Biomedical subjects

Y Tao

Publications and source records attributed to Y Tao.

At least 109 records · Page 6Linked to original sources

PubMed1997

Pain as a predictor of outcome in patients with operable pancreatic carcinoma.

BACKGROUND: The purpose of our study was to evaluate the relationship between pain and resectability and survival in patients with operable pancreatic carcinoma. METHODS: Pain, pain intensity, and pain location were prospectively assessed in newly diagnosed patients with operable adenocarcinoma of the pancreas. Patients were evaluated before their first operation at a large tertiary care cancer center. Pain factors were then correlated with outcomes of surgery, including resectability and survival. RESULTS: Seventy-seven patients with operable pancreatic carcinoma were evaluated before operation. With the Memorial Pain Assessment Card and a demographic questionnaire, an analysis of analgesic use and pain prevalence and intensity were quantitated. Twenty-two (29%) of 77 patients reported no pain. Fifty-five had mild to severe pain. Moderately severe or greater pain (Memorial Pain Assessment Card Tursky scores of 5 or greater or visual analogue self-assessment pain intensity scores greater than 30) was found in 20 patients. Twenty-six (34%) patients had resectable disease. Of the 51 patients who did not have resections, 35 had metastatic disease. Locoregional unresectable disease without metastases was found in 16 patients. Resectability was correlated with the presence of pain (p = 0.04). The median survival for all patients was 6.7 months. Not surprisingly, patients undergoing resection had a significantly better median survival than did those whose disease was unresectable (5.5 versus 15.1 months). Pain before operation significantly predicted survival (median survival for those with pain, 5.7 months; for those without pain, 15 months; p = 0.003). Even among patients who underwent resection, the presence of pain was associated with a worse survival (21.9 months versus 9.2 months; p = 0.045). In a multivariate analysis the two significant variables were inability to undergo resection and presence of any pain. CONCLUSIONS: The presence of pain in newly diagnosed patients with potentially operable pancreatic cancer is an ominous predictor of resectability and of survival. Even if the patient can undergo resection, the presence of preoperative pain is associated with a poor prognosis. Patients with operable pancreatic cancer who present with pain, even those whose evaluation shows a likelihood of resectability, are at high risk for recurrence with an impaired survival compared with those patients without pain.

Adenocarcinoma↗

PubMed1997

PAF antagonists as possible inhibitors of corneal epithelial defects and ulceration.

The extracellular matrix (ECM) plays a crucial role in cell adhesion, differentiation and wound-healing. Its stability is tightly controlled by enzymes that regulate the metabolism of its components (e.g collagen, fibronectin, laminin). We have found that in the cornea, a potent lipid inflammatory mediator platelet-activating factor (PAF) activates the expression of two metalloproteinases (MMP-1 and MMP-9) as well as urokinase-plasminogen activator (uPA). uPA is of particular interest because, as a serine protease, it is at the top of the protease cascade. PAF may contribute to the destruction of the ECM and the formation of epithelial defects and corneal ulcers by activating uPA and then proteases. We also investigated how several PAF antagonists with different binding affinities can block the expression of the uPA gene. Our results suggest that PAF antagonists with affinities for intracellular binding sites and/or specific structures derived from triazolobenzodiazepine could be of therapeutic use to limit the breakdown of the ECM and the development of ulcer formation.

Azepines↗

PubMed1997

Effects of garlic thioallyl derivatives on growth, glutathione concentration, and polyamine formation of human prostate carcinoma cells in culture.

