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Biomedical subjects

K Beardsall

Publications and source records attributed to K Beardsall.

7 recordsLinked to original sources
PubMed2003

Pericardial effusion and cardiac tamponade as complications of neonatal long lines: are they really a problem?

AIM: To estimate the frequency of pericardial effusion/cardiac tamponade associated with the use of neonatal percutaneous long lines (PLLs) over the past five years. METHOD: A retrospective nationwide postal survey, of all neonatal and special care units in the United Kingdom. RESULTS: Eighty two cases of pericardial effusion/cardiac tamponade were reported from the five year period, during which we estimate that 46 000 PLLs were inserted. The calculated frequency of pericardial effusion/cardiac tamponade occurring with PLLs was 1.8/1000 lines. There were 30 deaths, giving a fatality rate after pericardial effusion of 0.7/1000 lines. CONCLUSIONS: Pericardial effusion/cardiac tamponade is a serious but infrequent complication of PLL use.

Cardiac Tamponade↗
PubMed2000

Neonatal group B streptococcal infection in South Bedfordshire, 1993-1998.

BACKGROUND: Group B streptococcus (GBS) is now the leading cause of neonatal bacterial sepsis in the western world. The incidence of GBS infection in the United States has been determined, and guidelines produced and implemented for the prevention of neonatal infection. Neither incidence nor guidelines are currently established in the United Kingdom. AIM: To define the pattern of neonatal infection within one hospital (Luton and Dunstable Hospital). METHOD: A six year retrospective analysis was performed. RESULT: An incidence of early onset GBS of 1.15 per 1000 deliveries, comparable with that documented in the United States, was found.

Cross Infection↗
PubMed1999

Neonatal diabetes mellitus and cerebellar hypoplasia/agenesis: report of a new recessive syndrome.

Classical neonatal diabetes mellitus is defined as hyperglycaemia occurring within the first six weeks of life in term infants. Cerebellar agenesis is rare. We report three cases of neonatal diabetes mellitus, cerebellar hypoplasia/agenesis, and dysmorphism occurring within a highly consanguineous family. This constellation of abnormalities has not previously been described. Two of these cases are sisters and the third case is a female first cousin. The pattern of inheritance suggests this is a previously undescribed autosomal recessive disorder. Prenatal diagnosis of the condition in this family was possible by demonstration of the absence of the cerebellum and severe IUGR.

Cerebellum↗
PubMed1998

Are neuronal intranuclear inclusions the common neuropathology of triplet-repeat disorders with polyglutamine-repeat expansions?

Neuronal intranuclear inclusions have been found in the brain of a transgenic mouse model of Huntington's disease and in necropsy brain tissue of patients with Huntington's disease. We suggest that neuronal intranuclear inclusions are the common neuropathology for all inherited diseases caused by expansion of polyglutamine repeats. We also suggest that patients with a pathological diagnosis of neuronal intranuclear hyaline inclusion disease may also have polyglutamine repeat expansions.

Animals↗
PubMed1996

Renal length in sickle cell disease: observations from a cohort study.

Renal length has been measured by ultrasound in 237 subjects with homozygous sickle cell (SS) disease, 147 with sickle cell-hemoglobin C (SC) disease, and in 78 age-matched controls with a normal hemoglobin (AA) genotype. As expected, renal length increased with age in all genotypes but mean length was significantly greater in SS disease compared with SC disease (mean difference 4.3 mm after adjustment for height) and significantly greater in both genotypes than in AA controls (SS/AA difference 9.2 mm, SC/AA difference 5.0 mm after adjustment for height). Examination of relationships between renal length and some hematological indices (hemoglobin, fetal hemoglobin, reticulocyte counts, alpha thalassemia status) in SS or SC disease showed only a significant negative correlation with hemoglobin and positive correlation with reticulocyte count in SS disease. Further analysis suggested that the stronger relationship was between renal length and high reticulocyte count. The mechanism of renal enlargement is unknown although glomerular hypertrophy and increased renal blood volume are likely contributors.

Adolescent↗
PubMed1992

Nerve growth factor selectively prevents excitotoxin induced degeneration of striatal cholinergic neurones.

Selective neuronal death is a prominent feature of human neurodegenerative disease both of genetic and idiopathic origin. Huntington's disease is characterised by the selective degeneration of striatal projection neurones, with the relative preservation of a variety of interneurones. The ability of the endogenous excitotoxin, quinolinic acid, to produce a pattern of selective neuronal cell death was investigated using immunocytochemical and histochemical techniques. We find that the large striatal, cholinergic interneurones are relatively spared, and that this sparing can be enhanced by the co-administration of the neurotrophin, nerve growth factor (NGF). Further, a single co-injection of NGF will selectively prevent both the cell death and morphological changes that occur within cholinergic cells when assessed 2 weeks later. These results suggest that an interaction between growth factors and excitotoxins can dramatically modify patterns of selective neuronal death.

Animals↗