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Biomedical subjects

J del Castillo

Publications and source records attributed to J del Castillo.

At least 19 recordsLinked to original sources
PubMed2000

Epidemiological, clinical and control investigations on field porcine coccidiosis: clinical, epidemiological and parasitological paradigms?

For several reasons, we are convinced that the parasitologist community must look again at porcine neonatal coccidiosis. We find it surprising that this disease is seldom addressed, and that assumptions are not always supported by clinico-epidemiological analysis. For example, the relationship between diarrhoea and the excretion of oocysts during experimental infection versus field infection is not questioned. Lindsay et al. review parasitological knowledge of this disease in the latest (1999) edition of Diseases of swine. Although this paper is divided into two parts, we have three distinct objectives: (1) to bring to the debate our experience in the medical control of this disease; (2) to propose a diagnostic methodology; (3) to raise some questions on various clinical, epidemiological and parasitological unknowns.

Animals↗
PubMed1999

The prolonged hematologic effects of a single injection of PEG-rHuMGDF in normal and thrombocytopenic mice.

A single injection of > or =10 microg/kg PEG-rHuMGDF in mice causes a dose-dependent increase in circulating platelets beginning on day 3 and peaking on days 5-6. The mean platelet volume and platelet distribution width at doses > or =100 microg/kg initially increase in a dose-dependent fashion and later decrease. However, the mean platelet volume does not change when platelets are incubated with PEG-rHuMGDF in vitro. The number of marrow megakaryocytes increases in a dose-dependent fashion as early as day 1 and peaks on day 3. Marrow megakaryocyte colony-forming units (CFU-Meg) do not increase on days 1-3 at a dose of 100 microg/kg (a dose that increases platelet numbers two- to threefold and may be clinically relevant), but the relative frequency of high ploidy megakaryocytes and the proportion of large marrow megakaryocytes (29-50 microm in diameter) increases. After a dose of 1,000 microg/kg the percentage of megakaryocytes in mitosis peaks at 24-48 hours and the percentage of megakaryocytes incorporating BrdU is maximal at 48 hours, the relatively delayed peak of BrdU incorporation most likely representing endomitosis. The relative frequency of type II and III megakaryocytes peaks on days 3 and 4, respectively. Pharmacokinetic analysis of PEG-rHuMGDF shows peak serum concentrations at 2-4 hours and a terminal half-life of 11.4+/-2.5 hours. A single injection of PEG-rHuMGDF ameliorates carboplatin-induced megakaryocytopenia and thrombocytopenia in a dose-response dependent fashion. In conclusion, a single injection of PEG-rHuMGDF increases megakaryocyte and platelet production in normal and myelo-suppressed mice.

Acetylcholinesterase↗
PubMed1999

PEG-rHuMGDF promotes multilineage hematopoietic recovery in myelosuppressed mice.

PEG-rHuMGDF administered to normal mice is a lineage-specific growth factor for megakaryocytes and platelets as judged by morphologic examination of hematologic cells in marrow and peripheral blood smears. The purpose of this study was to document that PEG-rHuMGDF in myelosuppressed mice promotes multilineage hematopoietic recovery. High-dose 5-fluorouracil (5-FU) in mice results in profound myelosuppression and 0-30% survival. Mice receiving a single dose of PEG-rHuMGDF (1000 microg/kg) 1 day after 5-FU (225 mg/kg) demonstrate an increased survival (76% vs 27% in control mice at 14 days). Compared to surviving controls, PEG-rHuMGDF-treated mice not only show the expected higher platelet counts, but also increased marrow colony-forming unit granulocyte-macrophage, increased multilineage marrow cellularity, and increased neutrophil, monocyte, and lymphocyte counts in peripheral blood. PEG-rHuMGDF- and vehicle-treated mice both develop hepatic abscesses after 5-FU treatment, but the abscesses in the PEG-rHuMGDF-treated mice contain more neutrophils, suggesting that myeloid reconstitution contributes to their survival. Furthermore, survival in 5-FU-treated mice is significantly improved by granulocyte colony-stimulating factor and antibiotics, suggesting that infection rather than thrombocytopenia is the predominant cause of death. PEG-rHuMGDF after 5-FU promotes survival accompanied by accelerated lymphohematopoietic repopulation, suggesting that PEG-rHuMGDF, a lineage-specific thrombopoietic factor in normal mice, promotes multilineage hematopoietic recovery in myelosuppressed mice.

