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Biomedical subjects

K Hu

Publications and source records attributed to K Hu.

At least 73 records · Page 4Linked to original sources
PubMed2000

[Effects of the occlusal splint on stress distribution of the mandible with temporomandibular joint disorders].

OBJECTIVE: To investigate the biomechanical mechanism of occlusal splint therapy of temporomandibular joint disorders (TMD). METHODS: The changes of stress distribution on the mandible with TMD before and after occlusal splint therapy were simulated and analyzed by three-dimensional finite element method. RESULTS: Occlusal splint influenced the character of stress distribution on the mandible. It might distinctly decrease maximum and minimum principal stresses on each region of the mandible with TMD, among which the stress on condylar surface of ill side was reduced more significantly, and the stress distribution of bilateral condyles was close to equality and balance. Meanwhile, the stress symmetry on every position of the mandible was improved slightly. CONCLUSIONS: Occlusal splint can alleviate even eliminate the injury to the temporomandibular joint, and make unbalance of joint inner environment adjusted and restored by improving the stress distribution. This is primarily thought to be one of the main biomechanical mechanism of occlusal splint treatment.

Biomechanical Phenomena↗
PubMed1999

Endothelial dysfunction in chronic myocardial infarction despite increased vascular endothelial nitric oxide synthase and soluble guanylate cyclase expression: role of enhanced vascular superoxide production.

BACKGROUND: Endothelial dysfunction of the peripheral vasculature is a well-known phenomenon in congestive heart failure that contributes to the elevated peripheral resistance; however, the underlying mechanisms have not yet been clarified. METHODS AND RESULTS: Dilator responses, the expression of protein and mRNA of the endothelial nitric oxide synthase (eNOS), inducible NOS (iNOS), and soluble guanylate cyclase (sGC), and superoxide anion (O(2)(-)) and peroxynitrite production were determined in aortic rings from Wistar rats 8 weeks after myocardial infarction and compared with those in sham-operated animals. In rats with heart failure, the concentration-response curve of the endothelium-dependent vasodilator acetylcholine (after preconstriction with phenylephrine) was significantly shifted to the right, and the maximum relaxation was attenuated. Determination of expression levels of the 2 key enzymes for NO-mediated dilations, eNOS and sGC, revealed a marked upregulation of both enzymes in aortas from rats with heart failure, whereas iNOS expression was not changed. Pretreatment with exogenous superoxide dismutase partially restored the acetylcholine-induced relaxation in aortas from rats with heart failure. Aortic basal and NADH-stimulated O(2)(-) production assessed by use of lucigenin-enhanced chemiluminescence was significantly elevated in rats with chronic myocardial infarction. Peroxynitrite-mediated nitration of protein tyrosine residues was not different between the 2 groups of rats. CONCLUSIONS: These results demonstrate that endothelial dysfunction in ischemic heart failure occurs despite an enhanced vascular eNOS and sGC expression and can be attributed to an increase in vascular O(2)(-) production by an NADH-dependent oxidase. By inactivation of NO, O(2)(-) production appears to be an essential mechanism for the endothelial dysfunction observed in heart failure.

Acetylcholine↗
PubMed1999

Immunization with amyloid-beta attenuates Alzheimer-disease-like pathology in the PDAPP mouse.

Amyloid-beta peptide (Abeta) seems to have a central role in the neuropathology of Alzheimer's disease (AD). Familial forms of the disease have been linked to mutations in the amyloid precursor protein (APP) and the presenilin genes. Disease-linked mutations in these genes result in increased production of the 42-amino-acid form of the peptide (Abeta42), which is the predominant form found in the amyloid plaques of Alzheimer's disease. The PDAPP transgenic mouse, which overexpresses mutant human APP (in which the amino acid at position 717 is phenylalanine instead of the normal valine), progressively develops many of the neuropathological hallmarks of Alzheimer's disease in an age- and brain-region-dependent manner. In the present study, transgenic animals were immunized with Abeta42, either before the onset of AD-type neuropathologies (at 6 weeks of age) or at an older age (11 months), when amyloid-beta deposition and several of the subsequent neuropathological changes were well established. We report that immunization of the young animals essentially prevented the development of beta-amyloid-plaque formation, neuritic dystrophy and astrogliosis. Treatment of the older animals also markedly reduced the extent and progression of these AD-like neuropathologies. Our results raise the possibility that immunization with amyloid-beta may be effective in preventing and treating Alzheimer's disease.

