Neonatal anthropometric charts: what they are, what they are not.
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Anthropometry↗
Biomedical subjects
C Fabris
Publications and source records attributed to C Fabris.
Postnatal weight increase and growth velocity of very low birthweight infants.
BACKGROUND: Only a few studies have dealt with postnatal growth velocity of very low birthweight (VLBW) infants. OBJECTIVE: To analyse weight growth kinetics of VLBW infants from birth to over 2 years of age. PATIENTS: A total of 262 VLBW infants were selected; inaccurate estimate of gestational age, major congenital anomalies, necrotising enterocolitis, death, and loss to follow up within the first year were the exclusion criteria. METHODS: Body weight was recorded daily up to 28 days or up to discontinuation of parenteral nutrition, weekly up to discharge, then at 1, 3, 6, 9, 12, 18, and 24 months of corrected age. Individual growth profiles were fitted with a seven constant, exponential-logistic function suitable for modelling weight loss and weight recovery, two peaks, and the subsequent slow decrease in growth velocity. RESULTS: After a postnatal weight loss, all infants showed a late neonatal peak of growth velocity between the 7th and 21st weeks; most also experienced an early neonatal peak between the 2nd and 6th week. VLBW infants who were small for gestational age and those with major morbidities grew less than reference VLBW infants who were the appropriate size for gestational age without major morbidities: at 2 years of age, the difference in weight was about 860 g. The more severe growth impairment seen in VLBW infants with major morbidities is almost entirely due to the reduced height of the late neonatal peak of velocity. CONCLUSIONS: The growth model presented here should be a useful tool for evaluating to what extent different pathological conditions or nutritional and medical care protocols affect growth kinetics.
Aging↗
Mycobacterium tuberculosis isolates belonging to katG gyrA group 2 are associated with clustered cases of tuberculosis in Italian patients.
Fifty-one consecutive isolates of Mycobacterium tuberculosis, collected during a 2-year period in the north-east of Italy, were subjected to IS6110-RFLP analysis to detect the presence of clusters and assigned to one of the three genotypic groups delineated by single nucleotide polymorphisms in the genes katG and gyrA. All the isolates collected from the local population belonged to group 2 or 3, while group 1 isolates were found only in specimens collected from African immigrants. Clustered cases of tuberculosis, which are likely to be related to recently transmitted infection, were found to be significantly associated with katG gyrA group 2. In the local situation, strains belonging to this group may therefore present a higher risk of transmission.
Adult↗
Use of IgG Avidity test in case definitions of toxoplasmosis in pregnancy.
A survey network for congenital toxoplasmosis (TOXO-NET) was set up in December 1996 in Piedmont (Italy). Participants were asked to classify the infections in pregnant mothers and newborns by the criteria of the European Network on Congenital Toxoplasmosis published by Lebech in 1996. Because the IgG Avidity test is largely employed as a 2nd level test in toxoplasmosis diagnosis and it could be helpful to date infection, the co-ordinators of TOXO-NET suggested including it in the "case definition" of "probable" infection and "unlikely" infection. 117 cases of toxoplasmosis in pregnancy divided into the risk categories under Lebech's criteria were re-examined using the "new" case definitions. 77 out of 117 (65.8%) Toxoplasma gondii infections during pregnancy could be defined with only one serum sample using the IgG Avidity test. The IgG Avidity test proved a useful method to classify the Toxoplasma gondii infections in pregnancy, especially when we had only one serum sample.
Animals↗
A high neonatal serum eosinophil cationic protein level is a risk factor for atopic symptoms.
