Conditional knockout of ITGB4 in bronchial epithelial cells directs bronchopulmonary dysplasia.

Neonatal respiratory system disease is closely associated with embryonic lung development. Our group found that integrin ß4 (ITGB4) is downregulated in the airway epithelium of asthma patients. Asthma is the most common chronic respiratory illness in childhood. Therefore, we suspect whether the deletion of ITGB4 would affect fetal lung development. In this study, we characterized the role of ITGB4 deficiency in bronchopulmonary dysplasia (BPD). ITGB4 was conditionally knocked out in CCSP-rtTA, Tet-O-Cre and ITGB4f/f triple transgenic mice. Lung tissues at different developmental stages were collected for experimental detection and transcriptome sequencing. The effects of ITGB4 deficiency on lung branching morphogenesis were observed by fetal mouse lung explant culture. Deleting ITGB4 from the airway epithelial cells results in enlargement of alveolar airspaces, inhibition of branching, the abnormal structure of epithelium cells and the impairment of cilia growth during lung development. Scanning electron microscopy showed that the airway epithelial cilia of the ß4ccsp.cre group appear to be sparse, shortened and lodging. Lung-development-relevant factors such as SftpC and SOX2 significantly decreased both mRNA and protein levels. KEGG pathway analysis indicated that multiple ontogenesis-regulating-relevant pathways converge to FAK. Accordingly, ITGB4 deletion decreased phospho-FAK, phospho-GSK3ß and SOX2 levels, and the correspondingly contrary consequence was detected after treatment with GSK3ß agonist (wortmannin). Airway branching defect of ß4ccsp.cre mice lung explants was also partly recovered after wortmannin treatment. Airway epithelial-specific deletion of ITGB4 contributes to lung developmental defect, which could be achieved through the FAK/GSK3ß/SOX2 signal pathway.

[Research progress of lung aging in chronic respiratory diseases].

Cell aging is an extremely complex process, which is characterized by mitochondrial structural dysfunction, telomere shortening, inflammatory microenvironment, protein homeostasis imbalance, epigenetic changes, abnormal DNA damage and repair, etc. Aging is usually accompanied by structural and functional damage of tissues and organs which further induces the occurrence and development of aging-related diseases. Aging includes physiological aging caused by increased age and pathological aging induced by a variety of factors. Noteworthy, as a target organ directly contacting with the outside air, lung is more prone to various stimuli, causing pathological premature aging which is lung aging. Studies have found that there is a certain proportion of senescent cells in the lungs of most chronic respiratory diseases. However, the underlying mechanism by which these senescent cells induce lung senescence and their role in chronic respiratory diseases is still obscure. This paper focuses on the causes and classification of lung aging, the internal mechanism of lung aging involved in chronic respiratory diseases, and the application of anti-aging treatments in chronic respiratory diseases. We hope to provide new research ideas and theoretical basis for the clinical prevention and treatment in chronic respiratory diseases.

Airway epithelial integrin ß4-deficiency exacerbates lipopolysaccharide-induced acute lung injury.

Airway epithelial cells, the first barrier of the respiratory tract, play an indispensable role in innate immunity. Integrin ß4 (ITGB4) is a structural adhesion molecule that is involved in the pathological progression of acute inflammatory diseases and is downregulated in asthmatic patients. Research has shown that endothelial ITGB4 has proinflammatory properties in acute lung injury (ALI). However, the role of epithelial ITGB4 in a murine ALI model is still unknown. This study investigated the role of ITGB4 in lipopolysaccharide (LPS)-induced ALI. We found that ITGB4 in the airway epithelium had remarkably increased after the introduction of LPS in vivo and in vitro. Then, we constructed airway epithelial cell-specific ITGB4 knockout (ITGB4-/- ) mice to study its role in ALI. At a time point of 12 h after the tracheal injection of LPS, ITGB4-/- mice showed increased macrophages (mainly M1-type macrophages) and neutrophil infiltration into the lungs; inflammation-related proteins including interleukin (IL)-6, tumor necrosis factor, and IL-17A were significantly elevated compared to their levels in ITGB4+/+ mice. Furthermore, we investigated the role of ITGB4 in the anti-inflammatory response. Intriguingly, in the ITGB4-/- + LPS group, we found significantly reduced expression of anti-inflammatory factors, including IL-10 messenger RNA (mRNA) and ARG-1 mRNA. We also observed that monocyte chemotactic protein (MCP-1) increased significantly both in vivo and in vitro. Airway epithelium activates macrophages, most likely driven by MCP-1, which we confirmed in the coculture of epithelia and macrophages. These phenomena indicate that ITGB4 in airway epithelial cells plays an important role in the process of inflammation and activation of macrophages in ALI. Overall, these data demonstrated a novel link between airway epithelial ITGB4 and the inflammatory response in LPS-induced ALI.

