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Bovine leukemia virus (BLV) is a retrovirus that primarily infects dairy cows. Although few studies have also used the tax gene, phylogenetic studies of BLV use mostly the env gene. The aim of this work was to establish the circulating genotypes of BLV in specialized dairy cattle from Antioquia, Colombia. Twenty blood samples from Holstein Friesian cows were collected, and their DNA was isolated. A PCR was performed for a partial region of the env and tax genes. A phylogenetic analysis was carried out using the maximum likelihood and Bayesian methods for both genes. Nineteen sequences were identified as genotype 1 by env and tax genes. Only one sequence was clustered with genotype 3 and had the highest proportion of different nucleotide sites compared to other strains. Four amino acid substitutions in the 134 amino acid residue fragment of the Env protein were identified in the Colombian sequences, and three new amino acid substitutions were reported in the 296 amino acid residue fragment of the Tax protein. R43K (Z finger), A185T (Activation domain), and L105F changes were identified in the genotype 3 sample. This genotype has been reported in the United States, Japan, Korea, and Mexico, but so far, not in Colombia. The country has a high rate of imported live animals, semen, and embryos, especially from the United States. Although it is necessary to evaluate samples from other regions of the country, the current results indicate the presence of two BLV genotypes in specialized dairy herds.
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Hemoglobin S is caused by a nucleotide change in HBB gene (HBB:c.20A>T, p.Glu6Val), is presented in diverse forms: simple carriers (HbSA), homozygotes (HbSS) also known as sickle cell anemia, and compound heterozygotes with other ß-hemoglobinopathies. It is worldwide distributed, in Mexico, is frequently observed in the southern states Guerrero, Oaxaca and Chiapas. Elevated fetal hemoglobin (HbF) is associated with mild phenotype; single-nucleotide variants (SNVs) in modifier genes, such as BCL11A, HBG2, HBBP1 pseudogene and HBS1L-MYB intergenic region, upregulate HbF synthesis. The aim of this study was to identify HbF regulating genetic variants in HbSS and HbSA Mexican subjects. We studied 39 individuals (HbSS = 24, 61%, HbSA = 15, 39%) from Chiapas (67%) and Guerrero (33%), peripheral blood was collected in ethylenediamine tetraacetic acid (EDTA) for molecular and hematological studies, DNA was isolated by salting-out technic and genotyping was performed through allelic discrimination by real time polymerase chain reaction (RT-PCR) using Taqman® probes for 15 SNV (in BCL11A: rs6706648, rs7557939, rs4671393, rs11886868, rs766432, rs7599488, rs1427407; HBS1L-MYB: rs28384513, rs7776054, rs9399137, rs4895441, rs9402686, rs1320963; HBG2: rs7482144; and HBBP1: rs10128556). The obtained data were analyzed using IMB SPSS v.22.0 software. All minor alleles were observed in frequencies over 0.05, the most frequent was rs9402686 (0.82), while the less frequent was rs101028556 (0.08). In HbSS group, the mean fetal hemoglobin was 11.9 ± 5.9% and was significantly elevated in BCL11A rs11886868 wildtype homozygotes and in carriers of HBS1L-MYB intergenic region rs7776054 (p = 0.04 and p = 0.03, respectively). In conclusion, in HbSS Mexican patients, two SNVs were observed related to increased HbF; BCL11A rs11886868 and HBS1L-MYB rs7776054.
Sickle cell anemia (SCA) is one of the most common types of hemoglobinopathies in people of African ancestry, it is caused by homozygosity of HbS mutation (HBB:c.20A>T). It is known that fetal hemoglobin plays a key role in decreasing HbS polymerization which damages the erythrocyte structure and is responsible for the characteristic hemolytic crises endured by these patients. Single-nucleotide variant (SNV) in genes that regulate fetal hemoglobin (HbF) after birth have been associated with its increment, thus ameliorating the hematologic phenotype of this pathology and other ß-hemoglobinopathies. Therefore, in this study, we identified, for the first time in Mexican patients with SCA (HbSS) and HbS carriers (HbSA), the presence of 15 SNVs on BCL11A, HBS1L-MYB and HBG2; all HbSS patients had anemia and elevated HbF; 2 variants were related to increased HbF rs11688888C of BCL11A and rs7776054G of HBSIL-MYB; and finally, all minor alleles were found at a frequency higher than 0.05.
