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Biomedical subjects

C C Huang

Publications and source records attributed to C C Huang.

At least 307 records · Page 17Linked to original sources
PubMed1997

A multidisciplinary pulmonary rehabilitation program for patients with moderately severe chronic obstructive pulmonary disease.

A multidisciplinary pulmonary rehabilitation program was conducted for 13 outpatients (mean age 66 +/- 6.7 yr) with moderately severe chronic obstructive pulmonary disease. Changes in pulmonary function and blood gas data were not significant. Exercise capability, including 6-minute walking distance (WkD6), maximal work load (WkLmax), endurance time, and maximum heart rate, improved significantly (p < 0.05), as did subjective symptoms and quality of life. Of the observed changes, only baseline PaO2 and oxygen saturation were positively correlated with changes in maximum heart rate. The initial maximum heart rate was inversely related to both the absolute and percentage improvement. There were no significant relationships between improvement in WkD6 and age, initial arterial blood gas, or pulmonary function, but a significant relationship was found between baseline forced expired volume in the first second (FEV1) and percentage change in WkLmax. Our results indicate that patients with moderately severe chronic obstructive pulmonary disease can improve their exercise capacity, subjective symptoms, and quality of life through a pulmonary rehabilitation program. All patients can increase their endurance, regardless of their initial exercise performance. Maximum heart rate and FEV1 are predictors of exercise capability improvement.

Aged↗
PubMed1997

Malakoplakia of the prostate: a case report.

Malakoplakia is an unusual chronic inflammatory disease that was first discovered in the urinary bladder but has subsequently been described in other sites. Characteristic gross and microscopic features of the lesions have been well described. The diagnosis of this tumor-like lesion can only be established by pathologic examination of the involved tissue. A case of prostatic malakoplakia with characteristic gross and microscopic features is reported in a 59-year-old man who presented with urinary frequency and a diminished urinary stream. Clinically the condition mimicked carcinoma of the prostate gland and the patient underwent a radical retropubic prostatectomy. Postoperative recovery was uneventful. The clinical and pathological findings, differential diagnosis and pertinent literature are reviewed. Preoperative needle biopsy or intraoperative frozen section for tissue diagnosis is recommended to avoid unnecessary radical surgery for this type of tumor-like lesion.

Humans↗
PubMed1996

Effects of occupational dust exposure on the respiratory health of Portland cement workers.

The object of this study was to assess the relationship between occupational Portland cement dust exposure and respiratory health. Respiratory symptoms and ventilatory function were studied in a group of 591 male Portland cement workers employed in four cement plants. The prevalence of chronic respiratory symptoms was higher in exposed than in control workers. The exposed group had a significantly lower mean forced vital capacity (FVC), forced expiratory volume at 1 s (FEV1), and forced expiratory flows after exhalation of 50% and 75% of the vital capacity (FEF50, FEF75) than the control group. The data suggest that occupational exposure to Portland cement dust may lead to higher prevalence of chronic respiratory symptoms and the reduction of ventilatory capacity.

Adult↗
PubMed1996

Inhibition of calcium channels in rat hippocampal CA1 neurons by conantokin-T.

Effects of conantokin-T, a 21 amino acid peptide toxin isolated from the fish-hunting cone snail Conus tulipa, on the high-voltage-activated Ca2+ channel currents were studied in acutely dissociated rat hippocampal CA1 neurons using whole-cell voltage clamp-recording technique with 5 mM Ba2+ as the charge carrier. Conantokin-T inhibited the whole-cell Ba2+ current (IBa) in a concentration-dependent manner. The nimodipine (20 microM) and omega-agatoxin-IVA (0.2 microM) block of IBa were abolished in the presence of conantokin-T (3 microM); however, conantokin-T (3 microM) did not affect the block of IBa induced by 3 microM omega-conotoxin-GVIA. These results indicate that conantokin-T is a potent but wide-spectrum Ca2+ channel antagonist.

Animals↗
PubMed1996

The effects of induced apneic episodes on cerebral cortical oxygenation in newborn piglets.

