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Biomedical subjects

H L Wang

Publications and source records attributed to H L Wang.

At least 91 records · Page 5Linked to original sources

Interrelationship between periodontics and adult orthodontics.

The purpose of this review article is to provide the dental practitioner with an understanding of the interrelationship between periodontics and orthodontics in adults. Specific areas reviewed are how periodontal tissue reacts to orthodontic forces, influence of tooth movement on the periodontium, effect of circumferential supracrestal fiberotomy in preventing orthodontic relapse, effect of orthodontic bands on the periodontium, specific microbiology associated with orthodontic bands, mucogingival considerations and time relationship between orthodontic and periodontal therapy. In addition, the relationship between orthodontics and implant restorations (e.g., using dental implants as orthodontic anchorage) will be discussed.

Adult↗

Evaluation of a bioactive glass alloplast in treating periodontal intrabony defects.

This study evaluated the use OF bioactive glass (BG) for repairing/regenerating periodontal intrabony defects. Fourteen systemically healthy patients participated. Each patient had 2 contralateral sites with > or = 6 mm clinical probing depth and radiographic evidence of an intrabony defect. One defect was treated with flap debridement plus BG (test) and the other with flap debridement alone (control). Baseline measurements included gingival index (GI), plaque index (PI), position of the free gingival margin (S/FGM), clinical attachment level (CAL), probing depth (PD), and mobility. At the time of surgery and at surgical reentry (9 to 13 months later), hard tissue measurements included: stent to defect base, bone crest to defect base, and defect width at the bone crest. One-way repeated ANOVA was used to analyze the treatment effect. Friedman's test was used to detect any significant changes of GI, PI and mobility at different time periods (baseline, 3 months, 6 months, and reentry). For multivariate analysis, the random coefficients mixed effect model was applied to adjust the intra-correlation effect. Both treatments resulted in decreased PD and gain of CAL. These changes were only significant (P < 0.05) for the BG treated sites (PD reduction = 1.24+/-0.43 mm, CAL gain = 0.87+/-0.38 mm) from baseline. Defect fill was significant for test (1.1+/-0.4 mm) and control (1.4+/-0.4 mm) alike (P < or = 0.01). Although BG treated sites had more PD reduction and CAL gain than debridement only controls, there were no statistically significant differences between groups for any parameter measured. Further studies are required to clarify the beneficial effects, if any, of BG alloplast in treating periodontal intrabony defects.

Adult↗

Use of biodegradable polylactic acid barrier materials in the treatment of grade II periodontal furcation defects in humans--Part I: A multicenter investigative clinical study.

This study evaluated two bioresorbable polylactic acid barriers (Epi-Guide and Guidor) to determine if design differences were of therapeutic significance in the treatment of Grade II furcation defects in humans. Forty patients with bilaterally matched, Grade II furcation defects in maxillary or mandibular first or second molars were treated in a multicenter study. Comprehensive initial periodontal therapy, followed by defect debridement and root preparation, preceded randomized membrane placement. Data collected from all three investigative centers were pooled and analyzed using an analysis of variance appropriate for a counterbalancing design. Both barrier types produced measurable improvements of clinical probing values. Barrier exposure scores taken through the eighth week postoperative revealed that Epi-Guide was less likely to become exposed than Guidor. The findings of this study, which was conducted over a 12-month period, demonstrated that Epi-Guide and Guidor were comparable as measured by clinical probing determinations.

Absorbable Implants↗

A morphometric analysis of the furcation region of mandibular molars.

