Coastal phytoplankton blooms expand and intensify in the 21st century.

Phytoplankton blooms in coastal oceans can be beneficial to coastal fisheries production and ecosystem function, but can also cause major environmental problems1,2-yet detailed characterizations of bloom incidence and distribution are not available worldwide. Here we map daily marine coastal algal blooms between 2003 and 2020 using global satellite observations at 1-km spatial resolution. We found that algal blooms occurred in 126 out of the 153 coastal countries examined. Globally, the spatial extent (+13.2%) and frequency (+59.2%) of blooms increased significantly (P < 0.05) over the study period, whereas blooms weakened in tropical and subtropical areas of the Northern Hemisphere. We documented the relationship between the bloom trends and ocean circulation, and identified the stimulatory effects of recent increases in sea surface temperature. Our compilation of daily mapped coastal phytoplankton blooms provides the basis for global assessments of bloom risks and benefits, and for the formulation or evaluation of management or policy actions.

Application of 5T glutamate chemical exchange saturation transfer imaging in brain tumors: preliminary results.

PURPOSE: Glutamate chemical exchange saturation transfer (GluCEST) is a non-invasive CEST imaging technique for detecting glutamate levels in tissues. We aimed to investigate the reproducibility of the 5T GluCEST technique in healthy volunteers and preliminarily explore its potential clinical application in patients with brain tumors. METHODS: Ten volunteers (4 males, mean age 29 years) underwent three 5T GluCEST imaging scans. The reproducibility of the three imaging GluCEST measurements was assessed using one-way repeated measures analysis of variance (ANOVA), generalized estimating equations, and linear mixed models. Twenty-eight patients with brain tumors (10 males, mean age 54 years) underwent a single GluCEST scan preoperatively, and t-tests were used to compare the differences in GluCEST values between different brain tumors. In addition, the diagnostic accuracy of GluCEST values in differentiating brain tumors was assessed using the receiver work characteristics (ROC) curve. RESULTS: The coefficients of variation of GluCEST values in healthy volunteers were less than 5% for intra-day, inter-day, and within-subjects and less than 10% for between-subjects. High-grade gliomas (HGG) had higher GluCEST values compared to low-grade gliomas (LGG) (P < 0.001). In addition, cerebellopontine angle (CPA) meningiomas had higher GluCEST values than acoustic neuromas (P < 0.001). The area under the curve (AUC) of the GluCEST value for differentiating CPA meningioma from acoustic neuroma was 0.93. CONCLUSION: 5T GluCEST images are highly reproducible in healthy brains. In addition, the 5T GluCEST technique has potential clinical applications in differentiating LGG from HGG and CPA meningiomas from acoustic neuromas.

Author Correction: Global land change from 1982 to 2016.

In this Letter, errors in Supplementary Table 1 have been corrected.

Global land change from 1982 to 2016.

Land change is a cause and consequence of global environmental change1,2. Changes in land use and land cover considerably alter the Earth's energy balance and biogeochemical cycles, which contributes to climate change and-in turn-affects land surface properties and the provision of ecosystem services1-4. However, quantification of global land change is lacking. Here we analyse 35 years' worth of satellite data and provide a comprehensive record of global land-change dynamics during the period 1982-2016. We show that-contrary to the prevailing view that forest area has declined globally5-tree cover has increased by 2.24 million km2 (+7.1% relative to the 1982 level). This overall net gain is the result of a net loss in the tropics being outweighed by a net gain in the extratropics. Global bare ground cover has decreased by 1.16 million km2 (-3.1%), most notably in agricultural regions in Asia. Of all land changes, 60% are associated with direct human activities and 40% with indirect drivers such as climate change. Land-use change exhibits regional dominance, including tropical deforestation and agricultural expansion, temperate reforestation or afforestation, cropland intensification and urbanization. Consistently across all climate domains, montane systems have gained tree cover and many arid and semi-arid ecosystems have lost vegetation cover. The mapped land changes and the driver attributions reflect a human-dominated Earth system. The dataset we developed may be used to improve the modelling of land-use changes, biogeochemical cycles and vegetation-climate interactions to advance our understanding of global environmental change1-4,6.

