Another case of prenatally diagnosed 48,XYY,+21.
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Adult↗
Biomedical subjects
A Lin
Publications and source records attributed to A Lin.
A randomized trial of extra-amniotic saline infusion versus laminaria for cervical ripening.
OBJECTIVE: To compare extra-amniotic saline infusion versus laminaria for cervical ripening and labor induction. METHODS: Patients of at least 34 weeks' gestation with a Bishop score of 3 or less were randomized to either laminaria ripening for 6 hours or more followed by oxytocin induction versus initiation of extra-amniotic saline infusion at the start of oxytocin induction. Indications for induction included 41 weeks' gestation or greater, hypertensive disease, diabetes, oligohydramnios, suspect fetal growth, and nonreassuring fetal testing. RESULTS: There were no significant differences in maternal age, race, parity, gestational age, or indications for induction between the two groups (extra-amniotic saline infusion group, n = 26, laminaria group, n = 26). After only 3 hours of oxytocin induction, patients in the extra-amniotic saline infusion group achieved an identical distribution of Bishop scores compared with the patients in the laminaria group after 6 hours or more of pre-induction ripening as well as 3 hours of oxytocin induction. There were no differences in rates of cesarean delivery (extra-amniotic saline infusion 35%, laminaria 35%), infectious complications, or neonatal outcomes between the two groups. The induction-to-delivery interval (+/- standard deviation) was significantly shortened with extra-amniotic saline infusion (extra-amniotic saline infusion 12.9 +/- 5.7 hours versus laminaria 16.9 +/- 7.1 hours, P = .03). In addition, fewer cesarean deliveries were performed for failed inductions (cervix less than 5 cm dilated) in the extra-amniotic saline infusion group (one of 26 versus six of 26, P = .049). CONCLUSION: Extra-amniotic saline infusion offers potential advantages over the use of laminaria. Extra-amniotic saline infusion saves a significant amount of time both by obviating the need for pre-induction cervical ripening and in shortening the induction-to-delivery interval. Also, fewer patients required cesarean delivery for failed induction of labor with extra-amniotic saline infusion.
Adult↗
Production of type II ribotoxins by Aspergillus species and related fungi in Taiwan.
A molecular investigation was conducted on the production of type II ribotoxin of the species Aspergillus and related fungi in Taiwan. Species that carried ribotoxin were confirmed by (1) cross-reactivity to anti-alpha-sarcin serum; (2) Southern dot hybridization; (3) PCR amplification of genomic DNA with specific primers; and (4) analysis of ribotoxic activity. Five new strains, A. clavatus, A. oryzae var. effusus, A. ostianus, A. tamarii, and Neosartorya fischeri var. spinosa, were identified to contain an alpha-sarcin-like ribotoxin. These positive strains exhibit ribotoxic activity by cleaving ribosomes and generating an alpha-fragment.
Animals↗
Adsorption of charged non-albumin bound drugs by amorphous silica.
We investigated the in vitro drug adsorption of PQ 10150 sodium silicate gel (AIS, Santa Clara, CA) with particle size of 230 microns and surface area of 400 m2/g. We observed 99% to 88% adsorption of gentamicin; a mean 91% of disopyramide; a mean 89% of quinidine at low concentration, falling to 75% at higher concentration. Insulin was 88% adsorbed at low concentrations but less so (65%) at higher concentrations. We observed a mean 83% adsorption of procainamide, a mean 84% of N-acetyl procainamide, 74% of lidocaine, 73% of amitriptyline, and 44% of desipramine. We found an average of 14% reduction of total digoxin concentration when serum containing digoxin (2 to 33 ng/mL) was exposed to sodium silicate, while the reduction in free digoxin concentration was 16%. Five percent ethosuximide was also removed. The adsorption of theophylline, phenobarbital, acetaminophen, phenytoin, ethylene glycol, methotrexate, salicylate, thiocyanate and diazepam was minimal and not significant. We conclude that significant amounts of charged, non-albumin bound drugs can be removed by PQ 10150 sodium silicate gel.
Adsorption↗
[Treatment of maxillofacial vascular malformation by arterial embolism and application of sclerosing agent].
30 cases of large cavernous and racemose hemangioma of the maxillofacial were treated selectively with arterial embolism of the tumor and inject Xiaozhiling into the tumor, from November 1990 to November 1993. This method has exact effect either to racemose or to cavernous hemangioma, without facial defect and functional damage. All the patients were followed up 6 months to 3 years. 27 cases were cured, 1 failed, 1 gave up treatment, 1 died of complication. Its mechanism, indications, prevention of complications and recurrence were discussed.
