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Biomedical subjects

D B Singer

Publications and source records attributed to D B Singer.

At least 37 records · Page 2Linked to original sources
PubMed1988

Pregnancy-induced hypertension and congenital adrenal hypoplasia.

Adrenal weights and histologic features in an autopsy population of 759 fetuses and neonates were correlated with the presence or absence of pregnancy-induced hypertension. Hypoplastic fetal adrenals with normal proportions of fetal and adult cortical layers (miniature histologic type) had combined adrenal weights less than 1 g, and were noted in 11 fetuses and neonates born to 39 mothers with pregnancy-induced hypertension, two born to 35 mothers with suggested pregnancy-induced hypertension, and 45 born to 685 mothers with no pregnancy-induced hypertension. Hypoplastic fetal adrenals were associated significantly with pregnancy-induced hypertension by chi 2 analysis (P less than .01). When a more stringent criterion for fetal adrenal hypoplasia was used (combined adrenal weight/body weight ratio of less than 1:1000), five cases were associated with pregnancy-induced hypertension, three with suggested pregnancy-induced hypertension, and seven with normal maternal blood pressures (P less than .001). This study confirms the relationship between pregnancy-induced hypertension and reduced fetal adrenal mass. We speculate that reduced production of dehydroepiandrosterone sulfate by the small adrenals may be related to maternal hypertension.

Adrenal Glands↗
PubMed1986

Neonatal sepsis due to nontypable Haemophilus influenzae.

From August 1980 through July 1984, 19 neonates had sepsis due to Haemophilus influenzae. Onset of disease occurred within 48 hours after birth of all the neonates. One neonate was born at term and 18 were born prematurely, including seven neonates born before 28 weeks' gestation. Eight neonates and one fetus died, six of them within 24 hours of birth. Acute chorioamnionitis was present in the placentas. Those neonates with the most severe placental inflammation survived while all of those who died had moderate or only mild chorioamnionitis. Acute villitis was noted in the placentas of three neonates who died. Respiratory distress syndrome (in 15 neonates) and pneumonia (in 15 neonates) were noted in 18 liveborn patients. Nine mothers had fever, six of them with genitourinary infections and one with septicemia due to H influenzae. All isolates of H influenzae were submitted for serologic typing and none were typable. In 14 cases, isolates were biotyped yielding eight with biotype II, four with biotype III, and one each with biotypes IV and V. Neonatal sepsis due to nontypable H influenzae is now nearly as common as sepsis due to group B Streptococcus. Both organisms produce diseases with many features in common, especially fulminant courses with respiratory distress and pneumonia, and often have a fatal outcome.

Anti-Bacterial Agents↗
PubMed1986

Effect of insulin on the size of skeletal muscle fibers of fetal rhesus monkey.

Increased body weight of insulin-treated fetuses is largely attributed to increased muscle mass. Skeletal muscle from fetal rhesus monkeys was analyzed for differences in the sizes of muscle fibers from monkeys treated in utero with high or low doses of insulin and compared to control (non-insulin-treated) animals. The results indicate no significant difference among the various groups studied and suggest that hyperplasia, not hypertrophy, of skeletal muscle fibers is responsible for the observed increase in muscle mass.

Animals↗
PubMed1986

Perinatal group B streptococcal infection in midgestation.

In a series of 32 fetuses and neonates studied at autopsy at Women and Infants Hospital, group B streptococcus (GBS) was isolated from the right atrial blood or from the lung. Eleven or 34% (5 stillborn fetuses and 6 liveborn infants) were delivered in midgestation, between 18 and 28 weeks, and all weighed less than 1000 g. Maternal clinical features in GBS infection during midgestation included vaginal hemorrhage in 4 and premature rupture of membranes in 8. The high rate of fetal death associated with this infection in midgestation (45%) bears emphasizing. Reproductive loss among mothers with previous pregnancies seems to be a risk factor for subsequent perinatal loss due to GBS. Of 17 pregnancies among these 11 mothers, only 3 resulted in living children. Colonized mothers with GBS are usually treated late in the third trimester, if at all. This study indicates that attention must be directed to midgestation, at least among the high-risk group.

Female↗
PubMed1986

Hepatic erythropoiesis in infants of diabetic mothers: a morphometric study.

Hepatic erythropoietic tissue is inversely proportional to the gestational age both in infants of diabetic mothers and in control cases. Hepatic erythropoietic and indices range from 17.8 in fetuses and babies before 28 weeks' gestational age to about 1.0 in fetuses and babies at 40-42 weeks' gestational age. The decline with gestational age is gradual in the last 10-12 weeks of in utero development. Infants of diabetic mothers who are normally grown have normal amounts of erythropoiesis in their livers. At term, large infants of diabetic mothers have excessive hepatic erythropoiesis. Hypoxia, a frequent feature in infants of diabetic mothers, is probably responsible for the increased erythropoiesis, but an alternate mechanism may be that hyperinsulinemia directly stimulates erythroid precursors or erythropoietin production.

Birth Weight↗
PubMed1985

Prepartum diagnosis of traumatic fetal-maternal hemorrhage.

The diagnosis of significant fetal-maternal hemorrhage due to abdominal trauma was made upon detection of fetal red cells in the maternal circulation before delivery, and prompted immediate intervention despite an equivocal fetal monitor tracing. Histologic examination of the placenta identified the area of disruption of the fetal circulation, and the clinical condition of the neonate confirmed the diagnosis. A test for fetal-maternal hemorrhage would be appropriate in the evaluation of any pregnant woman sustaining trauma to the abdomen.

Abdominal Injuries↗
PubMed1985

Hemorrhage in cardiac conduction tissue in premature infants.

