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Biomedical subjects

M Yao

Publications and source records attributed to M Yao.

At least 55 records · Page 3Linked to original sources

Amino acid residues in ribonuclease MC1 from bitter gourd seeds which are essential for uridine specificity.

The ribonuclease MC1 (RNase MC1), isolated from seeds of bitter gourd (Momordica charantia), consists of 190 amino acids and is characterized by specific cleavage at the 5'-side of uridine. Site-directed mutagenesis was used to evaluate the contribution of four amino acids, Asn71, Val72, Leu73, and Arg74, at the alpha4-alpha5 loop between alpha4 and alpha5 helices for recognition of uracil base by RNase MC1. Four mutants, N71T, V72L, L73A, and R74S, in which Asn71, Val72, Leu73, and Arg74 in RNase MC1 were substituted for the corresponding amino acids, Thr, Leu, Ala, and Ser, respectively, in a guanylic acid preferential RNase NW from Nicotiana glutinosa, were prepared and characterized with respect to enzymatic activity. Kinetic analysis with a dinucleoside monophosphate, CpU, showed that the mutant N71T exhibited 7.0-fold increased K(m) and 2.3-fold decreased k(cat), while the mutant L73A had 14.4-fold increased K(m), although it did retain the k(cat) value comparable to that of the wild-type. In contrast, replacements of Val72 and Arg74 by the corresponding amino acids Leu and Ser, respectively, had little effect on the enzymatic activity. This observation is consistent with findings in the crystal structure analysis that Asn71 and Leu73 are responsible for a uridine specificity for RNase MC1. The role of Asn71 in enzymatic reaction of RNase MC1 was further investigated by substituting amino acids Ala, Ser, Gln, and Asp. Our observations suggest that Asn71 has at least two roles: one is base recognition by hydrogen bonding, and the other is to stabilize the conformation of the alpha4-alpha5 loop by hydrogen bonding to the peptide backbone, events which possibly result in an appropriate orientation of the alpha-helix (alpha5) containing active site residues. Mutants N71T and N71S showed a remarkable shift from uracil to guanine specificity, as evaluated by cleavage of CpG, although they did exhibit uridine specificity against yeast RNA and homopolynucleotides.

Amino Acid Sequence↗

PTEN/MMAC1/TEP1 mutations in human primary renal-cell carcinomas and renal carcinoma cell lines.

Extensive allelotyping studies have implicated several tumor-suppressor loci on chromosomes 3p, 5q, 6q, 8p, 9pq, 10q, 11q, 14q, 17p, 18q and 19p in human kidney tumorigenesis. The PTEN (also called MMAC1 and TEP1) gene, a candidate tumor suppressor located at chromosome 10q23.3, is mutated in a variety of sporadic malignancies as well as in patients with Cowden disease. To investigate the potential role of the PTEN gene in renal tumorigenesis, we searched for abnormalities of the gene in 68 primary renal-cell carcinomas (RCCs) as well as in 17 renal carcinoma-derived cell lines, using DNA-SSCP, sequencing and microsatellite analysis. Five of 68 (7.5%) primary RCCs exhibited intragenic mutations (3 missense, 1 deletion and 1 splice-site), and 1 of 17 (5.9%) cell lines had an insertion mutation. Loss of heterozygosity of the PTEN gene occurred in 25% of primary RCCs, including the 3 cases with intragenic mutation and the 1 PTEN-mutated cell line. Clinical and histopathological examinations revealed that 4 of the 5 primary tumors with PTEN mutation were high-grade, advanced clear-cell RCCs with distant metastases or renal vein tumor invasions, resulting in poor prognostic courses. The other was a low-stage papillary/chromophilic RCC. Our data suggest that PTEN mutation is observed in a subset of RCCs and that, especially in clear-cell RCCs, it occurs as a late-stage event and may contribute to the invasive and/or metastatic tumor phenotype.

Carcinoma, Renal Cell↗

Heart failure and apoptosis: electrophoretic methods support data from micro- and macro-arrays. A critical review of genomics and proteomics.