Quantifying H&E staining results, grading and predicting IDH mutation status of gliomas using hybrid multi-dimensional MRI.

OBJECTIVE: To assess the performance of hybrid multi-dimensional magnetic resonance imaging (HM-MRI) in quantifying hematoxylin and eosin (H&E) staining results, grading and predicting isocitrate dehydrogenase (IDH) mutation status of gliomas. MATERIALS AND METHODS: Included were 71 glioma patients (mean age, 50.17 ± 13.38 years; 35 men). HM-MRI images were collected at five different echo times (80-200 ms) with seven b-values (0-3000 s/mm2). A modified three-compartment model with very-slow, slow and fast diffusion components was applied to calculate HM-MRI metrics, including fractions, diffusion coefficients and T2 values of each component. Pearson correlation analysis was performed between HM-MRI derived fractions and H&E staining derived percentages. HM-MRI metrics were compared between high-grade and low-grade gliomas, and between IDH-wild and IDH-mutant gliomas. Using receiver operational characteristic (ROC) analysis, the diagnostic performance of HM-MRI in grading and genotyping was compared with mono-exponential models. RESULTS: HM-MRI metrics FDvery-slow and FDslow demonstrated a significant correlation with the H&E staining results (p < .05). Besides, FDvery-slow showed the highest area under ROC curve (AUC = 0.854) for grading, while Dslow showed the highest AUC (0.845) for genotyping. Furthermore, a combination of HM-MRI metrics FDvery-slow and T2Dslow improved the diagnostic performance for grading (AUC = 0.876). DISCUSSION: HM-MRI can aid in non-invasive diagnosis of gliomas.

The feasibility of half-dose contrast-enhanced scanning of brain tumours at 5.0 T: a preliminary study.

PURPOSE: This study investigated and compared the effects of Gd enhancement on brain tumours with a half-dose of contrast medium at 5.0 T and with a full dose at 3.0 T. METHODS: Twelve subjects diagnosed with brain tumours were included in this study and underwent MRI after contrast agent injection at 3.0 T (full dose) or 5.0 T (half dose) with a 3D T1-weighted gradient echo sequence. The postcontrast images were compared by two independent neuroradiologists in terms of the signal-to-noise ratio (SNR), contrast-to-noise ratio (CNR) and subjective image quality score on a ten-point Likert scale. Quantitative indices and subjective quality ratings were compared with paired Student's t tests, and interreader agreement was assessed with the intraclass correlation coefficient (ICC). RESULTS: A total of 16 enhanced tumour lesions were detected. The SNR was significantly greater at 5.0 T than at 3.0 T in grey matter, white matter and enhanced lesions (p < 0.001). The CNR was also significantly greater at 5.0 T than at 3.0 T for grey matter/tumour lesions, white matter/tumour lesions, and grey matter/white matter (p < 0.001). Subjective evaluation revealed that the internal structure and outline of the tumour lesions were more clearly displayed with a half-dose at 5.0 T (Likert scale 8.1 ± 0.3 at 3.0 T, 8.9 ± 0.3 at 5.0 T, p < 0.001), and the effects of enhancement in the lesions were comparable to those with a full dose at 3.0 T (7.8 ± 0.3 at 3.0 T, 8.7 ± 0.4 at 5.0 T, p < 0.001). All subjective scores were good to excellent at both 5.0 T and 3.0 T. CONCLUSION: Both quantitative and subjective evaluation parameters suggested that half-dose enhanced scanning via 5.0 T MRI might be feasible for meeting clinical diagnostic requirements, as the image quality remains optimal. Enhanced scanning at 5.0 T with a half-dose of contrast agents might benefit patients with conditions that require less intravenous contrast agent, such as renal dysfunction.

The mortality impacts of current and planned coal-fired power plants in India.

