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Biomedical subjects

A Firpo

Publications and source records attributed to A Firpo.

14 recordsLinked to original sources
PubMed1997

Microsporidium-associated sinusitis.

Two cases of biopsy-proven Microsporidium-associated chronic sinusitis in HIV-seropositive patients are presented. Spores of Septata intestinalis were identified by light microscopy and confirmed by electron microscopy in each case. Both patients displayed severe deficiencies of nasal mucosa CD4-positive cells, demonstrated by immunohistochemical methods. Only two other cases of Septata intestinalis-associated sinusitis have been reported previously. Our observations agree with the theory that functional defects in local mucosal immunity may partially explain the acquisition of opportunistic mucosal infections in many HIV-seropositive patients.

AIDS-Related Opportunistic Infections↗
PubMed1995

Characterization of the tobacco glycoprotein surface binding property of heart and skeletal muscle cells. I. Modulation of the heart cell membrane TGP interaction by anti-TGP IgG.

Monolayers of L6 rat skeletal myoblast cells formed surface binding isotherms with the purified tobacco leaf glycoprotein TGP1 and the enriched cigarette tar glycoprotein TGP2. Scatchard analysis showed that the binding in the range of the limited concentrations tested was to a single class molecule and the calculated affinity constant (Kd) for TGP1 and TGP2 showed similar values (9.78 x 10(-13) M and 3.09 x 10(-13) M, respectively). The bound TGPs were almost totally displaced by excess nonradiolabeled molecules. The calculated Bmax of the L6 myoblast monolayer was 2.93 fmol for TGP1 and 0.217 fmol for TGP2 per 32.2 mm2. Guinea pig heart sarcolemma binding isotherms were also formed with radiolabeled TGP1 and TGP2. The interaction of tobacco leaf TGP1 with the heart cell membranes was irreversible because only 15-20% of the bound TGP1 was displaced by 100-fold, non-labeled molecules but the interaction of tar TGP2 with heart sarcolemma was reversible and probably saturable. The heart sarcolemma TGP2 affinity constant (Kd) was 5.88 x 10(-7) M and the Bmax, 2.45 x 10(-8) M per 12.5 micrograms sarcolemma. Pretreatment of heart sarcolemma with increasing concentrations of leaf TGP1 did not displace tar TGP2 binding but its absorption on the membrane resulted in increased TGP2 sarcolemma attachment by a complex and unexplained mechanism. Increasing concentrations of the sera of 10 of 15 guinea pigs (67%) that received mainstream emissions of tobacco smoke from a University of Kentucky cigarette smoking machine for 152 days, displaced cigarette tar TGP2 heart cell sarcolemma attachment and this inhibition was significantly different from that produced by the sera of sham smoked and of non-exposed animals (Mann-Whitney test, p = 0.0082). Staphylococcus protein A inhibited the displacement of TGP2 produced by the sera of cigarette smoke exposed guinea pigs and this observation indicated that this action was mediated by IgG molecules. The specific immunoprecipitation of a radiolabeled surface epitope of the L6 myoblast monolayers pretreated with TGP1 or TGP2 by immune IgG against TGP2 and by the IgG of an antiserum against standard TGP showed that the tobacco glycoproteins attached to a unit polypeptide of the plasma membrane of the muscle cells of approximately 76 kDa. These data support the notion that TGP molecules in cigarette smoke are absorbed systemically on smoking and may have a direct toxic effect when they attach to the surface TGP binding proteins of heart and skeletal muscle cells.

Animals↗
PubMed1992

Pediatric AIDS and perinatal HIV infection in Zaire: epidemiologic and pathologic findings.

HIV infection in women and children is a special problem in Zaire and in other countries where heterosexual transmission is predominant. Nearly half of the cases of HIV infection are in women 15 to 30 years old and as many as seven infected infants may be born each year. Whether or not infected at birth, these children have mothers, and often fathers, who are infected and likely to die while they are still very young. Such orphaned children, as well as those whose families cannot provide adequate food and health care, add to the problematic economies of developing countries. The problems of children of HIV-infected mothers in developing countries may be compounded further by factors directly related to their mother's disease. Infected mothers who are sick may produce insufficient levels of antibodies and be unable to provide their children with adequate natural passive immunity before birth. Their infants may also receive inadequate levels of breast-milk-derived antibodies possibly enhancing their already increased susceptibility to perinatal infections, and lastly, the volume of breast milk produced by these mothers may be inadequate for the nutrition of these infants. All these factors may further compromise the already difficult task of distinguishing those infants of HIV-infected mothers who are ill because they are infected from those who are ill because of their mother's disease. Regardless of the mechanisms accounting for the increased vulnerability of infants of HIV--seropositive and AIDS-afflicted mothers to perinatal infections, infant mortality can be expected to increase significantly as a direct consequence of the progression of the HIV pandemic throughout Africa and possibly other developing countries; this in populations already with a total under five-years-of-age mortality rate exceeding 15%. The association of chorioamnionitis with HIV seropositivity and with the clinical status of the mother seems to suggest that impaired maternal immunity increases the risk of premature birth, its consequent lower birth weight, and to HIV or other perinatally acquired infections. The identification of women at higher risk of chorioamnionitis and their treatment might provide a means to decrease the risk of premature delivery and possibly reduce the rate of HIV transmission to their infants. The pathologic changes in organs of infants and children with HIV infection require in-depth, systematic study to better define the natural history of perinatal HIV disease and infection.(ABSTRACT TRUNCATED AT 400 WORDS)

