Gotowe bibliografie tematyczne / JHMC

Gotowa bibliografia na temat „JHMC”

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Data publikacji: 26 lipca 2024

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Artykuły w czasopismach na temat "JHMC"

1

Moreno, Sindy C., Justin To, Hajoon Chun i Ivan M. Ngai. "Vertical Transmission of COVID-19 to the Neonate". Infectious Diseases in Obstetrics and Gynecology 2020 (12.11.2020): 1–5. http://dx.doi.org/10.1155/2020/8460672.

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Objective. To estimate the incidence rate of vertical transmission of coronavirus disease 2019 (COVID-19) to the neonate during the third trimester. Study Design. We conducted a retrospective observational study of pregnant women diagnosed with COVID-19 during the third trimester, who delivered at Flushing Hospital Medical Centre (FHMC) or Jamaica Hospital Medical Centre (JHMC) between March 20, 2020, and April 30, 2020. The study participants were symptomatic pregnant women diagnosed with COVID-19 via positive SARS-CoV-2 RNA, real-time reverse transcription-polymerase chain reaction (SARS-CoV-2 rRT-PCR) test. Evidence of vertical transmission was assessed in the neonate via a SARS-CoV-2 rRT-PCR test, with nasopharyngeal swab samples collected on the neonates after 24 hours of birth. The exclusion criteria for this study were maternal or neonate records without SARS-CoV-2 rRT-PCR test results, neonates not delivered at FHMC or JHMC, and foetuses with suspected foetal anomalies or incomplete medical records. Results. We identified 19 symptomatic pregnant women diagnosed with COVID-19, including two women with twin pregnancies. Seven patients (36.8%) were delivered via cesarean. 12 patients (63.1%) presented in spontaneous labour, and 8 (38.1%) had preterm delivery. No maternal intensive care unit admission, maternal sepsis, or maternal mortality was observed. Twenty-one neonates were evaluated for COVID-19 after birth. SARS-CoV-2 rRT-PCR test results were negative in 100% of the neonates. Thirteen neonates (61.9%) were admitted to the neonatal intensive care unit. Prematurity was the most common cause of NICU admission 6 (46.1%), with a length of stay of 5.5 ± 6.4 days. No invasive mechanical ventilation, neonatal sepsis, or neonatal mortality was observed. Conclusion. In our cohort, symptomatic COVID-19 during the third trimester of pregnancy was not associated with vertical transmission to the neonate.
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Kyuwa, Shigeru, Yoh-ichi Tagawa, Shinwa Shibata, Kunio Doi, Kenji Machii i Yoichiroh Iwakura. "Murine Coronavirus-Induced Subacute Fatal Peritonitis in C57BL/6 Mice Deficient in Gamma Interferon". Journal of Virology 72, nr 11 (1.11.1998): 9286–90. http://dx.doi.org/10.1128/jvi.72.11.9286-9290.1998.

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ABSTRACT Gamma interferon-deficient (IFN-γ−/−) mice with a C57BL/6 background were infected intraperitoneally with mouse hepatitis virus strain JHM (JHMV). In contrast to IFN-γ-+/− and IFN-γ+/+ mice, JHMV persisted in IFN-γ−/− mice and induced death during the subacute phase of the infection. Unexpectedly, infected IFN-γ−/− mice showed severe peritonitis accompanying the accumulation of a viscous fluid in the abdominal and thoracic cavities in the subacute phase. Destructive changes of hepatocytes were not observed. Administration of recombinant IFN-γ protracted the survival time of IFN-γ−/− mice after JHMV infection. These results demonstrate that IFN-γ plays a critical role in viral clearance in JHMV infection. They also show that a resultant persistent JHMV infection induces another form of disease in IFN-γ−/− mice, which bears a resemblance to feline infectious peritonitis in cats.
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Walsh, Kevin B., Lewis L. Lanier i Thomas E. Lane. "NKG2D Receptor Signaling Enhances Cytolytic Activity by Virus-Specific CD8+ T Cells: Evidence for a Protective Role in Virus-Induced Encephalitis". Journal of Virology 82, nr 6 (26.12.2007): 3031–44. http://dx.doi.org/10.1128/jvi.02033-07.

