Pylephlebitis combined with septic shock secondary to acute nonperforated appendicitis: a case report.

Pylephlebitis, which is a type of septic thrombophlebitis of the portal vein, is a rare and life-threatening complication that commonly occurs following appendicitis. However, nonspecific abdominal complaints and fever can impede the diagnosis of pylephlebitis. Timely use of appropriate antibiotics and anticoagulants is paramount for treating this condition. We present a case of pylephlebitis and septic shock caused by acute nonperforated appendicitis. A 32-year-old man presented with migratory right lower abdominal pain. Blood cultures showed the presence of Escherichia coli. Blood test results showed increased bilirubin concentrations and coagulation factor abnormalities. A computed tomographic abdominal scan showed that the portal vein had a widened intrinsic diameter. After intensive care treatment with antibiotics, antishock therapy, anticoagulants, and other supportive treatments, the infection was monitored, the abdominal pain disappeared, and the jaundice subsided. Laparoscopic appendectomy was performed. Histopathology showed acute suppurative appendicitis, and no abnormalities were observed during the follow-up period after discharge. A multidisciplinary approach is mandatory for the decision-making process in the presence of pylephlebitis caused by appendicitis to obtain a correct diagnosis and prompt treatment. Similarly, the timing of appendectomy is important for minimizing intra- and postoperative complications.

Burden and trends of mental disorders in China from 1990 to 2019: findings from the Global Burden of Disease Study 2019.

PURPOSE: Mental disorders remain the leading causes of disability worldwide. We aimed to determine the burden and trends of mental disorders in China from 1990 to 2019. METHODS: The incidence, prevalence, and disability-adjusted life years (DALYs) of mental disorders at national level of China were examined by age, sex, and subcategories. Temporal trends in the age-standardized rates for incidence, prevalence, and DALYs were assessed by the average annual percentage change (AAPC). All estimates are presented as numbers and age-standardized rates, with 95% uncertainty intervals (UIs). RESULTS: The number of incident cases due to mental disorders increased from 42.90 million to 52.72 million, the number of prevalent cases increased from 132.63 million to 160.16 million, and the number of DALYs increased from 15.64 million to 20.29 million during 1990-2019. Decreasing trends were observed in the age-standardized rates for incidence, prevalence and DALYs. Anxiety and depressive disorders were more frequent in women, while ADHD, conduct disorder, and autism spectrum disorders were more common in men. Compared with 1990, the age-specific incidence rates were higher in individuals under 14 years and over 55 years, whereas rates were lower in those aged 15-49 years in 2019. CONCLUSION: The number of incident cases, prevalent cases, and DALYs due to mental disorders gradually increased in China from 1990 to 2019. Anxiety and depressive disorders were the leading causes of burden due to mental disorders, which affected women more than men. Mental disorders deserve greater attention in health policy decision making.

Core-shell CoCuOx@MOx (MNb, Ti and Ce) catalysts with outstanding durability and resistance to H2O for the catalytic combustion of o-dichlorobenzene.

Configuring Co-based catalysts with excellent activity, durability, anti-H2O capability and superior chlorine resistance is an effective strategy for catalytic combustion of CVOCs. In this work, we elaborated a CoCuOx catalysts with the same core but different shell. The CoCuOx dodecahedron surface was successfully coated with shells of Nb2O5, TiO2, and CeO2 using a range of conventional synthesis methods. The prepared core-shell catalysts (CoCuOx@TiO2 and CoCuOx@Nb2O5) were found to generate plentiful acid sites and abundant lattice oxygen species, indicating a strong interaction between the core and shell layers that resulted in a significant enhancement of catalytic activity. Additionally, by-products generation was successfully controlled by acid sites and lattice oxygen species. More importantly, the core-shell structure design significantly improved the thermal stability and anti-H2O capability of the catalysts. Furthermore, the possible formation pathways and reaction mechanisms were proposed based on in-situ FTIR and selectivity analysis.

Development of free 25-hydroxyvitamin D3 assay method using liquid chromatography-tandem mass spectrometry.