[Research progress of respiratory syncytial virus (RSV) infection and respiratory diseases in infancy].

Lower respiratory tract infection (LRTI) induced by respiratory syncytial virus (RSV) is an important cause of hospitalization for infants. Compared with adults, infants are more likely to cause serious respiratory diseases after RSV infection due to the specific immature airway structure and immune system. The balance of immune resistance and immune tolerance of the host is critical to effective virus clearance and disease control. This paper reviews the relationship between RSV infection and respiratory diseases in infancy, the influence factors of the high pathogenicity of RSV infection in early life, as well as the research progress of anti-RSV therapy, and expands the specific molecular events regulating immune resistance and immune tolerance. We expect to present new ideas for the prevention and treatment of RSV-related respiratory diseases in clinical practice.

[Progress of epithelial-mesenchymal transition in respiratory system and the modulatory mechanism of cell adhesion].

Epithelial-mesenchymal transition (EMT) plays an important role in the development and pathogenesis of respiratory system. Epithelial cells are characterized by well-developed, intercellular contacts, whereas EMT triggers the sequential destabilization of cell-cell adhesive junctions. The dynamic remodeling of the epithelial cell adhesion molecules is important for maintaining the integrity and normal function of epithelium. This paper reviews the research progress of EMT in lung development, lung injury repair and chronic lung diseases, and summarizes the effect of cell junctions and cell adhesion molecules on EMT molecular events.

[The research progress of integrin ß4].

Integrin is a transmembrane receptor that mediates the connection between cells and their external environment, such as extracellular matrix (ECM). Integrin ß4 (ITGß4) plays a number of functions due to its special structures: forms α6ß4 with ITGα6 subunit and participates in the formation of hemidesmosomes; mediates cell-to-cell matrix interaction and cell-to-cell interaction, cell proliferation and survival, as well as migration and invasion. Also, ITGß4 participates in various disease processes by activating multiple signaling pathways. In this paper, the structure, physiological function and function of ITGß4 in respiratory system, tumor, nervous system and other related diseases will be reviewed.

Bombesin Receptor-Activated Protein (BRAP) Modulates NF-κB Activation in Bronchial Epithelial Cells by Enhancing HDAC Activity.

Our previous studies provided evidence that bombesin receptor-activated protein (BRAP), encoded by C6ORF89, is widely expressed in human airway epithelial cells and may play a role in the stress response of lung epithelia. In this study, we demonstrated that BRAP has a regulatory effect on NF-κB transcriptional activity in cultured human bronchial epithelial cells (HBECs). BRAP overexpression by gene transfer inhibited both basal and inducible NF-κB transcriptional activity in HBECs, whereas BRAP knockdown had the opposite effect. BRAP was shown to regulate NF-κB activity by enhancing histone deacetylase (HDAC) activity. In addition, BRAP might increase HDAC activity that leads to NF-κB activation via its putative C-terminal domain. Our study suggests that the BRAP protein is an important regulator of immune and inflammatory responses in the human airway epithelium.

[Allergens-induced sensitization alters airway epithelial adhesion molecules expression in mice].

