Quantifying the contributions of natural and anthropogenic dust sources in Shanxi Province, northern China.

Dust storms have direct or indirect impacts on climate change and human health. Identifying and quantifying natural/anthropogenic dust sources can facilitate effective prevention and control of dust events. Based on surface real-time PM10 monitoring data, satellite remote sensing and the HYSPLIT model, this study determined the specific timing, coverage and sources of dust events in Shanxi Province, Northern China. Thus, a composite fingerprinting technique was established to quantify potential dust sources and dust contributions of single dust events. The dust oxidation model was validated, indicating that the composite fingerprinting technique was well suited to the study region. The results show that natural dust sources (67%) contributed more to the study region than anthropogenic dust sources. They were mainly from the northwest and north of the study region. Particularly, the contributions of Taiyuan (TY) and Linfen (LF) accounted for the largest (82%) and smallest (55%) proportions, respectively, both exceeding 50%. Anthropogenic dust sources contributed 33%, mainly from the east and south of the study region. The contribution of anthropogenic dust sources increased in the study region from north to south. In terms of potential dust sources, the Tengger Desert and Badain Jaran Desert (TDBD) contributed the most (26%), followed by the Otindag Sandy Land (OL) (22%). The Taklimakan Desert (TD) contributed the least (2%). The Middle Farmland region of the Hexi Corridor (HMF) in the west (15%) had the largest proportion of anthropogenic dust sources. Differences in the regional contribution of potential dust sources mainly resulted from winter winds, surface drought severity and particle size. At an insignificant distance from the study region, the contribution of potential dust sources was larger in the west than in the east and increased from south to north overall. These methods and findings can contribute to improving the ecological environment in Northern China.

[Glaucoma-related adverse events and their associated factors after cataract surgery in congenital cataracts: a review and update].

Congenital cataract is one of the main causes of blindness in children. Glaucoma-related adverse event (GRAE) is a serious complication of congenital cataract extraction. Its occult onset can cause irreversible damage to the optic nerve, its related factors are, however, not clear. In recent years, with the deepening of research, we have a more comprehensive understanding of the risk factors of glaucoma-related adverse events. This paper summarizes in detail the impact of its risk factors: ocular anatomical features, surgical design, other ocular and systemic diseases on GRAE, and systematically summarizes its diagnostic criteria, treatment and prognosis, in order to provide a comprehensive reference of research-related factors affecting GRAE after cataract surgery and indication for the vacancy in scientific research and to establish a prediction model for the incidence of postoperative GRAE based on the analysis of influencing factors, and precisely predict the prognosis of children after surgery cataract in clinical aspect.

[Study on the Protective effect and mechanism of Nicotinamide Riboside on lung injury in paraquat intoxicated mice].