The free hormone hypothesis has triggered controversies regarding the measurement of free vitamin D metabolites, such as free 25-hydroxyvitamin D (25(OH)D), as a suitable indicator for total vitamin D for clinical use. This issue can be addressed by developing a precise and accurate method for free 25(OH)D measurement. In the present study, a novel assay method for free 25(OH)D3 based on liquid chromatography-tandem mass spectrometry (LC-MS/MS) was developed. Sample preparation first involved ultrafiltration to remove vitamin D-binding protein-bound and albumin-bound 25(OH)D, followed by extraction with a column, derivatization, evaporation, dissolution, and injection into the LC-MS/MS system. The coefficient of variation of repeatability and reproducibility obtained were 3.8-4.5% and 4.8-5.9%, respectively. Satisfactory linearity (r=0.999) was obtained up to 80 pg/ml. The lower quantification limit was 0.97 pg/ml and the S/N ratio on the peak of 1.0 pg/ml sample was 24.8 (which is more than the acceptable value of 10). The recovery rate was between 84.5 and 92.4% with a negligible matrix effect (94.5-104.9%). Levels of free 25(OH)D3, but not total 25(OH)D3, in the serum of the patients with chronic kidney disease (CKD) and hepatic cirrhosis (HC) were substantially lower than those in healthy subjects. The correlation coefficient between total and free 25(OH)D3 was 0.738 in all samples, while the linear regression equations were different between the patients with CKD and HC. In conclusion, LC-MS/MS assay for free 25(OH)D3 might be useful to evaluate high-throughput methods, including ELISA.

Dual specificity phosphatase 22 relates to skin lesion degree and biologics history, while its longitudinal elevation during treatment reflects better outcome in psoriasis patients.

BACKGROUND: Dual specificity phosphatase 22 (DUSP22) plays an important role in the regulation of immune and inflammation, but its correlation with clinical features and treatment outcome in psoriasis patients is still unclear. This study was to investigate the longitudinal change of DUSP22 with time, as well as its association with disease activity and treatment response in psoriasis patients. METHODS: Totally, 120 psoriasis patients, 50 patients with other skin inflammations as disease controls (DCs), and 50 health controls (HCs) were recruited. Serum samples were collected from psoriasis patients at baseline, month (M)1, M3, and M6 after initiation of etanercept-based treatment as well as from DCs and HCs after enrollment to assess DUSP22 level by enzyme-linked immunosorbent assay. RESULTS: DUSP22 was lower in psoriasis patients than in HCs and DCs (both p < 0.001). Besides, in psoriasis patients, DUSP22 was associated with lower psoriasis area severity index (PASI) score (p = 0.001) and systemic biological treatment history (p = 0.023), but not with other demographics, disease characteristics, or treatment history (all p>0.05). In addition, DUSP22 was increased with time (p < 0.001) in total patients. Moreover, DUSP22 at M3 (p = 0.004) and M6 (p < 0.001) was higher in response patients than in non-response patients evaluated by PASI 75. Additionally, DUSP22 at M3 (p < 0.001) and M6 (p = 0.003) was also increased in response patients compared with non-response patients evaluated by PASI 90. CONCLUSION: DUSP22 decreases and negatively correlates with disease activity, while its longitudinal elevation with time reflects satisfactory treatment response in psoriasis patients.

Circ-IGF1R plays a significant role in psoriasis via regulation of a miR-194-5p/CDK1 axis.

Psoriasis is a skin disorder that is classed as an autoimmune disease. It is characterized by excessive proliferation, abnormal migration and differentiation of keratinocytes, as well as inflammatory cell infiltration. Circular RNAs (circRNAs/circ) have been reported to play an important role in several aspects of psoriasis. Thus in the present study, the role of circ-insulin-like growth factor 1 receptor (circ-IGF1R) in the development of psoriasis was assessed, and the involvement of microRNA (miR)-194-5p was also investigated as its expression was downregulated in psoriasis. StarBase analysis and dual luciferase reporter assays confirmed the interaction between circ-IGF1R with miR-194-5p. The increased expression of circ-IGF1R and decreased expression of miR-194-5p were further confirmed by reverse transcription-quantitative polymerase chain reaction in interleukin (IL-22)-stimulated HaCaT cells. The increased proliferation, migration and invasion, as well as decreased apoptosis, caspase 3 activity and cleaved-caspase 3/caspase 3 ratio were observed in IL-22-stimulated HaCaT cells. Conversely, transfection of circ-IGF1R-small interfering (si)RNA resulted in significantly increased expression of miR-194-5p with or without stimulation of IL-22 in HaCaT cells, and also overcame the effects of the miR-194-5p inhibitor. Additionally, transfection of circ-IGF1R-siRNA inhibited cell proliferation, migration and invasion, which were reversed by transfection of a miR-194-5p inhibitor. Similarly, circ-IGF1R-siRNA promoted apoptosis, caspase 3 activity and the cleaved-caspase 3/caspase 3 ratio, which were reversed by miR-194-5p inhibitor. These results showed that circ-IGF1R could affect the proliferation, apoptosis, migration and invasion of IL-22-stimulated HaCaT cells by regulating the expression of miR-194-5p. Based on TargetScan prediction and dual luciferase reporter assays, it was shown that cyclin-dependent kinase (CDK)1 was targeted by miR-194-5p. Additionally, the expression of CDK1 was upregulated following stimulation with IL-22 in HaCaT cells at the mRNA and protein levels. Transfection of miR-194-5p mimic or miR-194-5p inhibitor negatively regulated CDK1 expression in the IL-22 induced HaCaT cells. In conclusion, circ-IGF1R-siRNA could inhibit the cell proliferation, migration and invasion, and induce apoptosis by regulating the miR-194-5p/CDK1 axis. circ-IGF1R may thus serve as a potential treatment target for psoriasis.

