Aging acceleration of balsamic vinegar applying micro-oxygenation technique.

The effect of micro-oxygenation (MOX) technique on quality and sensorial characteristics of balsamic vinegar was investigated, aiming to aging acceleration. Aging experiments were conducted using a multiple diffuser micro-oxygenator for up to 6 months with an oxygen flow of 30 mg/L/month, including oak chips (1 g/L) or not. Barrel maturation was simultaneously carried out. Quality, nutritional, sensorial characteristics and the aromatic profile of all aged vinegars were evaluated throughout aging. MOX accelerated the alteration of aging indices. Volatile compounds of fruity aroma and wine were decreased, while the fatty/buttery and caramel aroma compounds were increased. Similar compounds of 1.5-year barrel maturation were developed within 6 and 5 months applying MOX without or with oak chips, respectively. MOX resulted in reduction of the aging time to 1/3 compared to the corresponding one in barrels, considered as an attractive approach for vinegar-producing industries, mimicking and accelerating the long and costly barrel aging.

Genetic variants of surfactant proteins A, B, C, and D in bronchopulmonary dysplasia.

BPD_28D (O2 dependency at 28 days of life) and BPD_36W (O2 dependency at 36 wks post-menstrual age) are diseases of prematurely born infants exposed to mechanical ventilation and/or oxygen supplementation. In order to determine whether genetic variants of surfactant proteins (SPs-A, B, C, and D) and SP-B-linked microsatellite markers are risk factors in BPD, we performed a family based association study using a Greek study group of 71 neonates (<30 wks gestational age) from 60 families with, 52 BPD_28D and 19 BPD_36W, affected infants. Genotyping was performed using newly designed pyrosequencing assays and previously published methods. Associations between genetic variants of SPs and BPD subgroups were determined using Transmission Disequilibrium Test (TDT) and Family Based Association Test (FBAT). Significant associations (p

Macroglossia, transient neonatal diabetes mellitus and intrauterine growth failure: a new distinct entity?

A newborn infant, small for her gestational age with macroglossia and transient insulinopenic diabetes mellitus is described. Two similar cases have been found in the literature. Flat glucose tolerance test results were found in the mother, the mechanism of which was not disclosed; there was no evidence of hyperinsulinism or malabsorption syndrome and the response of plasma growth hormone, and cortisol, and of urinary epinephrine to insulin-induced hypoglycemia was adequate. It is suggested that the triad of intrauterine growth retardation, macroglossia, and transient neonatal diabetes mellitus constitutes a distinct clinical entity. The link to the maternal abnormalities of carbohydrated homeostasis remains speculative.

Outbreak of colonization of neonates with Enterobacter sakazakii.

An outbreak of colonization of 11 neonates with Enterobacter sakazakii occurred in a neonatal intensive care unit from the 10 September to 17 October 1984. During this period Ent. sakazakii was isolated from throat and rectal swabs and tracheal aspirates, but not from blood, of the neonates. The duration of colonization ranged from 2 to 8 weeks. The isolates were resistant to amikacin and to tobramycin, but sensitive to gentamicin. Four of the 11 colonized neonates had clinical signs of severe sepsis and one of meningitis and four died in spite of intensive chemotherapy. The source and the mode of spread of Ent. sakazakii remained unknown as it was not found on the hands of staff or in the inanimate environment of the unit. Ent. sakazakii may be implicated in severe infections in neonates and should be included when screening clinical specimens.

Determination of slime-producing S. epidermidis specific antibodies in human immunoglobulin preparations and blood sera by an enzyme immunoassay: correlation of antibody titers with opsonic activity and application to preterm neonates.