The multiple causes and multiple consequences of mammalian heart failure make it an attractive proposition for analysis using gene array technology, especially where the failure is idiopathic in nature. However, gene arrays also hold potential artefacts, particularly when gene expression levels are low, and where changes in expression levels are modest. Also, at present, the number of genes available on arrays is not large enough to prevent potential sampling deficiencies. Thus, it may not be wise to place too much reliance on quantitative interpretations of gene array data. Also, recently doubts were raised about the qualitative reliability of array genes. Electrophoretic methods are slow, cumbersome and complex but they can provide confirmation that the trends and numbers arising from the new gene arrays are reliable. In this overview, we compare gene array data with data from protein activity assays such as zymograms, Western blots, two-dimensional electrophoresis, and immunohistochemistry. Similar or complementary data from the same heart tissues analyzed by either microarrays or macroarrays can be reassuring to those interested in reliable molecular analyses of normal and failing hearts. Similar principles will apply to other tissues and cells.

Animals↗

In vitro protein binding studies with BMS-204352: lack of protein binding displacement interaction in human serum.

BMS-204352, a maxi-K channel opener, is currently under development for the treatment of stroke. Protein binding of BMS-204352 was determined in sera from several species, namely, rat, monkey, dog, and human. Data indicated that the compound was shown to be highly protein bound in serum from all species (ca. 99.6%). In order to test for the potential for drug-drug interactions and competitive displacement of BMS-204352 by diazepam, phenytoin, propranolol, and warfarin, in vitro experiments were performed using spiked human serum and ex vivo human plasma samples. Protein binding was determined using equilibrium dialysis for 4 h at maximal therapeutic concentrations for each drug alone or in appropriate combination in spiked serum samples. Ex vivo samples from a clinical BMS-204352 study (0, 1, and 24 h) were dialyzed separately after addition of diazepam, phenytoin, propranolol, or warfarin. Drug content in biological matrices was measured for radioactivity using liquid scintillation counting. Results indicated that (1) addition of diazepam, phenytoin, propranolol, or warfarin did not alter the free fraction of BMS-204352; (2) BMS-204352 did not displace diazepam, phenytoin, propranolol, or warfarin from their protein binding sites, and (3) comparison of ex vivo plasma samples after BMS-204352 dosing indicated no impact of BMS-204352 and/or its metabolites on the free fraction of diazepam, phenytoin, propranolol, or warfarin. In conclusion, the potential for a drug-drug interaction due to alterations in protein binding with BMS-204352 is unlikely.

Animals↗

Apoptosis of ventricular and atrial myocytes from pacing-induced canine heart failure.

OBJECTIVE: Rapid ventricular pacing in dogs results in a low output cardiomyopathic state similar to idiopathic dilated cardiomyopathy in man. Cell death by apoptosis may play an important role in the loss of cardiac function. This study investigates the molecular pathways involved in the regulation of apoptosis in dogs with pacing-induced heart failure. METHODS: Apoptosis was identified by terminal transferase nick end-labelling (TUNEL) in the ventricles and atria of dog hearts affected by rapid-ventricular pacing. Western blots were used to determine expression of the components involved in the initiation (Fas, Fas-Ligand, FADD), regulation (Bcl-2, Bax) and execution (caspase-2 and caspase-3) of apoptosis. RESULTS: Pacing-induced heart failure resulted in a significant increase in the number of ventricular and atrial myocyte nuclei undergoing apoptosis as measured by TUNEL. Compared to the samples from control hearts (n=6) the expression of Bcl-2, an inhibitor of apoptosis, was significantly reduced in ventricles from five dogs with pacing-induced heart failure. No change in the expression of the apoptotic inducer Bax was detected. Fas and FADD were significantly elevated in all paced ventricles, and Fas-L was only detected in the paced hearts. Both caspase-2 and caspase-3 were elevated following ventricular pacing. CONCLUSIONS: We have identified components of the signalling pathways along which apoptosis proceeds following the induction of heart failure in dogs. Apoptosis was also detected in the atria raising the possibility that, like human dilated cardiomyopathy, the molecular changes are global.

