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Biomedical subjects

M Fu

Publications and source records attributed to M Fu.

At least 55 records · Page 3Linked to original sources

[Preliminary study on orthodontic treatment before and after distraction osteogenesis].

OBJECTIVE: To get some guidelines for the orthodontic treatment before and after distraction osteogenesis (DO). METHODS: DO was performed in 4 patients maxilla and two for mandible. The patients were aged from 19 to 25 (average 21.5). We try to sum up the procedures and clinical experiences of pre- and post-surgery orthodontics. RESULTS: The procedures and experiences obtained are the followings: 1. Pre-surgery orthodontics for DO is simplified as alignment of dental arch in a short period. 2. Post-surgery orthodontics for DO is more complicated and peculiar. The main task is to make the opened posterior teeth occlude as soon as possible by light force vertical elastics. At the same time, some cross elastics may be needed for correction of posterior occlusal relationship. 3. Expansion of upper arch may be needed in some patients because of constricted dental arch. 4. Class II or III elastics may be used for prevention of relapse after DO. CONCLUSIONS: DO is a new technique in orthognathic surgery. Post-surgery orthodontics is more complicated and important in the treatment course.

Adult↗

[The change of genioglossus muscle activity of OSAS patients with and without snoreguard].

OBJECTIVE: The effect of snoreguard on the genioglossus (GG) muscle activity of OSAS patients was investigated. METHODS: Fifteen male patients with mild to severe OSAS were diagnosed by overnight polysomnographic and GG EMG studies, and reexamined with snoreguard. GG muscle activities of these patients with and without snoreguard were compared. RESULTS: The results revealed that the overnight GG muscle activity decreased significantly and the fluctuating GG muscle activity was improved effectively by the treatment of snoreguard. CONCLUSION: The treatment mechanisms of mandibular advancing appliance on OSAS are mechanical enlargement of upper airway and the passivity of GG muscle during treatment.

Adult↗

[Individual studies of parent-offspring similarity in Class II division 1 malocclusion].

OBJECTIVE: To study the parent-offspring similarity of class II division 1 malocclusion. METHODS: On the basis of family units, the polygonic curves and superimposed graphs of parents with those of the offspring were compared. RESULTS: (1) Craniofacial structure of most parents of the class II division 1 patients have class II convex tendency. (2) The curves of the offspring resemble one or two of the parent's in 84% of the families, and the resemblance mainly concentrates in skeleton. CONCLUSIONS: (1) Class II division 1 malocclusion is characterized by familial aggregativity. (2) High probability of heredity exists in parent-offspring similarity, and we believe that hereditary factors dominate in skeletal area while in dental area there is a higher probability that environmental factors dominate.

Female↗

[Study on the content of serum HDL subclasses in obese subjects].

OBJECTIVE: To investigate the change of the contents of serum HDL subclasses in obese subjects. METHODS: Contents of serum HDL subclasses in healthy controls(n = 64) and obese subjects(n = 58) were determined by two-dimensional gel electrophoresis associated with immunodetection method. RESULTS: The pre-beta 1 HDL, HDL3c and HDL3b contents increased significantly (P < 0.001) and the HDL2b content decreased significantly (P < 0.001) in obese subjects as compared with those in healthy controls. In male obese subjects, the pre-beta 1 HDL and HDL3c levels were significantly higher(P < 0.01 and P < 0.05, respectively) and HDL2b level was significantly lower(P < 0.05), compared with those in female obese subjects. In male control subjects, the level of pre-beta 1 HDL was significantly higher than that in female subjects. In obese subjects, the concentrations of BMI and serum TG had positive correlation with those of pre-beta 1 HDL(r = 0.382, P < 0.001), HDL3c(r = 0.232, P < 0.05) and HDL3b(r = 0.294, P < 0.01) and negative correlation with that of HDL2b(r = -0.304, P < 0.01). CONCLUSION: The particle size of HDL in obese subjects showed a general shift toward smaller size, which indicated that the maturation of HDL could be abnormal in obese subjects. The particle size of HDL was found to be smaller in both obese and control male subjects than in female subjects, suggesting that sex seems to be related to the contents of serum HDL subclasses.

Adult↗

[Clinical application and evaluation of polymerase chain reaction-microwell plate hybridization assay in the detection of Mycobacterium tuberculosis].

