Enoyl coenzyme a hydratase 1 attenuates aortic valve calcification by suppressing Runx2 via Wnt5a/Ca2+ pathway.

The morbidity and death rates of calcified aortic valves|calcific aortic valve (CAV) disease (CAVD) remain high for its limited therapeutic choices. Here, we investigated the function, therapeutic potential, and putative mechanisms of Enoyl coenzyme A hydratase 1 (ECH1) in CAVD by various in vitro and in vivo experiments. Single-cell sequencing revealed that ECH1 was predominantly expressed in valve interstitial cells and was significantly reduced in CAVs. Overexpression of ECH1 reduced aortic valve calcification in ApoE-/- mice treated with high cholesterol diet, while ECH1 silencing had the reverse effect. We also identified Wnt5a, a noncanonical Wnt ligand, was also altered when ECH1 expression was modulated. Mechanistically, we found that ECH1 exerted anti-calcific actions through suppressing Wnt signaling, since CHIR99021, a Wnt agonist, may significantly lessen the protective impact of ECH1 overexpression on the development of valve calcification. ChIP and luciferase assays all showed that ECH1 overexpression prevented Runx2 binding to its downstream gene promoters (osteopontin and osteocalcin), while CHIR99021 neutralized this protective effect. Collectively, our findings reveal a previously unrecognized mechanism of ECH1-Wnt5a/Ca2+ regulation in CAVD, implying that targeting ECH1 may be a potential therapeutic strategy to prevent CAVD development.

Study on the underlying molecular mechanism of benzene-induced nervous system damage in mice based on tandem mass tag (TMT) proteomics.

Benzene is known to be a common toxic industrial chemical, and prolonged benzene exposure may cause nervous system damage. At present, there were few studies on benzene-induced neurological damage. This research aimed to identify the protein biomarkers to explore the mechanism of nervous system damage caused by benzene. We established a benzene poisoning model of C57 mice by gavage of benzene-peanut oil suspension and identified differentially expressed proteins (DEPs) in brain tissue using tandem mass tag (TMT) proteomics. The results showed a significant weight loss and decrease in leukocyte and neutrophil counts in benzene poisoning mice compared to the control group. We also observed local cerebral oedema and small vessel occlusion in the cerebral white matter of benzene poisoning mice. TMT proteomic results showed that a total 6,985 proteins were quantified, with a fold change (FC) > 1.2 (or < 1/1.2) and P value <0.05 were considered as DEPs. Compared with the control group, we identified 43 DEPs, comprising 14 upregulated and 29 downregulated proteins. Kyoto encyclopedia of genes and genomes (KEGG) pathway analysis results showed that the candidate proteins were mainly involved in cholesterol metabolism, complement and coagulation cascades, african trypanosomiasis, PPAR signaling pathway, and vitamin digestion and absorption. Three proteins, 2-hydroxyacylsphingosine 1-beta-galactosyltransferase (UGT8), Apolipoprotein A-I (APOA1) and Complement C3 (C3) were validated using immunoblotting and immunohistochemical. In conclusion, our study preliminarily investigated the mechanism of benzene toxicity to the nervous system by analyzing DEPs changes in the brain.

Inhibition of HSP20 Ameliorates Steatotic Liver Disease by Stimulating ERK2-Dependent Autophagy.

HSP20 emerges as a novel regulator of autophagy in the heart. Nonetheless, the detailed function of HSP20 in the liver and its effect on autophagy remain unknown. Here, we observed that HSP20 expression is increased in liver tissues from mice and patients with metabolic dysfunction-associated steatotic liver disease (MASLD), formerly known as nonalcoholic fatty liver disease. Liver-specific downregulation of HSP20 mitigates hepatic steatosis and insulin resistance in obese mice, while upregulating HSP20 promotes lipid deposition and hepatocyte cell death. Mechanistically, liquid chromatography-tandem mass spectrometry revealed that HSP20 interacts with phosphorylated extracellular regulated protein kinase 2 (ERK2) and prevents its dephosphorylation by dual specificity phosphatase 6, leading to ERK2-mediated repression of autophagy and resulting in aggravated saturated fatty acid (SFA)-triggered hepatocyte death. Importantly, such adverse effects could be ameliorated by ERK inhibitor. Our data reveal a framework of how HSP20 increases susceptibility of SFA-induced liver injury through enhancing ERK2 phosphorylation, which represents a plausible therapeutic intervention to combat MASLD.

