DLK1 promoted ischemic angiogenesis through notch1 signaling in endothelial progenitor cells.

Delta like non-canonical Notch ligand 1 (DLK1), as a member of epidermal growth factor-like family, plays a critical role in somatic growth, tissue development and possibly tissue renewal. Though previous studies had indicated that DLK1 contributed to adipogenesis and myogenesis, it's still controversial whether DLK1 affects angiogenesis and how it interacts with Notch signaling with numerous conflicting reports from different models. Based on our preliminary finding that DLK1 expression was up-regulated in mice ischemic gastrocnemius and in the border zone of infarcted myocardium, we administered either recombinant DLK1 (rDLK1) or PBS in C57BL/6 mice after establishment of hindlimb ischemia (HLI) and myocardial infarction (MI), respectively. Exogenous rDLK1 administration significantly improved both blood perfusion of mice ischemic hindlimbs and muscle motor function on the 3rd, 7th day after HLI, by promoting neovascularization. Similar effect on neovascularization was verified in mice on the 28th day after MI as well as improvement of cardiac failure. Correspondingly, the number of CD34+KDR+ cells, indicated as endothelial progenitor cells (EPCs), was significantly in mice ischemic gastrocnemius by rDLK1 administration, which was abrogated by DAPT as the specific inhibitor of Notch intracellular domain (NICD). Furthermore, bone marrow mononuclear cells were obtained from C57BL/6 mice and differentiated to EPCs ex vivo. Incubation with rDLK1 triggered Notch1 mRNA and NICD protein expressions in EPCs as exposed to hypoxia and serum deprivation, promoting EPCs proliferation, migration, anti-apoptosis and tube formation. Otherwise, rDLK1 incubation significantly decreased intracellular and mitochondrial reactive oxygen species, increased ATP content and mitochondrial membrane potential, downregulated short isoform of OPA-1 expression whereas upregulated mitofusin (-1, -2) expression in EPCs by Notch1 signaling, which were all abrogated by DAPT. In summary, the present study unveils the pro-angiogenesis and its mechanism of rDLK1 through activation of Notch1 signaling in endothelial progenitor cells.

PBL teaching in ultrasonography resident standardization training in the COVID-19 pandemic.

OBJECTIVE: To study the effect of the problem-based learning (PBL) method in ultrasonography (US) resident standardization training during the COVID-19 pandemic. METHODS: Fifty residents were divided into two groups to participate in a 30-day US training program. The residents in the observation group underwent PBL combined with the lecture-based learning (LBL) method, while the residents in the control group experienced the LBL method alone, with 25 residents in each group. A basic theoretical test, practical examination, and questionnaire were used to evaluate the teaching effect of the PBL + LBL method and the LBL method alone. RESULTS: The basic theoretical pretest score of the observation group was not significantly different from that of the control group. However, the posttest theoretical score and practical score were significantly higher in the observation group than in the control group (P < 0.01). The results of the questionnaire showed that the resident satisfaction level in the observation group with PBL combined with the LBL method was 96%, which was significantly higher than that of the control group with the LBL method alone (80%) (P < 0.05). CONCLUSION: The combination of PBL with the LBL method has obvious advantages over the LBL method alone in regard to the training of US residents during the COVID-19 pandemic.

Overexpression of four MiTFL1 genes from mango delays the flowering time in transgenic Arabidopsis.

BACKGROUND: TERMINAL FLOWER 1 (TFL1) belongs to the phosphatidylethanolamine-binding protein (PEBP) family, which is involved in inflorescence meristem development and represses flowering in several plant species. In the present study, four TFL1 genes were cloned from the mango (Mangifera indica L.) variety 'SiJiMi' and named MiTFL1-1, MiTFL1-2, MiTFL1-3 and MiTFL1-4. RESULTS: Sequence analysis showed that the encoded MiTFL1 proteins contained a conserved PEBP domain and belonged to the TFL1 group. Expression analysis showed that the MiTFL1 genes were expressed in not only vegetative organs but also reproductive organs and that the expression levels were related to floral development. Overexpression of the four MiTFL1 genes delayed flowering in transgenic Arabidopsis. Additionally, MiTFL1-1 and MiTFL1-3 changed the flower morphology in some transgenic plants. Yeast two-hybrid (Y2H) analysis showed that several stress-related proteins interacted with MiTFL1 proteins. CONCLUSIONS: The four MiTFL1 genes exhibited a similar expression pattern, and overexpression in Arabidopsis resulted in delayed flowering. Additionally, MiTFL1-1 and MiTFL1-3 overexpression affected floral organ development. Furthermore, the MiTFL1 proteins could interact with bHLH and 14-3-3 proteins. These results indicate that the MiTFL1 genes may play an important role in the flowering process in mango.