Acquired Immunodeficiency Syndrome↗
PubMed1991

Lymphoid germinal centers are reservoirs of human immunodeficiency virus type 1 RNA.

When radiolabeled RNA was used for in situ hybridization, human immunodeficiency virus type 1 (HIV-1) RNA was found in high concentrations in germinal centers of lymphoid tissues from patients with HIV-1 infection. Most of the signal from hybridized probe was independent of specific cells, being found in the extracellular space of germinal centers in all lymphoid tissues examined from adult patients with Centers for Disease Control (CDC) class II and III disease or pediatric patients with CDC class P-2A disease. Lymphoid tissues from adult patients with CDC class IV infections or pediatric patients with CDC class P-2D disease (including autopsy material) lacked intact germinal centers, and HIV-1 RNA was then found only in rare, isolated cells, with some tissues having no detectable HIV-1 RNA. Thus, in the early stages of HIV infection, germinal centers serve as important reservoirs of free virus in the interstitial spaces, and this reservoir disappears as the germinal centers involute with advancing disease.

Adenoids↗
PubMed1990

Cellular control of IgE induction by a polyphenol-rich compound. Preferential activation of Th2 cells.

The polyphenol group rutin (R) appears to influence isotype expression, because R-BSA conjugates induce anti-BSA responses in mice that show a significant decrease in hemagglutinating antibodies (HA) to BSA, as compared to mice immunized with BSA. However, the level of IgE antibodies to BSA is unaltered. To determine if suppressor cells for isotypes other than IgE are induced by R-BSA, cell transfers were performed. The results were consistent with the view that the decrease in HA titer to BSA in R-BSA immunized mice is not due to the activation of suppressor cells for isotypes other than IgE. Inasmuch as the IgE response in mice is associated with the production of IL-4 by Th2 cells, we analyzed the factors produced by spleen cells cultured with R-BSA. We found that supernatant from spleen cells cultured with R-BSA contained IL-4 as determined by the enhanced expression of Fc epsilon R (CD23) on B cells. This enhancement was inhibited by 11B11, the anti-IL-4 mAb. IL-2, a product of Th1 cells, was not detected in these supernatants. Moreover, IL-4 mRNA, but not IL-2 mRNA, was detected by Northern blot analysis of RNA from spleen cells cultured with R-BSA. Taken together the data suggest that the polyphenol containing compounds preferentially activate Th2 cells, thereby favoring IgE production.

Animals↗
PubMed1989

The effect of interleukin-1 alpha and tumor necrosis factor alpha on the secretion of human chorionic gonadotropin by JAR human choriocarcinoma cells.

The regulation of human chorionic gonadotropin (hCG) secretion by placental trophoblasts is incompletely understood. A recent study reports that Interleukin-1 beta (IL-1 beta) stimulates hCG production in vitro by human, first trimester, placental trophoblasts, but not by a human choriocarcinoma cell line. Human decidua has been shown to produce IL-1 alpha and beta, and Tumor Necrosis Factor alpha (TNF alpha). The precise role(s) of these proteins in pregnancy is unknown. In the present study, hCG production by human choriocarcinoma cells (JAR) was evaluated in the presence of recombinant human IL-1 alpha (rHIL-1 alpha) and rHTNF alpha. hCG production was increased by rHIL-1 alpha in a dose-dependent manner, and heat-inactivation of this cytokine abolished the effect. Equimolar quantities of rHTNF alpha failed to influence hCG production or cell viability. IL-1 may be important in the regulation of hCG production by human trophoblasts, and therefore may play a physiologic role in pregnancy. Furthermore, TNF does not appear to participate in the regulation of the production of this hormone by human choriocarcinoma cells. This is the first demonstration of a divergence of activity of these two cytokines in the reproductive process.

Choriocarcinoma↗
PubMed1989

Cardiac malformations in trisomy-18: a study of 41 postmortem cases.

