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K Hu

Publications and source records attributed to K Hu.

At least 91 records · Page 5Linked to original sources

[Ion chromatography of L-ascorbic acid, sulfite and thiosulfate using their postcolumn reactions with cerium (IV) and fluorescence detection of cerium (III)].

An ion chromatographic method was used to separate the species of L-ascorbic acid, sulfite and thiosulfate in their mixtures. This method is based on the separation of each anion in their mixtures by using a separation column, and then on the fluorimetric measurement of cerium (III) formed by a postcolumn reaction of cerium (IV) with the species of L-ascorbic acid, sulfite and thiosulfate in the effluent. The optimal conditions for separating and determining the above three species have been established. By using a 3 mmol/L carbonate eluent, the species of L-ascorbic acid, sulfite and thiosulfate could be eluted at the proper retention times of 1.7, 2.6 and 5.0 min, respectively, and these three anions could be separated completely. The effects of the concentrations of cerium (IV) and sulfuric acid in the postcolumn reaction solution on the chromatographic peak-height were tested in order to obtain the optimal peak-height. It was found that the peak-height at first increases rapidly with an increase in the concentration of cerium (IV) and sulfuric acid respectively up to a certain concertation, then increases slowly. These critical concentrations of cerium (IV) and sulfuric acid also depend on the amount of the analyte injected. Meanwhile the baseline signals of the sepectra increase with an increase in the concentration of cerium (IV). Some concentrations above the critical concentration of sulfuric acid could be selected as the optimal concentration of sulfuric acid, but the concentration of cerium (IV) should be optimized by establishing a compromise between the higher peak-height and the lower baseline signal. The detection limit of this method was found to be 1 mumol/L for thiosulfate when an amount of 100 microL analyte was injected.

Ascorbic Acid↗

[Photocurrent spectra of undoped LECSIGaAs].

Extrinsic photocurrent spectra of undoped LECSIGaAs have been measured to investigate the deep levels in this material. A broad photocurrent response band M1 ranging from 0.40 to 0.70 eV has been observed. M1 band reveals five peaks at 0.46, 0.49, 0.56, 0.65 and 0.69 eV, respectively. The onset thresholds for the 0.46, 0.49, 0.56 and 0.69 eV peaks are 0.44, 0.47, 0.51 and 0.67 eV, respectively. It is likely that M1 band is due to different deep levels and each of these deep levels has a concentration larger than 10(14) cm(-3). The origin of M1 band is discussed and possible associations of the 0.44, 0.47 and 0.51 eV thresholds with copper acceptor, EL3 and oxygen donor are presented. The relationship between M1 band and the photoresponse behavior of drain current of GaAs field effect transistor was also investigated.

English Abstract↗

Hydralazine prevents endothelial dysfunction, but not the increase in superoxide production in nitric oxide-deficient hypertension.

Dilator responses, superoxide anion-production, endothelial nitric oxide (NO) synthase and soluble guanylyl cyclase expression were determined in aortic rings from Wistar rats treated for 5 weeks either with the NO synthase inhibitor NG-nitro-L-arginine-methylester (L-NAME), L-NAME plus hydralazine or placebo. In the L-NAME-treated group, acetylcholine-induced relaxation was significantly attenuated whereas it was nearly normal in the L-NAME/hydralazine group. This difference was even more pronounced following inhibition of the endogenous superoxide dismutase using diethyldithiocarbamate. Aortic superoxide production was significantly elevated in both L-NAME-treated groups and hydralazine had no acute effect on superoxide formation. Expression of endothelial NO synthase was similar in all three groups whereas the attenuated soluble guanylyl cyclase expression in rats treated with L-NAME was nearly normalised by concomitant hydralazine treatment. These results demonstrate that in NO-deficient hypertension hydralazine treatment improves vasodilator responses but not the increased superoxide production.

Acetylcholine↗

Overexpression of the sarcolemmal calcium pump in the myocardium of transgenic rats.

