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Biomedical subjects

H M Liu

Publications and source records attributed to H M Liu.

At least 73 records · Page 4Linked to original sources
PubMed1997

Direct surgery of carotid cavernous fistulae and dural arteriovenous malformations of the cavernous sinus.

OBJECTIVE: To save the patency of the internal carotid artery (ICA) during the treatment of carotid cavernous fistulae or cavernous sinus dural arteriovenous malformations, direct surgery of the cavernous sinus after failure of endovascular treatment was attempted in this study. METHODS: A total of 78 patients with carotid cavernous fistulae or cavernous sinus dural arteriovenous malformations were treated. Obliteration of the fistulous rent and preservation of the ICA were the therapeutic goals. All patients, except one in whom acute bleeding occurred, received endovascular treatment as the first treatment. In 18 (23.4%) of these 77 patients, it was not possible to obliterate the fistulous rents without sacrificing the ICAs. The 18 patients and the 1 patient with acute bleeding underwent direct surgery to open the cavernous sinus. RESULTS: Various methods, including suturing or clipping the fistulae, sealing the fistulae with fascia and acrylate glue, and packing the cavernous sinus were applied. In each of three complicated cases, the cavernous segment of the ICA was trapped and an intracranial bypass from the petrous segment to the supraclinoid segment was performed. There was nor mortality, and the most common morbidity was transient oculomotor palsy, which occurred in eight patients. Follow-up angiography revealed that the ICAs or bypass grafts were thrombosed in 5 of the 19 patients who had undergone surgery. CONCLUSION: In this series, the overall ICA patency rate of patients who underwent embolization and surgery was 94%, and the obliteration rate of the fistulae was 100%. Direct surgery of the cavernous sinus as a complimentary treatment of embolization can increase the preservation rate of the ICA.

Adolescent↗
PubMed1997

Polymorphic markers of the glycogen debranching enzyme gene allowing linkage analysis in families with glycogen storage disease type III.

Glycogen storage disease type III (GSD-III), an autosomal recessive disease, is caused by deficient glycogen debranching enzyme (GDE) activity. We identified three polymorphic markers in the GDE gene using single strand conformation polymorphism (SSCP) analysis and DNA sequencing. They were -10G/A in the 5' non-translated region of exon 3,2001 + 8C/T in intron 16, and 3199C/T (P1067S) in exon 25. Two polymorphic markers (-10G/A and 2001 + 8C/T) were highly informative in both controls and GSD-III patients with heterozygosity values of 0.50 and 0.46, respectively. The third marker (3199C/T) had a heterozygosity value of 0.26. Restriction analysis of the PCR amplified genomic DNA products in two GSD-III families showed for the first time the potential use of these markers for carrier detection and prenatal diagnosis in this disease.

Base Sequence↗
PubMed1997

Churg-Strauss syndrome presented as multiple intracerebral hemorrhage.

Intracerebral hemorrhage is an uncommon sequel of Churg-Strauss syndrome. We describe a 27 y old Taiwanese male patient who was clinicopathologically diagnosed as Churg-Strauss syndrome. The patient experienced a sudden onset of blurring of vision and slowness of motion and speech. Magnetic resonance imaging of the brain revealed lobar hemorrhage on right parieto-occipital and left parietal areas. The cause of cerebral hemorrhage was probably due to poorly controlled high blood pressure and vasculitis. He received pulse therapy of methylprednisolone and cyclophosphamide followed by oral prednisolone. His neurological symptoms responded well to such a regimen. Cerebral hemorrhage is a major cause of morbidity and death in patients with Churg-Strauss syndrome. Uncontrolled high blood pressure may cause cerebral hemorrhage. Careful monitor of blood pressure is critical for the management of Churg-Strauss syndrome patients.

Adult↗
PubMed1997

[Studies on the molecular epidemiology of poliovirus type 1 in China].

A strain of poliovirus type 1 isolated from an endemic in Shandong Province in 1988 and three strains of poliovirus type 1 isolated from an endemic in Xinjiang in 1990 were analysed by dot blot hybridization with Sabin I specific probe and PCR amplification with Sabin I specific primers. They were proved to be non-Sabin-like poliovirus. The nucleotide sequences of VP1-2A junction region of four poliovirus type 1 isolates were analysed. It was found that the nucleotide diversity of four isolates with Sabin I was equal to or greater than 16.7%. This finding proved that they were wild polioviruses and greatly different fromSabin I. It was also found that the nucleotide sequence diversity among three strains from Xinjiang was very small (less than 2.6%) with identical amino acid sequences. This indicated that the three Xinjiang strains belonged to the same genotype. While the difference of Shandong strain from the three Xinjiang strains was between 14. 0% to 15.33% in nucleotide sequence and 2.0% to 4.0% in amino acids. This indicated that Shandong strain was apparently different from three Xinjiang strains and it belonged to another wild genotype which had a different history of evolution.

