Cholecystokinin B receptor agonists alleviates anterograde amnesia in cholecystokinin-deficient and aged Alzheimer's disease mice.

BACKGROUND: As one major symptom of Alzheimer's disease (AD), anterograde amnesia describes patients with an inability in new memory formation. The crucial role of the entorhinal cortex in forming new memories has been well established, and the neuropeptide cholecystokinin (CCK) is reported to be released from the entorhinal cortex to enable neocortical associated memory and long-term potentiation. Though several studies reveal that the entorhinal cortex and CCK are related to AD, it is less well studied. It is unclear whether CCK is a good biomarker or further a great drug candidate for AD. METHODS: mRNA expressions of CCK and CCK-B receptor (CCKBR) were examined in two mouse models, 3xTg AD and CCK knock-out (CCK-/-) mice. Animals' cognition was investigated with Morris water maze, novel object recognition test and neuroplasticity with in-vitro electrophysiological recording. Drugs were given intraperitoneally to animals to investigate the rescue effects on cognitive deficits, or applied to brain slices directly to explore the influence in inducement of long-term potentiation. RESULTS: Aged 3xTg AD mice exhibited reduced CCK mRNA expression in the entorhinal cortex but reduced CCKBR expression in the neocortex and hippocampus, and impaired cognition and neuroplasticity comparable with CCK-/- mice. Importantly, the animals displayed improved performance and enhanced long-term potentiation after the treatment of CCKBR agonists. CONCLUSIONS: Here we provide more evidence to support the role of CCK in learning and memory and its potential to treat AD. We elaborated on the rescue effect of a promising novel drug, HT-267, on aged 3xTg AD mice. Although the physiological etiology of CCK in AD still needs to be further investigated, this study sheds light on a potential pharmaceutical candidate for AD and dementia.

Association between the insufficient improvement of the quantitative flow ratio and worsening outcomes in ST-segment elevated myocardial infarction: a multicentre prospective cohort study.

Background: Improved coronary physiological function after percutaneous coronary intervention (PCI) has been shown to improve prognosis in stable ischaemic heart disease, but has not yet been explored in ST-segment elevated myocardial infarction (STEMI). The study sought to determine whether an improvement in the quantitative flow ratio (QFR) could improve the prognosis of STEMI patients undergoing primary PCI. Methods: Patients diagnosed with STEMI who were receiving primary PCI were recruited for the study. Those with thrombolysis in myocardial infarction (TIMI) flow <2 after wiring were excluded. The ΔQFR was calculated using the following formula: ΔQFR = post-PCI QFR - pre-stent QFR. The primary endpoint was the composite event, including recurrent myocardial infarction (MI) and acute heart failure (AHF). Results: In total, 515 STEMI patients with a median follow-up of 364 days were enrolled in the study. Based on the cut-off value from the receiver operator characteristic (ROC) curve, the patients were divided into the following two groups: the lower ΔQFR group (≤0.25, N=332); and the normal ΔQFR group (>0.25, N=183). Patients with a lower ΔQFR had a relatively higher rate of MI/AHF (10.5% vs. 4.4%, P=0.019) and AHF (7.2% vs. 2.7%, P=0.044). A lower ΔQFR was significantly associated with a higher incidence of MI/AHF [hazard ratio (HR) =2.962, 95% confidence interval (CI): 1.358-6.459, P=0.006, respectively] after adjusting for potential confounders. Pre-stent angiographic microvascular resistance [odds ratio (OR) =1.027, 95% CI: 1.022-1.033, P<0.001] and the stent-to-vessel diameter ratio <1.13 (OR =1.766, 95% CI: 1.027-3.071, P=0.04) were independent predictors of a lower ΔQFR. Conclusions: An insufficient improvement in the QFR contributes to worsening outcomes and might be a useful tool for risk stratification in STEMI.

Response surface optimization of sludge dewatering process: synergistic enhancement by ultrasonic, chitosan and sludge-based biochar.