Animals↗
PubMed1997

Anemia and perinatal death result from loss of the murine ecotropic retrovirus receptor mCAT-1.

The mCAT-1 gene encodes a basic amino acid transporter that also acts as the receptor for murine ecotropic leukemia viruses. Targeted mutagenesis in embryonic stem cells has been used to introduce a germ-line null mutation into this gene. This mutation removes a domain critical for virus binding and inactivates amino acid transport activity. Homozygous mutant pups generated from these cells were approximately 25% smaller than normal littermates, very anemic, and died on the day of birth. Peripheral blood from homozygotes contained 50% fewer red blood cells, reduced hemoglobin levels, and showed a pronounced normoblastosis. Histological analyses of bone marrow, spleen, and liver showed a decrease in both erythroid progenitors and mature red blood cells. Mutant fetal liver cells behaved normally in in vitro hematopoietic colony-forming assays but generated an anemia when transplanted into irradiated C.B.-17 SCID mice. Furthermore, reconstitution of the white cell compartment of SCID mice by mutant fetal liver cells was less complete than that observed with a mixed population of wild-type and heterozygous fetal liver cells. Primary embryo fibroblasts from mutant mice were completely resistant to ecotropic retrovirus infection. Thus, mCAT-1 not only appears to be the sole receptor for a group of murine ecotropic retroviruses associated with hematological disease but also plays a critical role in both hematopoiesis and growth control during mouse development.

Anemia↗
PubMed1996

Systemic hematologic effects of PEG-rHuMGDF-induced megakaryocyte hyperplasia in mice.

PEG-rHuMGDF injected daily in normal mice causes a rapid dose-dependent increase in megakaryocytes and platelets. At the same time that platelet numbers are increased, the mean platelet volume (MPV) and platelet distribution width (PDW) can be either decreased, normal, or increased depending on the dose and time after administration. Thus, PEG-rHuMGDF at a low dose causes decreases in MPV and PDW, MGDF at an intermediate dose causes an initial increase followed by a decrease in MPV and PDW, and PEG-rHuMGDF at higher doses causes an increase in MPV and PDW followed by a gradual normalization of these platelet indices. In addition to the expected thrombocytosis after 7 to 10 days of daily injection of high doses of PEG-rHuMGDF, a transient decrease in peripheral red blood cell numbers and hemoglobin is noted accompanied in the bone marrow by megakaryocytic hyperplasia, myeloid hyperplasia, erythroid and lymphoid hypoplasia, and deposition of a fine network of reticulin fibers. Splenomegaly, an increase in splenic megakaryocytes, and extramedullary hematopoiesis accompany the hematologic changes in the peripheral blood and marrow to complete a spectrum of pathologic features similar to those reported in patients with myelofibrosis and megakaryocyte hyperplasia. However, all the PEG-rHuMGDF-initiated hematopathology including the increase in marrow reticulin is completely and rapidly reversible upon the cessation of administration of PEG-rHuMGDF. Thus, transient hyperplastic proliferation of megakaryocytes does not cause irreversible tissue injury. Furthermore, PEG-rHuMGDF completely ameliorates carboplatin-induced thrombocytopenia at a low-dose that does not cause the hematopathology associated with myelofibrosis.

Anemia↗
PubMed1996

A prospective study of in-line skating: observational series and survey of active in-line skaters--injuries, protective equipment, and training.