Adolescent↗
Differential activation of ERK and JNK mitogen-activated protein kinases by Raf-1 and MEKK.
Growth factors activate mitogen-activated protein kinases (MAPKs), including extracellular signal-regulated kinases (ERKs) and Jun kinases (JNKs). Although the signaling cascade from growth factor receptors to ERKs is relatively well understood, the pathway leading to JNK activation is more obscure. Activation of JNK by epidermal growth factor (EGF) or nerve growth factor (NGF) was dependent on H-Ras activation, whereas JNK activation by tumor necrosis factor alpha (TNF-alpha) was Ras-independent. Ras activates two protein kinases, Raf-1 and MEK (MAPK, or ERK, kinase) kinase (MEKK). Raf-1 contributes directly to ERK activation but not to JNK activation, whereas MEKK participated in JNK activation but caused ERK activation only after overexpression. These results demonstrate the existence of two distinct Ras-dependent MAPK cascades--one initiated by Raf-1 leading to ERK activation, and the other initiated by MEKK leading to JNK activation.
3T3 Cells↗
Acute inflammatory injury in the lung precipitated by oxidant stress induces fibroblasts to synthesize and release transforming growth factor-alpha.
Although transforming growth factor-alpha (TGF-alpha) is widely distributed in transformed cells and in some normal cells and much is known about its structure and metabolism, there is little information about its physiological actions. TGF-alpha is not thought to be synthesized by nontransformed fibroblasts, but it is thought to be a mitogen for these and epithelial cells (Derynck, R. (1986) J. Cell. Biochem. 32, 293-304). We report here that fibroblasts obtained from hamsters with oxidant-induced lung injury release TGF-alpha at levels comparable with those reported for transformed cells. In conditioned media, one isoform of 18 kDa was recognized by a monoclonal antibody to mature TGF-alpha; five isoforms ranging from 18 to 42 kDa were recognized in cell lysates. Conditioned media from these fibroblasts stimulated tyrosine phosphorylation of the epidermal growth factor (EGF)/TGF-alpha receptor, competed with radioactive EGF for binding sites on A431 cells, and were mitogenic for mesenchymal and epithelial cells. This mitogenic activity could be almost completely blocked by anti-TGF-alpha. Conditioned media from normal lung fibroblasts exhibited none of these activities. Using normal lung fibroblasts, we found that TGF-alpha synthesis could be induced in vitro with 25 nmol/ml EGF, suggesting that the induction in vivo may have been due, in part, to a stimulation by EGF (or TGF-alpha) released by other cell types such as alveolar macrophages recruited to the injury site. TGF-alpha is, in general, a mitogen for epithelial cells (Derynck, 1986); more specific to acute injury in the lung, it may affect the proliferation (Ryan, R. M., Mineo-Kuhn, M. M., Kromer, C. M., and Finkelstein, J. N. (1994) Am. J. Physiol. 266, L17-L23) and metabolic activities (Whitsett, J. A., Weaver, T. E., Lieberman, M. A., Clark, J. G., and Daugherty, C. (1987) J. Biol. Chem. 262, 7908-7913) of alveolar epithelial type II cells. This is, we believe, the first report of a fibroblast-derived TGF-alpha induced with oxidant injury. If this response was ubiquitously manifested in other tissues, then fibroblast-derived TGF-alpha might be an important determinant of the epithelial and mesenchymal hyperplasia commonly observed in tissue repair.
Acute Disease↗
Three unrelated cases of paracentric inversions of 1p in individuals with abnormal phenotypes.
Paracentric inversions, involving a rearrangement within one chromosome arm, are rare. Although carriers of balanced paracentric inversions should theoretically not be at risk for abnormal offspring, such cases have been reported. We report on 2 unrelated cases of inherited paracentric inversions of 1p with breakpoints at p32 and p36.1 and p32.3 and p36.22 in individuals with abnormal phenotypes. Another case of 2 abnormal monozygotic twins with a de novo paracentric inversion of 1p with breakpoints at p22 and p34 is presented as well.
