Fetal fibronectin and preterm labor.
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Biomedical subjects
Publications and source records attributed to S A Friedman.
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This prospective, nested, case-control study investigated whether maternal plasma fetal fibronectin reflects reduced trophoblastic invasion at 16 to 20 weeks in women who later have preeclampsia. Concentrations of fetal fibronectin were 8.7 +/- 2.6 micrograms/ml in women with preeclampsia and 8.1 +/- 2.5 micrograms/ml in matched controls (p greater than 0.5). These results are discussed.
This is the case report of an eighty-seven-year-old woman who was seen because of swelling of her left upper extremity and breast of one week's duration. She had a history of severe arthritis of the knees and had been wheelchair-bound for seven years. Venography showed compression of the cephalic vein and thrombosis of the distal basilic vein with extension into the axillary and subclavian veins. To the author's knowledge, this is the first case report of venous thrombosis in association with subluxation of the shoulder.
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Treatment of this pathophysiologically poorly understood disease is controversial. Despite this uncertainty, the goals of management of the patient with preeclampsia and eclampsia are diagnosis, stabilization, and delivery of the baby. Stabilization refers to both mother and fetus and should include the prevention of eclampsia or the recurrence of eclamptic seizures. There are empiric data supporting the use of magnesium sulfate for the management of preeclampsia and eclampsia in North America, but there are few data to support its efficacy as a classic anticonvulsant. Until controlled trials are completed, we suggest that magnesium sulfate continue to be used in preeclampsia, with the addition of established anticonvulsant medications when eclampsia occurs. Data on established antiepileptic drugs such as diazepam and phenytoin support their use in treating patients with eclamptic seizures. As stated in an earlier review, "in treating preeclampsia, magnesium sulfate therapy may have a role and may moderate factors leading to eclampsia. Whether magnesium sulfate therapy may have some as yet unproved effect on epileptogenic foci or seizure propagation is not the important issue for the physician caring for the eclamptic patient. Until adequately designed therapeutic trials are available, it is our opinion that treatment should be based on the use of anticonvulsant drugs of established efficacy in seizure control and prophylaxis (p. 1363)."
Current concepts of the pathogenesis of preeclampsia involve the generalized dysfunction of maternal vascular endothelial cells. We measured the endothelial isoform of fibronectin as a marker of endothelial cell injury throughout pregnancy in a prospective, case-control study. Nineteen women met strict criteria for the diagnosis of preeclampsia. Nineteen normal pregnant women, and 19 women with gestational hypertension but without other stigmata of preeclampsia (transient hypertension) were selected from the same cohort and matched according to race, age, nulliparity, and gestational age at delivery. Plasma levels of cellular fibronectin were significantly elevated in women meeting strict clinical and biochemical criteria for preeclampsia but not in women with normal pregnancies or transient hypertension. Moderate but significant elevations in mean levels were found in the second trimester in women destined to have preeclampsia, as compared with matched normal and transient hypertension groups (p less than 0.05). The results indicate that elevated plasma levels of cellular fibronectin are not simply the result of increased blood pressure but reflect a maternal insult specific to the syndrome of preeclampsia. Elevation of the mean concentration during the midtrimester is consistent with the hypothesis that endothelial cell injury is a specific lesion that occurs early in the course of preeclampsia, before clinical signs and symptoms.
Ultrasound has become an effective tool for evaluating the inferior vena cava. The authors report 3 cases that illustrate the difficulty in diagnosing partially adherent clots, which may have a high propensity for pulmonary embolism.
Preeclampsia is a complex clinical syndrome, with hypertension representing but one manifestation. Pathogenetically important events in the development of preeclampsia include incomplete trophoblastic invasion of the maternal spiral arteries, poor trophoblastic perfusion, elaboration of a putative endothelial cell toxin, and endothelial cell injury with resulting activation of coagulation, impairment of vasodepressor function, and altered endothelial permeability. These changes lead to the clinical signs and symptoms, which occur relatively late in the course of preeclampsia. The primary immunologic, genetic, and biochemical basis of preeclampsia remains speculative.
Pregnancies complicated by collagen vascular diseases present a challenge to the obstetrician, internist, and other consulting physicians caring for the patient. Although most pregnancies complicated by these disorders result in satisfactory outcomes, a significant number develop manifestations sufficiently serious to require admission to an intensive care unit. Such manifestations include lupus nephritis, CNS lupus, ARDS, massive alveolar hemorrhage, scleroderma renal crisis, pulmonary hypertension, severe myositis, and diffuse vasculitis. Of the numerous therapeutic options available, many may be used to optimize maternal and perinatal outcome.