The plasma membrane calmodulin-dependent calcium ATPase (PMCA) is a calcium-extruding enzyme controlling Ca2+ homeostasis in nonexcitable cells. However, its function in the myocardium is unclear because of the presence of the Na+/Ca2+ exchanger. We approached the question of the physiological function of the calcium pump using a transgenic "gain of function" model. Transgenic rat lines carrying the human PMCA 4 cDNA under control of the ventricle-specific myosin light chain-2 promoter were established, and expression in the myocardium was ascertained at the mRNA, protein, and functional levels. In vivo hemodynamic measurements in adult homozygous animals showed no differences in baseline and increased cardiac performance recruited by volume overload compared with controls. No differences between transgenic and control cardiomyocytes were found in patch clamp voltage dependence, activation/inactivation behavior of the L-type Ca2+ current, or fast [Ca2+]i transients (assessed by the Fura-2 method). To test whether the PMCA might be involved in processes other than beat-to-beat regulation of contraction/relaxation, we compared growth processes of neonatal transgenic and control cardiomyocytes. A 1.6- and 2.3-fold higher synthesis rate of total protein was seen in cells from transgenic animals compared with controls on incubation with 2% FCS for 24 hours and 36 hours, respectively. An effect of similar magnitude was observed using 20 micromol/L phenylephrine. A 1.4-fold- and 2.0-fold-higher protein synthesis peak was seen in PMCA-overexpressing cardiomyocytes after stimulation with isoproterenol for 12 hours and 24 hours, respectively. Because pivotal parts of the alpha- and beta-adrenergic signal transduction pathways recently have been localized to caveolae, we tested the hypothesis that the PMCA might alter the amplitude of alpha- and beta-adrenergic growth signals by virtue of its localization in caveolae. Biochemical as well as immunocytochemical studies suggested that the PMCA in large part was colocalized with caveolin 3 in caveolae of cardiomyocytes. These results indicate that the sarcolemmal Ca2+-pump has little relevance for beat-to-beat regulation of contraction/relaxation in adult animals but likely plays a role in regulating myocardial growth, possibly through modulation of caveolar signal transduction.

Animals↗

Effects of indirect light and propranolol on melatonin levels in normal human subjects.

An indirect lighting protocol was developed to measure nocturnal melatonin suppression by light in normal human subjects. Goals were to minimize both discomfort due to staring intensely at a bright light source, and behavioral variation due to wandering gaze. Subjects sat with a bank of five full-spectrum light sources placed behind them. Lights reflecting off the surfaces before each subject produced a hemisphere of light that measured 500 lx +/- 5%. Subjects retired to bed in darkness by midnight and then sat in the hemisphere of light from 02.00 h to 04.00 h. Blood for melatonin was drawn at 20-30-min intervals from midnight to 06.00 h. Plasma melatonin was measured by radioimmunoassay. The indirect lighting protocol was used to compare the effects of 500 lx light to dark (21 subjects) and to study varying light intensities from 300 to 2000 lx (7 subjects). We studied the effects of the sitting posture in very dim light of 20-30 lx (6 subjects). We also studied the effects of propranolol plus dark and propranolol plus 500 lx light on melatonin levels. Subjects received placebo, 10 mg propranolol or 40 mg propranolol orally at 23.00 h, and were then exposed to either the dark or light condition. Melatonin levels obtained with the indirect lighting protocol were consistent with studies using direct lighting; light of 500 lx significantly suppressed nocturnal melatonin and suppression was dose related between 300 and 2000 lx. Sitting in dim light had no significant effect on melatonin suppression when compared with the supine posture in the dark in six subjects. Propranolol caused a dose-dependent decrease in melatonin levels in both the dark and the light. There was no relationship between suppression of melatonin by propranolol and suppression by light.

Adolescent↗

Clinical course of rectal bleeding following I-125 prostate brachytherapy.

PURPOSE: Despite the occurrence of some rectal complications in most large series of patients treated with radiation, there is surprisingly little information regarding their management. We report here the clinical course of such patients after I-125 brachytherapy, in an effort to help delineate a rational management policy. METHODS AND MATERIALS: 109 patients with stage T1 to T2 prostatic carcinoma and Gleason score 2 to 7 were treated with I-125 implantation from 1988 through 1995. No external radiation was given. The prescribed minimum radiation dose to the prostate was 140 to 160 Gy. RESULTS: Nineteen of 109 patients (actuarial incidence: 19%) developed persistent, bright red rectal bleeding, from 1 to 28 months following I-125 implantation. Most occurred in the early part of the implant experience. Bleeding resolved in 6 of the 19 patients, from 9 to 48 months from the time of onset. Nine patients were treated with steroid enemas. Laser coagulation was used in three patients, and six patients had no intervention. There was no obvious difference in the resolution rate between groups. There was no obvious difference in the rectal wall radiation for patients who did or did not experience resolution of their bleeding. CONCLUSION: Persistent, minor radiation-related bleeding after prostate brachytherapy can be a source of consternation to patients. They should be reassured that spontaneous healing is likely to occur eventually in a large portion of patients, and should be cautioned against invasive treatment, unless absolutely necessary.

