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Featured researches published by Asad U. Sheikh.


American Journal of Obstetrics and Gynecology | 1992

Long-term outcome in fetal hydrops from parvovirus B19 infection

Asad U. Sheikh; Joseph M. Ernest; Michael O’Shea

Parvovirus B19 infection in the fetus is associated with anemia and hydrops and can result in fetal death. Fetal transfusion has been used in an attempt to improve outcome; however, it is associated with its own perinatal morbidity. We report two cases of fetal parvovirus B19 infection that were confirmed by polymerase chain reaction for parvovirus B19 deoxyribonucleic acid in umbilical cord blood. Ultrasonographic signs of compromise were observed at 30 and 24 weeks of gestation. Both fetuses were hydropic and one fetus was also anemic. Serial sonograms demonstrated that the hydrops resolved spontaneously over 3 to 5 weeks after diagnosis. One infant was delivered at 32 weeks of gestation as a result of idiopathic preterm labor. The other infant was delivered at term. Both infants appeared relatively normal at birth and have developed normally in the first year of life. Thus fetal hydrops in association with parvovirus B19 infection does not always lead to poor long-term outcome. A conservative approach without in utero therapy may be appropriate for the management of some of these fetuses.


American Journal of Obstetrics and Gynecology | 1993

Myocardial infarction during pregnancy: Management and outcome of two pregnancies

Asad U. Sheikh; Margaret Harper

OBJECTIVE Each year in the United States approximately 500,000 women die from ischemic heart disease. However, there are < 100 reported cases of myocardial infarction occurring during pregnancy. The current management of these patients is empiric, with pulmonary artery catheterization during labor being frequently reported. STUDY DESIGN In the past year we have managed and delivered two such patients, including the first reported case of myocardial infarction with a triplet gestation. RESULTS Both patients had clinical and laboratory signs of myocardial infarction and underwent coronary angiography. They subsequently had preeclampsia and were prematurely delivered of viable fetuses. One patient had angina pectoris during labor and was successfully treated with sublingual nitroglycerin. Neither patient suffered reinfarction or heart failure. Invasive hemodynamic monitoring was not used, and the mode of delivery was determined solely on obstetric indications. CONCLUSION In pregnant patients with myocardial infarction, invasive central monitoring is unnecessary in patients with good cardiac function and reserve and the mode of delivery should be based on obstetric indications.


American Journal of Obstetrics and Gynecology | 2000

Human immunodeficiency virus infection: In situ polymerase chain reaction localization in human placentas after in utero and in vitro infection

Asad U. Sheikh; Bruno M. Polliotti; Richard K. Miller

OBJECTIVE We compared localization of human immunodeficiency virus type 1 within human placentas infected in utero with localization within human placental explants infected in vitro. STUDY DESIGN Placental tissues from 3 cases of vertical transmission of human immunodeficiency virus type 1 were studied. Human placental explants from 6 term pregnancies not complicated by human immunodeficiency virus type 1 infection were infected in vitro with human immunodeficiency virus type 1(Ba-L). Sections from each placental explant and each placenta infected in utero were analyzed for human immunodeficiency virus type 1 localization by means of in situ polymerase chain reaction. RESULTS Human immunodeficiency virus type 1 was primarily localized within syncytiotrophoblast, Hofbauer cells, and extravillous mononuclear cells in placental tissue sections from cases of in utero infection. Within placental explants human immunodeficiency virus type 1 deoxyribonucleic acid was found in syncytiotrophoblast and Hofbauer cells. The distributions of viral localization were similar in placentas infected in utero and placental explants infected in vitro. CONCLUSION Human immunodeficiency virus type 1 can be localized to specific human placental cells (eg, syncytiotrophoblast) after either in utero or in vitro infection, which demonstrates the specificity and selectivity of human immunodeficiency virus infection in the human placenta.


Placenta | 1998

HIV-1 INFECTION OF HUMAN PLACENTAL VILLOUS TISSUE IN VITRO

Bruno M. Polliotti; Asad U. Sheikh; Shambavi Subbarao; S. Keesling; George R. Lee; Joseph Caba; Maurice Panigel; Richard C. Reichman; Andre J. Nahmias; Richard K. Miller