OBJECTIVES: 1) To assess the relationship between types of injuries incurred and training and protective equipment worn by adults injured while in-line skating; 2) to observe the type and amount of protective equipment worn by in-line skaters while skating; and 3) to survey active in-line skaters about formal training, protective equipment, and history of injuries incurred, and the effect of such injuries on the protective equipment subsequently worn. METHODS: A prospective study of consecutive adult patients presenting to the ED for evaluation of in-line skating injuries; a consecutive-series observational study of active in-line skaters to assess protective equipment worn; and a survey of selected active in-line skaters. Eighty-five adult patients were included who presented with a history of injury related to in-line skating to the EDs of an urban academic medical center, a suburban academic-affiliated hospital, and a community hospital. Four hundred eleven active in-line skaters on the Chicago lakefront were observed for protective equipment worn, 91 of whom participated in the survey. RESULTS: Of those presenting to the ED with injuries, only 15% indicated that they had received formal in-line skating instruction. Of the ED patients, 50% wore no protective equipment; overall, 6% wore a helmet; 44%, wrist protection; 23%, knee protection; and 19%, elbow protection. Only 2% wore all of the above equipment. The primary mechanism of injury reported was a loss of balance (58%); others included collision with objects (25%), collision with bicycles (11%), and collision with cars (5%). Fractures or dislocations occurred in 48% of the patients; 6% had head injuries necessitating CT scans. Those who wore no protective gear were more likely to require hospital admission (p < 0.05). Of the 411 in-line skaters observed, 157 (38%) wore no protective equipment. Compared with the injured group presenting to the ED, fewer observed participants were without protection (p < 0.05). Among those surveyed, prior injury was not associated with the subsequent use of protective gear. CONCLUSION: Patients who present to the ED for evaluation of in-line skating injuries have a high incidence of fractures/dislocations. Few injured or surveyed in-line skaters had formal training. Use of protective equipment by injured skaters was associated with a decreased likelihood of hospitalization. Observed in-line skaters more commonly wore protective gear than did those who presented to the ED with injuries.

Athletic Injuries↗
PubMed1995

Megakaryocyte growth and development factor ameliorates carboplatin-induced thrombocytopenia in mice.

Megakaryocyte growth and development factor (MGDF) administered intraperitoneally (IP) to mice causes a dose-dependent thrombocytosis accompanied by a decrease in mean platelet volume. MGDF increases the number of megakaryocytes in the bone marrow and spleen. MGDF does not affect the circulating number of leukocytes. Carboplatin, a chemotherapeutic agent that causes thrombocytopenia in humans, administered to mice as a single IP injection at a nonlethal dose causes a significant, but reversible thrombocytopenia. The carboplatin-induced thrombocytopenia is accompanied by an increase in circulating endogenous MGDF that precedes the return of circulating platelets to a normal level. MGDF mRNA is constitutively present in the liver. After carboplatin treatment, hepatic MGDF mRNA does not increase in concordance with circulating MGDF. Circulating soluble MGDF receptor levels (c-mpl) do not change significantly during the course of carboplatin-induced thrombocytopenia. MGDF injected IP once daily beginning 1 day after injection of carboplatin reverses carboplatin-induced thrombocytopenia in a dose-dependent fashion. The normalization of circulating platelet numbers in carboplatin plus MGDF-treated mice is accompanied by a normalization of megakaryocyte numbers in the bone marrow. In conclusion, MGDF, by increasing the number of marrow megakaryocytes and circulating platelets is an effective therapy for carboplatin-induced thrombocytopenia in mice.

Animals↗
PubMed1995

Hematologic effects of stem cell factor (SCF) and leukemia inhibitory factor (LIF) in vivo: LIF-induced thrombocytosis in SCF-primed mice.