This study examined furcation dimensions and morphology in first and second mandibular molar teeth. One hundred thirty-four extracted human mandibular molars with divergent roots were selected. Teeth were viewed at 7X magnification on a dissecting microscope interfaced with a computer equipped with a state-of-the-art histomorphometry software program. Various aspects of furcation anatomy were measured and recorded. Data were examined by using analysis of variance for all paired comparisons. For nonparametric data, the Kruskal Wallis test was used. Results indicated that 61.94% of buccal and 50.75% of lingual molar surfaces presented with cervical enamel projections (CEPs), with the highest frequency noted in second molars. CEPs ranged from 0.98 mm to 1.33 mm, whereas root trunk heights varied between 2.23 mm and 2.93 mm. Generally, lingual molar surfaces had longer root trunks when compared to buccal surfaces. Root separation increased by approximately 0.5 mm at each 1-mm increment apical to the furcal roof. This study provides new information regarding the furcal anatomy of mandibular molar teeth and supplements previous reports that suggest the CEP is a common problem which must be addressed by clinicians when treating molar teeth.

Analysis of Variance↗

Guided tissue regeneration. Absorbable barriers.

Over the past 15 years, techniques aimed at regeneration of lost periodontal tissue have become widely used and accepted in clinical practice. Among these techniques are those which use the principles of guided tissue regeneration (GTR), wherein barriers (i.e., membranes) are used to control cell and tissue repopulation of the periodontal wound. A variety of non-absorbable and absorbable barriers have been developed and used for this purpose, with a trend in recent years toward increased use of absorbable GTR materials. This article describes the evolution of absorbable barrier materials and overview materials available for clinical use today. In addition, advantages and disadvantages of these materials are discussed, as well as possible new developments in barrier-based GTR therapy.

Absorption↗

Slow-channel myasthenic syndrome caused by enhanced activation, desensitization, and agonist binding affinity attributable to mutation in the M2 domain of the acetylcholine receptor alpha subunit.

We describe a novel genetic and kinetic defect in a slow-channel congenital myasthenic syndrome. The severely disabled propositus has advanced endplate myopathy, prolonged and biexponentially decaying endplate currents, and prolonged acetylcholine receptor (AChR) channel openings. Genetic analysis reveals the heterozygous mutation alphaV249F in the propositus and mosaicism for alphaV249F in the asymptomatic father. Unlike mutations described previously in the M2 transmembrane domain, alphaV249F is located N-terminal to the conserved leucines and is not predicted to face the channel lumen. Expression of the alphaV249F AChR in HEK fibroblasts demonstrates increased channel openings in the absence of ACh, prolonged openings in its presence, enhanced steady-state desensitization, and nanomolar rather than micromolar affinity of one of the two binding sites in the resting activatable state. Thus, neuromuscular transmission is compromised because cationic overloading leads to degenerating junctional folds and loss of AChR, because an increased fraction of AChR is desensitized in the resting state, and because physiological rates of stimulation elicit additional desensitization and depolarization block of transmission.

Acetylcholine↗

Expression of a binding protein for FGF is associated with epithelial development and skin carcinogenesis.

Fibroblast growth factors (FGF)-1 and -2 are found in most embryonic and adult normal and tumor tissues, where they are immobilized in the extracellular matrix (EM). Mobilization of these FGFs is part of a tightly controlled process resulting in the activation of high-affinity receptors. Recently, we have shown that a novel human FGF-binding protein (FGF-BP) mediates the release of immobilized FGF-2 from the EM. Here we isolated genomic and cDNA clones of the mouse FGF-BP homologue and studied its expression during embryonic development and skin carcinogenesis. The murine gene contains two exons that generate a 1.2 kb mRNA and predicts an 18 kDa secreted protein that is 63% identical to its human homologue. FGF-BP mRNA expression during embryogenesis is restricted to skin, intestine and lung. In the developing skin, FGF-BP expression starts at embryonic day 9, reaches peak levels perinatally and is downregulated during postnatal development. Development regulation in the intestine is similar, but in lungs and ovaries high expression was also observed in the adult. FGF-BP mRNA expression in the adult skin is dramatically increased during early stages of carcinogen-induced transformation in vivo and by ras-activation in vitro. Finally, mouse FGF-BP binds to FGF-2 and can function as a modulator of FGF in FGF-responsive cells. Our results suggest a potential function of FGF-BP during development and tumorigenesis.

Amino Acid Sequence↗

Bacterial scavengase p20 is structurally and functionally related to peroxiredoxins.

