[Epidemic situation of imported malaria in Chengdu City from 2012 to 2016].

Objective To understand the malaria epidemic situation in Chengdu City, so as to provide the evidence for effectively carrying out the malaria elimination work. Methods The data of imported malaria in Chengdu City from 2012 to 2016 were collected from the Disease Surveillance Information Reporting System of Chinese Center for Disease Control and Prevention and analyzed respectively. Results A total of 240 imported malaria cases were reported in Chengdu City from 2012 to 2016. In detail, 68.75% of the cases were falciparum malaria cases, 20.41% were vivax malaria cases, 2.50% were quartan malaria cases, 6.25% were ovale malaria cases, and 2.08% were mixed Plasmodium infections. Among them three patients died, with a mortality of 1.25%. All of the cases were infected overseas, among which 224 patients returned from Africa and 16 patients from Southeast Asia. The annual average morbidity was 0.28/100 000, and there was a significantly difference among annual average morbidities (χ2 = 23.87, P < 0.001). There were malaria cases reported in every month, and no significantly difference among seasons (χ2 = 0.833, P > 0.05). Conclusion The number of overseas imported malaria in Chengdu City increases year by year. The effective measures to control the overseas imported malaria should be strengthened to consolidate the achievements of malaria elimination.

Insights on Flow Behavior of Foam in Unsaturated Porous Media during Soil Flushing.

One-dimensional column and two-dimensional tank experiments were carried out to determine (1) the physics of foam flow and propagation of foaming gas, foaming liquid, and foam; (2) the pressure distribution along foam flow and the effect of media permeability, foam flow rate and foam quality on foam injection pressure; and (3) the migration and distribution property of foam flow in homogeneous and heterogeneous sediments. The results demonstrated that: (1) gas and liquid front were formed ahead of the foam flow front, the transport speed order is foaming gas > foaming liquid > foam flowing; (2) injection pressure mainly comes from the resistance to bubble migration. Effect of media permeability on foam injection pressure mainly depends on the physics and behavior of foam flow; (3) foam has a stronger capacity of lateral spreading, besides, foam flow was uniformly distributed across the foam-occupied region, regardless of the heterogeneity of porous media.

Transport characteristics of nanoscale zero-valent iron carried by three different "vehicles" in porous media.

This study investigated the transport properties of nanoscale zero-valent iron (Fe(0)) (nZVI) carried by three vehicles: water, sodium dodecyl sulfate (SDS) solution, and SDS foam. Batch experiments were conducted to assess the sedimentation capability of nZVI particles in these three vehicles. Column experiments were conducted to investigate the transport properties of nZVI in porous media formed with different sizes of sand (0.25 mm to 0.5 mm, 0.5 mm to 0.9 mm, and 0.9 mm to 1.4 mm). Three main results were obtained. First, the batch experiments revealed that the stabilities of nZVI particles in SDS solution and SDS foam were improved, compared with that of nZVI particles in water. Moreover, the sedimentation of nZVI in foam was closely associated with the foam drainage volume. The nZVI content in foam was similar to that in the original foaming suspension, and the nZVI particle distribution in foam became significantly more uniform at a stirring speed of 3000 r/min. Second, the transport of nZVI was enhanced by foam compared with water and SDS solution for 0.25 mm to 0.5 mm diameter sand. For sand with diameters of 0.5 mm to 0.9 mm and 0.9 mm to 1.4 mm, the mobility of nZVI carried by SDS solution was optimal, followed by that of nZVI carried by foam and water. Thus, the mobility of nZVI in finer sand was significantly enhanced by foam, compared with that in coarse sand. In contrast, compared with the bare nZVI suspension and nZVI-laden foam, the spatial distribution of nZVI particles carried by SDS solution was significantly uniform along the column length. Third, the SDS concentration significantly influenced the migration of nZVI in porous media. The enhancement in the migration of nZVI carried by SDS solution was greater at an SDS dose of 0.25% compared with that at the other three doses (0.2%, 0.5%, and 1%) for sand with a 0.25 mm to 0.5 mm diameter. Increased SDS concentrations positively affected the transport of nZVI by foam for sand with a 0.25 mm to 0.5 mm diameter, and the SDS concentrations for enhancing the mobility of nZVI carried by SDS foam satisfied the following order: 1% > 0.5% > 0.25% > 0.2%. Thus, SDS solution and SDS foam were better vehicles than water for delivering nZVI particles to porous media for contamination remediation.

