Aldo Ângelo Moreira Lima

Household food access and child malnutrition: Results from the eight-country MAL-ED study

BackgroundStunting results from decreased food intake, poor diet quality, and a high burden of early childhood infections, and contributes to significant morbidity and mortality worldwide. Although food insecurity is an important determinant of child nutrition, including stunting, development of universal measures has been challenging due to cumbersome nutritional questionnaires and concerns about lack of comparability across populations. We investigate the relationship between household food access, one component of food security, and indicators of nutritional status in early childhood across eight country sites.MethodsWe administered a socioeconomic survey to 800 households in research sites in eight countries, including a recently validated nine-item food access insecurity questionnaire, and obtained anthropometric measurements from children aged 24 to 60 months. We used multivariable regression models to assess the relationship between household food access insecurity and anthropometry in children, and we assessed the invariance of that relationship across country sites.ResultsAverage age of study children was 41 months. Mean food access insecurity score (range: 0–27) was 5.8, and varied from 2.4 in Nepal to 8.3 in Pakistan. Across sites, the prevalence of stunting (42%) was much higher than the prevalence of wasting (6%). In pooled regression analyses, a 10-point increase in food access insecurity score was associated with a 0.20 SD decrease in height-for-age Z score (95% CI 0.05 to 0.34 SD; p = 0.008). A likelihood ratio test for heterogeneity revealed that this relationship was consistent across countries (p = 0.17).ConclusionsOur study provides evidence of the validity of using a simple household food access insecurity score to investigate the etiology of childhood growth faltering across diverse geographic settings. Such a measure could be used to direct interventions by identifying children at risk of illness and death related to malnutrition.

Zinc and glutamine improve brain development in suckling mice subjected to early postnatal malnutrition.

OBJECTIVE The effect of zinc and glutamine on brain development was investigated during the lactation period in Swiss mice. METHODS Malnutrition was induced by clustering the litter size from 6-7 pups/dam (nourished control) to 12-14 pups/dam (undernourished control) following birth. Undernourished groups received daily supplementation with glutamine by subcutaneous injections starting at day 2 and continuing until day 14. Glutamine (100 mM, 40-80 microL) was used for morphological and behavioral studies. Zinc acetate was added in the drinking water (500 mg/L) to the lactating dams. Synaptophysin and myelin basic protein brain expressions were evaluated by immunoblot. Zinc serum and brain levels and hippocampal neurotransmitters were also evaluated. RESULTS Zinc with or without glutamine improved weight gain as compared to untreated, undernourished controls. In addition, zinc supplementation improved cliff avoidance and head position during swim behaviors especially on days 9 and 10. Using design-based stereological methods, we found a significant increase in the volume of CA1 neuronal cells in undernourished control mice, which was not seen in mice receiving zinc or glutamine alone or in combination. Undernourished mice given glutamine showed increased CA1 layer volume as compared with the other groups, consistent with the trend toward increased number of neurons. Brain zinc levels were increased in the nourished and undernourished-glutamine treated mice as compared to the undernourished controls on day 7. Undernourished glutamine-treated mice showed increased hippocampal gamma-aminobutyric acid and synaptophysin levels on day 14. CONCLUSION We conclude that glutamine or zinc protects against malnutrition-induced brain developmental impairments.

Spinal cord transection modifies ileal fluid and electrolyte transport in rats.

Spinal cord injury (SCI) is associated with severe autonomic changes, including inhibition of gastrointestinal (GI) motility. GI motility changes are known to affect electrolytes transport and these changes have not been adequately studied after SCI. We studied the ileal permeability to fluid and electrolytes in rats submitted to experimental spinal cord transection (SCT), between T4 and T5, throughout the first week after SCT. SCT increased ileal secretion of Na+ (P<0.05) and decreased the Cl(-) absorption during the first week post SCI (P<0.05). Water transport was also significantly altered, leading to increased water secretion following the Na+ gradient. Ileal secretion of K+ was significantly increased 1 and 7 days after spinal cord injury. To our knowledge, the present findings are the first direct evidence that SCT alters ileal electrolyte transport in rats. Further studies are necessary to evaluate the mechanisms involved in this phenomenon.

