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21.
Leukotriene B4 (LTB4) and the protein kinase C activator, 4-beta-phorbol dibutyrate (PDBu), both induced a pronounced and concentration-dependent stimulation of hydrogen peroxide (H2O2) generation by purified guinea pig peritoneal eosinophils in the concentration range 1 nM-1 microM. The LTB4 response was inhibited competitively by the specific LTB4 receptor antagonist, U-75302, with a KB of 25 nM, while the concentration-response curves for both stimuli were shifted rightwards (3.8-fold and 2.8-fold for LTB4 and PDBu, respectively) by the competitive protein kinase C inhibitor, 1-O-hexadecyl-2-O-methylglycerol at a concentration of 300 microM. LTB4 appears, therefore, to induce respiratory burst in eosinophils via a receptor-mediated mechanism involving protein kinase C. 相似文献
22.
M I Goodwin 《Acta orthopaedica Scandinavica》1990,61(2):187-188
23.
24.
C W Twiston-Davies M I Goodwin P J Baxter 《The Journal of bone and joint surgery. British volume》1990,72(3):510-511
We report a double-blind study of the effectiveness of indomethacin suppositories in the relief of postoperative pain and the reduction in demand for opiate analgesia following orthopaedic procedures. 相似文献
25.
A W Perry C W Goodwin J L Finkelstein M R Madden T J Krizek 《The Journal of burn care & rehabilitation》1988,9(5):490-491
During excisions of acute burn wounds, attention to aesthetic detail often is secondary to the goal of rapid gross coverage. Expeditious approximation of adjacent skin grafts has long presented a problem to surgeons. Some surgeons simply place the grafts next to each other, relying on the intervening areas to "scar in". Others use staples to hold grafts together. These staples, however, can become buried under healed grafts and can cause "foreign body" reactions in the months and years ahead. In addition, staples cause bleeding beneath the newly placed grafts, contributing to hematoma formation. Still other surgeons suture or tape adjacent pieces of skin graft together, a tedious exercise. The cosmetic result of these techniques is often less than optimal resulting in the unfortunately familiar "patchwork quilt" appearance of grafts interweaved among scars. Vascular clips have proven to be useful for holding adjacent pieces of skin graft together. 相似文献
26.
27.
BACKGROUND: The goal of this investigation was to determine the association between self-reported childhood trauma and physical disorders among adults in the United States. METHOD: Data were drawn from the National Comorbidity Survey (N=5877). Multiple logistic regression analyses were used to determine the associations between childhood physical abuse, sexual abuse, and childhood neglect and the likelihood of specific physical disorders among adults. RESULTS: Childhood physical abuse, sexual abuse and neglect were associated with a statistically significantly increased risk of a wide range of physical illnesses during adulthood. After adjusting for demographic characteristics, lifetime anxiety and depressive disorders, alcohol and substance dependence, and all types of trauma: results showed that childhood physical abuse was associated with increased risk of lung disease (OR= 1.5 (1.1, 2.2)), peptic ulcer (OR= 1.5 (1.03, 2.2)) and arthritic disorders (OR= 1.5 (1.1, 2.2)); childhood sexual abuse was associated with increased risk of cardiac disease (OR = 3.7 (1.5, 9.4)); and childhood neglect was associated with increased risk of diabetes (OR=2 2 (1.1, 4.4)) and autoimmune disorders (OR =4.4 (1.7, 11.6)). CONCLUSIONS: Consistent with previous work, these results suggest that self-reported childhood trauma is associated with increased risk of a range of physical illnesses during adulthood. Future research that includes replication of these findings using prospectively assessed physical and mental disorders with objectively measured biological data using a longitudinal design, including other known risk factors for these diseases and more detailed information on specific forms of abuse, is needed to understand the potential mechanisms of these links. 相似文献
28.