The cardiac malformations in 41 karyotyped and autopsy cases of trisomy-18 are presented in detail. The salient findings were a ventricular septal defect in all cases; tricuspid valve anomalies in 33 cases (80%); pulmonary valve anomalies in 30 (70%); aortic valve malformations in 28 (68%); mitral valve anomalies in 27 (66%); polyvalvular disease (that is, malformations of more than one valve) in 38 (93%); a subpulmonary infundibulum (conus) in 40 (98%); a bilateral conus with a short subaortic infundibulum in 1 case with double outlet right ventricle (this being the only documented case of bilateral infundibulum in trisomy-18); double outlet right ventricle in 4 cases (10%), three having a subpulmonary infundibulum only and all 4 having mitral atresia; tetralogy of Fallot in 6 cases (15%), 2 having pulmonary atresia; and a striking absence of transposition of the great arteries and inversion at any level (visceral or cardiac), findings that appear to be characteristic of all trisomies. These data suggest that excessive chromosomal material (as in trisomies) may result in situs solitus at all levels. The malformations of the atrioventricular and semilunar valves were characterized by redundant or thick myxomatous leaflets, long chordae tendineae and hypoplastic or absent papillary muscles. The ventricular septal defect was associated with anterosuperior conal septal malalignment in 25 cases (61%). On the basis of the characteristic valvular lesions, the type of ventricular septal defect and the absence of transposition or inversions, two-dimensional echocardiographic diagnosis of trisomy-18 in the fetus may become possible.

Chromosomes, Human, Pair 18↗
PubMed1989

Enrichment of right-side-out Trypanosoma cruzi plasma membrane vesicles.

A simple method to prepare a high yield of Trypanosoma cruzi plasma membrane vesicles (PMV) from epimastigotes and metacyclic trypomastigotes is described. The method may be applicable to other protozoa. Solid-phase immunoassay to bind surface T. cruzi epitopes showed that this preparation was enriched with 80-82% PMV and that most of these were right-side out (81-92%). The method was based on the extraction of extrinsic proteins and subpellicular tubules with mild high and low ionic strength buffers without detergents (pH 7.4) and on the differential centrifugation of PMV based on their specific density (1.049 g/ml, 4 degrees C). Transmission electron microscopy of PMV pellets showed a heterogeneous population of vesicles without other significant cytoskeletal contaminants. T. cruzi PMV were also enriched with an ouabain- and oligomycin-insensitive magnesium-ATPase and contained an adenylyl cyclase, preserved for at least 3 months at -70 degrees C in storage buffer. Measurements of the [14C]-dextran and the 3H2O space indicated that T. cruzi PMV were not sealed, explaining why Lubrol PX and NaF failed to stimulate the adenylyl cyclase activity further and why T. cruzi PMV were unable to concentrate 86Rb in flow dialysis assays. No detectable DNA and RNA was found. The preparation was not capable of removing 51Cr or [3H]glucosamine from live L6 myoblast surfaces in physiologic conditions and acid phosphatase was extracted by this method. The contaminating fraction (18-20% by immunoassay) consisted of endoplasmic reticulum membranes with NADH oxidase activity and of kinetoplast membranes with cytochrome c oxidase and oligomycin sensitive magnesium-ATPase activity. The biologically active T. cruzi PMV retained the ability of living forms to trigger the alternate pathway of complement by releasing the Bb activation fragment from human Factor B.

Animals↗
PubMed1989

Interleukin-1 alpha and tumor necrosis factor alpha cause placental injury in the rat.

Bacterial endotoxins (LPS) causes placental injury and fetal demise in pregnant animals. Because several biological effects of LPS are mediated by interleukin-1 (IL-1) and tumor necrosis factor (TNF), the hypothesis that these cytokines could cause placental injury similar to that seen in LPS-treated pregnant rats was tested. On day 12 of gestation, rats were injected intraperitoneally with saline, LPS, native or heat-inactivated (HI) rHIL 1 alpha, or rH-TNF alpha. Seven days later, grossly abnormal implantation sites and fetal demise were observed in rats injected with rHIL-1, rHTNF, or LPS but not in those injected with saline or HI-cytokines. Necrosis of placental, decidual, and fetal tissues was observed in cytokine-treated animals. The necrosis was more severe in LPS-treated rats, in which no fetal remains were identifiable. These data suggest that IL-1 and TNF may play a role in the fetoplacental injury observed in LPS-treated pregnant rats.

Animals↗
PubMed1984

Coordinate induction of cytochrome P-448 mediated mixed function oxidases and histopathologic changes produced acutely in chick embryo liver by polychlorinated biphenyl congeners.