Objective: To investigate the protective effect and mechanism of Nicotinamide Riboside (NR) on lung injury caused by Paraquat intoxicated mice. Methods: Eighty clean male BALB/C mice were selected and averagely divided forty mice into 4 groups with 10 mice in each group, PQ group was given 25% PQ solution (60 mg/kg) by one-time gavage. PQ+NR group were intraperitoneally injected with NR solution (300 mg/kg) 1 hour before given the same amount of PQ solution (60 mg/kg) by one-time gavage, The Control group were given the same amount of saline by one-time gavage, The same amount of NR was intraperitoneally injected before NR group were given saline by one-time gavage. Observed and recorded general condition of PQ intoxicated mice. Observed and recorded the death of mice every half an hour and counted the mortality and drew survival curve of each group after 72 hours exposure. another forty mice were averagely divided and treated by the same way. After 24 hours of modelling, mice were anaesthetized and killed. Then blood was extracted after eyeball was removed. The changes of TNF-a、IL-6 and MPO in serum of mice were detected by ELISA.Two lung tissues were removed from the chest and used to measure the D/W ratio of the lung. The pathological changes of lung were observed and scored under light microscope.The levels of SOD, MDA and Caspase-3 in lung tissues were determined by chemical colorimetry. The expression of Sirt1 and Nrf2 in lung tissues was detected by Western-blot. Results: Compared with the Control group and the NR group, the mice in the PQ group had a poor general condition, such as depression, crouching, skin disorder and reduced activity, food, urine and feces. The symptoms in the PQ+NR group were reduced compared with the PQ group. The survival rate at 72 hours after exposure: 80% in the PQ+NR group and 40% higher than that in the PQ group (P=0.029) . Compared with Control group and NR group, the D/W ratio (0.09±0.07) , lung pathology score under light microscope (11.80±0.37) , TNF-a (39.89±1.48) pg/ml、IL-6 (77.29±2.38) pg/ml、MPO (0.31±0.01) µg/ml、SOD (6.62±0.30) U/mgprot、MDA level (1.21±0.14) mmol/mgprot, Caspase-3 activity (356.00± 27.16) %, Sirt1 and Nrf2 protein expression (1.02±0.14、0.82±0.06) were significantly decreased in PQ group (P=0.004、0.023) ; Compared with PQ group, PQ+NR group significantly increased the D/W ratio (0.10±0.10) , decreased the pulmonary pathology score under light microscope (7.400.51) , decreased TNF-a (33.00± 0.65) pg/ml、IL-6 (52.23±4.23) pg/ml、MPO leve (0.23±0.01) µg/mll, increased SOD leve (9.28±0.45) U/mgprotl, decreased MDA level (0.78±0.02) mmol/mgprot, decreased Caspase-3 activity (222.80±7.59) %, and increased the protein expressions of Sirt1 and Nrf2 (1.62±0.16、1.06±0.04) (P=0.048、0.035) . Conclusion: NR can prolong the survival time of PQ poisoned mice; NR intervention can effectively inhibit the inflammatory response, peroxidation injury and apoptosis of PQ poisoned mice; NR intervention can upregulate the expression of Sirt1 and Nrf2 protein and effectively reduce the lung injury of PQ poisoning.

[The epidemic and prevention of plagues in modern Shanghai].

It was found that a variety of plagues were prevalent in Shanghai at the end of the Qing Dynasty and the beginning of the Republic of China, by analysing and synthesising the epidemic situation, the causes of the epidemic, the social impact, and prevention and control measures. These plagues led to serious social harm and economic losses. Their causes were believed closely related to some factors, such as urban environment, population flow, and climate changes. Their prevention appeared to be applicable and effective. The Shanghai concession and Chinese authorities organised society to fight against plagues and stabilise the social order. Charity organisations of the local communities were also involved in social support. It was found that more can be done in studies on interdisciplinary synthesis, comparative study of epidemic prevention measures of managers, and of traditional Chinese medicine prevention and treatment.

[Study on the protective effect and mechanism of somatostatin on renal injury in paraquat intoxicated mice].

