Low-level echogenicity in intraventricular hemorrhage versus ventriculitis

Serial cranial sonograms of 55 neonates with large perinatal intraventricular/intraparenchymal hemorrhages and moderate-to-severe posthemorrhagic hydrocephalus were reviewed. In all 55 patients, the ventricles were initially enlarged and filled with anechoic cerebrospinal fluid, which contained discrete hyperechoic fragments of hematoma. Between 7 and 25 days after the initial hemorrhagic episode, however, diffuse, low-level echogenicity appeared in the ventricles of 34 patients. The low-level echogenicity was transient and persisted for 7-59 days (average, 18 days). In 32 patients, low-level echogenicity was a benign finding associated with prior intraventricular hemorrhage. In two patients, the low-level echogenicity was associated with ventriculitis. Low-level echogenicity appeared, increased, then cleared, but reappeared with the onset of ventriculitis in these two patients. Thickening of the ependyma and abnormal periventricular echogenicity, signs of inflammation, were also present. Although low-level echogenicity may commonly be a benign finding, the possibility of ventriculitis should not be ignored.     

The regulation of hemopoiesis in long-term bone marrow cultures. II. Stimulation and inhibition of stem cell proliferation

The isolation of a DNA synthesis inhibitor (NBME fraction IV) and stimulator (RBME fraction III) specific for the hemopoietic stem cell (CFU-s) from freshly isolated normal adult and regenerating murine bone marrow, respectively, has been well documented. We have utilized long- term liquid bone marrow cultures in a further analysis of the role of these factors in the regulation of CFU-s proliferation. Our results show that shortly after feeding, at a time when the cultured CFU-s are actively proliferating, high levels of the hemopoietic stem cell proliferation stimulator fraction III can be isolated from the culture medium. In contrast, the presence of essentially noncycling CFU-s found in cultures fed 8-10 days previously correlates with high levels of the hemopoietic stem cell inhibitor fraction IV. These results suggest that a certain balance between these factors determines CFU-s proliferation in the long-term cultures. In support of this, DNA synthesis in actively cycling CFU-s in the long-term cultures is inhibited for at least 3 days by the addition of excess NBME fraction IV (inhibitor). Furthermore, DNA synthesis in noncycling cultured CFU-s is stimulated for at least 5 days by the addition of RBME fraction III (stimulator).     

Response to influenza virus vaccination in vertical HIV infection

OBJECTIVE: To assess the antibody response to influenza vaccine of children vertically infected with HIV. DESIGN: Prospective study in HIV infected children vaccinated during the winter of 1994-5. SETTING: Family HIV clinic at St Mary's Hospital, Paddington. SUBJECTS: 25 children, aged 1-11 years, vertically infected with HIV. MAIN OUTCOME MEASURES: Responses to influenza antigens (H1N1-A/Taiwan/1/86, H3N2-A/Shandong/9/93, B/Panama/45/ 90) were tested by haemagglutination inhibition. Antibody responses were assessed according to clinical symptoms and immune function, stratified according to the 1994 revised classification for HIV infection in children. RESULTS: 23 children (92%) had either very low or no detectable antibody before vaccination. New protective antibody responses were made by 10 children (40%): in seven to a single antigen, in two to two antigens, and in one to all three antigens. For each antigen there was an overall small increase in the mean geometric titre of antibody produced, but this only reached a protective level for antigen H1N1 and for children with minimal symptoms. Less symptomatic children were significantly more likely to produce a protective antibody response to influenza vaccination. No association was found between immune function, as measured by CD4 count, and vaccine response. CONCLUSIONS: Only vaccination of the least symptomatic HIV infected children against influenza is likely to be effective. This will not only protect them against influenza, but will also protect other more immunosuppressed and vulnerable members of their families.     

Inhibitory synaptogenesis in mouse somatosensory cortex

It is widely believed that inhibitory synapses are not present or present in only small numbers in the rodent cerebral cortex during the early postnatal period when the cortex is being innervated by thalamocortical fibers. Quantitative electron microscopy was carried out on the posteromedial barrel subfield of mouse somatosensory cortex from postnatal day 4 (P4) when thalamocortical innervation of the barrels is becoming established, through to sexual maturity (>P32), and in adulthood. Both asymmetrical (putatively excitatory) and symmetrical (putatively inhibitory) synapses were present in all layers from P4. The symmetrical synapses were immunoreactive for GABA at all ages. There was a progressive increase in both asymmetrical and symmetrical synapses up to P32, density in all layers increasing 16-fold, with the production of asymmetrical synapses leading and greatly outstripping that of symmetrical. From P32 to P120, the oldest age studied, synaptic numbers declined by 18% to 13 times the P4 level, but this affected predominantly layers II/III, IV and V, and mainly involved asymmetrical synapses. The relative percentage of asymmetrical to symmetrical synapses from P4 to P8 was 57%/43% but at P32 it was 89.5%/10.5% and in adulthood 85.4%/14.6%. These data indicate that inhibitory synaptogenesis in the rodent cortex begins earlier than previously thought, a basis for inhibition being present from the earliest period. Pruning of all synapses occurs well after thalamocortical innervation is established and inhibitory synapses are less affected by the pruning process.      

Tailored hormonal therapy in secretory adrenocortical cancer

Mitotane is often considered the front-line hormonal therapyof adrenocortical carcinoma (ACC). An illustrative case concerningthis issue and the rationale to ponder other alternatives isreported. A 69 year-old woman, diagnosed with ACC was admittedwith hypertensive crisis, supraventricular tachycardia, congestiveheart-failure, diarrhoea and rabdomyolisis. Two years earlier,she had undergone