O Clostridium difficile como agente indutor de diarréia inflamatória

Clostridium difficile has been pointed out as an important agent of diarrheal diseases associated with antibiotic use. However, due to its complexity, the physiopathology of these diseases is only partially elucidated, although a series of scientific works has demonstrated the importance of toxins A and B in the pathogenesis of the inflammatory diarrhea induced by this microorganism. The inflammatory mechanisms involved in the biological activities of these toxins are complex. There are some studies demonstrating that toxin B has no enterotoxic activity in vivo. However, this toxin causes dose-dependent eletrophysiologic and morphologic modifications of human colonic mucosa in vitro. In addition, toxin B stimulates the synthesis of potent inflammatory mediators by monocytes and macrophages. The effects provoked by toxin A on the intestinal mucosa are quite evident and are characterized by intense fluid secretion and by inflammatory cell accumulation, such as macrophages, mast cells, lymphocytes and neutrophils, with the consequent release of mediators such as prostaglandins, leukotrienes, platelet activating factor, nitric oxide and cytokines. Key-words: Clostridium difficile. Toxins A and B. Diarrhea. Inflammation. Marcos Fábio G. Rocha, José Júlio C. Sidrim e Aldo Ângelo M. Lima Clostridium difficile as an inflammatory diarrhea inducer agentO Clostridium difficile tem sido apontado como um importante agente causador de doencas diarreicas associadas ao uso de antimicrobianos. Contudo, em razao da sua complexidade a fisiopatologia dessas doencas ainda se encontra apenas parcialmente esclarecida, muito embora, uma serie de trabalhos cientificos demonstrem a importância das toxinas A e B na patogenese da diarreia inflamatoria induzida por esse microrganismo. Os mecanismos inflamatorios envolvidos nas atividades biologicas dessas toxinas sao bastante complexos. Existem alguns estudos relatando que a toxina B e desprovida de efeitos enterotoxicos, in vivo. No entanto, essa toxina provoca, de forma dose-dependente, alteracoes eletrofisiologicas e morfologicas na mucosa colonica humana, in vitro. Ademais, a toxina B estimula a sintese de potentes mediadores inflamatorios, por monocitos e macrofagos. Os efeitos provocados pela toxina A sobre a mucosa intestinal sao bastante evidentes e caracterizam-se por uma intensa secrecao de fluidos e por um grande acumulo de celulas inflamatorias, do tipo macrofagos, mastocitos, linfocitos e neutrofilos, com a consequente liberacao de seus mediadores, tais como prostaglandinas, leucotrienos, fator de agregacao plaquetaria, oxido nitrico e citocinas.Clostridium difficile has been pointed out as an important agent of diarrheal diseases associated with antibiotic use. However, due to its complexity, the physiopathology of these diseases is only partially elucidated, although a series of scientific works has demonstrated the importance of toxins A and B in the pathogenesis of the inflammatory diarrhea induced by this microorganism. The inflammatory mechanisms involved in the biological activities of these toxins are complex. There are some studies demonstrating that toxin B has no enterotoxic activity in vivo. However, this toxin causes dose-dependent eletrophysiologic and morphologic modifications of human colonic mucosa in vitro. In addition, toxin B stimulates the synthesis of potent inflammatory mediators by monocytes and macrophages. The effects provoked by toxin A on the intestinal mucosa are quite evident and are characterized by intense fluid secretion and by inflammatory cell accumulation, such as macrophages, mast cells, lymphocytes and neutrophils, with the consequent release of mediators such as prostaglandins, leukotrienes, platelet activating factor, nitric oxide and cytokines.

Multirresistência a antimicrobianos mediada por plasmídios R em cepas de Shigella flexneri isoladas no nordeste do Brasil

In Shigella strains were studied the molecular mechanism that mediated the multiply antibiotic-resistance. Twenty-six strains of Shigella flexneri were utilised in this investigation. These strains were submitted to disk diffusion test, mating experiments and plasmid isolation. In relation to antibiotics resistance standard it was observed that all Shigella flexneri strains were resistant to at least, three antibiotics tested. From twenty-six Shigella flexneri strains donors submitted to conjugation process, 34.6% (nine strains) resulted in variable frequency of transconjugants. From strains that conjugated, 100%, transferred the resistance factor acquainted with ampicillin. Being that, in all transconjugants which were observed, just one plasmid with 23.1 Kb was evidenced. This plasmid found in all strains was characterised as the cause of resistance to ampicillin.