Brachytherapy↗

Urinary incontinence in patients who have a TURP/TUIP following prostate brachytherapy.

PURPOSE: To determine urinary morbidity in patients who have transurethral resection of the prostate (TURP) after 125I brachytherapy. MATERIALS AND METHODS: A total of 109 patients with Stage T1-T2 prostatic carcinoma were treated with 125I implantation from 1991 through 1995. Ten patients underwent TURP/transurethral incision of the prostate (TUIP) after brachytherapy to relieve urinary obstruction refractory to nonsurgical management. RESULTS: Patients who developed refractory urinary retention had a slightly larger preimplant prostate volume than those who did not (62 vs. 54 ml; p = 0.16). Seven of the 10 patients developed some degree of permanent urinary incontinence following TURP/TUIP. Urinary incontinence was mild in three patients [Late Effects Normal Tissue Radiation Oncology Group (LENT) score = 1] and severe in four additional patients (LENT score = 3). There was no obvious relationship between the degree of incontinence and use of TURP vs. TUIP, amount of tissue resected, or time between brachytherapy and TURP/TUIP. In five patients for whom detailed urethral radiation dose information was available, the doses were higher than generally recommended. CONCLUSION: Permanent urinary incontinence is common in patients who require a TURP or TUIP after prostate brachytherapy. Its cause is apparently multifactorial and may include the degree of physical damage to the urinary sphincters and the radiation dose to the urethral region.

Brachytherapy↗

Long-term effects of beta-adrenergic blocking agent treatment on hemodynamic function and left ventricular remodeling in rats with experimental myocardial infarction: importance of timing of treatment and infarct size.

OBJECTIVES: This study was designed to assess the long-term effects of a beta1-selective beta-adrenergic blocking agent on mortality, in vivo hemodynamic function, left ventricular volume and wall stress in post-myocardial infarction (MI) rats. BACKGROUND: Beta-blockers have shown beneficial results in clinical studies after MI. However, the underlying mechanism is not yet understood, and experimental studies have shown conflicting results. METHODS: Bisoprolol (60 mg/kg body weight per day) was given 30 min or 14 days after MI or sham operation. RESULTS: The mortality rate was reduced only in early bisoprolol-treated rats (29% vs. 46% in untreated rats, p < 0.05). Heart rate was equally reduced in all treatment groups, and the maximal rate of rise of left ventricular systolic pressure (dP/dt(max)) decreased in sham rats and in rats with a small to moderate infarct size. Stroke volume index was unchanged in sham rats and in rats with a small to moderate infarct with early or late bisoprolol treatment and increased in rats with a large infarct in the late bisoprolol group. Left ventricular volume was increased by bisoprolol in sham rats and rats with a small infarct but not in rats with a large infarct. CONCLUSIONS: Treatments starting early (30 min) or late (14 days) after coronary artery ligation with bisoprolol increased left ventricular volume in sham rats and in rats with a small infarct but not in rats with a large infarct. Late bisoprolol treatment improved stroke volume index, and early bisoprolol treatment reduced diastolic wall stress, in rats with a large myocardial infarct. Thus, bisoprolol effects on remodeling and cardiac performance after myocardial infarction strongly depend on infarct size and timing of treatment. This finding may explain previous controversial results that did not consider infarct size and timing of treatment.

Adrenergic beta-Antagonists↗

Three-dimensional 31P magnetic resonance spectroscopic imaging of regional high-energy phosphate metabolism in injured rat heart.

The purpose of this study was to measure the spatially varying 31P MR signals in global and regional ischemic injury in the isolated, perfused rat heart. Chronic myocardial infarcts were induced by occluding the left anterior descending coronary artery eight weeks before the MR examination. The effects of acute global low-flow ischemia were observed by reducing the perfusate flow. Chemical shift imaging (CSI) with three spatial dimensions was used to obtain 31P spectra in 54-microl voxels. Multislice 1H imaging with magnetization transfer contrast enhancement provided anatomical information. In normal hearts (n = 8), a homogeneous distribution of high-energy phosphate metabolites (HEP) was found. In chronic myocardial infarction (n = 6), scar tissue contained negligible amounts of HEP, but their distribution in residual myocardium was uniform. The size of the infarcted area could be measured from the metabolic images; the correlation of infarct sizes determined by histology and 31P MR CSI was excellent (P < 0.006). In global low-flow ischemia (n = 8), changes of HEP showed substantial regional heterogeneity. Three-dimensional 31P MR CSI should yield new insights into the regionally distinct metabolic consequences of various forms of myocardial injury.