This study investigated whether naturally occurring garlic derivatives and synthetic S-cysteinyl compounds that resemble garlic constituents have antiproliferative effects on human prostate carcinoma (LNCaP) cells. Studies also examined whether S-allylmercaptocysteine and S-allylcysteine affect two important molecular targets, namely reduced glutathione and polyamines. Results showed that S-allylmercaptocysteine (50 mg/L) diminished LNCaP cell growth whereas the antiproliferative effect of S-allylcysteine was not as pronounced. Studies using synthetic S-cysteinyl analogues revealed that growth inhibition was most effective with compounds containing a disulfide or an active diallyl moiety. Marginal to no inhibitory effect was observed with monosulfinic analogues. Both S-allylmercaptocysteine and S-allylcysteine caused an increase in LNCaP cell reduced glutathione concentrations. Putrescine and spermine concentrations decreased and spermidine increased 3 d after S-allylmercaptocysteine treatment. At 5 d after S-allylmercaptocysteine treatment, polyamine concentrations were similar to those of saline-treated controls. Diminished cell growth and altered polyamine concentrations suggest that S-allylmercaptocysteine may impede the polyamine synthesizing enzyme, ornithine decarboxylase, either by enhancing the formation of reduced glutathione, a known inhibitor of ornithine decarboxylase, or by reacting directly with ornithine decarboxylase at its nucleophilic thiol moiety. Because S-allylcysteine also increases reduced glutathione formation but does not significantly inhibit growth, the latter mechanism may be more likely for this compound. These data provide further evidence that nonessential nutrients derived from garlic may modulate tumor growth. Further research is required on effects of garlic derivatives in vivo before information from the present studies can be used to assist in the development of effective nutritional strategies for preventing progression of prostate cancer.

Antineoplastic Agents, Phytogenic↗

PubMed1997

Subunit composition determines E2F DNA-binding site specificity.

The product of the retinoblastoma (Rb) susceptibility gene, Rb-1, regulates the activity of a wide variety of transcription factors, such as E2F, in a cell cycle-dependent fashion. E2F is a heterodimeric transcription factor composed of two subunits each encoded by one of two related gene families, denoted E2F and DP. Five E2F genes, E2F-1 through E2F-5, and two DP genes, DP-1 and DP-2, have been isolated from mammals, and heterodimeric complexes of these proteins are expressed in most, if not all, vertebrate cells. It is not yet clear whether E2F/DP complexes regulate overlapping and/or specific cellular genes. Moreover, little is known about whether Rb regulates all or a subset of E2F-dependent genes. Using recombinant E2F, DP, and Rb proteins prepared in baculovirus-infected cells and a repetitive immunoprecipitation-PCR procedure (CASTing), we have identified consensus DNA-binding sites for E2F-1/DP-1, E2F-1/DP-2, E2F-4/DP-1, and E2F-4/DP-2 complexes as well as an Rb/E2F-1/DP-1 trimeric complex. Our data indicate that (i) E2F, DP, and Rb proteins each influence the selection of E2F-binding sites; (ii) E2F sites differ with respect to their intrinsic DNA-bending properties; (iii) E2F/DP complexes induce distinct degrees of DNA bending; and (iv) complex-specific E2F sites selected in vitro function distinctly as regulators of cell cycle-dependent transcription in vivo. These data indicate that the specific sequence of an E2F site may determine its role in transcriptional regulation and suggest that Rb/E2F complexes may regulate subsets of E2F-dependent cellular genes.

Animals↗

PubMed1997

Endometrial thickness in tamoxifen-treated patients: correlation with clinical and pathologic findings.