Due to the colloidal stability, the high compressibility and the high hydration of extracellular polymeric substances (EPS), it is difficult to efficiently dehydrate sludge. In order to enhance sludge dewatering, the process of ultrasonic (US) cracking, chitosan (CTS) re-flocculation and sludge-based biochar (SBB) skeleton adsorption of water-holding substances to regulate sludge dewaterability was proposed. Based on the response surface method, the prediction model of the specific resistance to filtration (SRF) and sludge cake moisture content (MC) was established. The US cracking time and the dosage of CTS and SBB were optimized. The results showed that the optimal parameters of the three were 5.08 s, 10.1 mg/g dry solids (DS) and 0.477 g/g DS, respectively. Meantime, the SRF and MC were 5.4125 × 1011 m/kg and 76.8123%, which significantly improved the sludge dewaterability. According to the variance analysis, it is found that the fitting degree of SRF and MC model is good, which also confirms that there is significant interaction and synergy between US, CTS and SBB, and the contribution of CTS and SBB is greater. Moreover, the process significantly improves the sludge's calorific value and makes its combustion more durable.

Characteristics and evaluation of heavy metal pollution in a soil-wheat system of an arid oasis city in northwest China.

In this paper, the Cu and Ni accumulation and contamination levels in agricultural soils and wheat around a smelter in Jinchang City in northwest China were investigated with a combination of field investigations and indoor analytical tests, using a soil-wheat system as the study area. The average Cu and Ni contents in the soil were 119.50 mg kg-1 and 123.40 mg kg-1, respectively, both of which exceeded the local soil background values. The Cu and Ni contents in 46.15% o and 26.92% of sampling sites, respectively, exceeded the screening values for soil contamination risk in agricultural land in China. The average Cu content in different parts of wheat was in the order of roots (24.22 mg kg-1) > leaves (20.11 mg kg-1) > husks (5.51 mg kg-1) > grains (4.05 mg kg-1) > stalks (3.74 mg kg-1). Furthermore, the average Ni content ranked as leaves (24.64 mg kg-1) > roots (21.12 mg kg-1) > husks (6.95 mg kg-1) > stalks (1.75 mg kg-1) > grains (0.38 mg kg-1). The health risk evaluation showed that with average hazard index values of 0.88 for adults and 1.04 for children for Cu and Ni in wheat grain, wheat in this region is unlikely to pose a health risk to adults but may pose a lesser health risk to children. The Ni bio-concentration and translocation factors in the husk and leaves of wheat were greater than those of Cu and smaller than those of Cu in the other parts of wheat. The results of this study provide basic data for the remediation of heavy metal contamination in local agricultural soils.

Visually or auditorily induced seizures involve the activation of nonhippocampal brain areas and hippocampal removal does not alleviate seizures in a mouse model of temporal lobe epilepsy.

OBJECTIVE: Several studies have attributed epileptic activities in temporal lobe epilepsy (TLE) to the hippocampus; however, the participation of nonhippocampal neuronal networks in the development of TLE is often neglected. Here, we sought to understand how these nonhippocampal networks are involved in the pathology that is associated with TLE disease. METHODS: A kainic acid (KA) model of temporal lobe epilepsy was induced by injecting KA into dorsal hippocampus of C57BL/6J mice. Network activation after spontaneous seizure was assessed using c-Fos expression. Protocols to induce seizure using visual or auditory stimulation were developed, and seizure onset zone (SOZ) and frequency of epileptic spikes were evaluated using electrophysiology. The hippocampus was removed to assess seizure recurrence in the absence of hippocampus. RESULTS: Our results showed that cortical and hippocampal epileptic networks are activated during spontaneous seizures. Perturbation of these networks using visual or auditory stimulation readily precipitates seizures in TLE mice; the frequency of the light-induced or noise-induced seizures depends on the induction modality adopted during the induction period. Localization of SOZ revealed the existence of cortical and hippocampal SOZ in light-induced and noise-induced seizures, and the development of local and remote epileptic spikes in TLE occurs during the early stage of the disease. Importantly, we further discovered that removal of the hippocampi does not stop seizure activities in TLE mice, revealing that seizures in TLE mice can occur independent of the hippocampus. SIGNIFICANCE: This study has shown that the network pathology that evolves in TLE is not localized to the hippocampus; rather, remote brain areas are also recruited. The occurrence of light-induced or noise-induced seizures and epileptic discharges in epileptic mice is a consequence of the activation of nonhippocampal brain areas. This work therefore demonstrates the fundamental role of nonhippocampal epileptic networks in generating epileptic activities with or without the hippocampus in TLE disease.

Microvascular and Prognostic Effect in Lesions With Different Stent Expansion During Primary PCI for STEMI: Insights From Coronary Physiology and Intravascular Ultrasound.

