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H T Ma

Publications and source records attributed to H T Ma.

At least 19 recordsLinked to original sources
PubMed2003

The enhancement of TiO2 photocatalytic activity by hydrogen thermal treatment.

In this study, conventional TiO2 powder was heated in hydrogen (H2) gas at a high temperature as pretreatment. The photoactivity of the treated TiO2 samples was evaluated in the photodegradation of sulfosalicylic acid (SSA) in aqueous suspension. The experimental results demonstrated that the photodegradation rates of SSA were significantly enhanced by using the H2-treated TiO2 catalysts and an optimum temperature for the H2 treatment was found to be of 500-600 degrees C. The in situ electron paramagnetic resonance (EPR) signal intensity of oxygen vacancies (OV) and trivalent titanium (Ti3+) associated with the photocatalytic activity was studied. The results proved the presence of OV and Ti3+ in the lattice of the H2-treated TiO2 and indicated that both were contributed to the enhancement of photocatalytic activity. Moreover, the experimental results presented that the EPR signal intensity of OV and Ti3+ in the H2-treated TiO2 samples after 10 months storage was still significant higher than that in the untreated TiO2 catalyst. The experiment also demonstrated that the significant enhancement occurred in the photodegradation of phenol using the H2-treated TiO2.

Benzenesulfonates↗
PubMed2001

Expression of functional receptor-coupled TRPC3 channels in DT40 triple receptor InsP3 knockout cells.

The TRPC3 channel, an intensively studied member of the widely expressed transient receptor potential (TRP) family, is a Ca(2+)-conducting channel activated in response to phospholipase C-coupled receptors. Despite scrutiny, the receptor-induced mechanism to activate TRPC3 channels remains unclear. Evidence indicates TRPC3 channels interact directly with intracellular inositol 1,4,5-trisphosphate receptors (InsP(3)Rs) and that channel activation is mediated through coupling to InsP(3)Rs. TRPC3 channels were expressed in DT40 chicken B lymphocytes in which all three InsP(3)R genes were deleted (DT40InsP(3)R-k/o). Endogenous B-cell receptors (BCR) coupled through Syk kinase to phospholipase C-gamma (PLC-gamma) activated the expressed TRPC3 channels in both DT40w/t and DT40InsP(3)R-k/o cells. The diacylglycerol (DAG) analogue 1-oleoyl-2-acetyl-sn-glycerol (OAG) also activated TRPC3 channels independently of InsP(3)Rs. BCR-induced TRPC3 activation was blocked by the PLC enzymic inhibitor, U-73122, and also blocked by wortmannin-induced PLC substrate depletion. Neither U-73122 nor wortmannin modified either OAG-induced TRPC3 activation or store-operated channel activation in DT40 cells. Cotransfection of cells with both G protein-coupled M5 muscarinic receptors and TRPC3 channels resulted in successful M5 coupling to open TRPC3 channels mediated by PLC-beta. We conclude that TRPC3 channels are activated independently of InsP(3)Rs through DAG production resulting from receptor-mediated activation of either PLC-gamma or PLC-beta.

Androstadienes↗
PubMed2001

Assessment of the role of the inositol 1,4,5-trisphosphate receptor in the activation of transient receptor potential channels and store-operated Ca2+ entry channels.

