Single-cell transcriptomics reveals writers of RNA modification-mediated immune microenvironment and cardiac resident Macro-MYL2 macrophages in heart failure.

BACKGROUND: Heart failure (HF), which is caused by cardiac overload and injury, is linked to significant mortality. Writers of RNA modification (WRMs) play a crucial role in the regulation of epigenetic processes involved in immune response and cardiovascular disease. However, the potential roles of these writers in the immunological milieu of HF remain unknown. METHODS: We comprehensively characterized the expressions of 28 WRMs using datasets GSE145154 and GSE141910 to map the cardiac immunological microenvironment in HF patients. Based on the expression of WRMs, the immunological cells in the datasets were scored. RESULTS: Single-cell transcriptomics analysis (GSE145154) revealed immunological dysregulation in HF as well as differential expression of WRMs in immunological cells from HF and non-HF (NHF) samples. WRM-scored immunological cells were positively correlated with the immunological response, and the high WRM score group exhibited elevated immunological cell infiltration. WRMs are involved in the differentiation of T cells and myeloid cells. WRM scores of T cell and myeloid cell subtypes were significantly reduced in the HF group compared to the NHF group. We identified a myogenesis-related resident macrophage population in the heart, Macro-MYL2, that was characterized by an increased expression of cardiomyocyte structural genes (MYL2, TNNI3, TNNC1, TCAP, and TNNT2) and was regulated by TRMT10C. Based on the WRM expression pattern, the transcriptomics data (GSE141910) identified two distinct clusters of HF samples, each with distinct functional enrichments and immunological characteristics. CONCLUSION: Our study demonstrated a significant relationship between the WRMs and immunological microenvironment in HF, as well as a novel resident macrophage population, Macro-MYL2, characterized by myogenesis. These results provide a novel perspective on the underlying mechanisms and therapeutic targets for HF. Further experiments are required to validate the regulation of WRMs and Macro-MYL2 macrophage subtype in the cardiac immunological milieu.

Transcriptomic Analysis Revealed Antimicrobial Mechanisms of Lactobacillus rhamnosus SCB0119 against Escherichia coli and Staphylococcus aureus.

Lactic acid bacteria were reported as a promising alternative to antibiotics against pathogens. Among them, Lactobacillus rhamnosus could be used as probiotics and inhibit several pathogens, but its antibacterial mechanisms are still less known. Here, L. rhamnosus SCB0119 isolated from fermented pickles could inhibit bacterial growth or even cause cell death in Escherichia coli ATCC25922 and Staphylococcus aureus ATCC6538, which was mainly attributed to the cell-free culture supernatant (CFS). Moreover, CFS induced the accumulation of reactive oxygen species and destroyed the structure of the cell wall and membrane, including the deformation in cell shape and cell wall, the impairment of the integrity of the cell wall and inner membrane, and the increases in outer membrane permeability, the membrane potential, and pH gradient in E. coli and S. aureus. Furthermore, the transcriptomic analysis demonstrated that CFS altered the transcripts of several genes involved in fatty acid degradation, ion transport, and the biosynthesis of amino acids in E. coli, and fatty acid degradation, protein synthesis, DNA replication, and ATP hydrolysis in S. aureus, which are important for bacterial survival and growth. In conclusion, L. rhamnosus SCB0119 and its CFS could be used as a biocontrol agent against E. coli and S. aureus.

Natural selection and genetic diversity of domain I of Plasmodium falciparum apical membrane antigen-1 on Bioko Island.

