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COMMERCE BUSINESS DAILY ISSUE OF JULY 14,1995 PSA#1388National Institutes of Health, Division of Research Contracts, 6100
Executive Blvd., MSC 7540, Room 6E01, Bethesda, Maryland 20892- 7540 A -- MOLECULAR ANALYSES OF AUTOPSY SPECIMENS FROM SIDS AND CONTROL
INFANTS TO ASCERTAIN MIDDLE EAR INFECTION SOL NIH-DC-95-13 POC Jonathan
Ferguson, Contract Specialist, (301) 496-4487. The National Institute
on Deafness and Other Communication Disorders, National Institutes of
Health, intends to conduct a comparative study of molecular analyses of
autopsy specimens from children who were determined to have died from
Sudden Infant Death Syndrome (SIDS) and a control group of children who
died from other causes. The purposes of the study is to determine if
there are certain infectious agents, both viral (influenza,
parainfluenza, respiratory syncytial, rhino, and adenovirus) and
bacterial (hemophilus influenzae, streptococus pneumoniae, and
moraxella catarrhalis), that are more frequently recovered from
children who die from SIDS than from other causes. Multiplex polymerase
chain reaction assays will be employed to look for bacterial and viral
upper respiratory tract pathogens in nasopharyngeal and middle-ear
specimens collected at autopsy. A minimum of four specimens
(mucopithelial or mucoperiosteal from both right and left middle ears,
the anterior aspect of the nasal cavity, the posterior aspect of the
nasopharynx, and eustachian tube and brain stem) shall be collected
from each autopsied patient for molecular microbiological analyses. A
three year cost reimbursement type contract is anticipated. The
solicitation is scheduled to be issued on or about September 1, 1995.
A copy of the solicitation may be obtained by sending a written request
referencing the above RFP number. Only one RFP shall be sent to each
requesting organization. All responsible sources may submit a proposal
which shall be considered by the Government. (0193) Loren Data Corp. http://www.ld.com (SYN# 0007 19950713\A-0007.SOL)
A - Research and Development Index Page
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