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Biomedical subjects

C C Huang

Publications and source records attributed to C C Huang.

At least 325 records · Page 18Linked to original sources
PubMed1996

Posttraumatic gluteal epidermal cyst with ischiorectal and presacral extension.

An unusual case of rapid-growing posttraumatic gluteal epidermal cyst with ischiorectal and presacral extension is reported. Pertinent clinical history and magnetic resonance imaging allowed accurate preoperative diagnosis. Cautious complete excision was important to prevent recurrence. To our knowledge, posttraumatic gluteal epidermal cyst with this unusual clinical presentation has not been described previously.

Adult↗
PubMed1996

Dopa-responsive dystonia: clinical and family study in Taiwanese.

We report the clinical features of four female patients with dopa-responsive dystonia (DRD), and the survey of the family members. The patients were 2 sisters and 2 sporadic patients from 3 families. Their age of onset ranged between 5 and 13 years. The clinical manifestation was characterized by limb dystonia which was relieved by L-dopa treatment. Diurnal fluctuation disappeared 15 years later in one patient. There was a wide spectrum of Parkinsonian features and variability of dystonia. Response of L-dopa was still excellent 20 years later. In survey of the family members, there was neither bradykinesia, rigidity, tremor nor dystonia.

Adult↗
PubMed1996

Investigations on the mechanism of tetrahydro-9-aminoacridine-induced presynaptic inhibition in the rat amygdala.

Tetrahydro-9-aminoacridine, a centrally acting anticholinesterase, has been reported to improve clinical conditions of certain patients with Alzheimer's disease. A previous study from our laboratory suggested that tetrahydro-9-aminoacridine presynaptically inhibited synaptic transmission. In the present study, the mechanism responsible for presynaptic inhibition mediated by tetrahydro-9-aminoacridine was studied in the rat amygdalar slice preparation using intracellular recording techniques. Bath application of tetrahydro-9-aminoacridine reversibly suppressed the excitatory postsynaptic potential. Tetrahydro-9-aminoacridine's inhibitory action was unaffected by the pretreatment of slices with baclofen (5 microM), suggesting that it did not act by eliciting the release of GABA, which binds presynaptic GABAB receptors to inhibit glutamate release. The synaptic depressant effect of tetrahydro-9-aminoacridine was blocked in the presence of 4-aminopyridine. The action of 4-aminopyridine could be reversed by reducing extracellular Ca2+ concentrations from a control level of 2.5 to 0.5 mM, suggesting that tetrahydro-9-aminoacridine inhibits excitatory postsynaptic potentials by acting directly at the terminals to decrease a Ca2+ influx. The L-type Ca2+ channel blocker nifedipine (50 microM) had no effect on tetrahydro-9-aminoacridine-induced presynaptic inhibition. However, the depressant effect of tetrahydro-9-aminoacridine was partially occluded in slices pretreated with the N-type Ca2+ channel blocker omega-conotoxin GVIA (1 microM). It is concluded that a reduction in omega-conotoxin GVIA-sensitive Ca2+ currents contributes to tetrahydro-9-aminoacridine-mediated presynaptic inhibition. After exposure to bicuculline, a GABAA receptor antagonist, afferent stimulation evoked epileptiform bursts. Occasionally, spontaneous bursts similar in waveform to synaptically triggered bursts also occurred in disinhibited slices. Application of tetrahydro-9-aminoacridine reversibly reduced the burst duration in a concentration-dependent manner. These results suggest that tetrahydro-9-aminoacridine possesses anticonvulsant activity against disinhibited bursts.

4-Aminopyridine↗
PubMed1996

Carbachol induces inward current in neostriatal neurons through M1-like muscarinic receptors.