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ABSTRACT Inoculation with the neurotropic JHM strain of mouse hepatitis virus (JHMV) into the central nervous system (CNS) of mice results in an acute encephalitis associated with an immune-mediated demyelinating disease. During acute disease, infiltrating CD8+ T cells secrete gamma interferon (IFN-γ) that controls replication in oligodendrocytes, while infected astrocytes and microglia are susceptible to perforin-mediated lysis. The present study was undertaken to reveal the functional contributions of the activating NKG2D receptor in host defense and disease following JHMV infection. NKG2D ligands RAE-1, MULT1, and H60 were expressed within the CNS following JHMV infection. The immunophenotyping of infiltrating cells revealed that NKG2D was expressed on ∼90% of infiltrating CD8+ T cells during acute and chronic disease. Blocking NKG2D following JHMV infection resulted in increased mortality that correlated with increased viral titers within the CNS. Anti-NKG2D treatment did not alter T-cell infiltration into the CNS or the generation of virus-specific CD8+ T cells, and the expression of IFN-γ was not affected. However, cytotoxic T-lymphocyte (CTL) activity was dependent on NKG2D expression, because anti-NKG2D treatment resulted in a dramatic reduction in lytic activity by virus-specific CD8+ T cells. Blocking NKG2D during chronic disease did not affect either T-cell or macrophage infiltration or the severity of demyelination, indicating that NKG2D does not contribute to virus-induced demyelination. These findings demonstrate a functional role for NKG2D in host defense during acute viral encephalitis by selectively enhancing CTL activity by infiltrating virus-specific CD8+ T cells.
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Dickey, Laura L., Colleen Worne, Jessica Glover, Joshua Daugherty, Thomas Lane i Ryan M. O’Connell. "MicroRNA-155 enhances T-cell trafficking and antiviral effector function in a model of coronavirus-induced neurologic disease". Journal of Immunology 196, nr 1_Supplement (1.05.2016): 55.12. http://dx.doi.org/10.4049/jimmunol.196.supp.55.12.

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Abstract Micro-RNAs (miRNAs) are non-coding RNAs that modulate cellular gene expression at the post-transcriptional level. These molecules are becoming increasingly recognized as important in helping tailor T-cell responses following viral infection. We therefore sought to examine the functional role of miR-155 in a model of viral-induced demyelination. Intracranial injection with the neurotropic JHM strain of mouse hepatitis virus (JHMV) results in an acute encephalomyelitis followed by an immune-mediated demyelinating disease. Compared to wild-type mice, JHMV-infected mice deficient in miR-155 (miR-155−/−) developed delayed but exacerbated disease concomitant with increased morbidity/mortality, weight loss, and spinal cord demyelination. In addition, miR-155−/− mice had decreased total and virus-specific CD4+ and CD8+ T-cell accumulation within the CNS during the acute phase of disease. Furthermore, IFN-γ and TNF-α production, as well as and cytolytic function, were impaired in CD8+ cells from miR-155−/− mice. These results identify miR-155 as a key mediator of disease development and recovery in a model of virus-induced neurological disease.
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Grist, Jonathan Jeffrey, Brett S. Marro i Thomas Lane. "Inducible expression of CXCL1 within the CNS amplifies demyelination in pre-clinical models of multiple sclerosis". Journal of Immunology 196, nr 1_Supplement (1.05.2016): 139.13. http://dx.doi.org/10.4049/jimmunol.196.supp.139.13.

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Abstract The functional role of the ELR+ chemokine CXCL1 in host defense and disease in two pre-clinical mouse models of the human demyelinating disease multiple sclerosis (MS) was assessed. Mice in which expression of CXCL1 is under the control of a tetracycline-inducible promoter active within GFAP-positive cells were generated and infected intracranially with the neurotropic JHM strain of mouse hepatitis virus (JHMV) or immunized with myelin oligodendrocyte glycoprotein (MOG)35-55 to induce experimental autoimmune encephalomyelitis (EAE). In both JHMV-induced neurologic disease and EAE, overexpression of CXCL1 by astrocytes resulted in increased clinical disease severity. Immunophenotyping cells infiltrating into the central nervous system (CNS) revealed a selective increase in Ly6G+CD11b+ neutrophils (but not Ly6G−Ly6C+CD11b+ monocytes) present within the CNS. In JHMV infected mice and MOG35-55-immunized mice, the T cell response to antigen with regard to proliferation and cytokine production was not altered, nor was trafficking into the CNS affected. In both models, increased CXCL1 expression within the CNS resulted in increased morbidity that correlated with selectively elevated neutrophil infiltration, diminished numbers of mature oligodendrocytes, and an increase in the severity of demyelination. Neutrophil ablation in CXCL1-transgenic mice reduced the severity of demyelination in mice arguing a role for these cells in white matter damage. Collectively, these findings illustrate that sustained CXCL1 expression amplifies the severity of white matter damage and neutrophils can contribute to this process in two different mouse models of MS.
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Parra, Beatriz, David R. Hinton, Norman W. Marten, Cornelia C. Bergmann, Mark T. Lin, Camillia S. Yang i Stephen A. Stohlman. "IFN-γ Is Required for Viral Clearance from Central Nervous System Oligodendroglia". Journal of Immunology 162, nr 3 (1.02.1999): 1641–47. http://dx.doi.org/10.4049/jimmunol.162.3.1641.

