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Biomedical subjects

G Alexander

Publications and source records attributed to G Alexander.

At least 73 records · Page 4Linked to original sources
PubMed1994

THE SHIFT IN VISUAL PIGMENT DOMINANCE IN THE RETINAE OF JUVENILE COHO SALMON (ONCORHYNCHUS KISUTCH): AN INDICATOR OF SMOLT STATUS

Smolting juvenile coho salmon were sampled to determine (1) whether a correlation between hypo-osmoregulatory ability and visual pigment composition existed and (2) whether the hormone 3,5,3'-tri-iodothyronine (T3) was playing a role in the visual pigment conversion process. Plasma sodium levels of seawater-challenged fish (30 ) indicated that there was a 5 week period of optimal ability to excrete excess plasma sodium ions (hypo-osmoregulation) in the late spring/early summer that represented the 'window of opportunity' for the entry or introduction to sea water of the salmon. Early in the smoltification process, the vitamin-A2-based visual pigment porphyropsin increased its dominance in the retinae, and radioimmunoassay of plasma indicated that T3 levels were at a maximum prior to this increase in porphyropsin. As the parr­smolt transformation continued, there was a steady decrease in the relative amounts of porphyropsin, indicating that the retinae were favouring the acquisition of rhodopsin. Rhodopsin dominance virtually coincided with the period of best hypo-osmoregulatory ability. Subsequently, the salmon showed a loss of hypo-osmoregulatory ability and concomitant increases in the amount of porphyropsin in the retina were observed. The relationship between the visual pigment shift and the smoltification process is discussed in terms of preparation for migration and thyroid hormone involvement, and the use of retinal visual pigment composition as an index of smolt status is proposed.

Journal Article↗
PubMed1993

Liver transplantation in European patients with the hepatitis B surface antigen.

BACKGROUND: The role of liver transplantation in patients positive for the hepatitis B surface antigen (HBsAg) is controversial because of the high rate of recurrent hepatitis B virus (HBV) infection. It has not been determined whether this risk is greater for certain patients and whether the administration of anti-hepatitis B surface antigen (anti-HBs) immune globulin is beneficial. METHODS: We conducted a retrospective study at 17 European centers of 372 consecutive HBsAg-positive patients who underwent liver transplantation between 1977 and 1990. Recurrence of HBV infection was defined as the reappearance of HBsAg in serum. RESULTS: For all 334 patients with follow-up data, the mean (+/- SE) three-year actuarial risk of recurrence of HBV was 50 +/- 3 percent. The risk was 67 +/- 4 percent among 163 patients with HBV-related cirrhosis, 32 +/- 5 percent among 110 patients with cirrhosis related to hepatitis delta virus, 40 +/- 16 percent among 14 patients with fulminant hepatitis delta infection, and 17 +/- 7 percent among 39 patients with fulminant HBV infection (P < 0.001). Among the patients with HBV-related cirrhosis, the risk of HBV recurrence was greatest (83 +/- 6 percent) in those who were seropositive for HBV DNA at the transplantation and lowest (58 +/- 7 percent) in those with neither HBV DNA nor hepatitis B e antigen detectable in serum. With respect to the use of passive prophylaxis with anti-HBs immune globulin, the risk of HBV recurrence was 75 +/- 6 percent among the 67 patients given no immunoprophylaxis, 74 +/- 5 percent among the 83 treated for two months, and 36 +/- 4 percent among the 209 treated for six months or longer (P < 0.001). In a multivariate analysis the predictors of a lower risk of HBV recurrence were the long-term administration of the immune globulin, hepatitis delta virus superinfection, and acute liver disease. For the entire study cohort, survival was 75 percent at one year and 63 percent at three years, but for those in whom HBV infection recurred, survival was 68 percent at one year and 44 percent at three years. CONCLUSIONS: In this retrospective study of HBsAg-positive patients, liver transplantation had better results in those who had fulminant hepatitis or delta virus superinfection. An absence of viral replication at the time of transplantation and long-term immunoprophylaxis were associated with a reduced risk of recurrent HBV infection and reduced mortality.

Actuarial Analysis↗
PubMed1992

Activation of the classical complement pathway in spontaneous bacterial peritonitis.

To investigate the possibility that low complement concentrations in the plasma and ascites of patients with severe liver disease could be secondary to complement consumption, complement activation was studied in 32 patients with severe liver disease, 11 of whom had spontaneous bacterial peritonitis (SBP). In patients with SBP, plasma C3 and C4 were significantly lower than in uninfected patients (mean values 0.74 v 1.13 g/l, p less than 0.01 and 0.20 v 0.28 g/l, p less than 0.05 respectively). Plasma complement activation via the classical pathway, as shown by C4d/C4, was significantly increased in patients with SBP compared with uninfected patients (37.3 v 22.2, p less than 0.01) as was C3d/C3 (14.0 v 8.11, p less than 0.01), but there was no significant difference in Ba/B between SBP and uninfected patients. Ascitic C3 concentrations were higher in patients without SBP than in infected patients (0.37 v 0.08 g/l, p less than 0.05), as were factor B values (0.11 v 0.03 g/l, p less than 0.05). There was no significant difference in ascitic C4 concentrations in patients with SBP compared with uninfected patients (0.03 v 0.07 g/l). Although consumption of C3, as shown by C3d/C3 in ascites, was increased in infected patients compared with uninfected patients (79.1 v 36.1, p less than 0.05), there was no difference in ascitic complement activation between the groups for either the classical or alternative pathways. In SBP, decreased plasma C3 and C4 are primarily caused by increased activation of the classical pathway and not impaired hepatic synthesis. Activation and consumption of C3 is one factor causing the low ascitic C3 concentrations observed in SBP.

