Two cases of "recovery" in Kanner syndrome.
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Biomedical subjects
Publications and source records attributed to M Prior.
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Despite the dramatic increase of depression and suicidal behavior in children, research within this field is limited. Suicide is the 10th leading cause of death in children aged 1 through 14 years. For each child who completes the act of suicide, there are at least 50 more who attempt it. It is difficult to collect statistics on suicide in children owing to the lack of standard criteria for determining suicide in this age group and the myths that surround childhood suicide deaths. Children of all ages, including infants, can experience depression, but it will be manifested differently across each age group, especially from the infant to the school-aged child. Factors that identify children at risk for suicide include family history, loss of a loved one before the age of 12, violence, decreased family ties, and increased family pressures. Prevention strategies need to be accessible to the child both at home and in school. A variety of community-based suicide prevention programs are available for children and adults to assist children in overcoming suicidal feelings.
This study investigated the hypothesis that children sustaining a mild closed head injury have a higher prevalence of premorbid behavioural problems than children in the general community. The prevalence of emotional and behavioural problems among children with a mild closed head injury was compared with the prevalence of problems in children with a severe closed head injury, children in the general community, and children referred to a psychiatric outpatient clinic. The results showed that the children with a mild head injury did not have significantly more premorbid emotional and behavioural problems than other children in the community. The children with a mild head injury also had significantly fewer emotional and behavioural problems than children referred to a psychiatric outpatient clinic. The results suggest that the common assumption that children with a mild closed head injury have a higher prevalence of premorbid emotional and behavioural problems than other children in the general community may not be correct.
BACKGROUND: Iloprost therapy for severe peripheral obstructive arterial disease (POAD) has demonstrated to be effective in reducing the need for amputation. However the feasibility of a 28-day infusion regimen in less severe stages of the disease is poor due to the length in hospital stay. A randomized, controlled, parallel-group pilot study was carried out with the aim to evaluate clinical and circulatory effects of Iloprost, a stable prostacyclin analogue, administered with two different infusion schedules to patients with POAD at Leriche Fontaine stage III. METHODS: Twenty patients 16 males and 4 females, mean age 66 +/- 6 years) with objective signs of POAD, rest pain for at least two weeks and posterior tibial artery pressure > 50 mmHg, were randomized to either Iloprost i.v. infusion up to 2 ng/Kg/min for 6/h/day for 28 days (Group A) or to Iloprost i.v. infusion up to 1.5 ng/Kg/min for 16/h/day for 7 days (Group B). At baseline (before starting first infusion) after 7 days (for group B only, end of therapy) and after 28 days (end of therapy for Group A, end of study for Group B) the following parameters were evaluated: walking distance, rest pain and analgesic consumption, plethysmographyc parameters (first flow, peak flow and peak flow time) and laser Doppler parameters (rest flow, post ischemic flow). RESULTS: After 28 days, both Iloprost infusion schedules increased walking capacity (maximum walking distance/pain free walking distance +119/+84% +199/+85% respectively, for Group A and B respectively) reduced ischemic pain (-45% and -48% respectively for Group A and B) and analgesic consumption and improved plethysmographyc and laser Doppler parameters. Tolerability seemed to be better in Group B, suggesting that the lower dose and the shorter duration of the therapy period might result in reduced incidence of headache thus, in principle, increasing patient acceptability. CONCLUSIONS: The results of this pilot study, if confirmed by larger trials, could have important positive implications in terms of costs, patient comfort and management.
The role of endothelial dysfunction in the pathogenesis of diabetic microangiopathy is reviewed. Reversible alterations in microcirculation, consisting of increased capillary pressure, blood flow and endothelial permeability, can be detected at an early stage in diabetes mellitus. Irreversible structural modifications of the vascular wall, such as thickening of the basal membrane due to the extracellular accumulation of proteins, take place at later stages. Atherosclerosis further affects microcirculation in diabetes mellitus by decreasing autoregulatory capacity and blood flow reserve. Endothelial dysfunction has been observed to precede the onset of microvascular lesions, as demonstrated by reduction in the vasodilatory response to vasoactive agents and by alterations in the antithrombotic properties of the endothelium. Experimental data available so far suggest that endothelial dysfunction may be directly related to hyperglycemia. Abnormalities in lipoprotein metabolism, generation of glycation end products, and increased oxidative stress may also be responsible for the endothelial dysfunction in diabetes mellitus. Insulin resistance appears to be related to endothelial dysfunction in non-insulin-dependent diabetes mellitus through a reduction in the biological activity of endothelial-derived nitric oxide.
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