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Abstract Infection of the central nervous system (CNS) by the JHM strain of mouse hepatitis virus (JHMV) is a rodent model of the human demyelinating disease multiple sclerosis. The inability of effective host immune responses to eliminate virus from the CNS results in a chronic infection associated with ongoing recurrent demyelination. JHMV infects a variety of CNS cell types during the acute phase of infection including ependymal cells, astrocytes, microglia, oligodendroglia, and rarely in neurons. Replication within the majority of CNS cell types is controlled by perforin-dependent virus-specific CTL. However, inhibition of viral replication in oligodendroglia occurs via a perforin-independent mechanism(s). The potential role for IFN-γ as mediator controlling JHMV replication in oligodendroglia was examined in mice deficient in IFN-γ secretion (IFN-γ0/0 mice). IFN-γ0/0 mice exhibited increased clinical symptoms and mortality associated with persistent virus, demonstrating an inability to control replication. Neither antiviral Ab nor CTL responses were diminished in the absence of IFN-γ, although increased IgG1 was detected in IFN-γ0/0 mice. Increased virus Ag in the absence of IFN-γ localized almost exclusively to oligodendroglia and was associated with increased CD8+ T cells localized within white matter. These data suggest that although perforin-dependent CTL control virus replication within astrocytes and microglia, which constitute the majority of infected CNS cells, IFN-γ is critical for control of viral replication in oligodendroglia. Therefore, different mechanisms are used by the host defenses to control virus replication within the CNS, dependent upon the phenotype of the targets of virus replication.
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Lin, Mark T., David R. Hinton, Norman W. Marten, Cornelia C. Bergmann i Stephen A. Stohlman. "Antibody Prevents Virus Reactivation Within the Central Nervous System". Journal of Immunology 162, nr 12 (15.06.1999): 7358–68. http://dx.doi.org/10.4049/jimmunol.162.12.7358.

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Abstract The neurotropic JHM strain of mouse hepatitis virus (JHMV) produces an acute CNS infection characterized by encephalomyelitis and demyelination. The immune response cannot completely eliminate virus, resulting in persistence associated with chronic ongoing CNS demyelination. The contribution of humoral immunity to viral clearance and persistent infection was investigated in mice homozygous for disruption of the Ig μ gene (IgM−/−). Acute disease developed with equal kinetics and severity in IgM−/− and syngeneic C57BL/6 (wt) mice. However, clinical disease progressed in IgM−/− mice, while wt mice recovered. Viral clearance during acute infection was similar in both groups, supporting a primary role of cell-mediated immunity in viral clearance. In contrast to wt mice, in which infectious virus was reduced to below detection following acute infection, increasing infectious virus was recovered from the CNS of the IgM−/− mice following initial clearance. No evidence was obtained for selection of variant viruses nor was there an apparent loss of cell-mediated immunity in the absence of Ab. Passive transfer of anti-JHMV Ab following initial clearance prevented reactivation of infectious virus within the CNS of IgM−/− mice. These data demonstrate the clearance of infectious virus during acute disease by cell-mediated immunity. However, immunologic control is not maintained in the absence of anti-viral Ab, resulting in recrudescence of infectious virus. These data suggest that humoral immunity plays no role in controlling virus during acute infection, but plays an important role in establishing and maintaining CNS viral persistence.
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Stohlman, Stephen A., David R. Hinton, Beatriz Parra, Roscoe Atkinson i Cornelia C. Bergmann. "CD4 T Cells Contribute to Virus Control and Pathology following Central Nervous System Infection with Neurotropic Mouse Hepatitis Virus". Journal of Virology 82, nr 5 (19.12.2007): 2130–39. http://dx.doi.org/10.1128/jvi.01762-07.