Objective: To investigate the protective effect of somatostatin (SS) on acute kidney injury (AKI) of paraquat (PQ) poisoned mice and its mechanism. Methods: From December 2017 to April 2018, a total of 48 SPF male BALB/C mice were selected and randomly divided into 4 groups, with 12 mice in each group: Control group, SS group (20 mg/kg SS was injected 1 hour before and 3 hours after gavage with normal saline) , PQ group (2% PQ 60 mg/kg by gavage) and PQ+SS group (Intragastric administration was performed with 2% PQ solution of 60 mg/kg, and 20 mg/kg SS was administered 1 h before and 3 h after intragastric administration) , 12 mice in each group were observed for the general situation and behavioral effects. After 24 hours of modeling, mice were sacrificed.Then blood was extracted after eyeball was removed, and both kidneys were removed by laparotomy. Serum IL-6, TNF-α and MPO levels were determined by ELISA. The characteristic pathological changes of toxic renal tubular injury were observed under light microscope and scored accordingly. The changes of NF-κB expression were detected by Western-Blot, SOD, Caspase-3 and malondialdehyde (MDA) were detected by chemical colorimetry. Results: Mice in Control group and SS group showed normal general conditions and behaviors; Mice in PQ group were significantly worse than those in Control group, showing decreased feeding and activity, dry fur, hair shedding and listless spirit; The above symptoms in the mice of PQ+SS group were alleviated compared with the PQ group. Under the light microscope, the renal tissue structure of PQ group was obviously disordered and severely damaged, and the nephropathy score was (6.14±0.72) . The performance of PQ+SS group under light microscope was improved compared with PQ group, and nephropathy score (4.36±0.42) decreased (P<0.05) . Compared with the Control group, serum TNF-α (39.89±3.32) pg/ml, IL-6 (77.29±4.77) pg/ml, renal NF-κB (2.29±0.097) , MPO (0.31±0.017) µg/ml, MDA (0.91±0.03) mmol/mg prot, and Caspase-3 (376.51±8.24) % levels were significantly increased in the PQ group, while the level of renal SOD (2.36±0.73) U/mg prot was significantly decreased (P<0.05) . Compared with the PQ group, serum TNF-α (33.82±1.57) pg/ml, IL-6 (58.49±5.89) pg/ml, renal NF-κB (0.84±0.05) , MPO (0.22±0.01) µg/ml, MDA (0.72±0.05) mmol/mg prot, Caspase-3 (327.32±21.93) % decreased significantly, and renal SOD (4.90±0.81) U/mg prot increased significantly in the PQ+SS group (P<0.05) . Conclusion: PQ poisoning can lead to AKI in mice, while SS can reduce AKI caused by PQ poisoning, improve the general survival state of PQ poisoned mice, and play a certain protective role in kidney injury caused by PQ poisoning, which may be achieved by inhibiting oxidative stress response, inflammatory response and apoptosis caused by poisoning.

Evidence of s-wave superconductivity in the noncentrosymmetric La7Ir3.

Superconductivity in noncentrosymmetric compounds has attracted sustained interest in the last decades. Here we present a detailed study on the transport, thermodynamic properties and the band structure of the noncentrosymmetric superconductor La 7 Ir 3 (T c ~ 2.3 K) that was recently proposed to break the time-reversal symmetry. It is found that La7Ir3 displays a moderately large electronic heat capacity (Sommerfeld coefficient γ n ~ 53.1 mJ/mol K2) and a significantly enhanced Kadowaki-Woods ratio (KWR ~32 µΩ cm mol2 K2 J-2) that is greater than the typical value (~10 µΩ cm mol2 K2 J-2) for strongly correlated electron systems. The upper critical field Hc2 was seen to be nicely described by the single-band Werthamer-Helfand-Hohenberg model down to very low temperatures. The hydrostatic pressure effects on the superconductivity were also investigated. The heat capacity below T c reveals a dominant s-wave gap with the magnitude close to the BCS value. The first-principles calculations yield the electron-phonon coupling constant λ = 0.81 and the logarithmically averaged frequency ω ln = 78.5 K, resulting in a theoretical T c = 2.5 K, close to the experimental value. Our calculations suggest that the enhanced electronic heat capacity is more likely due to electron-phonon coupling, rather than the electron-electron correlation effects. Collectively, these results place severe constraints on any theory of exotic superconductivity in this system.

[Textual criticism and discrimination on the naming of"Five-abstention Soup of Medical Professional"from the Han-tomb of the Marquis of Haihun].