Ectopic thyroid tissue: An unusual cause of intracardiac mass.

Intracardiac ectopic thyroid tissue is an extremely rare condition, with only 37 cases reported in the English literature. We present a case of intracardiac ectopic thyroid adenoma and briefly review the published reports.

Insight into the Pro-inflammatory and Profibrotic Role of Macrophage in Heart Failure With Preserved Ejection Fraction.

The prevalence of heart failure (HF) with preserved ejection fraction (HFpEF) is higher than that of HF with reduced/midrange ejection fraction (HFrEF/HFmrEF). However, no evidence-based guidelines for managing HFpEF have been generated. The current body of knowledge indicates that fibrosis and inflammation are important components of the cardiac remodeling process in HFpEF. In addition, macrophages potentially play an important role in pro-inflammatory and profibrotic processes in HFpEF patients, whereas HFpEF comorbidities could be a driving force for systemic microvascular inflammation and endothelial dysfunction. Under such circumstances, macrophages reportedly contribute to inflammation and fibrosis through 3 phases namely, inflammation, repair, and resolution. Signal transduction pathway-targeted therapies using animal experiments have generated important discoveries and breakthroughs for understanding the underlying mechanisms of HFpEF. However, only a handful of studies have reported promising results using human trials. Further investigations are therefore needed to elucidate the exact mechanisms underlying HFpEF and immune-pathogenesis of cardiac fibrosis.

Ginkgo biloba extracts prevent aortic rupture in angiotensin II-infused hypercholesterolemic mice.

Abdominal aortic aneurysms (AAAs) are a chronic vascular disease characterized by pathological luminal dilation. Aortic rupture is the fatal consequence of AAAs. Ginkgo biloba extracts (GBEs), a natural herb extract widely used as food supplements, drugs, and cosmetics, has been reported to suppress development of calcium chloride-induced AAAs in mice. Calcium chloride-induced AAAs do not rupture, while angiotensin II (AngII)-induced AAAs in mice have high rate of aortic rupture, implicating potentially different mechanisms from calcium chloride-induced AAAs. This study aimed to determine whether GBE would improve aortic dilation and rupture rate of AngII-induced AAAs. Male apolipoprotein E (apoE) -/- mice were infused with AngII and administered either GBE or its major active ingredients, flavonoids and ginkgolides, individually or in combination. To determine the effects of GBE in mice with established AAAs, male apoE-/- mice were firstly infused with AngII for 28 days to develop AAAs, and then administered either GBE or vehicle in mice with established AAAs, which were continuously infused with AngII for another 56 days. GBE, but not the two major active components separately or synergistically, prevented aortic rupture, but not aortic dilation. The protection of GBE from aortic rupture was independent of systolic blood pressure, lipid, and inflammation. GBE also did not attenuate either aortic rupture or progressive aortic dilation in mice with established AAAs. GBE did not reduce the atherosclerotic lesion areas, either. In conclusion, GBE prevents aortic rupture in AngII-infused hypercholesterolemic mice, but only in the early phase of the disease development.

Triterpenoid Saponins from Anemone rivularis var. Flore-Minore and Their Anti-Proliferative Activity on HSC-T6 Cells.