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Anemia Falciforme , Hemoglobina Fetal , DNA Intergênico , Ácido Edético , Hemoglobina Fetal/genética , Hemoglobina Falciforme/genética , Heterozigoto , Homozigoto , Humanos , México , Nucleotídeos , Polimorfismo de Nucleotídeo Único , Proteínas Repressoras/genéticaRESUMO
Bovine leukemia virus (BLV) is a retrovirus that affects primarily milky cows. Animals serologically positive to BLV show a Th1 cytokine profile with a predominance of interferon gamma (IFN-γ). IFN-γ has antiviral activity through mechanisms such as resistance to infection, inhibition of viral replication and apoptosis. The objective of this work was to determine the transcription levels of IFN-γ and its relationship with proviral load and persistent lymphocytosis in a population of Holstein cows of the province of Antioquia, Colombia. IFN-γ transcription levels were evaluated by qPCR in 140 Holstein cows. A one-way analysis of variance and a Student's t test were used to evaluate the differences between the means. The amount of IFN-γ mRNA found in BLV-positive cows was lower than in BLV-negative cows. Moreover, in the group of infected cows a lower level of IFN-γ mRNA expression was found in BLV and persistent lymphocytosis cows (BLV+PL) compared with BLV and aleukemia cows (BLV+AL). The level of IFN-γ mRNA expression was lower in cows with high proviral load (HPL) compared to cows with low proviral load (LPL). BLV infection is related to abnormal expression of IFN-γ mRNA, although IFN-γ has antiviral activity, its expression is affected by high proviral load. Keywords: cytokine; immune system; leukemia; bovine leukemia virus.
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Leucose Enzoótica Bovina/imunologia , Interferon gama/genética , Linfocitose/veterinária , Carga Viral , Animais , Bovinos , Colômbia , Leucose Enzoótica Bovina/genética , Humanos , Vírus da Leucemia Bovina , Linfocitose/genética , Provírus , RNA MensageiroRESUMO
The coronavirus disease 2019 (COVID-19) is caused by the severe acute respiratory syndrome coronavirus2 (SARS-CoV-2) virus. COVID-19 affected more than 6million persons worldwide in fewer than 4 months, after the report of the first cases in China in December 2019. The relation of the disease caused by SARS-Cov-2 to immunosuppressive treatment used in different gastrointestinal disorders is uncertain, resulting in debate with regard to suspending immunosuppressive therapy to improve infection outcome. Said suspension implies the inherent risk for graft rejection or autoimmune disease exacerbation that can potentially worsen the course of the infection. Based on the presently available evidence, a treatment stance has been established for patients with gastrointestinal diseases that require immunosuppressive therapy.
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Infecções por Coronavirus/complicações , Imunossupressores/efeitos adversos , Imunossupressores/uso terapêutico , Hepatopatias/tratamento farmacológico , Pancreatopatias/tratamento farmacológico , Pandemias , Pneumonia Viral/complicações , COVID-19 , Humanos , Hepatopatias/complicações , Transplante de Fígado , Transplante de Pâncreas , Pancreatopatias/complicaçõesRESUMO
INTRODUCTION: Beta-thalassemia (ß-thal) is frequent in Mexican patients with microcytosis and hypochromia. We report three novel mutations and analyze the actual mutational spectrum in Mexican population. METHODS: One hundred and forty-nine ß-thal Mexican mestizo patients were studied (154 alleles). ARMS-PCR was performed to identify Cd39C>T, IVS1:1G>A, IVS1:110G>A, -28A>C, initiation codonA>G and IVS1:5G>A mutations, and gap-PCR for δß-thal Spanish type. DNA sequencing of HBB gene was carried out in negative samples for the initial screening. RESULTS: Fifteen different HBB gene mutations were observed in 148 alleles; three of them are novel: -90C>G, 20 bp deletion (at codons 78/85), and IVS2:2T>G; the mutation IVS1:6T>C that was observed for first time in our population; and eleven previously described mutations. Six alleles showed normal HBB sequence. To date, a total of 21 different mutations have been observed in Mexican patients; the four most frequent mutations are of Mediterranean origin: Cd39C>T (37.2%), IVS1:1G>A (17.3%), IVS1:110G>A (13.9%), and δß-thal Spanish type (9.0%), which represent 77.4% of the total studied alleles. CONCLUSION: Considering the novel mutations -90C>G, -20 bp Cd78/85, IVS2:2T>G and the first observation of IVS1:6T>C, the molecular spectrum of ß-thal in Mexicans comprises 21 different mutations, confirming the high allelic heterogeneity in Mexicans.