Retracted: Role of Paeonol in an Astrocyte Model of Parkinson Disease.

The authors wish to retract the article. In this article, they found that astrocytes that were pretreated with paeonol significantly rescued MPP+-induced cell viability reduction, and inhibited up-regulation of cell apoptosis, caspase-1 activity, COX2, iNOS, and Bax/Bcl-2 ratio, as well as p-JNK and p-ERK. These findings suggest that paeonol is a neuroprotective agent suitable for use in treatment of PD. However, in subsequent research, they examined the protein levels of p-JNK/p-ERK/p-P38 in different groups. Results showed that in the MPP+ groups, not all these protein levels were higher than those in the control group, because of the flawed data presentations. They also used western blot analysis to assess protein levels of Bax and Bcl-2 in astrocytes. Compared with the control group, Bax protein level was increased, while Bcl-2 protein level was decreased after treatment with MPP+, and these changes were not reversed by paeonol. Based on the above, they ascertained that there must have been some serious mistake in their experiment. As a result, all authors agreed to retract this article. Reference: Maosheng Ye, Yuxin Yi, Shixing Wu, Yong Zhou, Dongji. Role of Paeonol in an Astrocyte Model of Parkinson Disease. Med Sci Monit, 2017; 23: 4740-4748. DOI: 10.12659/MSM.906716.

Zafirlukast attenuates advanced glycation end-products (AGEs)-induced degradation of articular extracellular matrix (ECM).

Zafirlukast, a leukotriene receptor antagonist, has been shown to exert a wide range of effects including anti-asthmatic, anti-inflammatory and oral anti-bacterial. Osteoarthritis is one of the most prevalent age-related public health burdens in the modern world. In the present study, we applied zafirlukast in the treatment of human primary chondrocytes and found that it exerts potent anti-osteoarthritic effects. Zafirlukast inhibited AGEs-induced degradation of the articular extracellular matrix by suppressing expression of MMPs, ADAMTS, NOX-4, generation of ROS, and activation of NF-κB via the IκBα/JNK/AP-1 pathway through targeted inhibition of CysLTR1. These findings suggest that zafirlukast possesses a protective effect against AGEs- induced damage and dysfunction in human chondrocytes.

Inhibition of MiRNA-125b Decreases Cerebral Ischemia/Reperfusion Injury by Targeting CK2α/NADPH Oxidase Signaling.