Adult↗
PubMed1992

Lead exposure and child behavior.

OBJECTIVES: Unlike cognitive impairments associated with lead exposure, lead-associated child behavior problems have been difficult to specify, particularly in young children. METHODS: The Child Behavior Checklist (CBCL) and the Center for Epidemiologic Studies Depression Scale were used as the outcome and confounding variables, respectively, of major interest. These measures were examined with respect to blood lead levels of 201 African-American children aged 2 through 5 years. RESULTS: In comparison with the low exposed group, the high exposed group (two consecutive blood lead levels greater than or equal to 15 micrograms/dL) had a significantly higher mean CBCL Total Behavior Problem Score (TBPS) and Internalizing and Externalizing scores; when other factors, including maternal depressive symptomatology, were controlled for, regression procedures indicated a .18-point TBPS increase for each unit increase in lead and a 5.1-point higher TBPS in the high exposed group; children in this group were 2.7 times more likely to have a TBPS in the clinical range. CONCLUSIONS: Through its use of a standardized parent-report measure of behavior and its consideration of maternal morale in multiple linear and logistic regression procedures, this study provides further evidence of lead's detrimental effect on child behavior at levels typical of present-day exposure.

Academies and Institutes↗
PubMed1992

Moving from health care research to action.

Although the United States spends more on health care than any country in the world, access to that care is becoming increasingly difficult. The National Cancer Institute and other federal agencies are sponsoring innovative research for delivering effective medical services, particularly to underserved populations. Models of successful collaboration between private and public sectors concerned with health care can be adapted and implemented at the national, state, and local levels. However, other measures are needed to ensure access to adequate health care for all Americans. Minimal but effective regulations are needed to ensure quality control, reduce duplication of services, and minimize cost increases. Public and private sectors also need to consider ways to extend adequate health insurance coverage to all Americans and to provide compensation for preventive services.

Cost Control↗
PubMed1991

Fungal infection: a common, unrecognised complication of acute liver failure.

The true incidence and clinical relevance of fungal infection was ascertained in a prospective study of 50 consecutive patients with acute liver failure. Fungal infection was present in 16 (32%) patients (15 candida, one aspergillus) and in seven was considered the major cause of death. All six untreated died, while five of ten patients treated with anti-fungal therapy survived. The diagnosis was made on positive cultures from at least one significant site or on histological evidence of tissue invasion. All 16 had concomitant bacterial infection and shared features suggestive of a clinical syndrome: deterioration in coma grade after initial improvement; pyrexia unresponsive to antibiotics; established renal failure; and a markedly elevated white cell count. Fungal infection is a common, serious complication of acute liver failure and therapy is indicated for those with positive cultures. A prophylactic trial would be justified in those surviving 5 days, especially, with established renal failure.

Acute Disease↗
PubMed1991

Arterial-venous pH differences and tissue hypoxia in patients with fulminant hepatic failure.

OBJECTIVE: A recent report suggested that, for hypotensive patients, tissue acidemia is best monitored by simultaneous estimates of arterial pH, mixed venous pH, and bicarbonate. This method of detecting tissue acidemia may therefore apply to fulminant hepatic failure patients, who are known to have a high frequency of covert tissue hypoxia. In the present study, both arterial pH and mixed venous pH and bicarbonate were compared in 22 patients with fulminant hepatic failure. Blood samples were drawn from the pulmonary artery and radial artery and this blood was analyzed to determine oxygen delivery and consumption. The arterial pH, mixed venous pH, and bicarbonate were compared using an oxygen flux test to determine the optimal method of demonstrating tissue hypoxia in this group of patients. DESIGN: A prospective study. SETTING: The Liver Unit of our institution. PATIENTS: Patients (n = 22) with fulminant hepatic failure admitted between January 1989 and January 1990. INTERVENTIONS: Patients were studied before and after an infusion of prostacyclin. MEASUREMENTS AND RESULTS: The findings of this study suggest that pH and bicarbonate differences in arterial and mixed venous blood samples were not indicative of tissue hypoxia in patients with fulminant hepatic failure. By contrast, measurement of oxygen consumption after the infusion of prostacyclin, with the demonstrated increase in oxygen uptake, provided a more accurate indication of covert tissue hypoxia. CONCLUSIONS: In critically ill patients with a hyperdynamic circulation, such as those patients with fulminant hepatic failure, an oxygen flux test remains the best method of determining the presence of covert tissue hypoxia.

