analyzing protein content of whole wheat flour were established based on corresponding spectral data, and according to the performance about the calibration coefficient and the root mean square error of cross validation (RMSEV) of every calibration, the effects of MSC pretreatment spectral region on PLSR calibration results were investigated and the pretreatment spectral regions were optimized by comparing theperformance of more calibration models. For the optimized calibration, the calibration coefficient and the RMSECV improved compared with the calibration established based on the spectral data corrected using MSC in the fixed region of calibration. The correlation coefficient can be raised from 0.96 to 0.98 and RMSECV can be decreased from 0.37% to 0.32%. The results show that the capability of MSC on correcting the spectral interference information of non-chemical absorption can be influenced by preprocessing spectral regions, the performance of calibration model can be improved by optimizing the MSC pretreatment spectral region, and the appropriate pretreatment spectral region is prerequisite to obtain the best calibration results while using MSC for near-infrared spectra analysis.

[Study on the best detector-distance of noninvasive biochemical examination by Monte Carlo simulation].

The present paper studies the best detector-distance to improve the near-infrared spectrum signal intensity of the dermis layer and eliminate the interference of the epidermis and subcutaneous layer. First, we analyzed the organizational structure of the skin and calculated the tissue optical parameters of different layers. And we established the Monte Carlo model with the example of glucose absorption peak at 2 270 nm. Then, we used the Monte Carlo method to simulate the light transmission rules in the skin, obtaining the average path length, the average visit depth and the fractions of absorbed energy at each layer with the change in critical angle and detector-distance. The results show that when the photons are incident at an angle less than 45 degrees, you can ignore the effect of the incident angle on photon transmission path, and when the detector-distance is 1 mm, the fraction of absorbed photon energy by the dermis layer is the largest, while it can ensure more energy received by detector. We determined that the best detector-distance is 1mm, which successfully avoids the interference of the epidermis spectral information and obtains large amounts of blood in the dermis layer, which is conducive to the near-infrared non-invasive measurement of biochemical components and the subsequent experiments.

C-reactive protein is a predictor for lower-extremity deep venous thrombosis in patients with primary intracerebral hemorrhage.

OBJECTIVE: Our study aimed to determine whether there exists an association between low-grade systemic inflammation, as measured by serum C-reactive protein (CRP), and the risk of lower-extremity deep venous thrombosis (LEDVT) in patients with primary intracerebral hemorrhage (ICH). METHODS: This observational study was retrospectively conducted on patients with primary ICH who were presented to two tertiary medical centers between January 2021 and August 2022. The primary outcome was detecting LEDVT occurrence within 14 days from the onset of the acute ICH episode. Weighted logistic regression and restricted cubic spline models were employed to estimate the association between CRP and LEDVT following 1:1 propensity score matching (PSM). RESULTS: Of the 538 patients with primary ICH who met the inclusion criteria, 76 (14.13%) experienced LEDVT. Based on the cut-off levels of CRP measured upon admission from the receiver operating characteristic (ROC) curve, patients with primary ICH were categorized into two groups: (i) CRP < 1.59 mg/L and (ii) CRP ≥ 1.59 mg/L. After 1:1 PSM, the LEDVT events occurred in 24.6% of patients with CRP ≥ 1.59 mg/L and 4.1% of patients with CRP < 1.59 mg/L (P < 0.001). ROC curve revealed the area under the ROC curve of 0.717 [95% confidence interval (CI) 0.669-0.761, P < 0.001] for CRP to predict LEDVT with a sensitivity of 85.71% and specificity of 56.29%. After adjusting for all confounding variables, the occurrence of LEDVT in ICH patients with higher CRP levels (≥ 1.59 mg/L) was 10.8 times higher compared to those with lower CRP levels (95% CI 4.5-25.8, P < 0.001). A nonlinear association was observed between CRP and an increased risk of LEDVT in the fully adjusted model (P for overall < 0.001, P for nonlinear = 0.001). The subgroup results indicated a consistent positive link between CRP and LEDVT events following primary ICH. CONCLUSIONS: Higher initial CRP levels (CRP as a dichotomized variable) in patients with primary ICH are significantly associated with an increased risk of LEDVT and may help identify high-risk patients with LEDVT. Clinicians should be vigilant to enable early and effective intervention in patients at high risk of LEDVT.