To explore the relationship between the epithelial adhesion molecules and immune responses of airway epithelium, we observed the expression of integrin ß4 and intercellular adhesion molecule-1 (ICAM-1) in the mice airway epithelium after sensitization with allergens. BALB/c mice were sensitized with intraperitoneal injection of ovalbumin (OVA) or house dust mite (HDM) and then developed airway hyper-responsiveness as determined by barometric whole-body plethysmography. Both OVA and HDM sensitization led to increases of the number of peripheral leukocytes as well as inflammatory cells infiltration in lungs. OVA sensitized mice showed more severe inflammatory cells infiltration than HDM sensitized mice. Immunohistochemistry analysis of mice lung tissues revealed that sensitization with both allergens also led to a decrease of integrin ß4 expression and an increase of ICAM-1 expression in airway epithelia. OVA sensitized mice showed a more significant increase of ICAM-1 expression compared with HDM sensitized mice. siRNA mediated silencing of integrin ß4 gene in 16HBE cells resulted in an up-regulation of ICAM-1 expression. Our results indicate a possible role of airway epithelial adhesion molecules in allergen-induced airway immune responses.

Role of bombesin receptor activated protein in the antigen presentation by human bronchial epithelial cells.

Bombesin receptor activated protein (BRAP) was identified in a bacterial two-hybrid screen for proteins interacting with bombesin receptor subtype-3 (BRS-3). We found that BRAP is widely expressed in the airway epithelium of human lungs and may play a role during the stress response of lung epithelium. In this work, we explored the potential roles of BRAP in the antigen presenting function of human bronchial epithelial cells (HBECs). Overexpression of a BRAP recombinant protein in a human bronchial epithelial cell line resulted in a reduction of FITC-OVA uptake by HBECs, which indicated that the antigen uptake ability is inhibited. The analysis of the protein expression of surface molecules including B7 homologs and the major histocompactability complex (MHC) class II molecules showed that the expression levels of HLA-DR and B7DC increased while the levels of B7-H1 and B7.2 decreased. Since those surface molecules are all related to antigen presenting process, the altered expression pattern of those molecules provides further evidence showing that BRAP overexpression leads to a change in antigen presenting function of HBECs. Moreover, overexpression of BRAP in HBECs caused a decrease of co-cultured lymphocytes proliferation and a changed pattern of cytokines produced by lymphocytes in the presence of FITC-OVA, which indicated that changes in the maturation pattern and functions of co-cultured lymphocytes were induced by BRAP overexpression. Overall, our results suggested that overexpression of BRAP may play a role during the antigen presenting process of bronchial epithelium by inhibiting the antigen uptake ability of bronchial epithelial cells.

Nonstructural protein-1 of respiratory syncytial virus regulates HOX gene expression through interacting with histone.

Human respiratory syncytial virus (RSV), a major cause of severe respiratory diseases, constitutes an important risk factor for the development of subsequent asthma. In searching for its mechanism, the present study was designed to screen the interacting proteins of two important nonstructural (NS) proteins in human BECs. The subcellular localization and the effects of NS on HOX gene expression were also examined. The results showed that NS1 was distributed throughout the nucleus and cytoplasm, while NS2 was mainly distributed in cytoplasm of BECs. NS1 interacted specifically with host histone H2BD, inducing histone ubiquitination and subsequent HOX gene expression. In conclusion, the results of the present study indicated that RSV NS-1 induces HOX gene expression, through histone ubiquitination in a BEC cell line, which may provide a novel conception for understanding the relationship between severe RSV bronchiolitis during early life and the development of subsequent asthma.

[Heavy Metal Pollution and Health Risk Assessment in Karst Basin Around a Lead-Zinc Mine].

Water quality is one of the most important environmental issues in the sustainable development of karst areas. To investigate heavy metal pollution and assess health risk in karst water basins around mines, 18 groups of water samples were collected from the river and groundwater in the Sidi River karst basin, and the concentrations of nine types of heavy metals(Cu, Pb, Zn, Cd, Mn, Fe, As, Cr, and Sr) were determined. Sample data were analyzed using principal component analysis, correlation analysis, water quality index, the Nemerow comprehensive pollution index, hazard quotient, and hazard index. The results showed that the Sidi River was slightly alkaline. The farther the river water samples were from the tailings reservoir, the lower were the concentrations of Cu, Pb, Zn, Cd, Mn, Fe, As, and Sr in the river water. Principal component and correlation analyses showed that heavy metals in the Sidi River karst basin mainly came from mine discharge(55.42%), carbonate weathering dissolution(21.41%), and human activities(14.72%). Eighty-two percent of the samples in the river and all the samples in the groundwater were excellent water. The Nemerow comprehensive pollution index in the river was 4.12 with strong pollution. All the hazard indices were below 1, and Pb, Zn, As, Cd, and Cr were potentially threatening metals in the Sidi River karst basin. The concentration of heavy metals changed significantly after entering the karst conduit, indicating that the unique properties of the karst aquifer affected the spatial variation of the heavy metal concentration. The results of this study can provide data reference for water resource prevention and human health protection in the Sidi River karst basin and similar karst basins.

