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Biomedical subjects

B K Pal

Publications and source records attributed to B K Pal.

At least 19 recordsLinked to original sources
PubMed2006

Lymphatic filariasis: possible pathophysiological nexus with oxidative stress.

Wuchereria bancrofti-mediated lymphatic filariasis is widely prevalent. Diversity in immune response presumably may lead to myriad clinical presentations, such as overt chronic filariasis, occult filariasis with atypical systemic manifestation and asymptomatic microfilariae carrier state. Anticipated oxidative stress during inflammatory response to infective conditions might complicate the immune response and thus might alter the disease outcome. The present study was carried out to assess the status of oxidative stress in different clinical presentations of bancroftian filariasis. Twenty-five microfilariae carriers and 30 cases each of chronic filariasis and occult filariasis were compared to 30 endemic normal individuals. Serum malondialdehyde level and superoxide dismutase enzyme activity were measured by spectrophotometric methods and levels of filarial antigen were measured by ELISA. In the filarial cases, the levels of these parameters were assayed again after treatment with diethylcarbamazine citrate (DEC). Results showed significant (P<0.05) association of oxidative stress with chronic and occult filariasis but not with microfilarial carriers. DEC therapy in both clinical cases and carriers resulted in a significant reduction of oxidative stress associated with decreased antigen level (P<0.01). These findings suggest the possible involvement of oxidative stress in filarial disease pathology.

Adult↗
PubMed1998

Monitoring retroviral RNA dimerization in vivo via hammerhead ribozyme cleavage.

We have used a strategy for colocalization of Psi (Psi)-tethered ribozymes and targets to demonstrate that Psi sequences are capable of specific interaction in the cytoplasm of both packaging and nonpackaging cells. These results indicate that current in vitro dimerization models may have in vivo counterparts. The methodology used may be applied to further genetic analyses on Psi domain interactions in vivo.

3T3 Cells↗
PubMed1991

The effect of temperature and oligonucleotide primer length on the specificity and efficiency of amplification by the polymerase chain reaction.

The polymerase chain reaction (PCR) is most effectively performed using a thermostable DNA polymerase such as that isolated from Thermus aquaticus. Since temperature and oligonucleotide length are known to control the specificity of oligonucleotide hybridization, we have investigated the effect of oligonucleotide length, base composition, and the annealing temperature on the specificity and efficiency of amplification by the PCR. Generally, the specificity of PCR is controlled by the length of the oligonucleotide and/or the temperature of annealing of the primer to the template. An empirical relationship between oligonucleotide length and ability to support amplification was determined. This relationship allows for the design of specific oligonucleotide primers. A model is proposed which helps explain the observed dependence of PCR on annealing temperature and length of the primer.

Base Sequence↗
PubMed1989

Allele-specific enzymatic amplification of beta-globin genomic DNA for diagnosis of sickle cell anemia.

A rapid nonradioactive approach to the diagnosis of sickle cell anemia is described based on an allele-specific polymerase chain reaction (ASPCR). This method allows direct detection of the normal or the sickle cell beta-globin allele in genomic DNA without additional steps of probe hybridization, ligation, or restriction enzyme cleavage. Two allele-specific oligonucleotide primers, one specific for the sickle cell allele and one specific for the normal allele, together with another primer complementary to both alleles were used in the polymerase chain reaction with genomic DNA templates. The allele-specific primers differed from each other in their terminal 3' nucleotide. Under the proper annealing temperature and polymerase chain reaction conditions, these primers only directed amplification on their complementary allele. In a single blind study of DNA samples from 12 individuals, this method correctly and unambiguously allowed for the determination of the genotypes with no false negatives or positives. If ASPCR is able to discriminate all allelic variation (both transition and transversion mutations), this method has the potential to be a powerful approach for genetic disease diagnosis, carrier screening, HLA typing, human gene mapping, forensics, and paternity testing.

Alleles↗
PubMed1983

Wild mouse retrovirus-induced neurogenic paralysis in laboratory mice. I. Virus replication and expression in central nervous system.

Ecotropic wild mouse retrovirus (1504 M)-induced neurogenic paralytic disease has been studied in inbred strains of mice. The major criterion for the successful transmission of the disease in the laboratory strains of mice is inoculation of high titer ecotropic virus in FV-1n strains of mice at newborn stage (less than or equal to 1 day old), Hybridization studies using 1504 M viral cDNA as probe indicate that in nonparalyzed mice, the inoculated virus replicates primarily in spleen tissue, whereas virus replication is evident in both spleen and central nervous system (CNS) tissue of paralyzed mice. Our studies on virus gene expression indicate that both viral gag gene product p30 and env gene product gp70 are expressed in brain, spinal cord and spleen tissues of paralyzed mice. Together, these results indicate that inoculation of neurotropic wild mouse virus into FV-1n strains of newborn laboratory mice is necessary for the establishment of infection in CNS tissue leading to virus replication and expression and resulting in the paralytic disease.