OBJECTIVE: To evaluate the clinical application and feasibility of polymerase chain reaction-microwell plate hybridization assay in the detection of Mycobacterium tuberculosis. METHODS: 1130 specimens with strong suspicion for mycobacterium tuberculosis were collected from the hospitals and were detected by fast bacilli stain, culture, PCR-electrophoresis and PCR-microwell plate hybridization respectively. The laboratory results were analyzed in combination with the symptoms and signs of patients and the observations on treatment. Also detected were 100 samples from the clinically evidenced non-tuberculosis patients. RESULTS: In the 100 samples collected from the patients without tuberculosis, the PCR-hybridization method and culture method did not detect Mycobacterium tuberculosis, but the fast bacilli stain method and PCR-electrophoresis method brought out one and two false-positive results respectively. The results of testing the 1030 clinical samples which probably contained Mycobacterium tuberculosis demonstrated that the PCR-hybridization method had the highest positive rate (481/1030) among the four methods, and the positive rates of the other three methods were PCR-electrophoresis (406/1030), culture (365/1030) and fast bacilli stain (256/1030) in proper order. The chi-square test showed that there were significant difference between the PCR-hybridization method and the other three methods respectively (P < 0.0083 or P < 0.0017). CONCLUSION: PCR-Hybridization method is specific, sensitive, accurate and fast in detecting mycobacterium tuberculosis; it is worthy to be used clinically.

Evaluation Studies as Topic↗

Role of calcineurin in angiotensin II-induced cardiac myocyte hypertrophy of rats.

OBJECTIVE: The present study investigated the role of calcineurin in angiotensin II(AngII) -induced cardiac myocyte hypertrophy of rats. METHOD: The primary cardiac myocytes were cultured under the standard conditions. The calcineurin activity in AngII-treated cardiomyocytes was tested by using PNPP; protein synethsis rate was assessed by 3H-leucine incorporation; atrial natriuretic factor(ANF) mRNA level was determined by Northern blot analysis. Cell viability was estimated by lactate dehydrogenase (LDH) levels in cultured medium and by dyed cell numbers. RESULT: After stimulation of 10, 100 and 1 000 nmol/L of AngIi, calcineurin activities in the cardiomyocytes were increased by 13%, 57% (P < 0.05) and 228% (P < 0.01) respectively, compared with control group. Cyclosporin A(CsA), a specific inhibitor of calcineurin, markedly inhibited the calcineurin activity and decreased the 3H-leucine incorporation in AngII-treated cardiomyocytes in a dose-dependent manner. It was also found that CsA slightly reduced the mRNA level of ANF gene in AngII-stimulated cardiomyocytes. CONCLUSION: During AngII-induced cardiac myocyte hypertrophy, calcineurin signal pathway is activated, and inhibition of the pathway can attenuate AngII-induced cardiac myocyte hypertrophy, which suggests that the calcineurin signal pathway may play an important role in AngII-induced myocardial hypertrophy of rats.

Angiotensin II↗

[Fluorescence quenching method for the determination of p-hydroxyphenylpyruvic acid].

A fluorescence quenching method for the determination of p-hydroxyphenylpyruvic acid with trytophan in the medium pH 11.01 NH3-NH4Cl is studied. The calibration curve is linear for p-hydroxyphenylpyruvic acid from 0 to 15 micrograms.mL-1 with lambda ex/lambda em = 285/356 nm. The detection limit is 0.37 microgram.mL-1. Twenty replicate determinations of solutions containing 10 micrograms.mL-1 p-hydroxyphenylpyruvic acid show a relative standard deviation of 1.2%. This method can be applied to the determination of p-hydroxyphenylpyruvic acid in serum with satisfactory results.

Calibration↗

Aminoanthraquinones as novel ligands at the polyamine binding site on the N-methyl-D-aspartate receptor complex.

As part of a drug discovery program using high-throughput radioligand-binding assays, aminoanthraquinones were identified as potential modulators of N-methyl-D-aspartate (NMDA) receptor function. Aminoanthraquinones may represent a novel class of polyamine binding site ligands with a unique pharmacophore and may facilitate the rational design of novel NMDA-receptor modulators.

Anthraquinones↗

The integrin-linked kinase regulates the cyclin D1 gene through glycogen synthase kinase 3beta and cAMP-responsive element-binding protein-dependent pathways.