We examine the health implications of electricity generation from the 2018 stock of coal-fired power plants in India, as well as the health impacts of the expansion in coal-fired generation capacity expected to occur by 2030. We estimate emissions of SO2, NOX, and particulate matter 2.5 µm (PM2.5) for each plant and use a chemical transport model to estimate the impact of power plant emissions on ambient PM2.5 Concentration-response functions from the 2019 Global Burden of Disease (GBD) are used to project the impacts of changes in PM2.5 on mortality. Current plus planned plants will contribute, on average, 13% of ambient PM2.5 in India. This reflects large absolute contributions to PM2.5 in central India and parts of the Indo-Gangetic plain (up to 20 µg/m3). In the south of India, coal-fired power plants account for 20-25% of ambient PM2.5 We estimate 112,000 deaths are attributable annually to current plus planned coal-fired power plants. Not building planned plants would avoid at least 844,000 premature deaths over the life of these plants. Imposing a tax on electricity that reflects these local health benefits would incentivize the adoption of renewable energy.

The disruption of white matter integrity of systemic striatal circuits in alcohol-dependent males with physiological cue reactivity.

Alcohol dependence (AD) is a chronic and relapsing disorder. Conditioned cues associated with the rewarding properties of drugs could trigger motivational/physiological reactions and render subjects vulnerable to relapse. Striatal circuit dysfunction has been implicated in alcohol addiction behaviours. However, little is known about the striatal tracts structural connectivity changes underlying cue induced reactivity in AD. In our present study, we recruited 51 patients with AD; 31 individuals had physiological response. We used seed-based classification by probabilistic tractography with nine target masks to explore the white matter integrity of striatal circuits in physiological responders (N = 31), non-responders (N = 20), and healthy controls (N = 27). Compared with healthy controls, physiological responders showed lower fractional anisotropy (FA) and/or higher mean diffusivity in the striatum-dorsolateral prefrontal cortex (dlPFC), striatum-ventral lateral prefrontal cortex, striatum-supplementary motor area (SMA), and striatum-insular. Considering age and smoking are potential nuisances to diffusion parameters, an analysis of covariance also was conducted and similar results were found. We also found the cue-induced physiological response was negatively associated with the FA of the striatum-SMA (r = -0.287; p = 0.045) and left striatum-dlPFC (r = -0.253; p = 0.079) in AD. In our study, we found abnormal integrity of striatal circuit structural connectivity in AD with physiological cue reactivity, especially trajectory from prefrontal cortex and insular. We also found the FA of striatal tracks was negatively associated with the degree of cue reactivity. Our findings provide further evidence for reduced white matter integrity of striatal circuits for cue reactivity in male individuals with AD.

Curcumin alleviates ketamine-induced oxidative stress and apoptosis via Nrf2 signaling pathway in rats' cerebral cortex and hippocampus.

AIMS: To investigate curcumin's protective effect on nerve damage caused by ketamine anesthesia via the Nrf2 signaling pathway. Rats and PC12 cells were used in this experiment to investigate the mechanism of nerve injury caused by ketamine anesthesia. Furthermore, our findings suggest that curcumin may affect oxidative stress and apoptosis by targeting the Nrf2 pathway, thereby alleviating the nerve injury caused by ketamine. METHODS: The rat cerebral cortex and hippocampus were stained with Nissl and immunohistochemistry to determine the number of neurons and the expression of Caspase-3, Bcl-2, and Bax. CCK-8 assay was used to determine the optimal concentration of ketamine, curcumin, and H2 O2 in PC12 cells. Flow cytometry was used to detect changes in reactive oxygen species and the rate of apoptosis in each group. To determine whether Nrf2 entered the nucleus, immunofluorescence was used. Both tissues and cells were subjected to RT-PCR and Western blotting detection at the same time. The levels of oxidative stress were determined using a malondialdehyde (MDA) and superoxide dismutase (SOD) assay kit. RESULTS: Ketamine reduced the number of neurons in the cortex and hippocampus of rats. The proteins Bax and Caspase-3 were upregulated, while Bcl-2 was down-regulated in the cortex and hippocampus. The viability of PC12 cells has decreased. MDA content increased while SOD activity decreased in cortex, hippocampus, and PC12 cells. Ketamine had an effect on the expression of some genes in the Nrf2 signaling pathway as well as apoptosis. Curcumin pretreatment may be able to prevent ketamine-induced damage. CONCLUSIONS: The oxidative stress and apoptosis caused by ketamine during growth of the cerebral cortex, hippocampus, and PC12 cells may be decreased by curcumin's activation of the Nrf2 signaling pathway. Our research provides a potential strategy for the secure administration of anesthetics in medical settings.