OBJECTIVE: This study was performed to evaluate sonographic measurements of endometrial thickness in postmenopausal breast cancer patients being treated with tamoxifen and to correlate endometrial thickness with pathology, symptoms, and duration of tamoxifen treatment. MATERIALS AND METHODS: Pelvic sonograms and medical records of 91 postmenopausal breast cancer patients being treated with tamoxifen were retrospectively reviewed. Histologic results were available in 46 patients (51%). Endometrial thickness was measured in anteroposterior dimension and was considered normal when less than 8 mm. Endometrial thickness was then correlated with histopathologic findings, symptoms, and duration of tamoxifen treatment. RESULTS: Forty-seven examinations (52%) showed endometrial thickness of less than 8 mm and 44 examinations (48%) showed endometrial thickness of 8 mm or more. Endometrial biopsy was performed in 10 women (21%) in whom the endometrial thickness was less than 8 mm, revealing seven normal endometria, one endometrial polyp, and two insufficient samples. Endometrial biopsy was performed in 36 women (82%) in whom endometrial thickness was 8 mm or more, revealing three cases with more than one diagnosis. In this group, diagnoses included 14 normal endometria, 12 endometrial polyps, four endocervical polyps, three hyperplasias, two endometrial cancers, one papillary syncytial metaplasia, one cystic change, one inflammatory debris, and one insufficient sample. Postmenopausal bleeding prompted 20 studies, 12 of which revealed endometrial thickness of 8 mm or more. We found no difference in endometrial thickness of patients who had bleeding versus those who had no bleeding. Endometrial thickness increased with the duration of tamoxifen treatment. Seventy-three women being treated with tamoxifen for less than 5 years had a median endometrial thickness of 5 mm, and 44% of biopsies yielded abnormal results. Eighteen women receiving tamoxifen 5 years or longer had a median endometrial thickness of 14 mm, and 58% of endometrial biopsies in this group were abnormal. The two endometrial cancers occurred in women who were treated with tamoxifen for 6 years. Correlation between duration of tamoxifen use and endometrial thickness was significant (p < .026). CONCLUSION: The majority of women being treated with tamoxifen were asymptomatic, but 48% of sonograms revealed an endometrial thickness of 8 mm or more. Endometrial polyps, the most common abnormality, were diagnosed in 33% of biopsies performed for endometrial thickness of 8 mm or more. Endometrial thickness showed no correlation with symptoms, but we found a statistically significant correlation between increased endometrial thickness and duration of tamoxifen treatment that was longer than 5 years.

Antineoplastic Agents, Hormonal↗

PubMed1997

Effect of radix Salviae miltiorrhizae on extracellular adenosine and evaluation of its protective efficacy in ischemic reperfusion rat--microdialysis, HPLC and histopathologic studies.

The effects of Radix Salviae Miltiorrhizae (RSM) on extracellular adenosine (Ade) and its metabolites, i.e. inosine, hypoxanthine and xanthine, were studied with microdialysis and HPLC techniques during cerebral ischemia-reperfusion induced by 4-vessel occlusion in rat brain. Histological examination of hippocampus was performed 6 h after reperfusion. ECF (extracellular fluid) adenosine and its metabolites were compared between the controls (n = 6) and RSM-treated rats (n = 6). Basal level of Ade and its metabolites release were not greatly affected by pretreatment with RSM, and no significant difference as compared with the sham-operated (n = 6). Ade and its metabolites were dramatically increased after ischemia, and decreased near basal-level and its metabolites remained high at the end of reperfusion. In the RSM-treated animals, the tendency of changes of Ade and its metabolites was just the same as in the controls, but the magnitudes of changes were significantly lower at some different time points. In sham-operated animals, no changes were observed at different time points both during ischemia (30 min.) and reperfusion (60 min.). Histopathological findings demonstrated that RSM pretreatment results in better histologic preservation of the pyramidal cells in the postischemic reperfusion CA1 sector both qualitatively and quantitatively. These results indicated that RSM protects against cerebral ischemia reperfusion injury.

Adenosine↗

PubMed1997

[Dynamic study on blood lead levels of pregnant women and infants in a district of Beijing].

Under strict quality control, the authors investigated the levels of PbB among 270 women from early pregnancy to delivery and their infants. The mean PbB levels of the first three months of pregnancy and delivery is 45.0 microg/L and 64.8 microg/L respectively. Analysis shows an increase of mean PbB level in the period of gestation, and a significant increase in the last three months. The mean PbB level of umbilical cord is 51.9 microg/L (10.4% umbilical cord PbB > 100 microg/L). The mean PbB level of infants increases with the months, it increases significantly after six months. Regression analysis confirmed the positive correlation between the PbB levels of first three and second three months of gestation, the PbB of delivery and umbilical cord, the PbB of umbilical coral and infants. The correlation coefficient of the PbB level of delivery and umbilical cord, the PbB level of infants at six months and at twelve months is 0.80 and 0.47 respectively.

