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Biomedical subjects

M Espinoza

Publications and source records attributed to M Espinoza.

At least 19 recordsLinked to original sources

An adaptive input-output modeling approach for predicting the glycemia of critically ill patients.

In this paper we apply system identification techniques in order to build a model suitable for the prediction of glycemia levels of critically ill patients admitted to the intensive care unit. These patients typically show increased glycemia levels, and it has been shown that glycemia control by means of insulin therapy significantly reduces morbidity and mortality. Based on a real-life dataset from 15 critically ill patients, an initial input-output model is estimated which captures the insulin effect on glycemia under different settings. To incorporate patient-specific features, an adaptive modeling strategy is also proposed in which the model is re-estimated at each time step (i.e., every hour). Both one-hour-ahead predictions and four-hours-ahead simulations are executed. The optimized adaptive modeling technique outperforms the general initial model. To avoid data selection bias, 500 permutations, in which the patients are randomly selected, are considered. The results are satisfactory both in terms of forecasting ability and in the clinical interpretation of the estimated coefficients.

Aged↗

Population genetic data for 18 STR loci in Costa Rica.

Allele frequencies for 18 STR autosomal loci (D3S1358, VWA, FGA, D8S1179, D21S11, D18S51, D5S818, D13S317, D7S820, D16S539, TH01, TPOX, CSF1PO, Penta D, Penta E, D19S433, D2S1338 and SE33) were obtained from a sample of 191-500 unrelated individuals from Costa Rica, Central America.

Costa Rica↗

Cyclosporine-associated leukoencephalopathy in organ transplant recipients: experience of three clinical cases.

Leukoencephalopathy is a structural alteration of cerebral white matter mainly involving damage to myelin. Several reports have linked cyclosporine (CsA) with this alteration. The clinical features vary from qualitative alterations of consciousness to neurological deficits. Magnetic resonance imaging (MRI) of the brain demonstrates the damage to the white matter, which is essential for the differential diagnosis. We describe three clinical cases of leukoencephalopathy. The first case is a 43-year-old man received a cadaveric kidney transplant using immunosuppression with of mycophenolate mofetil, prednisone, and CsA. Four months later he developed meningism and bilateral sixth nerve palsy. The second case is a 50-year-old man with a cadaveric kidney transplant received immunosuppressive treatment with azathioprine and prednisone. As a result of gouty arthritis of the ankle, azathioprine was replaced with CsA to allow addition of allopurinol. Two weeks later he developed confusion and personality changes. The third case is a 16-year-old man received a orthotopic liver transplant. Postoperatively he suffered generalized tonic-clonic seizures. In all patients the CsA levels were toxic and signs of neurological alterations were present on MRI. All patients recovered rapidly after CsA withdrawal.

Adolescent↗

Impact of pregnancy on the function of transplanted kidneys.

INTRODUCTION: This study reviewed the course of pregnancies in terms of impact on renal function and delivery-related data among women who received kidney transplants in our unit. METHODS: We reviewed the medical records of women transplanted between 1982 and 2002 who became pregnant. We recorded the data of medical, obstetrical, and transplant-related complications, plasma creatinine levels, and blood pressures at baseline, delivery, and 12 months after delivery. RESULTS: Thirty women had 37 pregnancies. Immunosuppressive protocols included cyclosporine, ketoconazole, azathioprine, and prednisone in 22 patients or azathioprine and prednisone in 15. Renal function decreased significantly: mean creatinine levels at baseline, delivery, and after 1 year were: 1.19 +/- 0.38 mg/dL; 1.44 +/- 0.70 mg/dL; and 1.38 +/- 0.53 mg/dL, respectively (P = .023 and P = .004 vs baseline respectively). Systolic and diastolic blood pressures at delivery were higher than at baseline (134 +/- 19 and 86 +/- 14 mm Hg vs 126 +/- 21 and 79 +/- 13 mm Hg (P = .029 and P = .053, respectively). These values normalized 1 year later (128 +/- 21 and 80 +/- 16). Decreased use of antihypertensive drugs were the cause of poor blood pressure control (1.8 +/- 1.3 vs 0.9 +/- 0.7, P < .01). Blood pressure control improved following delivery. The most frequent complications were preeclampsia (18.9%), intrahepatic cholestasis (13.5%), and urinary tract infections (13.5%). There were five rejection episodes. Seven miscarriages took place and one mole. Eleven pregnancies were uncomplicated. CONCLUSION: Renal transplantation is the best treatment for fertile women with end-stage renal disease who want to become pregnant. However, pregnancy is risky for the mother, fetus, newborn, and allograft.

Blood Pressure↗

[Reference values of growth hormone binding protein (GHBP) for a normal pediatric population].