Activation of adenosine A3 receptor attenuates progression of osteoarthritis through inhibiting the NLRP3/caspase-1/GSDMD induced signalling.

The specific adenosine A3 receptor (A3AR) agonist (CF101) has potential for inflammation and pain in various disease, such as arthritis, cancer and neuropathic pain, while the role of A3AR in post-traumatic OA and the underlying mechanism is largely unknown. CF101 was orally administrated in OA rats induced by anterior cruciate ligament transection (ACLT) surgery, and the rat primary chondrocytes were stimulated by hydrogen peroxide (H2 O2 , 300 µM). Histologic grading system was performed for detecting cartilage degeneration and immunohistochemistry for determining pyroptosis. The moleculars associated with cartilage homeostasis and inflammatory cytokines were analysed; moreover, the activation of NLRP3 inflammasome was determined. CF101 treatment significantly attenuated OA cartilage damage, OA-related pain and cartilage pyroptosis. Chondrocytes stimulated by H2 O2 evoked ROS release, thereby promoting the activation of NLRP3 inflammasome and facilitating the cleavage of GSDMD, which ultimately resulted in the mass release of pro-inflammatory cytokines including IL-1ß and IL-18, and production of matrix hydrolase. The pre-treatment with CF101 powerfully inhibited the above process both in vivo and in vitro. Our findings demonstrated that activation of A3AR attenuates OA progression and relieves pain perception through suppression of cartilage degradation and inhibition of ROS/NLRP3/GSDMD signalling, indicating pyroptosis is a potential candidate for OA treatment.

Bioenergetics and abnormal functional connectivity in psychotic disorders.

Psychotic Disorders such as schizophrenia (SZ) and bipolar disorder (BD) are characterized by abnormal functional connectivity (FC) within neural networks such as the default mode network (DMN), as well as attenuated anticorrelation between DMN and task-positive networks (TPN). Bioenergetic processes are critical for synaptic connectivity and are also abnormal in psychotic disorders. We therefore examined the association between brain energy metabolism and FC in psychotic disorders. 31P magnetization transfer spectroscopy from medial prefrontal cortex (MPFC) and whole-brain fMRI data were collected from demographically matched groups of SZ, BD, and healthy control (HC) subjects. The creatine kinase (CK) reaction flux calculated from spectroscopy was used as an index of regional energy production rate. FC maps were generated with MPFC as the seed region. Compared to HC, SZ showed significantly lower CK flux, while both BD and SZ patients showed decreased anticorrelation between MPFC and TPN. CK flux was significantly correlated with FC between MPFC and other DMN nodes in HC. This positive correlation was reduced modestly in BD and strongly in SZ. CK flux was negatively correlated with the anticorrelation between MPFC and TPN in HC, but this relationship was not observed in BD or SZ. These results indicate that MPFC energy metabolism rates are associated with stronger FC within networks and stronger anticorrelation between networks in HC. However, this association is decreased in SZ and BD, where bioenergetic and FC abnormalities are evident. This pattern may suggest that impairment in energy production in psychotic disorders underlies the impaired neural connectivity.

Near doubling of Brazil's intensive row crop area since 2000.

Brazil has become a global leader in the production of commodity row crops such as soybean, sugarcane, cotton, and corn. Here, we report an increase in Brazilian cropland extent from 26.0 Mha in 2000 to 46.1 Mha in 2014. The states of Maranhão, Tocantins, Piauí, Bahia (collectively MATOPIBA), Mato Grosso, Mato Grosso do Sul, and Pará all more than doubled in cropland extent. The states of Goiás, Minas Gerais, and São Paulo each experienced >50% increases. The vast majority of expansion, 79%, occurred on repurposed pasture lands, and 20% was from the conversion of natural vegetation. Area of converted Cerrado savannas was nearly 2.5 times that of Amazon forests, and accounted for more than half of new cropland in MATOPIBA. Spatiotemporal dynamics of cropland expansion reflect market conditions, land use policies, and other factors. Continued extensification of cropland across Brazil is possible and may be likely under current conditions, with attendant benefits for and challenges to development.

