Biomedical subjects

N D Barkar

Publications and source records attributed to N D Barkar.

6 recordsLinked to original sources

PubMed2002

Pathways that control cortical F-actin dynamics during secretion.

Chromaffin cells possess a mesh of filamentous actin underneath the plasma membrane which acts as a barrier to the chromaffin vesicles access to exocytotic sites. Disassembly of cortical F-actin in response to stimulation allows the movement of vesicles from the reserve pool to the release-ready vesicle pool and, therefore, to exocytotic sites. The dynamics of cortical F-actin is controlled by two mechanisms: a) stimulation-induced Ca2+ entry and scinderin activation and b) protein kinase C (PKC) activation and MARCKS phosphorylation as demonstrated here by experiments with recombinant proteins, antisense olygodeoxynucleotides and vector mediated transient expressions. Under physiological conditions (i.e., cholinergic receptor stimulation followed by Ca2+ entry), mechanism (a) is the most important for the control of cortical F-actin network whereas when Ca2+ is released from intracellular stores (i.e., histamine stimulation) cortical F-actin is regulated mainly by mechanism b.

Actins↗

PubMed1991

[Identification of a protective epitope--a fragment of Lassa virus nucleoprotein].

Several peptides from Lassa virus glyco- and nucleoproteins were predicted as probable T-cell epitopes. Their synthesis was performed by solid phase method. The study of possible protective effect in vivo with Lassa-sensitive CBA mice revealed protective epitope within the 277-303 nucleoprotein region. Further studies reduced the protective epitope structure to the 287-300 nucleoprotein fragment.

Amino Acid Sequence↗

PubMedDate not supplied

[Relationship between bound and free amino acids in the brain of growing rats].

Total pool of glutamate, glutamine and GABA in the hemispheres increases during postnatal life of rats, the increase being due to that in free and bound forms of amino acids. In the cerebellum of 1-day rats, the content of free and bound glu, gln asp, GABA, bound ala and free gly is lower, whereas the level of free glu and ala, bound gly is higher than in mature animals. To the end of the 1st week, total amino acid content decreases, except GABA, which is increased. Aminon acid content begins to increase at the 21th and 28th days of postnatal life.

Aging↗

PubMedDate not supplied

[Lassa and Mozambique viruses: cross protection in experiments on mice and action of immunosuppressants on experimental infections].

The pathogenicity of Mozambique virus for random-bred mice and CBA mice was studied. In contrast to Lassa virus, intracerebral inoculation of newborn zandom-bred mice with Mozambique virus (1000 PFU/mouse) results in death of the animals. The pathogenic properties of both viruses for adult CBA mice were found to be similar: intracerebral inoculation of the viruses caused death of the animals within 6-8 days, but not intraperitoneal inoculation. With the latter, they produced a population of immunocompetent cells protecting syngeneic recipient mice against the lethal intracerebral inoculation of the homologous virus. Cross-protection experiments demonstrated that intraperitoneal inoculation of Lassa virus protected 70% of mice against the lethal infection with Mozambique virus, and intraperitoneal inoculation of Mozambique virus protected 45% of mice against Lassa virus. Cyclophosphamide exerted no protective effect in Mozambique virus-infected mice. Cyclosporin A exerted no therapeutic effect in mice lethally infected with Lassa or Mozambique virus.

Animals↗

PubMedDate not supplied

[Effect of immunosuppression on the development and outcome of an acute infection in mice caused by administration of the Lassa virus].

In experimental infection of mice with Lassa virus, the infectious virus could be detected in all the organs and brain tissues tested. Histopathological lesions were demonstrated in cerebral and spinal cord tissues only. Roentgen irradiation in a dose of 500 R and cyclophosphamide protected mice against a lethal Lassa virus dose. Cyclosporin A in various doses exerted no effect on the outcome of the acute infection. The adoptive transfer of splenocytes from mouse donors inoculated intraperitoneally prevented the development of lethal disease symptoms and death of mice-recipients. It is suggested that immunocompetent cells are involved in the development and outcome of experimental infection of mice with Lassa virus.

Acute Disease↗

PubMedDate not supplied

[Pathogenicity of the Lassa virus for laboratory mice].

Pathogenicity for randombred and inbred mice of various age groups of the standard Lassa virus and the virus enriched with defective interfering particles (DIP) was studied. The standard Lassa virus inoculated intracerebrally caused 100% death of C3H/Sn mice aged up to 4 weeks and 60%-70% death of randombred white mice aged 3-4 weeks. BALB/C mice were found to be nonsusceptible to the virus, and its lethality for C57BL/6 and AKR mice varied within the range of 30%-60%. Lassa virus enriched with DIP caused no death of the susceptible animals and showed poor protective activity against the standard virus.

Aging↗