PubMed Health⌕ Search

Biomedical subjects

M Ortiz

Publications and source records attributed to M Ortiz.

At least 19 recordsLinked to original sources
PubMed1995

Steel factor (c-kit ligand) promotes the survival of hematopoietic stem/progenitor cells in the absence of cell division.

It is known that the majority of primitive hematopoietic progenitors are in a noncycling quiescent state. In addition, normal hematopoietic progenitors and progenitor cell lines show an absolute dependence on growth factors for their survival in vitro, yet the effect of growth factors on progenitor cell survival has not been separated from effects on both proliferation and differentiation. Using an in vitro assay system, we examined whether growth factors could promote the survival of stem cells in culture in the absence of cell division. These studies show that steel factor (SLF) and, to a lesser extent, interleukin-3 (IL-3) directly promoted the survival of elutriated bone marrow progenitor cells (countercurrent centrifugal elutriation [CCE]-27) that are enriched for primitive hematopoietic progenitors that respond to the combination of SLF plus IL-3. Furthermore, SLF promoted the survival of short-term reconstituting cells (STRC), and long-term reconstituting cells (LTRC) with trilineage reconstitution potential in vivo. In comparison, granulocyte colony-stimulating factor (G-CSF), IL-6, leukemia inhibitory factor, IL-11, IL-1, granulocyte macrophage CSF (GM-CSF), and macrophage CSF (M-CSF) had no effect on the survival of these cells. In the presence of mitotic inhibitors (nocodazole or aphidicolin), SLF promoted the survival of CCE-27 progenitor cells that respond to the combination of SLF plus IL-3 in vitro and STRCs and LTRCs that are detected in vivo. Taken together, these data show that SLF can directly promote the survival of hematopoietic progenitor cells in the absence of cell division.

Animals↗
PubMed1995

Prevalence of intestinal parasite infections among individuals with mental retardation in New York State.

The prevalence of intestinal parasite infection among program participants of the New York State Office of Mental Retardation and Developmental Disabilities for the period 1986-1987 was estimated, and demographic factors associated with increased risk for infection were identified. The overall prevalence of infection was 7.3%. The two most prevalent infections were Enterobius vermicularis (4.5%) and strongyloides stercoralis (1.2%). Males and individuals with severe or profound mental retardation were twice as likely to be positive for the presence of intestinal parasites as females and individuals with mild/moderate retardation. The relatively low prevalence found in this study compared with previous surveys suggests that management of parasitic infection is improving in conjunction with developments in delivery of medical and habilitative services.

Adolescent↗
PubMed1994

The growth response of Lin-Thy-1+ hematopoietic progenitors to cytokines is determined by the balance between synergy of multiple stimulators and negative cooperation of multiple inhibitors.

The present studies investigated the balance of positive and negative growth signals in direct regulation of hematopoiesis. Interleukin-3 (IL-3) combined with Steel factor (SLF) optimally stimulated proliferation of Lin-Thy-1+ murine bone marrow progenitors in single-cell assays, and that proliferation was inhibited more than 90% by transforming growth factor-beta 1 (TGF-beta 1). Colony-stimulating factor-1 (CSF-1), granulocyte-macrophage colony-stimulating factor (GM-CSF), IL-1, or IL-6 as a third stimulatory growth factor was incapable of counteracting the TGF-beta 1-mediated inhibition of IL-3-plus-SLF-stimulated growth, while G-CSF slightly enhanced the number of TGF-beta 1-resistant clones. As a fourth factor, only IL-1 could partially overcome the TGF-beta 1-induced growth inhibition. While the presence of a cocktail of five additional stimulatory growth factors did not enhanced the frequency of single Lin-Thy-1+ progenitors proliferating in response to IL-3 plus SLF, the number of responding progenitors in the presence of TGF-beta 1 was enhanced nine-fold. Furthermore, tumor necrosis factor-alpha (TNF-alpha) and interferon-gamma (IFN-gamma), but not macrophage inflammatory protein-1 alpha (MIP-1 alpha), cooperated with TGF-beta 1 to reverse the proliferative effects of multiple stimulatory cytokines, resulting in 76% inhibition. Thus, the direct effects of single inhibitory factors on hematopoietic progenitor cell growth can be reversed by multiple stimulatory growth factors, and negative growth factors can directly cooperate to suppress progenitor cell growth stimulated by multiple positive-acting factors.