Receptor-specific delivery of protein antigen to dendritic cells by a nanoemulsion formed using top-down non-covalent click self-assembly.

A new class of targeted and immune-evading nanocarrier made using only biological components and facile processes is assembled in a bottom-up fashion. Simple top-down sequential addition of immune-evading or receptor-specific antibody elements conjugated to biosurfactant protein DAMP4 promotes self-assembly at an interface previously formed in the presence of peptide surfactant AM1, leading to a functional display at the interface through non-covalent molecular self-assembly.

Mechanisms of surfactant-enhanced air sparging in different media.

This article presents the results of a laboratory investigation of the mechanisms of surfactant-enhanced air sparging (SEAS) in different media. Two kinds of media (medium sand and gravel) were used in one-dimensional column experiments, designed to determine (1) the functional relationship between the air saturation and surface tension of water during SEAS, and (2) the contaminant removal mechanisms in different air travel modes (channels and bubbles) under different surface tension values. The results demonstrated that when air traveled in the form of channels, a decrease in surface tension accordingly reduced capillary pressure in porous media. Air saturation therefore increased, thereby considerably improving contaminant removal. The variations in removal efficiency under different surface tension values coincide with the trend of air saturation change. When air traveled in the form of bubbles, the SEAS-induced air saturation in the column was directly affected by foam stability and foamability, rather than by the surface tension of water. Surfactant addition improved only the contaminant removal rate, but the decrease in lingering concentration was insignificant. The results of this study can serve as theoretical bases for SEAS application in contaminated sites.

Extrusion based rapid prototyping technique: an advanced platform for tissue engineering scaffold fabrication.

Advances in scaffold design and fabrication technology have brought the tissue engineering field stepping into a new era. Conventional techniques used to develop scaffolds inherit limitations, such as lack of control over the pore morphology and architecture as well as reproducibility. Rapid prototyping (RP) technology, a layer-by-layer additive approach offers a unique opportunity to build complex 3D architectures overcoming those limitations that could ultimately be tailored to cater for patient-specific applications. Using RP methods, researchers have been able to customize scaffolds to mimic the biomechanical properties (in terms of structural integrity, strength, and microenvironment) of the organ or tissue to be repaired/replaced quite closely. This article provides intensive description on various extrusion based scaffold fabrication techniques and review their potential utility for TE applications. The extrusion-based technique extrudes the molten polymer as a thin filament through a nozzle onto a platform layer-by-layer and thus building 3D scaffold. The technique allows full control over pore architecture and dimension in the x- and y- planes. However, the pore height in z-direction is predetermined by the extruding nozzle diameter rather than the technique itself. This review attempts to assess the current state and future prospects of this technology.

Proteomic analysis of clear cell renal cell carcinoma. Identification of potential tumor markers.

OBJECTIVE: To identify new tumor specific proteins of renal cell carcinoma (RCC) using proteomic analysis. METHODS: Nine renal cell carcinomas were resected and these surgical operations were carried out from June 2007 to September 2008 in the Urology Department of the Second Affiliated Hospital of Soochow University, Suzhou, Jiangsu Province, China. The cancer tissues and para-cancer normal tissues were preserved in liquid nitrogen. We analyzed the RCC tissues and para-cancer normal tissues by 2-dimensional polyacrylamide gel electrophoresis (2D-PAGE). The 16 differentially expressed protein spots (p<0.05 by Student t-test) were identified by matrix assisted laser desorption ionization/time of flight mass spectrometry and tandem mass spectrometry. RESULTS: Six proteins were down regulated and 10 proteins were up regulated in clear cell RCC compared with corresponding normal kidney tissue. The down regulated proteins were calbindin, ester hydrolase C11orf54, alcohol dehydrogenase, ammecr1-like protein, adenosine diphosphate (ADP)/adenosine-5'-triphosphate (ATP) translocase 3 and leucine-tyrosine-arginine (LYR) motif-containing protein 5. The up regulated proteins were hypoxia inducible domain family member 1A, glutathione S-transferase P, thioredoxin-dependent peroxide reductase, peroxiredoxin-6, CD2-associated protein, annexin A5, gamma-enolase, retinal dehydrogenase 1, vimentin, and protein-glutamine gamma-glutamyltransferase 2. CONCLUSION: The data provide potential tumor markers for diagnosis of RCC.