The effects of carbachol on rat neostriatal neurons were examined in the slice and the freshly dissociated neuron preparations using intracellular and whole-cell voltage-clamp recording methods. Superfusion of carbachol (30 microM) produced a depolarization concomitant with an increase in the rate of spontaneous action potentials. This depolarization was associated with an increase in the input resistance. The carbachol-induced membrane depolarization was blocked by pirenzepine (1 microM), a selective M1 muscarinic receptor antagonist. In other experiments, we observed that carbachol induced a transient inward current on the freshly dissociated neostriatal neuron at a holding potential of -60 mV in a concentration-dependent manner underlying the whole-cell voltage-clamp mode. The inward current caused by carbachol was not reduced by tetrodotoxin (1 microM), calcium-free recording solution or Cd2+ (100 microM). However, it was blocked by Ba2+ (100 microM). In addition, the carbachol-induced inward current reversed polarity at about the potassium equilibrium potential. The whole-cell membrane inward current in response to voltage-clamp step from -90 to -140 mV was reduced by 30 microM carbachol. With stronger hyperpolarization beyond the potassium equilibrium potential, carbachol produced a progressively greater reduction in membrane current. This inhibitory effect was also abolished by Ba2+ (100 microM). A concentration of 30 microM carbachol-induced inward current could be reversibly antagonized by the M1 muscarinic receptor antagonist pirenzepine (0.1-1 microM), with an estimated IC50 of 0.3 microM. However, other muscarinic receptor subtype (M2 or M3) antagonists could also block the carbachol-induced inward current. The rank order of antagonist potency was: pirenzepine (M1 antagonist) > 4-diphenylacetoxy-N,N-methyl-piperidine methiodide (M3/M1 antagonist) > gallamine (M2 antagonist). Based on these pharmacological data, we concluded that carbachol can act at M1-like muscarinic receptors to reduce the membrane K+ conductances and excite the neostriatal neurons.

Animals↗
PubMed1996

A new approach to the treatment of true-combined endodontic-periodontic lesions by the guided tissue regeneration technique.

Clinicians often have difficulty in the diagnosis and treatment of the combined endodontal and periodontal (endo-perio) lesion. A case of an endo-perio true-combined lesion on a maxillary premolar was first treated with conventional endodontic therapy. Periodontal surgery was then completed, which included scaling and root planing and apical curettage on the tooth. The facial bony defect was then filled with a decalcified freeze-dried bone allograft mixed with tetracycline powder. A non-resorbable Teflon membrane was then used to cover the bone material and the periodontal flap sutured over this. This combined treatment resulted in minimal probing depth (2 mm), maximal clinical attachment gain (8 mm), as well as radiographic evidence of alveolar bone gain. This case report demonstrates that proper diagnosis, followed by removal of etiological factors and utilizing the guided tissue regeneration technique combined with osseous grafting, will restore health and function to a tooth with severe attachment loss caused by an endo-perio lesion.

Adult↗
PubMed1996

Heat shock proteins in middle ear cholesteatoma.

Heat shock proteins (HSPs), particularly HSP60 and HSP70, may have integral roles in several aspects of the pathogenesis of acquired cholesteatoma. Cholesteatoma is usually associated with an inflammatory reaction occurring in the middle ear cavity, leading to proliferation, differentiation, and programmed cell death of keratinocytes. The presence of HSP60 and HSP70 in cholesteatoma was demonstrated by the immunoblotting assay with specific anti-HSP60 and anti-HSP70 antibodies after protein extraction. The distribution of HSP60 and HSP70 in the cholesteatoma tissues was studied immunohistochemically with paraffin-embedded sections. HSP60 and HSP70 appeared to be localized in the cytoplasm of keratinocytes in all layers of the epithelium of cholesteatoma. Moreover, HSP70 was found in the nucleus of keratinocytes. Both HSPs were not labeled in the epidermis of the external ear canal skin or normal facial skin, except for significant staining on keratinocytes of hair follicles in facial skin. High density of HSP60 and HSP70 may be induced by the inflammatory reaction and immune responses in the middle ear cavity during the clinical development of cholesteatoma. Induction of HSP60 and HSP70 in cholesteatoma epithelium may also be related to hyperproliferation and active differentiation of basal keratinocytes, which cause the accumulation of keratin debris, a characteristic feature of cholesteatoma. In the nucleus of keratinocytes, HSP70 may act to stabilize p53 protein, which functions as a negative regulator of cellular proliferation and is crucial to apoptosis of keratinocytes. This study demonstrates HSPs in cholesteatoma and suggests important roles for HSPs in the clinical development of cholesteatoma.

