Aflatoxin: Is it a neglected threat for formula-fed infants?

In the present study, the risk of exposure to aflatoxin in infants fed breast milk and formula was investigated. For this purpose, aflatoxin B₁ (AFB₁) was determined in the serum of both breast-fed and formula-fed infants. Serum AFB₁ positivity was significantly higher in the formula-feeding (F) group than the breast-feeding (B) group (42.8 vs 8.5%, P <0.01). The AFB, concentration in different commercial formulas was also determined. Aflatoxin B₁ was found in seven of the eight newly opened packages of different brands of formula. The concentrations showed a statistically significant increase at the 30th day after opening the packages (P <0.01). Although AFB₁ concentrations in the formulas were found to be within acceptable limits for most countries, still, its existence must be carefully evaluated because future influences of very small amounts of aflatoxin on the growing organism have not been fully elucidated. Therefore, it was again concluded that for infants, human milk is safer than commercial formulas because of the lower contamination risk of aflatoxin. Also, commercial formulas must be regularly examined by authorities for the possible risk of aflatoxin contamination.     

Should sperm donors be paid? A survey of the attitudes of the general public

Gamete donation in assisted reproduction is an accepted treatment option for certain infertile couples. Traditionally, men donating spermatozoa have been paid a nominal fee, whilst women donating oocytes have not. The issue of payment for sperm donors has recently attracted attention following the Human Fertilisation and Embryology Authority's (HFEA) suggestion that such payment may be withdrawn. Prior to the final meeting of the HFEA working party which is examining this issue, here we report the results of a survey designed to solicit opinion on whether sperm donors should be paid, to identify social or other factors which influence this opinion, and to examine the influence of financial incentive on potential donors. We surveyed 717 individuals in three distinct groups: the general public, students (potential donors), and infertility patients (potential recipients). The majority of the potential donor group (students) was in favour of paying sperm donors, as were infertility patients. In contrast the general public was not. The opinion of the general public on this issue was influenced by their prior knowledge of whether donors were paid: those of the general public favouring the payment of sperm donors had a prior awareness that such payments were made. Although not in favour of paying sperm donors, the general public overwhelmingly approved of the use of donated spermatozoa for the treatment of infertile couples, and thought that ways should be sought to increase the availability of donor spermatozoa for the treatment of infertility and for research purposes. Within the potential donor group (students), the majority indicated that financial reward was an important factor which would influence their decision to donate spermatozoa. As the majority of both the potential recipients and potential donors feels that sperm donors should be paid, perhaps the views of these groups should carry significant weight when the decision whether or not to withdraw payment is taken. This is especially the case in view of the fact that the majority of the general public is in favour of the use of donated spermatozoa for the treatment of infertile couples.      

Presynaptic gating of postsynaptically expressed plasticity at mature thalamocortical synapses

Thalamocortical (TC) projections provide the major pathway for ascending sensory information to the mammalian neocortex. Arrays of these projections form synaptic inputs on thalamorecipient neurons, thus contributing to the formation of receptive fields (RFs) in sensory cortices. Experience-dependent plasticity of RFs persists throughout an organism's life span but in adults requires activation of cholinergic inputs to the cortex. In contrast, synaptic plasticity at TC projections is limited to the early postnatal period. This disconnect led to the widespread belief that TC synapses are the principal site of RF plasticity only in neonatal sensory cortices, but that they lose this plasticity upon maturation. Here, we tested an alternative hypothesis that mature TC projections do not lose synaptic plasticity but rather acquire gating mechanisms that prevent the induction of synaptic plasticity. Using whole-cell recordings and direct measures of postsynaptic and presynaptic activity (two-photon glutamate uncaging and two-photon imaging of the FM 1-43 assay, respectively) at individual synapses in acute mouse brain slices that contain the auditory thalamus and cortex, we determined that long-term depression (LTD) persists at mature TC synapses but is gated presynaptically. Cholinergic activation releases presynaptic gating through M(1) muscarinic receptors that downregulate adenosine inhibition of neurotransmitter release acting through A(1) adenosine receptors. Once presynaptic gating is released, mature TC synapses can express LTD postsynaptically through group I metabotropic glutamate receptors. These results indicate that synaptic plasticity at TC synapses is preserved throughout the life span and, therefore, may be a cellular substrate of RF plasticity in both neonate and mature animals.     

Postsynaptic depolarisation enhances transmitter release and causes the appearance of responses at "silent" synapses in rat hippocampus

Recent data indicate that most "silent" synapses in the hippocampus are "presynaptically silent" due to low transmitter release rather than "postsynaptically silent" due to "latent" receptors of alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid type (AMPARs). That synapses bearing only N-methyl-d-aspartate (NMDAR) receptors do exist is suggested by the decreased number of transmission failures during postsynaptic depolarisation and by the presence of NMDA-mediated excitatory postsynaptic currents (EPSCs) in synapses silent at rest. We tested whether these effects could be due to potentiated transmitter release at depolarised postsynaptic potentials rather than removal of Mg(2+) block from NMDARs. Using whole-cell recordings of minimal EPSCs from CA1 and CA3 neurones of hippocampal slices we confirmed decreased incidence of failures at +40 mV as compared with -60 mV. This effect was associated with a gradual increase of EPSC amplitude after switching to +40 mV and with a decrease of paired-pulse facilitation. In initially silent synapses, potentiation of pharmacologically isolated AMPAR-mediated EPSCs was still observed at +40 mV and this persisted after stepping back to -60 mV. All above effects were blocked when the cell was dialysed with the Ca(2+) chelator BAPTA (20 mM). These observations are difficult to reconcile with the "latent AMPAR" hypothesis and suggest an alternative explanation, namely that the reduction in failure rates at positive potentials is due to potentiation of transmitter release following Ca(2+) influx through NMDARs. Our results suggest that silent synapses can be mainly "presynaptically" rather than "postsynaptically silent" and thus increased transmitter release rather than insertion of AMPARs is a major mechanism of early long-term potentiation maintenance.     

Quinone-induced DNA single strand breaks in a human colon carcinoma cell line

It has been demonstrated that synthetic quinones, such as menadione, cause DNA damage in different cell systems, possibly being mediated by free radicals generated during redox cycling. It has been suggested that the damage caused could be related to tumor induction in different sites. To our knowledge it has not yet been demonstrated that the natural quinones, vitamin K1 and K2, exert the same activity. Using a colon carcinoma cell line, HT-29, we examined the extent of DNA damage induced by menadione, vitamin K1 and K2. Menadione caused significant DNA damage at low concentrations (25-200 microM) with a linear correlation of r = 0.95. In the presence of dicoumarol, a DT-diaphorase inhibitor, the damage was detected at concentrations five times lower indicating that free radicals generated during the redox cycling play a key role. Neither vitamin K1, incorporated in micelles, nor K2 caused detectable single strand breaks with respect to the controls either in the presence or in absence of dicoumarol. Our results demonstrate that, despite their redox cycling properties, the natural forms of vitamin K do not cause DNA damage in HT-29 cells as menadione does in the experimental conditions used.