Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound

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Query: EC:2.7.10.1 (ERK)
95,504 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Infection with Schistosoma mansoni induces humoral and T cell mediated responses and leads to a delayed hypersensitivity that results in granulomatous inflammatory disease around the parasite eggs. Regulation of these responses resulting in a reduction in this anti-egg inflammatory disease is apparently determined by idiotypic repertoires of the patient, associated with genetic background and multiple external factors. We have previously reported on idiotype/anti-idiotype-receptor interactions in clinical human schistosomiasis. These findings support a hypothesis that anti-SEA cross-reactive idiotypes develop in some patients during the course of a chronic infection and participate in regulation of anti-SEA cellular immune responses. We report here on experiments which extend those observations to the regulation of granulomatous hypersensitivity measured by an in vitro granuloma model. T cells from chronic intestinal schistosomiasis patients were stimulated in vitro with anti-SEA idiotypes and assayed in an autologous in vitro granuloma assay for modulation of granuloma formation. These anti-SEA idiotype reactive T cells were capable of regulating autologous in vitro granuloma formation. Both CD4 and CD8 T cells could be activated to regulate granuloma formation. This regulatory activity, initiated with stimulatory anti-SEA idiotypic antibodies, was antigenically specific and was dependent on the presence of intact (F(ab')2) immunoglobulin molecules. The ability to elicit this regulatory activity appears to be dose dependent and is more easily demonstrated in chronically infected intestinal patients or SEA sensitized individuals.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Human schistosomiasis mansoni: studies on in vitro granuloma modulation. 134 21

Maternal lung edema due to the use of beta-mimetic tocolytic agents is a well-documented complication. The risk increases if several other factors are present: infectious diseases, the use of inhaled anesthetics, EPH gestosis, hydramnios, twin gestation and preexisting cardiovascular disease. The complications induced by beta-mimetic tocolytic agents can be reduced by remembering their side effects and contraindications and restricting fluid intake. During obstetric general anesthesia in patients undergoing tocolysis, the infusion of large amounts of saline, as is widely practised today, is strictly contraindicated.
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PMID:[Maternal pulmonary edema as an anesthesia complication after intravenous tocolysis and stimulating of lung maturation]. 135 38

Beachey, Edwin H. (National Institute of Allergy and Infectious Diseases, Bethesda, Md.), and Roger M. Cole. Cell wall replication in Escherichia coli, studied by immunofluorescence and immunoelectron microscopy. J. Bacteriol. 92:1245-1251. 1966.-Cell wall components of four different strains of Escherichia coli (B; B/r, try(-); O5; and O86:B7) were labeled with homologous fluorescent antibodies (FLG); the way the label was dispersed on further growth in media free of antibody was followed by fluorescence microscopy. Fluorescence diminished diffusely along longitudinal wall but remained bright at cell poles (or cross walls); newly formed cross walls did not fluoresce. In agreement, reverse labeling (preincubation in unlabeled antibody, followed by staining on the slide with homologous FLG) showed that stainability of longitudinal wall increased gradually and diffusely with increased time of incubation, whereas polar wall remained nonfluorescent or stained only faintly; newly formed poles (or cross walls), on the other hand, stained brightly. These observations were confirmed by electron microscopy, after immunoferritin labeling. Although the mode of cross-wall formation remained unclear, our findings refuted reported ideas of segmental or polar growth of cell wall in E. coli and supported the idea of wall replication by diffuse intercalation, as described for Salmonella.
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PMID:Cell wall replication in Escherichia coli, studies by immunofluorescence and immunoelectron microscopy. 533 68

Each of several strains of fixed rabies virus was found to replicate to high titers in C1300 mouse neuroblastoma (clone NA) cells, without adaptation. Rabies serogroup Lagos bat, Mokola, and Duvenhage viruses also replicated efficiently in NA cells. Kotonkan and Obodhiang viruses replicated efficiently after adaptation, to titers not previously obtained in vitro. Infection in NA cells was frequently more cytopathic than in BHK-21 cells, allowing titration of Kotonkan and Obodhiang viruses by plaque assay. Duvenhage virus caused syncytium formation. Serial propagation of rabies viruses at a high multiplicity of infection in NA cells led to a rapid decline in virus yields; similar "autointerference" has not previously been demonstrated with rabies virus in other cell systems. Rabies virus infection in NA cells exhibited extreme sensitivity to interference by experimentally added defective interfering virions. Although several strains of attenuated rabies virus consistently reverted rapidly to virulence after propagation in NA cells, other strains of attenuated rabies and rabies serogroup viruses acquired increased virulence at a more gradual rate or not at all, suggesting that diverse characters may control virulence. When attenuated Flury HEP rabies virus was serially propagated at a low multiplicity of infection in either NA cells or suckling mouse brain, virulence appeared at a very variable rate, indicating that these systems may selectively enhance replication of randomly occurring virulent virus mutants.
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PMID:Rabies serogroup viruses in neuroblastoma cells: propagation, "autointerference," and apparently random back-mutation of attenuated viruses to the virulent state. 738 May 49