Ezrin mediates c-Myc actions in prostate cancer cell invasion.

The forced overexpression of c-Myc in mouse prostate and in normal human prostate epithelial cells results in tumor transformation with an invasive phenotype. How c-Myc regulates cell invasion is poorly understood. In this study, we have investigated the interplay of c-Myc and androgens in the regulation of prostate cancer cell invasion. We found that c-Myc induces cell invasion and anchorage-independent growth by regulating ezrin protein expression in the presence of androgens. The activity of the ezrin promoter is controlled by androgens through c-Myc, which binds to a phylogenetically conserved E-Box located in the proximal promoter region. Besides, we also show that ezrin is an important regulator of c-Myc protein levels. These effects are achieved through androgen-induced changes in ezrin phosphorylation, which results in the regulation of downstream signals. These downstream signals involve the modulation of Akt and GSK-3beta activity resulting in increased c-Myc protein synthesis and inhibition of its degradation. In summary, we have shown a key role for ezrin as a mediator of c-Myc-induced tumorigenesis in prostate cancer cells.

Encapsulation of DNA and non-viral protein changes the structure of murine polyomavirus virus-like particles.

Asymmetrical-flow field flow fractionation with multiple-angle light scattering (AFFFF-MALS) was, for the first time, used to characterize the size of murine polyomavirus virus-like particles (MPV VLPs) packaged with either insect cell genomic DNA or non-viral protein. Encapsidation of both genomic DNA and non-viral protein were found to cause a contraction in VLP radii of gyration by approximately 1 nm. Non-viral protein packaged into VLPs consisted of a series of glutathione-S-transferase, His and S tags attached to the N-terminal end of the MPV structural protein VP2 (M(r) = 67108). Transmission electron microscopy analysis of MPV VLPs packaging non-viral protein suggested that VLPs grew in diameter by approximately 5 nm, highlighting the differences between this invasive technique and the relatively non-invasive AFFFF-MALS technique. Encapsulation of non-viral protein into MPV VLPs was found to prevent co-encapsidation of genomic DNA. Further investigation into why this occurred led to the discovery that encapsulation of non-viral protein alters the nuclear localization of MPV VLPs during in vivo assembly. VLPs were relocated away from the ring zone and the nuclear membrane towards the centre of the nucleus amongst the virogenic stroma. The change in nuclear localization away from the site where VLP assembly usually occurs is a likely reason why encapsidation of genomic DNA did not take place.

IGF-II regulates metastatic properties of choriocarcinoma cells through the activation of the insulin receptor.

Choriocarcinoma is a highly malignant tumor that can arise from trophoblasts of any type of gestational event but most often from complete hydatidiform mole. IGF-II plays a fundamental role in placental development and may play a role in gestational trophoblastic diseases. Several studies have shown that IGF-II is expressed at high levels in hydatidiform moles and choriocarcinoma tissues; however, conflicting data exist on how IGF-II regulates the behaviour of choriocarcinoma cells. The purpose of this study was to determine the contribution of the receptors for IGF-I and insulin to the actions of IGF-II on the regulation of choriocarcinoma cells metastasis. An Immuno Radio Metric Assay was used to analyse the circulating and tissue levels of IGF-I and IGF-II in 24 cases of hydatidiform mole, two cases of choriocarcinoma and eight cases of spontaneous abortion at the same gestational age. The JEG-3 choriocarcinoma cell line was used to investigate the role of IGF-II in the regulation of cell invasion. We found that mole and choriocarcinoma tissue express high levels of IGF-II compared to first trimester placenta. Both IGF-I and IGF-II regulate choriocarcinoma cell invasion in a dose dependent manner but through a different mechanism. IGF-II effects involve the activation of the InsR while IGF-I uses the IGF-IR. The positive effects of IGF-II on invasion are the result of enhanced cell adhesion and chemotaxis (specifically towards collagen IV). The actions of IGF-II but not those of IGF-I were sensitive to inhibition by the insulin receptor inhibitor HNMPA(AM)3. Our results demonstrate that the insulin receptor regulates choriocarcinoma cell invasion.

