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Biomedical subjects

R Traub

Publications and source records attributed to R Traub.

At least 19 recordsLinked to original sources
PubMed1998

Description of Songshupsylla, a new subgenus of Macrostylophora (Siphonaptera: Ceratophyllidae), with a discussion of its species groups.

The new subgenus Songshupsylla is erected to include certain species heretofore included in Macrostylophora s. lat. Ewing, 1929. The subgenus is further divided into 2 species groups according to their morphological characters and geographical distribution in the Paleartic and Oriental Regions. Brief descriptions of these species groups and the names of the Chinese taxa are given.

Animals↗
PubMed1996

Hypothesis: "Rogue cell"-type chromosomal damage in lymphocytes is associated with infection with the JC human polyoma virus and has implications for oncopenesis.

The hemagglutination inhibition antibody titers against the JC and BK polyoma viruses (JCV and BKV, respectively) are significantly elevated in individuals exhibiting "rogue" cells among their cultured lymphocytes. However, the elevation is so much greater with respect to JCV that the BKV elevation could readily be explained by cross reactivity to the capsid protein of these two closely related viruses. The JCV exhibits high sequence homology with the simian papovavirus, simian virus 40 (SV40), and inoculation of human fetal brain cells with JCV produces polyploidy and chromosomal damage very similar to that produced by SV40. We suggest, by analogy with the effects of SV40, that these changes are due to the action of the viral large tumor antigen, a pluripotent DNA binding protein that acts in both transcription and replication. The implications of these findings for oncogenesis are briefly discussed.

Adolescent↗
PubMed1996

Expression of multiple classes of the nuclear factor-1 family in the developing human brain: differential expression of two classes of NF-1 genes.

Nuclear factor-1 (NF-1) is a multifunctional protein that participates in both transcription and replication. NF-1 proteins exist as a family of proteins that share some common structural and functional features but also demonstrate organ and cell type specific expression. Based upon these characteristics, the family of NF-1 proteins is divided into four classes, A, B, C and D. Several NF-1 binding sites have been identified in the regulatory sequences of the human polyomavirus, JCV, which multiplies most efficiently in glial cells derived from human fetal brain. Nuclear proteins from these cultures bind specifically to these NF-1 sites. It is not known, however, which member(s) of the NF-1 family is expressed in cells susceptible to JCV infection. We have examined glial cells as well as HeLa cells, which are not permissive to JCV, for NF-1 expression. By RT-PCR analysis, all four classes of NF-1 are expressed in human fetal glial cells and HeLa cells. However, by Northern analysis the expression of class D gene is much higher in the glial cells than HeLa cells. Expression of the class C gene, first identified in HeLa cells as NF-1/CTF1, is barely detectable in glial cells but highly expressed in HeLa cells. The screening of cDNA libraries from two early human brain tissues resulted in the identification of a number of clones which appear to be related and belong to a single class of the NF-1 family, class D. Nucleotide sequence of one clone, designated NF-1/AT1, confirms this. The NF-1/AT1 protein was overexpressed in E coli and found to bind specifically to an NF-1 probe by gel shift analysis. Southern analysis of human fetal glial cells indicates that the NF-1/AT1 gene, class D, is derived from a different gene than NF-1/CTF1. These results suggest the possibility that genes or viruses, like JCV, which use NF-1 for their expression in human brain derived cells may preferentially use the NF-1 class D protein.

Amino Acid Sequence↗
PubMed1994

An increase in p50/p65 NF-kB binding to the HIV-1 LTR is not sufficient to increase viral expression in the primary human astrocyte.