Comparative study of high-performance mesophilic and thermophilic anaerobic membrane bioreactors in the co-digestion of sewage sludge and food waste: Methanogenic performance and energy recovery potential.

To support smart cities in terms of waste management and bioenergy recovery, the co-digestion of sewage sludge (SeS) and food waste (FW) was conducted by the anaerobic membrane bioreactor (AnMBR) under mesophilic and thermophilic conditions in this study. The biogas production rate of the thermophilic AnMBR (ThAnMBR) at the SeS to FW ratio of 0:100, 75:25, 50:50 and 100:0 was 2.84 ± 0.21, 2.51 ± 0.26, 1.54 ± 0.26 and 1.31 ± 0.08 L-biogas/L/d, inconspicuous compared with that of the mesophilic AnMBR (MeAnMBR) at 3.00 ± 0.25, 2.46 ± 0.30, 1.63 ± 0.23 and 1.30 ± 0.17 L-biogas/L/d, respectively. The higher hydrolysis ratio and the poorer rejection efficiencies of the membrane under thermophilic conditions, resulting that the permeate COD, carbohydrate and protein of the ThAnMBR was higher than that of the MeAnMBR. The lost COD that might be converted into biogas was discharged with the permeate in the ThAnMBR, which was partly responsible for the inconspicuous methanogenic performance. Furthermore, the results of energy recovery potential assessment showed that the energy return on investment (EROI) of the MeAnMBR was 4.54, 3.81, 2.69 and 2.22 at the four SeS ratios, which was higher than that of the ThAnMBR at 3.29, 2.97, 2.02 and 1.80, respectively, indicating the advantage of the MeAnMBR over the ThAnMBR in energy recovery potential. The outcomes of this study will help to choose a more favorable temperature to co-digest SeS and FW to support the construction of smart cities.

Humidity Enhances the Solid-Phase Catalytic Ability of a Bulk MOF-808 Metal-Organic Gel toward a Chemical Warfare Agent Simulant.

Zirconium-based metal-organic frameworks have emerged as promising materials for detoxifying chemical warfare agents (CWAs) due to their remarkable stability and porosity. However, their practical application is hindered by issues with their powder form and poor catalytic performance in solid-phase degradation. To address these challenges, herein, a granular MOF-808 metal-organic gel (G808) is prepared under optimized conditions for catalytic degradation of the simulant 2-chloroethyl ethyl sulfide (2-CEES), a sulfide blister agent, in a neat state under different humidity conditions. The detoxification performance of G808 toward 2-CEES is significantly enhanced as the content of water present increases. The half-life of 2-CEES decontaminated by G808 can be shortened to 816 s, surpassing those of many other benchmark materials. To confirm the mechanism of catalytic degradation, we used gas chromatography, gas chromatography-mass spectrometry, and theoretical calculations. The findings revealed that hydrolysis was the predominant route. Additionally, granular G808 was reusable and adaptable to high-moisture environments, making it an excellent protective material with practical potential.

Towards advanced simultaneous nitrogen removal and phosphorus recovery from digestion effluent based on anammox-hydroxyapatite (HAP) process: Focusing on a solution perspective.