The effect of different inspiratory oxygen levels (FiO2) on cortical oxygenation (pO2) during and after recovery from apnea, was investigated in 18 anesthetized, paralyzed, and mechanically ventilated newborn piglets. Heart rate (HR) and mean arterial blood pressure (MABP) were continuously monitored as the piglets were subjected to repeated episodes of apnea initiated by disconnecting the ventilator and terminated when HR decreased to less than 80 beats/min by reconnecting the ventilator. A closed cranial window was placed over the parietal cortex of the animals and cortical pO2 was measured optically by phosphorescence quenching. Apneic episodes induced in animals ventilated with 15%, 22% and 40% oxygen had mean duration's of apnea (time before HR decreased to less than 80 beats/min) of 80, 128 and 134 s, respectively. By the end of the apnea the MABP decreased to 82%, 64%, and 54% of control, respectively. The cortical pO2 decreased from control values of 24.1, 32.3 and 38.3 Torr at 15%, 22% and 40% oxygen, respectively, to 1.7 to 3.2 Torr at the end of the apneic episode. The duration of apnea necessary for the cortical pO2 to drop below 20.3 Torr was 18, 44 and 81 s at 15%, 22% and 40% oxygen, respectively. There was an inverse correlation between the rate of decline of cortical pO2 and baseline FiO2 levels. With reventilation, the cortical pO2 reached maximal values of 42.8, 51.9 and 57.2 Torr at 15%, 22%, and 40% oxygen, respectively, before returning to the pre-apnea values. The present results show that apnea of less than 30 s duration at an FiO2 of 22% do not result in significant cortical hypoxia in hemodynamically stable piglets. Increasing the FiO2 to above 22% may possibly increase the rate of recovery of tissue oxygenation but it also may facilitate post-hypoxic cortical hyperoxia, a factor that may predispose the immature brain to free radical injury.

Animals↗
PubMed1996

Inhibition of N-type calcium currents by lamotrigine in rat amygdalar neurones.

Lamotrigine (LAG) is a new anticonvulsant drug for the treatment of partial and secondarily generalized seizures. The present study was aimed at elucidating the possible involvement of Ca2+ channels in the action of LAG using whole-cell patch clamp recordings in acutely dissociated amygdalar neurones. Whole-cell Ca2+ currents (ICa) were elicited by 200 ms step commands from -70 mV to -10 mV. Application of LAG reduced the ICa by an average of 40.3 +/- 3.2%. The inhibition of ICa by LAG was markedly reduced or eliminated in the presence of the N-type Ca2+ channel blocker omega-conotoxin-GVIA (1 microM). These results suggest that LAG may exert its anticonvulsant effect through inhibition of presynaptic N-type Ca2+ channels, thereby reducing glutamate release.

Amygdala↗
PubMed1996

Involvement of the alpha subunit of farnesyl-protein transferase in substrate recognition.

Using photoaffinity labeling, we have identified a region in mammalian farnesyl-protein transferase (FPTase) involved in substrate recognition. The photolabel used (Compound 1) is a peptide containing the photoactive amino acid p-benzoylphenylalanine (Bpa). Upon exposure to UV light. Compound 1 inhibits FPTase activity in a time- and concentration-dependent manner. Photoinhibition of FPTase activity by Compound 1 is prevented by adding H-Ras to the reaction mixture, indicating that labeling is targeted to the enzyme active site. We used peptide mapping by HPLC, Edman sequencing, and matrix-assisted time-of-flight (MALDI-TOF) mass spectrometry to identify the site of interaction with radiolabeled Compound 1. These experiments indicate that a specific region of the alpha subunit of the enzyme, Asp110-Arg112, is involved in substrate binding and suggest that Glu111 is likely to be the residue covalently modified by the photoaffinity label. Sequence alignments between yeast and mammalian FPTases reveal that Glu111 is conserved. The implications of this finding are discussed in light of previous mutagenesis studies on FPTase.

Affinity Labels↗
PubMed1996

Mutual inhibitory effects between dopamine and carbachol on the excitatory synaptic transmission in the rat neostriatum.