The P1 partition region contains two large open reading frames that encode the proteins ParA and ParB. It was previously shown that ParA is essential for partition activity. Using a novel assay, we show that ParB protein is also an absolute requirement for partition and that it is active in trans to the partitioning plasmid. Development of complementation tests for parA and parB allowed us to assign a number of partition-defective point mutants of a P1 miniplasmid to the parA and parB cistrons. Using gene fusion techniques, it was shown that parA and parB constitute an operon controlled from a promoter proximal to the start of parA. Transcription from this promoter is autoregulated by a feedback loop that is sensitive to the ParA and ParB proteins in concert. The parB gene also appears to be expressed at a low level from a second promoter at the intercistronic boundary. This results in a low level of expression and tight autoregulation for the ParA protein and slightly less stringent control for ParB synthesis.
Puerperal ovarian vein thrombosis is a dangerous complication of childbirth and often leads to inferior vena cava thrombosis and multiple pulmonary emboli. Computed tomography of the abdomen is useful in early diagnosis. Two patients with typical computed tomographic features are presented.
An asymptomatic woman was evaluated because of a chest x-ray examination suggesting an aortic aneurysm. CT scan revealed proximal aortic dissection, which had apparently leaked into the pericardium. Increased use of CT scanning is expanding our knowledge of the clinical spectrum of aortic dissection.
The etiology of preeclampsia remains unknown. Because of their widespread and varied effects in the human body, prostaglandins--specifically PGI2, thromboxane A2, PGE, and PGF2 alpha--have come under much investigation as possible etiologic factors. The vasodilating, platelet-disaggregating prostaglandins (PGI2 and PGE) are increased during normal pregnancy and may account for many of the observed hemodynamic changes, which begin as early as the first trimester. In contrast, a relative increase in the vasoconstricting, platelet-aggregating prostaglandins (thromboxane A2 and PGF2 alpha) is seen in preeclampsia. The disruption in the delicate balance between these two opposing pairs of prostaglandins may play an important role in the causation of preeclampsia. The growing body of literature that deals with the relationship between prostaglandins and preeclampsia is discussed.
We have defined a minimal partition site, parS, from the plasmid P1. It contains sufficient cis-acting information to direct accurate segregation of low-copy-number plasmids that contain it as long as the two essential P1 Par proteins are supplied in trans. The site is, at most, 34 base pairs and contains a perfect 13-base-pair inverted repeat. Site-directed mutations were made within the repeat sequence that abolished activity whether or not the symmetry of the palindrome was maintained. Partition appears to be a competitive process, as differentially marked plasmids carrying the same type of partition site are not independently segregated but are randomly distributed with respect to each other. We have studied competition between plasmids carrying various fragments encompassing the parS site. As expected, two plasmids carrying the minimal parS site compete with each other. However, a sequence that lies to the left of the minimal parS site acts as a major modulator of this competition, changing the specificity of the competitive effect completely. Thus, this adjacent sequence appears to be an important determinant of the specificity of the wild-type P1 partition system without being necessary for its efficient function.
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A 56-year-old woman with no history of cardiac disease developed acute pulmonary edema following a subarachnoid hemorrhage. A constellation of findings, including elevated creatine kinase MB isoenzyme activity in the absence of electrocardiographic or scintigraphic evidence of acute myocardial infarction, elevated pulmonary artery wedge pressure, segmental wall motion abnormalities, and depressed ejection fraction of the left ventricle demonstrated by two-dimensional echocardiography and radionuclear ventriculography, pointed to a direct myocardial injury leading to cardiac failure. The evidence for cardiogenic origin of pulmonary edema provided by this case is in contrast to the belief that "neurogenic" pulmonary edema is of noncardiac origin.
Prior to the advent of two-dimensional echocardiography, atrial septal aneurysm was rarely diagnosed during life. In this article, two-dimensional echocardiography identified an atrial septal aneurysm as the site of intracardiac right-to-left shunting, causing hypoxemia in a patient with acute right ventricular infarction. In addition to this rare presentation, the patient also had systemic embolism, a known complication of atrial septal aneurysms.
The gam locus of bacteriophage lambda encompasses two coding sequences with the same reading frame and translational stop, one corresponding to an Mr 11646 polypeptide (gamS gene), the other to an Mr 16349 polypeptide (gamL gene). A DNA segment encoding gamS but not gamL was placed under lambda pR promoter control (regulated by the cIts857-coded repressor) on a multicopy plasmid, and an insertion mutation (gamS201) was constructed. Expression of gamS+, but not gamS201, inhibited Escherichia coli RecBC nuclease in vivo; the criteria were inhibition of chromosomal DNA degradation after UV irradiation and plating of T4 gene 2- phages. The recB+ C+ bacteria expressing gamS+ were completely or partially similar to recC- mutants with respect to certain phenotypes: defective plating of phages P1 and P2, ability to plate (in a recA- background) lambda red- gam- phages, reduced resistance to UV irradiation, defective SOS induction, decreased colony-forming ability.