The mechanism for coupling between Ca(2+) stores and store-operated channels (SOCs) is an important but unresolved question. Although SOCs have not been molecularly identified, transient receptor potential (TRP) channels share a number of operational parameters with SOCs. The question of whether activation of SOCs and TRP channels is mediated by the inositol 1,4,5-trisphosphate receptor (InsP(3)R) was examined using the permeant InsP(3)R antagonist, 2-aminoethoxydiphenyl borate (2-APB) in both mammalian and invertebrate systems. In HEK293 cells stably transfected with human TRPC3 channels, the actions of 2-APB to block carbachol-induced InsP(3)R-mediated store release and carbachol-induced Sr(2+) entry through TRPC3 channels were both reversed at high agonist levels, suggesting InsP(3)Rs mediate TRPC3 activation. However, electroretinogram recordings of the light-induced current in Drosophila revealed that the TRP channel-mediated responses in wild-type as well as trp and trpl mutant flies were all inhibited by 2-APB. This action of 2-APB is likely InsP(3)R-independent since InsP(3)Rs are dispensable for the light response. We used triple InsP(3)R knockout DT40 chicken B-cells to further assess the role of InsP(3)Rs in SOC activation. (45)Ca(2+) flux analysis revealed that although DT40 wild-type cells retained normal InsP(3)Rs mediating 2-APB-sensitive Ca(2+) release, the DT40InsP(3)R-k/o cells were devoid of functional InsP(3)Rs. Using intact cells, all parameters of Ca(2+) store function and SOC activation were identical in DT40wt and DT40InsP(3)R-k/o cells. Moreover, in both cell lines SOC activation was completely blocked by 2-APB, and the kinetics of action of 2-APB on SOCs (time dependence and IC(50)) were identical. The results indicate that (a) the action of 2-APB on Ca(2+) entry is not mediated by the InsP(3)R and (b) the effects of 2-APB provide evidence for an important similarity in the function of invertebrate TRP channels, mammalian TRP channels, and mammalian store-operated channels.

Adenosine↗
PubMed2000

Ca2+ entry mediated by store depletion, S-nitrosylation, and TRP3 channels. Comparison of coupling and function.

The mechanism for coupling between Ca(2+) stores and store-operated channels (SOCs) is an important but unresolved question. SOC-mediated Ca(2+) entry is complex and may reflect more than one type of channel and coupling mechanism. To assess such possible divergence the function and coupling of SOCs was compared with two other distinct yet related Ca(2+) entry mechanisms. SOC coupling in DDT(1)MF-2 smooth muscle cells was prevented by the permeant inositol 1,4,5-trisphosphate (InsP(3)) receptor blockers, 2-aminoethoxydiphenyl borate (2-APB) and xestospongin C. In contrast, Ca(2+) entry induced by S-nitrosylation and potentiated by store depletion (Ma, H-T., Favre, C. J., Patterson, R. L., Stone, M. R., and Gill, D. L. (1999) J. Biol. Chem. 274, 35318-35324) was unaffected by 2-APB, suggesting that this entry mechanism is independent of InsP(3) receptors. The cycloalkyl lactamimide, MDL-12, 330A (MDL), prevented SOC activation (IC(50) 10 micrometer) and similarly completely blocked S-nitrosylation-mediated Ca(2+) entry. Ca(2+) entry mediated by the TRP3 channel stably expressed in HEK293 cells was activated by phospholipase C-coupled receptors but independent of Ca(2+) store depletion (Ma, H.-T., Patterson, R. L., van Rossum, D. B., Birnbaumer, L., Mikoshiba, K., and Gill, D. L. (2000) Science 287, 1647-1651). Receptor-induced TRP3 activation was 2-APB-sensitive and fully blocked by MDL. Direct stimulation of TRP3 channels by the permeant diacylglycerol derivative, 1-oleoyl-2-acetyl-sn-glycerol, was not blocked by 2-APB, but was again prevented by MDL. The results indicate that although the activation and coupling processes for each of the three entry mechanisms are distinct, sensitivity to MDL is a feature shared by all three mechanisms, suggesting there may be a common structural feature in the channels themselves or an associated regulatory component.

Animals↗
PubMed2000

Requirement of the inositol trisphosphate receptor for activation of store-operated Ca2+ channels.

The coupling mechanism between endoplasmic reticulum (ER) calcium ion (Ca2+) stores and plasma membrane (PM) store-operated channels (SOCs) is crucial to Ca2+ signaling but has eluded detection. SOCs may be functionally related to the TRP family of receptor-operated channels. Direct comparison of endogenous SOCs with stably expressed TRP3 channels in human embryonic kidney (HEK293) cells revealed that TRP3 channels differ in being store independent. However, condensed cortical F-actin prevented activation of both SOC and TRP3 channels, which suggests that ER-PM interactions underlie coupling of both channels. A cell-permeant inhibitor of inositol trisphosphate receptor (InsP3R) function, 2-aminoethoxydiphenyl borate, prevented both receptor-induced TRP3 activation and store-induced SOC activation. It is concluded that InsP3Rs mediate both SOC and TRP channel opening and that the InsP3R is essential for maintaining coupling between store emptying and physiological activation of SOCs.