Androgens induce CD-9 in human prostate tissue.

Based on microarray analyses of LNCaP and LNCaP-r prostatic cell-lines we tentatively identified CD-9 as an androgen sensitive protein. This prompted us to characterize the androgen sensitivity and the correlation to malignancy of CD-9 at the protein level. Using Western blot, RT-PCR and immunohistochemistry the expression of CD-9 was analysed in LNCaP cells stimulated during increasing time by the synthetic androgen R1881 and also in 88 specimens of human prostate cancer tissues. Expression of CD-9 was induced by R1881 in LNCaP. CD-9 was immunolocalized in human prostate tissue sections representing non-malignant tissue as well as tumour areas. In non-malignant glands CD-9 immunoreactivity was observed at the apical and lateral cell borders of luminal epithelial cells. Basal epithelial cells were largely unstained. In tumour areas CD-9 staining intensity was variable and apparently not related to primary Gleason grade. In prostate tissue from a patient under androgen ablation therapy no staining was observed in luminal epithelial cells or in the tumour areas, but some staining was observed in basal epithelial cells. CD-9 is regulated by androgens in LNCaP and present in human prostate specimens. The expression is variable and changes in expression levels. These and earlier studies using other tissues indicate that CD-9 and its cellular localization could have an important role in prostate cancer cell development.

Pleiotropic effects of HIF-1 blockade on tumor radiosensitivity.

We have previously shown that radiation increases HIF-1 activity in tumors, causing significant radioprotection of the tumor vasculature. The impact that HIF-1 activation has on overall tumor radiosensitivity, however, is unknown. We reveal here that HIF-1 plays an important role in determining tumor radioresponsiveness through regulating four distinct processes. By promoting ATP metabolism, proliferation, and p53 activation, HIF-1 has a radiosensitizing effect on tumors. Through stimulating endothelial cell survival, HIF-1 promotes tumor radioresistance. As a result, the net effect of HIF-1 blockade on tumor radioresponsiveness is highly dependent on treatment sequencing, with "radiation first" strategies being significantly more effective than the alternative. These data provide a strong rationale for pursuing sequence-specific combinations of HIF-1 blockade and conventional therapeutics.

The relationship between hypoxia and angiogenesis.

Recent studies have generated a large amount of data supporting the hypothesis that hypoxia drives tumor angiogenesis. The relationship between the two is often considered a matter of supply and demand: ineffectively-vascularized tumor tissue becomes hypoxic, stimulating neoangiogenesis to improve the influx of oxygen, thereby diminishing the angiogenic drive. Although this paradigm is logically pleasing, much of what is known about tumor biology argues against such a straightforward relationship. In fact, some preclinical data convincingly shows that tumor hypoxia and angiogenesis do not always go hand in hand. It is important to begin to explore means of reconciling these discrepancies. Although poor oxygenation is a strong stimulus for tumor angiogenesis, (1) the pathogenesis of tumor hypoxia is much more complicated than the supply-demand paradigm lets on and (2) hypoxia is not necessarily sufficient or necessary for neovascularization to occur. These subtleties may help to explain why so much data disagrees with the current hypoxia-angiogenesis model and may begin to build a better understanding of the role hypoxia plays in tumor vascularization. This article will review what is known about hypoxia and angiogenesis in nononcological processes and will apply these lessons to tumor biology to more deeply describe their relationship.

Radiation activates HIF-1 to regulate vascular radiosensitivity in tumors: role of reoxygenation, free radicals, and stress granules.

Through a poorly understood mechanism, tumors respond to radiation by secreting cytokines capable of inhibiting apoptosis in endothelial cells, thereby diminishing treatment response by minimizing vascular damage. We reveal here that this pathway is governed by a major angiogenesis regulator, HIF-1. Following radiotherapy, tumor reoxygenation leads to: (1) nuclear accumulation of HIF-1 in response to reactive oxygen, and (2) enhanced translation of HIF-1-regulated transcripts secondary to stress granule depolymerization. The resulting increase in HIF-1-regulated cytokines enhances endothelial cell radioresistance. Inhibiting postradiation HIF-1 activation significantly increases tumor radiosensitivity as a result of enhanced vascular destruction. These data describe novel pathways contributing significantly to our understanding of HIF-1 regulation which may be major determinants of tumor radiosensitivity, potentially having high clinical relevance.