BACKGROUND/AIMS: Cerebral ischemia-reperfusion (I/R) injury involves multiple independently fatal terminal pathways. CK2α/NADPH oxidase is an important signaling pathway associated with ischemia-reperfusion injury, and miR-125b can regulate oxidative stress-related injury. In this study, we investigated whether the effect of miR-125b in rat brain I/R injury occurs through its modulation of the CK2α/NADPH oxidase pathway. METHODS: Rats were subjected to 2 h of cerebral ischemia followed by 24 h of reperfusion to establish an I/R injury model. Neurological deficit was evaluated using a five-point score. Infarct volume was evaluated with 2, 3, 5-triphenyltetrazolium chloride (TTC) staining, and RT-PCR was used to detect expressions of miR125b and CK2α. We then examined the association between miR-125b expression and the CK2α/NADPH oxidative signaling pathway in a PC-12 cell oxygen-glucose deprivation and reoxygenation (OGD/R) injury model. Transfection with miR-125b mimics, an miR-125b inhibitor, and luciferase reporter gene plasmid was accomplished using commercial kits. In these cells, Western blots were used to detect the levels of expression of CK2α, cleaved caspase-3, NOX2, and NOX4. RT-PCR was used to detect the expressions of CK2α, miR125b, NOX2, and NOX4. We evaluated Lactate Dehydrogenase (LDH) level, NADPH oxidase activity, and caspase-3 activity using commercial kits. Mitochondrial reactive oxygen species (ROS) were measured by fluorescence microscopy. For both PC-12 cells and rat brains, histological analyses were conducted to observe morphological changes, and apoptosis was measured using a commercial kit. RESULTS: I/R rats exhibited an increase in neurological deficit score, infarct volume, and cellular apoptosis, along with miR-125b elevation and CK2α downregulation. OGD/R treatment increased PC-12 cells' injuries, cellular apoptosis, and ROS levels. These changes were associated with miR-125b elevation, CK2α downregulation and activations of NOX2 and NOX4, mimicking our in vivo findings. All of these effects were reversed by the inhibition of miR-125b, confirming a strong correlation between miR-125b activity and the CK2α/NADPH oxidase signaling pathway. CONCLUSIONS: Based on these observations, we conclude that inhibition of miR-125b protects the rat brain from I/R injury by regulating the CK2α/NADPH oxidative signaling pathway.

Role of Paeonol in an Astrocyte Model of Parkinson's Disease.

BACKGROUND Parkinson's disease (PD) is characterized by a progressive degeneration of dopaminergic (DA) neurons in the substantia nigra pars compacta (SNc). Inflammation and neural degeneration are implicated in the pathogenesis of PD. Paeonol has been verified to attenuate inflammation. MATERIAL AND METHODS 1-methyl-4-phenylpyridnium ion (MPP+, 100 µM) was used to induce the cell model of PD in primary cultured astrocytes. Astrocyte cell viability and apoptosis were determined by 3-(4, 5-dimethyl-2-thiazolyl)-2, 5-diphenyl-2-H-tetrazolium bromide (MTT) assay and flow cytometry (FCM), respectively. Protein levels of cyclooxygenase-2 (COX-2) and inducible nitric oxide synthases (iNOS) in culture medium were tested by enzyme-linked immunosorbent (ELISA) assay. Protein levels of casapse-1, COX2, iNOS, B-cell lymphoma 2 (Bcl-2)-associated X protein (Bax), Bcl-2, and phosphorylated Jun N-terminal kinase (p-JNK)/phosphorylated extracellular signal-regulated kinase (p-ERK)/p-P38 were examined by Western blot. RESULTS Pretreatment with paeonol remarkably rescued MPP+-induced cell viability reduction, up-regulation of cell apoptosis, caspase-1 activity, COX-2, iNOS, and Bax/Bcl-2 ratio in primary astrocytes. Furthermore, paeonol repressed MPP+ -induced elevation of p-JNK/p-ERK in primary cultured astrocytes. CONCLUSIONS The present study found that paeonol protected cells from apoptosis by repressing the activation of the JNK/ERK related signalling pathway induced by MPP+ in astrocytes. We propose that paeonol is a neuroprotective agent for the treatment of PD patients, with great promise in the future.

[The Analgesia of Oxymatrine Affecting Calcium Channel and GABA Release].