Five previously undescribed triterpenoid saponins (1-5), along with eight known ones (6-13), were isolated from the whole plants of Anemone rivularis var. flore-minore. Their structures were clarified by extensive spectroscopic data and chemical evidence. For the first time, the lupane-type saponins (3 and 12) were reported from the Anemone genus. The anti-proliferative activity of all isolated saponins was evaluated on hepatic stellate cells (HSC-T6). Saponins 12 and 13, which possess more monosaccharides than the others, displayed potent anti-proliferative activity, with IC50 values of 18.21 and 15.56 µM, respectively.

Study on the biodegradation characteristics and mechanism of tetracycline by Serratia entomophila TC-1.

Microbial degradation is an important solution for antibiotic pollution in livestock and poultry farming wastes. This study reports the isolation and identification of the novel bacterial strain Serratia entomophila TC-1, which can degrade 87.8 % of 200 mg/L tetracycline (TC) at 35 °C, pH 6.0, and an inoculation amount of 1 % (v/v). Based on the intermediate products, a possible biological transformation pathway was proposed, including dehydration, oxidation ring opening, decarbonylation, and deamination. Using Escherichia coli and Bacillus subtilis as biological indicators, TC degraded metabolites have shown low toxicity. Whole-genome sequencing showed that the TC-1 strain contained tet (d) and tet (34), which resist TC through multiple mechanisms. In addition, upon TC exposure, TC-1 participated in catalytic and energy supply activities by regulating gene expression, thereby playing a role in TC detoxification. We found that TC-1 showed less interference with changes in the bacterial community in swine wastewater. Thus, TC-1 provided new insights into the mechanisms responsible for TC biodegradation and can be used for TC pollution treatment.

Epicardial fat in patients with metabolic syndrome: A systematic review and meta-analysis.

PURPOSE: Abnormally increased epicardial fat appears to be associated with an additional risk of major adverse cardiovascular events (MACEs) in the context of metabolic syndrome (MetS). However, evidence on the relationship between epicardial fat volumes (EFVs), epicardial fat thickness (EFT) and MetS remains inconsistent. METHODS: Specific searches of electronic databases from 1 January 2000 to 31 October 2022 were independently performed by two researchers. In this study, two quantification measures of epicardial fat were included: comparison of total computed tomography-based EFVs and EFT between two groups (individuals with and without MetS), estimating standardized mean difference (SMD) with corresponding 95 % confidence intervals (CIs) through a random-effects model analysis. The heterogeneity in the included studies was explored by meta-regression and subgroup analyses. RESULTS: The EFVs were significantly increased in MetS subjects compared with non-MetS subjects (SMD: 1.07, 95 % CI: 0.69-1.45, p < 0.001), and the EFT was also significantly larger in MetS patients than in the Non-MetS (SMD: 1.12, 95 % CI: 0.84-1.41, p < 0.001). We compared the Caucasian and American subgroups with the Asian and African subgroups, and the EFT was greater in the former subgroups (SMD: 1.32, 95 % CI: 0.44-2.20, p < 0.001). When comparing the EFT among the age subgroups, there was a significant SMD between adolescents and adults or elderly individuals (SMD: 1.21, 95 % CI: 0.84-1.52, p < 0.001). CONCLUSIONS: MetS patients tend to present greater EFT near the right ventricular free wall and greater total EFVs. Increased epicardial fat, an imaging biomarker, independently affects the onset of MetS.

A dual bacterial alliance removed erythromycin residues by immobilizing on activated carbon.

Removing erythromycin from the environment is a major challenge. In this study, a dual microbial consortium (Delftia acidovorans ERY-6A and Chryseobacterium indologenes ERY-6B) capable of degrading erythromycin was isolated, and the erythromycin biodegradation products were studied. Coconut shell activated carbon was modified and its adsorption characteristics and erythromycin removal efficiency of the immobilized cells were studied. It was indicated that alkali-modified and water-modified coconut shell activated carbon and the dual bacterial system had excellent erythromycin removal ability. The dual bacterial system follows a new biodegradation pathway to degrade erythromycin. The immobilized cells removed 95% of erythromycin at a concentration of 100 mg L-1 within 24 h through pore adsorption, surface complexation, hydrogen bonding, and biodegradation. This study provides a new erythromycin removal agent and for the first time describes the genomic information of erythromycin-degrading bacteria, providing new clues regarding bacterial cooperation and efficient erythromycin removal.