Alzheimer Disease↗
PubMed1999

Plaque-independent disruption of neural circuits in Alzheimer's disease mouse models.

Autosomal dominant forms of familial Alzheimer's disease (FAD) are associated with increased production of the amyloid beta peptide, Abeta42, which is derived from the amyloid protein precursor (APP). In FAD, as well as in sporadic forms of the illness, Abeta peptides accumulate abnormally in the brain in the form of amyloid plaques. Here, we show that overexpression of FAD(717V-->F)-mutant human APP in neurons of transgenic mice decreases the density of presynaptic terminals and neurons well before these mice develop amyloid plaques. Electrophysiological recordings from the hippocampus revealed prominent deficits in synaptic transmission, which also preceded amyloid deposition by several months. Although in young mice, functional and structural neuronal deficits were of similar magnitude, functional deficits became predominant with advancing age. Increased Abeta production in the context of decreased overall APP expression, achieved by addition of the Swedish FAD mutation to the APP transgene in a second line of mice, further increased synaptic transmission deficits in young APP mice without plaques. These results suggest a neurotoxic effect of Abeta that is independent of plaque formation.

Alzheimer Disease↗
PubMed1999

30 Gy may be an adequate dose in patients with anal cancer treated with excisional biopsy followed by combined-modality therapy.

BACKGROUND AND OBJECTIVES: There are a subset of patients with invasive anal cancers who undergo an excisional biopsy either before or after combined-modality therapy (CMT). The objective of this study is to determine whether these patients can be adequately treated with a lower dose of pelvic radiation therapy. METHODS: A total of 25 patients were treated with CMT either before or after an excisional biopsy. The four subsets included 8 patients with initial excision followed by CMT with 30-34 Gy (EX/30), 6 patients with initial excision followed by CMT with 45-50.4 Gy (EX/45), 10 patients treated by CMT with 30 Gy followed by an excision (30/EX), and 1 patient by CMT with 45 Gy followed by an excision (45/EX). RESULTS: For the total group, the actuarial 5-year disease-free survival was 78%, overall survival was 86%, colostomy-free survival was 91%, and local control was 82%. When patients received CMT either before or following an excision, the actuarial local control and survival results with 30-34 Gy vs. 45-50.4 Gy were similar. In contrast to radiation dose, in patients who received 30-34 Gy, the sequence of the excision (before or after CMT) did appear to have a borderline significant impact on local control. Actuarial 5-year local control was 100% for EX/30 vs. 67% for 30/EX (P = 0.08). CONCLUSIONS: Because of the small number of patients in each group and the retrospective nature of the analysis, it is difficult to draw definitive conclusions from this study. However, our data suggest that in patients who are selected to undergo an initial excisional biopsy followed by CMT, 30 Gy may be an adequate radiation dose. Local control may be higher in patients who undergo an excisional biopsy followed by CMT compared with the converse.

Adenocarcinoma↗
PubMed1999

Metabolism of polychlorinated dibenzo-p-dioxins by rat liver microsomes.

The in vitro metabolism of several chlorinated dibenzo-p-dioxin congeners (PCDDs) was studied using rat liver microsomes as a source of CYP 1 enzymes. The reactions were kinetically first order in both enzyme and substrate and showed a general trend toward decreasing reactivity with increasing chlorination. Michaelis-Menten kinetics were followed for 1-chlorodibenzo-p-dioxin (1-CDD); the reactivity of the enzyme preparation toward 1-CDD exactly paralleled its activity toward 7-ethoxyresorufin. The unreactive congeners 1,2,3,7,8-pentachlorodibenzo-p-dioxin (PeCDD) and 2,2'-dichlorobiphenyl (2,2'-DCB) acted as competitive inhibitors toward 1-CDD, with inhibition constants in the micromolar range, similar to the value of the Michaelis constant of 1-CDD. The inhibitory potency of furafylline, a mechanism-based inhibitor that is selective for CYP 1A2, declined in the order acetanilide (standard) > 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) > 1-CDD. We conclude that 1-CDD and 1,2,3,4-TCDD are oxidized almost exclusively by CYP 1A1, whereas 2,3,7,8-TCDD and 1,2,4,7,8-PeCDD are oxidized mainly by CYP 1A2. 1,2,3,7,8-PeCDD was oxidized too slowly for us to reach any conclusion about the P450 isozyme responsible.