A highly effective single-cell PCR method using a fluorescence-activated cell sorting (FACS)-based automated cell deposition unit (ACDU) that sorts single cells directly into PCR tubes was developed. To evaluate the sensitivity of this method, single ACH-2 cells (containing one HIV-1 genome per cell) were sorted, and 220 out of 228 samples (96.5%) were HIV DNA-positive by PCR. Furthermore, the number of samples accidentally containing more than one cell was determined by sorting single cells from a mixture of human cytomegalovirus (HCMV)-infected fibroblasts and ACH-2 cells. Multiplex nested PCR (nPCR) was then performed, detecting HCMV and HIV DNA simultaneously. From 66 sorted cells, 2 (3%) were double-positive for HIV and HCMV, 31 (47%) for HCMV alone, 30 (45.5%) for HIV alone and 3 (4.5%) were PCR-negative. The ACDU was then programmed to sort defined numbers of cells into PCR tubes. This is similar to classic dilution assays in that it allows the determination of the percentage of cells that was positive for a specific DNA. The accuracy of multiple cell deposition by the ACDU was evaluated by determining the percentage of HIV-positive cells in defined mixtures of ACH-2 and uninfected H9 cells. Infection rates determined by the ACDU correlated well with the rates expected from the given dilutions.
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PMID:Detection of DNA in single cells using an automated cell deposition unit and PCR. 877 56

We transfected human and rabbit peripheral blood mononuclear cells (PBMC) with the ACH molecular clone of human T-cell lymphotropic virus type 1 (HTLV-1) to study its in vitro and in vivo properties. PBMC transfected with ACH were shown to transfer infection to naive PBMC. ACH transformed rabbit PBMC, as indicated by interleukin-2-independent proliferation of a transfectant culture. This transformant culture was shown by flow cytometric analysis to be a CD4+ CD25+ T-lymphocyte population containing, as determined by Southern blot analysis, at least three integrated HTLV-1 proviral copies. HTLV-1 infection was produced in rabbits inoculated with ACH-transfected, irradiated PBMC. Inoculated rabbits seroconverted to positivity for antibodies against HTLV-1 and had steady or rising HTLV-1 enzyme-linked immunosorbent assay antibody titers. Western blot (immunoblot) analysis revealed sustained seroconversion of rabbits to positivity for antibodies against all major viral antigenic determinants. Infection of rabbits was further demonstrated by antigen capture assay of p24 in PBMC and lymph node cultures and PCR amplification of proviral sequences from PBMC. These data suggest that ACH, like wild-type HTLV-1, infects and transforms primary CD4+ T lymphocytes and is infectious in vivo. This clone will facilitate investigations into the role of viral genes on biological properties of HTLV-1 in vitro and in vivo.
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PMID:In vitro CD4+ lymphocyte transformation and infection in a rabbit model with a molecular clone of human T-cell lymphotrophic virus type 1. 879 75

The recent resurgence of TB together with the ongoing HIV epidemic has resulted in a larger number of infectious TB patients being admitted to US health care facilities. These patients have become a source for both nosocomial (patient-to-patient) and occupational (patient-to-health care worker) M. tuberculosis transmission. Infectious MDR-TB patients serve as even greater potential infectious sources because they often remain AFB smear and culture positive for months to years. The keys to the prevention of nosocomial and occupational transmission of M. tuberculosis is conducting a risk assessment for each area of the facility and instituting appropriate control measures, having a high index of suspicion by clinicians for infectious TB in those who present with consistent signs and symptoms, rapid triage of such patients to isolation areas and their appropriate clinical work-up, and the institution of effective antituberculous therapy. Infection control personnel should ensure that infectious TB patients are isolated in appropriate isolation rooms (i.e., negative pressure, greater than or equal to 6 ACH, and direct external exhaust of the room air). Health care workers with infectious TB patient contact should be instructed in the epidemiology of M. tuberculosis transmission, the role of respirators in protecting the health care worker from airborne inoculation, and the importance of periodic health care worker TST. The nosocomial TB outbreaks in the 1980s and 1990s document that M. tuberculosis can be transmitted to both patients and health care workers in US health care facilities when appropriate infection control measures are not fully implemented. Follow-up studies at some of these institutions, however, document that when infection control measures similar to the 1990 or 1994 CDC TB Guidelines are fully implemented, M. tuberculosis transmission to both patients and health care workers can be reduced or eliminated. Protection of both patients and health care workers from M. tuberculosis infection is dependent on an understanding and full implementation of the 1994 CDC TB Guidelines.
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PMID:Prevention of nosocomial transmission of Mycobacterium tuberculosis. 918 53