Slime-producing Staphylococcus epidermidis is responsible for severe infections in immunocompromised patients and, particularly, in premature infants who are transiently deficient in IgG. A sulfated polysaccharide with molecular mass of 20-kDa (20-kDa PS) has been recognized as the major polysaccharide component and antigenic determinant of S. epidermidis extracellular slime layer. The presence of adequate amounts of antibodies to 20-kDa PS in patients' sera would be of importance to prevent or treat slime-producing S. epidermidis bacteremia. Administration of intravenous immunoglobulin (IVIG) is considered to be a reasonable IgG replacement therapy and has been widely used to prevent or treat neonatal sepsis. Clinical trials have shown conflicting results on the efficacy of IVIGs and this phenomenon has been attributed to the variability of IVIG preparations in the content and opsonic activity of IgG against microorganisms of clinical importance. Monitoring of antibodies to distinct bacterial macromolecules, which are species-specific and responsible for bacterial infections, has not been performed previously. A highly precise and repeatable enzyme immunoassay was developed to determine quantitatively the levels of antibodies against the 20-kDa PS of S. epidermidis slime. The amount of 20-kDa PS specific antibodies found in 27 lots of an IVIG preparation (Sandoglobulin) correlated well with their in vitro opsonic activity against slime-producing S. epidermidis. The majority of lots (75%) having titers higher than 200 units/ml showed significant opsonic activity (50-75%) towards slime-producing S. epidermidis. Sandoglobulin lots with titers higher than 200 units/ml of 20-kDa PS specific IgG were administered as a prophylactic agent to low-birth weight (lower than 1700 g) preterm neonates immediately after birth. The levels of total and 20-kDa PS specific IgG in neonates' blood sera were significantly higher than those found in the control group, even 10 days after the last infusion. The rate of slime-producing S. epidermidis bacteremia in neonates who received IVIG was also considerably lower than those in the control group. The results of this study suggest that specific IgG titers estimated by the developed enzyme immunoassay may well be indicative of the IVIG opsonic activity against slime-producing S. epidermidis. Furthermore, administration of Sandoglobulin with titers higher than a cut-off value of 200 units/ml may significantly protect preterm neonates against slime-producing S. epidermidis bacteremia.

Human milk and intestinal host defense in newborns: an update.

In this update of the role of breast milk ingestion on passive and active protection of the human neonate, new observations and studies are presented that appear to support the concept that preterm and term infants should receive their mother's milk so far as possible. New objective evidence has been presented to support the role of breast milk in the protection of the newborn from intestinal and systemic infections. New concepts of the active role of breast milk growth factors on an accelerated development of the infant's own mucosal barrier function are presented, as well as preliminary data to support the role of breast milk growth factors in gut development. This new area of breast milk function, however, requires extensive clinical studies to support the practical value of breast milk in the development of the infant's own defenses.

Prothrombotic factors in neonates with cerebral thrombosis and intraventricular hemorrhage.

AIM: To investigate whether the factor V Leiden mutation (FVL), the prothrombin gene G20210A variant or the methylenetetrahydrofolate reductase (MTHFR) C677T genotype are risk factors for central nervous system (CNS) thrombosis or intraventricular hemorrhage (IVH) in neonates. METHODS: Thirteen full-term infants with cerebral infarct documented with magnetic resonance imaging were assessed with the whole spectrum of assays for thrombophilia including the three DNA-based prothrombotic factors. The frequency of congenital defects was compared with that observed in 38 healthy full-term infants. The genetic defects were also assessed in 55 premature neonates, gestational age <32 wk, 17 of whom developed IVH, grade II-IV. The remaining 38 premature neonates without IVH were used as controls. RESULTS: In the CNS thrombosis group: a prothrombotic factor was detected in 53% of patients and an underlying disease or a triggering event in 61.5%. The frequency of FVL in thrombosed neonates was higher (23%) than in the group of healthy full-term infants (10.5%), although it did not reach statistical significance. IVH developed in 30.9% of premature neonates. Apart from several maternal or neonatal risk factors for IVH, FII G20210A was found in a considerably higher prevalence in the cohort of neonates with IVH (12%) than in those without (2%), although the difference was not statistically significant. CONCLUSION: The pathogenesis of cerebral thrombosis or IVH in neonates is multifactorial. Along with underlying diseases or triggering events, congenital prothrombotic factors (FVL or FII G20210A) showed a trend towards a higher frequency in full-term infants with CNS thrombosis or premature neonates with IVH than in controls. However, their contribution to neonatal cerebral thrombosis or IVH remains to be determined.