Dissolved Heavy Metal Pollution and Assessment of a Karst Basin around a Mine, Southwest China.

Karst water quality is one of the most important environmental issues in karst areas. The study's purpose was to investigate dissolved heavy metal pollution and health risk assessment in karst water basins around mines. River water and groundwater samples were analyzed by principal component analysis, correlation analysis, water quality index, hazard quotient, and hazard index. Median concentrations of dissolved heavy metals in the Sidi River were similar to the world average with a slightly alkaline characteristic. The concentrations of most dissolved heavy metals in river water were higher than those in groundwater. The concentrations of Zn, Pb, and Cd around the mine exceeded the limits of drinking water indicators. The poor water quality samples with high water quality index values were distributed around the mine. Lead (Pb), Zn, As, Cd, and Cr were potentially threatening metals in the study area. The pollution level of dissolved heavy metals in the Sidi River was at a medium level compared with other rivers worldwide. Principal component analysis and correlation analysis showed that Cu, Pb, Zn, Cd, Mn, Fe, As, and Sr mainly came from mine drainage; Ca2+, Mg2+, and Cr mainly came from the contribution of carbonate rocks; Na+ and K+ were related to local human agricultural activities. The concentrations of dissolved heavy metals in groundwater were affected by karst aquifers. The results of this study can provide a data reference for water resources prevention and human health protection in the Sidi River's karst basin and similar karst basins.

Integrin-ß4 regulates the dynamic changes of phenotypic characteristics in association with epithelial-mesenchymal transition (EMT) and RhoA activity in airway epithelial cells during injury and repair.

Background: In airway disease such as asthma a hyperactive cellular event of epithelial-mesenchymal transition (EMT) is considered as the mechanism of pathological airway tissue remodeling after injury to the airway epithelium. And the initiation of EMT in the airways depends on the epithelial disruption involving dissolution and/or destabilization of the adhesive structures between the cells and ECM. Previously, we have shown that integrin-ß4, an epithelial adhesion molecule in bronchial epithelium is an important regulator of cell proliferation and wound repair in human airway epithelial cells. Therefore, in this study we aimed to investigate whether integrin-ß4 also regulates EMT phenotypes during injury and repair in airway epithelial cells of both wild type/integrin-ß4-/- mice in vivo and cultured cells treated with integrin-ß4/nonsense siRNA in vitro. Methods: We induced injury to the airway epithelial cells by either repeated exposure to ozone and mechanical scratch wound, and subsequently examined the EMT-related phenotypic features in the airway epithelial cells including biomarkers expression, adhesion and cytoskeleton reorganization and cell stiffness. Results: The results show that in response to injury (ozone exposure/scratch wound) and subsequent spontaneous repair (ozone withdrawal/wound healing) both in vivo and in vitro, the airway epithelial cells underwent dynamic changes in the epithelial and mesenchymal biomarkers expression, adhesion and cytoskeleton structures as well as cell stiffness, all together exhibiting enhanced EMT phenotypic features after injury and reversal of the injury-induced effects during repair. Importantly, these injury/repair-associated EMT phenotypic changes in airway epithelial cells appeared to be dependent on integrin-ß4 expression. More specifically, when integrin-ß4 was deficient in mice (integrin-ß4-/-) the repair of ozone-injured airway epithelium was impaired and the recovery of ozone-enhanced EMT biomarkers expression in the airway epithelium was delayed. Similarly, in the scratch wounded airway epithelial cells with integrin-ß4 knockdown, the cells were impaired in all aspects related to EMT during wound and repair including cell proliferation, wound closure rate, adhesion and cytoskeleton protein expression (vinculin and vimentin), mesenchymal-like F-actin reorganization, cell stiffness and RhoA activation. Conclusion: Taken together, these results suggested that integrin-ß4 may be essential in regulating the effects of injury and repair on EMT in airway epithelial cells via influencing both the cell adhesion to ECM and cells' physical phenotypes through RhoA signaling pathway.