Adult↗
PubMed1996

Structural motifs encoded by individual exons of the human neurokinin-1 receptor gene interact differentially with selective agonists and antagonists.

Three chimeric receptors were constructed by exchanging exons between human neurokinin NK1 and NK3 receptor genes. The N-terminal sequences of these chimeric receptors are encoded by exon 1, exon 1-2, or exon 1-3 of the NK1 receptor gene, whereas the remaining C-terminal sequences of these chimeric receptors are encoded by corresponding exons of the human NK3 receptor gene. Substance P bound with high affinities to all three chimeric receptors, suggesting that in addition to the common structures composed of conserved amino acid residues among neurokinin receptors, structural elements encoded by the first exon of the human NK1 receptor gene may also play an important role for substance P binding. On the contrary, potent NK1 antagonists L703,606 and SR140,333 did not show any detectable binding to these chimeric receptors. In accordance, sequences encoded by exon 4, and possibly exon 5, are likely to contain important structural motifs that may directly or indirectly influence the binding of these antagonists. Further comparison of the binding affinities of highly selective NK1 agonists, [Sar9, Met(O2)11] substance P, substance P methyl ester, and septide, revealed that each agonist may interact differently with the human NK1 receptor. These results show that the exon-exchanging technique can be a useful tool for studying structure-function relationships of receptors in which exon-intron junctions are fully conserved among receptor subtypes.

Amino Acid Sequence↗
PubMed1996

Chronic elemental mercury intoxication: neuropsychological follow-up case study.

In initial and follow-up investigations of neuropsychological function in a patient with elemental mercury intoxication, his scores were compared with those of a group of normal control subjects matched for sex, age and education. Each subject received a comprehensive neuropsychological examination including a personality inventory. On the initial examination the results indicated that the patient had a significant depression of performance intellectual functioning, impairments of attention, non-verbal short-term memory and visual judgement of angles and directions, psychomotor retardation and personality changes including depression, anxiety, desire to be alone, lack of interest and sensitivity to physical problems. Such an impairment picture is compatible with the previous observations of individuals with chronic exposure to elemental, organic or inorganic mercury. The follow-up study was undertaken about 1.5 years later. The results show that the patient's cognitive and personality functions were fully recovered. Our findings thus suggest a reversibility of impaired neuropsychological function in persons with elemental mercury poisoning if a prompt removal from the toxic environment is accomplished, together with proper medical treatment.

Adult↗
PubMed1996

Frequency of linear hyperechogenicity over the basal ganglia in young infants with congenital rubella syndrome.

Five young infants with congenital rubella syndrome (CRS) underwent cranial ultrasonographic examinations and/or computed tomographic examinations. Only two of these infants were small for their gestational age, and none of them were microcephalic at birth. Deafness and ocular lesions were found in four patients, and congenital heart disease was found in three. All had abnormal ultrasonographic findings: linear-shaped hyperechogenicity over the basal ganglia was noted for five patients, periventricular punctate hyperechogenicity was noted for three, and subependymal cysts were observed in two. Follow-up ultrasonograms for two of the patients showed progressively enlarging hyperechogenic lesions. Calcification was found in both patients examined by means of computed tomography. All patients became microcephalic, with profound global developmental delay. Intracranial calcifications are common findings in patients with CRS. Ultrasonography should be performed for high-risk neonates, regardless of their symptoms. The finding of linear hyperechogenicity over the basal ganglia should prompt a search for all congenital infections, including CRS.

Basal Ganglia↗
PubMed1996

Peritoneal nitric oxide is a marker of peritonitis in patients on continuous ambulatory peritoneal dialysis.