China↗

PubMed1997

[Allergic bronchopulmonary aspergillosis successfully treated with itraconazole].

A 67-year-old man was admitted to our hospital because of coughing, a low-grade fever, and abnormal shadows on a chest X-ray film. He had had asthma as a child, but had no asthmatic symptoms on admission. A CT scan showed collapse of the right middle lobe and mucoid impactions in the lingula. Bronchoscopy revealed thick mucus obstructing the right middle-lobe bronchus and the left upper-lobe bronchus. The eosinophil count and the IgE level were abnormally high. Aspergillus fumigatus was detected in his sputum. Tests for immediate skin reaction and precipitating antibody to aspergillus antigen were positive. After treatment with itraconazole he became asymptomatic. Radiographic abnormalities had resolved by 1 month after the start of treatment; a high resolution CT scan obtained after clinical improvement revealed central bronchiectasis. In this patient with allergic bronchopulmonary aspergillosis, a course of itraconazole alone was followed by satisfactory improvement.

Aged↗

PubMed1997

In vivo neurogenesis is inhibited by neutralizing antibodies to basic fibroblast growth factor.

While extracellular growth factors govern neuronal precursor mitosis in culture, little is known about their roles in regulating neurogenesis in vivo. Previously, we reported that subcutaneously administered basic fibroblast growth factor (bFGF) promoted neuroblast proliferation in P1 rat brain, in regions in which bFGF and FGF receptors are expressed during development. To define the role of endogenous bFGF in neurogenesis, we employed a neutralizing monoclonal antibody to the factor. In culture, bFGF-induced granule precursor proliferation was progressively inhibited by increasing concentrations of antibody. In contrast, heat-inactivated or nonneutralizing anti-bFGF antibodies were ineffective. The inhibition was specific for bFGF, since EGF-induced [3H]dT incorporation was not altered. To study effects in vivo, neutralizing antibody was administered to newborn rats via the cisterna magnum. Four hours after injection, DNA synthesis in cerebellum and hippocampus was decreased by 53% and 63%, respectively, suggesting that endogenous bFGF was involved in brain development. To define effects on neurogenesis specifically, granule cell precursors were isolated after antibody treatment. [3H]dT incorporation in granule precursors was decreased by 50%, indicating that the neutralizing antibody inhibited neuroblast proliferation in vivo. In contrast, no reduction was observed using nonneutralizing or the heat-inactivated antibodies. The inhibition of precursor proliferation following immunoneutralization of bFGF in vivo suggests that the endogenous factor normally regulates brain neurogenesis.

Animals↗

PubMed1997

Platelet-activating factor induces cyclooxygenase-2 gene expression in corneal epithelium. Requirement of calcium in the signal transduction pathway.