Activation of CFTR trafficking and gating by vasoactive intestinal peptide in human bronchial epithelial cells.

Cystic fibrosis transmembrane conductance regulator (CFTR) is an apical membrane chloride channel critical to the regulation of fluid, chloride, and bicarbonate transport in epithelia and other cell types. The most common cause of cystic fibrosis (CF) is the abnormal trafficking of CFTR mutants. Therefore, understanding the cellular machineries that transit CFTR from the endoplasmic reticulum to the cell surface is important. Vasoactive intestinal polypeptide (VIP) plays an important role in CFTR-dependent chloride transport. The present study was designed to observe the affection of VIP on the trafficking of CFTR, and channel gating in human bronchial epithelium cells (HBEC). Confocal microscopy revealed CFTR immunofluorescence extending from the apical membrane deeply into the cell cytoplasm. After VIP treatment, apical extension of CFTR immunofluorescence into the cell was reduced and the peak intensity of CFTR fluorescence shifted towards the apical membrane. Western blot showed VIP increased cell surface and total CFTR. Compared with the augmented level of total CFTR, the surface CFTR increased more markedly. Immunoprecipitation founded that the mature form of CFTR had a marked increase in HBEC treated with VIP. VIP led to a threefold increase in Cl(-) efflux in HBEC. Glibenclamide-sensitive and DIDS-insensitive CFTR Cl(-) currents were consistently observed after stimulation with VIP (10(-8) mol/L). The augmentation of CFTR Cl(-) currents enhanced by VIP (10(-8) mol/L) was reversed, at least in part, by the protein kinase A (PKA) inhibitor, H-89 and the protein kinase C (PKC) inhibitor, H-7, suggesting PKA and PKC participate in the VIP-promoted CFTR Cl(-) currents.

Involvement of integrin beta4 in ozone stress-induced airway hyperresponsiveness.

It is known that ozone stress can induce airway hyperresponsiveness (AHR). The underlying cellular and molecular mechanisms are not fully understood. We constructed a successive ozone-stressed rat model and showed that AHR caused by ozone stress presented as increased lung resistance (R(L)) to inhaled histamine but not baseline R(L). Meanwhile, structural disruption and decreased expression of integrin beta4 on airway epithelia were observed. Further regression analysis revealed a significant negative correlation between increases in R(L) to histamine (at 0.32 mg/ml) and mRNA expression of integrin beta4. Moreover, when integrin beta4 on human bronchial epithelial cells was knocked down, we found that reactive oxygen species was increased and apoptosis rates were higher. Overall, this study suggests that downregulation of integrin beta4 is important for the development ozone stress-induced AHR, presumably because it causes increased oxidative damage and epithelial apoptosis.

Wound repair and anti-oxidative capacity is regulated by ITGB4 in airway epithelial cells.

Integrin beta 4 (ITGB4) is a structural adhesion molecule which engages in maintaining the integrity of airway epithelial cells. Its specific cytomembrane structural feature strongly indicates that ITGB4 may engage in many signaling pathways and physiologic processes. However, in addition to adhesion, the specific biologic significance of ITGB4 in airway epithelial cells is almost unknown. In this article, we investigated the expression and functional properties of ITGB4 in airway epithelial cells in vivo and in vitro. Human bronchial epithelial cell line (16HBE14O-cells) and primary rat tracheal epithelial cells (RTE cells) were used to determine ITGB4 expression under ozone tress or mechanical damage, respectively. An ovalbumin (OVA)-challenged asthma model was used to investigate ITGB4 expression after antigen exposure in vivo. In addition, an ITGB4 overexpression vector and ITGB4 silence virus vector were constructed and transfected into RTE cells. Then, wound repair ability and anti-oxidation capacity was evaluated. Our results demonstrated that, on the edge of mechanically wounded cell areas, ITGB4 expression was increased after mechanical injury. After ozone stress, upregulation expression of ITGB4 was also detected. In the OVA-challenged asthma model, ITGB4 expression was decreased on airway epithelial cells accompanying with structural disruption and damage of anti-oxidation capacity. Besides, our study revealed that upregulation of ITGB4 promotes wound repair ability and anti-oxidative ability, while such abilities were blocked when ITGB4 was silenced. Taken together, these results showed that ITGB4 was a new interesting molecule involved in the regulation of wound repair and anti-oxidation processes for airway epithelial cells.