The cyclin D1 gene encodes the regulatory subunit of a holoenzyme that phosphorylates and inactivates the pRB tumor suppressor protein. Cyclin D1 is overexpressed in 20-30% of human breast tumors and is induced both by oncogenes including those for Ras, Neu, and Src, and by the beta-catenin/lymphoid enhancer factor (LEF)/T cell factor (TCF) pathway. The ankyrin repeat containing serine-threonine protein kinase, integrin-linked kinase (ILK), binds to the cytoplasmic domain of beta(1) and beta(3) integrin subunits and promotes anchorage-independent growth. We show here that ILK overexpression elevates cyclin D1 protein levels and directly induces the cyclin D1 gene in mammary epithelial cells. ILK activation of the cyclin D1 promoter was abolished by point mutation of a cAMP-responsive element-binding protein (CREB)/ATF-2 binding site at nucleotide -54 in the cyclin D1 promoter, and by overexpression of either glycogen synthase kinase-3beta (GSK-3beta) or dominant negative mutants of CREB or ATF-2. Inhibition of the PI 3-kinase and AKT/protein kinase B, but not of the p38, ERK, or JNK signaling pathways, reduced ILK induction of cyclin D1 expression. ILK induced CREB transactivation and CREB binding to the cyclin D1 promoter CRE. Wnt-1 overexpression in mammary epithelial cells induced cyclin D1 mRNA and targeted overexpression of Wnt-1 in the mammary gland of transgenic mice increased both ILK activity and cyclin D1 levels. We conclude that the cyclin D1 gene is regulated by the Wnt-1 and ILK signaling pathways and that ILK induction of cyclin D1 involves the CREB signaling pathway in mammary epithelial cells.

Activating Transcription Factor 2↗

Transgenic overexpression of caveolin-3 in skeletal muscle fibers induces a Duchenne-like muscular dystrophy phenotype.

It recently was reported that Duchenne muscular dystrophy (DMD) patients and mdx mice have elevated levels of caveolin-3 expression in their skeletal muscle. However, it remains unknown whether increased caveolin-3 levels in DMD patients contribute to the pathogenesis of DMD. Here, using a genetic approach, we test this hypothesis directly by overexpressing wild-type caveolin-3 as a transgene in mice. Analysis of skeletal muscle tissue from caveolin-3- overexpressing transgenic mice reveals: (i) a dramatic increase in the number of sarcolemmal muscle cell caveolae; (ii) a preponderance of hypertrophic, necrotic, and immature/regenerating skeletal muscle fibers with characteristic central nuclei; and (iii) down-regulation of dystrophin and beta-dystroglycan protein expression. In addition, these mice show elevated serum creatine kinase levels, consistent with the myo-necrosis observed morphologically. The Duchenne-like phenotype of caveolin-3 transgenic mice will provide an important mouse model for understanding the pathogenesis of DMD in humans.

Animals↗

Transforming growth factor-beta1 recruits histone deacetylase 1 to a p130 repressor complex in transgenic mice in vivo.

Transforming growth factor (TGF)-beta1 functions as a tumor suppressor in vivo. Using transgenic mice, we show that hepatic TGF-beta1 overexpression inhibits abundance of the cyclin-dependent kinase activating tyrosine phosphatase cdc25A protein. The reduction in cdc25A protein levels was associated with increased binding of histone deacetylase 1 to p130 in the hepatic extracts. In cultured cells, HDAC1/p130 overexpression inhibited activity of the cdc25A promoter through an E2F site. TGF-beta1 treatment enhanced p130 binding to the cdc25A promoter E2F site assessed in chromatin immunoprecipitation assays. Hepatic proliferation induced by partial hepatectomy was associated with a decrease in the amount of HDAC1 bound to p130, without a significant decrease in p130 abundance, suggesting that HDAC1 binding to p130 may be regulated by proliferative stimuli. The induction of cdc25A abundance induced by partial hepatectomy correlated with the induction of DNA synthesis. These studies suggest that TGF-beta1 may enhance HDAC1 binding to p130 in vivo, thereby inhibiting cdc25A gene expression. TGF-beta1 regulation of HDAC1/pocket protein associations may provide a link between chromatin remodeling proteins and cdk inhibition through induction of cdc25A in vivo.

Animals↗

Gut-enriched Krüppel-like factor represses cyclin D1 promoter activity through Sp1 motif.

Cancer cells differ from normal cells in many characteristics including loss of differentiation and uninhibited cell proliferation. Recent studies have focused on the identification of factors contributing to cell growth and differentiation. Gut-enriched Krüppel-like factor (GKLF or KLF4) is a newly identified eukaryotic transcription factor and has been shown to play a role in regulating growth arrest. We have previously shown that GKLF mRNA levels were significantly decreased in colon cancer tissues, and that over-expression of GKLF in colonic adenocarcinoma cells (HT-29) resulted in reduction of cyclin D1 (CD1) mRNA and protein levels. The current study was undertaken to determine the mechanisms by which GKLF inhibited CD1 expression. In a transient transfection system, GKLF suppressed CD1 promoter activity by 55%. Sequential deletion and site-directed mutation analysis of the CD1 promoter have identified the sequence between -141 and -66, a region containing an Sp1 response element, to be essential for GKLF function. By electrophoretic mobility gel shift assay, recombinant GKLF and nuclear extracts from HT-29 cells were found to bind to the Sp1 motif on the CD1 promoter. The inhibitory effect of GKLF on the CD1 promoter activity was completely abolished by excessive amount of Sp1 DNA and GKLF significantly reduced the stimulatory function of Sp1 suggesting that GKLF and Sp1 may compete for the same binding site on the CD1 promoter. These results indicate that GKLF is a transcriptional repressor of the CD1 gene and that the inhibitory effect of GKLF is, in part, mediated by interaction with the Sp1 binding domain on its promoter.