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ABSTRACT Replication of the neurotropic mouse hepatitis virus strain JHM (JHMV) is controlled primarily by CD8+ T-cell effectors utilizing gamma interferon (IFN-γ) and perforin-mediated cytotoxicity. CD4+ T cells provide an auxiliary function(s) for CD8+ T-cell survival; however, their direct contribution to control of virus replication and pathology is unclear. To examine a direct role of CD4+ T cells in viral clearance and pathology, pathogenesis was compared in mice deficient in both perforin and IFN-γ that were selectively reconstituted for these functions via transfer of virus-specific memory CD4+ T cells. CD4+ T cells from immunized wild-type, perforin-deficient, and IFN-γ-deficient donors all initially reduced virus replication. However, prolonged viral control by IFN-γ-competent donors suggested that IFN-γ is important for sustained virus control. Local release of IFN-γ was evident by up-regulation of class II molecules on microglia in recipients of IFN-γ producing CD4+ T cells. CD4+ T-cell-mediated antiviral activity correlated with diminished clinical symptoms, pathology, and demyelination. Both wild-type donor CD90.1 and recipient CD90.2 CD4+ T cells trafficked into the central nervous system (CNS) parenchyma and localized to infected white matter, correlating with decreased numbers of virus-infected oligodendrocytes in the CNS. These data support a direct, if limited, antiviral role for CD4+ T cells early during acute JHMV encephalomyelitis. Although the antiviral effector mechanism is initially independent of IFN-γ secretion, sustained control of CNS virus replication by CD4+ T cells requires IFN-γ.
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Matsuyama, Shutoku, i Fumihiro Taguchi. "Receptor-Induced Conformational Changes of Murine Coronavirus Spike Protein". Journal of Virology 76, nr 23 (1.12.2002): 11819–26. http://dx.doi.org/10.1128/jvi.76.23.11819-11826.2002.

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ABSTRACT Although murine coronavirus mouse hepatitis virus (MHV) enters cells by virus-cell membrane fusion triggered by its spike (S) protein, it is not well known how the S protein participates in fusion events. We reported that the soluble form of MHV receptor (soMHVR) transformed a nonfusogenic S protein into a fusogenic one (F. Taguchi and S. Matsuyama, J. Virol. 76:950-958, 2002). In the present study, we demonstrate that soMHVR induces the conformational changes of the S protein, as shown by the proteinase digestion test. A cl-2 mutant, srr7, of the MHV JHM virus (JHMV) was digested with proteinase K after treatment with soMHVR, and the resultant S protein was analyzed by Western blotting using monoclonal antibody (MAb) 10G, specific for the membrane-anchored S2 subunit. A 58-kDa fragment, encompassing the two heptad repeats in S2, was detected when srr7 was digested after soMHVR treatment, while no band was seen when the virus was untreated. The appearance of the proteinase-resistant fragment was dependent on the temperature and time of srr7 incubation with soMHVR and also on the concentration of soMHVR. Coimmunoprecipitation indicated that the direct binding of soMHVR to srr7 S protein induced these conformational changes; this was also suggested by the inhibition of the changes following pretreatment of soMHVR with anti-MHVR MAb CC1. soMHVR induced conformational changes of the S proteins of wild-type (wt) JHMV cl-2, as well as revertants from srr7, srr7A and srr7B; however, a major proportion of these S proteins were resistant to proteinase K even without soMHVR treatment. The implications of this proteinase-resistant fraction are discussed. This is the first report on receptor-induced conformational changes of the membrane-anchored fragment of the coronavirus S protein.
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Watanabe, Rie, Shutoku Matsuyama i Fumihiro Taguchi. "Receptor-Independent Infection of Murine Coronavirus: Analysis by Spinoculation". Journal of Virology 80, nr 10 (15.05.2006): 4901–8. http://dx.doi.org/10.1128/jvi.80.10.4901-4908.2006.

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ABSTRACT A highly neurovirulent murine coronavirus JHMV (wild-type [wt] JHMV) is known to spread from cells infected via the murine coronavirus mouse hepatitis virus receptor (MHVR) to cells without MHVR (MHVR-independent infection), whereas a mutant virus isolated from wt JHMV, srr7, spread only in an MHVR-dependent fashion. These observations were obtained by the overlay of JHMV-infected cells onto receptor-negative cells that are otherwise resistant to wt JHMV infection. MHVR-independent infection is hypothetically thought to be attributed to a naturally occurring fusion activation of the wt JHMV S protein, which did not occur in the case of srr7. Attachment of S protein on cells without MHVR during the S-protein activation process seems to be a key condition. Thus, in the present study, we tried to see whether wt JHMV virions that are attached on MHVR-negative cells are able to infect those cells. In order to make virions attach to the cell surface without MHVR, we have used spinoculation, namely, the centrifugation of cells together with inoculated virus at 3,000 rpm for 2 h. This procedure forces viruses to attach to the cell surface, as revealed by quantitative estimation of attached virions by real-time PCR and also facilitated wt JHMV infection to MHVR-negative cells, but failed to do so for srr7. Virions of both wt and srr7 attached on MHVR-negative cells by spinoculation were facilitated for infection in the presence of a soluble form of MHVR that induces conformational changes of both wt and srr7. It was further revealed that wt JHMV S1, but not srr7, was released from the cell surface when S protein was expressed on cells. These observations support the hypothesis that attachment of the virion to MHVR-negative cells is a critical step and that a unique feature of wt JHMV S1 to be released from S2 in a naturally occurring event is involved in an MHVR-independent infection.
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Rozprawy doktorskie na temat "JHMC"

