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21.
Hypospadias trends in two US surveillance systems 总被引:6,自引:0,他引:6
OBJECTIVE: Hypospadias is a common congenital anomaly, the cause of which is unknown. Unexplained increases in the rates of hypospadias occurred in five European countries in the 1970s and 1980s. We examined data from two birth defects surveillance systems in the United States for evidence of similar trends. METHODOLOGY: The Metropolitan Atlanta Congenital Defects Program (MACDP) provided birth prevalence rates from 1968 to 1993. The nationwide Birth Defects Monitoring Program (BDMP) provided rates from 1970 to 1993. MACDP data are population-based and could be categorized by the severity of the hypospadias. BDMP data allowed analysis of rate trends for the four census regions of the United States. RESULTS: Data from both surveillance systems showed an approximate doubling of hypospadias rates in the 1970s and 1980s. MACDP data showed that the rate of severe cases increased while the ratio of mild to severe cases decreased. BDMP data showed that hypospadias rates increased markedly in all four regions of the United States. CONCLUSIONS: The observed increases are unlikely to be attributable to increased sensitivity of the surveillance systems or the identification of more mild cases by physicians over time, because either trend would have increased rather than decreased the ratio of mild to severe cases. If real, these trends represent the largest number of cases and the first report of an increase in hypospadias rates outside of Europe. Additional investigation of a possible increase in hypospadias rates is warranted. 相似文献
22.
Gonzales AJ; Christensen JG; Preston RJ; Goldsworthy TL; Tlsty TD; Fox TR 《Carcinogenesis》1998,19(7):1173-1183
23.
Guo RJ; Wang Y; Kaneko E; Wang DY; Arai H; Hanai H; Takenoshita S; Hagiwara K; Harris CC; Sugimura H 《Carcinogenesis》1998,19(9):1539-1544
Mutations in the transforming growth factor beta type II receptor
(TGFbetaRII) gene have been detected in several human cancer types
exhibiting microsatellite instability. Using intron primers previously
reported for examination of the entire coding region of the TGFbetaRII
gene, 29 sporadic gastric cancers were screened with non-radioactive single
strand conformation polymorphism and subsequent DNA sequencing analysis.
Mutations of the TGFbetaRII gene were detected in three out of 29 tumors
(10%). Two cases showed deletions in a polyadenine tract in both alleles
and was positively associated with replication error. One case had an
insertion of GA dinucleotide sequence in one allele. Mutations of the
TGFbetaRII gene were restricted to exon 3 and other coding regions were not
affected. Loss of heterozygosity was detected by analyzing a polymorphic
site in intron 2. Three out of nine (33%) informative cases, which were all
of intestinal type and advanced cases, showed loss of heterozygosity but
neither TGFbetaRII mutation nor replication error was found in these cases.
Immunoreactivity of TGFbetaRII in tumor tissues was reduced to a different
extent in the gastric cancer with genetically abnormal transforming growth
factor. Although the numbers studied are small, homozygous (A)10 deletion
or loss of heterozygosity of TGFbetaRII is involved in tumorigenesis and
progression of at least some part of sporadic gastric cancer.
相似文献
24.
25.