BACKGROUND: Plasmodium falciparum apical membrane antigen-1 (PfAMA-1) is a promising candidate antigen for a blood-stage malaria vaccine. However, antigenic variation and diversity of PfAMA-1 are still major problems to design a universal malaria vaccine based on this antigen, especially against domain I (DI). Detail understanding of the PfAMA-1 gene polymorphism can provide useful information on this potential vaccine component. Here, general characteristics of genetic structure and the effect of natural selection of DIs among Bioko P. falciparum isolates were analysed. METHODS: 214 blood samples were collected from Bioko Island patients with P. falciparum malaria between 2011 and 2017. A fragment spanning DI of PfAMA-1 was amplified by nested polymerase chain reaction and sequenced. Polymorphic characteristics and the effect of natural selection were analysed using MEGA 5.0, DnaSP 6.0 and Popart programs. Genetic diversity in 576 global PfAMA-1 DIs were also analysed. Protein function prediction of new amino acid mutation sites was performed using PolyPhen-2 program. RESULTS: 131 different haplotypes of PfAMA-1 were identified in 214 Bioko Island P. falciparum isolates. Most amino acid changes identified on Bioko Island were found in C1L. 32 amino acid changes identified in PfAMA-1 sequences from Bioko Island were found in predicted RBC-binding sites, B cell epitopes or IUR regions. Overall patterns of amino acid changes of Bioko PfAMA-1 DIs were similar to those in global PfAMA-1 isolates. Differential amino acid substitution frequencies were observed for samples from different geographical regions. Eight new amino acid changes of Bioko island isolates were also identified and their three-dimensional protein structural consequences were predicted. Evidence for natural selection and recombination event were observed in global isolates. CONCLUSIONS: Patterns of nucleotide diversity and amino acid polymorphisms of Bioko Island isolates were similar to those of global PfAMA-1 DIs. Balancing natural selection across DIs might play a major role in generating genetic diversity in global isolates. Most amino acid changes in DIs occurred in predicted B-cell epitopes. Novel sites mapped on a three dimensional structure of PfAMA-1 showed that these regions were located at the corner. These results may provide significant value in the design of a malaria vaccine based on this antigen.

Internal Versus External Drainage With a Pancreatic Duct Stent For Pancreaticojejunostomy During Pancreaticoduodenectomy for Patients at High Risk for Pancreatic Fistula: A Comparative Study.

BACKGROUND: The aim of this study was to determine whether internal or external drainage with a pancreatic duct stent is the optimal pancreaticojejunostomy method to prevent pancreatic fistula (PF) after pancreaticoduodenectomy (PD) for subgroups of patients at high risk for PF. MATERIALS AND METHODS: A total of 495 patients who underwent PD were reviewed. Univariate and multivariate analyses were used to identify risk factors for PF after PD. We further compared the incidence of PF and outcomes between the internal and external drainage groups for subgroups of patients at high risk for PF. RESULTS: There was no difference in the incidence of complications according to the Clavien-Dindo classification or the rate of PF after PD in both groups (P = 0.961 and P = 0.505, respectively). The incidence of mortality was 3.8% in the internal drainage group and 3.9% in the external drainage group (P = 0.980). Univariate and multivariate analyses identified male gender (odds ratio [OR] = 2.93; 95% confidence interval [CI], 1.78-4.83; P = 0.000), pancreatic duct diameter (<3 mm) (OR = 2.58; 95% CI, 1.57-4.23; P = 0.000), and soft pancreatic texture (OR = 2.92; 95% CI, 1.71-4.98; P = 0.000) as independent risk factors for PF after PD. No differences in the incidence of PF for the subgroups of patients with one, two, or three risk factors were observed between the internal and external drainage groups (P = 0.334, P = 1.000, and P = 0.936, respectively). No differences in total complications, delayed gastric emptying, postpancreatectomy hemorrhage, biliary fistula, infection complications, reoperation, perioperative mortality, or postoperative hospital stay were noted. In addition, liquid loss and tube-related complications occurred in the external drainage group. CONCLUSIONS: Internal drainage is the optimal method to prevent PF after PD for subgroups of patients at high risk for PF because the surgical procedure is simple and prevents liquid loss and tube-related complications associated with external drainage. However, no differences in the incidence of PF and other complications after PD were observed between the two approaches.

[Effect of Xiaoai Jiedu Recipe on mIRNA Expression Profiles in H22 Tumor-bearing Mice].