Animals↗

The three-dimensional structure of septum site-determining protein MinD from Pyrococcus horikoshii OT3 in complex with Mg-ADP.

BACKGROUND: In Escherichia coli, the cell division site is determined by the cooperative activity of min operon products MinC, MinD, and MinE. MinC is a nonspecific inhibitor of the septum protein FtsZ, and MinE is the supressor of MinC. MinD plays a multifunctional role. It is a membrane-associated ATPase and is a septum site-determining factor through the activation and regulation of MinC and MinE. MinD is also known to undergo a rapid pole-to-pole oscillation movement in vivo as observed by fluorescent microscopy. RESULTS: The three-dimensional structure of the MinD-2 from Pyrococcus horikoshii OT3 (PH0612) has been determined at 2.3 A resolution by X-ray crystallography using the Se-Met MAD method. The molecule consists of a beta sheet with 7 parallel and 1 antiparallel strands and 11 peripheral alpha helices. It contains the classical mononucleotide binding loop with bound ADP and magnesium ion, which is consistent with the suggested ATPase activity. CONCLUSIONS: Structure analysis shows that MinD is most similar to nitrogenase iron protein, which is a member of the P loop-containing nucleotide triphosphate hydrolase superfamily of proteins. Unlike nitrogenase or other member proteins that normally work as a dimer, MinD was present as a monomer in the crystal. Both the 31P NMR and Malachite Green method exhibited relatively low levels of ATPase activity. These facts suggest that MinD may work as a molecular switch in the multiprotein complex in bacterial cell division.

Adenosine Diphosphate↗

Ribosomal protein L5 has a highly twisted concave surface and flexible arms responsible for rRNA binding.

Ribosomal protein L5 is a 5S rRNA binding protein in the large subunit and plays an essential role in the promotion of a particular conformation of 5S rRNA. The crystal structure of the ribosomal protein L5 from Bacillus stearothermophilus has been determined at 1.8 A resolution. The molecule consists of a five-stranded antiparallel beta-sheet and four alpha-helices, which fold in a way that is topologically similar to the ribonucleoprotein (RNP) domain. The molecular shape and electrostatic representation suggest that the concave surface and loop regions are involved in 5S rRNA binding. To identify amino acid residues responsible for 5S rRNA binding, we made use of Ala-scanning mutagenesis of evolutionarily conserved amino acids occurring in the beta-strands and loop regions. The mutations of Asn37 at the beta1-strand and Gln63 at the loop between helix 2 and beta3-strand as well as that of Phe77 at the tip of the loop structure between the beta2- and beta3-strands caused a significant reduction in 5S rRNA binding. In addition, the mutations of Thr90 on the beta3-strand and Ile141 and Asp144 at the loop between beta4- and beta5-strands moderately reduced the 5S rRNA-binding affinity. Comparison of these results with the more recently analyzed structure of the 50S subunit from Haloarcula marismortui suggests that there are significant differences in the structure at N- and C-terminal regions and probably in the 5S rRNA binding.

Amino Acid Sequence↗

SPARC expression in primary human renal cell carcinoma: upregulation of SPARC in sarcomatoid renal carcinoma.

SPARC (secreted protein acidic and rich in cysteine, also called osteonectin, BM-40, and 43K protein) is a matricellular protein and is associated with cell-matrix interactions during cell proliferation and extracellular remodeling. It is also implicated in the neovascularization, invasion, and metastasis of human malignancies. To investigate a potential role of the SPARC in renal tumorigenesis, we examined primary renal cell carcinomas (RCCs) for SPARC expression by Northern blot analysis and for protein distribution by immunohistochemistry. We found that 6 (100%) of 6 sarcomatoid and 25 (70%) of 36 clear-cell carcinomas had enhanced SPARC transcription compared with that of the corresponding normal kidney tissue. In contrast, papillary and chromophobe RCCs characterized by a hypovascular or avascular tumor phenotype had undetectable SPARC expression. Immunohistochemical analysis showed that SPARC was strongly stained in the cytoplasm of the sarcomatoid neoplastic cells in sarcomatoid RCCs, whereas it was expressed only in the vascular endothelial cells and fibroblasts in clear-cell RCCs. SPARC staining intensity in the stromal cells was increased in the invading portion in some clear-cell RCCs. These findings suggest that tumor development, including neovascularization and invasion in clear-cell RCCs, might be regulated by SPARC from stromal endothelial cells and fibroblasts and that sarcomatoid transformation from common-type RCCs is associated with upregulation of SPARC expression; SPARC may contribute to its aggressive tumor phenotype.

