Computed tomography for the diagnosis of gastroesophageal varices and risk assessment in patients with cirrhosis: a systematic review and meta-analysis.

PURPOSE: This meta-analysis aimed to evaluate the diagnostic accuracy of computed tomography (CT) for gastroesophageal varices (GEVs) and identify high-risk GEVs in patients with cirrhosis. METHODS: A comprehensive search of databases identified 28 studies reporting on CT-based diagnosis for GEVs confirmed via endoscopy. Meta-analyses were conducted to calculate the pooled sensitivity (SEN) and pooled specificity (SPE), positive likelihood ratio (PLR) and negative likelihood ratio (NLR), diagnostic odds ratio (DOR), and the area under the curve (AUC). RESULTS: Based on the number of patients (or varices), the pooled SEN, SPE, PLR, NLR, DOR, and AUC of CT-based diagnosis were estimated at 0.91 (0.92), 0.81 (0.45), 4.82 (1.67), 0.11 (0.17), 42.47 (10.26), and 0.93 (0.94), respectively, for any GEV and at 0.89 (0.89), 0.90 (0.79), 8.86 (4.28), 0.12 (0.14), 75.71 (30.19), and 0.95 (0.85), respectively, for high-risk GEVs. Subgroup analyses indicated that CT had a higher diagnostic accuracy for esophageal varices compared with gastric varices (AUC: 0.93 vs. 0.89, P < 0.05), and the 64-slice CT yielded superior SEN compared with 16-slice and <16-slice CT (AUC: 0.97 vs. 0.92 and 0.82, respectively, P < 0.05). Prospective studies demonstrated higher diagnostic accuracy than retrospective studies (AUC: 0.95 vs. 0.90, P < 0.05). Regarding variceal size, a cut-off of 3 mm and 5 mm discriminated between low- and high-risk individuals, respectively, with high diagnostic accuracy (AUC: 0.992 vs. 0.997, P > 0.05). CONCLUSION: CT demonstrates promising diagnostic accuracy for identifying GEVs and distinguishing high-risk GEVs in patients with cirrhosis. Further research validating optimal variceal size cut-offs is warranted to enhance clinical utility. CLINICAL SIGNIFICANCE: Such a high diagnostic accuracy of CT scans for predicting varices is clinically meaningful for patients with cirrhosis accompanied by portal hypertension. If high-risk varices are identified at CT scans, early intervention would be helpful to reduce the risk of variceal bleeding.

'Environmental standard limit concentration' arsenic exposure is associated with anxiety, depression, and autism-like changes in early-life stage zebrafish.

Arsenic is a worldwide environmental pollutant that can impair human health. Previous studies have identified mental disorders induced by arsenic, but the environmental exposure concentrations in the early life stages associated with these disorders are poorly understood. In the present study, early-life stage zebrafish were used to explore the effects on mental disorders under 'environmental standard limit concentrations' arsenic exposures of 5, 10, 50, 150, and 500 µg/L. The results showed that arsenic exposure at these concentrations changed the locomotor behavior in larval zebrafish and was further associated with anxiety, depression, and autism-like behavior in both larval and juvenile zebrafish. Changes were noted at benchmark dose limit (BMDL) concentrations as low as 0.81 µg/L. Transcriptomics showed that immediate early genes (IEGs) fosab, egr1, egr2a, ier2b, egr3, and jund were decreased after arsenic exposure in larval and juvenile zebrafish. Nervous system impairment and anxiety, depression, and autism-like behaviors in early-life stage zebrafish at 'environmental standard limit concentrations' may be attributed to the downregulation of IEGs. These findings in zebrafish provided new experimental support for an arsenic toxicity threshold for mental disorders, and they suggest that low levels of environmental chemicals may be causative developmental factors for mental disorders.

Paroxetine induced larva zebrafish cardiotoxicity through inflammation response.

Paroxetine (PRX) is a common antidepressant drug which widely existence in natural environment. Numerous studies in the past few decades have focused on the beneficial effects of PRX on depression, however, the toxic properties and the potential mechanisms remain unclear. In this study, zebrafish embryos were exposed to 1.0, 5.0, 10 and 20 mg/L of PRX from 4 to 120-hour-post-fertilization (hpf), and it showed that PRX exposure caused adverse effects in zebrafish embryos, including decreased body length, blood flow velocity, cardiac frequency, cardiac output and increased burst activity and atria area. Meanwhile, the Tg (myl7: EGFP) and Tg (lyz: DsRed) transgenic zebrafish were used to detect the cardiotoxicity and inflammation response of PRX. Moreover, the heart development associated genes (vmhc, amhc, hand2, nkx2.5, ta, tbx6, tbx16 and tbx20) and inflammatory genes (IL-10, IL-1ß, IL-8 and TNF-α) were up-regulated after PRX challenge. In addition, Aspirin was used to alleviate the PRX-induced heart development disorder. In conclusion, our study verified the PRX induced inflammatory related cardiotoxicity in larva zebrafish. Meanwhile, the current study shown the toxic effects of PRX in aquatic organism, and provide for the environmental safety of PRX.