Background: While coronary stent implantation in ST-elevation myocardial infarction (STEMI) can mechanically revascularize culprit epicardial vessels, it might also cause distal embolization. The relationship between geometrical and functional results of stent expansion during the primary percutaneous coronary intervention (pPCI) is unclear. Objective: We sought to determine the optimal stent expansion strategy in pPCI using novel angiography-based approaches including angiography-derived quantitative flow ratio (QFR)/microcirculatory resistance (MR) and intravascular ultrasound (IVUS). Methods: Post-hoc analysis was performed in patients with acute STEMI and high thrombus burden from our prior multicenter, prospective cohort study (ChiCTR1800019923). Patients aged 18 years or older with STEMI were eligible. IVUS imaging, QFR, and MR were performed during pPCI, while stent expansion was quantified on IVUS images. The patients were divided into three subgroups depending on the degree of stent expansion as follows: overexpansion (>100%), optimal expansion (80%-100%), and underexpansion (<80%). The patients were followed up for 12 months after PCI. The primary endpoint included sudden cardiac death, myocardial infarction, stroke, unexpected hospitalization or unplanned revascularization, and all-cause death. Results: A total of 87 patients were enrolled. The average stent expansion degree was 82% (in all patients), 117% (in overexpansion group), 88% (in optimal expansion), and 75% (in under-expansion). QFR, MR, and flow speed increased in all groups after stenting. The overall stent expansion did not affect the final QFR (p = 0.08) or MR (p = 0.09), but it reduced the final flow speed (-0.14 cm/s per 1%, p = 0.02). Under- and overexpansion did not affect final QFR (p = 0.17), MR (p = 0.16), and flow speed (p = 0.10). Multivariable Cox analysis showed that stent expansion was not the risk factor for MACE (hazard ratio, HR = 0.97, p = 0.13); however, stent expansion reduced the risk of MACE (HR = 0.95, p = 0.03) after excluding overexpansion patients. Overexpansion was an independent risk factor for no-reflow (HR = 1.27, p = 0.02) and MACE (HR = 1.45, p = 0.007). Subgroup analysis shows that mild underexpansion of 70%-80% was not a risk factor for MACE (HR = 1.11, p = 0.08) and no-reflow (HR = 1.4, p = 0.08); however, stent expansion <70% increased the risk of MACE (HR = 1.36, p = 0.04). Conclusions: Stent expansion does not affect final QFR and MR, but it reduces flow speed in STEMI. Appropriate stent underexpansion of 70-80% does not seem to be associated with short-term prognosis, so it may be tolerable as noninferior compared with optimal expansion. Meanwhile, overexpansion and underexpansion of <70% should be avoided due to the independent risk of MACEs and no-reflow events.

Non-stenting strategy is not inferior to stent implantation in patients with acute ST-segment elevated myocardial infarction and high thrombus burden and intermediate stenotic culprit lesion.

BACKGROUND: According to European Society of Cardiology (ESC) as well as American College of Cardiology/American Heart Association (ACC/AHA) guidelines, primary stenting is recommended for patients with acute ST-segment elevation myocardial infarction (STEMI); however, in-stent thrombosis is a life-threatening early adverse event that could lead to acute myocardial infarction (AMI) or even cardiac death. On the other hand, in-stent restenosis is a late adverse event that could result in recurrent readmission and revascularization. We compared a non-stenting (NS) strategy to a stenting (S) strategy in terms of incidence of major adverse cardiac events (MACEs) for patients with acute STEMI and high thrombus burden. METHODS: We performed a post hoc analysis of our prior multicenter, prospective cohort study (ChiCTR1800019923) among 51 eligible patients with acute STEMI and high thrombus burden. All participants received percutaneous coronary intervention (PCI) with a deferred-stenting strategy (second procedure performed within 48-72 h after primary PCI). Either NS or S strategies were carried out among patients. Primary outcomes were follow-ups of MACEs at 1, 3, 6, and 12 months. Intravenous ultrasound (IVUS) and quantitative flow ratio (QFR) evaluation were performed. RESULTS: In our post hoc analysis of 51 patients (21 with NS and 30 with S), baseline clinical and interventional characteristics were well matched between the 2 groups, to the exception of culprit lesion length. Incidence of MACEs was not significantly different between the 2 strategies in-hospital (P=0.56) and in follow-ups at 1 (P=0.41), 3 (free of events), 6 (P=0.71), and 12 (P=0.68) months. Culprit lesions of NS tended to be "low-risk" [minimum lumen area (MLA) 4.27±1.02 vs. 3.80±1.32 mm2, P=0.36] and plaque burden (70.79%±6.46% vs. 76.97%±6.76%, P=0.03) when compared with culprit lesions of S in IVUS evaluation. Evaluation of QFR showed more sufficient physiological reperfusion improvement with NS than with S [two-dimensional (2D) QFR: 0.85±0.09 vs. 0.79±0.13, P=0.10 and 3D QFR: 0.86±0.08 vs. 0.78±0.15, P=0.02]. CONCLUSIONS: The NS strategy did not increase MACEs in-hospital and at 1, 3, 6, and 12 months. The NS can be a safe option when meeting certain criteria for patients with STEMI and a high thrombus burden.