Blotting, Northern↗

Mutation of von Hippel-Lindau tumor suppressor gene in a sporadic endolymphatic sac tumor.

Endolymphatic sac tumor (ELST) is a low-grade adenocarcinoma of the temporal bone that is presumed to originate from the endolymphatic system. Although ELSTs are extremely rare in the general population, a significant number of studies have documented the occurrence of ELST among patients with von Hippel-Lindau (VHL) disease. Because of the rarity of the tumor, however, few cases of ELST have been analyzed for mutations of the VHL tumor suppressor gene. In this study, we reported a Japanese male patient with sporadic ELST, along with a molecular genetic analysis of the VHL gene. The light microscopic and immunohistochemical features and clinical presentations were typical of ELST. Sequencing studies of the tumor DNA disclosed a G to T substitution of nucleotide 564, which resulted in an amino acid substitution (Trp to Cys). This is the first report of the VHL gene mutation in a sporadic Japanese case of ELST.

Adenocarcinoma↗

A randomized trial confirming the efficacy of reduced dose recombinant tissue plasminogen activator in a Chinese myocardial infarction population and demonstrating superiority to usual dose urokinase: the TUCC trial.

BACKGROUND: Reports from Japan suggest effective myocardial infarction (MI) treatment in Asian patients with much lower doses of tissue plasminogen activators (tPA) than used in European and American regimens. Because increasing doses of fibrinolytics lead to increased bleeding complications, identification of patients who respond to reduced doses is of importance. We conducted a trial in the People's Republic of China in which reduced-dose recombinant tPA was compared with the standard local therapy, urokinase. METHODS: Four hundred patients with acute MI within 12 hours of symptom onset were to be randomized to an 8-mg bolus of recombinant tPA followed by a 42-mg 90-minute infusion or 1.5 million units of urokinase as a 30-minute infusion. Patients received aspirin and heparin and underwent angiography to determine infarct artery patency 90 minutes after the start of therapy. RESULTS: The Data and Safety Monitoring Board recommended premature termination after 342 patients were recruited. Infarct artery patency (grade 2 or 3) occurred in 79% of patients receiving recombinant tPA and in 53% of patients receiving urokinase (P <.001); Thrombolysis in Myocardial Infarction (TIMI) grade 3 flow was 48% and 28%, respectively (P <.001). The higher-patency-rate recombinant tPA growth had better posttreatment left ventricular ejection fractions, 58.6% versus 54.7%, P <.01. Adverse events were infrequent and not significantly different in the 2 groups. CONCLUSIONS: This study confirms that a substantially lower dose of recombinant tPA is effective in Asian patients compared with that required in Western patients even after consideration of body weight. Specific dose-response studies should be performed with fibrinolytic regimens to avoid overdosage with its attendant risks of excess bleeding.

Aged↗

The structure of the archaebacterial ribosomal protein S7 and its possible interaction with 16S rRNA.

Ribosomal protein S7 is one of the ubiquitous components of the small subunit of the ribosome. It is a 16S rRNA-binding protein positioned close to the exit of the tRNA, and it plays a role in initiating assembly of the head of the 30S subunit. Previous structural analyses of eubacterial S7 have shown that it has a stable alpha-helix core and a flexible beta-arm. Unlike these eubacterial proteins, archaebacterial or eukaryotic S7 has an N-terminal extension of approximately 60 residues. The crystal structure of S7 from archaebacterium Pyrococcus horikoshii (PhoS7) has been determined at 2.1 A resolution. The final model of PhoS7 consists of six major alpha-helices, a short 3(10)-helix and two beta-stands. The major part (residues 18-45) of the N-terminal extension of PhoS7 reinforces the alpha-helical core by well-extended hydrophobic interactions, while the other part (residues 46-63) is not visible in the crystal and is possibly fixed only by interacting with 16S rRNA. These differences in the N-terminal extension as well as in the insertion (between alpha1 and alpha2) of the archaebacterial S7 structure from eubacterial S7 are such that they do not necessitate a major change in the structure of the currently available eubacterial 16S rRNA. Some of the inserted chains might pass through gaps formed by helices of the 16S rRNA.