Adenosine Triphosphate↗

Quantitative regional blood volume studies in rat myocardium in vivo.

Many pathophysiological processes in the myocardium are in close relation to changes of the regional blood volume and regional myocardial blood flow or perfusion. Only few methods exist to obtain quantitative values for these parameters. Quantitative regional blood volume (RBV) studies in rat myocardium are presented using snapshot fast low angle shot (FLASH) inversion recovery T1 measurements with two different blood pool contrast agents, gadolinium diethylenetriaminopentaacetic acid (Gd-DTPA) albumin and Gd-DTPA polylysine. In contrast to previous attempts, each snapshot FLASH image acquisition was ECG-triggered under breathhold conditions. To measure relaxation times shorter than a heart cycle, each T1 sequence was repeated two times with different delays between inversion pulse and first image acquisition. The experiments were performed on a Bruker Biospec 70/21 using a homogeneous transmitter coil and a circularly polarized surface receiver coil, a special ECG trigger unit, and a respirator that is controlled by the pulse program. Based on a fast exchange model RBVm maps were calculated from the relaxation time maps for different concentrations of the two blood pool contrast agents. A significant dependence of the RBVm values on blood T1 was found. This is in accordance with a model that has been developed recently relating the dependence of RBVm on T1 of blood to perfusion. For Gd-DTPA albumin, the application of the model to the experimental data yields realistic values for RBV and perfusion. The values, which are in accordance with literature data, were obtained at highest contrast agent concentrations i.e., lowest relaxation times of blood (ca. 200 ms).

Albumins↗

Changes of myocardial high-energy phosphates with the cardiac cycle during acute or chronic myocardial stress.

Whether changes of cardiac high-energy phosphate concentrations occur over the cardiac cycle remains controversial. The hypothesis was that such cyclical changes are accentuated during acute or chronic myocardial stress. Isolated rat hearts were perfused under four conditions: (1) control, (2) inotropic stimulation by doubling of perfusate [Ca2+], (3) acute hypoxia (buffer PO2 approximately 150 torr), and (4) failing, chronically infarcted hearts. 31P-MR spectra were obtained at seven time points of the cardiac cycle. Under control conditions, cyclical changes ("cycling") of ATP (11+/-3%*, *P < 0.05) and phosphocreatine (9+/-2%*) were detected, inorganic phosphate cycling did not reach statistical significance. At high [Ca2+] perfusion, cycling of phosphocreatine (9+/-5%*) was not accentuated, cycling of ATP and inorganic phosphate did not reach significance. During acute hypoxia, cycling of ATP (10+/-4%*) and inorganic phosphate (11+/-4%*) occurred, but cyclical changes of phosphocreatine were not significant. In chronically infarcted hearts, the extent of cyclical changes of ATP, phosphocreatine, and inorganic phosphate was not accentuated. Thus, in perfused rat heart, small oscillations of high-energy phosphates during the cardiac cycle are detectable, but such changes are not accentuated during acute or chronic stress. The concentrations of high-energy phosphates over the cardiac cycle are tightly regulated.

Acute Disease↗

Changes of creatine kinase gene expression in rat heart post-myocardial infarction.