Abnormalities, Multiple↗
c-Jun N-terminal phosphorylation correlates with activation of the JNK subgroup but not the ERK subgroup of mitogen-activated protein kinases.
c-Jun transcriptional activity is stimulated by phosphorylation at two N-terminal sites: Ser-63 and -73. Phosphorylation of these sites is enhanced in response to a variety of extracellular stimuli, including growth factors, cytokines, and UV irradiation. New members of the mitogen-activated protein (MAP) kinase group of signal-transducing enzymes, termed JNKs, bind to the activation domain of c-Jun and specifically phosphorylate these sites. However, the N-terminal sites of c-Jun were also suggested to be phosphorylated by two other MAP kinases, ERK1 and ERK2. Despite these reports, we find that unlike the JNKs, ERK1 and ERK2 do not phosphorylate the N-terminal sites of c-Jun in vitro; instead they phosphorylate an inhibitory C-terminal site. Furthermore, the phosphorylation of c-Jun in vivo at the N-terminal sites correlates with activation of the JNKs but not the ERKs. The ERKs are probably involved in the induction of c-fos expression and thereby contribute to the stimulation of AP-1 activity. Our study suggests that two different branches of the MAP kinase group are involved in the stimulation of AP-1 activity through two different mechanisms.
Animals↗
Tricholin, a new antifungal agent from Trichoderma viride, and its action in biological control of Rhizoctonia solani.
Tricholin, a ribosome-inactivating protein isolated from the culture broth of Trichoderma viride, has been shown to exert fungicidal effects on Rhizoctonia solani through a multi-hit kinetic interaction. Tricholin causes a parallel cessation of growth, uptake of amino acids, and protein biosynthesis. The in vivo mode of action of tricholin on protein synthesis and cell growth appears to be attributed to the diminishing of the polysome formation in R. solani through damage to large ribosomal subunits. These results concur with previous data and prove that tricholin is an effective inhibitor of protein synthesis. The efficacy of tricholin as an antibiotic agent was estimated to have a duration of approximately 42 hours.
Antifungal Agents↗
[Epidemiology and control of hookworm infection in Fujian province].
Fujian province has been known to be endemic for mixed hookworm infection with Ancylostoma duodenale as the predominant species. The infection rate was 50% before 1980. As a result of mass treatment starting from 1980, the infection rate was decreased in most areas. And, infection foci were changed from sweet potato fields to the banana, sweatcane and asparagus fields where the infection rate tended to increase. It is stressed that the current endemic characteristics of hookworm infection should be paid more attention in implementing the control programme of hookworm infection.
Adolescent↗
Hydrolysis of ribosomes by electrophoretically blotted ribotoxin.
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Electrophoresis, Polyacrylamide Gel↗
The significance of eccentric foci of hyperpigmentation ('small dark dots') within melanocytic nevi. Analysis of 59 cases.
BACKGROUND AND DESIGN: Fifty-nine melanocytic nevi with eccentric foci of hyperpigmentation ("small dark dots") that measured primarily 1 to 2 mm in diameter were prospectively examined to determine the histologic correlates of the dark dots. RESULTS: Forty-one (69%) of the dark dots were due to increased melanin in epidermal melanocytes and/or keratinocytes, usually accompanied by melanophages; of these 41, six (15%) were associated with slight or moderate melanocytic nuclear atypia. Fifteen (25%) of the dark dots were due to increased dermal pigment that was either superficial or deep. Three (5%) of the dark dots were due to melanoma arising within a nevus. CONCLUSIONS: A small percentage of "small dark dots" within melanocytic nevi are due to melanoma. Biopsy specimens of nevi with small dark dots should be sectioned to ensure histologic examination of this focus of hyperpigmentation.
Adolescent↗
Purification and properties of a human platelet inositol 1,4,5-trisphosphate 3-kinase.