Amino Acid Sequence↗
PubMed1996

Local injection of kainic acid causes widespread degeneration of NADPH-d neurons and induction of NADPH-d in neurons, endothelial cells and reactive astrocytes.

Nitric oxide (NO), a diffusible gas, is a messenger molecule that mediates vascular dilatation and neural transmission. The enzyme nitric oxide synthase (NOS) present in neurons is activated by Ca2+ influx associated with activation of glutamate receptors. Cultured cortical neurons containing NOS are selectively vulnerable to injury by kainic acid (KA). However, the relationship between NOS neurons and excitotoxicity under in vivo conditions is not entirely clear. In the present study, we examined the time course and spatial distribution of changes in NOS neurons caused by an intracortical microinjection of KA in adult rats. NADPH-diaphorase (NADPH-d) histochemistry was used as a marker for NOS and the neuronal changes were correlated with changes in glial cells and endothelial cells. We demonstrated a rapid loss of NADPH-d neurons in the lesion center and degeneration of NADPH-d neurons and nerve terminals throughout ipsilateral cortex and hippocampus; the striatal neurons appeared to be unaffected. Subsequent to cortical neuronal degeneration, new NADPH-d activity appeared in proliferative reactive astrocytes and in endothelial cells at lesion periphery, and in neuronal groups at lesion periphery, in ipsilateral entorhinal cortex and bilateral hippocampus. These findings indicate that neurons expressing NADPH-d in cerebral cortex and hippocampus are selectively vulnerable to KA toxicity in vivo. The subsequent induction of NOS in neural and non-neural cells may be regarded as an adaptive response to the kainate-induced brain lesion.

Animals↗
PubMed1996

Mutations in exon 3 of the glycogen debranching enzyme gene are associated with glycogen storage disease type III that is differentially expressed in liver and muscle.

Glycogen storage disease type HI (GSD-III), an autosomal recessive disease, is caused by deficient glycogen debranching enzyme (GDE) activity. Most GSD-III patients are GDE deficient in both liver and muscle (type IIIa), and some GSD-III patients have GDE absent in liver but retained in muscle (type IIIb). The molecular basis for this enzymatic variability is largely unknown. In the present study, the analysis of the GDE gene in three GSD-IIIb patients by single-strand conformation polymorphism (SSCP), DNA sequencing, restriction analysis, and family studies, revealed each of them as being a compound heterozygote for two different mutations. The first mutant alleles in all three patients involved mutations in exon 3 at amino acid codon 6 of the GDE protein. Two had an AG deletion at nucleotides 17 and 18 of the GDE cDNA (17delAG) which resulted in change of subsequent amino acid sequence and a truncated protein (25X); the other had a C to T transition at nucleotide 16 of the cDNA which changed a Glutamine codon to a stop codon (Q6X). The 17delAG mutation was also found in 8 of the 10 additional GSD-IIIb patients. The Q6X mutation was found in one of the remaining two GSD-IIIb patients. These two mutations were not found in any of the 31 GSD-IIIa patients, 2 GSD-IIId patients, nor 28 unrelated normal controls. The second mutant alleles in each of the three GSD-IIIb patients were R864X, R1228X, and W68OX. The R864X and R1228X were not unique for GSD-IIIb as they were also found in GSD-IIIa patients (frequency of 10.3% and 5.2% in Caucasian patients, respectively). Our data demonstrated that both IIIa and IIIb had mutations in the same GDE gene and established for the first time the molecular basis of GSD-III that differentially expressed in liver and muscle. The striking and specific association of exon 3 mutations with GSD-IIIb may provide insight into mechanisms controlling tissue-specific expression of the GDE gene. The identification of exon 3 mutations has clinical significance as well because it distinguished GSD-IIIb from IIIa hence permitting diagnosis from a blood sample rather than a more invasive muscle biopsy.

Base Sequence↗
PubMed1996

A new fluorescent histological marker for ischemic neurons, EA 50: correlated with Fos and Jun/AP-1 immunoreactivity.

