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Query: UMLS:C0162871 (
abdominal aortic aneurysm
)
8,664
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Cells have been isolated from liver tumours that have arisen in control C3H/He mice, in mice given 10 micrograms diethylnitrosamine (DEN) during the neonatal period or in mice given a diet containing phenobarbitone (PB) to allow a daily intake of 85 mg/kg/day. The cells were grown to the 8 degrees subculture when their growth characteristics were investigated in monolayer culture and following suspension in soft agar and on transplantation into nude mice. In addition, DNA was isolated from the cultures and from tumours that grew in nude mice and analysed for mutations at codon 61 of the Ha-ras oncogene. All cells derived from DEN-induced hepatocellular carcinomas (HCC) demonstrated a lack of density inhibition of growth in monolayer culture, grew in soft agar and formed tumours in nude mice with an average mean latency of 29 days. Three of the seven lines showed mutations in Ha-ras: two were CAA-->
AAA
transversions and one showed a CAA-->CTA transversion. In contrast, cells isolated from eosinophilic nodules in mice given PB showed inhibition of growth at confluence, did not grow in soft agar and only four of eight formed tumours in nude mice with a mean average latent period of 181 days. Cells grown from HCC in mice given PB showed a lack of density inhibition of growth, however, they did not grow in soft agar nor did they form tumours in nude mice. A single spontaneous HCC from a control mouse showed a similar growth pattern to HCC cells isolated from mice given PB. Cells from a basophilic nodule, taken from a control untreated mouse grew vigorously in culture and in soft agar and formed tumours in nude mice with a latency of 6 days. None of the cells isolated from control mice or from mice given PB showed evidence of mutations at codon 61 of Ha-ras. These data confirm that there are fundamental differences in the biology of cells grown from tumours that develop in mice under different treatment regimes. These studies also demonstrate the utility of cell culture and molecular biology in addressing the fundamental mechanism of mouse hepatic neoplasia.
Carcinogenesis 1994
Sep
PMID:Growth characteristics and Ha-ras mutations of cell cultures isolated from chemically induced mouse liver tumours. 752 81
An analogue of Hoechst 33258, bearing a phenolic hydroxyl group in the meta rather than para position, was designed using molecular graphics to introduce hydrogen-bonding potentials between this OH group and the C = O group of cytosine-9 and the NH2 group of guanine-4', of the opposite strand of the B-DNA duplex, d(CGCGAATTCGCG)2. This derivative (meta-Hoechst) was synthesized in seven steps and characterized. Its binding to DNA was assessed by measurements of melting temperatures (Tm) and found to be similar in strength and AT preference to the parent Hoechst 33258 at this gross level. The AT preference of meta-Hoechst and Hoechst 33258 was probed further using hydroxyl radical footprinting on the tyrT DNA fragment, for which clear footprints were detected at AAT,
AAA
and ATAT runs, as for netropsin and distamycin. Hydroxyl radical footprinting was carried out on a trimer of CGCGAATTCGCG cloned into a longer DNA fragment, for which clear footprints for both Hoechst 33258 and meta-Hoechst were detected in regions with four or more contiguous AT base pairs. Three cell lines derived from haematological malignancies were more sensitive to both Hoechst 33258 and meta Hoechst than lines derived from solid tumours, but there was no significant difference between the activity of these two Hoechst derivatives.
Anticancer Drug Des 1995
Sep
PMID:Synthesis, DNA binding, footprinting and in vitro antitumour studies of a meta-hydroxy analogue of Hoechst 33258. 757 88
Animal experiments in the 80's demonstrated the feasibility of the concept first inaugurated by Dotter in 1969 of the endovascular implantation of a stent-graft prosthesis for the treatment of
abdominal aortic aneurysm
. In September 1990 Parodi was the first to treat a patient with an
AAA
using the implantation of a TPEG (transluminal placed endovascular stented graft). The rapid development of a variety of different devices can be observed since resulting in about 400 such prosthesis being implanted world wide for the treatment of
AAA
. The experience accumulated so far shows that severe complications can be avoided if morphology-based criteria are considered for the various treatment options (
AAA
classification type I, type IIa-c, type III). Despite considerable lethal incidents, technical mishaps and severe complications to date, the potential of TPEG for a structured approach to the treatment of
AAA
has to be evaluated. Prerequisites are 1) a competent team based on a close mutual cooperation of vascular surgeons and interventional radiologists, 2) a careful selection of patients, 3) TPEG to be performed in especially equipped operation theatres permitting the immediate application of conventional surgery if necessary, and 4) the implantation to be performed as a clinical study with flawless documentation of the procedure and follow-up.