Amino Acid Sequence↗

Dietary energy density and weight regulation.

Dietary energy density (ED) has been suggested as an important determinant of energy intake and, therefore, energy regulation. This review summarizes published studies on the effects of dietary ED on hunger, satiety, energy intake, and body weight in healthy individuals, and compares the relative effects of ED manipulated by dietary fat only, fat and fiber, water, and type of sweetener. In short-term studies, consumption of low-ED foods promotes satiety, reduces hunger, and decreases energy intake with no marked differences between different dietary manipulations used to change ED. In addition, low-ED diets promote moderate weight loss in long-term studies. In studies lasting longer than 6 months, weight loss was more than three times as great in individuals consuming diets both low in fat and high in fiber compared with diets only low in fat (-3.4 kg versus -1.0 kg). Combined, these studies suggest that diets low in fat and high in fiber may be the most effective low-ED diets for promoting weight loss. Further research is needed on the effects of dietary ED by changing water or sweetener content.

Body Composition↗

Fungal malignant otitis externa due to Scedosporium apiospermum.

Malignant otitis externa (MOE) is an infection of the external auditory canal that invades the skull base. Aspergillus species fungi were the pathological organism in 21 of 23 reported cases of fungal MOE. We report on a 21-year-old man with end-stage acquired immunodeficiency syndrome (AIDS) and fungal MOE caused by Scedosporium apiospermum. Fungal MOE is most common in patients with end-stage AIDS and hematologic malignancies. Granulation tissue is not a common finding in these patients, and the infectious process often starts in the mastoid air cells or middle ear space, as opposed to the external auditory canal. Surgical debridement and amphotericin B are the mainstays of therapy; resolution of the infection depends greatly on the severity of the underlying disease.

Acquired Immunodeficiency Syndrome↗

A family with von Hippel-Lindau disease revealed by pheochromocytoma.

Von Hippel-Lindau (VHL) disease is an inherited neoplastic disease characterized by a predisposition to develop retinal angiomas, central nervous system hemangioblastomas, renal cell carcinomas, pancreatic cysts and pheochromocytomas. Recently, we encountered three members of the same family who each had both VHL disease and pheochromocytoma. As in all three patients we suspected pheochromocytoma, the diagnosis of VHL disease should be considered. The possible presence of VHL disease was initially investigated in all three patients based on the presence of pheochromocytoma. A mutational analysis of the VHL gene revealed the presence of a missense mutation, consisting of a G to A transversion, at nucleotide 713 in all three patients. This germline point mutation in the VHL gene is often detected in type 2 VHL disease with pheochromocytoma. Genetic analysis seems to be useful for early detection of VHL disease, even when the formal criteria for diagnosis of this disease are lacking.

Adrenal Gland Neoplasms↗

Role of pancreatic polypeptide as a market of transplanted insulin-producing fetal pig cells.