Animals↗
PubMed1999

Functional and energetic consequences of chronic myocardial creatine depletion by beta-guanidinopropionate in perfused hearts and in intact rats.

Oral feeding with the creatine analogue beta-guanidinopropionate (beta-GP) reduces myocardial phosphocreatine and creatine concentrations by about 80%in vitro, this is accompanied by reduced contractile performance. We hypothesized, thus, that beta-GP feeding leads to hemodynamic changes in vivo characteristic of heart failure. beta-GP was fed to Wistar rats for up to 8 weeks. In isolated hearts, function was measured isovolumically, myocardial energetics were followed with (31)P-NMR spectroscopy. In vivo hemodynamics were measured with Millar-Tip-catheters and an electromagnetic flow probe. Beta-GP feeding did not alter heart weight. In vitro, diastolic pressure-volume curves indicated structural left ventricular dilatation, and a 36% reduction of left ventricular developed pressure was found; phosphocreatine was reduced by approximately 80%, ATP unchanged and creatine kinase reaction velocity ((31)P-MR saturation transfer) decreased by approximately 90%. The total creatine pool (high-pressure liquid chromatography) was reduced by up to approximately 70%. In contrast to in vitro findings, in vivo cardiac hemodynamics (including left ventricular developed pressure, d P/d t(max), cardiac output and peripheral vascular resistance) at rest and during acute volume loading showed no alterations after beta-GP feeding. The only functional impairment observed in vivo was a 14% reduction of maximum left ventricular developed pressure during brief aortic occlusion. In the intact rat, cardiac and/or humoral compensatory mechanisms are sufficient to maintain normal hemodynamics in spite of a 90% reduction of creatine kinase reaction velocity. However, chronic beta-GP feeding leads to structural left ventricular dilatation.

Adenosine Diphosphate↗
PubMed1999

Chronic high-dose creatine feeding does not attenuate left ventricular remodeling in rat hearts post-myocardial infarction.

OBJECTIVE: In heart failure, cardiac energy metabolism is compromised. The failing myocardium is characterized by reduced contents of both phosphorylated (phosphocreatine) and non-phosphorylated (free) creatine content as well as decreased energy reserve via creatine kinase (creatine kinase reaction velocity). These changes may contribute to cardiac dysfunction. The purpose of the present study was to determine whether chronic feeding with high-dose dietary creatine prevents the derangement of energy metabolism and the development of left ventricular remodeling in a rat model of heart failure, i.e. post-myocardial infarction (MI). METHODS AND RESULTS: Rats were subjected to sham operation or left coronary artery ligation. Surviving rats were fed with 0% (untreated) or 3% creatine (related to weight of diet) for 8 weeks. Creatine feeding increased serum creatine levels significantly approximately 2-fold. Thereafter, hearts were isolated, perfused and left ventricular pressure-volume curves obtained. Steady state and dynamic (CK reaction velocity) high-energy phosphate metabolism was determined with 31P NMR spectroscopy. In both MI groups (treated n = 8, untreated n = 7), pressure-volume curves were shifted right- and downward compared to both sham groups (treated n = 5, untreated n = 7), i.e. creatine had no effect on left ventricular remodeling. Likewise, similar reductions of phosphocreatine, free creatine and creatine kinase reaction velocity (untreated sham 12.0 +/- 0.7 mmol/lxs; untreated MI 7.8 +/- 0.7*; treated sham 13.6 +/- 1.0; treated MI 7.2 +/- 1.1*; *p < 0.025 sham vs. MI) were found in both MI groups. CONCLUSIONS: Chronic creatine feeding of post-MI rats is ineffective in preventing the functional and energetic derangements occurring post-MI. Inspite of increased serum creatine levels, neither the normal nor the failing heart accumulates additional creatine.