Clinical evaluation, biochemistry and genetic polymorphism analysis for the diagnosis of lactose intolerance in a population from northeastern Brazil

OBJECTIVE: This work aimed to evaluate and correlate symptoms, biochemical blood test results and single nucleotide polymorphisms for lactose intolerance diagnosis. METHOD: A cross-sectional study was conducted in Fortaleza, Ceará, Brazil, with a total of 119 patients, 54 of whom were lactose intolerant. Clinical evaluation and biochemical blood tests were conducted after lactose ingestion and blood samples were collected for genotyping evaluation. In particular, the single nucleotide polymorphisms C>T-13910 and G>A-22018 were analyzed by restriction fragment length polymorphism/polymerase chain reaction and validated by DNA sequencing. RESULTS: Lactose-intolerant patients presented with more symptoms of flatulence (81.4%), bloating (68.5%), borborygmus (59.3%) and diarrhea (46.3%) compared with non-lactose-intolerant patients (p<0.05). We observed a significant association between the presence of the alleles T-13910 and A-22018 and the lactose-tolerant phenotype (p<0.05). After evaluation of the biochemical blood test results for lactose, we found that the most effective cutoff for glucose levels obtained for lactose malabsorbers was <15 mg/dL, presenting an area under the receiver operating characteristic curve greater than 80.3%, with satisfactory values for sensitivity and specificity. CONCLUSIONS: These data corroborate the association of these single nucleotide polymorphisms (C>T-13910 and G>A-22018) with lactose tolerance in this population and suggest clinical management for patients with lactose intolerance that considers single nucleotide polymorphism detection and a change in the biochemical blood test cutoff from <25 mg/dL to <15 mg/dL.

Gingerol suppresses sepsis-induced acute kidney injury by modulating methylsulfonylmethane and dimethylamine production

Acute kidney injury (AKI) and metabolic dysfunction are critical complications in sepsis syndrome; however, their pathophysiological mechanisms remain poorly understood. Therefore, we evaluated whether the pharmacological properties of 6-gingerol (6G) and 10-gingerol (10G) could modulate AKI and metabolic disruption in a rat model of sepsis (faecal peritonitis). Animals from the sham and AKI groups were intraperitoneally injected with 6G or 10G (25 mg/kg). Septic AKI decreased creatinine clearance and renal antioxidant activity, but enhanced oxidative stress and the renal mRNA levels of tumour necrosis factor-α, interleukin-1β, and transforming growth factor-β. Both phenol compounds repaired kidney function through antioxidant activity related to decreased oxidative/nitrosative stress and proinflammatory cytokines. Metabolomics analysis indicated different metabolic profiles for the sham surgery group, caecal ligation and puncture model alone group, and sepsis groups treated with gingerols. 1H nuclear magnetic resonance analysis detected important increases in urinary creatine, allantoin, and dimethylglycine levels in septic rats. However, dimethylamine and methylsulfonylmethane metabolites were more frequently detected in septic animals treated with 6G or 10G, and were associated with increased survival of septic animals. Gingerols attenuated septic AKI by decreasing renal disturbances, oxidative stress, and inflammatory response through a mechanism possibly correlated with increased production of dimethylamine and methylsulfonylmethane.

l-Arginine and Its Use in Ameliorating Cryptosporidium parvum Infection in Undernourished Children

Crysptosporidiosis has been associated with persistent diarrhea and growth faltering (even without overt diarrhea) in children living in endemic areas of malnutrition and enteric infections in the developing world. The treatment is still unsatisfactory and therefore nutritional interventions are an attractive way to ameliorate the disease burden, especially in undernourished children. Herewith, we discuss the benefits of arginine supplementation to improve C. parvum infection outcomes in murine models. Clinical studies are warranted to confirm these findings, which may potentially benefit children at risk in the developing world.

Effects of oocyte source, cell origin, and embryo reconstruction procedures on in vitro and in vivo embryo survival after goat cloning

The birth of cloned goats has been well documented, but the overall goat cloning efficiency by somatic cell nuclear transfer procedures is still low, which may be further intensified in extreme environments. The aim of this study was to produce cloned goats under the conditions of the Brazilian SemiArid region, in a transgenic program for the expression of human lysozyme in the milk to target childhood diarrhea and malnutrition, comparing the effects of oocyte source, cell type, and embryo reconstruction procedures on in vitro and in vivo embryo survival after cloning by micromanipulation or by handmade cloning. The use of in vitro-matured oocytes resulted in more viable embryos after cloning than in vivo-matured cytoplasts, but no differences in pregnancy rates on day 23 were seen between oocyte sources (77.5 vs. 77.8%, respectively). The presence or absence of the zona pellucida for embryo reconstruction (78.8 vs. 76.0%, respectively) did not affect pregnancy outcome after transfer. However, pregnancy rate on day 23 was higher for embryos chemically activated by a conventional than a modified protocol (88.1 vs. 50.0%), and for embryos reconstructed with mesenchymal stem cells and fetal fibroblasts (100.0 and 93.3%) than with adult fibroblasts (64.7%). Although most pregnancies were lost, the birth of a cloned female was obtained from embryos reconstructed by micromanipulation using non-transgenic control cells and in vitro-matured oocytes with intact zona pellucida, after conventional activation and transfer at the 1-cell stage.