AIM: To show whether neonatal eosinophil counts (EC) and eosinophil cationic protein (ECP) can be used in assessing the risk of atopy, alone or in combination with family history of atopy (FHa). PATIENTS AND METHODS: A group of 63 newborns was included: 38 with FHa, 25 without FHa. A blood sample was collected on the 4th day of life for EC and ECP evaluation. Clinical follow-up was conducted after 1, 3, 6, 12, 18, 24 and 36 mo. The chi2 test and the Student's t-test were used to compare dichotomic and continuous variables, respectively. Variables shown to be significant by univariate analysis were evaluated with a multivariate regression model and the relative risks (RR) were estimated. RESULTS: Twenty-six newborns (41%) displayed atopic manifestations during the follow-up. Twenty-one (55%) of 38 newborns with FHa displayed atopic symptoms versus 5/25 (20%) without FHa (p 0.012). Neither EC nor serum ECP levels were significantly different between newborns with FHa and newborns without. ECP levels did not differ between newborns with single heredity and newborns with dual heredity. EC did not differ significantly between newborns who developed atopy and those who did not. Instead, serum ECP levels were significantly higher in newborns who developed atopy (mean 27.9 microU/l vs 16.8 microU/l). Atopic manifestations appeared in 16 (62%) of 26 newborns with ECP > or = 18 microU/l compared with 10 (27%) of 37 with ECP < 18 microU/l (p = 0.006). In the multivariate regression model, with ECP < 18 microU/l and no FHa as reference class, the class 1 (no FHa and ECP > or = 18 microU/l) has a low RR (1.4), class 2 (FHa and ECP < 18 microU/l) an intermediate RR (2.7) and class 3 (FHa and ECP > or = 18 microU/l) a very high RR (16.3). CONCLUSIONS: Neonatal serum ECP levels, in contrast with EC, were significantly higher in newborns who developed atopic manifestations during follow-up. The risk of atopy was about twice as great when ECP was > or = 18 microU/l (and four times as great in multivariate analysis). When serum ECP was combined with FHa, the RR for newborns with FHa and ECP > or = 18 microU/l was 16 times greater than for those without FHa and ECP < 18 microU/l. The identification of newborns at "extremely high atopic risk" (FHa and ECP > or = 18 microU/l) may be expecially useful--in clinical practice--in newborns with only one atopic parent or sibling, for whom it is not universally agreed that dietary and environmental prevention measures should be applied.
Blood Proteins↗
Photosensitizing properties of a boronated phthalocyanine: studies at the molecular and cellular level.
A synthetic procedure has been developed for the preparation of a Zn-phthalocyanine peripherally substituted with a dodecaborane. The absorption spectrum of the derivative is typical of the phthalocyanine chromophore. Moreover, the boronated phthalocyanine exhibits a high photosensitizing efficiency against a model biological substrate, such as N-acetyl-L-tryptophanamide, and a singlet oxygen quantum yield of 0.53 in dimethylformamide. Even though the presence of the dodecaborane moiety appears to decrease the affinity of the phthalocyanine for HT-1080 transformed human fibroblasts, the boronated phthalocyanine causes an essentially complete loss of cell viability upon irradiation with 600-700 nm light under mild conditions (1 microM concentration, 5-min irradiation at 10 mW/cm(2)).
Boron Compounds↗
Photosensitization with zinc (II) phthalocyanine as a switch in the decision between apoptosis and necrosis.
Photodynamic therapy (PDT) of tumors and other diseases is based on the uptake of a photosensitizing dye in target cells, which are damaged by reactive oxygen intermediates generated on irradiation with light in which the wavelengths match the dye absorption spectrum. PDT can induce cell death by necrosis and apoptosis both in vivo and in vitro, but the factors determining the contribution of either mechanism to the overall process are not completely defined. Our studies on the photosensitization of 4R transformed fibroblasts with the second-generation photosensitizer zinc (II) phthalocyanine (ZnPc) aim at determining the effect of important experimental parameters such as time of cell incubation (2 or 24 h) with ZnPc before irradiation and ZnPc concentration in the incubation medium on cell death. Furthermore, we propose possible correlations between the cell death mechanism and primary photo-damage sites; these are mainly determined by the intracellular localization of the photosensitizer. The mechanism of cell death was determined by both electron microscopy analysis of the morphological alterations induced by photosensitization and measurement of caspase 3 activation. The initial photodamage sites were determined by measuring the activities of several functions typical of mitochondria, lysosomes, Golgi apparatus, cytosol, and plasma membrane. The intracellular localization of ZnPc after 2- or 24-h incubation was determined by fluorescence microscopy. Necrosis, associated with early loss of plasma membrane integrity and complete depletion of intracellular ATP, represents the prevailing mode of death for 4R cells dark-incubated for 2 h with ZnPc and irradiated with light doses reducing viability by 99.9%. In contrast, irradiation performed 24 h after ZnPc incubation causes only partial inhibition of plasma membrane activities, and cell death occurs largely by apoptosis. ZnPc is mainly localized in the Golgi apparatus after 2- and 24-h incubation, and in all of the cases this compartment represents a primary target of photodamage. Only after prolonged incubation is mitochondrial localization of ZnPc clearly detected by fluorescence microscopy; this could be a determining factor for promotion of apoptosis. Our data demonstrate that it is possible to modulate the mechanism of cell death by appropriate protocols; this may be relevant for enhancing the therapeutic efficacy of PDT.