PURPOSE: To investigate the effect of the inflammatory mediator platelet-activating factor (PAF) in the induction of the inducible prostaglandin H synthase-cyclooxygenase-2 (COX-2) gene expression in corneal epithelium. METHODS: Rabbit corneas were incubated in organ culture with or without carbamyl PAF (cPAF, 100 nM). The effects of PAF antagonist BN50730 (10 microM), protein synthesis inhibitor cycloheximide (CHX; 30 micrograms/ml), RNA synthesis inhibitor actinomycin D (50 micrograms/ml), and tumor promoter phorbol ester (TPA); (100 nM) were tested. Total RNA for corneal epithelium was analyzed by Northern blot analysis using mouse COX-2 cDNA fragments labeled with 32P as probes. Western blots were performed using mouse monoclonal antibodies. Primary cultures of rabbit corneal epithelium were loaded with the fluorescent dye fluo-3 AM and changes in intracellular calcium concentration [Ca2+]i were analyzed by laser scanning confocal microscopy. RESULTS: Platelet-activating factor induction of COX-2 expression was detectable by Northern blot analysis at 2 hours, peaked at 4 hours, and remained increased for as long as 8 hours. At 16 hours, there was a marked increase in COX-2 expression. The effect was abolished by the PAF antagonist. TPA also induced COX-2 gene expression. Neither PAF-nor TPA-induced expression was inhibited by CHX. In a Ca(2+)-free medium, there was a 50% inhibition of COX-2 gene induction by PAF. The calcium ionophore A23187 also caused an increase in expression of COX-2 messenger RNA; this did not occur in Ca(2+)-free medium. Confocal microscopy imaging showed that after the addition of PAF, there was a transient increase in [Ca2+]i in corneal epithelial cells that peaked between 30 and 60 seconds. The increase was inhibited in the presence of BN50730 or in a Ca(2+)-free medium. A23187 also caused a transient increase in [Ca2+]i that was not altered in cells previously treated with PAF or BN50730. CONCLUSIONS: PAF may enhance prostaglandin synthesis in the corneal epithelium by increasing COX-2 gene expression. This increase is by means of transcriptional activation of the gene and results in increased COX-2 protein formation. Influx of Ca2+ due to PAF stimulation is required to induce the COX-2 gene. A PAF antagonist abolishes all PAF effects and could be of therapeutic value by modulating ocular inflammation at the level of COX-2 gene expression.

Aniline Compounds↗

PubMed1997

[Changes of NMDA receptor gene expression in infection brain injury induced by Bordetella pertussis in rats].

N-methyl-D-aspartate receptors (NMDAR) in cerebral cortexes of rat brain injury induced by Bordetella pertussis (Bp) were measured by methods of Northern blot analysis and [3H] MK-801 radioligand-receptor binding to study changes and effects of NMDAR1 of gene expression in the infection brain injury. The affinity (Kd) of NMDAR in Bp group was significantly decreased [30.5 +/- 3.0 nmol.L-1 (Bp), 43.1 +/- 4.2 nmol.L-1 (NS), P < 0.05], but expression of NMDAR1 mRNA and binding site density (Bmax) of NMDAR observed no significant differences between the experimental and the control group (P > 0.05), respectively. The results suggest that NMDAR1 was activated with high affinity functionally, but no changes in binding site density and transcriptional expression of NMDAR1 occured in the infection brain injury.

Animals↗

PubMed1997

[Delayed brain injury induced by Bordetella pertussis in rats].

To induced new model of delayed infection brain injury, we divided randomly 40 adult male Sprague-Dawley rats into four groups: bordetella pertussis (BP) groups, and normal sailine (NS) groups in 4 h (n = 10) and 24 h (n = 10), respectively, injected BP at 0.2 ml.kg-1 which contained the bacilli in 10.8 x 10(9).ml-1 into the rat left internal carotid artery of BP groups, and injected at the equal volume as control in the same way into NS groups. The water content (WC), Evans blue content (EB), cations of sodium, potassium, calcium in the brain tissues were measured and the morphologic changes in the hippocampal CA1 were detected by electron microscopy. These results were shown as follows: the left hemisphere of BP group in 4 h was characterized by the brain edema which predominated in swollen, necrotic astroglial cells, endothelial cells, and insignificant increase of contents of sodium, calcium and decrease of potassium; BP group in 24 h was characterized by dark cells, the brain edema also existed in astroglial cells. These results indicate that a delayed infection brain injury model is performed successfully by injection with BP into the left internal carotid artery of rats. The model is characterized by the features of delayed neuronal death and mixed type brain edema.

Animals↗

PubMed1996

Neurogenesis in neonatal rat brain is regulated by peripheral injection of basic fibroblast growth factor (bFGF).