Adenocarcinoma↗

The cyclin D1 gene is transcriptionally repressed by caveolin-1.

The cyclin D1 gene encodes the regulatory subunit of the holoenzyme that phosphorylates and inactivates the retinoblastoma pRB protein. Cyclin D1 protein levels are elevated by mitogenic and oncogenic signaling pathways, and antisense mRNA to cyclin D1 inhibits transformation by the ras, neu, and src oncogenes, thus linking cyclin D1 regulation to cellular transformation. Caveolins are the principal protein components of caveolae, vesicular plasma membrane invaginations that also function in signal transduction. We show here that caveolin-1 expression levels inversely correlate with cyclin D1 abundance levels in transformed cells. Expression of antisense caveolin-1 increased cyclin D1 levels, whereas caveolin-1 overexpression inhibited expression of the cyclin D1 gene. Cyclin D1 promoter activity was selectively repressed by caveolin-1, but not by caveolin-3, and this repression required the caveolin-1 N terminus. Maximal inhibition of the cyclin D1 gene promoter by caveolin-1 was dependent on the cyclin D1 promoter T-cell factor/lymphoid enhancer factor-1-binding site between -81 to -73. The T-cell factor/lymphoid enhancer factor sequence was sufficient for repression by caveolin-1. We suggest that transcriptional repression of the cyclin D1 gene may contribute to the inhibition of transformation by caveolin-1.

Amino Acid Sequence↗

p300 and p300/cAMP-response element-binding protein-associated factor acetylate the androgen receptor at sites governing hormone-dependent transactivation.

The androgen receptor (AR) is a sequence-specific DNA-binding protein that plays a key role in prostate cancer cellular proliferation by dihydrotestosterone and the induction of secondary sexual characteristics. In this study we demonstrate that the AR can be modified by acetylation in vitro and in vivo. p300 and p300/cAMP-response element-binding protein acetylated the AR at a highly conserved lysine-rich motif carboxyl-terminal to the zinc finger DNA-binding domain. [(14)C]acetate-labeling experiments demonstrated that AR acetylation by p300 in cultured cells requires the same residues identified in vitro. Point mutation of the AR acetylation site (K632A/K633A) abrogated dihydrotestosterone-dependent transactivation of the AR in cultured cells. Mutation of the p300 CH3 region or the p300/cAMP-response element-binding protein histone acetylase domain reduced ligand-dependent AR function. The identification of the AR as a direct target of histone acetyltransferase co-activators has important implications for targeting inhibitors of AR function.

Acetylation↗

Cell-cycle dysregulation and the molecular mechanisms of prostate cancer.

Prostate cancer is the most common cause of non-cutaneous cancer in men and although frequently latent is the second commonest cause of death. Screening for the disease was historically based on symptoms of urethral obstruction, clinical examination of the prostate gland and serum measurements of prostate specific antigen. As prostate cancer growth in the early stages is enhanced by androgens, the mainstay of therapy has been androgen ablation by pharmaco-therapeutic or surgical means. The subsequent development of androgen therapy resistant prostate cancer in many patients, for whom therapeutic options remain limited, has led researchers to focus attention on understanding the molecular genetics of prostate cancer. The array of genetic abnormalities observed in prostate tumors, which include changes in components of the cell cycle, suggest the disease is quite heterogeneous and may require further sub-classification based on genetic markers. Such analyses may lead to identification of relevant new prognostic and therapeutic indicators. The advent of transgenic mouse models of prostate cancer may provide a critical tool for the implementation of rational genetic based therapeutics and alternate drug design.

Animals↗

Myocardial oxygen consumption modulates adenosine formation by canine right ventricle in absence of hypoxia.