Summary The role of the placenta in the materno-fetal transmission of HIV-1 infection remains unexplained despite continuing progress. Among the many different experimental models (animal, isolated cells, placental tissue and isolated placental perfusion), we have selected human placental villous tissue culture as the one closest to the in utero condition associated with HIV infectivity and allowing experimentation for an adequate period of time The aim of this study was to investigate infectivity of several HIV-1 strains in human placental explants. Two laboratory strains, Ba-L and IIIB, and VI-5 (isolated from an HIV-positive baby) were utilized. Ba-L and VI-5 were Non-Syncytium-Inducing (NSI), and IIIB was Syncytium-Inducing (SI). Placental explants (first trimester and full term) were incubated for 24 hours with free virus of each strain, then intensively rinsed to remove the inoculum. After an additional five days of culture, explants were examined for infection by detection of p24 in the culture medium and by PCR amplification of viral DNA using two pairs of gag gene primers. Ba-L and VI-5 (NSI) infected both first and third trimester placental tissue. Positive indications of viral infection included increasing p24 production during the third day post-inoculation, which remained sustained for three days; and positive DNA-PCR detection in explants on day 6. As a control for infectivity, p24 increases could be completely abolished using HIV-Ig. Strain IIIB (SI) did not infect placental tissue as determined by lack of p24 release and absence of viral DNA by PCR detection. Free HIV-1 could infect the intact human placental villus and, as observed in vivo , NSI HIV-1 strains appeared more successful in infecting in vitro human placental tissue of first and third trimesters.


Placenta | 1998

In situ PCR discriminates between infected and uninfected human placental explants after in vitro exposure to HIV-1

Asad U. Sheikh; Bruno M. Polliotti; Richard K. Miller

Summary Reliable identification of HIV-1 infection in the human placenta has been limited by inadequate sensitivity or specificity of available techniques. In situ PCR technology has been demonstrated to reliably detect HIV-1 infection in a variety of tissues. Experience with ISPCR in placentae is limited. The aim of this study was to evaluate the utility of ISPCR in detecting HIV-1 infection in placental explants exposed to free virus. Two viral strains, HIV IIIB and HIV Ba-L, were used. First and third trimester placental explants were exposed for 24 hours and then cultured in virus free media for an additional 4 days. Infectivity was assessed by detection of p24 and standard PCR. Tissue sections were also analyzed by ISPCR for infection. First and third trimester tissues exposed to HIV Ba-L were infected according to the p24 and PCR assays. Infected syncytiotrophoblast, Hofbauer cells and stromal cells were identified with ISPCR in these tissues. In contrast, neither the first nor the third trimester tissues are infected after exposure to HIV IIIB according to p24 or PCR assays. The HIV IIIB tissues were uninfected according to ISPCR analysis as well. Results of ISPCR and standard assays for infectivity correlated consistently for infected and uninfected tissues. Thus, ISPCR is a reliable tool in assessing HIV-1 infectivity of placentae. These data support the clinical observation that differences in infectivity of the conceptus is at least partially dependent upon the viral strain.


Placenta | 1998

THE ROLE OF THE PLACENTA IN THE VERTICAL TRANSMISSION OF HIV AND OTHER INFECTIOUS AGENTS - A Workshop Report -

Richard K. Miller; Peter Ebbesen; Edwina J. Popek; Bruno M. Polliotti; Asad U. Sheikh; Drucilla Roberts; Vladimir Zachar; Andre J. Nahmias; Jash Unadkat

Summary It was obvious to all in attendance that the dialogue concerning not only HIV but all infectious agents must be continued as part of these international placental conferences. It was noted with pleasure that significant advances have occurred since the meeting of the Rochester Trophoblast Conference in 1992. Enhanced efforts by not only placentologists but also microbiologists, molecular biologists, pathologists, obstetricians, neonatologists, pharmacologists and those in related disciplines continue to be required for the anticipated breakthroughs necessary for the prevention of the vertical transmission of serious infections in the newborn such as HIV. All of the presentations emphasized the essential role of the placenta in modulating the infectivity of the conceptus. It was concluded that placentae from all stages of gestation are at risk of infection by certain viral strains which appear to specifically infect the placenta, e.g., HIV.


American Journal of Obstetrics and Gynecology | 1997

Effects of chronic infusion of angiotensin II on renin and blood pressure in the late-gestation fetal sheep

John R. Stanley; Carlos E. Giammattei; Asad U. Sheikh; Jennifer L. Green; Timothy J. Zehnder; James C. Rose


Annals of Medicine | 1995

Clinical picture and consequences of fetal parvovirus B19 infection.

Asad U. Sheikh; J.M. Ernest


Teratology | 2000

Role of the placenta in fetal HIV infection

Richard K. Miller; Bruno M. Polliotti; Todd S. Laughlin; Shelley Gnall; Sachio Iida; Marlene Carneiro; Kimberly Lord; Yan Ding; Asad U. Sheikh


Methods of Molecular Biology | 2000

In situ PCR detection of HIV expression in the human placenta.

Asad U. Sheikh; Bruno M. Polliotti; Richard K. Miller

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Todd S. Laughlin

University of Rochester Medical Center

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Drucilla Roberts

Baylor College of Medicine

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Edwina J. Popek

Baylor College of Medicine

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J.M. Ernest

Wake Forest University

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