UNLABELLED: Circulating concentrations of the high affinity growth hormone binding protein (GHBP) may be a marker of GH receptor density as well as GH sensitivity. GOAL: To determine values of GHBP for a normal Chilean pediatric population. METHODS: We determined GHBP levels in 73 males and 73 females between 4 to 15.5 years and 4 to 16.8 years respectively, divided in 7 groups according to age and puberal status. RESULTS: The population was normally distributed in weight, height and body mass index (BMI). GHBP activity increased up to Tanner IV in males and Tanner III in females, and decreased slightly thereafter in Tanner V and IV respectively. There was a significant difference between GHBP levels of preschool children and those found in Tanner II to V in both sexes (p < 0.05). In addition, we found a positive correlation between GHBP vs weight, height and BMI (p < 0.001) in males and females. CONCLUSION: The availability of this methodology allows us to establish the normative value of GHBP in our population and provides useful information to interpret GH circulating levels in children with growth disorders.

Adolescent↗

Macrophage migration inhibitory factor release by macrophages after ingestion of Plasmodium chabaudi-infected erythrocytes: possible role in the pathogenesis of malarial anemia.

Human falciparum malaria, caused by Plasmodium falciparum infection, results in 1 to 2 million deaths per year, mostly children under the age of 5 years. The two main causes of death are severe anemia and cerebral malaria. Malarial anemia is characterized by parasite red blood cell (RBC) destruction and suppression of erythropoiesis (the mechanism of which is unknown) in the presence of a robust host erythropoietin response. The production of a host-derived erythropoiesis inhibitor in response to parasite products has been implicated in the pathogenesis of malarial anemia. The identity of this putative host factor is unknown, but antibody neutralization studies have ruled out interleukin-1beta, tumor necrosis factor alpha, and gamma interferon while injection of interleukin-12 protects susceptible mice against lethal P. chabaudi infection. In this study, we report that ingestion of P. chabaudi-infected erythrocytes or malarial pigment (hemozoin) induces the release of macrophage migration inhibitory factor (MIF) from macrophages. MIF, a proinflammatory mediator and counter-regulator of glucocorticoid action, inhibits erythroid (BFU-E), multipotential (CFU-GEMM), and granulocyte-macrophage (CFU-GM) progenitor-derived colony formation. MIF was detected in the sera of P. chabaudi-infected BALB/c mice, and circulating levels correlated with disease severity. Liver MIF immunoreactivity increased concomitant with extensive pigment and parasitized RBC deposition. Finally, MIF was elevated three- to fourfold in the spleen and bone marrow of P. chabaudi-infected mice with active disease, as compared to early disease, or of uninfected controls. In summary, the present results suggest that MIF may be a host-derived factor involved in the pathophysiology of malaria anemia.

Anemia↗

Omental transplantation for Alzheimer's disease.

The acetylcholine, dopamine, serotonin and other neurotransmitters may be reduced in the subcommissural regions even in the early stages of Alzheimer's disease(AD), due to hypoperfusion of the anterior perforating and anterior choroidal arteries. This hypothesis was confirmed after the transplant of omental tissue on the optic chiasma, carotid crotch and anterior perforated space in a woman with moderate AD. Neurological improvement was better in the first week after the surgery than in the following months.

Alzheimer Disease↗

[Usefulness of the measurement of insulin-like growth factor (IGF-I) and IGF-1 binding protein-3 (IGFBP-3) for the diagnosis of growth hormone (GH) deficiency in children].

BACKGROUND: The diagnosis of GH deficiency (GHD) is based upon the results of GH stimulation tests, which have several drawbacks. AIM: To evaluate the usefulness of IGF-1 and IGFBP-3 for the diagnosis of GHD in prepuberal children. MATERIAL AND METHODS: We measured IGF-I and IGFBP-3 in three group of subjects: I. GHD (n: 24), height < -2SD for age (Z score, average +/- SD: -4.2 +/- 1.2), growth velocity < p10 (3.4 +/- 1.0 cm/year) and peak GH level on two GH stimulation tests < 7 ng/ml (1.2 +/- 0.6 ng/ml); II. Short non-GHD (NGHD, n: 32), height of -2.7 +/- 0.9 SD for age, growth velocity < p 25 (3.9 +/- 1.2 cm/year), and peak GH level on two GH stimulation tests > 7 ng/ml (15.3 +/- 6.9 ng/ml), y III. Normal school children (n: 35) with normal heights (-0.17 +/- 0.12 SD) were studied as controls. RESULTS: IGF-1 and IGFBP-3 were significantly lower in GHD than in NGHD and controls (p < 0.001), and in NGHD than in C (p < 0.001). We defined the normal range of both proteins as +/- 2 SD of the mean of the control group. Using this criteria, IGF-I was low in 21/24 GHD, and in 12/32 NGHD. IGFBP-3 was low in 22/24 GHD, and in 6/32 NGHD. Only 1 GHD patient had both exams in the normal range, suggesting that he is probably NGHD. 4/32 of the NGHD and both exams below normal range, suggesting that they are probably GHD. CONCLUSIONS: IGF-1 and IGFBP-3 are important tools for the diagnosis of GHD.