In this paper, the state-of-the-art information on the anammox-HAP process is summarized. The mechanism of this process is systematically expounded, the enhancement of anammox retention by HAP precipitation and the upgrade of phosphorus recovery by anammox process are clarified. However, this process still faces several challenges, especially how to deal with the âˆ¼ 11% nitrogen residues and to purify the recovered HAP. For the first time, an anaerobic fermentation (AF) combined with partial denitrification (PD) and anammox-HAP (AF-PD-Anammox-HAP) process is proposed to overcome the challenges. By AF of the organic impurities of the anammox-HAP granular sludge, organic acid is produced to be used as carbon source for PD to remove the nitrogen residues. Simultaneously, pH of the solution drops, which promotes the dissolution of some inorganic purities such as CaCO3. In this way, not only the inorganic impurities are removed, but the inorganic carbon is supplied for anammox bacteria.

PRMT4 Facilitates White Adipose Tissue Browning and Thermogenesis by Methylating PPARγ.

Obesity is a global health threat, and the induction of white adipose tissue (WAT) browning presents a promising therapeutic method for it. Recent publications revealed the essential role of protein arginine methyltransferase 4 (PRMT4) in lipid metabolism and adipogenesis, but its involvement in WAT browning has not been investigated. Our initial studies found that the expression of PRMT4 in adipocytes was upregulated in cold-induced WAT browning but downregulated in obesity. Besides, PRMT4 overexpression in inguinal adipose tissue accelerated WAT browning and thermogenesis to protect against high-fat diet-induced obesity and metabolic disruptions. Mechanistically, our work demonstrated that PRMT4 methylated peroxisome proliferator-activated receptor-γ (PPARγ) on Arg240 to enhance its interaction with the coactivator PR domain-containing protein 16 (PRDM16), leading to the increased expression of thermogenic genes. Taken together, our results uncover the essential role of the PRMT4/PPARγ/PRDM16 axis in the pathogenesis of WAT browning. ARTICLE HIGHLIGHTS: Protein arginine methyltransferase 4 (PRMT4) expression was upregulated during cold exposure and negatively correlated with body mass of mice and humans. PRMT4 overexpression in inguinal white adipose tissue of mice improved high-fat diet-induced obesity and associated metabolic impairment due to enhanced heat production. PRMT4 methylated peroxisome proliferator-activated receptor-γ on Arg240 and facilitated the binding of the coactivator PR domain-containing protein 16 to initiate adipose tissue browning and thermogenesis. PRMT4-dependent methylation of peroxisome proliferator-activated receptor-γ on Arg240 is important in the process of inguinal white adipose tissue browning.

Nano-Metal-Organic Framework Decorated With Pt Nanoparticles as an Efficient Theranostic Nanoprobe for CT/MRI/PAI Imaging-Guided Radio-Photothermal Synergistic Cancer Therapy.

The multifunctional theranostic nanoplatforms, which can realize changing the contrasts of medical images and enhance cancer therapies simultaneously, have attracted tremendous attention from chemists and medicine in past decades. Herein, a nanoscale metal-organic framework-based material was first synthesized and then decorated with platinum (NMOF545@Pt) successfully for multimodal imaging-guided synergistic cancer therapy. The obtained NMOF545@Pt is advantageous in shortening the longitudinal relaxation time (T1), enhancing photoacoustic effects, and elevating X-ray absorption efficiently. Thus, the enchantments of tripe imaging modalities, computed tomography (CT)/magnetic resonance imaging (MRI)/photoacoustic imaging (PAI), were realized with NMOF545@Pt administration simultaneously and can be cleared from the mice. Meanwhile, in vitro and in vivo experiments demonstrate that the synthesized NMOF545@Pt can dramatically increase photothermal therapy (PTT) and radiotherapy (RT) efficacy. Convincing evidence proves that tumor growth can be wholly inhibited without noticeable side effects or organ damage. The results demonstrated the promise of multifunctional nanocomposites NMOF545@Pt to improve biomedical imaging and synergistic tumor treatments.

Novel adipokine asprosin modulates browning and adipogenesis in white adipose tissue.