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Staněk, Martin. "Stanovení hodnoty JHMD, a.s". Master's thesis, Vysoká škola ekonomická v Praze, 2014. http://www.nusl.cz/ntk/nusl-193041.

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This thesis focuses on valuation of companies and enterprises. The value of the firm is useful not only during mergers and acquisitions but can be also a metric how to evaluate company's strategic and financial plans. The impact of strategic and financial decisions can be projected into a firm's value. The thesis contains theoretical part where all the basic models and concepts are presented and practical part which includes valuation of private owned company Jindřichohradecké místní dráhy a.s.
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Trujillo, Jonathan Anthony. "T cell responses to S-glutathionylated And heteroclitic viral epitopes and CCl2-mediated immune dysregulation in mice infected with a neurotropic coronavirus". Diss., University of Iowa, 2014. https://ir.uiowa.edu/etd/4775.

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Mice infected with neurotropic variants of the murine coronavirus, mouse hepatitis virus, (strains JHMV or J2.2–V–1) develop acute and chronic CNS infections, and provide a model system to study the pathogenesis of virus–induced neuroinflammation, mechanisms of virus persistence, and anti–viral immune responses in the CNS. Using the J2.2–V–1 model of CNS infection, we addressed the role of sustained CCL2 production during viral infection using mice in which CCL2 was expressed transgenically in oligodendrocytes. Tonic CCL2 expression in the CNS resulted in delayed kinetics of virus clearance, and converted what is typically a mild, nonlethal disease to acutely lethal encephalitis, with the majority of mice succumbing to the infection. CCL2 induced a rapid and dysregulated inflammatory response that was no longer protective and was unable to efficiently clear virus from the CNS. Infected CCL2 Tg mice had increased numbers of Foxp3–expressing CD4 T cells (Tregs) and of macrophages and microglia expressing elevated levels of YM–1, a marker for alternatively activated macrophages, and nitric oxide. Our results showed that CCL2 has effects beyond serving as a chemoattractant for leukocytes, and has effects on the composition and function of inflammatory cells at sites of infection. In a separate set of experiments, I identified and characterized two additional heteroclitic variants of the JHMV epitope S598 that induced CD8 T cells with greater antigen sensitivity to the native S598 determinant relative to the cells primed by the native epitope. One of these heteroclitic epitopes elicited a T cell response with nearly complete cross–reactivity towards the native peptide. The structural data show that these heteroclitic epitopes induced modest conformational changes in the local environment of the peptide–MHCI complex. I also provide data to support the notion that heteroclitic determinants augment functional avidity by increasing surface epitope density. Collectively, these data will help guide the design of heteroclitic epitopes in the setting of vaccine development. Lastly, I examined the consequences of oxidative stress induced by viral infection on antigen presentation. The brains of JHMV–infected mice were found to have signs of oxidative stress, with significantly decreased ratios of reduced (GSH) to oxidized (GSSG) glutathione, suggesting that there is an environment that is conducive for cysteine modification with oxidized glutathione. We found that virus–induced oxidative stress resulted in the presentation of both native and S–glutathionylated forms of the JHMV epitope S510 by infected cells. A subset of the S510–specific CD8 T cells failed to recognize the modified form of the epitope, suggesting that GSH–modification of a cysteine–containing viral epitope might interfere with T cell recognition. Further, GSH-modified peptides were identified in stressed human cells, including herpes virus–transformed B cells, suggesting that the modification is not limited to mouse cells. Collectively these findings have implications for both anti–viral immunity and anti–tumor immunity, where oxidative stress has been shown to play a role during infection and tumorgenesis.
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Houtman, Jacqueline Jaeger. "Pathogenesis of immune-mediated demyelination in mice infected with murine coronavirus JHM". 1996. http://catalog.hathitrust.org/api/volumes/oclc/36504710.html.