The interactions between dopamine and carbachol on the excitatory synaptic transmission were studied in rat neostriatal slices using an intracellular recording method. Excitatory postsynaptic potentials (EPSPs) were evoked by cortical stimulation. Application of dopamine (DA; 0.1 microM) or carbachol (0.1 microM) produced a dramatic and reversible inhibition of the EPSP amplitude. The inhibitory effect induced by carbachol was markedly attenuated in the presence of either DA (0.1 microM) or the selective D2 dopaminergic receptor agonist (+/-)-2-(N-phenylethyl-N-propyl) amino-5-hydroxytertralin (PPHT; 0.1 microM), but not by the D1 dopaminergic receptor agonist (+/-)-7, 8-dihydroxy-3-allyl-1-phenyl-2, 3, 4, 5-tetrahydro-1H-3-benzazepine (SKF-38393; 0.1 microM) or the D3 dopaminergic receptor agonist R(-)-(4aS, 10bS)-3, 4, 4a, 10b-tetrahydro-4-propyl-2H, 5H-[1] benzogyrano-[4,3-b]-1, 4-oxazin-9-ol (PD-128,907; 0.1 microM). Conversely, muscarinic receptor activation with carbachol (0.1 microM) also completely abolished the DA-induced depression of the EPSP amplitude. In addition, the inhibitory effect of DA on the carbachol-induced depression of the EPSP amplitude was antagonized by sulpiride (1 microM), a selective D2 dopaminergic receptor antagonist. However, D1 dopaminergic receptor antagonist (+/-)-7-bromo-8-hydroxy-3-methyl-1-phenyl-2, 3, 4, 5-tetrahydro-3-benzazepine (SKF-83566; 1 microM) did not affect DA's inhibition. Rp-adenosine-3',5'-cyclic monophosphothioate (Rp-cAMPS; 25 microM), a potent inhibitor of cAMP-dependent protein kinase A (PKA), alone decreased the amplitude of EPSP below baseline values and mimicked the inhibitory effect of DA on the carbachol-induced depression of the EPSP amplitude. Based on these findings, we conclude that the inhibitory effects of D2 dopaminergic receptor and muscarinic receptor activation on the excitatory synaptic transmission in the neostriatum are non-additive and therefore are antagonistic interactions. furthermore, the effect of muscarinic receptor stimulation will depend on the extent of D2 dopaminergic receptor activation and the modulation of the cellular PKA-dependent messenger system seems to contribute to their interactions.

Animals↗
PubMed1996

Blockade of isoproterenol-induced synaptic potentiation by tetra-9-aminoacridine in the rat amygdala.

The effects of tetrahydro-9-aminoacridine (THA) on beta-adrenoceptor activation-induced synaptic potentiation were studied in brain slices of the rat amygdala using intracellular recording techniques. To exclude the involvement of N-methyl-D-aspartate (NMDA) receptors, all the experiments were performed in the presence of NMDA receptor antagonist, D-APV (50 microM). Bath application of isoproterenol (Iso; 15 microM) results in a long-lasting enhancement of the amplitude of excitatory postsynaptic potentials (EPSPs) to 200 +/- 6% of baseline. Forskolin, which directly activates adenyl cyclase, produces a similar effect suggesting that Iso may act through a cyclic AMP-dependent mechanism. Pretreatment of the slices with THA (300 microM) completely abolishes the Iso- and forskolin-induced synaptic potentiation. We hypothesize that the locus of THA/beta-adrenoceptor interaction is presynaptic; the underlying mechanism is likely due to THA's depression of transmitter release via a presynaptic blockade of voltage-dependent Ca2+ channels.

Adrenergic beta-Agonists↗
PubMed1996

Reversal of the hydrogen bond to zinc ligand histidine-119 dramatically diminishes catalysis and enhances metal equilibration kinetics in carbonic anhydrase II.

Direct metal ligands to transition metals in metalloproteins exert a profound effect on protein-metal affinity and function. Indirect ligands, i.e., second-shell residues that hydrogen bond to direct metal ligands, typically exert more subtle effects on the chemical properties of the protein-metal complex. However, E117 of human carbonic anhydrase II (CAII), which is part of the E117-119-Zn(2+) triad, is a notable exception: E117-substituted CAIIs exhibit dramatically increased kinetics of zinc complexation, and the E117Q variant exhibits enormously diminished catalytic activity and sulfonamide affinity. The three-dimensional structures of zinc-bound and zinc-free E117Q CAII reveal no discrete structural changes in the active site that are responsible for enhanced zinc equilibration kinetics and decreased activity. Additionally, the structure of the acetazolamide complex is essentially identical to that of the wild-type enzyme despite the 10(4)-fold loss of enzyme-inhibitor affinity. We conclude, therefore, that the functional differences between E117Q and wild-type CAIIs arise from electrostatic and not structural differences in the active site. We propose that the E117Q substitution reverses the polarity of the residue 117-H119 hydrogen bond, thereby stabilizing H119 as a histidinate anion in the E117Q CAII holoenzyme. The additional negative charge in the first coordination sphere of the metal ion increases the pK(a) of the zinc-water ligand, destabilizes the transition state for CO(2) hydration, and facilitates the exchange of a zinc-histidine ligand with an additional water molecule by decreasing the stability of the tetrahedral zinc complex. These novel properties engineered into E117Q CAII facilitate the exploitation of CAII as a rapid and sensitive Zn(2+) biosensor.