Stem cell factor (SCF) administered as daily bolus injections in dose-response experiments in mice causes a progressive and dramatic dose-dependent panleukocytosis characterized by neutrophilia, eosinophilia, monocytosis, and lymphocytosis. SCF causes circulating platelet numbers to be dose-dependently increased after 2 weeks of daily injections. Leukemia inhibitory factor (LIF) administered as daily bolus injections in mice causes a peripheral leukopenia that is largely due to peripheral lymphopenia. LIF causes thrombocytosis peaking after approximately 1 w. Coinjection of SCF and LIF for 1 to 2 wk in mice does not cause a much greater thrombocytosis than the maximum thrombocytosis achievable with SCF or LIF alone. On the other hand, daily injection of SCF for 5 days followed by daily injection of LIF for 5 to 6 d in mice causes a very substantial increase in platelets that was lineage-specific in terms of not being accompanied by a generalized leukocytosis. In contrast, only a very modest thrombocytosis was noted in SCF-primed LIF-treated rats. LIF causes a large increase in the cytoplasmic volume of splenic megakaryocytes in mice, but not in rats. In conclusion, SCF-induced priming followed by LIF-induced maturation of megakaryocytes causes a substantial selective increase in the numbers of circulating platelets in mice.

Animals↗
PubMed1993

Granulocyte colony-stimulating factor crosses the placenta and stimulates fetal rat granulopoiesis.

We studied the effect of recombinant human granulocyte colony-stimulating factor (rhG-CSF) administration to pregnant rats upon fetal and neonatal myelopoiesis. Pregnant rats were treated with rhG-CSF twice daily for 2, 4, and 6 days before parturition. rhG-CSF crossed the placenta and reached peak fetal serum concentrations 4 hours after administration. Peak fetal serum levels were 1,000-fold lower than levels detected in the dam. Hematopoietic effects of rhG-CSF were assessed by cytologic analysis of the newborn blood, spleen, bone marrow, thymus, and liver. White blood cell counts were increased twofold to fourfold in newborns. This increase was due to circulating numbers of polymorphonuclear cells (PMN). rhG-CSF induced a myeloid hyperplasia in the newborn marrow consisting of immature and mature myeloid cells in the day-2 and day-4 treated pups. Bone marrow of pups treated for 6 days contained mostly hyper-segmented PMN with little or no increase in myeloid precursors. An increase in the number of postmitotic (PMN, bands, and metamyelocytes) and mitotic (promyeloblasts, myeloblasts, and metamyeloblasts) myeloid cells in the spleen of neonates was observed. No change was detected in splenic lymphocytes or monocytes. No effect of rhG-CSF was noted in the newborn liver or thymus. These results demonstrate that maternally administered rhG-CSF crosses the placenta and specifically induces bone marrow and spleen myelopoiesis in the fetus and neonate. The significant myelopoietic effects of rhG-CSF at low concentrations in the fetus suggest an exquisite degree of developmental sensitivity to this cytokine and may provide enhanced defense mechanisms to the neonate.

Animals↗
PubMed1993

Maternal administration of granulocyte colony-stimulating factor improves neonatal rat survival after a lethal group B streptococcal infection.

Maternally administered recombinant human granulocyte colony-stimulating factor (rhG-CSF) has been shown to cross the placenta and induce a peripheral neutrophilia and increases in the marrow and spleen neutrophil storage pools in fetal and newborn rats. In the present study, we have used this model system to investigate the efficacy of prenatally administered rhG-CSF on neonatal defense to a lethal challenge with Group B-beta hemolytic Streptococcus (GBS). Pregnant rats were injected with rhG-CSF twice daily beginning 6 days before parturition. At birth, all pups were infected with a dose of GBS that is lethal for 90% of infected pups (LD90). Survival was monitored daily for 5 days. Survival of infected pups from saline-treated mothers beyond 60 hours after infection was 10%. No difference in survival was observed among pups from mothers treated 2 and 4 days before parturition. In contrast, we determined that survival was 82.5% among infected pups from mothers treated for 6 days before parturition with rhG-CSF. Our results demonstrate that maternal administration of rhG-CSF augments neonatal defenses against a lethal bacterial challenge.