Deletion of Brca2 exon 27 causes hypersensitivity to DNA crosslinks,chromosomal instability,and reduced life span in mice 总被引:1,自引:0,他引:1
Donoho G Brenneman MA Cui TX Donoviel D Vogel H Goodwin EH Chen DJ Hasty P 《Genes, chromosomes & cancer》2003,36(4):317-331
The Brca2 tumor-suppressor gene contributes to genomic stability, at least in part by a role in homologous recombinational repair. BRCA2 protein is presumed to function in homologous recombination through interactions with RAD51. Both exons 11 and 27 of Brca2 code for domains that interact with RAD51; exon 11 encodes eight BRC motifs, whereas exon 27 encodes a single, distinct interaction domain. Deletion of all RAD51-interacting domains causes embryonic lethality in mice. A less severe phenotype is seen with BRAC2 truncations that preserve some, but not all, of the BRC motifs. These mice can survive beyond weaning, but are runted and infertile, and die very young from cancer. Cells from such mice show hypersensitivity to some genotoxic agents and chromosomal instability. Here, we have analyzed mice and cells with a deletion of only the RAD51-interacting region encoded by exon 27. Mice homozygous for this mutation (called brca2(lex1)) have a shorter life span than that of control littermates, possibly because of early onsets of cancer and sepsis. No other phenotype was observed in these animals; therefore, the brca2(lex1) mutation is less severe than truncations that delete some BRC motifs. However, at the cellular level, the brca2(lex1) mutation causes reduced viability, hypersensitivity to the DNA interstrand crosslinking agent mitomycin C, and gross chromosomal instability, much like more severe truncations. Thus, the extreme carboxy-terminal region encoded by exon 27 is important for BRCA2 function, probably because it is required for a fully functional interaction between BRCA2 and RAD51. 相似文献
29.
Localization of a gene for otosclerosis to chromosome 15q25-q26 总被引:5,自引:0,他引:5
Tomek MS; Brown MR; Mani SR; Ramesh A; Srisailapathy CR; Coucke P; Zbar RI; Bell AM; McGuirt WT; Fukushima K; Willems PJ; Van Camp G; Smith RJ 《Human molecular genetics》1998,7(2):285-290
Among white adults otosclerosis is the single most common cause of hearing
impairment. Although the genetics of this disease are controversial, the
majority of studies indicate autosomal dominant inheritance with reduced
penetrance. We studied a large multi- generational family in which
otosclerosis has been inherited in an autosomal dominant pattern. Five of16
affected persons have surgically confirmed otosclerosis; the remaining nine
have a conductive hearing loss but have not undergone corrective surgery.
To locate the disease- causing gene we completed genetic linkage analysis
using short tandem repeat polymorphisms (STRPs) distributed over the entire
genome. Multipoint linkage analysis showed that only one genomic region, on
chromosome 15q, generated a lod score >2.0. Additional STRPs were typed
in this area, resulting in a lod score of 3.4. STRPs FES (centromeric) and
D15S657 (telomeric) flank the 14. 5 cM region that contains an otosclerosis
gene.
相似文献
30.
Hendrickx J; Dams E; Coucke P; Lee P; Fernandes J; Willems PJ 《Human molecular genetics》1996,5(5):649-652
X-linked liver glycogenosis type II (XLG II) is a recently described X-
linked liver glycogen storage disease, mainly characterized by enlarged
liver and growth retardation. These clinical symptoms are very similar to
those of XLG I. In contrast to XLG I patients, however, XLG II patients do
not show an in vitro enzymatic deficiency of phosphorylase kinase (PHK).
Recently, mutations were identified in the gene encoding the liver alpha
subunit of PHK (PHKA2) in XLG I patients. We have now studied the PHKA2
gene of four unrelated XLG II patients and identified four different
mutations in the open reading frame, including a deletion of three
nucleotides, an insertion of six nucleotides and two missense mutations.
These results indicate that XLG II is due to mutations in PHKA2. In
contrast to XLG I, XLG II is caused by mutations that lead to minor
structural abnormalities in the primary structure of the liver alpha
subunit of PHK. These mutations are found in a conserved RXX(X)T motif,
resembling known phosphorylation sites that might be involved in the
regulation of PHK. These findings might explain why the in vitro PHK
enzymatic activity is not deficient in XLG II, whereas it is in XLG I.
相似文献