Acetazolamide↗
PubMed1996

Isoproterenol potentiates synaptic transmission primarily by enhancing presynaptic calcium influx via P- and/or Q-type calcium channels in the rat amygdala.

The effects of selective beta-adrenergic receptor agonist isoproterenol (Iso) on neuronal excitability and synaptic transmission were investigated in brain slices of rat amygdala. Iso (15 microM) produced a long-lasting enhancement of the EPSP that was not blocked by pretreatment with 20 microM D-2-amino-5-phosphonovalerate (D-APV) alone or D-APV in combination with kynuretic acid (1 mM). The sensitivity of postsynaptic neurons to the glutamate receptor agonist AMPA was unchanged by Iso pretreatment. Superfusion of Iso reversibly blocked the after-hyperpolarization (AHP) that followed a depolarizing current pulse and caused more action potential firing. Intracellular application of a selective inhibitor of the catalytic subunit of cAMP-dependent protein kinase A blocked the effect of Iso on the AHP, whereas Iso-induced potentiation was entirely normal in the same neuron. In addition, Iso decreased the magnitude of paired-pulse facilitation, which is consistent with a presynaptic mode of action. Substituting the Mg2+ for Ca2+ in the medium completely abolished the Iso-induced enhancement of the EPSP. The effect of Iso also was blocked by low concentrations of omega-agatoxin-IVA, but not by nifedipine or omega-conotoxin-GVIA. These results suggest that Iso enhances synaptic transmission in the amygdala via a presynaptic site of action: the mechanism underlying the potentiating effect likely is attributable to an increased Ca2+ influx through P- and/or Q-type Ca2+ channels.

Action Potentials↗
PubMed1996

Volume-activated taurine permeability in cells of the human erythroleukemic cell line K562.

The effects of hypotonic shock on cell volume, taurine influx and efflux were examined in the human erythroleukemic cell line K562. Cells exposed to hypotonic solutions exhibited a regulatory volume decrease (RVD) following rapid increases in cell volume. Cell swelling was associated with a increased taurine influx and efflux. The volume-activated taurine pathway was Na(+)-independent, and increased in parallel with increasing cell volume. The chloride channel blocker, 2,5-dichlorodiphenylamine-2-carboxylic acid (DCDPC), completely blocked the volume-activated taurine influx and efflux, while [dihydroindenyl)oxy]alkanoic acids (DIOA) and 5-nitro-2-(3-phenylpropylamino)benzoic acid (NPPB), an anion exchanger and anion channel blocker, respectively, also inhibited significantly. These results suggest that taurine transport is increased in response to hypotonic stress, which may be mediated via a volume-activated, DCDPC-sensitive anion channel.

Anions↗
PubMed1996

Presynaptic inhibition of excitatory neurotransmission by lamotrigine in the rat amygdalar neurons.

Lamotrigine (LAG) is a new antiepileptic drug which is licensed as adjunctive therapy for partial and secondary generalized seizures. In the present study, the mechanisms responsible for its antiepileptic effect were studied in rat amygdaloid slices using intracellular recording and whole-cell patch clamp techniques. Bath application of LAG (50 microM) reversibly suppressed the excitatory postsynaptic potentials (EPSPs) and currents (EPSCs) evoked by stimulating ventral endopyriform nucleus. Synaptic response mediated by the N-methyl-D-aspartate (NMDA) receptor (EPSPNMDA) was isolated pharmacologically by application of a solution containing non-NMDA receptor antagonist 6-cyano-7-nitroquinoxaline-2,3-dione (CNQX,10 microM) and gamma-aminobutyric acidA receptor antagonist bicuculline (20 microM). LAG produced a parallel inhibition of EPSPNMDA. Postsynaptic depolarization induced by alpha-amino-5-methyl-4-isoxazole propionate (AMPA) was not altered by LAG. In addition, LAG increased the ratio of the second pulse response to the first pulse response (P2/P1), which is consistent with a presynaptic mode of action. The L-type Ca+2 channel blocker nifedipine (20 microM) had no effect on LAG-induced presynaptic inhibition. However, the depressant effect of LAG was markedly reduced in slices pretreated with N-type Ca+2 channel blocker omega-conotoxin-GVIA (omega-CgTX-GVIA, 1 microM) or a broad spectrum Ca+2 channel blocker omega-conotoxin-MVIIC (omega-CgTX-MVIIC, 1 microM). It is concluded that a reduction in omega-CgTX-GVIA-sensitive Ca+2 currents largely contributes to LAG-induced presynaptic inhibition.