A lacquer vessel with the inscription of Yi gong wu jin tang (Five-abstention Soup of Medical Profession) has been unearthed from the Han-tomb of Marquis of Haihun, in which"Five abstentions"is related to the incantations and abstention therapies prevalent in the Qin and Han Dynasties. The"Five-abstention Law"is the five rituals and methods during the process of practicing incantations and abstentions therapies including"keeping one's thinking (cun si)","holding the breath(bi qi)","twirling eyes (nian mu)","stepping after Yu's sample (yu bu)"and"incanting and blessing (zhou zhu)". The"Five-abstention Law"uses the medium"soup"to achieve the purpose of treatment."Soup"refers either to"decoction"or to"magic water". The lacquer vessel with the inscription"Five-abstention Soup of Medical professional"could be an instrument for implementing the process of practising the"Five-abstention Law", reflecting the historical facts that Liu He, the Marquis Haihun did accept the incantations and abstention therapies.

Expression of microRNA-122 and microRNA-22 in HBV-related liver cancer and the correlation with clinical features.

OBJECTIVE: MicroRNAs (miR) participate in cell proliferation, apoptosis and transformation, as they can regulate gene expression and intracellular signal transduction for various physiological processes. MiR-122 and miR-22 are known to be related with occurrence and progression of hepatitis B virus (HBV)-related hepatocellular cancer (HCC). This study recruited HBV-related HCC patients, whose expression levels of miR-122 and miR-22 were determined to analyze the correlation with clinical and pathological indexes. PATIENTS AND METHODS: HBV-related HCC patients were enrolled, in parallel with patients suffering from benign liver disease and non-HBV-related HCC. Real-time PCR was employed to measure miR-122 and miR-22 expression levels. RESULTS: The relative expression levels of miR-122 and miR-22 in HBV-related HCC patients were 1.26 ± 2.73 and 5.49 ± 3.91, respectively, which were significantly lower than that in benign liver disease or non-HBV-related HCC patients (p < 0.05). No significant difference of serum miR-122 or miR-22 levels was found between benign liver disease and non-HBV-related HCC patients (p > 0.05). The miR-122 and miR-22 levels were negatively correlated with tumor size, lymph node metastasis, TNM stage, pathological type, differentiation grade, liver cirrhosis, AFP and HBV DNA, all of which were independent risk factors (p < 0.05). CONCLUSIONS: MiR-122 and miR-22 were downregulated in HBV-related HCC patients, and were related with tumor size, lymph node metastasis, TNM stage, pathological type, differentiation grade, liver cirrhosis, AFP and HBV DNA.

Pathway analysis of differentially expressed genes in human esophageal squamous cell carcinoma.

OBJECTIVE: Esophageal Squamous Cell Carcinoma (ESCC) is one of the most common human cancers with a particularly high incidence in certain regions of China. Differentially expressed genes (DEG) between the esophageal squamous carcinoma tissues and matched normal esophageal mucosal epithelial tissues can be detected by employing the gene microarray technology. This can aid the analysis of the underlying disease mechanism and can help to identify potentially critical genes as well as related molecular signalling pathways. MATERIALS AND METHODS: The potentially critical genes and related signal pathways are examined by bioinformatics analysis including Gene Ontology (GO) analysis, pathway analysis and signal transduction networks. Here, we performed microarray analysis with 8 pairs of ESCC and normal esophageal mucosal epithelial tissues. RESULTS: Compared to the control group, 347 and 203 genes were found to be up-regulated and down-regulated in the experimental group, respectively. Based on pathway analysis, 52 and 51 signal transduction pathways were involved in the up-regulated and the down-regulated genes, respectively. SLC27A6, RAB11A, ABCA8, JAM2, HNMT, GSTM1, and CDKN3, which play critical roles in regulating the expression of ESCC, were identified among the key genes involved in the signal transduction networks. CONCLUSIONS: Investigation of the mechanism underlying ESCC can provide a direction for the clinical prevention and treatment of ESCC.

Genetic polymorphisms of CCND1 and PTEN in progression of esophageal squamous carcinoma.