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Alelos , Mutação , Globinas beta/genética , Talassemia beta/genética , Adolescente , Adulto , Idoso , Criança , Pré-Escolar , Códon , Análise Mutacional de DNA , Éxons , Feminino , Heterogeneidade Genética , Genótipo , Humanos , Lactente , Íntrons , Masculino , México , Pessoa de Meia-Idade , Análise de Sequência de DNA , Adulto JovemRESUMO
INTRODUCTION: Alpha-thalassemia (α-thal) is a common monogenic disorder worldwide. In mixed ethnic populations, α-thal and beta-thalassemia (ß-thal) can be expected, sometimes giving complex phenotypes, which without molecular analysis are not easily explained. We performed the molecular identification of α- and ß-thal alleles in 51 Mexican patients with microcytosis, hypochromia, and normal or low levels of HbA2 . METHODS: Common deletional alleles (-α(3.7) , -α(4.2) , - -(SEA) , - -(MED) , - -(FIL) , - -(THAI) , -α(20.5) ) and α-triplication were studied by gap-PCR and nondeletional alleles (α(IVSI) ((-5nt)) , α2 (NcoI) , α1 (NcoI) ) by ARMS. ß-thal alleles Cd39 (C>T), IVS1:1 (G>A), IVS1:110 (G>A), and Spanish δß-thal were also investigated. DNA sequencing was performed on HBA2, HBA1, and HBB genes. Negative samples were subjected to MLPA. RESULTS: In 35 subjects, we identified the mutations, -α(3.7) , - -(SEA) , - -(FIL) , α(IVSI) ((-5nt)) , and ααα(anti3.7) and two novel deletion alleles - -(Mex1) (6.8-8.9 kb) and - -(Mex2) (77.6-135.7 kb). Four individuals also had a ß-thal allele (Cd39/IVS1:110). No α-thal alleles were observed in 16 subjects, but three had a ß-thal mutation Cd39, IVS1:110, and Spanish δß-thal. CONCLUSION: α-thal is relatively common in Mexican patients, the combination with ß-thal is sometimes unexpected, and this underlines the importance of performing molecular analysis for both α- and ß-genes defects in patients showing microcytic hypochromic anemia.
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Alelos , Anemia Hipocrômica/genética , Sequência de Bases , Hemoglobinas Glicadas/genética , Hemoglobinas Anormais/genética , Deleção de Sequência , Talassemia alfa/genética , Talassemia beta/genética , Feminino , Humanos , Masculino , MéxicoRESUMO
We investigated associations between vitamin D receptor (VDR) gene polymorphisms, FokI T>C (rs2228570), BsmI G>A (rs1544410), ApaI G>T (rs7975232), and TaqI T>C (rs731236), with bone mineral density (BMD) in postmenopausal Mexican-Mestizo women. Three hundred and twenty postmenopausal women participated, who were classified according to World Health Organization criteria as non-osteoporotic (Non-OP; N = 88), osteopenic (Opn; N = 144), and osteoporotic (OP; N = 88). BMD measurements at the lumbar (L1-L4) spine and at the left and right femoral neck were obtained by dual-energy X-ray absorptiometry. Single nucleotide polymorphisms (SNPs) were genotyped using real-time polymerase chain reaction and TaqMan probes. Genotype and allelic frequencies of the 4 VDR SNPs were similar among the 3 groups. Polymorphic allele frequencies were as follows: FokI (C) 0.53, 0.49, 0.56; BsmI (A) 0.26, 0.22, 0.23; ApaI (T) 0.43, 0.39, 0.44; TaqI (C) 0.27, 0.22, 0.23 for the Non-OP, Opn, and OP groups, respectively. Although no associations were found between the SNPs and BMD, based on the putative function of the FokI SNP, we constructed, for the first time, the haplotype with the 4 VDR SNPs, and found that the CGGT haplotype differed between the Non- OP and OP groups (21.8 vs 31.8%, P < 0.05). The risk analysis for this haplotype was nearly significant under the dominant model (OR = 1.783, 95%CI = 0.98-3.25, P = 0.058). This result suggests a possible susceptibility effect of the C allele of the FokI SNP for the development of osteoporosis in postmenopausal Mexican-Mestizo women.