Amygdala↗
PubMed1996

Variations of the left and middle hepatic veins: application in living related hepatic transplantation.

The anatomic variations of the middle hepatic vein (MHV) and left hepatic vein (LHV) in 200 patients with normal liver function were analyzed using ultrasonography to clarify the feasibility of resecting the left lobe or left lateral segment in living subjects for living related hepatic transplantation (LRHT). The MHV and LHV form a common trunk in 70% of cases but drain independently into the inferior vena cava (IVC) in 30%. In 7% of cases, the left median vein (LMV) drains into the MHV, in 32% of cases the anterior superior segmental vein (ASSV) that drains segment 8 flows into the MHV. The distance between the two confluence points (LHV flows into MHV or IVC and LMV flows into the MHV) ranged from 0.3 cm to 2.5 cm with an average of 0.75 cm. The diameter of the LMV at the point that flows into MHV ranged from 0.3 cm to 0.9 cm. with an average of 0.61 cm. The distance from the IVC to the confluence of the MHV and LHV ranged from 0 cm to 3.5 cm with an average of 1.5 cm in those cases whose MHV and LHV presented as common trunks. Preoperative delineation of this complex venous anatomy is of paramount importance because the hepatic veins have to be transected in the cutting plane of the liver. The location of this plane is determined by the optimal graft volume required, and both the graft and the remnant liver have to retain perfect function. The venous anatomy would change the cutting plane in the living donor and the surgical method of anastomosis for the recipient.

Adult↗
PubMed1996

Mediation of signal transduction in keratinocytes of human middle ear cholesteatoma by ras protein.

Immunolocalization was used to investigate the distribution of ras protein in both congenital and acquired cholesteatoma tissues. A pathological feature of middle ear cholesteatoma included accumulation of keratin debris due to active proliferation and differentiation of keratinocytes. Ras protein localized to the inner plasma membrane and cytoplasm of keratinocytes in all of the epithelial layers in both congenital and acquired cholesteatoma specimens. Keratinocytes in the basal layer were stained more intensely than their differentiated counterparts. Findings also demonstrated that receptors for epidermal growth factor, fibroblast growth factor, and plateletderived growth factor were present in the plasma membrane of keratinocytes. C-jun, a transcription factor was found in the nuclei of keratinocytes of the cholesteatoma epithelium. These findings indicate that ras protein plays a pivotal role in a signal transduction cascade between growth factor receptors in the plasma membrane and the transcription factor, c-jun, in the nuclei of keratinocytes during the growth of cholesteatoma.

Cholesteatoma, Middle Ear↗
PubMed1996

Middle ear catalase distribution in an animal model of otitis media.

Increasing evidence implicates free radicals in the pathogenesis of inflammatory disease, including otitis media. The anti-oxidant enzymes catalase, glutathione peroxidase and superoxide dismutase protect tissues from the destructive effects of free radicals. Our previous work has shown depressed levels of superoxide dismutase in the infected middle ears of a guinea pig model of otitis media in comparison with normal control ears. We studied the distribution and relative abundance of catalase in the middle ear of this animal model in an effort to elucidate the role free radicals play in the pathogenesis of otitis media. Catalase distribution was mapped immunohistochemically in the middle ears of guinea pigs with induced streptococcus otitis media, and compared with normal control ears. In the control ears, catalase was localized to the epithelium of the middle ear mucosa, with scant distribution in the submucosa. The infected ears demonstrated inflammatory cell invasion with hyperemia and submucosal edema. Catalase was localized to the epithelium and had scant distribution in the submucosa. This distribution was similar to that found previously with superoxide dismutase. Enzyme-linked immunosorbent assay of catalase demonstrated a mean value of 1.00 +/- 0.06 microgram/mg protein in the control ears, and 1.06 +/- 0.12 microgram/mg in the infected ears, but these two values were not statistically different.

Acute Disease↗