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Nkokoto, Mokela. "Analysis of the implementation of Johannesburg inner city renewal strategies". Thesis, 2007. http://hdl.handle.net/10539/2169.

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Student number: 0200613W Faculty of Engineering and the Built Environment Master of Property Development and Management.
This paper is a report on the research undertaken to evaluate the implementation of the Urban Renewal strategies that the City of Johannesburg adopted for the CBD renewal through the Blue IQ. The study was restricted to the views expressed by the general community, business community, Johannesburg Development Agency (JDA). Johannesburg Housing Company (JHC), Blue IQ, Gauteng Development Agency and Gauteng Economic Development Agency (GEDA), which are the main role players in the CBD renewal effort. There was administered questioner to the members of the Business and general communities that were randomly picked using the fish bowl method. Interviews were conducted with the senior executive staff of JDA. Blue IQ, JHC. Statistics derived from the above company s websites was used as well. The results of the study show that the renewal strategy has been largely successful in so far as a number of factors, which have contributed to the CBD decay such as poor infrastructure and slumps. There have also been considerable efforts to address acute shortage of parking space by private partners such as financial institutions. Although crime has decreased it is still posing a serious challenge as most people still consider the CBD high risk. However there is still a room for improvement, which includes: the enhancement of safety and security, the infrastructure maintenance policy and the enforcement of the municipality by laws and town planning scheme. Overall the strategies have also improved the economic performance of the city significantly though unemployment still remain high with the ever increasing number of people coming to seek opportunities.
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Książki na temat "JHMC"

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Couture, J. H. JHC Tesla handbook. San Diego, Ca. (10823 New Salem Point, San Diego 92126): JHC Engineering Co., 1988.

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Tuttle, W. C. Mystery at the JHC Ranch. South Yarmouth, Ma: Curley Pub., 1990.

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Congress, Joint Hospitality Industry, Barclays Bank i Henley Centre for Forecasting, red. Leisure in the new millennium: The Barclays and JHIC report produced by the Henley Centre, July 2000. London: Joint Hospitality Industry Congress, 2000.

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Ventriloquism [jhc]. PS Publishing, 2010.

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Dann, Jack. Junction [jhc]. PS Publishing, 2011.

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Morris, Edited by Mark. Cinema Futura [jhc]. PS Publishing, 2010.

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Urbis Morpheos [jhc]. Brand: PS Publishing, 2010.

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Shepard, Lucius. Viator Plus [jhc]. PS Publishing, 2009.

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Hautala, Rick. Reunion [signed jhc]. PS Publishing, 2009.

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Russell, R. B. Literary Remains [jhc]. PS Publishing, 2010.

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Części książek na temat "JHMC"

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Taguchi, F., S. Siddell, H. Wege, P. Massa i V. ter Meulen. "Characterization of JHMV Variants Isolated from RAT Brain and Cultured Neural Cells after Wild Type JHMV Infection". W Coronaviruses, 343–49. Boston, MA: Springer US, 1987. http://dx.doi.org/10.1007/978-1-4684-1280-2_43.

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Parra, Beatriz, Shawn Morales, Ramachristna Chandran i Stephen A. Stohlman. "B Cell Mediated Lysis of JHMV Infected Targets". W Advances in Experimental Medicine and Biology, 369–74. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1325-4_55.

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Stohlman, Stephen A., Qin Yao, Cornelia C. Bergmann, Stanley M. Tahara, Shigeru Kyuwa i David R. Hinton. "Transcription and Translation of Proinflammatory Cytokines Following JHMV Infection". W Advances in Experimental Medicine and Biology, 173–78. Boston, MA: Springer US, 1995. http://dx.doi.org/10.1007/978-1-4615-1899-0_28.

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Hayashi, M., K. Ishida, A. Maeda, Y. Kon, T. Mizutani, T. Watanabe, S. Arai i F. Okada. "Intramuscular Injection of Plasmid DNA Expressing mRNA7 Coding the Nucleocapsid Protein of JHMV Partially Protected Mice Against Acute Infection with JHMV". W Advances in Experimental Medicine and Biology, 693–99. Boston, MA: Springer US, 1998. http://dx.doi.org/10.1007/978-1-4615-5331-1_89.

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Taguchi, Fumihiro, Toshio Ikeda, Keiichi Saeki, Hideyuki Kubo i Tateki Kikuchi. "Fusogenic Properties of Uncleaved Spike Protein of Murine Coronavirus JHMV". W Coronaviruses, 171–75. Boston, MA: Springer US, 1994. http://dx.doi.org/10.1007/978-1-4615-2996-5_27.