Inflammatory mediators in perinatal asphyxia and infection.

AIM: To determine serum levels of interleukin-6 (IL-6), IL-1beta, tumor necrosis factor-alpha (TNF-alpha), soluble intercellular adhesion molecule-1 (sICAM-1) and C-reactive protein (CRP) in asphyxiated neonates and compare these inflammatory factors with those found in neonates with perinatal infection. METHODS: 88 neonates were studied, of whom 36 were asphyxiated, 18 were infected and the remaining 34 were controls. Peripheral blood samples were obtained on the 1st, 3rd and 5th postnatal days. RESULTS: Cytokines IL-6 and IL-1beta as well as sICAM-1 serum levels did not differ between asphyxiated and infected neonates; however, at most time periods, their values were significantly higher than controls. TNF-alpha was similar in the three groups of neonates. CRP serum values were significantly higher in the infected neonates than in the asphyxiated or control subjects. Among the 54 asphyxiated and infected neonates, 15 were considered as severe cases and 39 as mild. The severe cases, at most time periods, had significantly higher IL-6, IL-1beta and sICAM-1 levels compared with the mild ones. Through receiver operating characteristic curves the cut-off points, sensitivities, and specificities for distinguishing neonates at risk or at high risk for brain damage were established. CONCLUSION: Similar increases in serum levels of IL-6, IL-1beta and sICAM-1 were found in perinatally asphyxiated and infected neonates. As these increases correlated with the severity of the perinatal insults, neonates at high risk for brain damage might be detected.

Interleukin-8 and monocyte chemotactic protein-1 mRNA expression in perinatally infected and asphyxiated preterm neonates.

BACKGROUND: Inflammation due to perinatal infection (PI) and perinatal asphyxia (PA) may cause damage to various tissues and very often to the immature brain of the fetus and the newborn. Previously, we have shown that the neonatal immune system has the ability to produce increased chemokine protein levels in the serum during the inflammatory response caused by PI and PA. AIM: The aim of our present study was to investigate mRNA levels of the proinflammatory chemokines interleukin-8 (IL-8) and monocyte chemotactic protein-1 (MCP-1) in peripheral blood leukocytes from infected and asphyxiated neonates. METHODS: Forty-two premature neonates were studied; 11 with PI, 16 with PA and 15 without PA and PI, were used as controls. IL-8 and MCP-1 mRNA levels were investigated in whole blood and in phytohemagglutinin-activated lymphocytes using semi-quantitative polymerase chain reaction and real-time polymerase chain reaction, respectively. RESULTS: IL-8 mRNA levels were significantly increased in whole blood both during PA and PI, while MCP-1 mRNA levels were not. In vitro activated lymphocytes expressed significantly increased IL-8 mRNA levels during PI, whereas no increase was observed during PA. MCP-1 mRNA levels were significantly increased in activated lymphocytes during PA, while no increase was observed during PI. CONCLUSIONS: Our data show that chemokine mRNA levels expressed by activated lymphocytes during inflammation caused by PIs are different to those expressed during PAs. These findings might have important implications during the administration of specific chemokine antagonists in order to prevent or reduce tissue damage caused by inflammation.

Immune protection of human milk.

Human milk contains a very large number of specific and non-specific immunologic and nonimmunologic factors who provide passive and active protection to the newborn. The immunologic factors are either immunostimulatory or immunosuppressive. The immunostimulatory ones increase host defense mechanisms mainly against infective illness, and the immunosuppressive ones downregulate inflammation and the development of allergies. Furthermore, human milk has been found to promote intestinal growth and maturation and to have immunomodulating effects beyond infancy, later on in life. In conclusion, human milk represents a very valuable weapon for enhancing the immature immunologic system of the newborn and for strengthening its deficient host defense mechanisms against infective or other foreign agents.

Immunologic deficiencies in small-for-dates neonates.