Neurodevelopmental Toxicity of Emamectin Benzoate to the Early Life Stage of Zebrafish Larvae (Danio rerio).

Emamectin benzoate (EMB) is a widely used pesticide and feed additive in agriculture and aquaculture. It easily enters the aquatic environment through various pathways, thus causing adverse effects on aquatic organisms. However, there are no systematic studies regarding the effects of EMB on the developmental neurotoxicity of aquatic organisms. Therefore, the aim of this study was to evaluate the neurotoxic effects and mechanisms of EMB at different concentrations (0.1, 0.25, 0.5, 1, 2, 4 and 8 µg/mL) using zebrafish as a model. The results showed that EMB significantly inhibited the hatching rate, spontaneous movement, body length, and swim bladder development of zebrafish embryos, as well as significantly increased the malformation rate of zebrafish larvae. In addition, EMB adversely affected the axon length of motor neurons in Tg (hb9: eGFP) zebrafish and central nervous system (CNS) neurons in Tg (HuC: eGFP) zebrafish and significantly inhibited the locomotor behavior of zebrafish larvae. Meanwhile, EMB induced oxidative damage and was accompanied by increasing reactive oxygen species in the brains of zebrafish larvae. In addition, gene expression involvement in oxidative stress-related (cat, sod and Cu/Zn-sod), GABA neural pathway-related (gat1, gabra1, gad1b, abat and glsa), neurodevelopmental-related (syn2a, gfap, elavl3, shha, gap43 and Nrd) and swim bladder development-related (foxa3, pbxla, mnx1, has2 and elovlla) genes was significantly affected by EMB exposure. In conclusion, our study shows that exposure to EMB during the early life stages of zebrafish significantly increases oxidative damage and inhibits early central neuronal development, motor neuron axon growth and swim bladder development, ultimately leading to neurobehavioral changes in juvenile zebrafish.

The toxic effect of bisphenol AF and nanoplastic coexposure in parental and offspring generation zebrafish.

Microplastics (MPs) and bisphenol AF (BPAF) are two environmental pollutants that usually coexist in the natural environment. Studies of MPs or BPAF have gradually increased in recent years, but few studies have focused on the combination toxic effects. In this study, the subchronic model of adult zebrafish was exposed to 1 mg/L nanolevel microplastics and 200 µg/L BPAF for 45 days; the parental zebrafish were spawning every 3 days during exposure, and the effects of continuous poisoning were examined on the offspring after 1-9 spawns. The results showed that single BPAF exposure or BPAF and nanoplastic coexposure can both decrease the number of eggs laid and the locomotor behavior of parental zebrafish and impact the hatching rate, mortality, body length and locomotor behavior of offspring zebrafish, especially in 7-9 spawn. BPAF were accumulated in parental zebrafish intestinal in 334.62 ng/g in BPAF group and 594.52 ng/g in nm+BPAF group, and accumulated in whole offspring zebrafish for 281.6 ng/g in BPAF group and 321.46 ng/g in nm+BPAF group. Neurodevelopmental, inflammation, apoptosis and oxidative stress-related genes were also significantly increased after 7-9 spawn. In addition, the exacerbated accumulation in the BPAF+nm group in parental and offspring zebrafish may be the reason for the accelerated toxic effect in the present research. In this study, we investigated the combined effects of nanoplastics and BPAF on parental and offspring zebrafish in the aquatic environment to identify the accumulative toxic effects and provide new experimental support for assessing the effects of coexposure on aquatic organisms.

Examining ground and surface water changes in response to environmental variables, land use dynamics, and socioeconomic changes in Canada.

