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Biomedical subjects

Y K Liu

Publications and source records attributed to Y K Liu.

At least 91 records · Page 5Linked to original sources
PubMed1975

Folic acid deficiency in sickle cell anaemia.

Megaloblastic anaemia responding to folic acid has been reported in a number fo patients with sickle cell anaemia. The incidence of reduced serum and erythrocyte folate levels in such patients remains unclear, however. Serum and erythrocyte folate contents were measured microbiologically in patients with sickle cell anaemia as well as in two control groups with sickle cell trait or normal haemoglobin pattern. Low serum and erythrocyte folate values were significantly more common in 61 sickle-cell patients than in each of the two socio-economically-matched control groups including 61 subjects with Hb AS and 69 blacks with Hb AA. There was no correlation between serum folate and haematocrit or reticulocyte count. The erythrocyte folate, measured before and after removal of reticulocytes, remains a reliable indicator of deficiency of folic acid in sickle-cell patients despite variable degrees of reticulocytes. Folate therapy resulted in higher haematocrits in three of four sickle-cell patients with low serum and low erythrocyte folate values, but in only one of 12 patients with low serum folate and normal erythrocyte folate. These findings are consistent with other observations that folate requirement may be increased in chronic haemolytic disorders and suggest that erythrocyte folate values should be obtained in sickle-cell patients suspected of having folate deficiency.

Adolescent↗
PubMedDate not supplied

Marrow aplasia induced by colchicine. A case report.

A 70 year old male developed marrow aplasia and pancytopenia after receiving 10 mg of colchicine intravenously over a period of 5 days for acute gouty arthritis. Despite a fatal outcome, evidence of recovery of hematopoiesis was observed in the bone marrow 3 days after the last dose of the drug. The pathogenetic mechanism by which colchicine induced marrow aplasia in this patient remains unclear.

Aged↗
PubMedDate not supplied

Clinical and specular microscopic manifestations of iridocorneal endothelial syndrome.

PURPOSE: To investigate the correlation between the clinical pictures and the specular microscopic findings in patients with iridocorneal endothelial (ICE) syndrome. METHODS: The records of 15 patients with ICE syndrome who presented at the National Taiwan University Hospital between 1993 and 1996 were examined. The medical history, clinical pictures of the cornea, iris and anterior chamber angle, intraocular pressure, specular microscopic findings, and the correlation between clinical and specular microscopic findings were assessed. RESULTS: Endothelial changes in specular micrographs were found in all the patients, even in those patients with minimal angle involvement by peripheral anterior synechiae. Corneal decompensation resulting in corneal edema and bullae formation was the main cause of visual impairment. Neither ICE grading nor endothelial cell density correlated with corneal edema or intraocular pressure, but they correlated with the angle involvement in ICE syndrome. The intraocular pressure was difficult to control in 8 of these patients, even after treatment with anti-glaucoma agents and trabeculectomy, especially in the patients with Cogan-Reese syndrome. CONCLUSION: Although specular microscopy provides an invaluable method for the diagnosis of ICE syndrome, it is not a reliable tool for predicting prognosis. Close follow-up of intraocular pressure and early detection of glaucoma are important steps to preserve visual functions in patients with ICE syndrome.

Adult↗
PubMedDate not supplied

Fatigue response of lumbar intervertebral joints under axial cyclic loading.

A low-cycle fatigue of 11 lumbar intervertebral joints under axial compression is reported. The magnitude of the maximum compressive load ranged from 37 to 80% of the failure load. The maximum deformation, as a function of the number of cycles, showed two distinct results: one group showed a gradual, stable increase, and the other an abrupt, unstable increase. The before- and after-test radiographs showed a one-to-one correspondence between unstable specimens and generalized bony failure. The radiographs of 5-mm thick transverse endplate slices show crack propagation from the periphery of the subchondral bone inward. Removal of the organic matrix from the cracked specimens produced its physical disintegration into small particles, while normal controls and stable specimens retained their size and shape.

Adolescent↗
PubMedDate not supplied

Subcortical EEG changes in rhesus monkeys following experimental hyperextension-hyperflexion (whiplash).

A controlled study, involving EEG recordings from the scalp and chronically implanted electrodes in the cortex (ECoG), as well as from selected subcortical nuclei, was undertaken to investigate the neurophysiologic effects on rhesus monkeys following experimental whiplash (hyperextension of the head and neck). Sixteen animals, equally divided into four groups, were studied through the following protocol: (1) two animals within each group were whiplashed and then electrodes were implanted into the brain of one; (2) the second two animals were implanted with deep electrodes and then one was whiplashed. Weekly EEG follow-ups showed hippocampal spiking in three of the four whiplashed and then electrode-implanted animals and in one of implanted and then whiplashed animals 6 to 8 weeks postwhiplash. Several results deserve attention. (1) The "whiplash syndrome" owes part of its symptoms to EEG disturbances in the brain. (2) Prior to the onset of spiking, ie, 6 to 8 weeks postwhiplash, practically all scalp, cortical, and subcortical EEG recordings were normal. (3) When hippocampal EEG spiking did take place, only normal and mildly abnormal changes were seen in either the electrocorticogram (ECoG) or scalp electroencephalogram (EEG). (4) The growth and development of this trauma-induced hippocampal spiking followed the classic sequence for the spread of an epileptogenic focus. (5) This apparent subclinical form of posttraumatic epilepsy may be due to the combined effects of the whiplash plus the subcortical electrode placements further decreasing the already well-known, low-spiking threshold of the hippocampi.

Animals↗