Closely a primary infection of DC in vivo than other infection models. CBAs act by binding to DENV glycoproteins and subsequently interrupt the interaction between DENV and DC-SIGN. Our data provide more insight into the mechanism of action of the CBAs in MDDC and indicate the relevance of the carbohydrate-dependent entry pathway of DENV in primary human cells. It is important to further develop therapeutic concepts that may prevent DENV-induced diseases. Small-size non-peptidic analogues, such as PRM-S, should be further pursuit for this purpose. Undernutrition is a worldwide public health issue affecting more than one billion people, particularly in underdeveloped countries, where 25% of the undernourished population is children. Therefore, several recent studies have sought to correlate undernutrition in critical periods of development with various diseases in adulthood. Studies supporting the programming hypothesis have demonstrated that adverse fetal or neonatal environments such as undernutrition result in adaptative responses leading to structural and molecular alterations in various organs and tissues. The persistence of these modifications results in the development of several diseases in adult life, particularly affecting the cardiovascular and renal systems. These pathological situations are frequently associated with hypertension. The precise mechanism involved in increased blood pressure as a late consequence of metabolic programming is as yet unclear. Most experimental data indicate that hypertension is multifactorial and involves alterations in various organs including the kidney. Kidneys play a major role in the long-term control of arterial blood pressure by regulating Na intake/excretion. It has been reported that offspring from rats that are protein-restricted throughout gestation present with marked oligonephroenia, which can lead to a reduction in pressure natriuresis and consequent elevation of blood pressure. However, the reduced number of nephrons is not the sole cause of hypertension in the protein restriction model of programming. The intrarenal molecular machinery may also be altered, contributing to the programming of hypertension. This narrow period of pup development is considered one of the most important for the development of metabolic programming, and nephrogenesis is completed during this period. Fig. 1 demonstrates that despite the increased demand of lactation from an equal number of pups, the alimentary rhythm of 
undernourished mothers entailed two restrictions, low protein content of the diet and lower total food Pimozide intake with decreased available energy, which could cause metabolic programming in the offspring. The abnormal alimentary habit of undernourished mothers during lactation is probably due to low protein-associated hyperleptinemia, which could lead to satiety despite an increased energy demand as lactation ensued. The accompanying Mechlorethamine hydrochloride hypoprolactinemia contributed to the possible anorexigenic hormonal balance due to the orexigenic actions of prolactin. The reduced body mass of the offspring at weaning was a result of the low-protein induced lactogenesis failure. These maternal alimentary restrictions could contribute to the imprinting of metabolic programming of the progeny as they consistently consumed less of the normal diet despite it being offered ad libitum. This decreased food intake led to a reduced body mass throughout the growth period analyzed in the present study. Since the offspring food intake/body mass ratio after weaning remained permanently lower.