The outcomes in STEMI patients with high thrombus burden treated by deferred versus immediate stent implantation in primary percutaneous coronary intervention: a prospective cohort study.

BACKGROUND: No-/slow-reflow indicates worse outcomes in ST-elevation myocardial infarction (STEMI) patients with high thrombus burden. We examined whether deferred stenting (DS) strategy reduces no-/slow-reflow or major adverse cardiovascular events (MACEs) in primary percutaneous coronary intervention (pPCI) for patients with acute STEMI and high thrombus burden. METHODS: We performed an open-label, multi-center, prospective cohort study among eligible patients with acute STEMI and high thrombus burden who further received pPCI. All participants received PCI with DS (second procedure performed within 48-72 h) or immediate-stenting (IS) strategy. The primary outcome was the incidence of no-/slow-reflow. We evaluated MACEs and bleeding events during hospitalization and at 30- and 90-day follow-ups. RESULTS: We recruited 245 patients to this study, including 51 with DS and 194 with IS. Baseline clinical characters were comparable between the 2 strategies. Incidence of no-/slow-reflow defined by thrombolysis in myocardial infarction (TIMI) flow grade was not significantly different between the 2 strategies [DS: 5 (9.8%), IS: 33 (17.0%), P=0.21]. No-/slow-reflow by TIMI myocardial perfusion grade (TMPG) was less prevalent in DS [20 (39.2%) vs. 107 (55.2%), P=0.04]. No significant differences were found in recurrence of myocardial infarction (P=0.56), cardiac death (P=0.37), all-cause mortality (P=0.37), heart failure-induced readmission (P=0.35), or bleeding (P=0.61) between the 2 strategies in-hospital, and at 30- and 90-day follow-up. CONCLUSIONS: In STEMI patients with high thrombus burden who underwent pPCI, DS strategy reduced no-/slow-reflow of microcirculation. However, DS strategy did not reduce incidence of MACEs or bleeding.

Short-course Regimen for Subsequent Treatment of Pulmonary Tuberculosis: A Prospective, Randomized, Controlled Multicenter Clinical Trial in China.

PURPOSE: We designed a prospective, multicenter, randomized, controlled study to assess a 5-month regimen compared with the standard regimen on previously treated patients with pulmonary tuberculosis (TB). METHODS: We enrolled 917 sputum smear-positive patients undergoing additional treatment in 27 major tuberculosis hospitals in China. Patients were randomly assigned to a test group (n = 626)treated with a 5-month regimen of moxifloxacin, pasiniazid, rifabutin, ethambutol, and pyrazinamide or a reference group (n = 291) treated with an 8-month regimen of isoniazid, rifampicin, and streptomycin. All patients with a favorable response were followed up for 5 years after the end of treatment. FINDINGS: Of the study patients, 61 in the test group and 19 in the reference group had multidrug-resistant (MDR) TB. The treatment success rate in the study group was 74.12%, which was significantly higher than the 67.70% in the reference group (P = 0.04), whereas the treatment success rate of patients with MDR-TB was not significantly different between the test and reference groups (70.5% vs 63.1%, P =0.79). The adverse effects rates in the test and reference groups were 7.4% and 3.1%, respectively (P = .01). The difference in the TB recurrence rates between the group arm (9.6%) and the reference group (21.8%) was statistically significant (P < 0.001). IMPLICATIONS: The moxifloxacin, pasiniazid, rifabutin, ethambutol, and pyrazinamide test regimen yielded higher success and lower recurrence rates than the currently recommended isoniazid, rifampicin, and streptomycin regimen, but the rate of adverse effects was higher. ClinicalTrials.gov identifier: NCT02331823.

