GP facilitators and HIV infection. Shared care better for GPs and specialists.
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Biomedical subjects
Publications and source records attributed to E Murray.
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Since we started using ventricular assist devices (VAD) in July 1987 up to August 1993, 63 of 15,650 (0.4%) patients (pts) who underwent open heart surgery were supported postoperatively by VAD at out institution. Forty-three were male and 20 female, mean age 55.5 years. In 49 pts coronary artery bypass grafting (CABG), in 8 pts valve surgery, in 3 pts combined CABG and valve surgery and in 3 pts corrective procedures for congenital heart disease were performed. Perioperative myocardial infarction was the most frequent indication (73%). In 37 of the 63 pts (58.7%) a centrifugal (Biomedicus pump (group A) was used and in 26 pts (41.3%) a pulsatile Abiomed BVS 5000 (group B). Fourteen of 37 pts (38%) in group A were weaned from the VAD and all of them were discharged. Twenty-three pts were unable to be weaned and 19 of these pts died. The remaining 4 pts were transplanted successfully and subsequently 3 died and 1 was discharged. In all, 15 pts (39%) were long-term survivors. Sixteen of 26 pts (62%) in group B were weaned from VAD and 13 (50%) of them were discharged of whom 3 died. Ten patients were unable to be weaned and 7 of these died. The remaining 3 pts were transplanted successfully. In all, 16 pts (61.5%) were long-term survivors. The shorter the interval between beginning resuscitation and application of VAD the better the outcome. Younger age, VAD installation in OR, support time between 2 and 7 days and Abiomed pump, influence the survival rate positively.(ABSTRACT TRUNCATED AT 250 WORDS)
A new restriction endonuclease, Bsp24I, from Bacillus species 24, recognizing: [formula: see text] has been isolated. Its specificity and cleavage points were determined.
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The effects of 1,25-dihydroxyvitamin D3 [1,25(OH)2,D3], 1,25-dihydroxy-16ene-23yne-vitamin D3[1,25(OH)2-16ene-23yne-D3] (a synthetic analog) and retinoic acid on proliferation, protein synthesis, and alkaline phosphatase activity and mRNA were compared in two late-passage (P > 70) clonal rat osteoblastic cell lines (G2 and C12) in order to characterize variations in the basal and hormonally-regulated phenotypes. All agents inhibited proliferation (measured as cell number after 3 days of treatment) in late-passage (P > 70) G2 and C12 cells without inhibiting the rate of protein synthesis ([3H]leucine incorporation into TCA-precipitable protein) during the last 18 h of incubation. Basal and hormone-treated alkaline phosphatase activities were lower in late-passage G2 and C12 cells than those previously reported for early-passage G2 and C12 cells. 1,25(OH)2D3 and 1,25(OH)2-16ene-23yne-D3, up-regulated alkaline phosphatase activity in late-passage C12 cells and down-regulated it in late-passage G2 cells. The direction of these regulatory changes in late-passage cells was opposite to that reported for early passage of these clones, and changes were related to the levels of tissue-unspecific alkaline phosphatase mRNA normalized for actin mRNA. Effects of 1,25(OH)2D3 or 1,25(OH)2-16ene-23yne-D3 and retinoic acid were not additive, suggesting a competitive mechanism of action. It appears that increased sensitivity to the antiproliferative effects of regulatory hormones and defects in proliferation and specialization of the osteoblast are observed with increasing passage number in vitro in two model osteoblastic cell lines (G2 and C12).
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Injuries to the brachial plexus and subclavian artery are serious complications of shoulder girdle trauma. Due to the close anatomical relationship between the brachial plexus and the subclavian artery in the thoracic outlet, both structures are often simultaneously involved in shoulder girdle injuries. Isolated lesions of the subclavian artery or the brachial plexus can also occur, especially with clavicular fractures. When a false subclavian aneurysm leads to a gradually increasing compression of the brachial plexus, the neurological signs and symptoms develop insidiously after the traumatic event.
The objective was to determine the current use of their general practitioner (GP) by patients with human immunodeficiency virus (HIV) infection and whether such patients would be interested in having 'shared care' between a specialist HIV clinic and their GP. A questionnaire was administered to 203 HIV-positive men attending the HIV outpatient clinic of a central London teaching hospital. The main outcome measures were patient characteristics, numbers of patients registered with a GP, numbers of patients with a GP aware of their diagnosis, contacts with the GP in the last year and level of interest and shared care. Eighty-five per cent of patients were registered with a GP of whom 67% knew of the diagnosis. Those diagnosed for more than 2 years were significantly more likely to have an informed GP. A total of 73% of those registered had visited their GP in the previous year although only 27% had visited for an HIV-related problem. Only 19% had a GP actively involved in their HIV care. In all 51% of the patients indicated an interest in having shared care between the clinic and their GP. A high proportion of HIV patients are registered with and attend a GP although they rarely consult for HIV-related problems. A significant proportion of patients expressed interest in having shared care suggesting that there is the potential for increased GP involvement in the care of patients with HIV infection.