Canada's abundant and high-quality water resources support a growing human population, as well as thriving industrial and agricultural economies. However, recent intense drought conditions have raised concerns for current water resource availability. Patterns of long-term ground and surface water (GSW) changes, and their response to environmental conditions, land-use dynamics, and socioeconomic changes are not well-understood across this large and diverse country. To address this crucial gap, we identified regions of ground and surface water (GSW) changes in all the Provinces of Canada between 2002 and 2016 from the Gravity Recovery and Climate Experiment (GRACE) and Global Land Data Assimilation System (GLDAS) datasets. We explored the relationships between GSW changes and environmental, socioeconomic, and land-use dynamics over time. We found that all the Provinces of Canada gained a net 4.46 mm Liquid Water Equivalent (LWE) per year, equivalent to a total increase of 66.9 mm LWE. GSW increases were significantly associated with the normalized difference vegetation index and evapotranspiration rates. In contrast, GSW declines were significantly related to deforestation rate, urban expansion, and economic development (median household income). Despite apparent widespread post-drought recovery detected from 2002 to 2016, the rapid GSW declines were also observed in almost all of Western Canada and part of Ontario, amounting to a net loss of 66.13 mm. This indicates that a pronounced drought had emerged. It is anticipated that Canada will be experiencing more frequent and severe droughts under ongoing climate change and increasing demand for water resources.

Targeting Aß and p-Tau Clearance in Methamphetamine-Induced Alzheimer's Disease-Like Pathology: Roles of Syntaxin 17 in Autophagic Degradation in Primary Hippocampal Neurons.

Methamphetamine (Meth), a central nervous system (CNS) stimulant with strong neurotoxicity, causes progressive cognitive impairment with characterized neurodegenerative changes. However, the mechanism underlying Meth-induced pathological changes remains poorly understood. In the current study, Meth elicited a striking accumulation of the pathological proteins hyperphosphorylated tau (p-tau) and amyloid beta (Aß) in primary hippocampal neurons, while the activation of autophagy dramatically ameliorated the high levels of these pathological proteins. Interestingly, after the Meth treatment, Aß was massively deposited in autophagosomes, which were remarkably trapped in early endosomes. Mechanistically, syntaxin 17 (Stx17), a key soluble n-ethylmaleimide-sensitive fusion protein (NSF) attachment protein receptor (SNARE) protein responsible for autophagosome and mature endosome/lysosome fusion, was significantly downregulated and hindered in combination with autophagosomes. Notably, adenovirus overexpression of Stx17 in primary neurons facilitated autophagosome-mature endosome/lysosome fusion, which dramatically reversed the Meth-induced increases in the levels of p-tau, Aß, beta-secretase (Bace-1), and C-terminal fragments (CTFs). Immunofluorescence assays showed that Stx17 retarded the Meth-induced Aß, p-tau, and Bace-1 accumulation in autophagosomes and facilitated the translocation of these pathological proteins to lysosomes, which indicated the importance of Stx17 via enhanced autophagosome-mature endosome/lysosome fusion. Therefore, the current study reveals a novel mechanism involving Meth-induced high levels of pathological proteins in neurons. Targeting Stx17 may provide a novel therapeutic strategy for Meth-induced neurodegenerative changes.

Long-term exposure of zebrafish to bisphenol F: Adverse effects on parental reproduction and offspring neurodevelopment.

Bisphenol F (BPF), an alternative to bisphenol A (BPA) has potential endocrine and reproductive toxicity; however, the effects of environmental concentrations of BPF on the reproductive and developmental toxicity of offspring following parental exposure to BPF remain unclear. In the present study, the effects of life-cycle BPF exposure at environmental concentrations on zebrafish reproduction, offspring growth, and development were investigated. The results showed that the life-cycle of BPF exposure significantly elevated oxidative stress levels, increased gonadal apoptosis, and reduced zebrafish (F0) spawning. Notably, through maternal transfer, BPF exposure significantly affected offspring development. Developmental parameters such as hatching rate, spontaneous movements, heart rate, body length, and locomotor behavior decreased in zebrafish larvae (F1). In addition, the expression levels of genes related to oxidative stress, apoptosis, and neurodevelopment were altered in F1 larvae. Therefore, the present study provides evidence that BPF, even at environmental concentrations, can be potentially adverse in terms of reproductive defects and offspring neurodevelopmental disorders. Therefore, BPF, as a substitute for BPA, is worthy of in-depth evaluation.

The potential mechanism of BPF-induced neurotoxicity in adult zebrafish: Correlation between untargeted metabolomics and gut microbiota.