Obesity is an increasingly serious epidemic worldwide characterized by an increase in the number and size of adipocytes. Adipose tissue maintains the balance between lipid storage and energy utilization. Therefore, adipose metabolism is of great significance for the prevention, treatment and intervention of obesity. Asprosin, a novel adipokine, is a circulating hormone mainly secreted by white adipose tissue. Previous studies have shown that asprosin plays a role in fasting-induced homeostasis, insulin resistance, and glucose tolerance. However, whether it can regulate the metabolism of adipose tissue itself has not been studied. This study intended to examine the roles and potential mechanisms of asprosin in adipose regulation. We first demonstrated that the expression level of asprosin was significantly downregulated in subcutaneous white adipose tissue (scWAT) of high-fat diet (HFD)-fed or cold-stimulated mice. Overexpression of asprosin in scWAT reduced heat production, decreased expression of the browning marker uncoupling protein 1 (UCP1) and other browning-related genes, along with upregulation of adipogenic gene expression. Mechanistically, we found that Nrf2 was activated upon cold exposure, but this activation was suppressed after asprosin overexpression. In primary cultured adipocytes, adenovirusmediated asprosin overexpression inhibited adipose browning and aggravated lipid deposition, while Nrf2 agonist oltipraz could reverse these changes. Our findings suggest that novel adipokine asprosin negatively regulated browning and elevate lipid deposition in adipose tissue via a Nrf2-mediated mechanism. Asprosin may be a promising target for the prevention and treatment of obesity and other metabolic diseases.

Pri-miR-34b/c rs4938723 polymorphism is associated with a decreased risk of gastric cancer.

Previous studies have demonstrated that miR-34 family members are abnormally expressed in gastric cancer. Overexpression of the miR-34 family suppresses gastric carcinogenesis, whereas downregulation of the miR-34 family promotes tumorigenesis. p53 can bind to the promoter region of miR-34b/c, leading to an increase of miR-34b/c expression. Recently, a variant in the promoter region of pri-miR-34b/c (rs4938723) has been discovered, with the function of altering the binding efficiency of transcription factor GATA. The purpose of this study was to examine the role of the miR-34b/c rs4938723 and TP53 Arg72Pro polymorphisms in the susceptibility of gastric cancer. We analyzed the distribution of the two polymorphisms in 197 patients with gastric cancer and 289 age-, gender-, ethnicity-, and living area-matched controls using polymerase chain reaction-restriction fragment length polymorphism and DNA direct sequencing. We found that the CT and CT/CC genotypes of the miR-34b/c rs4938723 were associated with a significantly decreased risk of gastric cancer compared with the TT genotype (CT vs. TT: odds ratio [OR]=0.66; 95% confidence interval [95% CI], 0.45-0.97; and CT/CC vs. TT: OR=0.67; 95% CI, 0.47-0.97, respectively). Combined analysis showed that subjects carrying the miR-34b/c rs4938723 CT/CC and TP53 CG/CC genotypes had a 0.62-fold decreased risk to develop gastric cancer compared with subjects carrying the miR-34b/c rs4938723 TT and TP53 CG/CC genotypes (OR=0.62; 95% CI, 0.40-0.96). These findings suggest that the miR-34b/c rs4938723 may individually and jointly have a protective effect on the risk of gastric risk.

Lack of association between let-7 binding site polymorphism rs712 and risk of nasopharyngeal carcinoma.

Nasopharyngeal carcinoma (NPC) is characterized by its highly invasive and metastatic features. Therefore, screening genetic biomarkers of NPC to achieve early diagnose would be of great value for NPC therapy. Single nucleotide polymorphisms in let-7 miRNA binding site in 3' untranslated region of KRAS mRNA have been found to be associated with various cancer risks. In this study, we genotyped the frequency of KRAS rs712 to test its effect on NPC risk in a hospital-based case-control study in a Chinese population, with 188 histologically confirmed NPC patients and 356 cancer-free controls, using polymerase chain reaction-restriction fragment length polymorphism assay. There was no significant difference in the genotype and allele frequencies of the rs712 polymorphism between the NPC patients and the control group (GT vs. GG, OR 0.83, 95% CI 0.57-1.21; TT vs. GG, OR 1.27, 95% CI 0.58-2.75). Our data suggest that the KRAS rs712 polymorphism in let-7 miRNA binding site has no association with NPC risk. Further experiments with larger sample size or other polymorphism sites are needed to verify the result, especially in different ethnic groups.