Drivers of phenotypic variation in cartilage: Circadian clock genes.

Endogenous homeostasis and peripheral tissue metabolism are disrupted by irregular fluctuations in activation, movement, feeding and temperature, which can accelerate negative biological processes and lead to immune reactions, such as rheumatoid arthritis (RA) and osteoarthritis (OA). This review summarizes abnormal phenotypes in articular joint components such as cartilage, bone and the synovium, attributed to the deletion or overexpression of clock genes in cartilage or chondrocytes. Understanding the functional mechanisms of different genes, the differentiation of mouse phenotypes and the prevention of joint ageing and disease will facilitate future research.

Prospects of circadian clock in joint cartilage development.

Altering the food intake, exercise, and sleep patterns have a great influence on the homeostasis of the biological clock. This leads to accelerated aging of the articular cartilage, susceptibility to arthropathy and other aspects. Deficiency or overexpression of certain circadian clock-related genes accelerates the cartilage deterioration and leads to phenotypic variation in different joints. The process of joint cartilage development includes the formation of joint site, interzone, joint cavitation, epiphyseal ossification center, and cartilage maturation. The mechanism by which, biological clock regulates the cell-cycle, growth, metabolism, and other biological processes of chondrocytes is poorly understood. Here, we summarized the interaction between biological clock proteins and developmental pathways in chondrogenesis and provided the evidence from other tissues that further predicts the molecular patterns of these protein-protein networks in activation, proliferation, and differentiation. The purpose of this review is to gain deeper understanding of the evolution of cartilage and its irreversibility seen in damage and aging.

Puerarin inhibits the development of osteoarthritis through antiinflammatory and antimatrix-degrading pathways in osteoarthritis-induced rat model.

Puerarin is an isoflavone isolated from the medicinal plant Pueraria lobata. The purpose of this study was to study the antiinflammatory and antimatrix-degrading effects of puerarin in a rat osteoarthritis (OA) model and its protective effects on joints. The rat OA model was established by anterior cruciate ligament transection (ACLT) surgery. Rats (n = 40) were divided into nontreated OA, OA + celecoxib (2.86 mg/kg), OA + puerarin (50 and 100 mg/kg), and control groups. Two weeks after surgical induction, puerarin was administered by gavage daily for 8 weeks. After 8 weeks, macroscopic observation and histopathological images showed that cartilage damage was reduced after puerarin and celecoxib treatment, the intensity of Safranin O staining was high, and the OARSI scores were significantly reduced compared to the OA group. Puerarin reduced the expression of MMP-3, MMP-13, ADAMTS-5, and COX-2 in the cartilage tissue of ACLT rats, inhibited the production of IL-1ß, IL-6, and TNF-α inflammatory factors, increased Type II collagen content, and altered the expression of serum OA cartilage degradation/bone turnover biomarkers (CTX-I, CTX-II, COMP, and PIINP). Based on these findings, we speculate that puerarin supplement to attain recovery from OA damage.

The potential role of senescence in limiting fibrosis caused by aging.

Fibrosis-related diseases carry with them a high mortality rate and their morbidity increases with age. Recent findings indicate that induced senescence in myofibroblasts can limit or reduce myocardial fibrosis, cirrhosis, and idiopathic pulmonary fibrosis, while also accelerating wound healing. However, more senescent cells are accumulated as organisms age, which exacerbates aging-related diseases. These two contradictory theories inspired us to summarize papers on the restrictive effect of senescence on fibrosis and to input the key findings into simple software that we developed to assist with data organization and presentation. In this review, we illustrate that senescent cells secrete more matrix metalloproteinases to solubilize excess collagen, while chemokines and cytokines activate immune cells to eliminate senescent cells. In the elderly, it is perhaps more effective to limit fibrosis by inducing myofibroblast senescence and then removing senescent cells that are not cleared via normal mechanisms by antisenescence therapies.

Aberrant Brain Functional Connectivity Dynamic Responses to the Valsalva Maneuver in Heart Failure.