Responses of vascular endothelial cells to angiogenic signaling are important for tumor cell survival.

Neoplastic cells overexpress several angiogenic cytokines, which stimulate neovascularization. Whether the responses of the host endothelial cells to these signaling molecules affect tumor cells during early tumorigenesis has not been investigated. We investigated pre-angiogenic tumor cell survival and angiogenesis initiation by two murine tumor lines (4T1 mammary carcinoma and B16 melanoma), which constitutively expressed GFP, in dorsal skin-fold window chambers of mice treated with extracellular domain of Tie-2 (ExTek) or bFGF. ExTek reduced tumor cell survival, retarded tumor growth, and inhibited angiogenesis onset compared with controls. bFGF increased tumor cell survival and promoted earlier angiogenesis and tumor growth. Neither bFGF nor ExTek affected cell proliferation in vitro. RT-PCR showed mRNA expression of bFGF receptor 2 (FGFR2) IIIb, which does not bind bFGF efficiently, by 4T1 cells and B16 cells express FGFR1 but not FGFR2. B16 cells expressed angiopoietin (Ang) 2, but neither cell line expresses Ang1. Both tumor lines express VEGF. These findings suggested that effects of bFGF and ExTek on tumor cell survival and angiogenesis were not due to direct action but were instead a result of paracrine factors secreted by endothelial cells. These subsequent signals from endothelial cells promote early survival and proliferation of disseminated tumor cells before onset of angiogenesis.

Free split and segmental latissimus dorsi muscle transfer in one stage for facial reanimation.

The authors report the experience in facial reanimation using free innervated split and segmental latissimus dorsi muscle flap one-stage transfer in 86 patients with longstanding facial palsy. The segmental latissimus dorsi was taken from the distal part of the muscle so that the muscle flap had an ultra-long neurovascular pedicle of 13 to 17.5 cm in length. The muscle flap was made thinner by splitting the segmental muscle. The split segmental muscle flap was transferred to the paralyzed side of the face with its ultra-long neurovascular pedicle passing through a tunnel in the upper lip to the normal side of the face. The neurovascular pedicle of the muscle flap was anastomosed with the facial nerve, artery, and veins, respectively, on the normal side of the face. The operation was designed without the cross-facial nerve graft stage. From 1986 to October of 1997, 86 patients with long-standing facial paralysis were treated in our department. The duration of facial palsy in this series ranged from 1.5 to 51 years. A satisfactory result was obtained in 80 cases, evaluated at 8 months to 2 years postoperatively. The expression movement of the soft tissues of the face can be seen not only over transferred muscle but also on the paralyzed muscle covered by the splitting muscle flap. It is supposed that this is the result of muscle-muscle neurolization. Study of 66 specimens of latissimus dorsi muscle in the cadavers is discussed.

Association of celiac disease with microsatellite polymorphisms close to the tumor necrosis factor genes.

Celiac disease is tightly linked to the MHC class II region on chromosome 6. We have studied two highly polymorphic microsatellite loci, TNFa and b, near the TNF genes in the class III region of the MHC, for evidence of their association to CD, as compared to a control population. Our findings show that the microsatellite allele most significantly associated with the disease is TNFb3, which is found in 86.3% of CD patients versus 24.5% of controls, with allele frequencies of 0.5392 and 0.1290, respectively (p < 0.001). The TNFa2 allele had a frequency of 0.6122 in CD patients and 0.2627 in controls (p < 0.001), with phenotype frequencies of 87.8% and 50.0%, respectively. TNFa6 and -a11 and TNFb5 have significantly reduced frequencies in CD patients. TNFb3 shows a maximal level of linkage disequilibrium with HLA-DQB1*0201 in celiac patients. However, while the DQB1*0201/TNFa2 haplotype was strongly associated with CD, DQB1*0201 was not significantly in linkage disequilibrium with TNFa2, suggesting that TNFa2 is independently associated with CD. This association could have functional significance as TNFa2 has been correlated with high TNF production.