A let-7 KRAS rs712 polymorphism increases colorectal cancer risk.

Growing evidence has indicated that polymorphism present in the miRNA binding site of target gene can alter the ability of miRNAs to bind its target gene and modulate the development and progression of cancer. We aimed to investigate the association between let-7 KRAS rs712 polymorphism and the risk of colorectal cancer (CRC). The let-7 KRAS rs712 was analyzed in a case-control study, including 339 CRC patients and 313 age- and sex-matched controls; the relationship between the polymorphism and the clinicopathological features of CRC was also examined. Individuals carrying the let-7 KRAS rs712 TT genotype and T allele had an increased risk of developing CRC (TT vs. GG, adjusted OR = 2.18; 95% CI, 1.00-4.77; T vs. G, adjusted OR = 1.50; 95% CI, 1.15-1.96). Stratified analyses revealed that CRC patients with the let-7 KRAS rs712 TT genotype were more likely to have clinical stage III or IV disease (OR = 3.29, 95% CI, 1.32-8.20) and distant metastasis (OR = 4.70, 95% CI, 1.81-12.25). These findings provide evidence that the let-7 KRAS rs712 polymorphism may play crucial roles in the etiology of CRC.

Angiotensin II type I receptor A1166C polymorphism increases the risk of pregnancy hypertensive disorders: Evidence from a meta-analysis.

Pregnancy hypertensive disorders (PHDs) are considered to be a multifactorial and multisystemic disorder with a genetic predisposition. Alterations in the renin-angiotensin system are considered to play a significant role in the pathogenesis of the PHDs. However, results from published studies on the association between the angiotensin II type-1 receptor (AT1R) A1166C (rs5186) gene polymorphism and the risk of PHDs are conflicting. The aim of this meta-analysis was to investigate whether an association exists between AT1R A1166C gene polymorphism and PHDs in epidemiologic studies. We searched the PubMed, China National Knowledge Infrastructure (CNKI), and Chinese Biomedicine Literature (CBM) databases from their inception to July 2012. A total of 18 case-control studies, including a total of 1635 cases and 1934 controls, were available for this analysis. A significantly positive correlation was observed between the C allele and the AC/CC genotypes with PHDs in an overall comparison. In the subgroup analysis by ethnicity, the results suggested that the C allele and the AC/CC genotypes were associated with risk of PHDs in Asians. Our findings indicate that the AT1R gene 1166C allele and the AC/CC genotypes were positively associated with the PHDs, especially in Asians. However, well-designed multicenter studies with a larger sample size should be conducted to confirm the results.

The TLR9 gene polymorphisms and the risk of cancer: evidence from a meta-analysis.

BACKGROUND: Growing studies have revealed the association between polymorphisms in the Toll-like receptor 9 (TLR9) and susceptibility to cancer, however, the results remained inconsistent. METHODOLOGY/PRINCIPAL FINDINGS: To assess the effect of three selected SNPs (rs352140, rs5743836 and rs187084) in TLR9 on cancer, we performed a meta-analysis based on 11 case-control studies, including a total of 6,585 cancer cases and 7,506 controls. Summary odds ratios (OR) and corresponding 95% confidence intervals (CIs) for polymorphisms in TLR9 and cancer risk were estimated. Our meta-analysis indicated that rs352140 was associated with an increased cancer risk, especially in Caucasian. However, no significantly increased cancer risk was detected to be associated with rs187084 and rs5743836 either the overall or subgroup estimation. CONCLUSIONS: These meta-analysis results indicate that polymorphisms in TLR9 may play a role in cancer development.