Construction and application of highly efficient waste cooking oil degrading bacteria consortium in oily wastewater.

The treatment of cooking oil wastewater is an urgent issue need to be solved. We aimed to screen for efficient oil-degrading bacteria and develop a new microbial agent for degrading waste cooking oil in oily wastewater. Three extremely effective oil-degrading bacteria, known as YZQ-1, YZQ-3, and YZQ-4, were found by the enrichment and acclimation of samples from various sources and separation using oil degradation plates. The 16S rRNA sequencing analysis and phylogenetic tree construction showed that the three strains were Bacillus tropicus, Pseudomonas multiresinivorans, and Raoultella terrigena. Under optimal degradation conditions, the maximal degradation rates were 67.30 ± 3.69%, 89.65 ± 1.08%, and 79.60 ± 5.30%, respectively, for YZQ-1, YZQ-3, and YZQ-4. Lipase activity was highest for YZQ-3, reaching 94.82 ± 12.89 U/L. The best bacterial alliance was obtained by adding equal numbers of microbial cells from the three strains. Moreover, when this bacterial alliance was applied to oily wastewater, the degradation rate of waste cooking oil was 61.13 ± 7.30% (3.67% ± 2.13% in the control group), and COD removal was 62.4% ± 5.65% (55.60% ± 0.71% in the control group) in 72 h. Microbial community analysis results showed YZQ-1 and YZQ-3 were adaptable to wastewater and could coexist with local bacteria, whereas YZQ-4 could not survive in wastewater. Therefore, the combination of YZQ-1 and YZQ-3 can efficiently degrade oil and shows great potential for oily wastewater treatment.

Ectopic expression of two CAULIFLOWER genes from mango caused early flowering in Arabidopsis.

APETALA1 (AP1), CAULIFLOWER (CAL) and FRUITFULL (FUL) were homologous genes with redundant functions in the process of flower transformation and floral development in Arabidopsis. Two CALs genes, MiCAL1 and MiCAL2, were cloned from mango (Mangifera indica L.). Their full-length sequences contained 717 bp and 714 bp, encoding 239 and 238 amino acids, respectively. Both the MiCAL1 and MiCAL2 proteins contained typical MADS-box and K-box domains and therefore belonged to the CAL-like protein family. MiCAL1 and MiCAL2 were expressed in all tissues at the inflorescence elongation stage and flowering stage, with the highest expression in the leaves at the flowering stage. They had similar expression patterns during flower development, with the highest expression levels in leaves during flower differentiation and the lowest expression levels during fruit development. Overexpression of MiCAL1 and MiCAL2 resulted in significantly earlier flowering in Arabidopsis. Overexpression of MiCAL1 resulted in terminal flowers with normal flower organs, while overexpression of MiCAL2 induced partially variation in floral organs but had no effect on inflorescences. Yeast two-hybrid (Y2H) experiments showed that MiCAL1 and MiCAL2 can interact with several flower-related proteins as well as stress response proteins, such as SEP1, SVP1, SVP2, SOC1G and Di19-4. These results suggest that these two MiCALs genes may have an important influence on mango flowering.

Nerve growth factor induces cord formation of mesenchymal stem cell by promoting proliferation and activating the PI3K/Akt signaling pathway.