Chirurg 1995
Sep
PMID:[Endovascular reconstruction of infrarenal abdominal aortic aneurysm]. 758 58
There is evidence that the risk of
abdominal aortic aneurysm
(
AAA
) is greater in first-degree relatives of patients with the disorder than in the same age group of the general population. We conducted a 3-year study of siblings of
AAA
probands and siblings of a control group (cataract surgery patients) of the same age. Genetic information was obtained by interview from 126 probands and 100 controls; another family member was present at the interview. Medical records were obtained and further information verified before a sibling (over age 50) was assigned affected status. Of 427 siblings of probands, 19 (4.4%) had probable or definite
AAA
, compared with five (1.1%) of 451 siblings of controls. The lifetime cumulative risks of
AAA
at age 83 were 11.7% (SD 3.1) and 7.5% (4.1), respectively. The risk of
AAA
began at an earlier age and increased more rapidly for probands' siblings than for controls' siblings (p < 0.01, log-rank test). A risk comparison, based on the results of ultrasound screening of 54 geographically accessible siblings of probands and the 100 controls showed a similar pattern. Ten (19%) siblings of probands and eight (8%) controls had
AAA
on ultrasound (lifetime cumulative risk 60.8% [18.9] vs 14.9% [5.1], p = 0.01). These results show that familial factors influence the age of onset of
AAA
. We recommend routine ultrasound examination of siblings of patients with
AAA
.
Lancet 1995
Sep
02
PMID:Sibling risks of abdominal aortic aneurysm. 765 Oct 4
Constitutively activating mutations have recently been identified in the thyrotropin receptor (TSHR) of hyperfunctioning thyroid adenomas and familial hyperthyroidism. In the present study, we evaluated the frequency of constitutively activating TSHR mutations in a large series of autonomously functioning thyroid nodules (AFTNs) in Japan. Forty-five AFTNs (38 solitary hyperfunctioning thyroid adenomas and 7 toxic multinodular goiters) were analyzed. Genomic DNA was extracted from paraffin-embedded tissue sections, from which DNA fragments encoding the mutational hot spots of the receptor (the third cytoplasmic loop and the sixth transmembrane segment) were amplified by polymerase chain reaction. In the single-stranded conformation polymorphism (SSCP) analysis, only one hyperfunctioning adenoma (no. 21) displayed a migration abnormality. In sequence analysis, an unusual mutation of alternate three-base deletions at nucleotides 1953-1957 (
AAA
GAT ACC to AAG TCC), resulting in one amino acid deletion (Asp at 619) and one conservative amino acid substitution (Thr to Ser at 620), was identified in tumor DNA but not in leukocyte DNA of no. 21. Further, the normal sequence in these regions was confirmed in 10 randomly selected samples with normal migrating patterns in SSCP analysis. The functional property of the mutant with delta 619 and T620S (designated TSHR delta 619) was then evaluated with in vitro mutagenesis and transfection studies. Unexpectedly, however, there were no significant differences in TSH binding affinity, and basal and TSH-stimulated levels of cAMP and inositol 1,4,5-triphosphate between the TSHR delta 619 and the wt-TSHR. In conclusion, the incidence of the constitutively activating TSHR mutations in AFTNs appears to be low in Japan. The oncogenic potential of a novel somatic mutant TSHR delta 619 identified in a hyperfunctioning adenoma in this study is at present uncertain because of its intact function.
J Clin Endocrinol Metab 1995
Sep
PMID:Rarity of oncogenic mutations in the thyrotropin receptor of autonomously functioning thyroid nodules in Japan. 767 2
A 6.4-kb DNA fragment containing the DNA gyrase gyrA and gyrB genes was cloned and sequenced from the quinolone-susceptible Staphylococcus aureus type strain ATCC 12600. An expression plasmid was constructed by inserting the cloned genes into the Escherichia coli-S. aureus shuttle vector pAT19, and deletion plasmids carrying only functional gyrA and gyrB genes were derived from this plasmid. An efficient transformation system for S. aureus RN4220 was established by using these plasmids. Quinolone-resistant mutants of S. aureus RN4220 were isolated by three-step selection with quinolones. The first- and second-step mutants were considered to be transport mutants, and the third-step mutants were divided into five groups with respect to their resistance patterns and transformation results with gyrA and gyrB genes. Sequencing analysis of the resulting mutant gyrase genes showed that they had the following point mutations: group 1, Ser-84 (TCA) to Leu (TTA) in GyrA; group 2, Ser-84 (TCA) to Ala (GCA), Ser-85 (TCT) to Pro (CCT), or Glu-88 (GAA) to Lys (
AAA
) in GyrA; group 3, Asp-437 (GAC) to Asn (AAC) in GyrB; group 4, Arg-458 (CGA) to Gln (CAA) in GyrB; and group 5, Ser-85 (TCT) to Pro (CCT) in GyrA and Asp-437 (GAC) to Asn (AAC) in GyrB. When the gyrA and/or gyrB mutants were transformed with the wild-type gyrA and/or gyrB plasmids, they became quinolone susceptible, but transformants with the plasmids having the same mutations on the gyrA and/or gyrB genes did not confer susceptibility. These results indicate that mutations in both gyrA and gyrB can be responsible for quinolone resistance in S. aureus.