A better understanding of immune recognition of cells has led to identification of potential new targets on tumor cells. Noticeable successes in melanoma have been immunization with the GM2 ganglioside vaccine, and the identification of novel antigens such as MAGE, BAGE and GAGE recognized by T cells cloned from cancer patients with regressing disease. However, the unexpected finding that other antigens recognized by these T cells were overexpressed normal differentiation antigens such as tyrosinase. Pmel 17 and Melan A have led to vaccines developed against differentiation antigens expressed in other solid tumors. Monoclonal antibody, anti-idiotype and antigen based vaccines for colorectal target antigens 17-1A, CEA and 791Tgp72 are all in clinical development. Similarly HER2/neu and mucin overexpression in breast cancer represent promising targets. Mutations in tumor oncogenes or suppressor genes which lead to malignant transformation can also present tumor-specific antigens. The most effective vaccines against infectious disease are live viruses. The development of DNA vaccines which act like viruses in entering cells and show continuous production of antigens offers great potential for the future.
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PMID:Cancer vaccines. 939 16

Infection of a cell by human immunodeficiency virus type 1 (HIV-1) results in the formation of a reverse transcription complex in which viral nucleic acids are synthesized. Efficient disengagement of the reverse transcription complex from the cell membrane and subsequent nuclear translocation require phosphorylation of reverse transcription complex components by a virion-associated kinase. In this study, we identify the virion-associated kinase as mitogen-activated protein kinase (ERK/MAPK). Upon density gradient fractionation, MAPK, but not its activating kinase MEK, co-sedimented with viral particles. Expression of a constitutively active, but not kinase-inactive, MEK1 in virus producer cells was able to activate virion-associated MAPK in trans. Stimulation of virion-associated MAPK activity in trans by the mitogen phorbol myristate acetate (PMA) increased viral infectivity. Conversely, suppression of virion-associated MAPK by specific inhibitors of the MAPK cascade markedly impaired viral infectivity. These studies demonstrate regulation of an early step in HIV-1 infection by the host cell MAPK signal transduction pathway.
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PMID:Modulation of HIV-1 infectivity by MAPK, a virion-associated kinase. 956 43

Acute infectious disease presentations among many at-risk patient groups (eg, uninsured, homeless, and recent immigrants) are frequently seen in emergency departments. Therefore EDs may be useful sentinel sites for infectious disease surveillance. This article describes the background, development, and implementation of EMERGE ncy ID NET, an interdisciplinary, multicenter, ED-based network for research of emerging infectious diseases. EMERGE ncy ID NET was established in cooperation with the National Center for Infectious Diseases, Centers for Disease Control and Prevention (CDC) as part of the CDC's strategy to expand and complement existing disease detection and control activities. The network is based at 11 university-affiliated, urban hospital EDs with a combined annual patient visit census of more than 900,000. Data are collected during ED evaluation of patients with specific clinical syndromes, and are electronically stored, transferred, and analyzed at a central receiving site. Current projects include investigation of bloody diarrhea and the prevalence of Shiga toxin-producing Escherichia coli, animal exposures and rabies postexposure prophylaxis practices, seizures and prevalence of neurocysticercosis, nosocomial ED Mycobacterium tuberculosis transmission, and hospital isolation bed use for adults admitted for pneumonia or suspected tuberculosis. EMERGE ncy ID NET also was developed to be a mechanism for rapidly responding to new diseases or epidemics. Future plans include study of antimicrobial use, meningitis, and encephalitis, and consideration of other public health concerns such as injury and national and international network expansion.
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PMID:EMERGEncy ID NET: an emergency department-based emerging infections sentinel network. The EMERGEncy ID NET Study Group. 983 68


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