AIM: To investigate whether nerve growth factor (NGF) induced angiogenesis of bone marrow mesenchymal stem cells (MSCs) and the underlying mechanisms. METHODS: Bone marrow MSCs were isolated from femors or tibias of Sprague-Dawley rat, and cultured. The cells were purified after 3 to 5 passages, seeded on Matrigel-coated 24-well plates and treated with NGF. Tube formation was observed 24 h later. Tropomyosin-related kinase A (TrkA) and p75NTR gene expression was examined using PCR analysis and flow cytometry. Growth curves were determined via cell counting. Expression of VEGF and pAkt/Akt were analyzed with Western blot. RESULTS: NGF (25, 50, 100 and 200 µg/L) promoted tube formation of MSCs. The tubular length reached the maximum of a 2.24-fold increase, when the cells were treated with NGF (50 µg/L). NGF (50 µg/L) significantly enhanced Akt phosphorylation. Pretreatment with the specific PI3K inhibitor LY294002 (10 µmol/L) blocked NGF-stimulated Akt phosphorylation, tube formation and angiogenesis. NGF (25-200 µg/L) did not affect the expression of TrkA and vascular endothelial growth factor (VEGF), but significantly suppressed the expression of p75NTR. NGF (50 µg/L) markedly increased the proliferation of MSCs. CONCLUSION: NGF promoted proliferation of MSCs and activated the PI3K/Akt signaling pathway, which may be responsible for NGF induction of MSC angiogenesis.

Development of unenhanced CT-based imaging signature for BAP1 mutation status prediction in malignant pleural mesothelioma: Consideration of 2D and 3D segmentation.

OBJECTIVES: We aimed to explore the feasibility of 2D and 3D radiomics signature based on the unenhanced computed tomography (CT) images to predict BRCA1-associated protein 1 (BAP1) gene mutation status for malignant pleural mesothelioma (MPM) patients. MATERIALS AND METHODS: 74 patients with MPM were retrospectively enrolled (22 mutant BAP1, 52 wild-type BAP1 demonstrated by Sanger sequencing). The radiomic features were extracted respectively from the 2D and 3D segmentation of unenhanced pre-treatment CT images, and the dataset was randomly divided into training (n = 51) and test (n = 23) sets for radiomics model development and internal validation. The synthetic minority over-sampling technique (SMOTE) was used for data balancing in the training set. 2D or 3D features were sequentially selected by ICC > 0.8, correlation analysis (cut-value 0.7), univariate analysis or univariate logistic regression (LR), which were involved into multivariate LR for LR model construction. Following the comparison of the 2D and 3D models by the ROC analysis and Delong test for AUC, the calibration and clinical utility of 2D and 3D models were evaluated. RESULTS: 3D radiomic features showed better ICCs compared with 2D in both intra- (P < 0.001) and inter-observer (P < 0.001) analysis. 3D radiomic model based on selected features developed from a balanced training dataset presented a favorable predictive performance with AUC of 0.786 and 0.768 in the training and test sets, respectively. The predictive performance of 3D model was superior to 2D model (1 feature) both in the training (AUC 0.786 vs. 0.683, P = 0.036) and the test (AUC 0.768 vs.0.652, P = 0.441) set. The calibration curve and decision curves also indicate a better BAP1 prediction performance and clinical benefit for 3D model than that of 2D model. CONCLUSION: The developed unenhanced CT-based 3D radiomics signature is potential as a noninvasive marker for predicting BAP1 mutation status.

Isolation and functional characterization of three MiFTs genes from mango.

FLOWERING LOCUS T (FT) is a key integrator of environmental signals and internal cues and plays a central role in the photoperiod response mechanism in Arabidopsis. However, the function of FTs in Mangifera indica L. is unknown. In this study, we identified three MiFTs genes from mango and characterized their role in flowering regulation. The open reading frames of MiFT1, MiFT2, and MiFT3 are 540, 516, and 588 bp in length and encode 180, 172, and 196 amino acids, respectively; the genes belong to the PEBP family. MiFTs share the conserved exon/intron structure of FTs. The nucleotide sequence of MiFT1 is 90% identical to that of MiFT2 and 82% identical to that of MiFT3; MiFT2 and MiFT3 share 81% homology with each other. According to expression analysis, MiFTs were detected at different expression levels in all tested tissues. The expression levels of the three MiFTs were significantly different in leaves during flower development, and MiFT1 expression increased sharply in leaves and was significantly higher than that of the other two MiFTs during flower bud development. All three MiFTs showed daily cycles. Ectopic expression of the three MiFTs in transgenic Arabidopsis resulted in an earlier flowering genotype under long-day conditions, and MiFT1 had the strongest effect in promoting flowering. Additionally, overexpression of three MiFTs in Arabidopsis upregulated the expression levels of several flowering-related genes. Our results suggest that the three MiFTs have positive roles in promoting flowering and suggest that MiFT1 may acts as a key regulator in the flowering pathway.