Association of angiotensin-converting enzyme insertion/deletion polymorphism (rs4646994) with the risk of primary intracerebral hemorrhage.

BACKGROUND: Evidence has suggested that angiotensin-converting enzyme (ACE) may be involved in the etiology of primary intracerebral hemorrhage (PICH), but the underlying association between ACE I/D (rs4646994) polymorphism and PICH risk is still ambiguous. This meta-analysis was performed to quantitatively summarize the evidence for such a relationship. METHODS: Eligible studies were identified by searching PubMed, EMBASE, CNKI (China National Knowledge Infrastructure), CBM (Chinese biomedical literature database), and WANFANG databases within a range of published years from 1990 to August 2012. The odds ratio (OR) corresponding to the 95% confidence interval (CI) was used to assess the different associations. RESULTS: A total of 28 studies with 2806 cases and 3612 controls were included in this meta-analysis. The pooled examination displayed an overall increased PICH risk associated with ACE I/D polymorphism in a recessive model (OR = 1.80, 95% CI = 1.39-2.33, P < 0.001 for DD versus ID/II), however, this association was only present in Asians (OR = 1.91, 95% CI = 1.45-2.51, P < 0.001) and not in Caucasians (OR = 1.16, 95% CI = 0.55-2.44, P = 0.69). Hypertensive intracerebral hemorrhage (HICH) had a much greater risk (OR = 4.26, 95% CI = 2.87-6.32, P < 0.001) than general PICH (OR = 1.65, 95% CI = 1.25-2.18, P < 0.001) in Asians, and subgroup with controls excluding hypertension had a greater risk (OR = 2.65, 95% CI = 1.78-3.95, P < 0.001) than that including hypertension (OR = 1.50, 95% CI = 1.12-2.02, P = 0.01). CONCLUSIONS: This meta-analysis suggests that DD homozygote of ACE I/D polymorphism has an increased PICH risk in Asians, and may have a synergistic effect with hypertension.

Lack of association between TNFα rs1800629 polymorphism and schizophrenia risk: a meta-analysis.

Evidence has suggested that tumour necrosis factor α (TNFα) may be involved in the aetiology of schizophrenia, but the underlying association between TNFα-308G/A polymorphism (rs1800629) and schizophrenia risk is still ambiguous. This meta-analysis was performed to quantitatively summarise the evidence for such a relationship. Eligible studies were identified by searching PubMed, EMBASE, CNKI (China National Knowledge Infrastructure), CBM (Chinese Biomedical Literature Database) and WANFANG databases within a range of published years from 1990 to July 2012. The odds ratio (OR) corresponding to the 95% confidence interval (CI) was used to assess the different associations. Twenty-one studies with 4340 cases and 5745 controls were included in this meta-analysis. The pooled examination displayed that there was no significant association between TNFα-308G/A polymorphism and susceptibility to schizophrenia overall (OR=1.047, 95% CI=0.876-1.253, P=0.614 for A vs. G), and no difference in Caucasian subgroup (OR=1.041, 95% CI=0.815-1.331, P=0.747) and Asian subgroup (OR=1.057, 95% CI=0.807-1.386, P=0.686). Lack of association was also found in males (OR=0.862, 95% CI=0.413-1.797, P=0.692) and females (OR=0.797, 95% CI=0.579-1.097, P=0.163) with a dominant model. Taken together, this meta-analysis suggests that TNFα-308G/A polymorphism may not be associated with schizophrenia susceptibility.

The expression of neuroglobin in astrocytoma.

Neuroglobin (NGB) is a characterized heme globin that is widely expressed in the vertebrate central and peripheral nervous system as well as retina and endocrine tissues. However, to date, it is not determined whether functional NGB is expressed in cells of glia origin. In this study, we aimed to explore the detailed expression of NGB in a rat astrocytoma cell line (C6) and human astrocytoma cell line (U251) by reverse transcription-polymerase chain reaction, immunofluorescence, and Western blotting, and to detect the expression of NGB in human astrocytoma tissues by an immunohistochemical method. We found that NGB was present in a rat astrocytoma cell line (C6), human astrocytoma cell line (U251), and human astrocytoma tissues. The expression and potential roles of NGB in astrocytomas may provide insight into the mechanisms of tumor cells to adapt and survive in hypoxic microenvironments and also represent a novel therapeutic approach to astrocytomas.