Health is dependent upon good nutrition because of the interactions of immunologic function with nutritional status. Full-term neonates--and even more so prematures--present with various immaturities of their humoral and cellular immunologic mechanisms, particularly during the first days of life. Foetal growth retardation causes further deficiencies to the immature neonatal host defence mechanisms by decreasing thymic hormone activity and by reducing the numbers and activity of T and B-lymphocytes in their peripheral blood. Furthermore, very low levels of IgG 1 immunoglobulin and reduced bacteriocidal capacity of polymorphonuclear neutrophils have been found in small-for-dates neonates. Impaired immunocompetence in growth-retarded neonates is probably the main cause of the increased frequency and severity of infections they develop.

Parental nutrition in sick low-birth-weight neonates.

T. P. N. (aminoacids-glucose-fat) or aminoacids and glucose (A-G.) was given to 49 premature low-birth-weight neonates through peripheral veins for 7--42 days. The T. P. N. infusate contained glucose 12--20.5 g/kg/day and a standard dose of 2 g/kg/day for aminoacids and fat. The patients formed 4 groups: Twenty neonates were healthy but unable to tolerate oral feeding. Ten of them (group A) received T. P. N. and ten (Group B) received only A-G. Twenty nine neonates suffered from serious illness: 14 of them (Group C) received T. P. N. and 15 (Group D) A-G. In healthy neonates the weight gain was significantly higher in those who received T. P. N. than in those who took the same amount of calories but with A-G only. The addition of fat in parenteral nutrition is necessary in order to achieve a weight gain similar to that of intrauterine period. Fat is even more necessary in sick low-birth-weight neonates because they were found to be unable to tolerate high doses of glucose. Only part of the energy intake of the sick neonates could be covered with A-G. The present study has shown that parenteral nutrition can safely be given to sick low-birth-weight neonates without serious complications.

Chlorpromazine and lidocaine inhibit antibody-dependent cell-mediated cytotoxicity but not erythrocyte antibody rosette formation.

Pretreatment of human peripheral blood mononuclear cells with chlorpromazine and lidocaine reduces their ability to induce lysis of antibody-coated target cells. This effect of local anesthetics was not due to a reduction of binding of antibody-coated red cells to the mononuclear cells, but it was rather probably due to the inhibition of mobility of the Fc receptor on the cell membrane.

Phagocytosis and killing ability of Candida albicans by blood leucocytes of healthy term and preterm babies.

The phagocytosis and killing ability of leucocytes of 24 term and 22 preterm babies against Candida albicans were studies during the first 20 days of life because of the increased incidence of monilia infection at this time. The leucocytes of 14 adults aged 20 to 30 years served as controls. The phagocytosis ability of the leucocytes in adults, term, and preterm babies was not significantly different, mean values being respectively 66-7%, 57%, and 56-9%. The killing ability of the leycocytes in term and preterm babies was lower when compared with that of adult leucocytes (P less than 0-001 for term and P less than 0-01 for preterm infants). The mean value in adults was 27-5%, in term infants 9-7%, and in preterm infants 9-5%. It is suggested that as the addition of adult serum did not improve the candidacidal ability of newborn leucocytes, the killing defect should be sought in the leucocyte itself and not in serum factors.

Exchange transfusion in severe neonatal infection with sclerema.

Two critically ill newborn babies with severe infection associated with sclerema were successfully treated with appropriate antibiotics and repeated exchange transfusions.

Serum levels of lysozyme in term and preterm newborns.

Serum lysozyme levels were studied in term babies at the time of delivery and again between 7th and 30th postnatal days, and in preterm babies on the 1st, 3rd, and 5th postnatal days. Levels in term babies at delivery (mean 2.28 mug/ml) were similar to those found in adults, but they fell between the 7th and 30th postnatal days. In premature babies lysozyme levels on the first day of live (mean (0.82 mug/ml) were lower than in term babies. They tended to rise during the first 5 days, by which time they had reached levels found in term babies between the 7th and 30th days. The low lysozyme levels in preterm and in term babies after the first few days of life may contribute to the poor ability of the newborn baby to localize infection and to kill bacteria extracellularly.