Bisphenol F (BPF) is becoming the main substitute for bisphenol A (BPA) in plastics for food and beverage applications. Previous studies have demonstrated the neurotoxicity of BPF; however, its lifecycle toxicity and the underlying mechanisms remain poorly understood. In the current study, zebrafish were continuously exposed to BPF for four months from the embryo to adult stages in order to assess its neurotoxicity. Locomotor behaviors significantly decreased after BPF exposure, which was accompanied by a decrease in body weight, length, and hatching rate. Additionally, BPF increased the expression of inflammatory genes in the brain and destroyed the zebrafishes' intestinal integrity. Meanwhile, the 16S rRNA gene sequence results showed a significantly decreased microbiota abundance and diversity following BPF treatment. Neurotransmitter metabolites were also altered by BPF. Notably, the correlation analysis between microbiota and neurotransmitter metabolism verified that gut microbiota dysbiosis was closely related to the disturbance of neurotransmitter metabolites. Therefore, the present study evaluated the neurotoxicity of lifecycle exposure to BPF and unraveled a novel mechanism involving disturbance of neurotransmitter metabolism and gut dysbiosis, which may provide potential targets for BPF-mediated neurotoxicity.

Synchronous double primary hepatocellular carcinoma and intrahepatic cholangiocarcinoma: A case report and review of the literature.

RATIONALE: Presence of synchronous double hepatocelluar carcinoma (HCC) and intrahepatic cholangiocarcinoma (ICC) (sdpHCC-ICC) located separately within a single liver is extremely rare. The purpose of this study is to investigate the clinical, imaging, pathological characteristics, and prognosis of patients with sdpHCC-ICC, in order to enhance our understanding of the disease and improve diagnostic and therapeutic effect. PATIENT CONCERNS: A 49-year-old, female with the diagnosis of hepatitis B virus with obvious liver cirrhosis, was admitted to our hospital. On admission, the levels of α-fetoprotein and carbohydrate antigen 19-9 were found to be elevated. Abdominal ultrasonography and enhanced computed tomography revealed 2 solid masses located in segments (S) 4 and 6 of the liver, with malignant behaviors. DIAGNOSES: In the light of above investigations, preoperative diagnosis of multiple primary hepatocellular carcinomas was made. INTERVENTION: Hepatic resection of both segments was done. The resected specimens revealed the presence of well-defined tumors in segments 4 and 6 measuring 5.0 cm and 2.5 cm respectively. OUTCOMES: Histopathological examination confirmed the tumor of the 4th segment to be moderately and poorly differentiated ICC, and the tumor of the 6th segment to be poorly differentiated HCC. Immunohistochemically, the ICC in S4 was positive for CK19 and negative for Heppar-1, whereas the HCC in S6 was positive for Heppar-1 and negative for CK19. Unfortunately, metastasis to multiple organs and lymph nodes were observed 3 months later. The patient died of liver failure 16 months after surgery. LESSONS: The clinical characteristics of sdpHCC-ICC are usually atypical and nonspecific making its preoperative diagnosis quite difficult. Hepatitis B virus and hepatitis C virus infection were both the independent risk factor for the development of sdpHCC-ICC. In patients with chronic liver disease, careful observation with imaging is of utmost necessity. Tumor markers may also play a valuable role in the diagnosis. The definite diagnosis depends on pathological examination. Hepatic resection is considered the most effective mode of treatment. The prognosis of synchronous occurrence of double hepatic cancers is worse than either HCC or ICC, and the origin of the disease needs further study.

Mystery of methamphetamine-induced autophagosome accumulation in hippocampal neurons: loss of syntaxin 17 in defects of dynein-dynactin driving and autophagosome-late endosome/lysosome fusion.

Methamphetamine (METH), a psychoactive-stimulant facilitates massive accumulation of autophagosomes and causes autophagy-associated neuronal death. However, the underlying mechanisms involving METH-induced auto-phagosome accumulation remain poorly understood. In the current study, autophagic flux was tracked by mRFP-GFP-LC3 adenovirus, 900 µM METH treatment was found to significantly disrupt autophagic flux, which was further validated by remarkable increase of co-localized of LC3 and SQSTM1/p62, enhancement of LC3-II and SQSTM1/p62 protein levels, and massive autophagosome puncta aggregation. With the cycloheximide (CHX) treatment, METH treatment was displayed a significant inhibition of SQSTM1/p62 degradation. Therefore, the mRNAs associated with vesicle degradation were screened, and syntaxin 17 (Stx17) and dynein-dynactin mRNA levels significantly decreased, an effect was proved in protein level as well. Intriguingly, METH induced autophagosome accumulation and autophagic flux disturbance was incredibly retarded by overexpression of Stx17, which was validated by the restoration of the fusion autophagosome-late endosome/lysosome fusion. Moreover, Stx17 overexpression obviously impeded the METH-induced decrease of co-localization of the retrograded motor protein dynein/dynactin and autophagosome-late endosome, though the dynein/dynactin proteins were not involved in autophagosome-late endosome/lysosome fusion. Collectively, our findings unravel the mechanism of METH-induced autophagosome accumulation involving autophagosome-late endosome/lysosome fusion deficiency and that autophagy-enhancing mechanisms such as the overexpression of Stx17 may be therapeutic strategies for the treatment of METH-induced neuronal damage.