Human astrocytes can be infected with HIV-1 both in vivo and in vitro. The amount of HIV-1 p24 structural protein production is low in comparison to that of the macrophage. Several weeks following infection or transfection, however, cocultivation with uninfected lymphocytes or stimulation with the cytokines TNF-alpha and IL 1-beta will increase viral production from this cell type. In the present study we demonstrate that phorbol 12-myristate 13-acetate (PMA) also increases HIV-1 p24 production from the primary human astrocyte. Using electrophoretic mobility shift assay (EMSA) in combination with supershift studies using specific antibodies, we demonstrate that PMA, like TNF-alpha, increases the p50/p65 form of NF-kB. Furthermore we demonstrate that the protein kinase inhibitor H7 inhibits PMA- and TNF-alpha-associated increases in HIV-1 expression at a time when it has little to no inhibitory effect on the associated increases in p50/p65 NF-kB. Thus, unless p50/p65 NF-kB or its binding is affected by H7 in a manner that cannot be resolved by EMSA, an increase in this form of NF-kB is not always sufficient to increase HIV-1 expression from the astrocyte.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1994

Stimulation of HIV type 1 gene expression and induction of NF-kappa B (p50/p65)-binding activity in tumor necrosis factor alpha-treated human fetal glial cells.

In vitro, HIV-1 infection of human fetal glial cells initiates a noncytopathic, productive infection that results in a long-term persistence during which the viral genome remains latent. The cytokines tumor necrosis factor alpha (TNF-alpha) and interleukin 1 beta (IL-1 beta) reactivate HIV-1 gene expression in these cells, leading to production of infectious virus. Here we show that treatment of human fetal glial cells with TNF-alpha and IL-1 beta increase expression of the reporter gene chloramphenicol acetyltransferase (CAT) when placed under the control of the HIV-1 5' LTR. We also show that treatment of human fetal glial cells with TNF-alpha leads to increased binding of the nuclear transcription factor NF-kappa B (p50/p65) to a consensus kappa B-binding site present in the HIV-1 5'LTR. Our results suggest that TNF-alpha stimulation of HIV-1 gene expression in primary cultures of human fetal glial cells is mediated by an increase in binding of NF-kappa B (p50/p65) to the HIV-1 LTR. This is the first report documenting NF-kappa B-binding activity in primary cultures of human fetal glial cells.

Base Sequence↗
PubMed1992

Adjacent nuclear factor-1 and activator protein binding sites in the enhancer of the neurotropic JC virus. A common characteristic of many brain-specific genes.

JC virus is a neurotropic virus that causes the demyelinating disease progressive multifocal leukoencephalopathy in humans. In order to understand the neurotropic nature of this virus, we examined the binding of nuclear proteins to the viral regulatory region. A close association of nuclear factor-1 (NF-1) and Jun protein binding sites was found. These binding sites were either adjacent or overlapped each other. Depending on the order of binding, there was some interference of binding of the NF-1 protein by Jun even at a non-Jun binding site. This suggests that there may be a direct interaction between these proteins. Examination of the regulatory region of a number of genes expressed in the central and peripheral nervous systems revealed that many of these genes apparently have adjacent NF-1 and activator protein binding sites immediately upstream from the mRNA start site. Since it had been demonstrated that nuclear proteins from brain and non-brain cells could interact with these sites, it is probable that the NF-1- and Jun-related proteins which interact at these sites are involved in the basal activity of these genes. It appears that adjacent binding sites for NF-1 and Jun immediately upstream from the mRNA start site may be a characteristic of many genes expressed in the nervous system.

Base Sequence↗
PubMed1992

Interaction of the human polyomavirus, JCV, with human B-lymphocytes.

The human polyomavirus, JCV, is the causative agent of the central nervous system demyelinating disease progressive multifocal leukoencephalopathy (PML). The principal target of JCV infection in the central nervous system (CNS) is the myelinating oligodendrocyte. However, the site of JCV multiplication outside of the CNS and the mechanism by which virus gains access to the brain are not known. Recently, JCV infected B-lymphocytes have been demonstrated in PML patients in several lymphoid organs, in circulating peripheral lymphocytes, and in brain, suggesting a possible role of B-lymphocytes in the dissemination of virus to the brain. The experiments reported here were undertaken to understand more about the interactions of JCV with human B-lymphocytes. The data show that JCV is able to multiply in either Epstein-Barr virus transformed (EBV) or EBV negative human B cell lines resulting in production of infectious, progeny virions. In addition, nuclear proteins extracted from these B cells bind to similar nucleotides within the JCV regulatory region that are bound by nuclear proteins extracted from human fetal glial cells, the most susceptible host and principal target cell for JCV infection in vitro. It is not known, however, whether these DNA binding proteins from susceptible B cells and glial cells are similar.