Animals↗
Human proteome enhancement: high-recovery method and improved two-dimensional map of colostral fat globule membrane proteins.
The human milk fat globule membrane protein composition is still largely unknown, although it counts for 2-4% of the total milk protein content and contains several important biologically active components. The aim of this work was to create a two-dimensional electrophoresis (2-DE) map of the human milk fat globule membrane proteins, both integral and membrane-associated, and to identify and characterize as many protein components as possible. A new protocol for the solubilization and extraction of the human milk fat globule membrane proteins with a double extraction procedure is presented, and the results compared with the extraction methods reported in the literature. The proteins were separated, in the first dimension, by isoelectric focusing (IEF) in the pH range 3-10 on strips of 13 cm length and, in the second dimension, by Sodium dodecyl sulfate-polyacrylamide gel electrophoresis (SDS-PAGE) on 11.5% T homogeneous gels. A reproducible 2-DE map of integral and membrane-associated proteins was obtained and the first 23 spots, representing the major components, were identified by matrix assisted laser desorption/ionization-time of flight (MALDI-TOF) mass spectrometric analysis and/or by amino acid sequencing.
Electrophoresis, Gel, Two-Dimensional↗
Spontaneous rupture and successful removal of Silastic catheters in two low birth weight infants.
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Catheterization, Central Venous↗
Serum iron indices as a measure of iron deposits in chronic hepatitis C.
Serum iron indices are believed to be elevated in patients with hepatitis C virus (HCV) infection in connection to the presence of hepatic inflammation, though this hypothesis has never been formally tested. We studied 69 consecutive, unselected anti HCV antibody positive patients, aged 14 to 70 years. Iron, transferrin saturation and ferritin were measured in fasting serum samples. Histologically detectable iron (HDI) as well as histologic grading and staging were estimated semiquantitatively in liver biopsy samples. The median values for serum iron, transferrin saturation and serum ferritin were 24 micromol/l (range, 8-61), 29 percent (range, 6-77) and 170 microg/l (range, 1-954), respectively. At univariate analysis, all three serum iron indices were positively correlated with grading and staging scores, as well as with HDI in the liver; only serum iron was positively correlated with transaminases. At multivariate analysis, independent associations were found between serum iron and the grading score; ferritin and sinusoidal and portal HDI; transferrin saturation and total hepatic HDI. In conclusion, in hepatitis C, serum iron reflects the degree of current hepatic inflammation and necrosis, whereas the extent of progressive deposition of iron in sites of fibrosis is best reflected by serum ferritin. Transferrin saturation is the best predictor of the status of hepatic iron deposits.
Adolescent↗
Carriage of HFE mutations and outcome of surgical resection for hepatocellular carcinoma in cirrhotic patients.
BACKGROUND: Aggressive hepatocellular carcinoma (HCC) complicates frequently hereditary hemochromatosis, a disease for which a strong candidate gene, named HFE, has recently been identified. Patients with HCC who are heterozygotes for mutations in the HFE gene might have distinct features and a distinct disease course. METHODS: The presence of the 2 mutations associated with hereditary hemochromatosis (C282Y and H63D) was sought by restriction fragment length polymorphism in 61 cirrhotic patients (46 males and 15 females) who underwent resection for HCC at a single institution. RESULTS: There were 4 heterozygotes for the C282Y mutation and 6 homozygotes + 20 heterozygotes for the H63D mutation, with no compound heterozygotes. Carriage of >/= 1 HFE mutated allele was significantly more frequent in HCC patients than in 149 control subjects (44% vs. 29%, P = 0.005). Among C282Y heterozygotes, 3 of 4 were female, compared with 12 of 57 wild-type carriers (P = 0.015); no gender distribution existed among patients carrying H63D alleles (6 of 26 vs. 9 of 35, P = 0.813). Survival was longer for patients with wild-type HFE than for those with mutated HFE (67% vs. 22% at 3 years; hazard ratio = 0.42, 95% confidence interval = 0.21-0.80) (P < 0.01). The negative effect on survival that resulted from possessing >/= 1 HFE mutated allele was maintained even after adjustment for gender, age, presence of tumor capsule, presence of comorbid factors, Okuda stage, Edmonson grading, and number of lesions (P = 0.01). CONCLUSIONS: Testing for HFE mutations may help identify HCC patients with dismal prognoses for whom surgical resection may not represent the best treatment option.
