Why are children admitted to hospital?

The criteria for admitting children to hospital for medical care were examined in 399 consecutive, non-planned admissions to the Nottingham Children''s Hospital between October 1975 and January 1976. Sixty-one per cent of the children were referred direct to the casualty department by their parents. Over 20% were admitted primarily for social reasons, and many of the remainder came from homes judged to be at a disadvantage. The hospital medical services for children should be aware of the needs of parents as well as of the needs of sick children in their catchment area.     

Oxidative Stress Induces Mitochondrial Dysfunction in a Subset of Autism Lymphoblastoid Cell Lines in a Well-Matched Case Control Cohort

There is increasing recognition that mitochondrial dysfunction is associated with the autism spectrum disorders. However, little attention has been given to the etiology of mitochondrial dysfunction or how mitochondrial abnormalities might interact with other physiological disturbances associated with autism, such as oxidative stress. In the current study we used respirometry to examine reserve capacity, a measure of the mitochondrial ability to respond to physiological stress, in lymphoblastoid cell lines (LCLs) derived from children with autistic disorder (AD) as well as age and gender-matched control LCLs. We demonstrate, for the first time, that LCLs derived from children with AD have an abnormal mitochondrial reserve capacity before and after exposure to increasingly higher concentrations of 2,3-dimethoxy-1,4-napthoquinone (DMNQ), an agent that increases intracellular reactive oxygen species (ROS). Specifically, the AD LCLs exhibit a higher reserve capacity at baseline and a sharper depletion of reserve capacity when ROS exposure is increased, as compared to control LCLs. Detailed investigation indicated that reserve capacity abnormalities seen in AD LCLs were the result of higher ATP-linked respiration and maximal respiratory capacity at baseline combined with a marked increase in proton leak respiration as ROS was increased. We further demonstrate that these reserve capacity abnormalities are driven by a subgroup of eight (32%) of 25 AD LCLs. Additional investigation of this subgroup of AD LCLs with reserve capacity abnormalities revealed that it demonstrated a greater reliance on glycolysis and on uncoupling protein 2 to regulate oxidative stress at the inner mitochondria membrane. This study suggests that a significant subgroup of AD children may have alterations in mitochondrial function which could render them more vulnerable to a pro-oxidant microenvironment derived from intrinsic and extrinsic sources of ROS such as immune activation and pro-oxidant environmental toxicants. These findings are consistent with the notion that AD is caused by a combination of genetic and environmental factors.     

Turbinaria foliosasp. nov. (Fucales, Phaeophyceae) from the Sultanate of Oman, with a census of currently recognized species in the genus Turbinaria

Turbinaria foliosasp. nov. is described on the basis of several collections made from Dhofar, Sultanate of Oman. The new species is known only from southern Oman, a region of the northern Arabian Sea that is strongly impacted by the upwelling from the summertime monsoon. It is distinguished from other species of the genus by the shape of the leaves and by their loose, non‐congested arrangement. Air vesicles, embedded in the leaves, may be present, but more often are absent. A census of the currently recognized species in the genus Turbinaria is provided. Reference is made to Sargassum turbinarioides and Sargassum turbinati‐folium. These species possess discrete blades and spherical vesicles and thus conform to Sargassum.