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Densidade Óssea/genética , Osteoporose/genética , Polimorfismo de Nucleotídeo Único , Receptores de Calcitriol/genética , Idoso , Estudos de Casos e Controles , Feminino , Frequência do Gene , Estudos de Associação Genética , Haplótipos , Humanos , Indígenas Norte-Americanos/genética , México , Pessoa de Meia-Idade , Osteoporose/diagnóstico por imagem , RadiografiaRESUMO
Ad libitum feeding causes excessive follicular development and is associated with extensive metabolic changes in broiler - breeder hens. Restricting feed intake reduces excessive follicular development, but the mechanisms mediating this response are unknown. In the present study, the effects of feeding on follicular development in immature broil er - breeder hens were examined. There was an increase in the proportion of follicles 100 - 300, 300 - 500 and >500 μ m in diameter and a decrease in follicles <100 μ m in full - fed (FF) compared to restricted - fed (RF) hens. Increased follicular development in FF hens was associated with a greater expression of steroidogenic transcripts ( STAR, CYP11A1, HSD3B , and CYP19 ) within the ovarian cortex of FF hens. These transcripts represent markers of more advanced follicular development. However, increased follicular development in FF hens was not associated with changes in the expression of other factors previously implicated in follicular development, including those encoding TGF - beta ligands ( AMH, BMP6, BMP15 , or GDF9 ) or their signaling proteins (SMAD2/3 or SMAD1/5/9). Changes in histone modifications associated with proliferation, including trimethylated histone H3K4, trimethylated histone H3K27 , and acetylated histone H3K9 , we re also not different between treatment groups. However, feed restriction caused serine phosphorylation to localize strongly to the ovarian stroma of FF hens compared to RF hens. In contrast, phosphorylation of tyrosine residues localized more prominently to the surface of granulosa cells from RF hens. Thus, restricted feeding may enhance the efficiency of reproduction by suppressing early follicular development which is associated with changes in granulosa cell protein phosphorylation status.
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Animais , Células Estromais , Folículo Ovariano/anatomia & histologia , Fosforilação/fisiologia , Galinhas/classificação , Ração Animal/análiseRESUMO
Ad libitum feeding causes excessive follicular development and is associated with extensive metabolic changes in broiler - breeder hens. Restricting feed intake reduces excessive follicular development, but the mechanisms mediating this response are unknown. In the present study, the effects of feeding on follicular development in immature broil er - breeder hens were examined. There was an increase in the proportion of follicles 100 - 300, 300 - 500 and >500 μ m in diameter and a decrease in follicles <100 μ m in full - fed (FF) compared to restricted - fed (RF) hens. Increased follicular development in FF hens was associated with a greater expression of steroidogenic transcripts ( STAR, CYP11A1, HSD3B , and CYP19 ) within the ovarian cortex of FF hens. These transcripts represent markers of more advanced follicular development. However, increased follicular development in FF hens was not associated with changes in the expression of other factors previously implicated in follicular development, including those encoding TGF - beta ligands ( AMH, BMP6, BMP15 , or GDF9 ) or their signaling proteins (SMAD2/3 or SMAD1/5/9). Changes in histone modifications associated with proliferation, including trimethylated histone H3K4, trimethylated histone H3K27 , and acetylated histone H3K9 , we re also not different between treatment groups. However, feed restriction caused serine phosphorylation to localize strongly to the ovarian stroma of FF hens compared to RF hens. In contrast, phosphorylation of tyrosine residues localized more prominently to the surface of granulosa cells from RF hens. Thus, restricted feeding may enhance the efficiency of reproduction by suppressing early follicular development which is associated with changes in granulosa cell protein phosphorylation status.(AU)
