Transgenerational effects of childhood conditions on third generation health and education outcomes.

This paper examines the extent to which pre-puberty nutritional conditions in one generation affect productivity-related outcomes in later generations. Recent findings from the biological literature suggest that the so-called slow growth period around age 9 is a sensitive period for male germ cell development. We build on this evidence and investigate whether undernutrition at those ages transmits to children and grandchildren. Our findings indicate that third generation males (females) tend to have higher mental health scores if their paternal grandfather (maternal grandmother) was exposed to a famine during the slow growth period. These effects appear to reflect biological responses to adaptive expectations about scarcity in the environment, and as such they can be seen as an economic correctional mechanism in evolution, with marked socio-economic implications for the offspring.

IL-6 572 C/G, 190 C/T, and 174 G/C gene polymorphisms in children's malnutrition.

OBJECTIVES: The aim of the present study was to establish the correlations between the polymorphisms of the genes interleukin-6 (IL-6) 572, 190, and 174 in children's malnutrition. METHODS: We assessed 283 hospitalized children and divided them into 2 groups: group I (control) included 110 patients with normal nutritional status, median (range) age 10.90 (1-18) years; and group II consisted of 173 malnourished patients, median (range) age 10.70 (1-18) years. RESULTS: The 2 groups underwent IL-6 572 cytosine allele (C)/guanine allele (G), 190 C/thymine allele (T), and 174 G/C polymorphism testing, measurement of anthropometric indicators (mid-upper arm circumference and tricipital skinfold thickness [TST]), and paraclinical evaluation (protein, albumin). We observed that the GG and CG genotypes were more frequent in malnourished children for the IL-6 174 gene (P = 0.0001), whereas the CT heterozygous genotype was more frequent in the malnourished group for the IL-6 190 gene (P = 0.003). Body mass index (BMI), middle upper arm circumference (MUAC), TST, and low serum albumin levels correlated with the GG and CG genotypes of the IL-6 572 and IL-6 174 genes, and with the CT genotype of the IL-6 190 gene, in children with malnutrition, whereas the IL-6 190 TT genotype was a protective factor for malnutrition (P = 0.0001). CONCLUSIONS: Malnutrition is more frequently associated in children with IL-6 174 G allele carriers (GG and CG genotypes), whereas IL-6 190 TT genotype has a protective function. In malnourished children, the IL-6 572/190/174 GG/CT/CG, GG/CT/GG, GG/CC/GG, and GG/CC/CG combined genotypes are more frequent.

Correlación clínica- para-clínica en un escolar con hipertensión porta de etiología a esclarecer / Clinical-paraclinical in a school with portal hypertension to determine

La hipertensión porta (HTP) es el resultado del incremento de la presión dentro del sistema venoso porta. Se presenta con poca frecuencia en el paciente pediátrico pero es una de las mayores causas de morbilidad y mortalidad en el niño con enfermedad hepática. La mayoría de los pacientes con http presentan un estado hiperdinámico, lo cual aumenta el flujo venoso porta y mantiene la hipertensión. Puede ser secundaria a obstrucción a nivel prehepático, intrahepático o extrahehepático.

Portal hypertension (PH) is the result of increased pressure within the portal venous system. It occurs infrequently in the pediatric patient but it is a major cause of morbidity and mortality in children with liver disease. Most patients with PH have a hyperdynamic state, which increases venous flow and portal hypertension remains. May be secondary to obstruction at prehepatic, intrahepatic or extrahehepatic.

Stress and body mass index each contributes independently to tumor necrosis factor-alpha production in prepubescent Latino children.

This investigation extended prior work by determining if stress and body mass index (BMI) contributed independently to tumor necrosis factor-alpha (TNF-alpha) levels among prepubescent Latino children and if sex and family history of type 2 diabetes mellitus (T2DM) modified these relationships. Data were collected in South Florida from 112 nondiabetic school-aged Hispanic children, of whom 43.8% were obese (BMI >/= 95th percentile) and 51.8% presented with a family history of T2DM. Stressful life events were assessed via parental report using a life events scale. Plasma TNF-alpha levels were determined with enzyme-linked immunosorbent assay. The relative contributions of stress and BMI with TNF-alpha levels and the potential interaction effects of sex and family history of T2DM were analyzed with multiple linear regression analyses. Stress and BMI each accounted for a significant proportion of the unique variance associated with TNF-alpha. The association between stress and TNF-alpha was not modified by sex or family history of T2DM. These findings implicate BMI and stress as independent determinants of TNF-alpha (an inflammatory cytokine and adipocytokine) among Latino children. Future investigations should examine the potential roles of exercise, nutritional status, age, and growth hormone in explicating the relationship between TNF-alpha production and psychosocial distress and risk for infection among obese children.

Expression of cytokine mRNA in lymphocytes of malnourished children.

INTRODUCTION: Protein-calorie malnutrition represents a significant worldwide health problem and is associated with an increased risk for infections. The purpose of this study was to evaluate possible changes in type 1/type 2 responses balance in malnourished children. RESULTS: The data obtained in the present study showed that the expression levels of tumor necrosis factor-alpha, interleukin (IL)-4, and IL-10 were more highly, in contrast IL-2, gamma interferon, and IL-6 genes were expressed less in all groups of malnourished children compared with the well-nourished infected children. It is important to indicate that the data collected in the present work agree with the results obtained by different authors, who showed differences in the production of cytokines in malnourished children. CONCLUSION: In conclusion, the results suggest that alterations in the balance of type 1/type 2 immune responses exist in malnourished children, and this could be the reason that the immunological system of the malnourished children is incapable of eradicating infections.

Susceptibility to DNA damage induced by antibiotics in lymphocytes from malnourished children.

Infectious disease and malnutrition in children are public health problems in developing countries. Malnutrition is associated with higher levels of DNA damage, and this increased damage could be due to different factors, including the possibility that cells from malnourished children could be more susceptible to environmental damage. The aim of the present study was to evaluate the susceptibility of lymphocytes from malnourished children to DNA damage induced by antibiotics by using the comet assay. The same group of malnourished infected children were studied before and after a treatment period, and compared to a group of well-nourished infected children. Results showed that before and after drug treatment, tail length migration was two times greater in malnourished than in well-nourished children. The proportion of cells with high damage was also increased in malnourished children. Additionally in well-nourished and malnourished children, a cell subpopulation (non-damaged cells) more resistant to DNA damage induced by antibiotics was observed; this was more prevalent in the well-nourished children. Meanwhile, in malnourished children, a cell population seems to be more susceptible and reaches higher levels of DNA damage. This might help explain the impaired immune response observed in malnourished children. The increased DNA migration and the increased proportion of cells with higher levels of damage seem to indicate that malnourished children are more susceptible to DNA damage induced by drugs.