OBJECTIVE: To explore the analgesia of oxymatrine (OMT) affecting high voltage-dependent calcium channels (HVDCCs) and GABA release under neuropathic pain condition. METHODS: Totally 66 C57BL/6 mice were randomly divided into the sham-operation group, the model group, and the OMT group, 22 in each group. Neuropathic pain models were established by partial sciatic nerve ligation (PSNL). Hind paw plantar mechanical response threshold (MWT) was measured by up-and-down method with Von-Frey filament. mRNA expression of HVDCCs in brains and spinal cords was detected with Real-time PCR and concentration of GABA was determined using ELISA kit. RESULTS: Compared with day 0, the left hind paw MWTwas decreased on day 7, 10, and 14 in the model group (P < 0.05). Compared with the sham-operation group, the left hind paw MWT was significantly reduced in the model group on day 7 (P < 0.05). The MWT of PSNL ipsilateral hind paw was decreased on day 7 before OMT administration, when compared with day 0 (P < 0.05), and increased after OMT administration (P < 0.05). Compared with the sham-operation group, mRNA levels of Cav1.2, Cav1.3, Cav2.1, and Cav2.3 in brain tissues were increased and those of Cav2.2 were decreased significantly in the model group (P < 0.05). In spinal cord tissues, mRNA levels of Cav1.2 and Cav1.3 were increased, but those of Cav2.1, Cav2.2, and Cav2. 3 were decreased significantly in the model group, when compared with those of the sham-operation group (P < 0.05). Compared with the model group, mRNA levels of Cavl.2, Cavl.3, Cav2.1, and Cav2. 3 in brain tissues were decreased, and those of Cav2.2 were increased significantly in the OMT group (P < 0.05). In spinal cord tissues of the OMT group, mRNA levels of Cav1.3 decreased and those of Cav2.1, Cav2.2, and Cav2.3 increased significantly with statistical difference, when compared with those of the model group (P < 0.05). Compared with the sham-operation group, GABA levels in brain tissues decreased in the model group (P < 0.05). Compared with the model group, GABA levels in brain tissues increased in the OMT group (P < 0.05). There was no statistical difference in GABA levels of spinal cord tissues among these groups (P > 0.05). CONCLUSIONS: OMT had analgesic effect on neuropathic pain, which might be probably related to HVDDCs. Cav2.2 might directly affect GABA release.

[Study on analgesia of oxymatrine and its relation to calcium channels].

OBJECTIVE: To study whether the analgesis of oxymatrine (OMT) affects N-type voltage-gated calcium channels (VGCCs). METHODS: Totally 45 mice were randomly divided into the sham-operation group, the model group [established by partial sciatic nerve ligation (PSNL)] , and the OMT treatment group according to random digit table, 15 in each group. The dorsal root ganglions (DRG) were separated in PSNL pain model mice. Intracellular calcium concentration ([Ca2+]i) was determined with Fluo-3 AM immunofluorescent probe in cultured DRG neurons. Different protein expression levels of N-type (Cav2. 2) and L-type ( Cav1. 3) among VGCCs from brain and DRG tissues were detected with Western blot. RESULTS: Compared with the sham-operation group, [Ca2+]i, increased in cultured DRG neurons (P <0. 05) , protein expression levels of Cav2. 2 in the brain tissue increased (P <0. 05), protein expression levels of Cav2. 2 in DRG tissues decreased in the model group (P <0. 01). Compared with the model group, [Ca2+]i, decreased in cultured DRG neurons (P < 0. 05), protein expression levels of Cav2. 2 in the brain tissue decreased (P <0. 01), protein expression levels of Cav2. 2 in DRG tissues increased in the OMT treatment group (P <0. 01). There was no statistical difference in Cav1. 3 expressions in cultured DRG neurons and the brain (P >0. 05). CONCLUSION: Analgesic effect of OMT might be related to Cav2. 2 channel mediated calcium ion flux.

Sonic hedgehog and retinoic Acid induce bone marrow-derived stem cells to differentiate into glutamatergic neural cells.

Studies have showed that transplanted stem cells in the inner ear won't regenerate to replace the damaged sensory hair cells. They can spontaneously differentiate into mesenchymal cells and fibrocytes in the damaged inner ear. Only mature sensory cells of MSCs-derived possess the great potency for cell transplantation in the treatment of sensorineural hearing loss. So, we try to establish an efficient generation of the glutamatergic sensory neural phenotype for the cell transplantation of the hearing loss. We isolated MSCs from femoral and tibial bones according to their adherence to culture dishes. After purification, proliferation, and passaged, cells became homogeneous in appearance, showing more uniformity and grew in a monolayer with a typical spindle-shape morphology. The cell surface markers were assessed using FACS to characterize the isolated cells. For neural induction to harvest the glutamatergic sensory neurons, passage 3 MSCs were incubated with preinduced medium for 24 hr, and neural-induced medium for an additional 14 days. The cells exhibit a typical neural shape. RT-PCR analysis indicated that the mRNA levels of the neural cell marker nestin, Tau, MAP-2, ß-tubulin III, GluR-3, and GluR-4 were higher compared with primary MSCs. Immunohistochemistry and western-blotting proofed that nestin, MAP-2, ß-tubulin III, and GluR-4 proteins indeed exhibit their expression difference in the induced cells compared to the MSCs. We show an efficient protocol by the combined applications of Sonic Hedgehog (Shh) and Retinoic Acid (RA) to induce MSCs to differentiate into the glutamatergic sensory neuron which were identified from the morphological, biochemical, and molecular characteristics.