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Animais , Folículo Ovariano/anatomia & histologia , Fosforilação/fisiologia , Células Estromais , Galinhas/classificação , Ração Animal/análiseRESUMO
The corpus luteum (CL) is a transient endocrine organ that is essential for maintenance of pregnancy in both ruminants and primates. The cellular and endocrine mechanisms that regulate the CL in these species have commonalities and some distinct and intriguing differences. Both species have similar cellular content with large luteal cells derived from the granulosa cells of the follicle, small luteal cells from follicular thecal cells, and large numbers of capillary endothelial cells that form the vasculature that has an essential role in optimal CL function. Intriguingly, the large luteal cells in ruminants grow larger than in primates and acquire a capacity for high constitutive progesterone (P4) production that is independent of stimulation from LH. In contrast, the primate CL and the granulosa lutein cells from primates continue to require stimulation by LH/CG throughout the luteal phase. Although the preovulatory follicle of women and cows had similar size and steroidogenic output (10 to 20 mg/h), the bovine CL had about ten-fold greater P4 output compared to the human CL (17.4 vs. 1.4 mg/h), possibly due to the development of high constitutive P4 output by the bovine large luteal cells. The continued dependence of the primate CL on LH/CG/cAMP also seems to underlie luteolysis, as there seems to be a requirement for greater luteotropic support in the older primate CL than is provided by the endogenous LH pulses. Conversely, regression of the ruminant CL is initiated by PGF from the nonpregnant uterus. Consequently, the short luteal phase in ruminants is primarily due to premature secretion of PGF by the nonpregnant uterus and early CL regression, whereas CL insufficiency in primates is related to inadequate luteotropic support and premature CL regression. Thus, the key functions of the CL, pregnancy maintenance and CL regression in the absence of pregnancy, are produced by common cellular and enzymatic pathways regulated by very distinct luteotropic and luteolytic mechanisms in the CL of primates and ruminants.
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The corpus luteum (CL) is a transient endocrine organ that is essential for maintenance of pregnancy in both ruminants and primates. The cellular and endocrine mechanisms that regulate the CL in these species have commonalities and some distinct and intriguing differences. Both species have similar cellular content with large luteal cells derived from the granulosa cells of the follicle, small luteal cells from follicular thecal cells, and large numbers of capillary endothelial cells that form the vasculature that has an essential role in optimal CL function. Intriguingly, the large luteal cells in ruminants grow larger than in primates and acquire a capacity for high constitutive progesterone (P4) production that is independent of stimulation from LH. In contrast, the primate CL and the granulosa lutein cells from primates continue to require stimulation by LH/CG throughout the luteal phase. Although the preovulatory follicle of women and cows had similar size and steroidogenic output (10 to 20 mg/h), the bovine CL had about ten-fold greater P4 output compared to the human CL (17.4 vs. 1.4 mg/h), possibly due to the development of high constitutive P4 output by the bovine large luteal cells. The continued dependence of the primate CL on LH/CG/cAMP also seems to underlie luteolysis, as there seems to be a requirement for greater luteot ropic support in the older primate CL than is provided by the endogenous LH pulses. Conversely, regression of the ruminant CL is initiated by PGF from the nonpregnant uterus. Consequently, the short luteal phase in ruminants is primarily due to premature secretion of PGF by the nonpregnant uterus and early CL regression, whereas CL insufficiency in primates is related to inadequate luteotropic support and premature CL regression. Thus, the key functions of the CL, pregnancy maintenance and CL regression in the absence of pregnancy, are produced by common cellular and enzymatic pathways regulated by very distinct luteotropic and luteolytic mechanisms in the CL of primates and ruminants.