An inositol 1,4,5-trisphosphate 3-kinase (Ins(1,4,5)P3 3-kinase) has been purified 943-fold from a 30,000g human platelet extract and has a specific activity of 283 nmol/min/mg protein and an apparent Km for inositol 1,4,5-trisphosphate of 0.76 microM; the optimal pH for the enzymatic activity was 7.2. Under both denaturing and nondenaturing conditions, the kinase preparation contained two polypeptides, both of which exhibited Ca2+/calmodulin-dependent Ins(1,4,5)P3 3-kinase activity. In the presence and absence of calmodulin, Ins(1,4,5)P3 3-kinase exhibited a biphasic response to Ca2+, being stimulated between 10(-7) and 10(-6) M Ca2+ and inhibited when the Ca2+ level was further increased. Ins(1,4,5)P3 3-kinase was stimulated by calmodulin approximately 10-fold, requiring 55 nM calmodulin for a half-maximal effect. Calmodulin stimulation was immediately reversed upon chelation of Ca2+ by ethylene glycol bis (beta-amino-ethyl ether) N,N'-tetraacetic acid consistent with a mechanism of activation involving a direct interaction of calmodulin with Ins(1,4,5)P3 3-kinase. Since we have previously shown that Ins(1,4,5)P3 3-kinase can also be phosphorylated and consequently inactivated by protein kinase C in vitro (Lin, A. N., Barnes, S., and Wallace, R. W., 1990, Biochem. Biophys. Res. Commun. 170, 1369-1376), Ins(1,4,5)P3 3-kinase appears to be a key enzyme in the inositol phosphate signaling pathway and as such may play an important role in human platelet function.
Animals↗
5' distal and proximal cis-acting regulator elements are required for developmental control of a rice seed storage protein glutelin gene.
Using a homologous transgenic rice system it is demonstrated that 5' distal and proximal cis-acting transcriptional regulatory elements are required for developmental control of a rice seed storage protein glutelin gene. Analyses of gene expression of nine progressively truncated 5' promoter sequences in developing endosperm indicated the existence of at least one major positive element located from the -5.1 to -1.8 kb region. The functional importance of proximal elements in the context of 1.8 kb promoter was demonstrated by single substitution mutations in the TATA box (-28/-23), AACA motif (-73/-61), and protein-binding boxes I (-103/-86), II (-124/-110), III (-175/-158) and IV (-200/-217). A simultaneous mutation of five protein-binding sites (-410/-86) essentially eliminated the activity of the 1.8 kb promoter. Although temporal control of the Gt1 gene during endosperm development was retained in plants of constructs from -5.1 kb to -155 bp, spatial control of the glutelin gene was altered when the 5.1 kb promoter was deleted to -507 bp or -154 bp as the reporter gene activities of these constructs were detected in phloem of leaves, and in stems, sheaths and roots of plants.
Base Sequence↗
Identification of an oncoprotein- and UV-responsive protein kinase that binds and potentiates the c-Jun activation domain.
The activity of c-Jun is regulated by phosphorylation. Various stimuli including transforming oncogenes and UV light, induce phosphorylation of serines 63 and 73 in the amino-terminal activation domain of c-Jun and thereby potentiate its trans-activation function. We identified a serine/threonine kinase whose activity is stimulated by the same signals that stimulate the amino-terminal phosphorylation of c-Jun. This novel c-Jun amino-terminal kinase (JNK), whose major form is 46 kD, binds to a specific region within the c-Jun trans-activation domain and phosphorylates serines 63 and 73. Phosphorylation results in dissociation of the c-Jun-JNK complex. Mutations that disrupt the kinase-binding site attenuate the response of c-Jun to Ha-Ras and UV. Therefore the binding of JNK to c-Jun is of regulatory importance and suggests a mechanism through which protein kinase cascades can specifically modulate the activity of distinct nuclear targets.
3T3 Cells↗
Protein phosphatase 2A potentiates activity of promoters containing AP-1-binding elements.
The involvement of serine/threonine protein phosphatases in signaling pathways which modulate the activity of the transcription factor AP-1 was examined. Purified protein phosphatase types 1 (PP1) and 2A (PP2A) were microinjected into cell lines containing stably transfected lacZ marker genes under the control of an enhancer recognized by AP-1. Microinjection of PP2A potentiated serum-stimulated beta-galactosidase expression from the AP-1-regulated promoter. Similarly, transient expression of the PP2A catalytic subunit with c-Jun resulted in a synergistic transactivation of an AP-1-regulated reporter gene. PP2A, but not PP1, potentiated serum-induced c-Jun expression, which has been previously shown to be autoregulated by AP-1 itself. Consistent with these results, PP2A dephosphorylated c-Jun on negative regulatory sites in vitro, suggesting one possible direct mechanism for the effects of PP2A on AP-1 activity. Microinjection of PP2A had no effect on cyclic AMP (cAMP)-induced expression of a reporter gene containing a cAMP-regulated promoter, while PP1 injection abolished cAMP-induced gene expression. Taken together, these results suggest a specific role for PP2A in signal transduction pathways that regulate AP-1 activity and c-Jun expression.
Animals↗
Control of AP-1 activity by signal transduction cascades.
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Enzyme Activation↗