Objective To observe the mechanism of Xiaoai Jiedu Recipe (XJR) for fighting a- gainst hepatoma by detecting tumor miRNAs expression profiles in H22tumor-bearing mice. Methods To- tally 50 H22tumor-bearing mice were randomly divided into the model group, the low dose XJR group, the medium dose XJR group, the high dose XJR group, the Cisplatin group, 10 in each group. Different expressions of tumor tissues in H22 tumor-bearing mice under light microscope were detected using histopathological technique. Differentially expressed miRNAs of tumor tissue in H22tumor-bearing mice were detected by using miRNA chip technique. Differentially expressed miRNAs associated with antitumor mechanism of XJR were found out by statistical analysis. Results Histopathological results showed that reduced pathologic mitosis, smaller cancer cells, and obviously enhanced anti-cancer effect along with increased XJP dose. Results of miRNA chip analyses indicated XJP could significantly up-regulate the ex- pressions of miRNAs, such as miR-1298-5p, miR-874-3p, miR-721, miR-298-5p, miR-551b-5p, miR-346- 5p, miR-105, and so on. It could also down-regulate the expressions of miR-24-3p, miR-3963, miR-127- 3p, miR-434-5p, miR-1187, miR-468-3p, miR-221-5p, and miR-6695-5p. Conclusion XJP could fight a- gainst tumor possibly by regulating expressions of multiple miRNAs.

Microarray analysis on gene regulation by estrogen, progesterone and tamoxifen in human endometrial stromal cells.

Epithelial stromal cells represent a major cellular component of human uterine endometrium that is subject to tight hormonal regulation. Through cell-cell contacts and/or paracrine mechanisms, stromal cells play a significant role in the malignant transformation of epithelial cells. We isolated stromal cells from normal human endometrium and investigated the morphological and transcriptional changes induced by estrogen, progesterone and tamoxifen. We demonstrated that stromal cells express appreciable levels of estrogen and progesterone receptors and undergo different morphological changes upon hormonal stimulation. Microarray analysis indicated that both estrogen and progesterone induced dramatic alterations in a variety of genes associated with cell structure, transcription, cell cycle, and signaling. However, divergent patterns of changes, and in some genes opposite effects, were observed for the two hormones. A large number of genes are identified as novel targets for hormonal regulation. These hormone-responsive genes may be involved in normal uterine function and the development of endometrial malignancies.

Exosomal AC068768.1 enhances the proliferation, migration, and invasion of laryngeal squamous cell carcinoma through miR-139-5p/NOTCH1 axis.

Objective: Long non-coding RNAs (lncRNAs) are closely associated with the pathogenesis of laryngeal squamous cell carcinoma (LSCC). This study aimed to investigate the roles of AC068768.1 in LSCC. Methods: Exosomes were extracted by ultracentrifugation and identified by transmission electron microscopy (TEM) assay. The expression levels of mRNA and miRNA were determined by real-time quantitative polymerase chain reaction (RT-qPCR). Cellular functions were assesses through immunofluorescence, flow cytometry, colony formation, wound healing and transwell assays. Chromatin immunoprecipitation (ChIP) and luciferase assays were conducted to verify the binding of AC068768.1 by signal transducer and activator of transcription 3 (STAT3). Xenograft assays were performed to confirm the roles of AC068768.1 in LSCC, and hematoxylin-eosin (HE) staining was applied for histological analysis. Results: LSCC cell-derived exosomes induced M2-like tumor-associated macrophages (TAM2) polarization, which promoted the proliferation, migration, and invasion of LSCCs. Knockdown of exosomal AC068768.1 inhibited M2 polarization and suppressed LSCC aggressiveness both in vitro and in vivo. Moreover, AC068768.1 sponged miR-139-5p, inducing the upregulation of neurogenic locus notch homolog protein 1 (NOTCH1). LSCCs adapted to TAM2 polarization in the tumor microenvironment via AC068768.1-mediated activation of the NOTCH1 pathway. Additionally, NOTCH1 activated STAT3. Conclusion: The AC068768.1/miR-139-5p/NOTCH1/STAT3 axis promotes the metastasis of LSCC. This finding may provide a novel target for LSCC therapy.

Reduced syncytin-1 regulates trophoblast invasion and apoptosis in preeclampsia.