Comparison of glutathione reductase activity and the intracellular glutathione reducing effects of 13 derivatives of 1'-acetoxychavicol acetate in Ehrlich ascites tumor cells.

In a previous study, we showed that (1'S)-acetoxychavicol acetate ((S)-ACA) caused a rapid decrease in glutathione (GSH) levels less than 15 min after exposure. (S)-ACA-induced cell death was reversed by the addition of N-acetylcysteine. In the current study, we investigated the inhibitory activities of 13 derivatives of (S)-ACA on tumor cell viability, intracellular GSH level and GR activity. Correlations were found among a decrease in cell viability, intracellular GSH levels and the activity of GR in Ehrlich ascites tumor cells treated with the various ACA analogues. A test of the 13 derivatives revealed that the structural factors regulating activity were as follows: (1) the para or 1'-position of acetoxyl group (or other acyl group) was essential, (2) the presence of a C2'-C3' double or triple bond was essential, and (3) the S configuration of the 1'-acetoxyl group was preferable.

Combination of Zizyphus jujuba and green tea extracts exerts excellent cytotoxic activity in HepG2 cells via reducing the expression of APRIL.

Hepatocellular carcinoma is a type of tumor highly resistant to available chemotherapeutic agents. The treatment of hepatocellular carcinoma remains a challenge that needs new approaches in the future. In a previous study, we demonstrated that the chloroform fraction (CHCl(3)-F) from Z. jujuba has anticancer activity in human liver cancer cells (HepG2), and that combining CHCl(3)-F with green tea extracts (GTE) results in enhanced effects of anticancer activity in the cells. To further understand the mechanism of the anticancer activity of combining CHCl(3)-F and GTE in HepG2 cells, we investigated whether the addition of a mixture of CHCl(3)-F and GTE would affect the expression of APRIL (a proliferation-inducing ligand), which was expressed in HepG2 cells from 4 hours of incubation in vitro. We have shown that CHCl(3)-F and GTE enhanced anti-cancer activity by reducing the expression of APRIL. We speculate that the CHCl(3)-F and GTE mixture might provide a lead to a new drug design to treat hepatocellular carcinoma in the future.

1'-Acetoxychavicol acetate-induced cytotoxicity is accompanied by a rapid and drastic modulation of glutathione metabolism.

The effect of 1'-acetoxychavicol acetate (ACA), an anticarcinogenic compound naturally obtained from rhizomes and seeds of South East Asia plants, on the intracellular concentration of glutathione and the activities of enzymes related to glutathione metabolism was studied in Ehrlich ascites tumor cells. We showed in a previous study that ACA induced apoptosis in tumor cells and the cell death was reversed by the addition of N-acetlycysteine or glutathione ethylester. Here we found that ACA caused a rapid decrease in glutathione level in less than 10 min after ACA exposure. At the time, glutathione reductase activity was significantly inhibited and gamma-glutamyl cysteine increased by ACA exposure. These results show that ACA caused the decrease in the intracellular GSH levels in Ehrlich ascites tumor cells, suggesting that ACA-induced decrease of the cellular GSH levels can lead to growth arrest of cancer and enhancement of the efficacy other anticancer drugs.

Green tea extract enhances the selective cytotoxic activity of Zizyphus jujuba extracts in HepG2 cells.

Anticarcinogenic effects attributed to phytochemicals may be based on synergistic, additive, or antagonistic interactions of many compounds. In our previous study, we demonstrated that the chloroform fraction (CHCl(3)-F) from Z. jujuba has anticancer activity in HepG2 cells. In China, many people drink jujuba tea and believe in the synergic effects of jujuba and tea for better health. We therefore investigated the effects of CHCl(3)-F and green tea extract (GTE), and their underlying mechanisms of action in HepG2 cells. Our results showed that GTE enhanced the effect of CHCl(3)-F on cell viability in HepG2 cells, without cytotoxicity in rat hepatocytes, which was used as a normal cell model. Furthermore, combination of CHCl(3)-F and GTE caused an effect on G1 phase arrest but not on apoptosis. Interestingly, the mechanism of the G1 arrest was associated, not with an increase in p27(Kip1) levels and the hypohosphorylation of Rb, which are pathways used by CHCl(3)-F on G1 arrest in HepG2 cells, but with increases in p53 and p21(Waf1/Cip1) levels, and a decrease in cyclin E levels. Collectively, our findings suggest that combination of CHCl(3)-F and GTE produces an enhanced cell growth inhibition effect, and that the resultant G1 arrest was caused via a different mechanism as that of CHCl(3)-F treatment alone.