Exosomes derived from hypoxic bone marrow mesenchymal stem cells rescue OGD-induced injury in neural cells by suppressing NLRP3 inflammasome-mediated pyroptosis.

Exosomes have been shown to have therapeutic potential for cerebral ischemic diseases. In this study, we investigated the neuroprotective effects of normoxic and hypoxic bone marrow mesenchymal stromal cells-derived exosomes (N-BM-MSCs-Exo and H-BM-MSCs-Exo, respectively) on oxygen-glucose deprivation (OGD) injury in mouse neuroblastoma N2a cells and rat primary cortical neurons. The proportions of dead cells in N2a and primary cortical neurons after OGD injury were significantly increased, and N-BM-MSCs-Exo (40 µg/ml) could reduce the ratios, noteworthily, the protective effects of H-BM-MSCs-Exo (40 µg/ml) were more potent. Western blotting analysis indicated that N-BM-MSCs-Exo decreased the expression of NLRP3, ASC, Caspase-1, GSDMD-N, cleaved IL-1ß and IL-18 in N2a cells. However, H-BM-MSCs-Exo (40 µg/ml) was more powerful in inhibiting the expression of these proteins in comparison with N-BM-MSCs-Exo. Similar results were obtained in primary cortical neurons. Immunofluorescence assays showed that after N-BM-MSCs-Exo and H-BM-MSCs-Exo treatment, the co-localization of NLRP3, ASC, Caspase-1 and the GSDMD translocation from the nucleus to the cytoplasm and membrane after OGD injury were reduced in N2a cells and primary cortical neurons, and H-BM-MSCs-Exo had a more obvious effect. In addition, N-BM-MSCs-Exo and H-BM-MSCs-Exo significantly reduced lactate dehydrogenase (LDH) release and the IL-18 levels in cell culture medium in N2a cells and primary cortical neurons. Once again H-BM-MSCs-Exo induced these effects more potently than N-BM-MSCs-Exo. All of these results demonstrated that N-BM-MSCs-Exo and H-BM-MSCs-Exo have significant neuroprotective effects against NLRP3 inflammasome-mediated pyroptosis. H-BM-MSCs-Exo has a more pronounced protective effect than N-BM-MSCs-Exo and may be used to ameliorate the progression of cerebral ischemia and hypoxia injury in patients.

Titanium dioxide nanoparticle affects motor behavior, neurodevelopment and axonal growth in zebrafish (Danio rerio) larvae.

More attention has been recently paid to the ecotoxicity of titanium dioxide nanoparticles (nano-TiO2) owing to its common use in many fields. Although previous studies have shown that nano-TiO2 is neurotoxic, the mechanism is still largely unknown. In the present study, zebrafish embryos were exposed to 0.01, 0.1, and 1.0 mg/L nano-TiO2 and 1.0 mg/L micro-TiO2 for up to 6 days post-fertilization (dpf). Exposure to 1.0 mg/L nano-TiO2 significantly decreased the body length and weight of zebrafish larvae; however, the hatching and mortality rate of zebrafish embryos did not change. Behavioral tests showed that nano-TiO2 exposure significantly reduced the swimming speed and clockwise rotation times of the larvae. The results revealed that nano-TiO2 treatment adversely affected motor neuron axon length in Tg (hb9-GFP) zebrafish and decreased central nervous system (CNS) neurogenesis in Tg (HuC-GFP) zebrafish. Additionally, real-time polymerase chain reaction analysis demonstrated that genes associated with neurogenesis (nrd and elavl3) and axonal growth (α1-tubulin, mbp, and gap43) were significantly affected by nano-TiO2 exposure. In conclusion, our study demonstrated that early-life stage exposure of zebrafish to nano-TiO2 causes adverse neural outcomes through the inhibition of neurodevelopment and motor neuron axonal growth.