Actins↗
PubMed2000

Anti-goitrous effect of lecithin-bound iodine in propylthiouracil treated rats.

OBJECTIVE: Excess iodine and some iodine-containing compounds are known to affect various parameters of thyroid function. Lecithin-bound iodine (LBI) is a compound which induces involution of an enlarged thyroid. LBI was tested for its ability to affect thyroid ornithine decarboxylase (ODC) activity and apoptosis. METHODS: LBI was given orally to propylthiouracil-pretreated rats and the changes in ODC activity and apoptosis were observed. The thyroid apoptosis was detected by DNA laddering and flow cytometry. RESULTS: LBI suppressed the thyroid ODC activity within one hour after its administration and lowered slightly but significantly the thyroid putrescine levels at 3 h. The DNA cleavage ladder was evident at 3-6 h after LBI treatment. Propylthiouracil induced thyroid enlargement was reduced significantly at 3 days after chronic treatment with LBI. The thyroidal content of putrescine was also decreased after chronic treatment. These effects of LBI were essentially the same as those of excess iodide, while other iodinated compounds including amiodarone, iopanoic acid and erythrosine had no effect on the thyroid ODC activity. CONCLUSIONS: These results suggest that LBI may exert its anti-goitrous effects, consisting of the inhibition of ODC activity and apoptosis, in the form of inorganic iodide in vivo.

Animals↗
PubMed1999

Ca(2+) entry activated by S-nitrosylation. Relationship to store-operated ca(2+) entry.

The coupling between Ca(2+) pools and store-operated Ca(2+) entry channels (SOCs) remains an unresolved question. Recently, we revealed that Ca(2+) entry could be activated in response to S-nitrosylation and that this process was stimulated by Ca(2+) pool emptying (Favre, C. J., Ufret-Vincenty, C. A., Stone, M. R., Ma, H-T. , and Gill, D. L. (1998) J. Biol. Chem. 273, 30855-30858). In DDT(1)MF-2 smooth muscle cells and DC-3F fibroblasts, Ca(2+) entry activated by the lipophilic NO donor, GEA3162 (5-amino-3-(3, 4-dichlorophenyl)1,2,3,4-oxatriazolium), or the alkylator, N-ethylmaleimide, was observed to be strongly activated by transient external Ca(2+) removal, closely resembling activation of SOC activity in the same cells. The nonadditivity of SOC and NO donor-activated Ca(2+) entry suggested a single entry mechanism. Calyculin A-induced reorganization of the actin cytoskeleton prevented SOC but had no effect on GEA3162-induced Ca(2+) entry. However, a single entry mechanism could account for both SOC and NO donor-activated entry if the latter reflected direct modification of the entry channel by S-nitrosylation, bypassing the normal coupling process between channels and pools. Small differences between SOC and GEA3162-activated Ba(2+) entry and sensitivity to blockade by La(3+) were observed, and in HEK293 cells SOC activity was observed without a response to thiol modification. It is concluded that in some cells, S-nitrosylation modifies an entry mechanism closely related to SOC and/or part of the regulatory machinery for SOC-mediated Ca(2+) entry.

Animals↗
PubMed1998

Ca2+ pool emptying stimulates Ca2+ entry activated by S-nitrosylation.