Cyclin D1 (CCND1) plays a significant role in G1-S transition of cell cycle, and phosphatase and a tensin homologue (PTEN) negatively regulate cell cycle through phosphatidylinositol 3-kinase (PI3K)/AKT signaling. CCND1 and PTEN genetic polymorphisms might induce susceptibility to the occurrence of esophageal squamous cell carcinoma (ESCC). Three hundred and four ESCC patients and 413 healthy controls from Anyang, China, were enrolled in this study. All genotyping at CCND1 (807 G/A) and PTEN (rs701848 T/C and rs2735343 C/G) were identified by polymerase chain reaction-restriction fragment length polymorphism (PCR-RFLP) assay. Unconditional logistic regression model was used to analyze the correlation between the polymorphisms and the susceptibility to develop ESCC. Statistically significant differences were observed between cases and controls in distribution of genotypes or alleles at PTEN rs701848 T/C and rs2735343 C/G, with either haplotype TG or CG possessing notably higher proportion in cases than in the controls. However, such difference could not be found in the distribution of the polymorphisms at CCND1 807 G/A. In summary, the polymorphisms of PTEN rs701848 T/C and rs2735343 C/G might represent crucial modifying factors for development of ESCC.

The kinetic model and simulation of blood coagulation--the kinetic influence of activated protein C.

The paper described a limited part of the coagulation pathway, and in particular the inhibitory effects of activated protein C in the context of thrombin production. This is a computational modeling study with various assumption made of kinetic rates laws and their summation. The level of complexity and assumed parameters makes conclusions uncertain. However, an interesting outcome is that kinetic reaction rates may show oscillation behavior under particular, high levels of protein C feedback inhibition. The model would defy quantitative practical use, but could have predictive value as a qualitative descriptor of coagulation.

Dynamic model of the role of platelets in the blood coagulation system.

In order to confirm which process is the most important in the blood coagulation cascade, a dynamic model of the function of platelets in blood coagulation is provided based on biochemical experiments. A series of conclusions based on qualitative analysis and mathematical simulation are drawn about the influence of the activation rate of factor VIII and factor IX on the generation of thrombin (IIa). It is evident that the pro-coagulation stimulus must exceed a threshold value to initiate the coagulation cascade. The value is related to the rate of platelet activation, the binding constant d2. The stability of the fixed value is also related to the pro-coagulation stimulus. This article also evaluates the influence of the stimulus strength and the activated rate parameter of platelets on thrombin. The proportion of platelets activated at any given time is designated c. To each c, we obtain a maximum concentration of thrombin. It is evident that when the level of factor IX is below 1% of normal levels, the rate of thrombin generation reduces dramatically resulting in severe bleeding tendency.

Inhibitory effects of berberine on IK1, IK, and HERG channels of cardiac myocytes.

AIM: To study the effects of berberine on inward rectifier potassium current (IK1) and outward delayed rectifier potassium current (IK) of guinea pig ventricular myocytes, and on human ether-a-go-go related gene (HERG) channel expressed in Xenopus oocytes. METHODS: Whole cell patch-clamp and geneclamp techniques were used to record ionic currents. RESULTS: Berberine prolonged action potential duration (APD) and inhibited IK1 and IK in a concentration-dependent manner. Berberine 100 micromol/L increased APD90 from (450 +\- 48) ms to (888 +\- 90) ms (n = 6, P < 0.01), and inhibited IK1 by 65 % +\- 7 % (n = 6, P < 0.01). Berberine 50 micromol/L inhibited IK by 57 % +\- 6 %, IKtail by 53 % +\- 6 % (n = 6, P < 0.01). Berberine produced a voltage-dependent block on IK that increased with stronger depolarization, and once all channels were activated, there was no further block at positive potentials. Berberine blocked the HERG channels potently with an IC50 value of approximately 75 micromol/L. This block was voltage-dependent, suggesting that it probably bind to either open or inactivated HERG channels. CONCLUSION: Berberine prolonged APD and possessed blocking effect on IK1, IK, and HERG channel expressed in Xenopus oocytes. The antiarrhythmic mechanism of berberine is related to its inhibitory effects on IK1, IK, and HERG channel.