BACKGROUND: Patients with heart failure (HF) show abnormal autonomic activities, which may stem from altered functional connectivity (FC) between different brain sites. METHODS AND RESULTS: We evaluate insular and cerebellar FC with other brain areas, before, during, and after the Valsalva challenge, with functional magnetic resonance imaging in 35 HF and 35 control subjects. Significant insular FC emerged with striatum, thalamus, and anterior cingulate. While left and right cerebellar cortices showed significant FC with each other constituting the cerebellum network, the insula and cerebellum networks showed significant negative FC with each other at baseline, challenge, and recovery phases. The challenge induced increased FC within the insula and the cerebellum networks in both HF and controls. However, patients with HF showed more increased insular network FC, but less enhanced cerebellar FC. During the recovery phase, the negative FC between the insular network and cerebellum enhanced significantly in controls, but not in HF. Lower left ventricle ejection fraction was correlated with lower insula network FC, and impaired negative FC between cerebellum and the insula network in HF. CONCLUSIONS: Increased insular FC in patients with HF might contribute to exaggerated sympathetic tone. While impaired cerebellar FC and diminished negative interactions between cerebellum and insular systems may indicate impaired parasympathetic functions in HF.

Brain structural changes associated with aberrant functional responses to the Valsalva maneuver in heart failure.

Heart failure (HF) patients show inability to regulate autonomic functions in response to autonomic challenges. The autonomic deficits may stem from brain tissue injury in central autonomic regulatory areas, resulting from ischemic and hypoxic processes accompanying the condition. However, the direct evaluation of correlations between brain structural injury and functional timing and magnitude of neural signal patterns within affected areas, which may lead to impaired autonomic outflow, is unclear. In this study, we evaluate neural responses to the Valsalva maneuver with blood oxygen level-dependent functional magnetic resonance imaging in 29 HF patients and 35 control subjects and brain structural changes using diffusion tensor imaging-based mean diffusivity in a subsample of 19 HF and 24 control subjects. HF showed decreased neural activation in multiple autonomic and motor control areas, including cerebellum cortices, vermis, left insular, left putamen, and bilateral postcentral gyrus. Structural brain changes emerged in similar autonomic, as well as cognitive and mood regulation areas. Functional MRI responses in cerebellum and insula in HF subjects are delayed or decreased in magnitude to the challenge. The impaired functional responses of insular and cerebellar sites are correlated with the severity of tissue changes. These results indicate that the functions of insular and cerebellar regions, sites that are involved in autonomic regulation, are compromised, and that autonomic deficits in these areas have brain structural basis for impaired functions. Our study enhanced our understanding of brain structural and functional alterations underlying impaired autonomic regulations in HF subjects.

Abnormal functional connectivity of the amygdala is associated with depression in Parkinson's disease.

Depressive symptoms are common in Parkinson's disease (PD), but the pathophysiology and neural basis underlying depression in PD is not well understood. Abnormal functional connectivity of the amygdala with various cortical and subcortical areas has been observed in major depressive disorder, indicating that dysfunction of the corticolimbic network may be involved in the pathogenesis of major depressive disorder. However, little is known about alterations of amygdala functional connectivity in depressed PD patients. In the present study, 20 depressed PD patients, 40 nondepressed PD patients, and 43 matched healthy controls underwent neuropsychological tests and resting-state functional MRI scanning. Between-group differences in amygdala functional connectivity network were examined using t tests. Compared to the nondepressed PD patients, depressed PD patients showed increased left amygdala functional connectivity with the bilateral mediodorsal thalamus, right amygdala functional connectivity with the left superior temporal gyrus, and left calcarine gyrus. Compared to the healthy controls, the depressed PD group also showed increased left amygdala functional connectivity with the bilateral mediodorsal thalamus, but decreased left amygdala functional connectivity with the left putamen, left inferior frontal gyrus, and the right cerebellum, as well as decreased right amygdala functional connectivity with the left inferior orbitofrontal gyrus, the left gyrus rectus, and the right putamen. The increased connectivity between limbic regions and decreased connectivity between the corticolimbic networks may reflect impaired high-order cortical regulatory effects on the emotion-related limbic areas, which may lead to mood dysregulation. Our study should advance the understanding of neural mechanisms underlying depression in PD.