Animals↗
PubMed1992

Anti-muscarinic activity of a family of C11N5 compounds isolated from Agelas sponges.

In a search for potential target sites for C11N5 compounds obtained from marine sponges of the genus Agelas we evaluated their interaction with muscarinic acetylcholine receptors from rat brain membranes. In competition experiments with 3H-QNB these compounds displayed the following rank order of potency: sceptrin greater than oroidin greater than or equal to dibromosceptrin greater than or equal to clathrodin. Sceptrin (50 microM) was shown to be a competitive inhibitor of 3H-QNB binding as revealed by Scatchard analysis. The results demonstrate the ability of these compounds to interact with multiple target molecules in the micromolar range.

Alkaloids↗
PubMed1992

[Determination of plasma concentration of amiodarone and desethylamiodarone with high pressure liquid chromatography. Preliminary experience].

A simple specific and sensitive high pressure liquid chromatography method (HPLC) to measure amiodarone and desethylamiodarone is described. The plasma sample is deproteinized with acetonitrile and a 50 ul aliquote run in the HPLC system with reverse phase column (C-18). Methanol-ammonium hydroxide is used to separate and spectrophotometric measurements are read at 254 nm.95% of the drug present in plasma is extracted with this method, with a sensitivity of 0.03 ug/ml and a day to day variation under 3%. Preliminary measurements were analyzed in 14 subjects receiving amiodarone for treatment of supraventricular arrhythmia. With a mean dose of 267 +/- 116 (SD) mg/day, plasma levels of 1.3 +/- 0.6 ug.ml for amiodarone and 0.9 +/- 0.5 mg/ml for desethylamiodarone were obtained.

Adult↗
PubMed1991

Monoclonal antibody with specificity to a conserved epitope in the C-terminal domain of histone H1 variants.

A monoclonal type M-immunoglobulin (IgM) was generated in mice against a nuclease-urea extract of HeLa metaphase chromosomes. This antibody stains metaphase chromosomes from a variety of mammalian cultured cell types by indirect immunofluorescence. Antibody 12C7 reacts by western transfer technique with histone H1 in all the cell lines tested. The antibody cross-reacts with H1, and H1(0) in human cells. Proteolytic digestions of H1 suggest that the epitope is localized in the carboxy-terminal domain of the histone H1 molecule. Digestion with trypsin demonstrates that the antibody 12C7 does not react with the globular domain of histone H1. The C-terminal domain of H1 subtypes therefore seems to have a conserved determinant which does exist in H1, H1(0), and probably in H5. This antibody has applications in studying the role of that domain of H1 in processes like chromosome condensation and variations in chromatin structure which influence gene expression.

Antibodies, Monoclonal↗
PubMed1991

Heparin-induced hyperkalemia: a prospective study.

Heparin is frequently used for the prophylaxis and treatment of deep venous thromboembolism and it induces hypoaldosteronism leading to hyperkalemia, an uncommon adverse effect. In an intensive prospective drug monitoring study, 154 inpatients at the Internal Medicine Unit of Hospital Sotero del Río, Santiago, Chile, received heparin in the period between March and November 1990. Mean age of the patients was 65.8 +/- 12.9 years and 56.5% were female. Twenty-one (13.6%) patients developed heparin-induced adverse reactions. Thirteen events were hyperkalemia, 7 ecchymoses and 1 hematuria. The monitoring team and attending physicians have agreed to classify 9 heparin-induced hyperkalemia cases as probable and the other 4 as possible. No adverse reaction was fatal but 8 of the patients had severe hyperkalemia. Almost all reactions were dose-related. Hyperkalemia was more frequent in patients with diabetes mellitus, metabolic acidosis and long-term heparin therapy. The frequency of hyperkalemia did not correlate with age, sex, renal impairment or with previous use of anti-inflammatory drugs, heparin or aspirin.

Adolescent↗
PubMed1991

[Myocardial contraction and ventricular function in normal subjects evaluated with isotopic ventriculography and phase analysis].