Child↗

Tumor necrosis factor alpha as a uremic toxin: correlation with neuropathy, left ventricular hypertrophy, anemia, and hypertriglyceridemia in peritoneal dialysis patients.

Tumor necrosis factor alpha (TNF alpha) is usually excreted by the kidney. In dialysis patients, it accumulates. TNF alpha has been implicated in the pathogenesis of malnutrition, diabetic neuropathy, and erythropoietin resistance. We studied TNF alpha plasma levels in 49 stable peritoneal dialysis (PD) patients, with the aim of correlating those levels with the presence and severity of peripheral neuropathy, hypertrophic cardiomyopathy, and anemia. Kt/Vurea' residual renal creatinine clearance (CrC), nutritional markers, and general biochemistry were also determined. The average plasma level of TNF alpha was 67 +/- 32 pg/mL (range: 18.1-156.3 pg/mL; normal value 3-20 pg/mL). No correlation was observed between TNF alpha and KT/Vurea' but a negative correlation with CrC was seen (r: -0.37, p < 0.05). TNF alpha levels were higher in patients with neuropathy as compared to patients with normal results (72.5 +/- 32 pg/mL vs 44 +/- 22 pg/mL, p < 0.05). Patients with neuropathy also showed a lower CrC value (1.5 +/- 1.7 mL/min vs 3.9 +/- 2.6 mL/min, p < 0.01). TNF alpha levels were higher in patients with left ventricular hypertrophy (LVH) with respect to normal individuals (70.4 +/- 32 pg/mL vs 38.5 +/- 20.8 pg/mL, p < 0.05). Patients with severe LVH showed the lowest CrC value. A direct, significant relationship was found between TNF alpha levels and weekly erythropoietin dose (r: 0.41, p < 0.05). Patients with hypertriglyceridemia or taking lipid-lowering agents showed a positive linear correlation between TNF alpha and triglycerides (r = 0.7, n = 14, p < 0.05). These data suggest that accumulation of TNF alpha may contribute to the development or maintenance of some neurologic, hematologic, and cardiac complications of uremic syndrome. Loss of residual renal function conditions an increment in TNF alpha levels. These data continue to add support to the idea that TNF alpha may be considered a uremic toxin.

Adult↗

Induction of the chemokine beta peptides, MIP-1 alpha and MIP-1 beta, by lipopolysaccharide is differentially regulated by immunomodulatory cytokines gamma-IFN, IL-10, IL-4, and TGF-beta.

The macrophage occupies a central role in the host response to invasion, exerting its control over the developing inflammatory response largely through the elaboration of an assortment of endogenous mediators including many cytokines. The beta chemokine peptides, macrophage inflammatory protein [MIP]-1 alpha and MIP-1 beta, are two such effectors markedly up-regulated in macrophages following exposure to bacterial lipopolysaccharide (LPS). These highly homologous peptides, like the other members of the beta chemokine family, exhibit diverse but partially overlapping biological activity profiles, suggesting that the cellular participants and intensity of an inflammatory response may in part be regulated by selective expression of these chemokines. Studies reported here demonstrate that, in contrast to the "balanced" MIP-1 alpha/MIP-1 beta chemokine responses of LPS-stimulated macrophage cultures in vitro, circulating levels of MIP-1 beta are significantly higher than those of MIP-1 alpha following LPS administration in vivo. Further studies have revealed that several immunomodulatory cytokines known to be up-regulated in vivo as a consequence of exposure to an invasive stimulus (gamma-IFN, IL-10, IL-4, and transforming growth factor [TGF]-beta) down-regulated the LPS-induced release of MIP-1 alpha by macrophages in vitro, but spared the MIP-1 beta response. This altered pattern of secretion may explain, at least in part, the high circulating levels of MIP-1 beta relative to MIP-1 alpha observed in vivo in response to LPS challenge.

Animals↗

Effect of renutrition on the proliferation kinetics of PHA stimulated lymphocytes from malnourished children.

