Aortic saddle embolus. A twenty-year experience.

Clinical experience with aortic saddle embolus (ASE) is not extensive due to the relative infrequent lodging of emboli at the aortic bifurcation. During the period 1962-1982, 26 patients (mean age, 56 years) were treated at the UCLA Medical Center for ASE and followed from 2 to 158 months (mean, 45 months). These cases were reviewed in order to identify features of diagnosis, anticoagulation, and operation which impact on results. All 26 patients presented with bilateral lower extremity ischemia with or without extension of clot to the iliac bifurcation. Ninety-six per cent of emboli were of cardiac origin and one-third occurred in patients who had previous symptoms of chronic lower extremity ischemia. Rest pain and motor/sensory deficits were main complaints in 92% of the patients, but did not become manifest until more than 6 hours, unlike more distal emboli which have an earlier presentation. Preoperative angiography, even in the patient with a history of claudication, has a small role in planning the surgical approach to patients with ASE and, although performed in 11 patients, it influenced operation in only two. Operation within the "golden period" of 6 hours after embolization did not significantly influence outcome after ASE, since 20 patients were operated on more than 6 hours after embolization, with results similar to six patients who were operated on less than 6 hours after embolization. Early high-dose heparinization, used in all patients and maintained for a mean of 12 days, may have contributed to this effect. In 22 patients (85%) Forgarty catheter extraction via bilateral groin approaches was used with a mortality of 14%; only one death was directly attributed to the catheter embolectomy. In 15% of patients, a direct approach on the aorta was selected with a zero mortality rate. Postoperative functional result was excellent with an amputation rate of only 2% (one limb). Re-embolization occurred in seven patients (27%) after discharge, five of whom had not been maintained on Coumadin and two who were not anticoagulated adequately. The authors conclude that the keys to successful treatment of ASE include high dose heparin which is maintained through the perioperative period, embolectomy without preoperative angiography, and maintenance of long-term oral anticoagulation.     

Factor analysis of the items of the state-trait anxiety inventory

The present investigation was designed to determine by factor analysis the nature of the items that comprise the A-State and A-Trait scales of the State-Trait Anxiety Inventory. Three factors were identified. Factor I was defined exclusively by items from the A-State scale. The underlying dimension tapped by the scale was interpreted as state anxiety (how one feels at a particular moment in time); support thus was provided for Spielberger's A-State concept. Items from the A-Trait scale, however, identified two separate factors, neither of which was clearly consonant with Spielberger's concept of A-Trait. Factor II appeared to tap state anxiety according to how the individual generally feels or a typical level of state anxiety as remembered over an indefiniteperiod of time. Factor III was interpreted as a meamre of neuroticism.     

Durability of benefits of endovascular versus conventional abdominal aortic aneurysm repair

PURPOSE: Endovascular abdominal aortic aneurysm (AAA) repair is reported to result in less initial patient morbidity and a shorter hospital length of stay (LOS) when compared with conventional AAA repair. We sought to examine the durability of this result during the intermediate follow-up interval. METHODS: The records of all admissions for all patients who underwent AAA repair during a 26-month interval were reviewed. RESULTS: Three hundred thirty-seven (337) patients underwent procedures to repair AAAs (163 open and 174 endovascular). Endovascular procedures were performed with a variety of devices (Talent, 108; Ancure, 36; AneuRx, 26; Zenith, 2; and Cordis, 2) and configurations (141 bifurcated and 33 aortomonoiliac). The mean follow-up period was 10.6 months (endovascular repair) and 12.3 months (open repair). LOS did not significantly vary by device (P =.24 to P =.92) or configuration (P =.24). The initial median LOS for procedures was significantly shorter (P =.009) for endovascular repairs (5 days) than for open procedures (8 days). However, the patients who underwent endovascular repair were more likely to be readmitted during the follow-up interval when compared with patients who underwent open procedure. The readmission-free survival rate after AAA repair at 12 months was 95% for patients for open AAA repair versus 71% for patients for endovascular repair (P <.001). If the total hospital days were compared, including the initial and all subsequent AAA-related admissions, there was no significant difference for mean LOS for patients who underwent endovascular versus open AAA procedures (11 days versus 13.6 days; P =.21). The patients for endovascular AAA repair most commonly needed readmission for treatment of endoleak (n = 31), wound infection (n = 12), and graft limb thrombosis (n = 9). Although women had similar LOS to men for endovascular repair (P =.44), they had longer initial LOS for open AAA repair (15 versus 10 days; P =.03). After endovascular repair, women were more likely than men to be readmitted by 12 months (51% versus 71% readmission-free survival rate; P =.03) and they had longer LOS on readmission (13.2 versus 5.2 days; P =.006). No gender differences were identified for patients after open AAA repair regarding readmission-free survival rate (P =.09) or LOS on readmission (P =.98). CONCLUSION: Although initial LOS was shorter for the patients who underwent endovascular as compared with conventional AAA repair, this advantage was lost during the follow-up interval because of frequent readmission for the treatment of procedure-related complications, chiefly endoleak. These readmissions frequently involved the performance of additional invasive procedures. Gender differences existed regarding LOS and the likelihood of complications after open and endovascular AAA repair.     