Normal heart contraction was studied in 20 healthy subjects (14 males and 6 female, mean age 33 years). Rest radioventriculography and phase analysis were used. Ejection fraction was 66 +/- 7% for the LV and 53 +/- 7% for the RV (p < 0.0001). Peak filling rates in the first third of diastole were 1.6 +/- 0.6 EDV/sec for the LV and 0.7 +/- 0.3 EDV/sec for RV (p < 0.0001). Time to peak filling rate normalized for heart rate was 180 +/- 52 ms for the LV and 203 +/- 60 ms for the RV (p = 0.05). Filling fractions were 23 +/- 10% and 9 +/- 3%, respectively (p < 0.0001). Segmental motility was normal in all subjects. Phase analysis revealed faster emptying of the left atrium with phase angles of 171 +/- 13 degrees in the LA and 185 +/- 12 degrees in the RA (p = 0.00007). This difference may be related to faster diastolic events in the left ventricle. Phase angles for the LV and RV were -8.75 +/- 3 and -9.44 +/- 5 degrees, respectively (NS). We conclude that activation occurs earlier in the left atrium, proceeds through the septum and then synchronically over both ventricles.

Adolescent↗
PubMed1990

Tumor necrosis factor production by Kupffer cells requires protein kinase C activation.

Tumor necrosis factor (TNF) has been proposed as a primary inflammatory mediator of septic shock. In vitro and in vivo studies indicate that endotoxin- or lipopolysaccharide (LPS)-activated macrophages are a principle source of TNF; however, membrane signal transduction and intracellular pathways by which LPS triggers TNF production in macrophages are unclear. Recent evidence indicates that specific protein phosphorylation via activation of protein kinase C (PKC) is an early, critical step in the signaling of macrophage TNF production by phorbol esters. We hypothesize that PKC activation is also required in LPS-signaled Kupffer cell (KC) TNF production. Murine KCs were obtained by liver perfusion and digestion and then stimulated with LPS (Escherichia coli O111:B4) or LPS in the presence of H-7, a selective PKC inhibitor. Conditioned media was collected at 3 hr for assay of TNF utilizing the L929 cytolysis bioassay standardized to murine-rTNF-alpha. We found that H-7 inhibited significantly LPS signaled TNF release at a concentration of 10 microM, while H-8 (a cyclic nucleotide specific inhibitor) had no effect. The effect of H-7 was dose dependent and present at varying concentrations of LPS. Down regulation of PKC activity by preincubation of KCs with phorbol myristate acetate (PMA, a direct activator of PKC) also resulted in significantly reduced TNF release after LPS stimulation. The inhibitor H-7 (10 microM) also significantly inhibited LPS signaled prostaglandin E2 release in Kupffer cells. Total and specific intracellular protein phosphorylation was determined by trichloroacetic acid precipitation and SDS-polyacrylamide gel electrophoresis after labeling stimulated Kupffer cells with 32Pi. Total protein phosphorylation was not significantly altered by LPS stimulation; however, autoradiograms from PMA- and LPS-stimulated KCs demonstrate enhanced phosphorylation of a 40-kDa protein (2.7 +/- 0.9-fold) and a 33-kDa protein (3.1 +/- 1.0-fold) which were inhibited by H-7. We conclude that activation of PKC and protein phosphorylation are required steps in the signal transduction pathway of LPS-stimulated TNF production in Kupffer cells.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1990

Simple disturbance of the dam in the neonatal period can alter haloperidol-induced catalepsy in the adult offspring.

Three experiments were performed to determine whether apparently minimal disturbances of dams and litters would influence haloperidol-induced akinesia. In Experiment I, Long-Evans hooded rats (a) were left unmanipulated, (b) received nestcage relocation and observation, (c) received nestcage relocation/observation and maternal separation, or (d) received nestcage relocation/observation and pup handling. The male adult offspring received open-field testing and later received forepaw-on-dowel catalepsy testing following saline, morphine (20 mg/kg), or haloperidol (2 mg/kg). In Experiment II, hooded rats received (a) no manipulation, (b) nestcage relocation, (c) maternal separation, or (d) pup handling. At weaning, dams were tested in the open-field. Activity wheel locomotion of the offspring was assessed following saline or haloperidol for 3 days/week for 3 weeks; then, 5 and 7 days later, rats received haloperidol (0.5 mg/kg) and catalepsy testing. In both experiments, manipulations involving the dam reduced the offsprings' haloperidol-induced catalepsy, but, in Experiment II, a history of haloperidol administration distinguished between the effects of nestcage relocation and maternal separation. In Experiment III, Swiss albino mice received (a) no treatment, (b) nestcage relocation and maternal separation, (c) relocation/separation and mild cold stress of pups, (d) relocation/separation and pup handling, or (e) relocation/separation and severe cold stress of pups. Adult male mice received saline or haloperidol (2.5 mg/kg) and inclined grid catalepsy testing. Mice receiving relocation/separation and mice receiving relocation/separation and severe cold stress showed enhanced catalepsy versus control mice. Thus, it was concluded that seemingly innocuous events in infancy can influence the intensity of extrapyramidal side effects of neuroleptics in adulthood.