The fraction of lymphocytes that responded to phytohemagglutinin (PHA) stimulation and initiated cellular proliferation (stimulation index or SI) was determined in groups of healthy and severely malnourished children. SI was determined again in the latter group after a period of nutritional recovery. The proportion of interphasic cells showing PHA response was assessed adding bromodeoxyuridine to the culture, so proliferative nuclei appear big and stain light blue, with dispersed granular chromatin and apparent nucleoli, while non-proliferative nuclei look small, stain red, and have compact and homogeneous chromatin. In mitotic nuclei, differential staining of sister chromatids made it possible to distinguish cells that had gone through one, two and three or more proliferation cycles. Based on the data obtained from interphase nuclei and mitosis, the SI was estimated at 48 and 72 h of culture. SI were higher in lymphocytes from healthy children than in those from children with severe malnutrition, even after the period of nutritional recovery. However, the SI was significantly higher in lymphocytes from malnourished children after nutritional recovery. Although in these children more cells are stimulated, there seems to be still damage that causes a cycling delay.

Bromodeoxyuridine↗

Context-specific sensitization to naloxone-precipitated withdrawal in hamsters: effect of pimozide.

Three experiments were conducted to investigate the development of context-specific sensitization to naloxone-precipitated withdrawal in hamsters. In Experiment 1, animals in group M/S were given morphine (15 mg/kg) injections in a distinctive environment and saline in the home cage. Animals in group S/M were given saline in the distinctive environment and morphine in the home cage, and animals in group S/S were given saline in both environments. All groups were challenged subsequently with naloxone (0.4 mg/kg) in the distinctive environment and then observed for signs of opiate withdrawal. The results showed that group M/S gave more naloxone-precipitated withdrawal signs than each of the other groups, which did not differ from one another. Experiment 2 was designed to test the effect of pimozide on context-specific sensitization to naloxone-precipitated withdrawal. The design was similar to that of Experiment 1 but group P/M/S, which received an injection of pimozide (0.5 mg/kg) 4 h prior to morphine, was added. The results indicated that context-specific sensitization developed as in Experiment 1, except among animals treated with pimozide. Experiment 3 was designed to determine whether pimozide interferes with the development or the expression of context-specific sensitization. Six groups, differing in the frequency and timing of the pimozide injection, were employed. The results indicated that pimozide interfered with context-specific sensitization, whenever it was given. It is concluded that pimozide interferes with the expression of context-specific sensitization, although a separate effect on the development of sensitization is not ruled out.

Animals↗

Sister-chromatid exchange (SCE) and cell proliferation in lymphocytes from infected and non-infected children with severe protein calorie malnutrition (PCM).

The frequency of sister-chromatid exchanges (SCE) and the rate of cell proliferation were evaluated through differential staining of sister chromatids in mitogen-stimulated cultured lymphocytes sampled from five well-nourished children, from seven severely malnourished children infected with bacterium, and from 10 severely malnourished children following treatment for infection with antimicrobial drugs 2 weeks before blood sampling. The replication indices at 48 h of culture were higher in both groups of malnourished children than in the well-nourished children, indicating either a faster response to PHA and/or a shorter cell cycle in lymphocytes of these patients. The average frequency of SCE per mitosis was also significantly higher than in the control group. The mitotic index was similar in the three groups of children. The lack of significant difference in response between the two groups of malnourished children suggests that the effects observed at the cytogenetic level are caused by severe malnutrition per se, and not by any associated infection.

Cell Division↗

[Focal and segmental glomerulosclerosis in renal transplantation].

In 179 patients subjected to 186 renal transplants, 30 renal biopsies were performed due to the presence of a proteinuria over 3.5 g/24 h or due to a reduction in glomerular filtration rate. Six of these biopsies, coming from 5 patients, disclosed morphological alterations compatible with focal segmental glomeruloesclerosis. Five of these were due to recurrence of the primary disease (in four patients) and in all, massive proteinuria appeared from 1 to 23 days after transplantation. Two patients with three transplants, evolved to renal failure and required dialysis in a period 12 months as a mean. The third patient, developed a nephrotic syndrome without renal failure and died 14 months after the renal transplant due to a stroke. In the fourth patient, the nephrotic syndrome disappeared 38 days after the transplant and remained with minimal proteinuria until his last follow up visit two years later. The primary disease of the fifth patient is unknown; the nephrotic syndrome appeared 68 months after the transplant and remitted spontaneously in 2 months. The renal biopsy showed focal and segmental lesions with partial effacement of epithelial foot processes. It is concluded that focal segmental glomerulosclerosis recurrence in renal transplant occurs with early massive proteinuria and frequently leads to renal failure and graft loss in no more than two years.

Adolescent↗

Omental transplantation in the management of chronic traumatic paraplegia. Case report.

A 27 year old male patient with chronic traumatic paraplegia received an omental transplant to the spinal cord. During surgery we found 40 percent of the spinal cord hypotrophied, with vascular alterations and abundant scar tissue. Some neurological improvement already started a few days postoperatively. After 36 months of postoperative follow-up he presents with right crural monoparesis (grade 1-4), deep sensation and with sphincter control.

Adult↗