Adult↗
Identification of the human beta-casein C-terminal fragments that specifically bind to purified antibodies to bovine beta-lactoglobulin.
The presence of foreign proteins in human milk after the ingestion of bovine dairy products is thought to be one of the possible causes of allergic sensitization in exclusively breast-fed predisposed infants. The immunologic determination of bovine beta-lactoglobulin (LG) concentration in human milk has been reported by several researchers, but the results are conflicting. Moreover, a strong cross-reactivity between antibodies to bovine beta-LG and human milk proteins and peptides was reported, throwing doubt on the reliability of radioimmunoassay and enzyme-linked immunosorbent assay detection and quantification assays for bovine beta-LG in human milk. Thus, the goal of this study was to isolate human milk peptides with a molecular mass >or= 1,000 Da cross-reactive with antibodies to bovine beta-LG in order to identify possible common epitopes between human and bovine milk proteins. The proteins were first isolated by affinity chromatography with purified polyclonal antibodies to bovine beta-LG, followed by gel filtration fast phase liquid chromatography and reverse phase-high performance liquid chromatography purification of the components specifically bound in the affinity separation step. Affinity-bound peptides were identified by determining their amino acid sequence. All the sequenced peptides belonged to the C-terminal part of human beta-casein, which confirms the cross-reactivity of human milk proteins and peptides with antibodies to bovine beta-LG and allows the identification of possible common epitopes between the two proteins. No bovine beta-LG peptides with a molecular mass >or= 1,000 Da were found in our milk samples from healthy mothers on a diet rich in bovine milk and dairy products.
Journal Article↗
Endotoxin priming and liver damage by experimental duodenal obstruction in the rat.
To verify whether endotoxin (LPS) might act as a priming cofactor of liver injury caused by obstructing the duodenum, four groups of male Wistar rats were studied. The first two groups comprised rats in which a closed duodenal loop (CDL) was created: CDL, n = 6 and CDL + LPS, n = 7; the next two groups comprised sham-operated animals: Sham n = 6 and Sham + LPS, n = 6. LPS, 400 microg/kg bodyweight, was administered i.p. to the rats belonging to groups CDL + LPS and Sham + LPS, 24 h before laparotomy. Twenty-four hours after laparotomy the animals were killed. Damage to bile ducts, extent and grading of coagulative and lytic spotty necrosis in liver tissue were evaluated morphologically. Coagulative necrosis was severe in four of seven rats of the group CDL + LPS, mild in six of six rats of group CDL, and absent in four of six and five of six rats of groups Sham and Sham + LPS (chi2 32.8, P = 0.0001). The animals of group CDL + LPS had more frequently diffuse lytic spotty necrosis than the animals in the three other groups (chi2 9.57 P<0.01). The results of our study indicate that, in rodents subjected to a closed duodenal loop, priming with LPS exacerbates liver injury due to cholate stasis.
Alanine Transaminase↗
Prophylaxis of patent ductus arteriosus with ibuprofen in preterm infants.
UNLABELLED: The aim of our study was to evaluate whether the prophylactic use of ibuprofen would reduce the incidence of significant patent ductus arteriosus (PDA) and to confirm the effectiveness of ibuprofen as rescue treatment in closing PDA. Eighty preterm infants with gestational age less than 34 wk with infant respiratory distress syndrome (iRDS) were randomized to receive intravenous ibuprofen lysine (10 mg/kg, followed by 5 mg/kg after 24 and 48 h) either within 24 h of life (group A) or after echocardiographic diagnosis of PDA (group B). To evaluate the severity of RDS in each patient, we calculated the initial and highest values of Oxygenation Index (O.I. = mean airway pressure x FiO2 x 100/PaO2) and Ventilatory Index (V.I. = O.I. x mechanical respiratory rate). Other studied variables were ventilatory support, renal function, biochemical and haematological profiles, frequency of bronchopulmonary dysplasia (BPD), intraventricular haemorrhage (IVH), necrotizing enterocolitis (NEC) and retinopathy of prematurity (ROP). On the 3rd day of life, 8% (3/40) of patients of group A and 53% of patients (21/40) of group B (p < 0.0001) developed a significant PDA. Between patients of group B who presented PDA at 3 d of life 90% (19/21) had a closure of ductus arteriosus after ibuprofen treatment. Initial and highest values of O.I. and V.I. were similar in both groups A and B. No significant differences between the groups were observed in regard to respiratory support, renal function and frequency of BPD, IVH, NEC and ROP. Ibuprofen was not associated with adverse effects. CONCLUSION: Prophylactic treatment with ibuprofen reduces PDA occurrence in preterm infants with iRDS at 3 d of life in comparison with rescue treatment, but both modes are effective in closing the ductus without significant adverse effects.