Many major diseases of human brain involve deficiencies of select neuronal populations. As one approach to repair, we examined regulation of neurogenesis directly in vivo, employing postnatal day 1 (P1) cerebellar cortex, which is composed primarily of granule neurons and dividing precursors. We focused on basic fibroblast growth factor (bFGF), which stimulates precursor mitosis in culture and which is highly expressed in cerebellum during neurogenesis. Subcutaneous injection of bFGF increased [3H]thymidine ([3H]dT) incorporation, a marker for DNA synthesis, by 50% in whole cerebellar homogenates, suggesting that peripherally administered factor altered ongoing neural proliferation. Further, assay of isolated granule precursors revealed a 4-fold increase in [3H]dT incorporation following in vivo bFGF treatment, indicating that granule neuroblasts were the major bFGF-responsive population. Morphologic analysis indicated that twice as many granule precursors were in S-phase of the mitotic cycle after peripheral bFGF. To determine whether other neurogenetic populations respond to peripheral bFGF, we examined additional brain regions in vivo. bFGF stimulated DNA synthesis by 68% in hippocampus, and by > 250% in pontine subventricular zone (SVZ). In contrast, incorporation was not altered in basal pons or cerebral cortex, regions in which neurogenesis has already ceased. To define potential direct actions of peripherally administered factor, 125I-bFGF was used to study distribution. Intact 18 kDa 125I-bFGF was recovered from brain following peripheral injection, suggesting that the factor acted directly to stimulate mitosis in dividing neuroblasts. The stimulation of neuronal proliferation by exogenous bFGF suggests that the factor normally regulates neurogenesis, and provides new therapeutic approaches to promote functional recovery from nervous system diseases.

Animals↗

PubMed1996

Preliminary crystallographic studies of bacteriophage T4 fibritin confirm a trimeric coiled-coil structure.

Fibritin, a 52-kDa product of gene wac of bacteriophage T4, forms fibrous "whiskers" that connect to the phage tail and facilitate the later stages of phage assembly. Preliminary experiments suggest that fibritin is a trimer, and its predominant central part has a parallel alpha-helical coiled-coil structure. To investigate the oligomerization and function of fibritin, we have designed and studied two related deletion mutants, denoted M and E, that consist of its last 75 and 120 amino acids, respectively. Both proteins contain part of the coiled-coil region and the 29 amino acid carboxy-terminal domain essential for the trimerization of fibritin. The proteins are expressed as a soluble product in an Escherichia coli system. We have obtained crystals of fibritins M and E. Complete native X-ray diffraction data sets have been collected to 1.85 and 2.7 A resolution, respectively. The crystals have space group P3 with a=44.3 A, c=91.3 A (fibritin M) and R32 with a=41.2 A, b=358.7 A (fibritin E) in the hexagonal setting. Symmetry and packing considerations show that fibritin is a triple coiled coil.

Amino Acid Sequence↗

PubMed1996

Molecular cloning and functional expression of human deoxyhypusine synthase cDNA based on expressed sequence tag information.

Deoxyhypusine synthase is an NAD(+)-dependent enzyme that catalyses the formation of a deoxyhypusine residue on the eukaryotic initiation factor 5A (eIF-5A) precursor by transferring an aminobutyl moiety from spermidine to the epsilon-amino group of a unique lysine residue. We have recently cloned and characterized the Neurospora crassa deoxyhypusine synthase cDNA using a reverse genetics approach. A GenBank search showed that a stretch of the deduced amino acid sequence (96 amino acids) of Neurospora deoxyhypusine synthase matches a short human expressed sequence tag (EST), Z25337, with greater than 70% amino acid identity. Gene-specific primers based on this EST were used together with universal primers to obtain 1219 bp and 1078 bp cDNAs from a human cDNA library. The 1219 bp and 1078 bp sequences, each containing an open reading frame, encode polypeptides of respectively 368 and 321 amino acids. The short sequence is identical to the long one except that it is missing a stretch of 47 amino acids spanning residues 261-307. The 368-amino-acid sequence of human deoxyhypusine synthase shares a high degree of identity ( > 50%) and similarity ( > 60%) with that of the Neurospora and yeast deoxyhypusine synthases. After cloning into an expression vector, the 368-amino-acid recombinant protein exhibits high deoxyhypusine synthase activity. In contrast, the 321-amino-acid recombinant protein shows no detectable activity.