Cerebral ischemia/hypoxia induces ischemic neuronal changes characterized by nuclear pyknosis, cytoplasmic shrinkage, and basophilia. The ischemic neurons were shown to exhibit strong and persistent c-fos proto-oncogene. The ischemic neuronal changes and c-fos expression are thought to be the consequence of release of excessive glutamate by the ischemic neurons. In the present study, we investigated with immunohisto-chemistry the subcellular distribution of Fos and Jun/AP-1, the protein products of c-fos and c-jun proto-oncogenes, and compared them with histological changes shown by hematoxylin-eosin and by EA 50 stains. The latter is a stain mixture used traditionally in the Papani-colaou procedure and has a specific affinity for ischemic neurons. The active ingredient is eosin Y, a tetrabrominated derivative of fluorescein. With EA 50, the ischemic neurons stain red and emit a yellow fluorescence, while the non-ischemic neurons are green and non-fluorescent. The subcellular site of eosin Y binding corresponds with Fos and Jun/AP-1; all are concentrated in the nuclei and spread into the perikaryon, dendrites, and axons. The eosin Y-binding appears in neurons that have shown advanced ischemic changes. The dye is thus a good histological marker for damaged neurons, but requires freshly fixed tissues and paraffin sections of less than 4 microns thick. Preincubation of tissue sections in antibodies against Fos and Jun abolishes the eosin Y binding, suggesting that the dye may interact with Fos/Jun/AP-1 protein or other protein products in the ischemic neurons.

Animals↗
PubMed1996

Diagnosis and follow-up of carotid-cavernous fistulas by carotid duplex sonography and transcranial color Doppler imaging.

To investigate the suitability of extracranial carotid duplex (ECD) and transcranial color Doppler imaging (TCDI) in the diagnosis and follow-up of treatment in patients with carotid-cavernous fistulas (CCF), combined ECD and TCDI examinations were studied in seven patients with traumatic CCF. According to angiography, four patients had direct CCF, two indirect CCF and one both direct and indirect CCF. In ECD, hemodynamic parameters of the feeding artery showed an abnormally increased flow volume and decreased resistivity indices in five direct CCFs from the internal carotid artery and one indirect CCF from the external carotid artery. Direct visualization of the CCF was achieved in patients with direct CCF only, and revealed itself as a heterogeneous mosaic flash resulting from high flow velocities and turbulence. Patterns of venous drainage were detected via the transorbital and transforaminal windows in seven and five patients (four direct and one indirect CCF patients), respectively. These abnormal findings were improved or even normalized after successful treatment. In conclusion, combined ECD and TCDI examinations appear to be useful for the diagnosis and follow-up of CCF.

Adult↗
PubMed1996

Effects of isovolemic hemodilution on hemodynamics, cerebral perfusion, and cerebral vascular reactivity.

BACKGROUND AND PURPOSE: To verify the hemorheological effects of isovolemic hemodilution on hemodynamics and cerebral perfusion of normal humans, we tested the efficacy of isovolemic hemodilution in systemic hemodynamics and cerebral bood flow augmentation and its influences in vascular reserve. METHODS: Isovolemic hemodilution was studied in a total of 13 normal healthy subjects. Regional cerebral blood flow was measured by the xenon-enhanced CT method. Cerebral vascular activity was measured by acetazolamide challenge. These measurements, in association with hemorheological and hemodynamic monitoring, were analyzed before and after isovolemic hemodilution with low-molecular-weight dextran. RESULT: Our results showed significant change in hemodynamic parameters after isovolemic hemodilution, including tachycardia, a 24% increase of cardiac index, and decrease of peripheral vascular resistance. Both left and right heart work index increased as a consequence of increased cardiac index. Regional cerebral blood flow increased 35.0 +/- 2.5% at 3 hours after hemodilution and 20.2 +/- 3.9% at 1 week after hemodilution. Cerebral vascular reactivity decreased from 32.1 +/- 4.1% to 25.3 +/- 4.0% after hemodilution, implicating a certain degree of vasodilation in the process of hemodilution. The whole procedure of hemodilution was completed in 52 +/- 6 minutes, and the subjects did not report discomfort during the procedure. CONCLUSIONS: Isovolemic hemodilution in subjects with normal cerebral perfusion can augment cerebral blood flow efficiently in a rapid fashion, and this effect can last for at least a week. The mechanism of flow augmentation may be partially attributed to vasodilation, which could be manifested as tachycardia, increased cardiac output, and decreased cerebral vascular reactivity.

