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For five days, three groups of six premature infants each were fed human milk and given a daily dosage of one of the following: vitamin D3 (30 micrograms), 25-OH D3 (10 micrograms) and 1,25-OH D3 (0.5 micrograms). The infants in the groups were matched for gestational age and birthweight. Administration of 25-OH De or 1,25-(OH)2 D3 did not significantly modify the course of early neonatal hypocalcemia as compared with infants receiving vitamin C3. Mean plasma Ca +/- S. D. (mg/100 ml) decreased to nadir values at 48 hr (D3: 5.7 +/-1.2; 25 OH D3: 6.8 +/- 0.9; 1.25-(OH)2 D3: 6.7 +/-1.1). A progressive increase toward normal values was seen at 120 and 168 hr in the three groups. Mean plasma immunoreactive parathyroid hormone +/- S.D. (microliters Eq/ml) followed an opposite pattern with peak values at 48 hr (D3: 231 +/- 137; 25-OH D3: 281 +/- 138; 1,25-(OH)2 D3:211 +/- 149). Mean plasma +/- S.D. 25-OH values (ng/ml) were low at 1.2 hr (8.7 +/- 4.8) n: 16) and increased significantly after 7 days of D3 (18.2 +/- 4.2 P less than 0.001) and 25-OH D3 administration (46 +/- 10.3 P less than 0.001)/Mean plasma iCT +/- S.D. (pg/ml) reached peak values at 24 hr (D3: 457 +/- 186; 25-OH D3: 415 +/- 121; 1.25-(OH)2 D3: 443 +/- 183). These data suggest that the various forms of vitamin D are well absorbed in preterm infants and that administration of vitamin D metabolites during the first days of life is not warranted for they prophylaxis of early neonatal hypocalcemia.

Background: While mammalian embryos can adapt to their environments, their sensitivity overshadows their adaptability in suboptimal in vitro conditions. Therefore, the environment in which the gametes are fertilized or to which the embryo is exposed can greatly affect the quality of the embryo and consequently its implantation potential. Objectives: Since providing an optimal culture condition needs a deep understanding of the environmental effects, and regarding the fact that normal morphology fails to be a reliable indicator of natural embryo development, the current study aimed at comparing in vivo- and in vitro-derived blastocysts at the molecular level. Materials and Methods: In vivo and in vitro mouse blastocysts were obtained by flushing the uterine horns and in vitro fertilization/culture, respectively. Normal blastocysts of both groups were evaluated in terms of hatching rate and expression of three lineage-differentiation-, apoptosis-, and implantation-related genes. Results: The hatching rate was lower in In vitro fertilization (IVF)-produced blastocysts in comparison with that of the in vivo counterparts. More importantly, the study results indicated significant changes in the expression levels of eight out of ten selected genes, especially Mmp-9 (about -10.7-fold). The expression of Mmp-9 in trophoblast cells is required for successful implantation and trophoblast invasion. Conclusions: The current study, in addition to confirming that the altered gene expression pattern of in vitro-produced embryos resulted in normal morphology, provided a possible reason for lower implantation rate of in vitro-produced blastocysts regarding the Mmp-9 expression.

Methylenetetrahydrofolate reductase (MTHFR) synthesizes 5-methyltetrahydrofolate, a major methyl donor for homocysteine remethylation to methionine. Severe MTHFR deficiency results in marked hyperhomocysteinemia and homocystinuria. Patients display developmental delay and a variety of neurological and vascular symptoms. Cloning of the human cDNA and gene has enabled the identification of 29 rare mutations in homocystinuric patients and two common variants [677C>T (A222V) and 1298A>C (E429A)] with mild enzymatic deficiency. Homozygosity for 677C>T or combined heterozygosity for both polymorphisms is associated with mild hyperhomocysteinemia. In this communication, we describe four novel mutations in patients with homocystinuria: two missense mutations (471C>G, I153M; 1025T>C, M338T), a nonsense mutation (1274G>A, W421X), and a 2-bp deletion (1553delAG). We expressed the 1025T>C mutation as well as two previously reported amino acid substitutions [983A>G (N324S) and 1027T>G (W339G)] and observed decreased enzyme activity at 10%, 36%, and 21% of control levels, respectively, with little or no effect on affinity for 5-methyltetrahydrofolate. One of these mutations, 983A>G (N324S), showed flavin adenine dinucleotide (FAD) responsiveness in vitro. Expression of these mutations in cis with the 677C>T polymorphism, as observed in the patients, resulted in an additional 50% decrease in enzyme activity. This report brings the total to 33 severe mutations identified in patients with severe MTHFR deficiency.

Defense mechanism is a key concept in the psychoanalytic psychopathology of borderline personality disorder (BPD). Theoretical and empirical elaborations on this question are briefly reviewed and discussed with respect to process assessment of defense mechanisms; we put forward observer-rater methodology as an accurate means of assessing unconscious in-session processes. A sample of 25 patients presenting with BPD were interviewed, as were subjects from a matched control group without psychiatric symptoms (n = 25), using a psychodynamic interview paradigm. These interviews were transcribed and rated using the Defense Mechanisms Rating Scales. The results indicate that, compared to controls, patients with BPD used higher percentages of a action, borderline, disavowal, narcissistic, and hysteric defenses, along with lower levels of mature and obsessional defenses. Overall defensive functioning was significantly lower in the patients with BPD, compared to controls. Narcissistic defenses were related with symptom level. These results are discussed in light of previous studies on defensive functioning of BPD and the literature on psychoanalytic psychopathology. These results have several important clinical implications.

AbstractTo determine the role of familial factors in head and neck cancer, we analysed data from a hospital‐based case‐control study of squamous cell carcinoma of the head and neck in Brazil. There were 754 cases of squamous cell carcinoma of the head and neck (SCCHN) and 1,507 age‐ and gender‐matched hospital‐based controls with non‐malignant diseases. Subjects provided information on the occurrence of cancer in first‐degree relatives, as well as about other risk factors, including tobacco and alcohol consumption. Relative risks (RRs) were estimated for developing mouth, pharynx and larynx cancer when cancers in relatives were observed. RRs were adjusted for age, sex, city of admission and alcohol and tobacco consumption. The RR for developing SCCHN if a first‐degree relative had cancer at any site was significantly elevated at 1.97. The RR was 3.65 (95% Cl: 1.97–6.76) if the relative had head and neck cancer. Significantly elevated risks for developing head and neck cancer were associated with siblings with head and neck cancer (RR = 8.57) and, to a lesser extent, with fathers with head and neck cancer (RR = 2.49). There was no significantly increased risk associated with mothers with head and neck cancer, but these tumours were rare among mothers. Our data show that familial, possibly genetic, factors are important in the aetiology of head and neck cancer. © 1995 Wiley‐Liss, Inc.

Intracranial cysts are common findings on both computed tomography (CT) and magnetic resonance imaging (MRI) and represent a wide range of diagnoses. A cyst can be defined as a spherical growth with an epithelial lining, forming a cavity that is filled with fluid, cellular products, or debris. Histo