MR imaging of human brain at 3.0 T: preliminary report on transverse relaxation rates and relation to estimated iron content

PURPOSE: To determine the transverse relaxation rates R2 and R2' from several gray matter regions and from frontal cortical white matter in healthy human brains in vivo and to determine the relationship between relaxation rates and iron concentration [Fe]. MATERIALS AND METHODS: Six healthy adults aged 19-42 years underwent thin-section gradient-echo sampling of free induction decay and echo magnetic resonance (MR) imaging at 3.0 T. Imaging covered the mesencephalon and basal ganglia. RESULTS: Relaxation rates (mean +/- SD) were highest in globus pallidus (R2 = 25.8 seconds-1 +/- 1.1, R2' = 12.0 seconds-1 +/- 2.1) and lowest in prefrontal cortex (R2 = 14.4 seconds-1 +/- 1.8, R2' = 3.4 seconds-1 +/- 1.1). Frontal white matter measurements were as follows: R2 = 18.0 seconds-1 +/- 1.2 and R2' = 3.9 seconds-1 +/- 1.2. For gray matter, both R2 and R2' showed a strong correlation (r = 0.92, P < .001 and r = 0.90, P < .001, respectively) with [Fe]. Although the slopes of the regression lines for R2' versus [Fe] and for R2 versus [Fe] were similar, the iron-independent component of R2' (2.2 seconds-1 +/- 0.6), the value when [Fe] = 0, was much less than that of R2 (12.7 seconds-1 +/- 0.7). CONCLUSION: The small iron-independent component R2', as compared with that of R2, is consistent with the hypothesis that R2' has higher iron-related specificity.     

Macromolecule‐suppressed GABA‐edited magnetic resonance spectroscopy at 3T

Edited magnetic resonance spectroscopy makes possible noninvasive studies of the role of the inhibitory neurotransmitter GABA in the healthy brain and in disease processes. A major limitation of the methodology is coediting of macromolecular signals. Although it has previously been shown that macromolecular signal can be suppressed using a symmetrical editing scheme, this approach is rarely applied at field strength of 3T as insufficiently selective pulses result in loss of GABA signal (in addition to the intended suppression of macromolecular signal). In this article, the authors show that increasing the echo time to 80 ms lets more selective editing pulses be used, allowing for symmetric editing‐based suppression of coedited macromolecular signal without loss of GABA signal. The method is applied to acquire macromolecule‐suppressed GABA‐edited spectra in 10 healthy participants. Magn Reson Med, 2012. © 2012 Wiley Periodicals, Inc.     

Increased erythrocyte stearic acid desaturation in rats with chemically induced colorectal carcinomas

Our previous studies have demonstrated a desaturation of stearic acid related to oleic acid in the lipid layer of erythrocytes in patients with malignancies. This study investigated the stearic acid desaturation in red blood cell membranes of rats during the induction of colorectal tumours. Male Sprague-Dawley rats were injected weekly with dimethylhydrazine (DMH) and sacrificed at 4-week intervals. Blood was withdrawn via heart puncture, collected in EDTA bottle and erythrocytes separated by centrifugation. Total lipid extraction was carried out and analysed with gas liquid chromatography. In the control rats (injected with normal saline) the mean of the stearic to oleic acid ratio in erythrocyte membranes was 2.0±0.3 (n=28, range 1.51–2.62) compared to a mean of 0.94±0.16 (n=0.5–1.23) in tumour bearing rats (p< 0.001). The increased desaturation occurred in parallel with appearance of tumours. These data suggest the regulation of stearic acid desaturation is an important adaptive mechanism of membrane fluidity and could be a useful chemical marker for malignancy.     

Low birth weights contribute to high rates of early-onset chronic renal failure in the Southeastern United States

BACKGROUND: The southeastern United States is a region in which rates of cardiovascular and renal diseases are excessive. Within the Southeast, South Carolina has unusually high rates of end-stage renal disease (ESRD) in young people, with more than 70% of cases attributed to hypertension and diabetes. OBJECTIVE: To determine whether the increased vulnerability to early-onset ESRD might originate through impaired renal development in utero as measured by low birth weight. METHODS: Patients who were diagnosed with renal failure and undergoing dialysis from 1991 through 1996 were identified from the ESRD registry maintained by the Southeastern Kidney Council, Raleigh, NC. Birth weights reported on birth certificates were selected for the ESRD cases and non-ESRD controls who were born in South Carolina in 1950 and later. Birth weights were compared for 1230 cases and 2460 controls who were matched for age, sex, and race. RESULTS: Low birth weight was associated with ESRD among men and women as well as blacks and whites. Among people whose birth weight was less than 2.5 kg, the odds ratio for ESRD was 1.4 (95% confidence interval, 1.1-1.8) compared with people who weighed 3 to 3.5 kg. This association was present for renal failure resulting from diabetes, hypertension, and other causes. CONCLUSIONS: Low birth weights, which reflect adverse effects on development in utero, contribute to the early onset of ESRD in South Carolina. Since low birth weight increases the risk of ESRD from multiple causes, the data suggest that an adverse environment in utero impairs kidney development and makes it more vulnerable to damage from a range of pathological processes.     

Human dihydrofolate reductase gene is located in chromosome 5 and is unlinked to the related pseudogenes.

The chromosomal location of the human dihydrofolate reductase (DHFR; EC 1.5.1.3) gene that is amplified in a methotrexate-resistant human cell line has been investigated by screening a large number of human-mouse cell hybrids containing overlapping subsets of human chromosomes. A correlation of genomic blotting data with the chromosome constitution of the individual cell hybrids has allowed the assignment of the human DHFR gene to chromosome 5. This chromosome assignment has been confirmed by the observation of a concomitant loss of the human DHFR gene and of sensitivity to diphtheria toxin, a marker associated with chromosome 5, in two human-mouse cell hybrids selected for resistance to the toxin. Six EcoRI fragments of human DNA containing DHFR pseudogenes or other DHFR-related sequences have been assigned to chromosomes other than chromosome 5.