Adenosine Triphosphate↗
PubMed1999

A new pregnane glycoside from Dioscorea collettii var. hypoglauca.

During further bioactivity-guided fractionation, a new pregnane glycoside, hypoglaucin G (1), and a known compound, pregna-5, 16-dien-3beta-ol-20-one 3-O-alpha-L-rhamnopyranosyl-(1-->2)- [alpha-L-rhamnopyranosyl-(1-->4)] -beta-D-glucopyranoside (2), were isolated from the EtOH extract of Dioscorea collettii var. hypoglauca rhizomes, which induced morphological deformation of Pyricularia oryzae mycelia with minimum morphological deformation concentration values of 135 microM and 236 microM, respectively. The structure of 1 was established as 16beta-(4'-methyl-5'-O-beta-D-glucopyranosyl- pentanoxyl)-pre gn-5-en-3 beta-ol-20-one 3-O-alpha-L- rhamnopyranosyl-(1-->2)-[alpha-L-rhamnopyranosyl-(1-->4)]-beta-D- glucopyranoside on the basis of chemical evidence and spectral analysis, especially by 2D NMR techniques.

Antifungal Agents↗
PubMed1999

Antineoplastic agents. III: Steroidal glycosides from Solanum nigrum.

By bioactivity-guided fractionation, three known steroidal glycosides, beta 2-solamargine (1), solamargine (2), and degalactotigonin (3), were isolated from Solanum nigrum. Compounds 1-3 induced morphological abnormality in Pyricularia oryzae mycelia with MMDC (minimum morphological deformation concentration) values of 63.0, 38.5, and 97.2 microM, respectively. This is the first report on the isolation of 1 from this species and on the cytotoxicity of 1-3 on six cultured human solid tumor cell lines HT-29 (colon), HCT-15 (colon), LNCaP (prostate), PC-3 (prostate), T47D (breast), and MDA-MB-231 (breast) in vitro. The cytotoxic assay indicated that 2 is the main antineoplastic agent in S. nigrum. The structures of 1-3 were elucidated on the basis of chemical evidence and spectral analysis, especially by 2D-NMR analysis.

Antineoplastic Agents, Phytogenic↗
PubMed1999

Adenosine-induced activation of ATP-sensitive K+ channels in excised membrane patches is mediated by PKC.

Both protein kinase C (PKC) and adenosine receptor activation have been shown to enhance ATP-sensitive K+ (KATP) channels. The present studies were designed to determine whether PKC mediates adenosine effects on the KATP channel. The dependence of KATP channel activity (nPo) on intracellular ATP concentration ([ATP]i) was determined in excised rabbit ventricular membrane patches. External adenosine (100 microM in the pipette solution) significantly increased KATP nPo at all [ATP]i between 5 and 50 microM by decreasing channel sensitivity to [ATP]i (dissociation constant increased from 7.4 +/- 0.8 to 22.2 +/- 3.1 microM, P < 0.001), an effect blocked by the adenosine receptor antagonist 8-phenyltheophylline (10 microM). When the highly selective PKC blocker bisindolylmaleimide (BIM) was included in the internal (bath) solution, the KATP-stimulating action of adenosine was prevented. The addition of BIM to the superfusate rapidly inhibited KATP channels activated by adenosine. Endogenous PKC activation by phorbol 12,13-didecanoate (PDD), but not administration of the inactive congener 4alpha-PDD, enhanced KATP activity. Internal guanosine 5'-O-(2-thiodiphosphate) prevented KATP activation by adenosine, an effect which could be overridden by exposure to PDD. We conclude that PKC mediates adenosine activation of KATP channels in excised membrane patches in a membrane-delimited fashion.

Adenosine↗
PubMed1999

Effects of ACE inhibition and beta-receptor blockade on energy metabolism in rats postmyocardial infarction.