B-Lymphocytes↗
PubMed1992

[Comparative biological availability of two different ibuprofen granules].

Bioavailability of ibuprofen (CAS 15687-27-1) was investigated in 12 healthy volunteers who received 2 sachets of newly developed effervescent granules (Imbun), each containing 500 mg of ibuprofen lysine salt (corresponding to 292.6 mg of ibuprofen) as the test preparation and 1 sachet of commercially available granules containing 600 mg ibuprofen. Blood samples were withdrawn pre-dose and at 16 occasions until 10 h post dose. Ibuprofen plasma concentrations were assayed by HPLC using a proprietary column-switching technique. Maximum plasma concentrations, Cmax, and times of their occurrence, tmax, were taken from the plasma data directly, areas under the plasma level/time curves, AUC0-10, were calculated using the trapezoidal rule. Pharmacokinetic parameters were checked for significant differences using ANOVA with p = 0.05. When the test preparation was applied maximum ibuprofen levels of 60 +/- 17 micrograms/ml were reached at 27 +/- 17 min p. appl. while Cmax was 52 +/- 12 micrograms/ml at tmax = 94 +/- 27 min after application of the reference preparation. AUC values were 150 +/- 44 microgramsh/ml (test) and 148 +/- 33 microgramsh/ml (reference), respectively. Thus, relative bioavailability of ibuprofen was 101.8 +/- 16.3% (or 104.1 +/- 16.7% when the slight differences in doses were corrected for). Differences in extent of absorption as measured by AUC and Cmax proved to be insignificant whereas differences in absorption rate as measured by tmax were highly significant (p < 0.001).

Adult↗
PubMed1991

Dynorphin expression and Fos-like immunoreactivity following inflammation induced hyperalgesia are colocalized in spinal cord neurons.

Fos and Fos-related proteins are increased in spinal dorsal horn neurons following noxious stimulation. The laminar location of neurons that exhibit this increase is coincident with those that exhibit an increase in dynorphin in a rat model of peripheral inflammation and hyperalgesia. In order to determine whether the increase in Fos or related proteins and dynorphin occurs in the same dorsal horn neurons, two kinds of double-labeling methods were used: in situ hybridization histochemistry to label dynorphin mRNA autoradiographically, and immunocytochemistry to label Fos and Fos-related proteins, or a double immunocytochemical method that labeled Fos and Fos-related proteins and dynorphin peptide with distinct chromagens. With both methods more than 80% of the neurons in laminae I, II, V and VI exhibiting an increase in either dynorphin mRNA or peptide following peripheral inflammation also colocalized increased nuclear Fos-like immunoreactivity. However, the number of neurons displaying increased Fos-like immunoreactivity was substantially greater than the number of neurons colocalizing increased dynorphin. These data suggest that the activation of nuclear Fos and Fos-related proteins may be related to the induction of dynorphin gene expression in a subpopulation of spinal cord neurons following peripheral inflammation and hyperalgesia.

Animals↗
PubMed1989

Interaction of a nuclear factor-1-like protein with the regulatory region of the human polyomavirus JC virus.