Extracellular matrix metalloproteinase inducer (EMMPRIN) is present in smooth muscle cells of human aneurysmal aorta and is induced by angiotensin II in vitro.

The aim of the present study was to determine whether EMMPRIN (extracellular matrix metalloproteinase inducer) is present and is up-regulated in human aneurysmal aortas, and to assess a possible association with AngII (angiotensin II)-induced aneurysm formation. The presence of EMMPRIN was assessed in 41 surgical specimens from patients with a TAA (thoracic aortic aneurysm) (Type A aortic dissection, n=12; Type B aortic dissection, n=7; and TAA without dissection, n=7) or an AAA (abdominal aortic aneurysm, n=15) by immunohistochemistry. EMMPRIN expression in aortic aneurysm tissues was compared with 12 aortas obtained during autopsy (free of any vascular diseases), and scored for both staining intensity and the percentage of vascular cells stained. EMMPRIN protein levels in cultured human aortic SMCs (smooth muscle cells) following stimulation of AngII were analysed by Western blotting. Significant EMMPRIN immunoreactivity was detected in aortic aneurysm lesions from patients with TAAs and AAAs. In the aneurysmal wall, alpha-actin-positive SMCs were the main source of EMMPRIN. The frequency of EMMPRIN overexpression was significantly higher (P=0.026) in TAAs with dissection (68.4%) than TAAs without dissection (14.3%). AngII stimulation up-regulated the expression of EMMPIRN in cultured human aortic SMCs, which was suppressed by the addition of the AT1R (AngII type 1 receptor) antagonist losartan. In conclusion, the present study is the first to report the expression of EMMPRIN in aortic aneurysmal diseases, and we speculate that EMMPRIN may be important in the pathogenesis of these diseases. Whether these abnormalities are potential therapeutic targets deserve further investigation.

Diabetes mellitus: is it protective against aortic root dilatation?

OBJECTIVES: There is evidence of a negative association between diabetes and both abdominal aortic aneurysm and aortic diameter. However, little information is available on the relation between diabetes and aortic root diameter. METHODS: We studied 109 patients with type 2 diabetes. Two-dimensional echocardiography was used to measure the aortic root at the aortic annulus, the sinus of Valsalva, the sinotubular junction and the proximal part of the ascending aorta. Measured mean values were compared with 218 age- and sex-matched patients without diabetes. A comparison of the prevalence of aortic regurgitation between the 2 groups was also performed. RESULTS: In patients with diabetes, the mean aortic root dimensions were significantly smaller than in nondiabetic patients (p < 0.05). The prevalence of aortic root dilatation was significantly higher in nondiabetic subjects than in patients with diabetes (9.63 vs. 2.75%; p = 0.025). In the multivariable regression model, diabetes was a significant negative determinant of aortic root size at all measured sites. The prevalence of aortic regurgitation tended to be higher in nondiabetic subjects than in diabetic participants (11 vs. 18.8%); however, the difference did not achieve statistical significance (p = 0.071). CONCLUSIONS: In patients with diabetes, the aortic root dimension is significantly smaller than in patients without diabetes.

Green tea polyphenols attenuate hepatic steatosis, and reduce insulin resistance and inflammation in high-fat diet-induced rats.