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Schmidt, I., D. Ebner, M. A. Skinner, M. Pfleiderer, B. Schelle-Prinz i S. G. Siddell. "Structural Proteins of the Murine Coronavirus MHV-JHM". W Modern Trends in Virology, 75–82. Berlin, Heidelberg: Springer Berlin Heidelberg, 1988. http://dx.doi.org/10.1007/978-3-642-73745-9_9.

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Williamson, J., S. Kyuwa, F. I. Wang i S. Stohlman. "T Cell-Mediated Clearance of JHMV from the Central Nervous System". W Advances in Experimental Medicine and Biology, 557–63. Boston, MA: Springer US, 1990. http://dx.doi.org/10.1007/978-1-4684-5823-7_77.

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Ontiveros, Evelena, Lili Kuo, Paul Masters i Stanley Perlman. "Analysis of Nonessential Gene Function in Recombinant MHV-JHM". W Advances in Experimental Medicine and Biology, 83–89. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1325-4_13.

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Matsuyama, Shutoku, Rihito Watanabe i Fumihiro Taguchi. "Neurovirulence for Mice of Soluble Receptor-Resistant Mutants of Murine Coronavirus JHMV". W Advances in Experimental Medicine and Biology, 145–48. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1325-4_23.

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Zhang, Xuming. "Heterogeneity of Subgenomic mRNAs of a Mutant Mouse Hepatitis Virus Strain JHM2C". W Advances in Experimental Medicine and Biology, 541–46. Boston, MA: Springer US, 2001. http://dx.doi.org/10.1007/978-1-4615-1325-4_79.

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Streszczenia konferencji na temat "JHMC"

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Orf, Garry W. "Joint helmet-mounted cueing system (JHMCS) helmet qualification testing requirements". W Aerospace/Defense Sensing and Controls, redaktorzy Ronald J. Lewandowski, Loran A. Haworth i Henry J. Girolamo. SPIE, 1998. http://dx.doi.org/10.1117/12.317425.

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Bartak, Michalina, Anna Słońska, Marcin W. Bańbura i Joanna Cymerys. "Preliminary confirmation of alternative cellular receptor in neurons for mouse coronavirus (MHV-JHM)". W 1st International PhD Student’s Conference at the University of Life Sciences in Lublin, Poland: ENVIRONMENT – PLANT – ANIMAL – PRODUCT. Publishing House of The University of Life Sciences in Lublin, 2022. http://dx.doi.org/10.24326/icdsupl1.a001.

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Sakai, Akira, Hajime Koikegami, Siegfried Weisenburger, Guenther Roth, Norio Kanehira i Satoshi Komamine. "Comparison of Advanced Melting Process for HLW Vitrification, Joule-Heated Ceramic-Lined Melter (JHCM) and Cold-Crucible Induction Melter (CCIM)". W 2017 25th International Conference on Nuclear Engineering. American Society of Mechanical Engineers, 2017. http://dx.doi.org/10.1115/icone25-67807.

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High level waste (HLW) originating from reprocessing of spent fuel commercial power reactors contains more than 40 different elements. Vitrification into borosilicate glass at 1100 ∼1200°C is the process of choice. It is routinely used to immobilize the radioactive waste constituents in a chemically stable matrix for a final geological disposal. Melting process for commercial HLW glasses are variants of two basic designs. (1) The joule-heated ceramic-lined melter (JHCM) originally developed in the United States in 1973 and used in several nuclear sites in the world. (2) The hot-walled induction melter (HWIM), developed in France starting in 1962 and used in France and UK. These technologies, while effective, do pose limitations in waste form compositions and throughput rates. Particularly HLW originating from commercial spent fuel reprocessing usually contains noble metals elements such as ruthenium (Ru), rhodium (Rh), and palladium (Pd) which require special attention when this waste is vitrified. Recent advances to both of these baseline technologies are beginning to be used with large gains to ensure waste form flexibility, throughputs, and noble metals compatibility. The next generation JHCMs use a steeply sloped bottom and a subsidiary-heating bottom drain to allow these noble metals particles to be effectively flushed from the melter with higher waste loadings. Similar melters are being installed near Guangyuan/Sichuan province, China by German consortium team and being developed for the second K-Facility melter at Rokkasho by Japan Nuclear Fuel Limited (JNFL). As another example the advanced JHCMs will be installed in the Hanford WTP project having large glass pool surface area with rapid bubbling. Significant improvements on induction melters have also been implemented. AREVA recently installed a cold-crucible induction melter (CCIM) in combination with a rotary calciner at La Hague in France. This melter uses radio frequency induction to power the glass melt itself and water cooling of the outer surface maintains a frozen glass shell (skull) as the glass contact material. Because no permanent refractories or embedded electrodes are used, this design allows for high-temperature operation and can tolerate more corrosive melts, and uses a water-cooled, motor-driven mechanical stirrer to comply with noble metals behavior. This paper highlights some of these advances and suggests potential advantages and disadvantages of these next generation melter technologies comparing advanced JHCM with updated CCIM. In conclusion, these melters have made the technologies of choice for new HLW vitrification projects around the world.
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ABDULHAMID, HAKIM, PAUL DECONINCK i JÉRÔME MESPOULET. "CONCRETE CHARACTERIZATION FOR BALLISTIC THREAT". W 32ND INTERNATIONAL SYMPOSIUM ON BALLISTICS. Destech Publications, Inc., 2022. http://dx.doi.org/10.12783/ballistics22/36174.