We have initiated a study to identify host proteins which interact with the regulatory region of the human polyomavirus JC (JCV), which is associated with the demyelinating disease, progressive multifocal leukoencephalopathy. We examined the interaction of nuclear proteins prepared from different cell lines with the JCV regulatory region by DNA binding gel retardation assays. Binding was detected with nuclear extracts prepared from human fetal glial cells, glioma cells, and HeLa cells. Little or no binding was detected with nuclear extracts prepared from human embryonic kidney cells. Competitive binding assays suggest that the nuclear factor(s) which interacted with the JCV regulatory region was different from those which interacted with the regulatory region of the closely related polyomavirus SV40. We found three areas in the JCV regulatory region protected from DNase I digestion: site A, located just upstream from the TATA sequence in the first 98-base pair (bp) repeat; site B, located upstream from the TATA sequence in the second 98-bp repeat; and site C, located just following the second 98-bp repeat. There were some differences in the ability of the nuclear factor(s) from the two brain cell lines and HeLa cells to completely protect the nucleotides within the footprint region. The results from the DNase I protective studies and competitive DNA binding studies with specific oligonucleotides, suggest that nuclear factor-1 or a nuclear factor-1-like factor is interacting with all three sites in the JCV regulatory region. In addition, the results suggest that the nuclear factor which interacts with the JCV regulatory region from human brain cell lines is different from the factor found in HeLa cells.

Base Sequence↗
PubMed1989

Extension of JC virus host range to monkey cells by insertion of a simian virus 40 enhancer into the JC virus regulatory region.

A chimeric polyomavirus genome was constructed by inserting the 72- and the 21-bp repeats of simian virus 40 (SV40) into the JC virus (JCV) regulatory region on the late side of the JCV 98-bp repeats. Although the chimeric polyomavirus DNA was able to replicate very well in human fetal glial cells, deletions were found in sequences of the regulatory region. DNA sequence analysis of a selected clone indicated a 294-bp deletion from the original construction that retained the sequences for the JCV replication origin, 78 bp of one 98-bp repeat, 33 bp of one SV40 72-bp repeat, and one intact 72-bp repeat. Of significant interest was that this genome demonstrated an extended species and cell-type host range, producing infectious virus in human fetal brain and embryonic kidney as well as in rhesus monkey fetal and adult glial cells. However, the species host range was not extended beyond primate cells since the chimeric polyomavirus was unable to multiply in rodent glial cells. Analysis of the viral RNA transcripts from either kidney or glial cells indicated that the major start sites for early RNA mapped within the JCV sequences of the regulatory region and major start sites for late RNA mapped within the JCV and SV40 sequences. This extension of the JC virus host range was most likely attributable to changes in the regulatory region and not the viral T protein since a recombinant DNA clone which placed the coding sequences for the wild-type JCV T protein subject to regulation by the deleted chimeric regulatory region showed a similar extension of host range.

Animals↗
PubMed1989

Experimental transmission of murine typhus by Xenopsylla cheopis flea bites.

Transmission of Rickettsia typhi to rats by the bites of Xenopsylla cheopis (Rothschild) fleas was investigated. Procedures rigorously excluded the possibility of contamination of the host skin by flea faeces. Fleas with R. typhi infection (21-25 days post-infection) which fed through bolting cloth (45 min exposure to ten fleas) transmitted rickettsiae with a success rate of 20%. Infective fleas allowed free access to their host for 8 h (10-15 fleas/rat) gave transmission rates of 45-68%. They were also capable of inoculating R. typhi through a membrane of rat skin on a feeder. Only fleas which had been infected for 21 days or longer transmitted R. typhi orally. Oral transmission appeared to be the result of regurgitation of rickettsiae present in the foregut lumen rather than through salivary secretions.

Animals↗
PubMed1987

Antiviral antibodies in the sera of homosexual men: correlation with their lifestyle and drug usage.