Scavengase p20 was recently identified as a novel family of bacterial antioxidant enzymes possessing thioredoxin-linked thiol peroxidase activity. In this study, the Escherichia coli gene coding for scavengase p20 was isolated from three different strains and the nucleotide sequence was determined. Multiple alignment of amino acid sequence revealed that a previously unidentified Cys-61 is most conserved among all bacterial p20 scavengases and corresponds to the active site in the well-characterized peroxiredoxins. Phylogenetic analysis further supported that scavengase p20 is a novel subfamily of peroxiredoxins. Site-directed mutagenesis studies demonstrated that Cys-61 is indispensable for the antioxidant activities of scavengase p20. Taken together, our findings strongly suggest that the p20 scavengases are structurally and functionally related to peroxiredoxins.

Amino Acid Sequence↗

Scavengase p20: a novel family of bacterial antioxidant enzymes.

A novel antioxidant enzyme designated scavengase p20 was identified in various pathogenic bacteria through database searching for sequences strikingly homologous to a recently discovered Escherichia coli thiol peroxidase p20. The direct biochemical evidence for the existence of scavengase p20 in Haemophilus influenzae, Streptococcus pneumoniae and Helicobacter pylori was provided by protein microsequencing and by in vitro assays for antioxidant activities. Overlapping genes encoding scavengase p20 and superoxide dismutase were recognized in H. pylori and their functional implications are discussed.

Amino Acid Sequence↗

Vasoactive intestinal polypeptide enhances the GABAergic synaptic transmission in cultured hippocampal neurons.

The whole-cell mode of patch-clamp techniques was used to investigate the effect of vasoactive intestinal polypeptide (VIP) on spontaneous gamma-aminobutyric acid (GABA)-mediated inhibitory postsynaptic currents (IPSCs) of cultured hippocampal neurons. Application of VIP caused a significant increase in the frequency of spontaneous IPSCs with a reversible and dose-dependent manner. VIP had no effect on the mean amplitude and kinetic parameters of spontaneous IPSCs. In the presence of tetrodotoxin, VIP increased the frequency of miniature inhibitory postsynaptic currents (mIPSCs) without affecting their mean magnitude. Forskolin, but not its inactive analog 1,9-dideoxyforskolin, mimicked the stimulatory effect of VIP on spontaneous IPSCs and mIPSCs. VIP and forskolin failed to modulate GABAergic IPSCs in the presence of Rp-cAMPs, a cell permeable antagonist of cAMP-dependent protein kinase (PKA). Calcium channel blocker CdCl2 did not prevent VIP and forskolin from increasing the frequency of mIPSCs. These results suggest that the activation of presynaptic VIP receptor enhances the GABAergic synaptic transmission in cultured hippocampal neurons through the cAMP-PKA pathway and that VIP is likely to increase GABA release by directly stimulating the vesicular release apparatus.

2-Amino-5-phosphonovalerate↗

Complementation of and interference with Sindbis virus replication by full-length and deleted forms of the nonstructural protein, nsP1, expressed in stable transfectants of Hela cells.

Stable transfectants of Hela cells were isolated which expressed either the full-length 540-amino-acid Sindbis virus (SV) nonstructural protein, nsP1 (the form encoded by the mutant, SV(LM21)), or one of four forms with a carboxyl-terminal deletion. SV(LM21), in contrast to standard SV (SV(STD)), can replicate in Hela cells maintained in low-methionine (LM) medium. Expression of full-length nsP1(1-540), nsP1(1-492), or nsP1(1-448) resulted in complementation of SV(STD) when infected Hela cells were kept in LM medium after infection. In contrast, when cells were infected with SV(LM21) and maintained in LM medium, stable expression of any of the deleted forms of nsP1 interfered with the replication of virus. The ability of "cellular" nsP1 to complement SV(STD) in LM medium correlated with its methyltransferase activity.

Animals↗

Cloning, expression and CNS distribution of Kv4.3, an A-type K+ channel alpha subunit.