Non­alcoholic fatty liver disease (NAFLD) is characterized by hepatic steatosis, insulin resistance and inflammation; however, the exact pathogenesis of NAFLD is not fully understood. Green tea polyphenols (GTP) exhibit beneficial effects against metabolic syndrome. However, the effect of GTP on NAFLD remains largely unknown. The aim of the present study was to investigate the effects of GTP on NAFLD in high­fat diet (HFD)­induced rats. The NAFLD rat model was induced with a HFD for 8 weeks. A total of 30 adult male Sprague Dawley rats were randomly divided into three groups: i) Normal control group; ii) HFD group; and iii) HFD with GTP group. Hematoxylin and eosin and Oil Red O analyses were performed. The levels of alanine aminotransferase (ALT), aspartate amino-transferase (AST) and inflammatory cytokines in the serum, as well as oxidative stress markers and hepatic lipids in the liver were measured. In addition, parameters associated with glucose metabolism were also assessed. Western blotting and RT­qPCR were used to determine the expression levels of 5' adenosine monophosphate­activated protein kinase (AMPK). HFD­induced rats exhibited features associated with NAFLD. GTP intervention significantly reduced serum ALT and AST levels. Fasting serum glucose, insulin resistance and hepatic lipid levels were all decreased in the GTP­treated rats. GTP also significantly decreased the levels of TNF­α, IL­6 and malondialdehyde. In contrast, superoxide dismutase levels were increased in the liver. Furthermore, GTP also significantly increased phosphorylation of AMPK and attenuated histopathological changes indicative of injury in liver tissue. GTP has a protective effect on HFD­induced hepatic steatosis, insulin resistance and inflammation, and the underlying mechanism may involve the AMPK pathway.

Nanoscale Zero-Valent Iron and Chitosan Functionalized Eichhornia crassipes Biochar for Efficient Hexavalent Chromium Removal.

Sorption is widely used for the removal of toxic heavy metals such as hexavalent chromium (Cr(VI)) from aqueous solutions. Green sorbents prepared from biomass are attractive, because they leverage the value of waste biomass and reduce the overall cost of water treatment. In this study, we fabricated biochar (BC) adsorbent from the biomass of water hyacinth (Eichhornia crassipes), an invasive species in many river channels. Pristine BC was further modified with nanoscale zero-valent iron (nZVI) and stabilized with chitosan (C) to form C-nZVI-BC. C-nZVI-BC adsorbent showed high hexavalent chromium sorption capacity (82.2 mg/g) at pH 2 and removed 97.34% of 50 mg/L Cr(VI) from aqueous solutions. The sorption capacity of chitosan-nZVI-modified biochar decreased while increasing the solution pH value and ionic strength. The results of a sorption test indicated that multiple mechanisms accounted for Cr(VI) removal by C-nZVI-BC, including complexation, precipitation, electrostatic interactions, and reduction. Our study suggests a way of adding value to biomass waste by considering environmental treatment purposes.

Bone marrow mesenchymal stem cell transplantation combined with perindopril treatment attenuates infarction remodelling in a rat model of acute myocardial infarction.

OBJECTIVE: This study was performed to evaluate whether implantation of mesenchymal stem cell (MSC) would reduce left ventricular remodelling from the molecular mechanisms compared with angiotensin-converting enzyme inhibitors (ACEIs) perindopril into ischemic myocardium after acute myocardial infarction. METHODS: Forty rats were divided into four groups: control, MSC, ACEI, MSC+ACEI groups. Bone marrow stem cell derived rat was injected immediately into a zone made ischemic by coronary artery ligation in MSC group and MSC+ACEI group. Phosphate-buffered saline (PBS) was injected into control group. Perindopril was administered p.o. to ACEI group and MSC+ACEI group. Six weeks after implantation, the rats were killed and heart sample was collected. Fibrillar collagen was observed by meliorative Masson's trichome stain. Western Blotting was employed to evaluate the protein expression of matrix metalloproteinase (MMP)-2, matrix metalloproteinase (MMP)-9 in infarction zone. The transcriptional level of MMP2, MMP9 and tissue inhibitor of matrix metalloproteinase (TIMP)-1 in infarction area was detected by reverse transcriptase PCR (RT-PCR) analysis. RESULTS: The fibrillar collagen area, the protein expression of MMP2, MMP9 and the transcriptional level of MMP2, MMP9 mRNA in infarction zone reduced in MSC group, ACEI group, and MSC+ACEI group. No significant difference was detected in the expression of TIMP1 mRNA among the 4 groups. CONCLUSION: Both MSC and ACEI could reduce infarction remodelling by altering collagen metabolism.