Mechanism of growth inhibitory effect of Blumea balsamifera extract in hepatocellular carcinoma.

Blumea balsamifera is known to improve physiological disorders such as rheumatism and hypertension, but its anticancer activity has not been well elucidated. In this study, we found that Blumea balsamifera MeOH extract (BME) induced growth-inhibitory activity in rat and human hepatocellular carcinoma cells without cytotoxicity in rat hepatocytes which were used as a normal cell model. BME induced cell cycle arrest at the G1 phase via decreases in the expression of cyclin-E and phosphorylation of retinoblastoma protein. Furthermore, BME reduced the level of a proliferation-inducing ligand, that stimulates tumor cell growth. These findings suggest that BME has possible therapeutic potential in hepatoma cancer patients and that depletion of cellular APRIL is an important mechanism in the growth-inhibitory effect of BME.

Anticancer activities and mechanisms of Blumea balsamifera extract in hepatocellular carcinoma cells.

Blumea balsamifera (also known as sambong), a medicinal plant, is known to improve physiological disorders such as rheumatism and hypertension. However, its anticancer activity has not been well elucidated. In this study, we found that Blumea balsamifera MeOH extract (BME) induced growth inhibitory activity in rat and human hepatocellular carcinoma cells (McA-RH7777, HepG2, respectively) without cytotoxicity as in with rat hepatocytes used as a normal cell model. BME induced cell cycle arrest at G1 phase via decreases in expression of cyclin-E and phosphorylation of retinoblastoma (Rb) protein in both dose- and time-dependent manners. Furthermore, BME reduced the level of a proliferation related ligand (APRIL) which stimulates tumor cell growth. The anti-proliferative effect of BME was improved slightly but significantly by the treatment with recombinant human APRIL. These findings suggest that BME may have a possible therapeutic potential in hepatoma cancer patients and the depletion of cellular APRIL may be one of the important mechanisms on the growth inhibitory effect of BME.

(1'S)-Acetoxychavicol acetate and its enantiomer inhibit tumor cells proliferation via different mechanisms.

Elucidation of the mechanisms underlying potential anticancer drugs continues and unraveling these mechanisms would not only provide a conceptual framework for drug design but also promote use of natural products for chemotherapy. The biological effects of (1'S)-acetoxychavicol acetate ((S)-ACA) have been widely investigated. However, in most cases, a natural product or synthetic racemic compound was used in the study. In this study, we prepared (S)-ACA and its enantiomer (R)-ACA by a lipase-catalyzed esterification method and sought to determine the mechanisms of action of (S)-ACA and (R)-ACA in the growth inhibitory effect in Ehrlich ascites tumor cells (EATC). (S)-ACA caused an accumulation of tumor cells in the G1 phase of the cell cycle, which was accompanied by a decrease in phosphorylated retinoblastoma protein (Rb), an increase in Rb and a decrease in the phosphorylation of p27kip1. However, (R)-ACA caused an accumulation of tumor cells in the G2 phase of the cell cycle, an increase in hyperphosphorylated Rb and an increase in the phosphorylation of p27kip1. The results obtained in the present study demonstrate for the first time, to the best of our knowledge, that both (S)-ACA and (R)-ACA caused the inhibition of tumor cells growth but the inhibition was caused via different mechanisms.

[Revaluation of soil heavy metals pollution in Zhangshi irrigation area of Shenyang and analysis of Cd forms in soil].

This paper revaluated the situation of cadmium (Cd) pollution in rice field soils of Zhangshi irrigation area in Shenyang. The results indicated that the soil Cd pollution of test area was still quite serious. The Cd content in brown rice samples ranged from 0.435 to 0.855 mg x kg(-1), which exceeded the national criteria for food sanitation in China, and increased by 335%-755% compared with that 20 years ago. Brown rice Cd had a significant negative correlation with soil pH, and a positive correlation with soil available Cd. The decrease of soil pH induced more soil Cd transformed into available Cd which occupied 22.8%-52.0% of the total Cd and was easy to be absorbed by rice plant, inducing the Cd in brown rice exceeded national criteria. The pollutant Cd could transfer along with surface runoff, ground water and flying dust, making the pollution extend gradually.