The entry of Ca2+ following Ca2+ pool release is a major component of Ca2+ signals; yet despite intense study, how "store-operated" entry channels are activated is unresolved. Because S-nitrosylation has become recognized as an important regulatory modification of several key channel proteins, its role in Ca2+ entry was investigated. A novel class of lipophilic NO donors activated Ca2+ entry independent of the well defined NO target, guanylate cyclase. Strikingly similar entry of Ca2+ induced by cell permeant alkylators indicated that this Ca2+ entry process was activated through thiol modification. Significantly, Ca2+ entry activated by either NO donors or alkylators was highly stimulated by Ca2+ pool depletion, which increased both the rate of Ca2+ release and the sensitivity to thiol modifiers. The results indicate that S-nitrosylation underlies activation of an important store-operated Ca2+ entry mechanism.

Alkylating Agents↗
PubMed1997

Magnetic resonance imaging of tuberculous spinal infection.

The magnetic resonance imaging (MRI) characteristics of 15 cases of tuberculous (TB) spinal infection were reviewed. The commonest site was the lumbar spine (53.3%), often with three or more contiguous vertebrae involved (47%). Destruction of the vertebral body and the presence of paraspinal soft-tissue masses were noted in 73.3%. Posterior element abnormalities, which is a significant finding, were seen in 40%, a slightly lower incidence rate than in other reported series. Epidural disease (53.3%) and disc abnormalities (73%) were more frequent than was realized. The role of intravenous contrast is discussed. Intravenous gadolinium is useful because it increases diagnostic confidence by characterizing and delineating the disease process, detects reactivation in old and healed TB, helps in treatment management and may prove valuable in monitoring therapy. Magnetic resonance imaging should be considered to be the imaging modality of choice for patients with suspected tuberculous spinal infection.

Adult↗
PubMed1996

GLP-1 depolarizes the rat pancreatic beta cell in a Na(+)-dependent manner.

An intestinal hormone glucagon-like-peptide-1 (GLP-1) is a prominent candidate for incretin. In vitro experiment showed (Fridolf and Ahren, Mol. Cell. Endocrinol., 96 (1993) 85-90) that GLP-1 increased both insulin secretion and the efflux of 45Ca2+ in a Na(+)-dependent manner. Further, GLP-1 depolarizes the pancreatic beta cells in the presence of high concentration of glucose. Here, we report the effect of GLP-1 on the membrane potential with a physiological concentration of glucose in perforated patch clamp of primary cultured rat beta cells. 10 nM GLP-1 depolarized the beta cell, which was completely reversed by replacing Na+ with the impermeant molecule N-methyl-D-glucamine (NMDG). The Ca2+ channel blocker, Co2+ suppressed the Ca2+ spikes without hyperpolarizing the cell. GLP-1-induced insulin secretion in perifused islets was also suppressed by a prior replacement of Na+ with NMDG. In addition, GLP-1 slightly augmented the long-lasting Ba2+ current, which was reverted to the control level by a selective inhibitor of protein kinase A, H-89. These results indicate: (i) GLP-1 depolarizes the beta cell by activating the membrane Na+ permeability; (ii) GLP-1 slightly modulates the L-type Ca2+ channel probably through protein kinase A; and (iii) at least in part, these mechanisms may be involved in the insulin secretion induced by GLP-1.

Animals↗
PubMed1996

Effects of pancreastatin and somatostatin on secretagogues-induced rise in intracellular free calcium in single rat pancreatic islet cells.

Pancreastatin (PST) is known to inhibit glucose-stimulated insulin release both in vivo and in vitro, but it has not been determined whether PST acts directly on pancreatic B-cells and no study has been reported on the effect of PST on the intracellular free Ca2+ concentration ([Ca2+]i) in pancreatic islet cells. In the present study, by using the dissociated rat pancreatic B-cells, we examined the effects of PST on the increase in [Ca2+]i induced by several insulin secretagogues, and compared them with those of somatostatin (SRIF). PST (1-100 nM) dose-dependently inhibited the glucose-induced rise in [Ca2+]i in single pancreatic islet cells. SRIF (10 nM) also suppressed the glucose-induced rise in [Ca2+]i. These demonstrated direct inhibitory actions of PST and SRIF on the pancreatic B-cells. Acetylcholine (ACh, 10 microM) with 5.5 mM glucose induced a biphasic increase in [Ca2+]i in single islet cells. SRIF (10 nM) suppressed the second phase in [Ca2+]i increase without affecting the first phase. In contrast, PST (100 nM) had no effect on the ACh-induced response. Gastric inhibitory polypeptide (100 nM) with 5.5 mM glucose induced a rise in [Ca2+]i in single islet cells. SRIF inhibited this increase, but PST did not. Both PST and SRIF failed to affect the sustained rise in [Ca2+]i evoked by excess K+. These results suggest that PST and SRIF suppress the glucose-induced insulin secretion at least partly by inhibiting the rise in [Ca2+]i in pancreatic B-cells. Furthermore, PST may suppress the glucose-induced rise in [Ca2+]i via a mechanism different from that of SRIF.