A full-length K+ channel cDNA of Kv4.3, with an open reading frame of 611 amino acids, was isolated from rat hippocampus. Functional expression of Kv4.3 cDNA in Xenopus oocytes revealed an A-type K+ channel. In the central nervous system, Kv4.3 is most prominently expressed in the retrosplenial cortex, medial habenula, anterior thalamus, hippocampus, cerebellum, as well as lateral geniculate and superior colliculus, which are important for vision. The abundant expression of Kv4.3 in many CNS neurons supports its important role as a major component of subthreshold A currents in the control of action potentials and thus neuronal excitability.

Amino Acid Sequence↗

A site-directed mutagenesis study on the conserved alanine residue in the distal third intracellular loops of cholecystokininB and neurotensin receptors.

1. An alanine residue at the C-terminal tail of the third intracellular loop is highly conserved among various Gq protein-coupled receptors including rat cholecystokininB (CCKB) and neurotensin receptors. To investigate the functional significance of the conserved alanine in the activation of Gq proteins and phospholipase C (PLC) by CCKB and neurotensin receptors, the alanine residue was mutated in the present study. Subsequently, the ability of resulting mutant receptors to activate PLC was investigated by measuring the formation of inositol phosphates (IP) in COS-7 cells and recording Ca(2+)-activated chloride currents from Xenopus oocytes. 2. Site-directed mutagenesis was performed to mutate alanine at position 332 of rat CCKB receptor to glutamate. When the (A332E) mutant receptor was expressed in COS-7 cells and Xenopus oocytes, the efficacy and the potency of sulphated cholecystokinin octapeptide (CCK-8) to stimulate polyphosphoinositide hydrolysis in COS-7 cells and evoke calcium-dependent Cl- currents in oocytes were not significantly affected. 3. Alanine residue at position 302 of rat neurotensin receptor was also mutated to glutamate. When expressed in COS-7 cells and Xenopus oocytes, the resulting (A302E) mutant receptor was strongly defective in stimulating phosphatidylinositol turnover in COS-7 cells and evoking Ca(2+)-dependent chloride currents in oocytes. 4. In summary, the present study demonstrates that alanine residue at the C-terminus of third cytoplasmic domain is required for the full activation of Gq proteins and PLC by neurotensin receptors. However, in contrast to other Gq protein-coupled receptors, alanine at the distal third intracellular loop does not play a significant role in CCKB receptor activation of PLC.

Alanine↗

Basic amino acids at the C-terminus of the third intracellular loop are required for the activation of phospholipase C by cholecystokinin-B receptors.

In common with other Gq protein-coupled receptors, the third intracellular loop of the cholecystokinin-B (CCK-B) receptor contains three basic amino acids (K333/K334/R335) at the C-terminal segment. To determine the importance of these conserved basic residues in Gq-protein activation and stimulation of phospholipase C, these basic amino acids were mutated. Subsequently, the ability of resulting mutant receptors to activate phospholipase C was investigated by measuring inositol phosphate formation in COS-7 cells and recording Ca(2+)-activated Cl- currents from Xenopus oocytes. Site-directed mutagenesis was performed to mutate the three basic amino acids, K333/K334/R335, to neutral amino acids, M333/T334/L335. When the resulting mutant CCK-B receptors were expressed in COS-7 cells and Xenopus oocytes, sulfated cholecystokinin octapeptide (CCK-8) failed to induce inositol phosphate formation in COS-7 cells and evoke Ca(2+)-activated Cl- currents from oocytes. Each basic amino acid was also mutated (K333M, K334T, and R335L). All three single-point mutations resulted in a significant reduction in CCK-8-induced inositol phosphate formation and CCK-8-activated Ca(2+)-dependent Cl- currents. It is interesting that substituting the basic amino acids, K333/K334/R335, with three other basic residues, R333/R334/K335, did not change the maximal CCK-8-simulated inositol phosphate formation and the amplitude of CCK-8-evoked Ca(2+)-dependent Cl- currents. Radioligand-binding studies showed that the above-mentioned mutations did not affect the affinity for CCK-8 and receptor expression level in COS-7 cells. These findings suggest that basic amino acids at the C-terminus of the third cytoplasmic loop are required for the signal transduction by CCK-B receptors.