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Animais , Corpo Lúteo/anatomia & histologia , Endocrinologia/métodos , Folículo Ovariano/anatomia & histologia , Progesterona , Primatas/fisiologia , Ruminantes/fisiologiaRESUMO
The corpus luteum (CL) is a transient endocrine organ that is essential for maintenance of pregnancy in both ruminants and primates. The cellular and endocrine mechanisms that regulate the CL in these species have commonalities and some distinct and intriguing differences. Both species have similar cellular content with large luteal cells derived from the granulosa cells of the follicle, small luteal cells from follicular thecal cells, and large numbers of capillary endothelial cells that form the vasculature that has an essential role in optimal CL function. Intriguingly, the large luteal cells in ruminants grow larger than in primates and acquire a capacity for high constitutive progesterone (P4) production that is independent of stimulation from LH. In contrast, the primate CL and the granulosa lutein cells from primates continue to require stimulation by LH/CG throughout the luteal phase. Although the preovulatory follicle of women and cows had similar size and steroidogenic output (10 to 20 mg/h), the bovine CL had about ten-fold greater P4 output compared to the human CL (17.4 vs. 1.4 mg/h), possibly due to the development of high constitutive P4 output by the bovine large luteal cells. The continued dependence of the primate CL on LH/CG/cAMP also seems to underlie luteolysis, as there seems to be a requirement for greater luteot ropic support in the older primate CL than is provided by the endogenous LH pulses. Conversely, regression of the ruminant CL is initiated by PGF from the nonpregnant uterus. Consequently, the short luteal phase in ruminants is primarily due to premature secretion of PGF by the nonpregnant uterus and early CL regression, whereas CL insufficiency in primates is related to inadequate luteotropic support and premature CL regression. Thus, the key functions of the CL, pregnancy maintenance and CL regression in the absence of pregnancy, are produced by common cellular and enzymatic pathways regulated by very distinct luteotropic and luteolytic mechanisms in the CL of primates and ruminants.(AU)
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Animais , Corpo Lúteo/anatomia & histologia , Endocrinologia/métodos , Folículo Ovariano/anatomia & histologia , Progesterona , Ruminantes/fisiologia , Primatas/fisiologiaRESUMO
AIM: The purpose of this study was to estimate the effect sizes of drug interactions on plasma clozapine concentrations, adjusting for potentially confounding factors such as smoking. METHODS: The estimation was performed by using a mixed model, and a combination of unpublished (N=83) and published (N=172) data that included patients taking phenobarbital, valproic acid, fluvoxamine, fluoxetine, paroxetine, sertraline, citalopram and reboxetine, and patients not taking co-medications. RESULTS: The 255 patients provided a total of 415 steady-state trough plasma clozapine concentrations. Each patient provided 1 to 15 measures of plasma clozapine concentrations. Total plasma clozapine concentration, defined as the sum of plasma clozapine and norclozapine concentrations, was also investigated. A random intercept linear model of the natural log of plasma clozapine concentration with the natural log of dose and other variables as independent variables was built. The model confirmed that phenobarbital induces clozapine metabolism (effect size, E=-28%), and that fluoxetine (E=+42%), fluvoxamine (E=+263%) and paroxetine (E=+30%) inhibit it. Valproic acid appeared to inhibit clozapine metabolism in non-smokers (effect size, E=+16%), whereas it appeared to induce clozapine metabolism in smokers (E=-22%). The effect sizes of smoking on plasma clozapine concentration were -20% in patients not taking valproic acid, and -46% in patients taking valproic acid. Thus, smoking induces clozapine metabolism, and this induction may be stronger when the patient is taking valproic acid. The effect sizes allowed the computation of clozapine dose-correction factors for phenobarbital, 1.4 [95% confidence interval, CI, (1.1, 1.7)]; paroxetine, 0.77 (0.67, 0.89); fluoxetine, 0.70 (0.64, 0.78); fluvoxamine, 0.28 (0.22, 0.35); and valproic acid [0.86 (0.75, 1.0) in non-smokers, and 1.3 (0.96, 1.73) in smokers]. Sertraline, reboxetine and citalopram had no obvious effects. DISCUSSION: The results for total plasma clozapine concentrations are similar to those for plasma clozapine concentrations. The main limitations of this study were that the computed effect sizes reflect only the doses and treatment-durations of the co-medications studied, and that the substantial "noise" of the clinical environment may make it difficult to detect the effects of some variables, particularly those with small effect sizes. Gender was not significant probably due to its relatively small effect size in the studied population, and age was not significant probably due to the limited age variability. CONCLUSION: This article contributes to the clozapine literature by describing a possible interaction between taking valproic acid and smoking, which modifies plasma clozapine concentrations, by estimating the effect sizes of other compounds on plasma clozapine concentrations after correcting for confounders, and by providing dose-correction factors for clinicians.