Creatine kinase (CK) plays a crucial role in cardiac energy transduction. During chronic cardiac stress conditions leading to hypertrophy and/or heart failure, the profile of CK isoenzyme activities changes towards a fetal pattern with increases of BB- and MB-CK and decreases of MM-CK and mito-CK. Changes of myocardial CK gene expression are only indirectly reflected by measurements of CK activities. The purpose of this work was, therefore, to determine myocardial expression of B-, M- and sarcomeric mito-CK genes in an animal model of heart failure where hemodynamic alterations and CK system changes are well defined, that is, in the rat heart post-myocardial infarction. Intact residual left ventricular myocardium was harvested 2 months following infarction (MI; n = 7) or sham operation (sham; n = 6) after in vivo left-ventricular end-diastolic pressure (LVEDP) was recorded. Total CK activity was measured spectrophotometrically, CK isoenzyme distribution with agarose gel electrophoresis. Steady state mRNA levels coding for B-, M- and mito-CK genes were measured with quantitative PCR and were normalized for GAPDH expression. Total CK activity tended to be reduced in MI (5.51 +/- 0.62 IU/mg protein) compared to sham (6.77 +/- 0.24; P = 0.55). CK isoenzyme distribution showed an increase of fetal BB- + MB-CK (MI 22.0 +/- 3.1%, sham 15.1 +/- 1.0%; P < 0.05), no change of MM-CK and a decrease of mito-CK (27.0 +/- 1.5% sham, 20.8 +/- 2.0% MI: P < 0.05). Relative B-CK mRNA levels increased (sham 0.46 +/- 0.06, MI 1.03 +/- 0.09; P < 0.05) and M-CK mRNA levels decreased (sham 1.06 +/- 0.08. MI 0.66 +/- 0.09; P < 0.05) significantly post-MI. The increase of B-CK mRNA (r = 0.72; P = 0.009) and the decrease of M-CK mRNA (r = 0.76; P = 0.003) correlated significantly with in vivo LVEDP. Mito-CK mRNA levels remained unchanged after MI (sham 0.94 +/- 0.16, MI 0.98 +/- 0.09). Intact residual left-ventricular myocardium post-MI is characterized by increased B-CK-mRNA and reduced M-CK-mRNA expression.

Animals↗

[Transition of myocardial ischemia to heart failure].

Myocardial ischemia results in myocardial dysfunction. Recovery may be delayed ("stunning"), or persistent if perfusion remains reduced ("hibernation") and ischemia may go on to necrosis, thus, contributing to chronic heart failure. In addition, myocardium not directly affected by ischemia may undergo adaptive processes like hypertrophy and dilatation, which may result in chronic left heart failure. This process is characterized by hemodynamic, neurohumoral, and progressive morphologic changes of the heart which are closely interrelated. Hemodynamic changes basically consist of an increase in left ventricular filling pressure and a decrease in global ejection fraction, and, in most cases years after myocardial infarction, in an increase in systemic vascular resistance and right atrial pressure. Neurohumoral changes consist of an increase in plasma catecholamines, atrial natriuretic factor and vasopressin, and in an activation of the renin-angiotensin-system. Plasma endothelin-1 was recently reported to be increased in patients with heart failure, and prognosis was related to endothelin levels. Diminished response of vessels to endothelium (EDRF/NO) dependent vasodilatation suggests impairment of vascular endothelium in heart failure. Local changes of cardiac neurohumoral systems could contribute to structural changes of the heart, e.g., systemic activation to hemodynamic changes. Structural changes of the heart are characterized by an increase in volume and thickness of surviving myocardium and an expansion of ischemic and necrotic myocardium. Molecular control of these processes which include various cell types, such as cardiomyocytes and cardiofibroblasts, are currently an issue of intense research and could result in specific therapeutic importance.

Chronic Disease↗

Chronic effects of early started angiotensin converting enzyme inhibition and angiotensin AT1-receptor subtype blockade in rats with myocardial infarction: role of bradykinin.

OBJECTIVE: The long-term effects and mechanisms of early started angiotensin converting enzyme (ACE) inhibition post myocardial infarction (MI) are not well understood. Chronic effects of early ACE inhibition on hemodynamics, left ventricular diastolic wall stress and remodeling were, therefore, compared to that of angiotensin AT1-receptor subtype blockade in rats with experimental myocardial infarction. The contribution of bradykinin potentiation to both ACE inhibitor and angiotensin AT1-receptor subtype blockade was assessed by cotreatment of rats with a bradykinin B2-receptor antagonist. METHODS: MI was produced by coronary artery ligation in adult male Wistar rats. The ACE inhibitor, quinapril (6 mg/kg per day), or the angiotensin AT1-receptor subtype blocker, losartan (10 mg/kg per day), administered by gavage, and the bradykinin B2-receptor antagonist, Hoe-140 (500 micrograms/kg per day s.c.), administered either alone or in combination with quinapril or losartan, were started 30 min after MI and continued for eight weeks. RESULTS: Quinapril and losartan reduced left ventricular end-diastolic pressure and global left ventricular diastolic wall stress only in rats with large MI. Pressure volume curves showed a rightward shift in proportion to MI size that was not prevented by quinapril or losartan treatment. Only the ACE inhibitor reduced left ventricular weight and this effect was prevented by cotreatment with the bradykinin antagonist. Baseline and peak cardiac index and stroke volume index, as determined using an electromagnetic flowmeter before and after an acute intravenous volume load, were restored by quinapril, whereas losartan had no effects. CONCLUSION: Treatments starting 30 min after coronary artery ligation, with either quinapril or losartan, reduced preload only in rats with large MI. Despite this unloading of the heart, structural dilatation was not prevented by this early treatment. Only quinapril improved cardiac performance and reduced left ventricular weight and this effect was abolished by cotreatment with Hoe-140, suggesting an angiotensin II blockade-independent, but bradykinin potentiation-dependent, mechanism.