Nitric oxide plays an important role in mediating the inflammatory process. The aim of this study was to evaluate if nitric oxide production was increased during peritonitis in patients receiving continuous ambulatory peritoneal dialysis (CAPD), and the association with the prognosis. The study population comprised 21 patients with 22 episodes of peritonitis. Fifteen patients without peritonitis were controls. Nitrate was measured by HPLC and nitrite by the Griess method, to reflect nitric oxide production. Peritoneal dialysate effluent and plasma were collected from six patients during peritonitis and 1 week after treatment to study changes in dialysate:plasma ratio. In 15 patients, nitrite was measured during peritonitis and every 3 days for 2 weeks or until normalized for evolutional changes. The dialysate:plasma ratios of nitrate and nitrite during peritonitis were reduced 26% and 41.5%, respectively, after 1 week of treatment, indicating the peritoneal production of nitric oxide during peritonitis. In the evolutional study, a 5.1-fold increase of peak nitrite levels in bacterial peritonitis (n = 13) and a 2.5-fold increase in fungal peritonitis (n = 3) were observed compared to controls. Nitrite gradually declined to control levels (9.3 +/- 7.2 days) after effective antibiotic treatment, but took longer than to normalize leukocyte count in the peritoneal dialysate effluent (3.9 +/- 1.9 days). In four patients with refractory peritonitis (Candida infection in three, Acinetobacter infection in one), the nitrite levels remained elevated 2-fold despite treatment, and the catheters were removed. It is concluded that nitrite levels in peritoneal dialysate effluent may serve as a marker to assess treatment efficacy in CAPD patients with peritonitis.

Acinetobacter Infections↗
PubMed1996

Carbon disulfide induced polyneuropathy: sural nerve pathology, electrophysiology, and clinical correlation.

We report the clinical features, electrophysiological studies, sural nerve pathology and recovery course of carbon disulfide-(CS2) induced polyneuropathy in a 48-year-old man who worked in a viscose rayon plant. Sural nerve biopsy 2 years later still showed degeneration of both axon and myelin with a predominant loss of large myelinated fibers and remyelination. Electrophysiologic studies revealed mixed axonal and demyelinating polyneuropathy. To our knowledge, this is the first human report of sural nerve pathology in the recovery stage due to CS2 intoxication. After diagnosis, the patient was removed from the toxic environment. In the following three years, he showed part recovery predominantly in motor function compatible with the serial nerve conduction studies. We conclude that CS2 polyneuropathy may partly recover years after cessation of exposure.

Axons↗
PubMed1996

Differences in factors influencing the familial aggregation of febrile convulsion in population and hospital patients.

Socio-demographic data, initial clinical manifestations, outcome and family aggregation of febrile convulsion (FC) were compared between 85 population and 364 multicenter patients. More patients presented with clustering of seizures and had recurrence of FC in multicenter group than in population group. Multicenter patients had more fever episodes per year, more day-card attendance and a higher incidence of FC history in their parents. The odds ratio of FC in the siblings was 6:1 in population group and 12:1 in multicenter group. Lower socioeconomic status influenced the presence of FC in the sibling of population group. Instead, FC histories in the father and paternal cousins of probands had influence on the presence of FC in the siblings of multicenter group. We conclude that the population FC sample rather than the hospital sample is the more representative. And there are differences not only in the clinical manifestations but also in the effect of environmental and genetic influences on the family aggregation in population and hospital patients.

Adolescent↗
PubMed1996

Differential control of transcription by homologous homeodomain coregulators.

The human herpes simplex virus type 1 (HSV-1) transactivator VP16 and its homolog from bovine herpes-virus 1 (BHV-1) can each recruit the human homeodomain protein Oct-1 into a transcriptional regulatory complex. Here, we show that these two Oct-1 coregulators possess similar, if not identical, homeodomain recognition properties but possess different virus-specific cis-regulatory specificities: the HSV-1 VP-16 protein activates transcription from the HSV-1 VP16 response element, and the BHV-1 VP16 protein activates transcription from the BHV-1 VP16 response element. A distinct 3-bp segment, the D segment, lying 3' of the canonical TAATGARAT motif (where R is a purine) in the VP16 response element is responsible for the differential cis element recognition and transcriptional activation by these two homeodomain coregulators. These results demonstrate how a single homeodomain protein can direct differential transcriptional regulation by selective association with homologous homeodomain coregulators.