Tumour cell growth may be accelerated by protein kinase C (PKC) agonists
such as phorbol esters and receptor tyrosine kinases, but receptor tyrosine
kinases are in turn desensitized to growth factors by PKC agonists. To
clarify this apparent PKC bifunctionality, we have used phosphoantibodies
to determine the relationship between PKC- dependent phosphorylation events
affecting the ErbB2 oncoprotein in G8/DHFR 3T3 cells. Neither the kinetics
nor the extent of phorbol- induced juxtamembrane domain (Thr686)
phosphorylation vary directly with C-terminal (Tyr1222) dephosphorylation,
with Tyr1222 continuing to be dephosphorylated long after Thr686
phosphorylation has also declined. Platelet-derived growth factor (PDGF)
mimics the short-term effects of phorbol on Thr686 and Tyr1222
phosphorylation, and confocal microscopy reveals that both of these PKC
agonists induce rapid internalization of PKC-modified ErbB2. Phorbol causes
sustained cytoplasmic accumulation of PKC-phosphorylated receptors,
however, whereas PDGF triggers the appearance of this ErbB2 subset only
briefly. Metabolic labelling and co-precipitation studies fail to implicate
heterologous molecules in either the tyrosine dephosphorylation or
internalization of PKC-modified ErbB2. Taken in the context of earlier
juxtamembrane domain mutagenesis studies, these findings indicate that
phorbol-activated PKC may desensitize growth factor receptors to
extracellular ligands solely by triggering sustained receptor
internalization. We submit that PKC-dependent juxtamembrane domain
phosphorylation represents a physiological mechanism for shortening the
duration and enhancing the specificity of growth factor signalling by
promoting internalization of liganded and unliganded receptors,
respectively.
相似文献
26.
27.
Raymond J. Roberge 《Journal of occupational and environmental hygiene》2016,13(4):235-242
Face shields are personal protective equipment devices that are used by many workers (e.g., medical, dental, veterinary) for protection of the facial area and associated mucous membranes (eyes, nose, mouth) from splashes, sprays, and spatter of body fluids. Face shields are generally not used alone, but in conjunction with other protective equipment and are therefore classified as adjunctive personal protective equipment. Although there are millions of potential users of face shields, guidelines for their use vary between governmental agencies and professional societies and little research is available regarding their efficacy. 相似文献
28.
29.
Primary care nursing activities with patients affected by physical chronic disease and common mental disorders: a qualitative descriptive study
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30.
Platelet activation leads to the incorporation of 32[PO4(2-)] into bovine coagulation factor Va and recombinant human factor VIII. In the presence of the soluble fraction from thrombin-activated platelets and (gamma-32P) adenosine triphosphate, radioactivity is incorporated exclusively into the M(r) = 94,000 heavy chain (H94) of factor Va and into the M(r) = 210,000 to 90,000 heavy chains as well into the M(r) = 80,000 light chain of factor VIII. Proteolysis of the purified phosphorylated M(r) = 94,000 factor Va heavy chain by activated protein C (APC) gave products of M(r) = 70,000, 24,000, and 20,000. Only the intermediate M(r) = 24,000 fragment contained radioactivity. Because the difference between the M(r) = 24,000 and M(r) = 20,000 fragments is located on the COOH-terminal end of the bovine heavy chain, phosphorylation of H94 must occur within the M(r) = 4,000 peptide derived from the carboxyl-terminal end of H94 (residues 663 through 713). Exposure of the radioactive factor VIII molecule to thrombin ultimately resulted in a nonradioactive light chain and an M(r) = 24,000 radioactive fragment that corresponds to the carboxyl-terminal segment of the A1 domain of factor VIII. Based on the known sequence of human factor VIII, phosphorylation of factor VIII by the platelet kinase probably occurs within the acidic regions 337 through 372 and 1649 through 1689 of the procofactor. These acidic regions are highly homologous to sequences known to be phosphorylated by casein kinase II. Results obtained using purified casein kinase II gave a maximum observed stoichiometry of 0.6 mol of 32[PO4(2-)]/mol of factor Va heavy chain and 0.35 mol of 32[PO4(2-)]/mol of factor VIII. Phosphoamino acid analysis of phosphorylated factor Va by casein kinase II or by the platelet kinase showed only the presence of phosphoserine while phosphoamino acid analysis of phosphorylated factor VIII by casein kinase II showed the presence of phosphothreonine as well as small amounts of phosphoserine. The platelet kinase responsible for the phosphorylation of the two cofactors was found to be inhibited by several synthetic protein kinase inhibitors. Finally, partially phosphorylated factor Va was found to be more sensitive to APC inactivation than its native counterpart. Our findings suggest that phosphorylation of factors Va and VIIIa by a platelet casein kinase II- like kinase may downregulate the activity of the two cofactors. 相似文献