Animals↗
PubMed1993

Influence of formamide on the electrical and mechanical properties of the guinea pig ventricle.

1. Guinea pig papillary muscle in vitro upon exposure of Formamide (FMD) exerts a dose dependent positive inotropic effect. 2. The increase in tension developed by papillary muscle is associated with a marked decrease in the duration of the action potential. 3. The increase in extracellular calcium concentration does not modify the positive inotropic effect, but increases the duration of the action potential. 4. FMD markedly potentiate the increase in tension induced by caffeine 3 M suggesting a possible synergetic effect upon the release of Ca2+ ions from the S.R. 5. These experiments suggest that FMD increases the intracellular calcium concentration by exerting a direct action on intracellular calcium stores.

Action Potentials↗
PubMed1993

Pharmacological sensitivity of the articular capsule of the primary spines of Eucidaris tribuloides.

1. This paper describes the effects of several cholinergic agonists and antagonists, and of beta-phenylethylamine (PEA) and some of its derivatives, on the articular capsule, or ligament, of the primary spines of Eucidaris tribuloides. 2. Carbamylcholine (CCh), methacholine (MeACh), nicotine, and muscarine exert a stiffening effect similar to that of acetylcholine (ACh), although the time course of their actions varies widely. 3. Atropine induced stiffening and blocked and responses to muscarine and MeACh. The responses to MeACh were blocked also by 4-diphenylacetoxy-N-methylpiperidine, suggesting the presence in the ligament of type M3 muscarinic receptors, in addition to nicotinic ones. d-Tubocurarine induced stiffness of the ligament and failed to block the responses to ACh and nicotine. 4. While ACh induced only a slight desensitization, CCh caused a long-lasting blockade of the stiffening effects of the cholinergic agonists. This shows that the receptors for ACh have a site or sites that recognize the ester moieties of these molecules. 5. Eserine and neostigmine potentiate the responses to acetylcholine, indicating the presence of acetylcholinesterase in the ligament. 6. beta-Phenylethylamine, epinephrine, norepinephrine, and dopamine induce diphasic responses; usually a brief softening followed by a slow and irreversible stiffening of the ligament. 7. In contrast to the above, tyramine and octopamine elicit a simple softening of ligaments which are stiff as a result of handling or by exposure to cholinergic agonists. However, tyramine and octopamine do not soften ligaments which become stiff as a result of exposure to adrenergic agonists.

Acetylcholine↗
PubMed1993

Contractile properties of the articular capsule or ligament, in the primary spines of the sea-urchin Eucidaris tribuloides.

1. The articular capsule or ligament, of the primary spines of the sea-urchin Eucidaris tribuloides behaves as a classical excitable tissue, responding with a shortening or contracture to a variety of stimuli including the cholinergic agonists acetylcholine (ACh), methacholine (MeACh), carbamylcholine (CCh) and nicotine. 2. d-Tubocurarine failed to decrease the amplitude of the acetylcholine-induced contractures, while the contractures elicited by methacholine were blocked by atropine. Neostigmine, but not eserine, increased the amplitude of ACh-induced contractures, suggesting the presence of AChE in the preparation. 3. The cholinergic agonists induced contracture of the ligament, but had quite different kinetics, the rate of rise of the contracture being fastest for ACh and decreasing in the following order: CCh, MeACh and nicotine. 4. Tyramine and octopamine exert an inhibitory action on "catch" and a relaxing effect on the contracting ligament. 5. The time courses of the contractures elicited in the same preparation were virtually identical to those of "catch". Therefore, we propose that "catch" and contracture are only two different aspects of the same phenomenon; namely the contracture of the muscle fibers present in the ligament.

Acetylcholine↗
PubMed1993

Hematologic effects of stem cell factor alone and in combination with G-CSF and GM-CSF in vivo and in vitro in rodents.