Correlation Analysis of C-terminal telopeptide of collagen type II and Interleukin-1ß for Early Diagnosis of Knee Osteoarthritis.

OBJECTIVE: To analyze the correlation between the Kellgren-Lawrence (K-L) score of knee osteoarthritis (KOA) patients with different degrees and their urine concentration of C-terminal telopeptide of collagen type II (CTX-II) and interleukin-1ß (IL-1ß), and to further evaluate the diagnostic value of CTX-II and IL-1ß during the pathological process by producing an experimental osteoarthritis (OA) model in rabbits. METHODS: From 1 January 2017 to 31 December 2018, a total of 34 subjects (7 mild, 9 moderate, 9 severe arthritis patients, and 9 healthy individuals) comprising 16 men and 18 women were included in this study. Patients were diagnosed according to the American College of Rheumatology (ACR) criteria. The urine of all subjects was collected to detect the concentration of CTX-II and IL-1ß. The rabbits in the KOA group were subjected to protease (control group with saline) injection into the articular cavity of their right knees and immobilization with gypsum. We used radiological and histological examination to identify the KOA model. ELISA was applied to investigate the concentrations of CTX-II and IL-1ß in urine and serum, and Spearman's rank correlation analysis was used to analyze the correlation. RESULTS: There was no significant difference in the mean ages and body mass index (BMI) between groups. The mean ages of mild, moderate, and severe arthritis patients and healthy individuals were 54.29 ± 5.76, 58.44 ± 6.44, 59.89 ± 6.75, and 56.67 ± 4.18 years, respectively. The mean BMI of mild, moderate, and severe arthritis patients and healthy individuals were 23.59 ± 1.56, 23.57 ± 2.06, 24.46 ± 1.64, and 23.42 ± 1.35 kg/m2 , respectively. The Kellgren-Lawrence (K-L) score was higher with the aggravation of KOA. The K-L scores of mild, moderate, and severe KOA patients were 1.14 ± 0.38, 2.56 ± 0.53, and 3.63 ± 0.52, respectively. The KOA symptoms of patients became more severe, with not only increased K-L scores but also elevated concentrations of CTX-II and IL-1ß. Moreover, there was a positive correlation between CTX-II and IL-1ß of all subjects (r = 0.974, P < 0.001), between K-L score and urine concentration of CTX-II (r = 0.900, P < 0.001), and between K-L score and IL-1ß (r = 0.813, P < 0.001) of all subjects. Both were significantly increased in KOA group rabbits at all time points after surgery. The serum concentration of CTX-II and IL-1ß was elevated as early as in the 2nd week (3.69 and 4.25 times) and reached a peak (5.41 and 7.23 times) in the 4th week after surgery. Then, until 12 weeks after surgery, the CTX-II and IL-1ß concentrations in the KOA group were slightly reduced and remained around 4.5 and 6.3 times that in the control group. Moreover, there was a positive correlation between the serum concentration of IL-1ß and CTX-II (r = 0.967, P < 0.001). CONCLUSION: CTX-II and IL-1ß, which were significantly increased during the process of KOA, can be used as biomolecular markers to provide guidelines for early diagnosis and treatment of KOA.

Efficiency of Pb, Zn, Cd, and Mn Removal from Karst Water by Eichhornia crassipes.