Acetylcholine↗
PubMed1996

Acute inhibitory effect of excess iodide on ornithine decarboxylase in the thyroid of propylthiouracil-treated rats.

Polyamines such as putrescine, spermidine and spermine have been thought to play an important role in thyroid growth induced by goitrogens. Reduced biosynthesis of these polyamines might play a role in the antigoitrogenic effects of excess iodide. This study was designed to examine the effect of potassium iodide (KI) on ornithine decarboxylase (ODC), a rate-limiting enzyme in the biosynthesis of polyamines. Thyroidal ODC activity, protein content and mRNA were increased in rats made hypothyroid by 10 days of propylthiouracil treatment. The increase in ODC activity was suppressed after subcutaneous injection of KI (13mg/kg body weight); the apparent half-life of ODC activity after the treatment was estimated to be 19 min and the maximum suppression (90%) was seen 60 min after the treatment. On the other hand, administration of iodine-containing compounds including L-thyroxine, L-di-iodotyrosine,amiodarone, iopanoic acid and erythrosine showed no significant effect on ODC activity. The inhibitory effect of excess iodide was not reversed by pretreatment with dibutyryl cAMP and theophylline. The amount of immunoreactive ODC protein was reduced by iodide treatment (40%). However, the decrease was not as great as the decrease in ODC activity (90%). No significant change in thyroidal ODC mRNA content was seen 1 and 3 h following KI treatment. These results suggest that excess iodide reduces ODC activity in the rat thyroid gland by a post-transcriptional mechanism.

Animals↗
PubMed1995

MRI of intraspinal nerve sheath tumours presenting with sciatica.

The magnetic resonance imaging (MRI) characteristics of 14 intraspinal nerve sheath tumours (NST) presenting with sciatica were reviewed. The group comprised seven schwannomas, six neurofibromas and one perineuroma. The tumours were either iso- or hypointense with respect to spinal cord on T1-weighted (T1W) images; almost all tumours were hyperintense compared with spinal cord on T2-weighted (T2W) images. The tumours were all detectable on unenhanced T1W images. Nine NST were scanned following Gadolinium-Diethylenetriamine penta acetic acid (DTPA) injection and all showed intense enhancement. This aids differentiation from sequestrated disc fragments. Tumours were more likely to show homogeneous enhancement unless they were recurrent tumours. Rim enhancement occurs more commonly in schwannomas and this can be used to differentiate these from neurofibromas. However, on unenhanced images, schwannomas cannot be distinguished from neurofibromas. Four tumours occurred at T11-T12. There was poor correlation of the site of the lesion with the clinical findings. MRI studies in patients with sciatica should include the lower thoracic region especially if no protruded disc was found in the lumbar region.

Adolescent↗
PubMed1994

Case report: asymmetrical development of the gyri recti presenting as a suprasellar mass: case report and description of six further cases.

Asymmetrical appearances of normal anatomical structures can sometimes mimic pathology. We present a case where asymmetry of the gyri recti was interpreted as a suprasellar mass on axial CT scanning. The true nature of the apparent abnormality was revealed by coronal magnetic resonance imaging (MRI). We also present six further cases where asymmetrical gyri recti were noted as incidental findings on coronal MRI scans. This is a common, but important, normal anatomical variant, which should not be mistaken for pathology.

Adult↗
PubMed1993

Hypopituitarism after tuberculous meningitis in childhood.