OBJECTIVE: A total of 50 major bile duct injuries after laparoscopic cholecystectomy were managed by the Duke University Hepatobiliary Service from 1990-1992. The management of these complex cases is reviewed. SUMMARY BACKGROUND DATA: Laparoscopic cholecystectomy is the preferred method for removing the gallbladder. Bile duct injury is the most feared complication of the new procedure. METHODS: Review of videotapes, pathology, and management of the original operations were reviewed retrospectively, and the injuries categorized. Major biliary injury was defined as a recognized disruption of any part of the major extrahepatic biliary system. Biliary leakage was defined as a clinically significant biliary fistula in the absence of major biliary injury, i.e., with an intact extrahepatic biliary system. RESULTS: Thirty-eight injuries were major biliary ductal injuries and 12 patients had simple biliary leakage. Twenty-four patients had the classic type injury or some variant of the classic injury. A standard treatment approach was developed which consisted of ERCP for diagnosis, preoperative PTC with the placement of stents, CT drainage immediately after the PTC for drainage of biliary ascites, and usually Roux-en-Y hepaticojejunostomy with placement of O-rings for future biliary access if necessary. Major ductal injuries were high in the biliary system involving multiple ducts in 31 of the 38 patients. Re-operation was required in 5 of the 38 patients with particularly complex problems. CONCLUSIONS: Successful management of bile duct injury after laparoscopic cholecystectomy requires careful understanding of the mechanisms, considerable preoperative assessment by experts, and a multidisciplinary approach.
The pattern of expression of GFAP immunoreactivity in astrocytes of the juvenile rhesus monkey cortex was examined following infection with simian immunodeficiency virus (SIV). Blocks of cerebral cortex plus subjacent white matter from saline- and formalin-perfused brain were examined by peroxidase-linked immunochemical and immunofluorescence staining of deparaffinized sections. Strong GFAP immunoreactivity was found in astrocytic cells in both uninfected and SIV-infected juvenile macaque in the subpial cerebral cortex and in subcortical white matter, where GFAP-positive cells were abundant. GFAP staining of cortical layers 2-6 on the other hand was weak or absent in three uninfected controls and one infected animal without cognitive impairment, but moderate to strong in animals productively infected with SIV that demonstrated cognitive and/or motor impairment. These data demonstrate a cortical locus of astrocytic activation in rhesus monkeys infected with primate immunodeficiency virus isolate SIVB670 which, like HIV-1 in man, causes motor/cognitive impairment as well as immunodeficiency disease.
In a survey of a healthy population (n = 197), LDL cholesterol, plasma triglycerides and VLDL triglycerides were found to be substantially increased and plasma HDL cholesterol decreased in smokers. The lipid-associated atherogenic risk in smokers as assessed by the LDL/HDL ratio was significantly higher [2.89 (SD 1.18, n = 63)] than in non-smokers [2.38 (SD 0.98, n = 86) P < 0.01]. The lower HDL level found in smokers was explained by a lower HDL-2 subfraction as determined by analytical ultracentrifugation. HDL 2b, 2a and 3a, measured by gradient gel electrophoresis, were all lower in the smokers but this was only significant for HDL 2a. Smoking had no effect on Lp(a) levels. HDL cholesterol and HDL-2 were strongly negatively correlated whereas LDL cholesterol and LDL/HDL ratio were strongly positively correlated with the plasma triglyceride concentration. There was a small but significant reduction in plasma CETP activity [non-smokers 49% t/microliter (SD 17, n = 90), smokers 43% t/microliter (SD 17, n = 66) P < 0.05] but CETP activity was not correlated with any measure of HDL in this population. Smoking was found to be an important independent contributor to the variation in plasma triglyceride, HDL, HDL-2 and LDL/HDL ratio. After correcting for sex, age, BMI, alcohol consumption, oral contraceptive use and plasma triglycerides smoking was still found to be significantly associated with HDL and the LDL/HDL ratio. Upon adjustment for covariant factors the mean differences between smokers and non-smokers for HDL cholesterol, HDL-2 and LDL/HDL were 0.15 mM, 16 mg dl-1 and 0.39 respectively. There appeared to be important sex differences in the influence of smoking on plasma lipoproteins. In women the main impact of smoking was on triglyceride levels and they in turn affected LDL and HDL. In contrast, in men, smoking had little impact on triglycerides and affected HDL more directly. We conclude that smoking cigarettes has an important effect on plasma lipoprotein metabolism through multiple mechanisms.