Myocardial adenosine formation varies with myocardial oxygen consumption (MVO(2)), but whether concurrent hypoxia is required for adenosine formation is uncertain. Changes in right coronary (RC) perfusion pressure (RCP) produce directionally similar alterations in right ventricular (RV) MVO(2)and in RC venous P O(2)(P(v)O(2)), an index of myocardial P O(2). RCP was varied in 10 anesthetized, open chest dogs to determine if, under these conditions, RV formation of adenosine would increase with MVO(2)in absence of myocardial hypoxia. Dialysis probes were implanted in the mid myocardium of RV free wall for collecting dialysate samples for HPLC analyses to estimate interstitial adenosine and other purines. Coronary venous blood was sampled from a superficial vein draining the RC artery (RCA) perfusion territory. At 115+/-3 mmHg baseline RCP, RC blood flow (RCBF)=0.51+/-0.04 ml/min/g, MVO(2)=4.6+/-0.5 ml/min/100 g, P(v)O(2)=34+/-1.5 mmHg, and dialysate adenosine=0. 27+/-0.03microM. When RCP was lowered to 61+/-1 mmHg by adjusting an occluder on the proximal RCA, RCBF decreased to 0.36+/-0.03 ml/min/g, MVO(2)fell to 3.7+/-0.4 ml/min/100 g, lactate uptake remained positive, P(v)O(2)fell to 30+/-1.7 mmHg, and dialysate adenosine decreased to 0.20+/-0.03microM. Reactive hyperemia of 1.25+/-0.13 ml/min/g was observed when the RCA constriction was released, although dialysate adenosine had fallen. When RCP was elevated to 164+/-2 mmHg by inflating a balloon catheter in the descending aorta, RCBF increased to 0.70+/-0.06 ml/min/g, MVO(2)increased to 5.8+/-1. 0 ml/min/100 g, P(v)O(2)rose to 39+/-2.3 mmHg, and dialysate adenosine increased to 0.33+/-0.04microM. These data indicate that (1) RV oxygen demand varies with RCP; (2) if RV ischemia is absent, myocardial adenosine formation is modulated by MVO(2), with no requirement for hypoxia; (3) pressure-flow autoregulation is relatively ineffective in the RC circulation, where adenosine does not mediate and may even blunt autoregulation.

Adenosine↗

Cephalometric comparisons between Chinese and Caucasian patients with obstructive sleep apnea.

The purpose of this study was to compare two groups of adult men from different ethnic backgrounds and with obstructive sleep apnea; they were selected by matching age, gender, skeletal pattern, body mass index, and respiratory disturbance index. Pretreatment cephalometric radiographs and overnight polysomnograms of 30 Chinese and 43 Caucasian patients with Class II, Division 1 malocclusions were analyzed to investigate if there were craniofacial and upper airway structural differences between the two ethnic groups. The Chinese group, when compared with the group of Caucasian patients, revealed more severe underlying craniofacial skeletal discrepancies with significantly smaller maxilla and mandibles, more severe mandibular retrognathism, proclined lower incisors, increased total and upper facial heights, and steeper and shorter anterior cranial bases. However, no significant differences were found between the two groups in posterior facial height, ratio of upper to lower anterior facial height, and the position of hyoid bone, maxilla, and upper incisors. With regard to soft tissue and upper airway measurements, there were no significant ethnic differences in tongue and soft palate size, vertical length of oropharynx, and anteroposterior dimensions of the upper airway at most of the levels except for a larger super-posterior airway space, a larger nasopharynx and oropharynx cross-sectional area, and a smaller tongue height in the Chinese group. We conclude that there are a number of craniofacial and upper airway structures that differ between the two ethnic groups that may be relevant to the treatment of obstructive sleep apnea in various ethnic groups.

Asian People↗

Evolution in the treatment of choledochus cyst.

PURPOSE: The aim of this study was to reevaluate the results of the short jejunal interposition (Chicago-Beijing procedure) in the treatment of choledochus cyst and search for the way of further improvement. METHODS: A retrograde study of some 500 surgical cases was made. The immediate postoperative and 10-year follow-up results of the 3 main procedures used in 3 different time periods were compared. Twenty-five redo cases of the above-mentioned series and another 6 referred from other hospitals were analyzed specially for the main cause of complications. RESULTS: Ten-year uneventful follow-up occurred in more than 90% of cases after the Chicago-Beijing procedure, which was evidently superior to other 2 kinds of methods. Having solved the problems of the abnormal pancreatico-biliary communication and entero-biliary reflux, it remains the challenge of the anastomosis stricture. Malignancy degeneration disappeared dramatically after total excision of the cyst. CONCLUSIONS: Chicago-Beijing procedure proved to be the most reliable operation for choledochus cyst in comparison with the other 2 conventional methods in BCH. The prevention of anastomosis stricture should be emphasized for the further improvement of the surgical result.

Anastomosis, Roux-en-Y↗