Amino Acid Sequence↗

PubMed1996

Nitric oxide inhibits the initiation of cAMP pulsing in D. discoideum without altering receptor-activated adenylate cyclase.

We have previously demonstrated that nitric oxide (NO)-releasing compounds inhibit the differentiation and aggregation of D. discoideum cells (Tao et al., FEBS Lett. 314:49, 1992). In the present study, we demonstrate that treatment of intact cells with NO-releasing compounds inhibits their production of cAMP. This occurred even though the developmental expression of the known components necessary for proper cAMP signalling was unaffected. The inhibitory effects of NO-releasing compounds on cell aggregation were reversed by stimulating cells with pulses of cAMP. In response to an applied cAMP pulse, NO-treated cells displayed a normal signal relay response, indicating that receptor-activated adenylate cyclase activity was not inhibited by NO. This also argues that the processes of desensitization/resensitization occur normally in NO-treated cells. The data indicate that the developmental expression of the components of the chemotactic signalling occurs independently of cAMP production and that the activity of the adenylate cyclase may be regulated by cAMP/ cAMP-receptor independent pathway. These findings indicate both a new mechanism for the regulation of adenylate cyclase in D. discoideum and a novel means by which NO can function to alter cellular processes.

Adenylyl Cyclases↗

PubMed1996

Is there an error correcting code in the base sequence in DNA?

Modern methods of encoding information into digital form include error check digits that are functions of the other information digits. When digital information is transmitted, the values of the error check digits can be computed from the information digits to determine whether the information has been received accurately. These error correcting codes make it possible to detect and correct common errors in transmission. The sequence of bases in DNA is also a digital code consisting of four symbols: A, C, G, and T. Does DNA also contain an error correcting code? Such a code would allow repair enzymes to protect the fidelity of nonreplicating DNA and increase the accuracy of replication. If a linear block error correcting code is present in DNA then some bases would be a linear function of the other bases in each set of bases. We developed an efficient procedure to determine whether such an error correcting code is present in the base sequence. We illustrate the use of this procedure by using it to analyze the lac operon and the gene for cytochrome c. These genes do not appear to contain such a simple error correcting code.

Base Sequence↗

PubMed1996

Characterization of a vitellogenin receptor in white perch (Morone americana).

Receptors for white perch vitellogenin (wVTG) were characterized using wVTG, labeled in vivo with [3H]leucine or in vitro with 125I, and semipurified ovarian membranes. Specific binding of wVTG to the membranes was temperature-dependent, proportional to the amount of membrane, and saturable. Scatchard analyses revealed a single class of binding sites of low maximum binding capacity (MBC; approximately 35 pmol VTG/mg membrane protein) and high affinity (Kd approximately 400 nM), consistent with wVTG levels (540-2700 nM) circulating in maturing females. Ligand blotting revealed a receptor protein of M(r) approximately 157000 and a smaller protein, possibly its degradation product. Striped bass vitellogenin, chicken egg yolk very low density lipoprotein, and suramin displaced wVTG from its receptor, but BSA did not. No change in Kd was noted over the course of vitellogenesis in maturing perch, and MBC increased only slightly very late in the gametogenic cycle. The wVTG bound specifically to membranes prepared from liver, muscle, and mesenteric fat, but not to erythrocyte membranes. The Kd for ovary (394 nM) and liver (345 nM) were similar, but the Kd for muscle (1440 nM) was much higher.

Animals↗