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Antipsicóticos/sangue , Clozapina/sangue , Fatores de Confusão Epidemiológicos , Modelos Lineares , Transtornos Psicóticos/sangue , Antipsicóticos/uso terapêutico , Clozapina/análogos & derivados , Clozapina/uso terapêutico , Feminino , Humanos , Masculino , Transtornos Psicóticos/tratamento farmacológico , Valores de Referência , Pesos e MedidasRESUMO
OBJECTIVE: Asses if Abdominal Compartment Syndrome (ACS) increases the morbidity and mortality of the Pediatric Intensive Care Unit patients and if early recognition and intervention with decompressive therapy will alter outcome and decrease mortality. SETTING: Pediatric Intensive Care Unit of the University Pediatric Hospital-UPR. PATIENTS: All patients admitted to the PICU from July 1, 1999 to June 30, 2002 were enrolled in the study. Those having a distended and/or tense abdomen on physical examination were identified at risk for intra-abdominal hypertension (IAH). IAH was diagnosed if the intra-abdominal pressure (IAP) was above 10 mmHg and with ACS if the IAH was accompanied by: hemodynamic instability, oliguria or anuria, metabolic acidosis and respiratory deterioration. MEASUREMENTS AND MAIN RESULTS: 1052 patients were admitted to PICU. Ten patients with evidence of ACS were identified with an incidence of 0.9. Ages ranged from 6 weeks to 12.3 years. Peak intravesical pressure measurements ranged from 17 to 39 mmHg. Inspiratory pressure was raised from a mean of 21.2 to 32.0 cmH2O. The PCO2 increased from a mean of 35.1 to 63 torr and the pH decreased from a mean of 7.40 to 7.12. Overall mortality was 40for this patient population. CONCLUSIONS: The outcome of pediatric critical care patients depends on multiple variables. Now there is evidence that in a select group of patients IAH and ACS play a significant role in their morbidity and mortality. This makes it mandatory for clinicians taking care of this population to be increasingly aware of this condition.
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Humanos , Masculino , Feminino , Lactente , Síndromes Compartimentais/diagnóstico , Síndromes Compartimentais/terapia , Abdome , Criança , Pré-Escolar , Diagnóstico Precoce , Unidades de Terapia Intensiva PediátricaRESUMO
Five factor analyses with limitations explored the Suicidal Intent Scale (SIS) subscales reflecting suicidal behavior dimensions. This larger sample study conducts an exploratory factor analysis of the SIS. Two large samples of suicide attempters (N= 435 and N= 252) from a general hospital were studied. The validity of SIS subscales obtained from the factor analysis was investigated by examining the association between the subscales and clinical variables. There were two factors: expected lethality and planning. In both samples, male gender and depression tended to be associated with higher scores in both subscales (small to medium effect sizes). Hospitalization was associated with higher scores in both SIS subscales (medium to large effects) suggesting that these subscales were reasonably good predictors of suicide attempt severity. Clinicians assessing patient reports to establish the severity of suicide attempts need to ask questions regarding both dimensions: expected lethality and planning.
Assuntos
Tentativa de Suicídio/psicologia , Suicídio/psicologia , Adulto , Comportamento , Análise Fatorial , Feminino , Humanos , Masculino , Transtornos Mentais/psicologia , Escalas de Graduação Psiquiátrica , Recidiva , Reprodutibilidade dos Testes , Suicídio/estatística & dados numéricos , Tentativa de Suicídio/estatística & dados numéricosRESUMO
BACKGROUND: Both clinical and laboratory evidence in exposed seronegative (ESN) individuals to human HIV-1 has suggested the existence of mechanisms of natural resistance to the infection. A 32 base-pair deletion in the gene that codes for the CCR5, which is the main coreceptor for HIV-1, confers a high degree of resistance to HIV-1 infection. However, the genotype Delta32/Delta32 is present only in 2-4% of Caucasoid ESN individuals suggesting the existence of other mechanisms of protection. Mutations different from Delta32 have also been proposed as playing a role in resistance/susceptibility to this infection. OBJECTIVE: To screen for different mutations along the entire coding region of the ccr5 gene that can potentially explain the persistent seronegativity in a group of ESN individuals. STUDY DESIGN: Of a total of 86 individuals analyzed for Delta32 mutation by the PCR technique, 36 scored HIV seropositive (SP) and 50 were ESN. The entire group of ESN individuals was screened for other mutations in the ccr5 gene by single strand conformational polymorphism (SSCP) and DNA sequencing. RESULTS: The frequency of the mutant allele Delta32 was 4% (4/100) for ESN individuals and 4.2% (3/72) for SP individuals. The homozygous mutant genotype (Delta32/Delta32) was found in only 2% (1/50) of ESN individuals, but in no SP individuals. The heterozygous genotype was found in 8.3% (3/36) of SP individuals and in 4% (2/50) of ESN individuals. The differences in the allelic and genotypic frequencies among the groups were not statistically significant. A comparison between the observed and the expected genotypic frequencies showed that they were significantly different for the ESN group, suggesting a protective, yet indirect effect of the mutant genotype. CONCLUSIONS: The screening of the entire coding region of the ccr5 gene in all ESN did not revealed no other mutations that could account for resistance to HIV-1 infection. Although the CCR5 molecule is the most important coreceptor for HIV-1, mutations in this gene do not account for most of the cases of natural resistance to this virus that have so far been reported.