Animals↗
PubMed1996

TXA2 agonists inhibit high-voltage-activated calcium channels in rat hippocampal CA1 neurons.

Whole cell voltage clamp recordings were used to investigate the effects of thromboxane A2 (TXA2) agonists on the voltage-dependent Ca2+ currents in rat hippocampal CA1 neurons. TXA2 agonists [1S-[1 alpha, 2 beta(5Z), 3 alpha(1E, 3S*)4 alpha ]]-7-[3-[3-hydroxy-4-(4'-iodophenoxy)-1-butenyl]-7-oxabicyclo [2,2,1]heptan-2-yl]-5-heptenoic acid (I-BOP) and U-46619, reversibly suppressed the whole cell Ca2+ currents in a concentration-dependent manner. The effect was blocked by specific TXA2 receptor antagonist, SQ-29548. I-BOP as well as U-46619 inhibited both omega-conotoxin GVIA (CgTx)-sensitive and nimodipine sensitive Ca2+ currents but had no effect on CgTx/nimodipine insensitive Ca2+ currents. The I-BOP and U-46619 inhibition of Ca2+ currents was blocked by internal dialysis of hippocampal neurons with specific protein kinase C (PKC) inhibitors, NPC-15437 and PKC inhibitor-(19-36). Pretreatment of hippocampal neurons with either 5 micrograms/ml pertussis toxin (PTX) or 5 micrograms/ml cholera toxin (CTX) did not significantly affect the suppression of the Ca2+ currents by I-BOP and U-46619. Dialyzing with 1 mM guanosine 5'-O-(3-thiotriphosphate) or 1 mM GDP significantly attenuated the I-BOP or U-46619 action. These results demonstrate that TXA2 agonists inhibit both CgTx- and nimodipine-sensitive Ca2+ currents but not CgTx/nimodipine-insensitive currents in rat hippocampal CA1 neurons via a PTX- and CTX-insensitive G protein-coupled activation of the PKC pathway.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1996

Swelling-activated amino acid efflux in the human neuroblastoma cell line CHP-100.

1. The effects of hypoosmotic stress on cell volume and amino acid efflux were evaluated in the human neuroblastoma cell line CHP-100 with the Coulter Counter Multisizer and radiolabeled amino acid efflux, respectively. 2. CHP-100 cells swelled by approximately 35 +/- 5% (means +/- SE) when the osmolarity of the solution was decreased from 290 to 190 mOsm/kg H2O. The rapid swelling was followed by a biphasic regulatory volume decrease (RVD). 3. In cells loaded with 14C-taurine, hypoosmotic stress induced a 300 +/- 22% (n = 23, P < 0.05) increase in taurine efflux compared with controls. This efflux was inhibited by the chloride channel blockers 5-nitro-2-(3-phenylpropylamino)-benzoic acid (NPPB), 4,4'-diisothio-cyanostilbene-2,2'-disulfonic acid (DIDS), niflumic acid and by the volume-activated anion channel blocker tamoxifen. In addition, the swelling-activated taurine efflux was dependent upon extracellular calcium. 4. Similarly, in cells loaded with 14C-glycine, hypoosmotic stress significantly increased glycine efflux, which was also sensitive to NPPB. In contrast, efflux of 3H-glutamate was not significantly altered after hypoosmotic stress. 5. With the use of patch clamp recording techniques, Cl- channels were activated in cell attached patches after exposure to hypoosmotic solutions. 6. In nystatin perforated patches, permeability of the hypoosmotically activated anion channel was observed to be SCN- > I- > Br- > Cl- >> Glutamate. 7. It is concluded that in CHP-100 cells, anion channels are activated during hypoosmotic stress and these channels represent a pathway for efflux of amino acids.

Amino Acids↗