1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine Induced Parkinson's Disease in Mouse: Potential Association between Neurotransmitter Disturbance and Gut Microbiota Dysbiosis.

Recent studies have revealed significant roles of neurotransmitters and gut microbiota along the gut-brain axis in Parkinson's disease (PD); however, the potential mechanisms remain poorly understood. In the current study, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP) induced characteristic PD neurobehavior changes accompanied by increased α-synuclein, apoptotic protein Bim, and cleaved caspase-3 and decreased expression of tyrosine hydroxylase (TH). Meanwhile, the tryptophan (Trp) and tyrosine (Tyr) neurotransmitter metabolites involving kynurenine (KYN), serotonin (5-HT), and dopamine (DA) pathways were significantly changed in serum. Furthermore, the step-limited enzymes, which are responsible for the key metabolic pathways of these neurotransmitters, were obviously dysregulated. The 16S rRNA gene sequence results indicated that the abundance and diversity of the microbiota were obviously decreased in MPTP-treated mice, the presence of Ruminococcus, Parabacteroides and Parasutterella genera were obviously increased, while Coriobacteriaceae, Flavonifractor, Lachnospiraceae, Lactobacillaceae, and Rikenellaceae abundance was markedly decreased. The connectivity between the gut microbiota and neurotransmitter metabolism revealed that the gut microbiota dysbiosis was associated with disturbance of the DA, KYN, and 5-HT metabolic pathways. Therefore, our results provide evidence that gut-microbiota-brain axis disturbance may play an important role in PD development and targeting this axis might provide a promising therapeutic strategy for PD.

Methamphetamine induced neuroinflammation in mouse brain and microglial cell line BV2: Roles of the TLR4/TRIF/Peli1 signaling axis.

Methamphetamine (Meth), a highly addictive drug, can induce irreversible neuronal damage and cause neuropsychiatric and cognitive disorders. Meth's effects on modulating microglial neuroimmune functions and eliciting neuroinflammation have attracted considerable attention in recent years. Recent evident of the effect of the non-dependent domain containing adaptor inducing interferon (TRIF)/Pellino1 (Peli1) signaling axis on pro-inflammatory cytokine production provides novel clues for inflammation. Therefore, our study investigated Meth-induced neurotoxicity from a neuropathological perspective by examining TLR4-TRIF-Peli1 axis signaling activation. Meth significantly activated microglia accompanied by marked increase of TLR4 and TRIF expression, NF-kB and MAPK pathways activation and the production of IL-1ß, TNF-α and IL-6. Peli1 was involved in Meth-mediated neuroinflammation and knockdown of Peli1 strongly reversed NF-kB and MAPK pathways activation and pro-inflammatory cytokine excretion. Intriguingly, Peli1 upregulation induced by Meth was dependent on TRIF rather than the myloid differentiation factor 88 (MyD88) pathway, since the silencing of TRIF significantly suppressed Meth-induced Peli1 upregulation, while MyD88 knockdown had no obvious impact. Additionally, an in vivo study verified TLR4-TRIF-Peli1 axis activation and an enhanced level of downstream cytokine expression in the cortex after Meth treatment. Therefore, these findings provide new insight regarding the specific contributions of the TRIF-Peli1 pathway to Meth-mediated neuroinflammation.

Changes of ecosystem carbon stock following the plantation of exotic mangrove Sonneratia apetala in Qi'ao Island, China.

Carbon storage is one of the main objectives for mangrove afforestation. Planting of the exotic species Sonneratia apetala can rapidly increase the mangrove area and biomass. Here, we studied the change in vegetation and the soil carbon stocks along the chronosequence of S. apetala plantations in Qi'ao Island, China. Five sites, including rehabilitated S. apetala of different ages (1, 4, 9, and 15 years) and 40-year-old mature native Kandelia obovata forests were investigated. Vegetation biomass and the soil carbon content from 0 to 100 cm were analyzed. The ecosystem carbon density (vegetation and soil) was then calculated. A positive and linear relationship was observed between the vegetation carbon stocks and age of S. apetala. The 15-year-old S. apetala already had a similar biomass to 40-year-old K. obovata. However, its soil and ecosystem carbon densities remained lower than those of K. obovata. Different from K. obovata, the majority of the biomass of S. apetala was reserved within the stem. Mature K. obovata had a larger proportion of soil carbon stock to ecosystem carbon stock. S. apetala can accumulate biomass rapidly, but it had a lower ecosystem carbon stock than the native mature K. obovata.