INTRODUCTION: Preeclampsia is a pregnancy-specific disorder characterized by de novo development of hypertension and proteinuria over 20 weeks gestation that has been associated with the dysfunction of trophoblasts. Current evidence suggests that syncytin-1 plays an important role in the non-fusogenic biological activity of trophoblasts, except for specific fusogenic function. However, the underlying mechanism remains unclear. METHODS: The expression and location of syncytin-1 in normal and the late-onset preeclampsia placentas were detected by quantitative real-time PCR, western blotting and immunofluorescence. Morphological and apoptosis analysis were processed in placentas. The ex vivo extravillous explant culture model was used to explore the effect of syncytin-1 on EVT outgrowths. Real-time quantitative PCR and immunoblotting were used to calculate syncytin-1 levels in the trophoblast cells before and after syncytin-1 knockdown or overexpression. CCK-8 assay was used to detect the cell viability. TUNEL staining and immunoblotting were processed in trophoblast cells. Transwell assays and wound healing assays were utilize to assess the invasion and migration of trophoblastic cells. Conditional knockout of syncytin-a mouse model was conducted to present the change of placentas in vivo. The ex vivo extravillous explant culture model was used to explore the effect of syncytin-1 on EVT outgrowths. Western blotting was used to identify the key proteins of PI3K/Akt pathways and invasion-related proteins in trophoblast cells. RESULTS AND DISCUSSION: Here, reduced syncytin-1 was identified in the late-onset preeclampsia placentas. Reduced syncytin-1 may attenuates the EMT process by promoting apoptosis, inhibiting proliferation and invasion by suppressed PI3K/Akt pathway in trophoblast cells. Our findings provide novel insights into the non-fusogenic biological function of reduced syncytin-1 that may be involves in the pathogenesis of preeclampsia.

[Systems biology is a bridge of integrated traditional Chinese and Western medicine].

The integration of Chinese medicine (CM) and Western medicine (WM) is the only way for the development of medicine, and it is the best form for unifying systems theory and reductionism. In this paper, systems biology and its application in medical research were discussed. The authors put forward that systems biology may possibly interpret the scientific connotation of the complex theoretic systems of CM, which will make WM to well know the human body and disease. We hold that systems biology is a bridge of integrated CM and WM.

Indirect comparison of SGLT2 inhibitors in patients with established heart failure: evidence based on Bayesian methods.

AIMS: Head-to-head comparisons among SGLT2 inhibitors treatments in established heart failure remain absent. We conducted a systematic review of dedicated heart failure trials to assess indirectly the composite outcomes and individual clinical endpoints among SGLT2 inhibitor treatments. METHODS AND RESULTS: We systematically reviewed randomized controlled trials comparing SGLT2 inhibitors versus placebo in patients with established heart failure. A Bayesian approach to network meta-analysis was applied. Five trials including four treatment strategies were included in this study. The composite of cardiovascular death or hospitalization for heart failure showed no significant difference in the comparison between dapagliflozin and empagliflozin (OR 1.00, 95% CI 0.66-1.55), dapagliflozin and sotagliflozin (OR 1.54, 95% CI 0.91-2.65), and empagliflozin and sotagliflozin (OR 1.53, 95% CI 0.90-2.69). All-cause mortality showed no significant difference in the comparison between dapagliflozin and empagliflozin (OR 0.92, 95% CI 0.711-1.18), dapagliflozin and sotagliflozin (OR 1.05, 95% CI 0.68-1.59), and empagliflozin and sotagliflozin (OR 1.14, 95% CI 0.74-1.73). Cardiovascular death showed no significant difference in the comparison between dapagliflozin and empagliflozin (OR 0.94, 95% CI 0.71-1.23), dapagliflozin and sotagliflozin (OR 0.96, 95% CI 0.61-1.55), and empagliflozin and sotagliflozin (OR 1.03, 95% CI 0.64-1.66). Hospitalization for heart failure showed no significant difference in the comparison between dapagliflozin and empagliflozin (OR 1.13, 95% CI 0.64-1.97), dapagliflozin and sotagliflozin (OR 1.56, 95% CI 0.74-3.15), and empagliflozin and sotagliflozin (OR 1.39, 95% CI 0.68-2.78). CONCLUSIONS: In patients with established heart failure, there was no significant difference of the major efficacy outcomes among SGLT2 inhibitor treatments; however, sotagliflozin may be associated with the lowest risk of the composite of cardiovascular death or hospitalization for heart failure, and dapagliflozin may be associated with the lowest risk of all-cause and cardiovascular mortality.

The risk of all-cause death with dapagliflozin versus placebo: a systematic review and meta-analysis of phase III randomized controlled trials.