Six premature infants had hemorrhages that were limited to cardiac conduction tissues. Obstetric complications occurred in each; four were growth retarded, and four had perinatal asphyxia. Two babies survived beyond one week. Four survived less than 24 hours. Bradyrhythmias occurred in four. Extracardiac lesions included infections and renal failure in two infants, hyaline membrane disease in one, hypoplastic lungs in two (one with renal agenesis and placental amnion nodosum), and placental villous edema in two. Cardiac hemorrhage occurred in sinoatrial nodes (n = 1), atrioventricular nodes (n = 3), atrioventricular bundles (n = 3), left bundle branches (n = 5), and right bundle branches (n = 3). The lesions were macroscopic in five cases. These cases suggest that neonatal cardiac conduction tissues are vulnerable to hemorrhage, particularly if associated with perinatal insults. Such lesions may account for some idiopathic dysrhythmias in surviving babies.

Heart Conduction System↗
PubMed1984

X-linked recessive myotubular myopathy: I. Clinical and pathologic findings in a family.

Four neonatal deaths in one family were due to X-linked myotubular myopathy. The characteristic alterations in muscle, described in three cases, are marked fiber hypotrophy, size variability, and the presence of internal nuclei or pale areas. The diagnosis can be verified only by obtaining a careful genetic history. Previous occurrence of male neonatal death or stillbirth, or of hypotonia and respiratory insufficiency, is critical in the identification of suspected cases. There is morphologic justification for retaining the name "myotubular myopathy" to distinguish this X-linked disorder from other congenital conditions involving muscle weakness that have similar morphologic features.

Female↗
PubMed1984

X-linked recessive myotubular myopathy: II. Muscle morphology and human myogenesis.

The classification of centronuclear myotubular myopathies is controversial. Within this group of disorders, congenital X-linked recessive myotubular myopathy (XLMTM), characterized by marked cell hypotrophy and structural resemblance to fetal myotubes, represents a distinct entity. The histologic findings in verified and probable cases of XLMTM are reviewed. In addition, the ultrastructural features of muscle in one case of XLMTM are compared with those of normal fetal muscle at various developmental ages. In XLMTM both muscle and nerve show evidence of immaturity. Proliferation of the sarcotubular organelles in XLMTM, not observed in normal fetal muscle, may be due to impaired innervation.

Cell Nucleus↗
PubMed1984

Placentas in pregnancies complicated by maternal diabetes.

PDMs tend to be large and the size is generally in proportion to fetal size. Infarcts are both more numerous and more common in PDMs than in normal placentas. These reflect the in utero hypoxia found in IDMs. Placental infarcts are increased not only in cases of severe DM (classes D, F-R) but also mild and early DM (class A). We infer from this that maternal vascular disease may be present functionally long before pathologic changes can be detected by direct examination of vessels. More subtle evidence of hypoxia in PDMs, such as an increased number of syncytial knots, has been suggested by qualitative data but has not been confirmed by morphometric analysis. Other qualitative observations in PDMs include thickened basement membranes, flattened microvilli on trophoblasts, ectasia of capillaries and villous stromal edema; changes in intracellular organelles and structures include enlarged mitochondria, increased pinocytotic vesicles, and dilated profiles of endoplasmic reticulum. Quantitative morphometric analysis shows no differences between normal placentas and PDMs with regard to these changes. The transport and secretory functions of the placenta, especially important in pregnancy complicated by DM, are not addressed here. As our understanding of placental physiology enlarges, it will be useful to relate each function with its structural counterpart. Perhaps this review will in part provide rational data from which to proceed with the task.

Female↗
PubMed1984

Chronic hyperinsulinemia in the fetal rhesus monkey. Effects of physiologic hyperinsulinemia on fetal growth and composition.

One of the hallmarks of the hyperglycemic-hyperinsulinemic infant of the diabetic mother (IDM) is macrosomia and selective organomegaly. Primary hyperinsulinemia, with insulin levels similar to those observed in human IDMs at delivery, was produced in the fetal rhesus monkey during the last third of gestation. The effects of this physiologically relevant hyperinsulinemia, in the absence of hyperglycemia, on fetal growth were studied. Fetal macrosomia, with a 23% increase in total body weight, was observed in physiologically hyperinsulinemic fetuses. A similar 27% increase in weight was produced by fetal insulin levels that were 10 times higher. A logarithmic correlation was observed between fetal birth weight ratio and fetal plasma insulin concentration. In contrast to this increase in weight, skeletal growth, as measured by crown-heel length and head circumference, was not affected by hyperinsulinemia. Only cardiomegaly was found in the low-dose hyperinsulinemic fetuses, whereas cardiomegaly, hepatomegaly, and splenomegaly were produced by hyperinsulinemia in which insulin levels were in the highest range. Compositional analysis of heart and skeletal muscle indicated no differences in the protein, RNA and DNA concentration, or in the protein-to-DNA ratio in hyperinsulinemic fetuses. We interpret these data as indicating that fetal insulin plays the predominant role in controlling the normal, as well as the augmented, fetal weight characteristic of the human infant of the diabetic mother.

Animals↗
PubMed1983

Two lethal chondrodysplasias with giant chondrocytes.

Two infants, each with a different form of sporadic lethal chondrodysplasia, had multinucleated giant chondrocytes in resting cartilage. Both patients also had severe laryngeal stenosis and normal chromosomes. The radiographic abnormalities in one patient conformed to the recently delineated entity, atelosteogenesis (spondylohumerofemoral hypoplasia or giant cell chondrodysplasia); the other patient had an unclassified type of spondyloepiphyseal dysplasia. The findings in these two patients and the previously reported observations in spondylohumerofemoral dysplasia confirm that chondrocytic giant cells are a causally nonspecific phenomenon.

Cartilage↗