Adrenergic beta-Antagonists↗

Aggravation of left ventricular remodeling by a novel specific endothelin ET(A) antagonist EMD94246 in rats with experimental myocardial infarction.

An endothelin (ET(A)) antagonist reduced mortality and an ET(A) + ET(B) antagonist prevented left ventricular dilatation in rats with large myocardial infarction. This study tested the hypothesis that long-term blockade of the ET(A) receptor would have beneficial effects on left ventricular function and remodeling. Three hours after coronary artery ligation or sham operation in rats, EMD94246 (100 mg/kg/day, n=62) or placebo (n=62) was given by gavage. Eight weeks later, left ventricular hemodynamic measurements were performed and left ventricular volume determined with a double-lumen catheter after KCl-induced cardiac arrest. EMD94246 treatment had no effects on mortality or hemodynamic parameters. In rats with large infarcts, EMD94246 significantly increased left ventricular volume (2.5+/-0.1 vs. 2.2+/-0.1 ml/kg; p < 0.05). The nonpeptide ET(A)-selective antagonist EMD94246 promoted chronic left ventricular dilatation in rats with large myocardial infarction.

Animals↗

In vitro and In vivo characterization of a small-colony variant of the primary form of photorhabdus luminescens MD (Enterobacteriaceae)

A small-colony variant (Vsm) of the primary form (Vp) of Photorhabdus luminescens MD from in vitro and in vivo cultures is described. Unlike the primary form, Vp, the Vsm variant is not the preferred diet of its nematode symbiont, a Heterorhabditis sp., does not support development and reproduction of the nematode, and is less pathogenic than Vp to Galleria mellonella larvae. Vsm cells were carried by 25% of infective juveniles, but they comprised a very low percentage ( approximately 0.4%) of the total cells carried by the juvenile. In vitro subculture and in vivo injection into the larvae with either Vp or Vsm always produced a mixture of both Vp and Vsm. In nematode-bacterium-infected G. mellonella larvae, the Vp population in the hemocoel was high (4 x 10(9) to 5 x 10(9) CFU/g of wet insect tissue) at 24 h after infection, decreased about 10-fold by 48 h, and then regained a high level at day 5 before decreasing at day 7 and then remaining relatively constant through day 15 postinfection. The Vsm population, under the same conditions as those of Vp, increased gradually to a high level (9 x 10(8) CFU/g of wet insect tissue) at day 5 postinfection and then declined gradually through day 15.

Journal Article↗

Stress distribution in the mandible with unilateral condylar fracture.

OBJECTIVE: The purpose of this study was to investigate the influence of unilateral condylar neck fracture upon the stress distribution in the mandible and the temporomandibular joint (TMJ) to realize primarily the biomechanical mechanism of the temporomandibular joint disorders (TMD) caused by TMJ injury. METHODS: The character of stress distribution in the mandible of a normal human and a patient with TMD induced by unilateral condylar neck fracture followed by malpositioned healing was analyzed quantitatively and compared during centric occlusion by combining spiral computed tomography scanning technology with the three-dimensional finite element method. RESULTS: The patient with unilateral condylar neck fracture followed by malpositioned healing had unbalanced stress distribution in the mandible, such as differing nature and value of stress. The stress in the fractured side was higher than in the nonfractured side, in which the condyle was more evident. The maximum principal stress and minimum principal stress of each region in the fractured mandible were much higher than those in a normal mandible. Stress quality also differed. CONCLUSIONS: The abnormal stress changes after unilateral condylar neck fracture with malpositioned healing may be related to the effect of condylar shape change on masticatory muscle function and occlusion. TMJ injury not only damaged the condylar structure, but also compromised its biomechanic environment. It is preliminarily thought that unbalanced stress distribution, evidently increased stress, and varied stress character are biomechanic mechanisms of TMD. Condylar dislocated fracture should be treated promptly and properly to maintain the proper prognostic stress distribution.

Adult↗