Acetazolamide↗
PubMed1996

Evaluation of intracranial and extracranial carotid steno-occlusive diseases in Taiwan Chinese patients with MR angiography: preliminary experience.

BACKGROUND AND PURPOSE: We attempted to evaluate the location of vascular lesions in cases of cerebrovascular steno-occlusive diseases in Chinese persons living in Taiwan. METHODS: With three-dimensional time-of-flight magnetic resonance angiography (MRA) as a screening tool, 108 symptomatic patients with cerebrovascular steno-occlusive diseases were examined. Cardioembolic disease and cerebral hemorrhage cases were excluded. The degrees of stenosis of bilateral cervical carotid arteries and their major intracranial tributaries were recorded. They were categorized as nonsignificant stenosis (0% to 49%), significant stenosis (50% to 99%), and total occlusion. RESULTS: Our data revealed that 32.4% of the cases were normal in either cervical carotid arteries or their intracranial tributaries. In 24.1% of the cases, significant extracranial carotid stenosis or occlusion was the only finding on MRA. In 25.9% of the cases, only significant intracranial-tributary stenosis was found. In 17.6% of them, significant lesions were found in both extracranial and intracranial carotid artery tributaries. CONCLUSIONS: A racial difference between Chinese and white patients in location of lesion in cerebrovascular steno-occlusive diseases was confirmed. About one third of symptomatic Chinese patients living in Taiwan showed small-vessel disease. Approximately 24% of patients had only extracranial carotid disease, and about 26% had only intracranial carotid tributary disease. We need a larger series of patients to confirm these findings. However, MRA might be a good screening tool for steno-occlusive cerebrovascular disease, especially in persons of a race with more intracranial carotid disease, such as the Chinese.

Adult↗
PubMed1996

Kleine-Levin syndrome in a boy with Prader-Willi syndrome.

A 9 1/2-year-old Taiwanese boy with Prader-Willi syndrome had the following characteristics: difficulties with sucking, feeding and hypotonia during infancy, a dysmorphic face (triangular mouth, high arched palate, almond-shaped eyes and large head circumference with a relatively narrow bifrontal diameter), borderline intelligence, hypogonadism, hyperphagia, skin picking and truncal obesity. The boy experienced two hypersomnia episodes, at age 8 and 9 years, with both episodes lasting for 10 days. During the two episodes, he was found to have an exacerbated case of hyperphagia, pica, poor emotional control, stereotyped speech and agitated behavior upon awakening. After each episode, the boy had complete remission. Our findings show that the two episodes are compatible with Kleine-Levin syndrome. The relationship between the two syndromes, the Prader-Willi syndrome and the Kleine-Levin syndrome, deserves further study.

Child↗
PubMed1996

Kainate-induced brain lesion: similar local and remote histopathological and molecular changes as in ischemic brain infarct.

Cerebral ischemia/hypoxia induces histopathological changes characterized by nuclear and cytoplasmic condensation and sustained c-fos expression. The ischemic changes are thought to be initiated by excessive glutamate released by the ischemic neurons. However, no comparative study has been made between the pathological and molecular changes caused by local injection of excitotoxin and by ischemia. In the present study, we investigated the histopathological changes in rat brains induced by an intracerebral microinjection of kainic acid, a potent analogue of glutamate using two newly available markers for ischemic neurons: Fos immunohistochemistry and EA 50 stain. The rats were sacrificed at intervals from 1 hour (h) to 28 days. We demonstrated that the neurons at the site of injection developed changes typical of ischemia 1 h post-lesion: nuclear and cytoplasmic condensation, strong Fos immunoreactivity and positive EA 50 stain. By 1 day, the neurons underwent necrosis and an infarct-like picture was produced. The neuronal degeneration rapidly spread to the bilateral neocortex, CA3 and CA4 regions of hippocampus, piriform gyrus, amygdala and cerebellar Purkinje cells. After 3 days, there was neovascularization and macrophage production in the lesion center and astrocytic proliferation at the lesion periphery. The CA1 of hippocampus showed delayed neuronal necrosis typical of ischemia. Thus, intracerebral microinjection of KA induces similar histopathological and molecular changes as those occurring in brain infarct and is a simple and reliable model for studying changes related to focal brain infarct.

Animals↗