Assuntos
Infecções por HIV/genética , Soronegatividade para HIV/genética , HIV-1 , Receptores CCR5/genética , Alelos , Frequência do Gene , Infecções por HIV/imunologia , Soronegatividade para HIV/imunologia , Humanos , Imunidade Inata , MutaçãoRESUMO
BACKGROUND: In humans, measurement of maximum oxygen uptake is important because it is related to cardiovascular health. In Mexico there is scanty information in nationals and unfortunately such a data has been gathered from laboratory and field indirect methods ignoring reliability, validation and cross validation. PURPOSE: This study was designed to determine the validity and reliability of the 1,000 meters walk-run test in adults. METHODS: Fifty-one healthy subjects (31 men and 20 women) participated in four maximal tests; two in a laboratory on a treadmill for direct measurement of VO2max (L1 and L2) and twice in a track for distance walk-run time in 1,000 meters (C1 and C2). Values were analyzed by interclass correlation, Pearson product moment and "t" test. RESULTS: The VO2max in L1 y L2 were 2.67 and 2.70 L.min-1, (R = 0.97) and 44.2 and 46.2 mL.kg-1.min-1, meanwhile VO2max estimated from field were 44.2 and 46.2 mL.kg-1.min-1, (R = 0.98). Pearson correlation obtained from all subjects between laboratory and field test was of r = 0.88, without significant difference (P > 0.05). From those data we development the following equation: VO2max = 71.66-5.85 (t), where 71.66 and 5.85 are constants and t is the time employ in performing the test, R = -0.86, (p < 0.05). CONCLUSION: The 1,000 meters distance walk-run for time is highly reliable and valid test for estimation of VO2max in Mexican people. The test is safe, easy and short and can be administrated with a minimal amount of equipment. We propose its utilization in other population in order to perform cross validation.
Assuntos
Teste de Esforço , Consumo de Oxigênio , Adulto , Feminino , Humanos , MasculinoRESUMO
Repeated exposure to human immunodeficiency virus (HIV) does not always result in seroconversion. Modifications in coreceptors for HIV entrance to target cells are one of the factors that block the infection. We studied the frequency of Delta-32 mutation in ccr5 gene in Medellin, Colombia. Two hundred and eighteen individuals distributed in three different groups were analyzed for Delta-32 mutation in ccr5 gene by polymerase chain reaction (PCR): 29 HIV seropositive (SP), 39 exposed seronegative (ESN) and 150 individuals as a general population sample (GPS). The frequency of the Delta-32 mutant allele was 3.8% for ESN, 2.7% for GPS and 1.7% for SP. Only one homozygous mutant genotype (Delta-32/Delta-32) was found among the ESN (2.6%). The heterozygous genotype (ccr5/Delta-32) was found in eight GPS (5.3%), in one SP (3.4%) and in one ESN (2.6%). The differences in the allelic and genotypic frequencies among the three groups were not statistically significant. A comparison between the expected and the observed genotypic frequencies showed that these frequencies were significantly different for the ESN group, which indirectly suggests a protective effect of the mutant genotype (Delta-32/Delta-32). Since this mutant genotype explained the resistance of infection in only one of our ESN persons, different mechanisms of protection must be playing a more important role in this population.