Amino Acid Sequence↗

Mutation in the M1 domain of the acetylcholine receptor alpha subunit decreases the rate of agonist dissociation.

We describe the kinetic consequences of the mutation N217K in the M1 domain of the acetylcholine receptor (AChR) alpha subunit that causes a slow channel congenital myasthenic syndrome (SCCMS). We previously showed that receptors containing alpha N217K expressed in 293 HEK cells open in prolonged activation episodes strikingly similar to those observed at the SCCMS end plates. Here we use single channel kinetic analysis to show that the prolonged activation episodes result primarily from slowing of the rate of acetylcholine (ACh) dissociation from the binding site. Rate constants for channel opening and closing are also slowed but to much smaller extents. The rate constants derived from kinetic analysis also describe the concentration dependence of receptor activation, revealing a 20-fold shift in the EC50 to lower agonist concentrations for alpha N217K. The apparent affinity of ACh binding, measured by competition against the rate of 125I-alpha-bungarotoxin binding, is also enhanced 20-fold by alpha N217K. Both the slowing of ACh dissociation and enhanced apparent affinity are specific to the lysine substitution, as the glutamine and glutamate substitutions have no effect. Substituting lysine for the equivalent asparagine in the beta, epsilon, or delta subunits does not affect the kinetics of receptor activation or apparent agonist affinity. The results show that a mutation in the amino-terminal portion of the M1 domain produces a localized perturbation that stabilizes agonist bound to the resting state of the AChR.

Acetylcholine↗

Prevalence and genotype of hepatitis G virus in Chinese professional blood donors and hepatitis patients.

Prevalence of hepatitis G virus (HGV) was determined in a cohort of Chinese blood donors and hepatitis patients by the detection of viral RNA via reverse transcription-polymerase chain reaction. While HGV RNA was detected in only 1 of 150 healthy volunteers, the detection rate among professional blood donors was surprisingly high (21/265, 7.9%), and plasmapheresis was identified as a significant risk factor in this population. It was also shown that an elevated serum alanine aminotransferase level is not a reliable marker for HGV infection. Prevalences of HGV in patients with hepatitis C, with non-A-E hepatitis, and with hepatocellular carcinoma were relatively low (8.2%, 16.7%, and 6.1%, respectively). Striking sequence homology (>90%) shared by 5 HGV cDNA clones implicated that they belonged to the same genotype. Phylogenetic analysis of a 446-bp NS3 cDNA confirmed that this genotype was closely related to the prototype viruses.

Amino Acid Sequence↗

Sulbactam/cefoperazone versus cefotaxime for the treatment of moderate-to-severe bacterial infections: results of a randomized, controlled clinical trial.

We conducted a randomized, open-label, controlled, multicenter study to compare sulbactam/cefoperazone with cefotaxime in terms of efficacy and safety for the treatment of hospitalized patients with moderate-to-severe bacterial infections. More than two-thirds of the pathogens recovered from these patients produced beta-lactamase. Two hundred-seven (88.1%) of the 235 patients enrolled completed the study and were included in the efficacy and safety evaluations. One hundred-three patients received sulbactam/cefoperazone (2-4 g/d) administered in evenly divided doses every 12 hours by a 30-minute intravenous drip; 104 patients received cefotaxime (6-12 g/d) administered in evenly divided doses every 6 or 8 hours by a 30-minute intravenous drip. The overall efficacy rates (i.e., cure or markedly improved) were 95% for the sulbactam/cefoperazone group and 90% for the cefotaxime group (P = .186), whereas the bacterial eradication rates were 85% for the sulbactam/cefoperazone group and 81% for the cefotaxime group (P = .467). Both drug regimens were well tolerated. Sulbactam/cefoperazone is effective and safe for the treatment of moderate-to-severe bacterial infections caused mainly by beta-lactamase-producing organisms.

Adolescent↗