Transplantation of insulin-producing fetal pancreatic tissue into diabetic recipients has been shown to normalize blood glucose levels after several months. This time period is required for the growth and maturation of the fetal tissue so insulin levels cannot be used as a marker of graft function while the beta-cell is immature. Therefore, we have examined the use of another pancreatic endocrine hormone, pancreatic polypeptide (PP), to monitor graft function. The cell that produces this hormone has been shown to be the first mature endocrine cell in the fetal pancreas. Fetal pig pancreatic tissue, both in the form of 1 mm3 explants and islet-like cell clusters (ICCs), was transplanted into immunodeficient SCID mice and the levels of PP and insulin were measured in plasma and in the graft for up to 12 weeks. PP was detected in the untransplanted explants (0.58 pmol/mg) and ICCs (0.06 pmol/ICC) and the PP to insulin ratio was 2.7% and 5.8%, respectively. PP (but not porcine C-peptide, a marker of insulin secretion) was detectable in the plasma of SCID mice from 4 days to 3 weeks after transplantation, but not thereafter. The highest values were obtained at 4 days to 1 week. In the grafted tissue PP and insulin were present at all time points and the ratio of PP to insulin was 59%, 87%, 75%, 56%, 7%, 8%, and 7% at 4 days, 1, 2, 3, 6, 9, and 12 weeks, respectively. The decline in PP levels 3 weeks after transplantation was associated with beta-cell development in the graft. PP was also secreted by fetal pig pancreatic explants transplanted into diabetic NOD/SCID mice, with plasma levels measurable in the first week after the tissue was grafted. In immunocompetent BALB/c mice transplanted with the tissue, PP was detectable in plasma for 2 days after transplantation but not at 4 days, when cellular rejection commenced, or thereafter. We conclude that plasma PP levels can be used as a marker of the viability of fetal porcine pancreatic tissue in the first 3 weeks after it is transplanted into mice. These findings may have relevance to fetal pancreatic tissue transplanted into humans if suitable techniques can be developed to separate pig from human PP.

Animals↗

[Molecular genetic mechanism of the kidney cancer].

The oncogenic mechanisms of renal cell carcinoma(RCC) are becoming elucidated with recent advances in molecular biology. von Hipple-Lindau disease(VHL) tumor suppressor gene is mutated and inactivated frequently in clear cell type RCCs. The VHL protein forms a complex which shows a ubiquitin ligase activity. The lost of the ubiquitin ligase activity of VHL protein may be a key step for clear cell tumorigenesis. Papillary renal cell carcinomas are caused by activating mutation in the tyrosine kinase domain of the MET gene. This tumorigenic pathway is regulated by c-Src. Immunogene therapies have been started for the patients with advanced RCC. The information based on microarray and Serial Analysis of Gene Expression(SAGE) will provide novel diagnosis and therapy which focus on the tumorigenic mechanism of RCC in the near future.

Animals↗

"Hybrid" revascularization: video-thoracoscopy assisted MIDCAB combined with angioplasty.

A "hybrid" revascularization technique has been developed for cases in which a chronic total occlusion of the left anterior descending coronary artery (LAD) cannot be recanalized by percutaneous coronary intervention, but the lesions in the right coronary artery and/or left circumflex artery are very good candidates for angioplasty. This technique, which uses video-thoracoscopy assisted minimally invasive direct coronary artery bypass to recanalize the occluded LAD and angioplasty to dilate favorable lesions in other vessels, would achieve complete revascularization in selected patients with multi-vessel disease. In this preliminary study of four patients, angioplasty and stenting were successful in all patients without any complications; complete revascularization was achieved in all 4 patients. No recurrence of angina and no cardiovascular events developed during follow-up; this study therefore supports the belief that the "hybrid" revascularization technique is both feasible and safe.

Adult↗

mRNA and protein expression of Fas associated death domain protein in apoptosic hepatocyte induced by tumor necrosis factor-alpha.

OBJECTIVE: To study the expression of protein and mRNA of Fas associated death domain protein (FADD) in the apoptosic hepatocyte induced by D-galactosamine (GalN) and TNF-alpha. METHODS: Fulminant hepatic failure (FHF) was induced by injection of GalN into sensitized BALB/c mice by TNF-alpha. Hepatocyte apoptosis was examined by electric microscopy, in site end labeling (ISEL) and DNA electrophoresis on 1.5% agarose gel. The expression of protein and mRNA of FADD were detected by immunohistochemistry and PT-PCR. RESULTS: GalN/TNF-alpha may induce hepatocyte apoptosis, necrosis and liver failure. The expression of protein and mRNA of FADD were positively correlative with the apoptosic hepatocytes. CONCLUSION: TNF-alpha induces hepatocyte apoptosis by up regulation expression of FADD protein.

Adaptor Proteins, Signal Transducing↗