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Biomedical subjects

M A Lynch

Publications and source records attributed to M A Lynch.

At least 145 records · Page 8Linked to original sources
PubMed1977

Predicting child abuse: signs of bonding failure in the maternity hospital.

Fifty children referred to the Park Hospital because of actual or threatened abuse were compared with 50 controls born at the same maternity hospital. Five factors were significantly more common in the abused group than among their controls: (a) mother aged under 20 at birth of first child, (b) evidence of emotional disturbance, (c) referral of family to hospital social worker, (d) baby's admission to special care baby unit, (e) recorded concern over the mother's ability to care for child. Thirty-five of the abused group had two or more of these factors compared with only five of the control group. As these data were collected from information recorded routinely at the maternity hospital, it is possible to identify most abusing families when the child is born. Such identification must lead to a comprehensive assessment of each case followed by constructive preventive action.

Adolescent↗
PubMed1976

General practice observed. Child abuse and general practice.

In a general practice of 9250 patients with 1841 children under 10 there were 12 cases of actual abuse during 1973-6. In March 1976 30 children were at risk. A preventive scheme was set up and the short-term outcome was good. There were no cases of serious abuse among the children at risk.

Child Abuse↗
PubMed1975

Ill-health and child abuse.

Intensive therapeutic work with families, in which child abuse had occurred, suggested that bonding failure related in part to the pregnancy, perinatal experience, and early ill-health of the abused proband and parents. 25 consecutive unequivocally abused children who had 1 or more siblings were selected from our referrals. Six factors emerged as highly significantly over-represented in the proband biography as compared with the control sibling group: abnormal pregnancy, abnormal labour or delivery, neonatal separation, other separation in the first six months, illnesses in the first year of life, and illness in the mother in first year of life. These data suggest that treatment of parents during pregnancy the perinatal period, and early infancy may well be fruitful in the prevention of child abuse.

Adolescent↗
PubMedDate not supplied

Mechanisms underlying induction and maintenance of long-term potentiation in the hippocampus.

Long-term potentiation (LTP) in the hippocampus is accompanied by a number of changes on both sides of the synapse. It is now generally considered that the trigger for initiating LTP is the entry of calcium into the postsynaptic area through the NMDA-associated channel while the mechanism(s) underlying the maintenance of LTP are less well understood and probably involve contributions from both sides of the synapse.

Animals↗
PubMedDate not supplied

Alterations in Ca2+-dependent and Ca2+-independent release of catecholamines in preparations of rat brain produced by ethanol treatment in vivo.

Compared to preparations from control animals, superfused striatal slice preparations from brains of rats treated chronically with ethanol released a significantly greater fraction of stored [3H] dopamine on depolarisation in 40 mM K+. Similarly, the electrically-evoked release of [3H]-norepinephrine from cortical slices and of [3H]-dopamine from striatal slices is also increased, although with this mechanism of depolarisation the change is significant only in the case of [3H] norepinephrine release. In contrast to this tendency to enhancement of Ca2+-dependent depolarisation-induced release, a reduced fraction of stored [3H]-catecholamines was released from these preparations by the indirect sympathomimetics tyramine and (+)-amphetamine. The catecholamine release induced by these indirect sympathomimetics is largely independent of external Ca2+ and the results are interpreted as suggesting that chronic alcohol treatment changes the distribution of catecholamine neurotransmitters between storage pools in the nerve terminal which do or do not require Ca2+ entry for release.

Amphetamine↗
PubMedDate not supplied

Evidence that nerve growth factor plays a role in long-term potentiation in the rat dentate gyrus.

An inbred strain of Wistar rat (GH), which is deficient in nerve growth factor (NGF), was used to assess the possible role of NGF in the generation of long-term potentiation in perforant path-granule cell synapses. The data show that NGF was significantly decreased in the dentate gyrus of GH rats, that this deficit was accompanied by an impairment in long-term potentiation (LTP) and that intraventricular injection of NGF substantially reversed this impairment. Analysis of depolarization-induced glutamate release in synaptosomes prepared from dentate gyrus of control rats revealed that NGF alone was without effect, but in combination with the metabotropic glutamate receptor agonist, aminocyclopentane-1,3-dicarboxylic acid (ACPD), NGF induced a significant increase in release. This effect was occluded by prior induction of LTP, suggesting that the interaction between these agents may be required to enhance transmitter release which accompanies LTP in dentate gyrus. In contrast to the effect of NGF and ACPD on glutamate release in control rats, the combination of these agents had no effect on release in synaptosomes prepared from GH rats, which might be explained by the marked decrease in trk receptors in dentate gyrus of GH rats. It was concluded that the impaired ability of GH rats to sustain LTP is associated with a reduction in NGF concentration, a reduction in stimulated release of NGF and a decrease in trk receptors in dentate gyrus. It is proposed that these data indicate a role for NGF in the generation of long-term potentiation in perforant path-granule cell synapses.

Animals↗
PubMedDate not supplied

Interleukin-1 beta inhibits glutamate release in hippocampus of young, but not aged, rats.

The proinflammatory cytokine, interleukin-1, is synthesized in neuronal and glial cells and is released in response to stress/injury. IL-1 exerts profound effects on the central nervous system, which include an inhibitory effect on synaptic activity in hippocampus, a brain area expressing a high density of IL-1 receptors. We report that IL-1 beta has an inhibitory effect on KCl-stimulated release of glutamate and KC1-stimulated [45Ca] influx in synaptosomes prepared from hippocampus of 4-month-old rats. These effects were inhibited by the endogenous receptor antagonist, IL-1ra, and by the phospholipase A2 (PLA2) inhibitor, quinacrine, suggesting that IL-1 receptor activation is coupled to PLA2. An inhibitory effect of IL-1 beta on protein kinase C activity was also observed. KC1-induced calcium-dependent release and calcium influx, and protein kinase C activity were significantly decreased in hippocampal synaptosomes prepared from 22-month-old compared to 4-month-old animals. In contrast to the inhibitory effect of IL-1 beta in synaptosomes prepared from young adult animals, no effect was observed on release, calcium influx, or protein kinase C activity in synaptosomes prepared from aged animals. We report that there is an age-related increase in expression of IL-1 beta in hippocampus and propose that this change may underlie the attenuated responses to IL-1 beta in hippocampus of aged animals.

Age Factors↗
PubMedDate not supplied

Dietary antioxidant supplementation reverses age-related neuronal changes.

Evidence suggests that reactive oxygen species in brain may play a role in the development of age-related neuronal impairments, and that the increase in the concentration of the proinflammatory cytokine, interleukin-1beta (IL-1beta), in aged brain tissue, may also be a contributory factor. In this study, we have analyzed changes in enzymatic and nonenzymatic antioxidant levels, in parallel with interleukin-1beta concentration, in cortical tissue prepared from young and aged rats. We report that there was an age-related increase in the activity of superoxide dismutase without concomitant changes in the activity of catalase or glutathione peroxidase and an age-related decrease in the concentrations of alpha-tocopherol and ascorbate. These observations, coupled with age-related increases in lipid peroxidation and interleukin-1beta concentration, are consistent with a compromised antioxidant defense in cortex of aged rats, a proposal supported by the finding that these changes were not observed in cortical tissue prepared from rats fed on a diet supplemented with alpha-tocopherol and ascorbate for 12 weeks.

Aging↗