Hepatic histologic changes and induction of mixed function oxidases were examined and compared after administration to the chick embryo of four highly purified polychlorinated biphenyl (PCB) congeners: 3,4,3',4'-tetrachlorobiphenyl (TCB) and 3,4,5,3',4',5'-, 2,4,5,2',4',5'-, and 2,3,6,2',3',6'-hexachlorobiphenyls (HCBs). The major histopathologic change was hepatocyte swelling as evidenced by sinusoidal narrowing. It was observed within 24 hr after PCB administration at doses as low as 5 nmol/egg for 3,4,3',4'-TCB and 3,4,5,3',4',5'-HCB and only at doses of 5000 nmol/egg and higher for 2,4,5,2',4',5'-HCB. 2,3,6,2',3',6'-HCB was inactive. The histopathologic change was predominantly perivascular in distribution. It was accompanied by increased hepatic water content. Occasional hepatocytes showed nuclear pyknosis and cytoplasmic eosinophilia, but there was little histologic evidence of frank necrosis and no biochemical evidence, since serum glutamic-oxalic and glutamic-pyruvic transaminases and lactic dehydrogenase did not increase. Hepatic glutathione (GSH) levels were not significantly altered by 3,4,3',4'-TCB or 3,4,5,3',4',5'-HCB, indicating that GSH depletion does not have a significant role in the production of hepatotoxic changes by PCBs. Measurement of the degree of pathologic change indicated that 3,4,3',4'-TCB and 3,4,5,3',4',5'-HCB were three to four orders of magnitude more potent than 2,4,5,2',4',5'-HCB both as hepatotoxins and as inducers of the cytochrome P-448 mediated mixed function oxidases, aryl hydrocarbon hydroxylase, and 7-ethoxyresorufin deethylase. 2,3,6,2',3',6'-HCB was inactive as an inducer as well as as a hepatotoxin. The findings indicate that hepatotoxic changes are selectively produced in the chick embryo by those PCBs that also induce cytochrome P-448 mediated mixed function oxidases and in that respect resemble other manifestations of PCB toxicity (e.g., subcutaneous and pericardial edema and thymic involution) in both the chicken and other species. The results support the hypothesis that a common initial mechanism leads both to cytochrome P-448 type induction and to diverse manifestations of polyhalogenated hydrocarbon toxicity.

Animals↗
PubMed1982

Development of arachnoid villi and granulations in man.

The superior sagittal sinus and confluens sinuum of 27 fetuses and newborns ranging from postmenstrual intervals of 26-54 weeks were studied by scanning electron microscopy and histology. 26-week specimens showed oval depressions in the final portions of tributary veins to the sinus. Histologically there were arachnoid tissue clusters within the dural wall. The walls of the depressions were more irregular by the 30th week. Arachnoid villi were apparent by the 35th week and granulations were observed after the 39th weeks. The granulations increased in complexity as development proceeded.

Arachnoid↗
PubMedDate not supplied

Primary hyperaldosteronism in childhood due to unilateral macronodular hyperplasia. Case report.

We present the first report of primary hyperaldosteronism in childhood due to unilateral macronodular hyperplasia. A 10-year-old white boy with severe hypertension (150/100 mm Hg), hypokalemia (1.4 mEq/liter), and suppressed plasma renin activity (PRA) (less than 0.1 ng/ml/hr) demonstrated fixed PRA and aldosterone (aldo) levels that did not change with alteration of dietary sodium. The paradoxical decrease in serum aldo on assumption of upright posture suggested a tumor. Prolonged ACTH administration produced a continuous rise in blood pressure, but a transient rise in aldo. A minimal decrease in urinary aldo during dexamethasone administration was noted, excluding dexamethasone-suppressible hyperaldosteronism. Blood pressure normalized with spironolactone. Computerized transaxial tomography, iodocholesterol scanning, and adrenal venography were not diagnostic of a discrete adrenal lesion. Although hyperplasia is more common than an adenoma as a cause of hyperaldosteronism in childhood, a tumor was predicted, since adrenal vein hormone sampling with ACTH stimulation lateralized aldosterone secretion unequivocally to the left adrenal gland. However, left adrenalectomy revealed macronodular hyperplasia. Postoperatively, there was reversal of hypertension, hypokalemia, and hyperaldosteronism. Thus, in childhood, unilateral hypersecretion of aldosterone may result from nodular hyperplasia, rather than a discrete adenoma.

Adrenal Glands↗
PubMedDate not supplied

Cytology of ganglioglioma of the brain: a morphometric study.

This study describes and illustrates the application of the morphometric method in the classification of different types of cells in mixed populations. The nuclei of neoplastic cell and astrocytes, nonneoplastic monocytoid cells and lymphocytes in touch preparations of two gangliogliomas were measured. Two preoperative cerebrospinal fluid specimens from one of these cases were similarly evaluated. The mean nuclear area of some cell populations was statistically distinct and consistent in each preparation. Other cell populations showed considerable overlap in nuclear size and could not be separated on the basis of this parameter alone.

Astrocytes↗