Antimicrob Agents Chemother 1994
Sep
PMID:Quinolone resistance mutations in the DNA gyrase gyrA and gyrB genes of Staphylococcus aureus. 781 Oct 12
To determine the potential benefit of Dacron prostheses impregnated with silicon polymer, an elastomer-coated prosthetic graft (Intervascular [I]) was implanted in 30 patients with aortic occlusive arterial disease or infrarenal
abdominal aortic aneurysm
. These patients were compared with two other groups who underwent vascular reconstruction with either a knitted double-velour prosthesis (Meadow [M] or a knitted prosthesis (Bard-USCI [U]). The different prostheses were randomly allocated just prior to their insertion. Average blood loss was 1063.33 +/- 1065.69 ml for the I group, 888.33 +/- 575.85 ml for the M group, and 908.33 +/- 471.80 ml for the U group (NS). The duration of the operation was 160 +/- 56 minutes for the I group, 142 +/- 37 minutes for the M group, and 153 +/- 65 minutes for the U group (NS). The average follow-up was 12 months. As calculated by the actuarial method, primary patency at 36 months was 71.5% for the I group, 100% for the M group, and 98.2% for the U group (p < 0.001). Secondary patency was 73.7% for the I group and 100% for the M and U groups, respectively (p < 0.001). This study shows that the thrombogenicity of the elastomer-coated aortofemoral vascular prosthetic graft was significantly higher than that of the two other prostheses. Increased intraoperative blood loss and longer duration of operation were related to the aortic abnormality being treated (aneurysm or occlusion) rather than to the type of prosthetic graft being used.
Ann Vasc Surg 1994
Sep
PMID:Thrombogenicity of an elastomer-coated aortofemoral Dacron prosthetic graft in humans. 781 82
Acute aortic dissection and
abdominal aortic aneurysm
presenting as coexistent conditions is rare. We report a patient with a history of hypertension and acute severe back pain who had an acute aortic dissection extending into a preexisting 8 cm
abdominal aortic aneurysm
that was diagnosed by CT scan. There was no evidence of aortic rupture or leakage. The patient was treated with antihypertensive medication for 2 months to allow maturation of the acute dissection prior to elective repair of the
abdominal aortic aneurysm
. The repair was constructed to allow continued perfusion of both the true and false lumina by fenestration of the aortic septum at the proximal anastomosis. There were no postoperative complications. This case illustrates an unusual combination of aortic diseases. A management plan is described that safely treats both pathologic conditions.
Ann Vasc Surg 1994
Sep
PMID:Acute aortic dissection into a preexisting abdominal aortic aneurysm. 781 87
We report three cases in which ruptured aneurysm and aortocaval fistula went undetected until surgery was performed. Preoperative features suggestive of an arteriovenous fistula were not apparent in any of these patients; they all presented with cardiovascular collapse and all underwent emergency laparotomy after a ruptured
abdominal aortic aneurysm
was diagnosed. The fistula was discovered unexpectedly only after the aneurysmal sac was opened and the thrombus evacuated. In the first two patients the fistula was successfully sutured from within the aneurysmal sac. The first patient died 1 week postoperatively from rupture of a previously known associated thoracic aortic aneurysm and the second patient died during the operation from excessive blood loss. The third patient had a large fistula requiring an interposition synthetic graft to restore the continuity of the vena cava; the graft has remained patent 15 months postoperatively. Aortocaval fistula is an uncommon complication of aneurysmal aortic disease and may coexist with a rupture of the aneurysm into the retroperitoneum. In emergency cases such as ours it is usually discovered unexpectedly during the operation. The established method of treatment is to oversew the fistula from within the aneurysm; however, when the fistula is large reconstruction of the infrarenal inferior vena cava with an interposition synthetic graft is a good alternative to caval ligation.
Ann Vasc Surg 1994
Sep
PMID:Primary aortocaval fistula in association with ruptured aneurysms. 781 88
Between 1988 and 1993, 17 (3%) out of a total 654 patients underwent reoperation for control of haemorrhage following repair of
abdominal aortic aneurysm
in a vascular surgery unit. The first operation was performed for rupture in 12 cases and electively in five. The incidence of reoperation for postoperative bleeding was 1.7% following elective operation and 3.3% following emergency operation. Case-controls, matched for sex and primary operation, were identified. The mortality rate in those requiring reoperation was 58% compared with 23% in the control group (p = 0.037). Seven patients suffered progressive deterioration and died in the early postoperative period. Of the remaining ten patients, four suffered unexpected serious complications; two a fatal cerebro-vascular accident (CVA), one a fatal myocardial infarction (MI) and the fourth a non-fatal CVA. The patients requiring reoperation had greater blood loss (p < 0.05), greater transfusion requirements and lower core temperatures (p < 0.05) at the end of their first operation than the control group. All except one of the patients who bled had evidence of coagulopathy and had lower platelet counts than the control group both before and after the first operation. At reoperation there were multiple minor bleeding points in 11 patients, no active bleeding points in two patients and a discrete bleeding point in four patients. In conclusion, re-operation for control of postoperative haemorrhage is an uncommon complication which is strongly associated with coagulopathy, may predispose to "rebound" postoperative thrombotic episodes, and carries a poor prognosis.
Eur J Vasc Surg 1994
Sep
PMID:Postoperative haemorrhage following aortic aneurysm repair. 781 32
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