OBJECTIVE: To study the prevalence and pathogenesis of hypopituitarism following tuberculous meningitis in childhood. DESIGN: A retrospective cross-sectional study. SETTING: A university teaching hospital and a tuberculosis referral center. PATIENTS: Forty-nine patients, aged 23.4 +/- 6.0 years (mean +/- SD), who had tuberculous meningitis in childhood (age at diagnosis, 5.9 +/- 5.0 years) were studied. MEASUREMENTS: A detailed assessment of hypothalamic-pituitary function, including conventional stimulation tests and responses to four hypothalamic releasing hormones, was done. Magnetic resonance imaging of the hypothalamic-pituitary region was performed in patients with abnormal endocrine function. RESULTS: Ten patients were found to have abnormal pituitary function: Seven had growth hormone deficiency, four of whom also had gonadotropin deficiency; the other three had gonadotropin deficiency, corticotropin deficiency, and mild hyperprolactinemia, respectively; none had diabetes insipidus. Among those with growth hormone deficiency, a significant correlation (r = 0.749, P < 0.05) was found between the height standard deviation score and the age at diagnosis of tuberculous meningitis. Growth hormone, corticotropin, and gonadotropin responses to growth hormone releasing hormone, corticotropin releasing hormone, and gonadotropin releasing hormone, respectively, suggested a hypothalamic defect in five patients. Magnetic resonance imaging scans of the hypothalamic-pituitary region were abnormal in five patients. CONCLUSIONS: Hypopituitarism was documented in 20% of a small subset of patients years after recovery from tuberculous meningitis in childhood. The cause appears to be tuberculous lesions affecting the hypothalamus, pituitary stalk and, directly or indirectly, the pituitary itself. Early recognition and treatment can be beneficial.

Adolescent↗
PubMed1993

Induction of ornithine decarboxylase immunoreactivity in the male mouse kidney following testosterone treatment: an axial heterogeneity in the proximal tubule.

The effect of testosterone on the activity of ornithine decarboxylase (ODC), its protein level and immunocytochemical distribution were examined in the mouse kidney. Male BALB C mice at 8 weeks of age were used throughout. Fourteen hours before death, they received a subcutaneous injection of testosterone (1 mg/animal) or solvent to measure renal ODC activity or to detect the distribution of ODC immunoreactivity in the kidney. Renal ODC activity and the content of the enzyme were markedly increased after testosterone treatment. Histologically, few cells that were obviously immunoreactive to ODC were observed in the control animals and in the testosterone-treated animals a marked increase in ODC immunoreactivity was observed only in the cortex. ODC immunoreactive cells were located diffusely in the proximal tubule. In the pars recta, cells were stained weakly and homogeneously, while in the pars convoluta, the luminal surface of the cells showed stronger immunoreactivity. Moreover, many granule-like particles that were strongly ODC immunoreactive were observed inside the lumen of the pars convoluta. These results show that testosterone treatment induces an increase in ODC content in certain cells located in the proximal tubule of the cortex.

Animals↗
PubMed1992

Inhibitory effects of tetramethylpyrazine on platelets during cardiopulmonary bypass and arterial thrombus formation in dogs.

The corrected platelet count at the end of cardiopulmonary bypass (CPB) in nontreated dogs fell to 56.7% of the pre-operative level, while in tetramethylpyrazine (TMP, 10 mg.kg-1, iv)-treated dogs it fell to 82.8%. The number of alpha-granule membrane protein (GMP-140) which was expressed on the surface of activated platelets increased from the outset of CPB and reached the peak at the end of CPB in control dogs. But the number of GMP-140 molecules did not increase significantly throughout the operative procedure in TMP-treated dogs. In experimental thrombosis in dogs, the weight of the thrombus reduced to 23% of that in controls and the radioactivity ratio between the thrombus and blood was only 29% of that in controls at 4 h after iv injection of 125I-SZ-51 (a monoclonal antibody against GMP-140). These results indicate that TMP inhibits the platelet activation during CPB and arterial thrombosis.

Animals↗