[Inhibition of transmembrane K(+) currents in mammalian ventricular myocytes by antiarrhythmic agent RP62719].

The effect of RP62719 on the inward rectifier K(+) current (I(K1)),transient outward K(+) current (I(to)) and delayed outward K(+) current (I(K)) in isolated cardiac myocytes was determined using the whole cell patch clamp technique in guinea pig and dog. RP62719 decreased I(K1) with an inhibitory concentration 50 (IC(50) ) of 5.0+/-1.0 micromol/L at -100 mV in guinea pig ventricular cells. In dog ventricular myocytes, RP62719 inhibited Ito by 84+/-4.4% with an IC(50) of 1.2+/-0.51 micromol/L at +40 mV. In guinea pig ventricular cells, RP62719 decreased I(K): I(Kstep) by 50.0+/-8.3%%and I(Ktail) by 56.0+/-4.9% at +40 mV, respectively. RP62719 inhibited I(Kstep) with an IC(50) of 4.2+/-0.8 micromol/L and I(Ktail) with an IC(50) of 3.3+/-0.75 micromol/L. Thus it is suggested that the ionic mechanism of antiarrhymic effect by RP62719 may be due to its inhibition of I(K1),I(to) and I(K).

[Effects of glutamate on transient outward potassium current of dissociated hippocampal neurons in ca1 sector in rats].

The effects of glutamate on the transient outward potassium current of dissociated hippocampal CA(1) neurons of 7-10 d rats were studied by the whole-cell patch clamp technique. It was found that glutamate could block the transient potassium current in a dose- and time-dependent manner. The effect was partly voltage-dependent. These results suggest that glutamate may decrease the membrane conductance of K(+) channels in hippocampal neurons.

Effects of RP58866 on transmembrane K+ currents in mammalian ventricular myocytes.

AIM: To determine effects of RP58866 on inward rectifier K+ current (IKl), transient outward K+ current (Ito) and delayed outward rectifier K+ current (IK) in isolated cardiac myocytes. METHODS: In isolated ventricular myocytes of guinea pig and dog, the effect of RP58866 on IKl, Ito, and IK were observed by the whole cell voltage-clamp technique. RESULTS: RP58866 decreased IKl in a concentration-dependent manner, with an IC50 of (3.4 +/- 0.8) micromol.L-1 (n = 6) at -100 mV in guinea pig ventricular cells. In dog ventricular myocytes, RP58866 inhibited Ito with IC50 of (2.3 +/- 0.5) micromol.L-1 at +40 mV. In guinea pig ventricular cells, RP58866 at 100 micromol.L-1 decreased IK: IKstep by (58 +/- 13)% at +40 mV, and IKtail by (86 +/- 17)%, respectively. RP58866 inhibited IKstep with an IC50 of (7.5 +/- 0.8) micromol.L-1, and IKtail with an IC50 of (3.5 +/- 0.9) micromol.L-1. The envelope of tail analysis suggested that both IKr and IKs were inhibited. CONCLUSION: RP58866 inhibits IKl, Ito, and IK in cardiac myocytes with a similar potency, and is not a specific IKl inhibitor.

[Research on the mechanism of neuronal apoptosis in Alzheimer's disease and the effects of tetrohydroberberine on the apoptosis].

Apoptosis in Alzheimer's disease(AD) was studied by the techniques of immunohistochemistry, neuronal culture and patch clamp. The hippocampal neuronal apoptosis induced by beta-amyloid peptide (beta-AP) and its ionic mechanism were also observed. The results showed that neuronal apoptosis did exist in AD brains and beta-AP might induce the apoptosis by blocking the voltage-dependent K+ and Na+ channels, which were enhanced by nitric oxide(NO). In addition, tetrohydroberbine could protect against the apoptosis induced by beta-AP by reducing hippocampal neuronal intracellar free Ca2+.