This study experimentally investigated heavy metal removal and accumulation in the aquatic plant Eichhornia crassipes. Pb, Zn, Cd, and Mn concentrations, plant morphology, and plant functional groups were analyzed. Eichhornia crassipes achieved high removal efficiency of Pb and Mn from karst water (over 79.5%), with high proportion of Pb, Zn, and Cd absorption occurring in the first eight days. The highest removal efficiencies were obtained at initial Pb, Zn, Cd, and Mn concentrations of 1 mg/L, 2 mg/L, 0.02 mg/L, and 0.2 mg/L, respectively. Eichhornia crassipes exhibited a high bioconcentration factor (Mn = 199,567 > Pb = 19,605 > Cd = 3403 > Zn = 1913) and a low translocation factor (<1). The roots accumulated more Pb, Zn, Cd, and Mn than the stolons and leaves due to the stronger tolerance of roots. The voids, stomas, air chambers, and airways promoted this accumulation. Pb, Cd, Zn, and Mn likely exchanged with Mg, Na, and K through the cation exchange. C≡C, C=O, SO42-, O-H, C-H, and C-O played different roles during uptake, which led to different removal and accumulation effects.

Effects and Mechanisms of Calcium Ion Addition on Lead Removal from Water by Eichhornia crassipes.

Karst water is rich in calcium ions (Ca2+) and exhibits poor metal availability and low biodegradation efficiency. This study sought to analyze the effects and mechanisms of Ca2+ on lead (Pb) removal and absorption by Eichhornia crassipes (a floating plant common in karst areas). Moreover, the morphology and functional groups of E. crassipes in water were characterized via SEM, and FTIR. The results demonstrated that the removal rate of Pb in karst water (85.31%) was higher than that in non-karst water (77.04%); however, the Pb bioconcentration amount (BCA) in E. crassipes roots in karst water (1763 mg/kg) was lower than that in non-karst water (2143 mg/kg). With increased Ca2+ concentrations (60, 80, and 100 mg/L) in karst water, the Pb removal rate increased (85.31%, 88.87%, and 92.44%), the Pb BCA decreased (1763, 1317, and 1095 mg/kg), and the Ca BCA increased (6801, 6955, and 9368 mg/kg), which was attributed to PbCO3 and PbSO4 precipitation and competitive Ca and Pb absorption. High Ca2+ concentrations increased the strength of cation exchange, alleviated the fracture degree of fibrous roots, reduced the atrophy of vascular bundles, protected the cell wall, promoted C-O combined with Pb, enhanced the strength of O‒H, SO42-, C=O, and reduced the oxidization of alkynyl acetylene bonds.

[Regional Evolution and Control Factors of Karst Groundwater in Liulin Spring Catchment].

The Liulin Spring is one of the ten most famous karst springs in the Shanxi province. The abundant karst groundwater resources support the economic and social development in the Luliang Prefecture. Therefore, the study of evolution and control factors of karst groundwater is of great significance to the sustainable utilization of water resources in the watershed. For revealing the evolution and control factors of karst groundwater in the Liulin Spring area, the main ion components of 29 karst groundwater samples from spring supply area, runoff area, discharge area, and deep buried area were analyzed. The results showed that the temperature and Na+, Ca2+, Mg2+, Cl-, HCO3-, and SO42- concentrations increased continuously along the runoff route, from the recharge area to the runoff area, to the discharge area, and then to the deep burial area. K+, Na+, and Cl- mainly come from salt rock dissolution, and Ca2+, Mg2+, HCO3-, and SO42- mainly come from the dissolution of calcite, dolomite, and gypsum. Because they are controlled by the continuous dissolution of salt rock and gypsum, the concentration of Na+, Cl-, and SO42- in groundwater has increased greatly, with the maximum value being 50 times, 80 times, and 32 times of the minimum value, respectively. Under the influence of dedolomitization, the concentration of Ca2+ and HCO3- in groundwater does not change significantly, the maximum is 2-3 times of the minimum. In the recharge area and runoff area, Na+ and Cl- amounts are lower, and Ca2+ and HCO3- are the main cations and anions in the groundwater. However, in the discharge area and deep buried area, Cl- and Na+ exceed HCO3-, Ca2+, and Mg2+ and become the main anions and cations in the groundwater. The hydrochemical type changes from HCO3-Ca·Mg in the supply area to HCO3·SO4-Ca·Mg in the runoff area, to HCO3·SO4-Ca·Na·Mg in the recharge area, and finally to Cl·HCO3-Na·Ca, Cl·HCO3-Na, and Cl-Na·Ca in the deep burial area.