The association between MLH1 -93 G>A polymorphism of DNA mismatch repair and cancer susceptibility: a meta-analysis.

DNA mismatch repair, known as a fundamentally biological pathway, plays key roles in maintaining genomic stability, eliminating mismatch bases and preventing both mutagenesis in the short term and cancerogenesis in the long term. Polymorphisms of MLH1 in individuals may have an effect on the DNA repair capacity and therefore on cancer risk. Recently, emerging studies have been done to evaluate the association between MLH1 -93 G/A polymorphism and cancer risk in diverse populations. However, the results remain conflicting rather than conclusive. In this meta-analysis, we assessed reported studies of association between the MLH1 -93 G/A polymorphism and cancer risk including 13 691 cancer cases and 14 068 controls from 17 published studies. A borderline significant association between the MLH1 -93 G/A polymorphism and cancer risk was observed in overall analysis [heterozygote: odds ratio (OR) = 1.15; 95% confidence interval (CI) 1.05-1.26; homozygote: OR = 1.21; 95% CI, 1.04-1.40; dominant model: OR = 1.13; 95% CI 1.01-1.26; recessive model: OR = 1.21; 95% CI 1.07-1.35, respectively]. In subgroup analysis by ethnicity, significantly increased risks were found in Asian population and mixed population but not in Caucasian population. After stratified analysis according to the quality of literature, increased cancer risks were observed in the studies of lower quality but not in the studies of higher quality. Similarly, elevated cancer risks were observed in hospital-based studies but not in population-based studies. These findings showed no persuasive evidence that MLH1 -93 G/A polymorphism was associated with an increased risk of cancer. On the conservative standpoint, well-designed population-based studies with larger sample size in different ethnic groups should be performed to further confirm these results.

[Study on the distribution and location of neuroglobin in human tissues and cells].

OBJECTIVE: To explore the distribution and location of neuroglobin (NGB) and its function in human tissues and cells. METHODS: The distribution and localization of NGB in human tissues and cells were examined by immunohistochemical method. RESULTS: NGB-positive cells were mainly distributed in neurons of central nervous system and peripheral nervous system, and some in endocrine tissues and genital system. NGB-immunoreactive product located in the cytoplasm of these cells. CONCLUSION: The expression of NGB in human nervous tissues, some endocrine tissues and genital system suggested that NGB might play an important role in the utilizations of oxygen and physiological functions.

[The relationship of injury timing with the change of neuronal apoptosis and the expression of caspase-3 after brain contusion].

OBJECTIVE: To investigate and analyze the changes of neuronal-apoptosis and the expression of caspase-3 for finding out a new method of injury timing after brain contusion in human. METHODS: The tissue was stained by TUNEL for apoptosis and by immunohistochemistry for caspase-3. Image analysis technique was employed. RESULTS: The nerve cells stained positive by TUNEL and Caspase-3 immunohistochemistry were distributed in the penumbra and central area. Both these areas were in striking contrast with the distal area or those of control group. The positive staining was more prominente in penumbra area than in central area (P < 0.05). The changes of TUNEL staining and expression of Caspase-3 in penumbra area gradually increased with the survival period after injury; they were parallel to each other. There were linear relationships between the time of injury in 48 hours and the increase in the mean of integral optical density (IOD), the coefficient of correlation (r) being 0.93 and 0.69 for the two staining methods, and two linear regression formulae were induced, respectively. CONCLUSION: Observations on the increasing of neuronal apoptosis and Caspase-3 expression in relation with the survival period after injury could be utilized in the timing of brain contusion.