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This ongoing study aims at building a robust approach for reliable simulation of concrete behavior under ballistic impact of Kinetic Energy Penetrator (KEP) from concrete characterization to penetration efficiency. The Holmquist-Johnson-Cook concrete (JHC) material model is used combined with advanced capabilities of γ-SPH formulation available in IMPETUS AFEATM software. A common concrete used in building industry is considered for the study (~35MPa compressive strength). To limit the number of tests, only the most relevant data regarding the penetration phenomena have been investigated: quasi-static compression and dynamic oedometric compression tests have been realized. The impact test is conducted on a confined concrete cylinder at hypersonic speed. The test is instrumented to evaluate the model prediction in terms of projectile deceleration and depth of penetration. The numerical simulation results are in good correlation with the tests and higher impact speed up to 900 m/s will be investigated soon.
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Feng, Nan, ShaoBo Li i Qingsong Luo. "JHM-NC: a Joint Hierarchical Modulation and Network Coding Approach for Improving the System Performance in OFDM PON". W 2022 20th International Conference on Optical Communications and Networks (ICOCN). IEEE, 2022. http://dx.doi.org/10.1109/icocn55511.2022.9901311.

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Marra, James, Sergey Stefanovsky, Vladimir Lebedev i Dmitriy Suntsov. "The Results of Testing to Evaluate Crystal Formation and Settling in the Cold Crucible Induction Melter". W ASME 2009 12th International Conference on Environmental Remediation and Radioactive Waste Management. ASMEDC, 2009. http://dx.doi.org/10.1115/icem2009-16282.

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The Cold Crucible Induction Melter (CCIM) technology offers the potential to increase waste loading for High Level Waste (HLW) glasses leading to significant improvements in waste throughput rates compared to the reference Joule Heated Melter (JHM). Prior to implementation of a CCIM in a production facility it is necessary to better understand processing constraints associated with the CCIM. The glass liquidus temperature requirement and tolerance to crystal formation for processing in the CCIM is an open issue. Testing was conducted to evaluate crystal formation and crystal settling during processing in the CCIM to gain insight into the effects on processing. A high aluminum/high iron content glass composition with known crystal formation tendencies was selected for testing. A continuous melter test was conducted for approximately 51 hours. To evaluate crystal formation, glass samples were obtained from pours and from glass receipt canisters where the glass melt had varying residence time in the melter. Additionally, upon conclusion of the testing, glass samples from the bottom of the melter were obtained to assess the degree of crystal settling. Glass samples were characterized in an attempt to determine quantitative fractions of crystals in the glass matrix. Crystal identity and relative composition were determined using a combination of x-ray diffraction (XRD) and scanning electron microscopy coupled with energy dispersive spectroscopy (SEM/EDS). Select samples were also analyzed by digesting the glass and determining the composition using inductively coupled atomic emission spectroscopy (ICP-AES). There was evidence of crystal formation (primarily spinels) in the melt and during cooling of the collected glass. There was evidence of crystal settling in the melt over the duration of the melter campaign.
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Raporty organizacyjne na temat "JHMC"

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Gallagher, Hilary L., i Richard L. McKinley. Noise Attenuation Performance Assessment of the Joint Helmet Mounted Cueing System (JHMCS). Fort Belvoir, VA: Defense Technical Information Center, sierpień 2010. http://dx.doi.org/10.21236/ada582655.

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