The intravenous injection of rrSCF causes neutrophilia and lymphocytosis as well as the appearance of immature myeloid cells and occasional blast cells in the circulation. The marrow shows a left-shifted myeloid and erythroid hyperplasia as evidenced by increases in numbers of morphologically recognizable early myeloid and erythroid precursors. A decrease in the number of mature marrow neutrophils is noted, suggesting that the release of marrow neutrophils contributes to the peripheral neutrophilia. After 2 weeks of daily injections of rrSCF, the marrow demonstrates a remarkable mast cell hyperplasia accompanied by erythroid and lymphoid hypoplasia. rrSCF causes mast cells to appear in the circulation and causes a systemic increase in embryonic connective tissue-type mast cells. In vitro long-term culture of mouse marrow cells with rrSCF results in an outgrowth of mast cells. The coinjection of rrSCF and G-CSF for 1 week causes a synergistic increase in mature marrow neutrophils accompanied by a striking decrease in erythroid and lymphoid marrow elements. Spleens demonstrate increased granulopoiesis as well as erythropoiesis as compared to the spleens of rats treated with single growth factors. Splenic extramedullary erythropoiesis may act to compensate for the decrease in marrow erythropoiesis. The coinjection of rrSCF and G-CSF causes an increase in marrow mast cells at the end of 1 week, but the increase is much less than in rats treated with rrSCF alone. The combination of rrSCF and G-CSF causes a synergistic peripheral neutrophilia. In vivo daily administration of SCF plus GM-CSF results in a synergistic increase in marrow neutrophils, but not the striking synergistic increase in circulating neutrophils that is observed after SCF plus G-CSF. Colony-forming assays reveal a synergistic increase in CFU-GMs in the marrow, but not in peripheral blood, after coincubation with SCF plus GM-CSF as opposed to GM-CSF alone, demonstrating anatomic compartmentalization between a more primitive marrow CFU-GM subset and a more mature peripheral blood CFU-GM subset.

Animals↗
PubMed1992

Endotoxin-induced cytokine gene expression in vivo. IV. Expression of interleukin-1 alpha/beta and interleukin-1 receptor antagonist mRNA during endotoxemia and during endotoxin-initiated local acute inflammation.

After the intravenous (IV) injection of endotoxin, (lipopolysaccharide [LPS]), in the rat, interleukin-1 alpha/beta (IL-1 alpha/beta) mRNA expression peaks at 1 hour in whole organ RNA preparations of the lung, liver, spleen, and bowel. Interleukin-1 receptor antagonist (IL-1ra) mRNA peaks at 2 to 4 hours, consistent with the hypothesis that IL-1ra acts as an endogenous negative feedback mechanism to downregulate the proinflammatory effects of IL-1. After the intratracheal (IT) injection of LPS, however, IL-1 and IL-1ra mRNA levels in whole lung peak at 6 hours, concurrent with the maximum influx of neutrophils (PMNs) into the bronchoalveolar space. To address the cellular source of IL-1 and IL-1ra mRNA in the lung during acute pneumonitis, mRNA levels were studied in bronchoalveolar lavage (BAL) macrophages incubated with LPS in vitro for 6 hours as compared with BAL cells (95% PMNs) obtained 6 hours after IT injection of LPS. A much greater expression of IL-1 and IL-1ra mRNA was observed in PMN-rich BAL cells obtained after IT injection of LPS, suggesting that PMNs contribute substantially to IL-1 and IL-1ra mRNA expression. Fractionation of alveolar macrophage-enriched and PMN-enriched subpopulations from the BAL cells obtained at 6 hours after IT injection of LPS confirmed that neutrophils are a source of IL-1 and IL-1ra mRNA. The difference in the kinetics of IL-1 and IL-1ra mRNA expression in whole lung RNA preparations after IV and IT injections of LPS is due to the contribution of PMNs that appear in the lung in large numbers after IT injection. Finally, human peripheral blood PMNs were found to express IL-1ra mRNA and protein after in vitro incubation with LPS. PMNs may contribute to the up- and downregulation of their own accumulation by expressing both IL-1 and IL-1ra.

Animals↗