Animals↗
PubMed1983

Mink type C virus: biochemical characterization of the structural polypeptides.

Mink type C virions contained six major protein species of approximate M.W. of 90,000, 70,000, 30,000, 15,000, 12,000 and 10,000. The two largest polypeptides were glycosylated and the 12,000 M.W. polypeptide was the major phosphoprotein of the virion. Two-dimensional tryptic peptide map of the 30,000 M.W. major structural protein of MiLV showed a pattern distinct from those of analogous proteins from mouse and endogenous cat type C viruses. Significant peptide homology of this protein was, however, found with the corresponding protein of infectious feline type C virus (FeLV).

Animals↗
PubMed1982

Characterization of a highly oncogenic murine leukemia virus from wild mice.

We have isolated a highly lymphomagenic wild mouse virus by passage of a weakly oncogenic amphotropic murine leukaemia virus (MuLV-A) in NIH Swiss mice. This virus is similar in host range, interference and neutralization properties to that of the inoculated amphotropic virus but is distinct from it biochemically and causes lymphomas in 90-100% of mice within 1-2 months. Our results indicate that this highly oncogenic virus is a recombinant of wild mouse MuLV-A and sequences related to env gene region of the endogenous xenotropic virus of NIH Swiss mice.

Animals↗
PubMed1982

Binding characteristics of wild mouse type C virus to mouse spinal cord and spleen cells.

Binding characteristics of mouse spinal cord and spleen cells to naturally occurring, ecotropic (paralytogenic and lymphomagenic 1504M virus) and amphotropic (lymphomagenic 1504A virus) retroviruses of wild mice were investigated. 125I-labeled ecotropic (N-tropic) virus bound efficiently to both spinal cord and spleen cells from SWR/J mice (Fv-1n), but labeled amphotropic (N-tropic) virus bound efficiently only to spleen cells. The extent of binding of 1504M virus to the spinal cord cells was related to the time of incubation and to the amount of labeled input virus. 1504M virus bound to both glial and neuronal subpopulations of the spinal cord with almost equal efficiency. Binding of 125I-labeled 1504M virus to SWR/J mouse spinal cord cells was competitively inhibited by unlabeled homologous virus, whereas an excess of unlabeled 1504A virus inhibited only 10% of the ecotropic virus binding. Unlabeled 1504M virus almost completely inhibited the low-level binding of 125I-labeled 1504A virus to spinal cord cells. The different extent of binding of 1504M virus to spinal cord cells from different strains of mice (SWR/J, NIH Swiss, BALB/c-Jax, Lake Casitas wild, and CD-1) correlated with the susceptibility to paralysis in these strains of mice after inoculation with 1504M virus. Although the spinal cord cells of BALB/c mice contained a moderate amount of 1504M virus receptor sites, these mice were resistant to virus-induced paralysis because of their Fv-1b genotype. Our results indicate that the receptor sites for wild mouse ecotropic retrovirus are strain and organ specific and suggest that the presence of such receptors in central nervous system tissue may be a prerequisite for a successful virus infection and paralysis induction in Fv-1n mice.

Animals↗
PubMed1982

Characterization of genome structure of amphotropic and ecotropic wild mouse retroviruses.

We studied the RNA genomes of several wild mouse type C retroviruses by using RNase T1-oligonucleotide fingerprinting. The amphotropic and ecotropic viruses of field strain 1504 produced very similar oligonucleotide fingerprints, but each also had several unique oligonucleotides. All of these unique oligonucleotides were located in the env gene region and were probably responsible for the host range differences between these viruses, as well as the lymphomagenic and paralytogenic properties of the viruses. We obtained similar results with the amphotropic and ecotropic viruses of another field strain (4070), which was isolated from a mouse from a different trapping area. The amphotropic viruses of several field strains (strains 1504, 4070, and 1313) were more closely related than the ecotropic viruses of different strains (strains 1504, 4070, and 4996). These findings suggested that the genetic sequences of the amphotropic viruses are more conserved than those of ecotropic viruses isolated from the same wild mice.

Animals↗
PubMed1981

Natural killer cell activity in a population of leukemia-prone wild mice (Mus musculus).