Metabolic heterogeneity in low density lipoprotein (LDL) may be detected by examination of the daily urinary excretion rate of radioactivity after injection of trace-labeled lipoprotein. Two distinct pools are observed within LDL. The first (pool A) is cleared rapidly from the plasma, whereas the second (pool B) is catabolized more slowly. In the present study we examined LDL metabolism in seven hypercholesterolemic subjects (six women and one man) before and during fenofibrate therapy. Comparison with normocholesterolemic individuals showed that the pretreatment high LDL levels in the hypercholesterolemic subjects resulted from an accumulation of apoprotein-LDL (apo-LDL) mass in pool B (2,077 +/- 174 mg versus 787 +/- 70 mg in normal subjects, p < 0.002). Pool A apo-LDL was present at normal levels (approximately 1,000 mg), although its fractional catabolic rate was reduced (0.39 +/- 0.06 versus 0.61 +/- 0.03 pool/day in normal subjects, p < 0.01). Fenofibrate therapy (100 mg t.i.d. for 8 weeks) produced substantial reductions in plasma cholesterol (29%; p < 0.001), triglycerides (36%; p < 0.001), and LDL cholesterol (30%; p < 0.001). The latter was associated with a 30% decrease in circulating apo-LDL mass (2,312 +/- 200 mg versus 3,279 +/- 264 mg before treatment, p < 0.005). This resulted from a combination of two effects. First, although overall LDL apoprotein B production did not change, there was a shift from pool B to pool A. Pool A input was 400 +/- 74 mg/day pretreatment versus 706 +/- 62 mg/day on fenofibrate; pool B input was 422 +/- 35 mg/day pretreatment versus 258 +/- 41 mg/day on the drug. At the same time, catabolism of pool A rose from 0.39 +/- 0.06 to 0.66 +/- 0.08 pool/day (p < 0.05). We hypothesize that the shift from pool B to pool A resulted from a drug-induced decrease in the particle size of very low density lipoprotein made by the liver, which in turn favored the formation of more rapidly catabolized LDL. Overall, the rate of apo-LDL degradation by the receptor route (as detected using a combination of native and 1,2-cyclohexanedione-modified LDL tracers) rose 43% on the drug, whereas the amount cleared by the receptor-independent pathway did not change. Fenofibrate, therefore, appears not only to promote LDL catabolism via the receptor-mediated pathway but also, by lowering plasma triglyceride levels, inhibits the formation of slowly metabolized, potentially atherogenic LDL particles.
Between January 1988 and January 1992, 65 patients (pts) had a ventricle assist device (VAD) inserted in our clinic. In 24 pts a VAD was applied because of primarily unsuccessful weaning from cardiopulmonary bypass (Group A). In a further 24 pts (Group B) a VAD was installed for the therapy of refractive cardiogenic shock (CS) after initially successful cardiac surgery (n = 21) and after acute myocardial infarction (n = 3). Twelve pts were bridged to heart transplantation (Group C) and five had a VAD inserted for various other reasons (Group D). In 36 (55.4%) of the total 65 pts a nonpulsatile VAD (Biomedicus 540) was used: 10 in Group A; 20 in B, 3 in C and 3 in D. In 29 pts (44.6%) a pulsatile VAD (Abiomed BVS 5000) was used: 14 in Group A, 4 in B, 9 in C and 2 in D. Weaning rate and long-term survival rates were 50% and 46% respectively in Group A and 38% and 42% in Group B. Seven pts from Group C were transplanted and six are long-term survivors. Two pts (40%) in Group D were discharged from hospital. Major postoperative complications were bleeding (46%), thromboembolism (14%), multiple organ failure (11%), renal failure (11%), arterial embolism (4.6%), sepsis (3%). The results indicate that application of a VAD can be recommended in pts with postcardiotomy CS to allow recovery of cardiac function and in pts with irreversible ventricular damage as bridging to HTX.
Butorphanol was compared with fentanyl as the narcotic component of general anaesthesia for ambulatory laparoscopic surgery. This double-blind, randomized study enrolled 60 healthy women who received equianalgesic doses of fentanyl 1 microgram.kg-1 (F, n = 30) or butorphanol 20 micrograms.kg-1 (B, n = 30) prior to induction of anaesthesia. Tracheal anaesthesia was maintained with nitrous oxide/oxygen, isoflurane, and succinylcholine by infusion. Intraoperatively, patients who received B demonstrated lower pulse rate before and after intubation (P less than 0.05, P less than 0.01) and lower diastolic blood pressure after intubation (P less than 0.01). Anesthesiologists judged the maintenance phase as satisfactory more often with B (P less than 0.05). Postoperatively, there were no differences in analgesic need. No major side-effects occurred in either group. Among minor side-effects, patients who received B reported postoperative sedation more often, 77% vs 37% (P less than 0.01), which occurred during the first 45 min of recovery (P less than 0.05). Discharge times were not different. On the first postoperative day, more subjects who received B were satisfied with their anaesthesia experience (P less than 0.05). Butorphanol 20 micrograms.kg-1 is an acceptable alternative analgesic in general anaesthesia for ambulatory laparoscopy.
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