Animals↗
PubMed1990

Hepatic acute phase protein synthesis is indirectly regulated by tumor necrosis factor.

It has been proposed that tumor necrosis factor (TNF) is a direct regulator of postinjury hepatic protein synthesis. To test this hypothesis we investigated the total protein and specific acute phase protein synthesis response of murine hepatocytes to stimulation with mu-rTNF-alpha in vivo and in vitro. Total hepatocyte secretory protein synthesis was assessed by incorporation of [35-S] methionine into TCA-precipitated protein; and acute phase protein synthesis was assessed by induction of a 23-kD acute phase protein marker and by suppression of albumin synthesis determined by SDS-PAGE and autoradiography. We found that rTNF in vivo (8,000 units, IP injection) was associated with reduced total hepatocyte secretory protein synthesis (29 +/- 10%), increased synthesis of the 23-kD acute phase reactant (4.1 +/- 1.6-fold), and decreased albumin synthesis (0.68 +/- 0.2-fold) compared to saline-injected control animals. The in vitro stimulation of cultured murine hepatocytes directly with rTNF failed to demonstrate changes in total secretory protein synthesis or 23-kD protein; however, it did result in significant suppression of albumin synthesis (0.82 +/- 0.1-fold). In additional experiments, hepatocytes:nonparenchymal cell co-cultures stimulated with lipopolysaccharide (LPS) demonstrated protein synthesis changes similar to the in vivo TNF response including increased 23-kD protein and decreased albumin synthesis. These co-cultures demonstrated TNF production; however, addition of TNF antiserum during LPS stimulation had no effect on either 23-kD protein or albumin synthesis, despite the complete neutralization of TNF activity in the co-culture supernatants.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute-Phase Proteins↗
PubMed1990

[Post-traumatic hemobilia caused by arteriobiliary fistula. A case report and review of the literature].

One new case of post-traumatic hematobilia due to an arteriobilary fistula is reported. This etiology is relatively rare, and its diagnosis is sometimes difficult if the three signs: pain, bleeding and jaundice are not observed. The most effective paraclinical examination still is selective arteriogrpahy, which makes the diagnosis possible, accurately locates the fistula and sometimes allows hyperselective embolization, as it did in this case. The use of embolization for the treatment of post-traumatic hematobilia due to an arteriobiliary fistula reduces operative mortality for this disease, which still has a poor prognosis.

Adult↗
PubMed1989

Kinetic diversity of Na+ channel bursts in frog skeletal muscle.

Individual Na+ channels of dissociated frog skeletal muscle cells at 10 degrees C fail to inactivate in 0.02% of depolarizing pulses, thus producing bursts of openings lasting hundreds of milliseconds. We present here a kinetic analysis of 87 such bursts that were recorded in multi-channel patches at four pulse potentials. We used standard dwell-time histograms as well as fluctuation analysis to analyze the gating kinetics of the bursting channels. Since each burst contained only 75-150 openings, detailed characterization of the kinetics from single bursts was not possible. Nevertheless, at this low kinetic resolution, the open and closed times could be well fitted by single exponentials (or Lorentzians for the power spectra). The best estimates of both the open and closed time constants produced by either technique were much more broadly dispersed then expected from experimental or analytical variability, with values varying by as much as an order of magnitude. Furthermore, the values of the open and closed time constants were not significantly correlated with one another from burst to burst. The bursts thus expressed diverse kinetic behaviors, all of which appear to be manifestations of a single type of Na+ channel. Although the opening and closing rates were dispersed, their average values were close to those of alpha m and 2 beta m derived from fits to the early transient Na+ currents over the same voltage range. We propose a model in which the channel has both primary states (e.g., open, closed, and inactivated), as well as "modes" that are associated with independent alterations in the rate constants for transition between each of these primary states.

Animals↗