Chronic treatment with beta-receptor blockers or angiotensin-converting enzyme (ACE) inhibitors in heart failure can reduce mortality and improve left ventricular function, but the mechanisms involved in their beneficial action remain to be fully defined. Our hypothesis was that these agents prevent the derangement of cardiac energy metabolism. Rats were subjected to myocardial infarction (MI) or sham operation. Thereafter, animals were treated with bisoprolol, captopril, or remained untreated. Two months later, cardiac function was measured in the isolated heart by a left ventricular balloon (pressure-volume curves), and energy metabolism of residual intact myocardium was analyzed in terms of total and isoenzyme creatine kinase (CK) activity, steady-state levels (ATP, phosphocreatine), and turnover rates (CK reaction velocity) of high-energy phosphates (31P nuclear magnetic resonance) and total creatine content (HPLC). Bisoprolol and partially captopril prevented post-MI hypertrophy and partially prevented left ventricular contractile dysfunction. Residual intact failing myocardium in untreated, infarcted hearts showed a 25% decrease of the total, a 26% decrease of MM-, and a 37% decrease of the mitochondrial CK activity. Total creatine was reduced by 15%, phosphocreatine by 21%, and CK reaction velocity by 41%. Treatment with bisoprolol or captopril largely prevented all of these changes in infarcted hearts. Thus the favorable functional effects of beta-receptor blockers and ACE inhibitors post-MI are accompanied by substantial beneficial effects on cardiac energy metabolism.

Adenine Nucleotides↗
PubMed1999

[Effect of unilateral condylar fracture on stress distribution in the mandible].

OBJECTIVE: To investigate the effect of unilateral condylar fracture on stress distribution in the mandible in order to realize primarily the biomechanical mechanism of temporomandibular joint disorders (TMD) resulted in by joint injury. METHODS: The stress distributions in the mandible of a normal human and a patient with TMD induced by right condylar fracture following malposition healing were analyzed and compared quantitatively during centric occlusion by three-dimensional finite element method. RESULTS: The patient contained the unbalanced stress distribution in the mandible, such as different nature and value of stress. The stress in the fractured side was higher than the non-fractured side, in which condyle is more evident. The maximum principal stress and minimum principal stress of each region in his mandible were much higher than that in a normal mandible. Its stress quality changes also. The stress in his mandible was distributed asymmetrically. CONCLUSION: Unilateral condylar fracture not only damaged its structure, but also induced the badness of its biomechanical environment, in which condyle was the most sensitive region during the stresses in the mandible were changed. It was preliminarily thought that unbalanced stress distribution, evidently increased stress and varied stress character were one of biomechanical mechanism of TMD.

Adult↗
PubMed1999

[Effects of various condylar operations on its compressive mechanical property and bone density].

OBJECTIVE: To investigate the changes and relationship of condylar mechanical properties and its material character after various condylar operations. METHODS: Condylar compressive mechanical properties and its bone mineral content were analyzed quantitatively by compressive mechanical property measurement technique and dual energy X-ray absorptiometry in 6 and 6 adult dogs undergone either high shaping or reconstruction of condyles respectively, and compared with 12 normals. RESULTS: Condylar elastic--limit load and displacement, its largest load and displacement were the highest in control, but stiffness and bone mineral content were the highest in high-shaping group, all data were the lowest in the reconstruction ones. There was marked and extremely marked linear positive relativity among condylar elastic--limit load, largest load, stiffness and bone density, in which all relative coefficients exceeded 0.862. CONCLUSION: The changes of condylar shape induced by various operations directly influence its compressive mechanical properties and bone mineral content. There is linear positive relativity between condylar compressive mechanical properties and its bone mineral density.

Animals↗
PubMed1999

[An introduction of solvent-free(SPME) technique].

Solid-phase microextraction (SPME) is a solvent-free sample preparation technique in which a fused silica fiber coated with polymeric organic liquid is introduced into the sample. In this paper, theoretical aspects, operating models, factors of influencing sensitivity, applications and future development are introduced briefly with 19 references.

Chromatography, Gas↗