BACKGROUND: Dapagliflozin has proven cardioprotective and nephroprotective effects. However, the risk of all-cause death with dapagliflozin remains unclear. RESEARCH DESIGN AND METHODS: We performed a meta-analysis of phase III randomized controlled trials (RCTs) for the risk of all-cause death and safety events with dapagliflozin compared to placebo. PubMed and EMBASE were searched from inception to 20 September 2022. RESULTS: Five trials were included in the final analysis. Compared with the placebo, dapagliflozin demonstrated an 11.2% reduction in the risk of all-cause death (OR 0.88, 95% CI 0.81-0.94). No statistically significant difference in urinary tract infection (OR: 0.95, 95% CI: 0.78 to 1.17), bone fracture (OR: 1.06, 95% CI: 0.94 to 1.20), and amputation (OR: 1.01, 95% CI: 0.82 to 1.23) was observed between patients treated with dapagliflozin and placebo. Compared with placebo, dapagliflozin was associated with a significant reduction in acute kidney injury (OR: 0.71, 95% CI: 0.60 to 0.83), and increased the risk of genital infection (OR: 8.21, 95% CI: 4.19 to 16.12). CONCLUSIONS: Dapagliflozin was associated with significantly reduced all-cause death and increased genital infection. Dapagliflozin was safe concerning urinary tract infection, bone fracture, amputation, and acute kidney injury, compared with the placebo.

ERK/MAPK Signalling Pathway Regulates MMP2 Through ETS1 in Renal Clear Cell Carcinoma.

BACKGROUND: The c-ETS-1 (ETS1) expression is high in clear cell renal cell carcinoma (ccRCC) tissues; however, how it impacts ccRCC is currently unknown. METHOD: The online STRING web source was used to construct a protein network interacting with ETS1. The Cell Counting Kit-8 was used to detect the cell viability. A clonogenic assay, a wound-healing assay, and a Transwell assay were used to detect cell proliferation, invasion and migration abilities. Western blot was used to detect the expression of proteins. RESULT: The data showed the expression of ETS1 in ccRCC tissues to be significantly increased compared to adjacent tissues (p<0.05). The positive expression of ETS1 in ccRCC patients aged 20-100 was statistically significant compared to adjacent normal tissues (p<0.05). The grade of ETS1 positive expression (1-4) and lymph node metastasis (N1) in ccRCC were significantly higher than those in adjacent normal tissues (p<0.05). The tumour stage (stages 1-4) in ccRCC patients with positive ETS1 expression was significantly higher than that in adjacent normal tissues (p<0.05). Knockdown of ETS1 and PERK inhibitors significantly inhibited the proliferation, migration and invasion of ccRCC cells. Knockdown of ETS1 inhibited MMP-2 expression, and an extracellular signal-related kinase (ERK) inhibitor inhibited both ETS1 and MMP-2 expression. CONCLUSION: A high expression of ETS1 is associated with the progression of ccRCC. This study suggests that ETS1 promotes proliferation by increasing MMP2 expression in ccRCC, and combined knockdown of ETS1 and inhibition of ERK can significantly inhibit the proliferation, migration and invasion of ccRCC. ETS1 may be a therapeutic and prognostic target for renal cell carcinoma.

A pairwise radiomics algorithm-lesion pair relation estimation model for distinguishing multiple primary lung cancer from intrapulmonary metastasis.

Background: Distinguishing multiple primary lung cancer (MPLC) from intrapulmonary metastasis (IPM) is critical for their disparate treatment strategy and prognosis. This study aimed to establish a non-invasive model to make the differentiation pre-operatively. Methods: We retrospectively studied 168 patients with multiple lung cancers (307 pairs of lesions) including 118 cases for modeling and internal validation, and 50 cases for independent external validation. Radiomic features on computed tomography (CT) were extracted to calculate the absolute deviation of paired lesions. Features were then selected by correlation coefficients and random forest classifier 5-fold cross-validation, based on which the lesion pair relation estimation (PRE) model was developed. A major voting strategy was used to decide diagnosis for cases with multiple pairs of lesions. Cases from another institute were included as the external validation set for the PRE model to compete with two experienced clinicians. Results: Seven radiomic features were selected for the PRE model construction. With major voting strategy, the mean area under receiver operating characteristic curve (AUC), accuracy, sensitivity, and specificity of the training versus internal validation versus external validation cohort to distinguish MPLC were 0.983 versus 0.844 versus 0.793, 0.942 versus 0.846 versus 0.760, 0.905 versus 0.728 versus 0.727, and 0.962 versus 0.910 versus 0.769, respectively. AUCs of the two clinicians were 0.619 and 0.580. Conclusions: The CT radiomic feature-based lesion PRE model is potentially an accurate diagnostic tool for the differentiation of MPLC and IPM, which could help with clinical decision making.