Natural cell-mediated cytotoxicity against YAC-I targets was measured in splenocytes from leukemia-prone wild mice trapped near Lake Casitas (LC) in southern California. Cytotoxicity was mediated by cells that were non-adherent to nylon wool, non-phagocytic and resistant to thy-1.2 antiserum plus complement. Natural MuLV viremia in LC mice did not impair splenic cytotoxicity against TAC-I target cells, Cells infected with amphotropic and ecotropic MuLV of wild mouse origin were not appreciably lysed by LC splenic effectors. Although variable levels of cytotoxicity were detected against TAC-1 by normal spleen cells, consistently low levels of cytotoxicity against allogenic LC lymphoma, sarcoma and carcinoma targets were found using the same splenocytes. These results indicate that LC mice possess splenocytes with the characteristics of natural killer (NK) cells as defined in inbred mice. The resistance of LC-derived targets to lysis by LC NK cells suggests that NK cells may not be involved in natural tumor immunosurveillance or that the development of spontaneous tumors may involve escape from NK-mediated effector mechanisms.

Animals↗
PubMed1981

Immunopathology of natural and experimental lymphomas induced by wild mouse leukemia virus.

Naturally occurring lymphomas of Lake Casitas (LC) wild mice, and the lymphomas induced by LC murine leukemia virus (MuLV) in Swiss mice from the National Institutes of Health, displayed remarkably similar gross, microscopic, and functional characteristics. They spared the thymus, arose primarily in the splenic red pulp, became leukemic, and were comprised of stem cells lacking classic T- and B-cell markers. Cytoplasmic and surface immunoglobulin were undetectable in 34 of 35 spontaneous LC lymphomas and in any of ten LC MuLV-induced lymphomas in NIH Swiss mice. Assays for immunoglobulin secretion, complement (C'3) and Fc receptors, Thy 1.1,2 antigens, Ly 1,2 antigens, and erythroid and myeloid markers were negative on all of the spontaneous and experimental lymphomas. Cell lines were derived from five spontaneous lymphomas of LC mice. Three lines were characterized as null cells, one line as B cells, and one line as macrophages. All cell lines were diploid. The wild mouse spontaneous lymphomas, and lymphomas experimentally induced by LC MuLV in laboratory mice, provide a useful model for childhood acute lymphoblastic leukemia and for study of the early steps of B-lymphocyte differentiation.

Animals↗
PubMed1980

Akvr-1, a dominant murine leukemia virus restriction gene, is polymorphic in leukemia-prone wild mice.

We describe a restriction gene (Akvr-1, for AKR virus restriction) that is polymorphic for two alleles, Akvr-1R (restrictive) and Akvr-1r (susceptible), in a feral population of mice (Mus) musculus domesticus) at a squab farm near Lake Casitas (LC) in southern California. Akvr-1k is a dominant allele that exhibits 100% penetrance in prevention of viremia of AKR endogenous retrovirus and of virus-mediated lymphoma in LC (Akvr-1RR) X AKR F1 hybrids. The restriction phenotype segregates as a single Mendelian locus in backcrosses to AKR mice. Akvr-1R likewise is effective in restriction of NB-tropic Moloney murine leukemia virus-induced viremia and NB-tropic Friend virus-induced splenomegaly but fails to restrict expression or pathogenesis of LC-derived amphotropic retrovirus. Pleiotropic restriction of AKR, Friend, and Moloney ecotropic viruses, but not of amphotropic virus, suggests that the viral targets of Akvr-1 in the three ecotropic viruses are similar to each other and distinct from the target in the LC-amphotropic virus. The relationship of Akvr-1 to previously reported murine restriction loci Fv-1, Fv-2, and Fv-4 is discussed.

AKR murine leukemia virus↗
PubMed1978

RNA tumor virus phosphoproteins: primary structural analysis and identification of phosphopeptides.

Two-dimensional tryptic peptide mapping was used to compare the peptide sequences of the phosphoprotein (pp12) of cloned ecotropic and amphotropic wild mouse leukemia viruses, strains 1504 and 292. The maps of two ecotropic isolates were very similar to one another, as were the maps of two amphotropic isolates. There was also extensive similarity between the maps of this protein from ecotropic and amphotropic viruses, although characteristic peptide differences were readily recognized. These differences were consistent with the general type specificity of oncovirus phosphoproteins. The pp12 of the field isoalte of 292 virus contained five phosphopeptides, and the non-phosphorylated and variously phosphorylated species of this pp12 showed identical peptide maps, indicating differential phosphorylation of a single polypeptide.

Base Sequence↗