A reduction in reactive oxygen species contributes to dihydromyricetin-induced apoptosis in human hepatocellular carcinoma cells.

Reactive oxygen species (ROS) and cellular oxidant stress are considered inducers of carcinogenesis. However, the association of ROS with cancer is both complex and, at times, paradoxical. We assessed the effects of dihydromyricetin (DHM) on the induction of ROS accumulation and on the activation of the mitochondrial signaling pathway in human hepatoma HepG2 cells. The results indicated that DHM could reduce ROS accumulation in a concentration-dependent manner. Additionally, with increasing concentrations of DHM, the expression of proteins that participate in the cell apoptosis program increased in a concentration-dependent manner. Furthermore, we found that a low dose of H2O2 (10 nM) could reverse DHM-induced cell apoptosis. We observed the following critical issues: first, the cellular redox balance is vital in DHM-induced apoptosis of human hepatocellular carcinoma (HCC) cells, and second, ROS could function as a redox-active signaling messenger to determine DHM-induced cell apoptosis. In this study, we demonstrated that low levels of ROS are also critical for the function of HCC cells.

[Effect of Aß1-42 injection on hippocampus cells in rats and protective role of polygona-polysaccharose for Alzheimer's disease].

OBJECTIVE: To determine the effect of polygona-polysaccharose (PP) on learning and memory ability in rats with Alzheimer's disease (AD). METHODS: Forty five Sprague-Dawley rats were assigned into 3 groups. Rats in the sham-operated group were injected with normal saline. Rats in the Aß group were injected with Aß1-42. Rats in the PP group were injected with 16% PP solution for 45 days consecutively. The Morris water maze was used to investigate the ability of learning and memory in the rats. The effect of Aß and PP on the hippocampus cells was observed by HE and Congo red staining of methanol. RESULTS: Rats in the sham-operated group had no obvious morphological change; and morphology of rats in the PP group was basicaly normal. The layer of pyramidal cells in the Aß group was decreased. The cells appeared sparse and irregular and became smaller. Karyopyknosis and vacuolar degeneration cells were also found. More positive staining materials aggradated in the Aß group compared with the PP group by Congo red staining (P<0.05). CONCLUSION: Aß infusion into the hippocampus results in the impairment of the neuronal degeneration in the rats, which shows similar characterizations of AD. PP can reduce the deposition of Aß in the hippocampus.

Dihydromyricetin reduced Bcl-2 expression via p53 in human hepatoma HepG2 cells.

Dihydromyricetin (DHM) is a major active ingredient of flavonoids compounds. It exhibited anticancer activity and induced apoptosis in human hepatocellular carcinoma HepG2 cells according to our previous data. In this study, we investigated whether p53 is involved in DHM-triggered viability inhibition and apoptosis induction in cancer cells. MTT [3-(4, 5-Dimethylthiazol-2-yl)-2, 5-diphenyltetrazolium bromide] assay was employed to evaluate the viability of HepG2 cells after DHM treatment. Meanwhile, p53 small interfering RNA (siRNA) was adopted to silence p53 expression. Protein level of p53 and Bax/Bcl-2 were evaluated by western blot analysis. Cell counting assay showed that DHM inhibited HepG2 cell growth effectively in a time- and dose-dependent manner. P53 expression was significantly increased after DHM treatment, whereas Bcl-2 was reduced potently. Furthermore, after co-treatment with Pifithrin-α (PFT-α, p53 inhibitor), Bcl-2 expression was reversed. The expression of Bax was no significant change, which was also observed after p53 silence. These findings defined and supported a novel function that DHM could induce human hepatocellular carcinoma HepG2 cells apoptosis by up-regulating Bax/Bcl-2 expression via p53 signal pathway.

[Dispersion and analysis of odor pollution in landfill area under the enclosed operation condition].

Odor pollution of landfill site is a serious problem accompanied with the urbanization process that influences city life. Generally, odor emission points in landfill boundary are detected by experience, but the pollution intensity, distribution and variation in the scope of landfill boundary are difficulty to describe. In this research, odor emission points were disclosed with equal odor concentration curves that were delineated using electric nose and GPS instrument. The leakage of landfill gas and exhaust emission from biogas incineration torch was the main cause of the odor pollution in landfill area. Gas production evaluation suggested that the improvement of landfill gas consumption is the key point to control the odor pollution at the landfill site.