Gut microbiota interactions with antitumor immunity in colorectal cancer: From understanding to application.

Colorectal cancer (CRC) is one of highly prevalent cancer. Immunotherapy with immune checkpoint inhibitors (ICIs) has dramatically changed the landscape of treatment for many advanced cancers, but CRC still exhibits suboptimal response to immunotherapy. The gut microbiota can affect both anti-tumor and pro-tumor immune responses, and further modulate the efficacy of cancer immunotherapy, particularly in the context of therapy with ICIs. Therefore, a deeper understanding of how the gut microbiota modulates immune responses is crucial to improve the outcomes of CRC patients receiving immunotherapy and to overcome resistance in nonresponders. The present review aims to describe the relationship between the gut microbiota, CRC, and antitumor immune responses, with a particular focus on key studies and recent findings on the effect of the gut microbiota on the antitumor immune activity. We also discuss the potential mechanisms by which the gut microbiota influences host antitumor immune responses as well as the prospective role of intestinal flora in CRC treatment. Furthermore, the therapeutic potential and limitations of different modulation strategies for the gut microbiota are also discussed. These insights may facilitate to better comprehend the interplay between the gut microbiota and the antitumor immune responses of CRC patients and provide new research pathways to enhance immunotherapy efficacy and expand the patient population that could be benefited by immunotherapy.

A bibliometric and visual analysis of cancer-associated fibroblasts.

Background: Cancer-associated fibroblasts (CAFs) represent the predominant stromal component within the tumour microenvironment (TME), exhibiting considerable heterogeneity and plasticity that significantly impact immune response and metabolic reprogramming within the TME, thereby influencing tumour progression. Consequently, investigating CAFs is of utmost importance. The objective of this study is to employ bibliometric analysis in order to evaluate the current state of research on CAFs and predict future areas of research and emerging trends. Methods: Conduct a comprehensive search for scholarly publications within the Web of Science Core Collection database, encompassing the time period from January 1, 2001, to December 31, 2022. Apply VOSviewer, CiteSpace, R software and Microsoft Excel for bibliometric analysis and visualisation. Results: This study involved a comprehensive analysis of 5,925 publications authored by 33,628 individuals affiliated with 4,978 institutions across 79 countries/regions. These publications were published in 908 journals, covering 14,495 keywords and 203,947 references. Notably, there was a significant increase in articles published between 2019 and 2022. China had the highest count of articles, while the United States emerged as the most frequently cited country. The primary research institutions in this field were Shanghai Jiao Tong University, Harvard University, and the University of Texas MD Anderson Cancer Center. Sotgia, Federica and Lisanti, Michael P from the University of Manchester, and Martinet, Wim from the University of Antwerp were the most prolific and highly cited authors. The journal Cancers had the highest number of publications, while Cancer Research was the most frequently cited journal. Molecular, biology, immunology, medicine and genetics were the main research disciplines in the field of CAFs. Key directions in CAFs research encompassed the study of transforming growth factor-ß, Fibroblast Activation Protein, breast cancer, as well as growth and metastasis. The findings from the analysis of keyword co-occurrence and literature co-citation have revealed several emerging hotspots and trends within the field of CAFs. These include STAT3, multidrug resistance, pancreatic ductal adenocarcinoma, pan-cancer analysis, preclinical evaluation, ionizing radiation, and gold nanoparticles. Conclusion: Targeting CAFs is anticipated to be a novel and effective strategy for cancer treatment. This study provides a comprehensive overview of the existing research on CAFs from 2001 to 2022, utilizing bibliometric analysis. The study identified the prominent areas of investigation and anticipated future research directions, with the aim of providing valuable insights and recommendations for future studies in the field of CAFs.