Healthy homosexual men between the ages of 21 and 65 years, from the Washington, DC (n = 162), and New York City (n = 89) areas, were studied for antibodies in the serum against cytomegalovirus (CMV), herpes simplex virus (HSV) types 1 and 2, and Epstein Barr virus (EBV) viral capsid antigen (VCA). CMV-specific antibodies were assayed by enzyme-linked immunosorbent assay (ELISA), anti-HSV-1 and -2 antibodies were measured by indirect hemagglutination (IHA), and antibodies to EBV VCA were measured by the immunofluorescence assay. Antibodies to human T lymphotrophic virus III (HTLV-III) were detected by ELISA and Western blot procedures. T lymphocytes were enumerated using OKT4 monoclonal antibody. Healthy male volunteer blood donors (n = 90) matched for age range and race proportions were used as controls. The percentage of seropositive individuals in the homosexual group was higher (90-98%) for all the viruses tested than in the control group (47-87%). Comparisons of the geometric mean titers, expressed as reciprocal serum dilutions, of seropositive individuals in homosexual (H) vs control (C) group were as follows: CMV-IgG (ELISA) H = 1:794, C = 1:68; HSV-1 (IHA) H = 1:248, C = 1:14; HSV-2 (IHA) H = 1:56, C = 1:17; EBV-VCA (IFA) H = 1:385, C = 1:131. The homosexual group also showed a higher frequency of individuals with elevated titers than the control group. The CMV IgM antibody was prevalent in 17.7% of the homosexual group and 5% of the control group; arithmetic means for ELISA values for CMV IgM were 0.207 for the homosexual group and 0.05 for the control group. In the homosexual group, the anti-CMV antibody titers increased with age (P = 0.01) and with numbers of sex partners (P = 0.06). Both anti-HSV-1 and anti-HSV-2 antibodies correlated with the number of sex partners (P = 0.04 and P = 0.05, respectively). Neither age nor partner number correlated with response to EBV, and no particular sex act was related to the EBV VCA titer level. HTLV-III seropositivity was associated with higher herpes virus group antibody titers, probably because of life style cofactors. Among the HTLV-III-seropositive subjects, those with less than or equal to 400 T-helper lymphocytes/mm3 had lower antibody titers than those with greater than 400 T-helper lymphocytes/mm3 counts, suggesting an impaired immune response secondary to immunosuppression.

Adult↗
PubMed1985

Transovarial transmission of murine typhus rickettsiae in Xenopsylla cheopis fleas.

It has been generally accepted that infected fleas do not pass on Rickettsia mooseri, or indeed any other known pathogen, to their progeny. It is reported here that such transovarial transmission does occur in laboratory-infected Xenopsylla cheopis fleas. By means of the direct fluorescent antibody test, Rickettsia mooseri was observed in cells of the hemolymph of infected fleas. As many as 11 percent of the adults and 2.9 percent of the larvae of the generation reared therefrom, had demonstrable rickettsiae. Moreover, batches of the F1 fleas were capable of transmitting the infection to more than 18 percent of the rats they infested. The data support the contention that Xenopsylla cheopis fleas play an important role in the maintenance of murine typhus in rats in nature.

Animals↗
PubMed1985

Transmission of murine typhus rickettsiae by Xenopsylla cheopis, with notes on experimental infection and effects of temperature.

In studies on experimental infection of Rickettsia mooseri (= R. typhi) in Xenopsylla cheopis and laboratory rats, it was found that 10 days after the infectious feeding, the fleas were voiding feces that were infective to rats upon inoculation. The feces remained infective for at least the duration of the experiment, and a quantity as small as 0.2 micrograms of feces would result in seroconversion of 67% of the rats upon inoculation. Fleas were capable of transmitting the infection to rats as early as seven days after feeding on rickettsemic rats, but the rate of transmission was much higher late in the course of rickettsial development in the flea, e.g., virtually 100% by day 17. Fleas transmitted R. mooseri infection even when they fed on the host for a maximum of 30 min and were removed from the rats at least 25 min before they could be expected to deposit any feces. These and other data suggest that R. mooseri may be transmitted by X. cheopis by the feeding process, and not merely through contact with infective feces or crushed fleas. The ambient temperature had a profound effect upon rickettsial growth in the fleas. At 18 degrees C, the rickettsial content of the fleas was below detectable levels for at least ten days and remained low throughout, whereas at 24 degrees C and 30 degrees C the rickettsial titer was consistently two or three times greater. However, if, after six days, the fleas were transferred from an environment of 18 degrees C to one at 24 degrees C or 30 degrees C, the rickettsial growth increased by two or three logs within one week.

Animals↗