Age Factors↗
A pilot C282Y hemochromatosis screening in Italian newborns by TaqMan technology.
Hereditary hemochromatosis (HH) is a disorder of iron metabolism that leads to iron overload in middle age and can be caused by homozygosity for the C282Y mutation in the HFE gene. Preliminary studies have estimated the frequency of this mutation at 0.5-1% in Italy, but this has not been verified on a large sample. We analyzed 1,331 Italian newborns for the C282Y mutation in the HFE gene using dried blood spots (DBS) from the Neonatal Screening Center in Turin, Italy. The mutation was assessed using a semi-automatable 5'-nuclease assay (TaqMan technology). We detected 55 heterozygotes and no homozygotes in our sampling, resulting in an overall frequency of 2.1% +/- 0.6 for the C282Y allele. Differences in allele frequency were observed, and ranged from 2.7% +/- 1.3 in samples from Northern Italy, to 1.7% +/- 0.9 in samples from Central-Southern Italy. The low frequency of the at-risk genotype for iron overload suggests that genetic screening for HFE in Italy would not be cost effective. The present study, in addition to defining C282Y frequency, documents detection of the major HFE mutation on routine DBS samples from neonatal screening programs using a semi-automatable, rapid, reliable, and relatively inexpensive approach.
Base Sequence↗
Iron deposition and progression of disease in chronic hepatitis C. Role of interface hepatitis, portal inflammation, and HFE missense mutations.
Histologically detectable iron (HDI) and HFE mutations were searched for in liver biopsy specimens from 58 Italian patients with chronic hepatitis C, and morphologic features were compared to examine their reciprocal relation and their contribution to disease progression. HDI was evident in 48% of cases with features of nonhemochromatosis iron overload. Total, sinusoidal, and portal HDI increased with stage; grade was related to all iron scores because of the contribution of portal inflammation and interface hepatitis. HFE mutations were seen in 47% of patients with chronic hepatitis C and in 28% of control subjects; they were related to stage and the His63Asp mutation to portal HDI. On multivariate analysis, grade but not stage or HFE mutations was associated with HDI in all sites. Interface hepatitis with its sequelae (sinusoidal capillarization and microshunting) represents a major factor in iron deposition in chronic hepatitis C and justifies the features of HDI. HFE mutations are not responsible for HDI deposition but could favor the progression of virus-induced damage independently from interference with iron metabolism.
Adolescent↗
IgE cross-reactivity between human and cow's milk proteins in atopic breast-fed infants.
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Animals↗
Longitudinal distance standards of fetal growth. Intrauterine and Infant Longitudinal Growth Study: IILGS.
BACKGROUND: Most ultrasonographic fetal growth norms are derived from cross-sectional data or from longitudinal data treated as coming from cross-sectional studies, although only longitudinal models may detect particular aspects of fetal growth shape, such as peak of growth velocity. MATERIALS AND METHODS: The sample included 238 singleton normal pregnancies. All the fetal traits under study (biparietal diameter, occipito-frontal diameter, head circumference, femur diaphysis length and abdomen circumference) were measured according to the classical ultrasound techniques by highly trained operators. Individual growth profiles (made up of 5 to 9 measures) were taken at regular intervals between the 12th and the 40th week. Growth norms were traced by means of a two-stage linear model: (I) a 3-constant fetal growth function was fitted to each individual growth profile, (II) growth centiles were based upon the weighted mean and covariance matrix of the individual growth constants. RESULTS: Fetal growth curves show a sigmoid shape with a maximum slope (i.e. a peak growth velocity) which occurs earlier for head diameters (about 18 weeks), later for femur diaphysis length (20 weeks) and abdomen circumference (22 weeks). During intrauterine growth, all traits show a progressive increase in interindividual variability, which is more prominent for abdomen circumference. CONCLUSION: The mathematical model applied to a large sample of growth profiles provided a satisfactory description of the individual fetal development and its biological variability, and allowed the construction of longitudinal distance standards useful for clinical purposes.
Abdomen↗