Acid-Base Equilibrium↗
PubMed1991

Orthotopic liver transplantation at Addenbrooke's Hospital Cambridge 1968 to 1991.

Liver grafting is now established as the optimal treatment for patients with end-stage parenchymal liver disease. Twenty-three years of experience at a single center is presented. The 1-year actuarial patient survival rate for all cases transplanted in Cambridge has now risen from 10% in 1968 to 1970 to 80% in 1990 to 1991. Increasing numbers of patients are being referred for transplantation with an ever-increasing range of indications being developed. Many inborn errors of metabolism can now be cured by liver grafting. There is still, however, considerable scope for improvement in many areas of patient treatment from operative and postoperative care to long-term immunosuppressive management. Much remains to be done to minimize early sepsis- and rejection-related deaths and late immunosuppression-related morbidity.

Actuarial Analysis↗
PubMed1991

Intracranial and cerebral perfusion pressure changes before, during and immediately after orthotopic liver transplantation for fulminant hepatic failure.

Several centres that perform liver transplantation for fulminant hepatic failure have experience of patients who have not regained consciousness despite adequate graft function. In some of these, decerebration because of elevation in intracranial pressure was thought to have occurred intraoperatively or in the early post-operative period. In the present study six patients with fulminant hepatic failure who were transplanted had extradural monitors inserted before operation. Intracranial pressure had been controlled prior to transplantation and rose during the pre-clamp phase of the operation. Levels fell during the anhepatic phase but rose again during the reperfusion phase (p = 0.033). Overall, from the induction of anaesthesia to the reperfusion phase there was a significant increase in mean intracranial pressure (p less than 0.01). The cerebral perfusion pressure fell after induction of anaesthesia from a median 54 mmHg (range 46-62) to a median 35 mmHg (range 19-49, p less than 0.001) in the pre-clamp phase and remained low throughout the operation. During the first 10 hours after transplantation, three patients had further episodes of intracranial hypertension requiring treatment and it is important that monitoring should be continued through this period.

Adolescent↗
PubMed1991

Elevated plasma interleukin-6 and increased severity and mortality in alcoholic hepatitis.

Recent studies in alcoholic hepatitis have proposed a role for the cytokine tumour necrosis factor-alpha (TNF-alpha) a mediator of endotoxic shock in sepsis. In this study plasma levels of the closely related cytokine interleukin-6 (IL-6) were assayed in 96 samples from 58 patients with severe alcoholic hepatitis, and 69 patients in control groups (21 normal, 10 alcoholic without liver disease, 10 inactive alcoholic cirrhosis, 18 chronic liver disease, 10 chronic renal failure). Plasma IL-6 levels were markedly elevated in patients with alcoholic hepatitis when compared with all control groups (P less than 0.001). IL-6 levels were higher in patients who died (P = 0.04) and correlated with the features of severe disease including: increased grade of encephalopathy, increased neutrophil count, increased prothrombin ratio, hypotension, increased serum creatinine and increased serum bilirubin. Surprisingly, no correlation was found between levels of plasma IL-6 and plasma TNF-alpha or endotoxin, or the presence of infection; an inverse correlation was found between plasma IL-6 and serum globulins. These findings provide further evidence that the IL-6/TNF cytokine system is activated in severe alcoholic hepatitis and may mediate hepatic or extra-hepatic tissue damage.

Adult↗
PubMed1990

Prospective study of bacterial infection in acute liver failure: an analysis of fifty patients.

Fifty consecutive patients admitted with acute liver failure, minimal grade II encephalopathy, were studied prospectively to determine the incidence, timing and cause of bacterial infection, the relationship to clinical criteria for infection; and the influence of early microbiological diagnosis on clinical outcome. There were 53 proven bacterial infections in 40 patients, whereas in 5 of the remaining 10 patients infection was suspected on clinical grounds in the absence of significant cultures. Seven patients (14%) had more than one bacterial infection, and four patients had simultaneous infections caused by different organisms at each site. Fourteen infections (26.4%) were associated with bacteremia, and in six of these no source was found. Twenty-five infections (47.1%) arose from the respiratory tract, 12 (22.6%) from the urinary tract and 2 (3.7%) from central venous cannulas. Thirty-seven (69.8%) of the 53 infections were due to gram-positive bacteria; Staphylococcus aureus accounted for 19 (35.8%) of all the infections. Thirty patients died (60%), 28 of whom had bacterial infection at some time; in 24 of these the infection was diagnosed less than 24 hr before death. All nine deaths that occurred more than 7 days after admission were directly attributable to microbial infection. Clinical features such as elevated temperature and elevated peripheral white blood cell count were poor indicators of bacterial infection because these were absent in 30.2% of cases. These data show that there is a high incidence of bacterial infection early in the course of acute liver failure and suggest that prophylactic antimicrobial therapy, although unproven, might be justified.

Acute Disease↗