Influence of degenerative changes of intervertebral disc on its material properties and pathology.

OBJECTIVE: To investigate the material properties of normal and degenerated intervertebral discs (IVDs) and examine the effect of degenerative changes on IVD pathology. METHODS: A computer-based online search was undertaken to identify English articles about material properties of IVDs published from January 1950 to 2011 in PubMed database. The retrieved keywords included material properties, intervertebral disc and degeneration. Based on the principles of reliability, advancement and efficiency, the obtained data were primarily examined, and the original source was retrieved to read the full-text. Repetitive articles were excluded. The data of material properties of normal and degenerated IVDs were summarized and analyzed by meta-analysis. RESULTS: The data of Young's modulus, Poisson's ratio, shear modulus, hydraulic permeability and intradiscal pressure of normal and degenerated IVDs were obtained. Compared with normal IVDs, the Young's modulus and shear modulus of annulus fibrosus and nucleus pulposus were higher in degenerated IVDs, the Poisson's ratio was lower while the hydraulic permeability and intradiscal pressure were higher. Besides, the degeneration-related alterations in IVDs had an influence both on itself and other spinal structures, leading to diseases such as bulging disc, discogenic pain and spinal stenosis. Meanwhile, the heavy mechanical loading and injury indicated important pathways to IVD degeneration. CONCLUSIONS: To a certain extent, the degenerative changes of IVD influence its material properties. And the degeneration-related alterations of composition can cause structural failure of IVDs, leading to injuries and diseases.

Cervical spinal canal narrowing and cervical neurological injuries.

Cervical spinal canal narrowing can lead to injury of the spinal cord and neurological symptoms including neck pain, headache, weakness and parasthesisas. According to previous and recent clinical researches, we investigated the geometric parameters of normal cervical spinal canal including the sagittal and transverse diameters as well as Torg ratio. The mean sagittal diameter of cervical spinal canal at C(1) to C(7) ranges from 15.33 mm to 20.46 mm, the mean transverse diameter at the same levels ranges from 24.45 mm to 27.00 mm and the mean value of Torg ratio is 0.96. With respect to narrow cervical spinal canal, the following charaterstics are found: firstly, extension of the cervical spine results in statistically significant stenosis as compared with the flexed or neutral positions; secondly, females sustain cervical spinal canal narrowing more easily than males; finally, the consistent narrowest cervical canal level is at C(4) for all ethnicity, but there is a slight variation in the sagittal diameter of cervical spinal stenosis (less than or equal to 14 mm in Whites, less than or equal to 12 mm in Japanese, less than or equal to 13.7 mm in Chinese). Narrow sagittal cervical canal diameter brings about an increased risk of neurological injuries in traumatic, degenerative and inflammatory conditions and is related with extension of cervical spine, gender, as well as ethnicity. It is hoped that this review will be helpful in diagnosing spinal cord and neurological injuries with the geometric parameters of cervical spine in the future.

[Proteomics is the important technology platform of Chinese medicine pathogenesis research].

Pathogenesis is the core of the theoretical system in Chinese medicine (CM). Pathogenesis research is the breakthrough of the innovation and development of CM theories. Proteomics and CM pathogenesis were amazingly similar in aspects of integrity, dynamics, space, and complexity. It is of great significance using proteomics methods in studying CM pathogenesis essence and evolution laws, exploring the mechanisms of classical prescriptions or recipes with therapeutic efficacy, and promoting the modernization of CM.

[The application of metabonomics in modern studies of Chinese materia medica].

Metabonomics, a newly developing subject secondary to genomics, transcriptomics, and proteomics, is an important constituent part of systems biology. It is believed to be the final direction of the systems biology. It can be directly applied to understand the physiological and biochemical states by its "metabolome profile" as a whole. Therefore, it can provide a huge amount of information different from those originating from other "omics". In the modernization of Chinese materia medica research, the application of metabonomics methods and technologies has a broad potential for future development. Especially it is of important theoretical significance and application value in holistic efficacies evaluation, active ingredients studies, and safety research of Chinese materia medica.