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E E Powell

Publications and source records attributed to E E Powell.

At least 37 records · Page 2Linked to original sources

North Carolina mosquito records. I. Uncommon Aedes and Anopheles (Diptera: Culicidae).

New distribution records are provided for 10 mosquito species that are rare or uncommon in North Carolina: Aedes aegypti, Ae. cinereus, Ae. dupreei, Ae. fulvus pallens, Ae. hendersoni, Ae. mitchellae, Ae. thibaulti, Ae. tormentor, Ae. trivittatus, and Anopheles atropos. Biological notes are provided for habitats, behavior, and, in some cases, color patterns. Comments are also made about 6 additional species that are rare or uncommon in North Carolina.

Aedes↗

Peripheral blood chimerism following human liver transplantation.

The aim of this study was to prospectively investigate the peak levels and kinetics of donor leucocyte chimerism in human recipients following liver transplantation. The peak levels of chimerism were observed within the first 48 hours following transplantation and ranged from 0.15% to 20% of total peripheral blood mononuclear cells. In all but one patient, who developed graft versus host disease, there was an early peak level of chimerism that declined over time such that donor leukocytes were only intermittently detectable after 3 to 4 weeks. In 8 patients who had no episodes of graft rejection, the peak level of donor leukocyte chimerism ranged from 1.3% to 20% (mean +/- SEM; 5.5% +/- 2.1%). In 3 patients who were treated for episodes of acute graft rejection during the first four postoperative weeks, the peak level of donor leukocyte chimerism ranged from 0.15% to 0.2% (0.18 +/- 0.02, P = .012). The results demonstrate a marked variation in the total number of donor leukocytes detectable in the peripheral blood early after liver transplantation and also, that lower levels of chimerism may be associated with lower rates of initial graft acceptance and a higher incidence of acute rejection.

Adult↗

Human liver transplant perfusate: an abundant source of donor liver-associated leukocytes.

In vitro studies designed to examine the mechanisms of immune tolerance after liver transplantation in humans have been hampered by the difficulty in obtaining sufficient numbers of donor liver-associated leukocytes (LALs). We have investigated whether the ex vivo perfusion of donor livers releases a population of LALs that can be readily retrieved from the waste fluid. The mean number of cells recovered after Ficoll-Hypaque density-gradient separation was 2.6 +/- 0.5 x 10(8) cells, with a viability of 94% +/- 2%. The perfusate lymphocytes comprised mainly T cells (39% +/- 2%) with a very low CD4/CD8 ratio and natural killer (NK) cells (56% +/- 6%) with an increase in the proportion of the CD3-CD56+CD16- subset. The activation marker CD69 was present on the majority of the perfusate lymphocytes. These are the phenotypic characteristics that have been previously reported for lymphocytes isolated from hepatic sinusoids. In mixed lymphocyte reactions, the perfusate cells showed a marked increase in the ability to stimulate allogeneic responder cells, resulting in 353% +/- 78% (P = .003) greater incorporation of [3H]thymidine in responder cells when compared with stimulation by donor peripheral blood mononuclear cells. The results show that large numbers of viable donor lymphocytes can be readily isolated from the liver perfusate solution. These cells have the characteristics of liver-associated lymphocytes with a predominance of activated NK and CD8+ T cells. This population can now be used in in vitro assays to elucidate the influence of donor leukocytes on the development of graft acceptance.

Humans↗

Serum soluble CD23 but not IL8, IL10, GM-CSF, or IFN-gamma is elevated in patients with hepatitis C infection.

The increased frequency of autoantibodies and B cell non-Hodgkins lymphoma (B-NHL) in hepatitis C virus (HCV) infection suggests dysregulated humoral immunity. Soluble CD23 (sCD23) is involved in B cell activation and proliferation and the serum levels are raised in autoimmune diseases and B cell lymphoproliferative disease. We compared the serum levels of sCD23 in patients with HCV infection with those in patients with alcoholic cirrhosis (AC) and in healthy controls. Serum levels of interleukin (IL) 8, IL10, granulocyte macrophage-colony stimulating factor, and interferon-gamma were assessed simultaneously to check for generalized nonspecific immune stimulation. In contrast to the essentially normal serum levels of these latter cytokines, the levels of sCD23 were raised in the patients with HCV compared to those with AC and the normal controls (medians 34.0, 10.1, and 11.1 arbitrary units, respectively; HCV vs AC P < 0.0004, HCV vs controls P < 0.0001, AC vs controls P > 0.8). These results confirm HCV-induced humoral immune dysregulation and invite comparison with primary Sjögrens syndrome and Epstein-Barr virus infection, both of which are also associated with raised levels of serum sCD23, autoantibodies, and B-NHL.

Adult↗

Relative abundance and species composition of mosquito populations (Diptera:Culicidae) in a La Crosse virus-endemic area in western North Carolina.

Container surveys were conducted in 5 communities on the Cherokee Indian Reservation, an area of western North Carolina endemic for transmission of La Crosse (LAC) virus, to determine the potential for peridomestic mosquito breeding, the relative abundance of mosquito species, and the standing crop of mosquitoes per residence. Eleven species of mosquitoes were collected, but 80.9% of all mosquitoes reared from containers were Aedes triseriatus (Say). All communities averaged > 6 containers per residence, indicating that the potential for mosquito production was high. The Breteau index and mean standing crop of adults per residence in the 5 communities were highly concordant. LAC virus was isolated from 2 pools of 56 female and 36 male Ae. triseriatus adults that were reared from eggs collected by ovitraps. The minimum field infection rate was 0.26 per 1,000 adults tested. Aedes triseriatus, the most frequently collected blood-fed mosquito (98/112 blood-engorged specimens), fed predominantly on dogs (40.4%), rabbits (26.6%), and turtles (22.3%). Only 7.5% of the blood-fed mosquitoes had fed on eastern chipmunks. Peridomestic conditions on the Reservation appear to contribute to the maintenance of LAC virus transmission. Production of Ae. triseriatus occurs in artificial containers discarded around residences, and wooded areas immediately adjacent to residences provide resting cover for mosquitoes as well as suitable habitat for LAC virus reservoir hosts.

Aedes↗

Seasonal occurrence and abundance of Aedes triseriatus and other mosquitoes in a La Crosse virus-endemic area in western North Carolina.

The species composition and population abundance of mosquitoes were investigated from May to November in 1989 and 1990 on the Cherokee Indian Reservation, an area of western North Carolina endemic for transmission of La Crosse (LAC) virus. Mosquitoes representing 6 genera and 13 species were collected. Aedes triseriatus was the most abundant species collected, comprising over 98% of mosquitoes collected by ovitrapping and CO2-baited suction trapping, and 88% of resting adults collected by vacuuming vegetation and leaf litter. Culex restuans and Anopheles punctipennis were common but much less frequently collected. Host-seeking and resting Ae. triseriatus were most abundant in early to midsummer, whereas gravid Ae. triseriatus was most active in the fall. The previous occurrence of cases of LAC encephalitis was concordant with the seasonal activity of gravid but not host-seeking or resting Ae. triseriatus.

Aedes↗

Susceptibility to human type 1 diabetes at IDDM2 is determined by tandem repeat variation at the insulin gene minisatellite locus.

The IDDM2 locus encoding susceptibility to type 1 diabetes was mapped previously to a 4.1-kb region spanning the insulin gene and a minisatellite or variable number of tandem repeats (VNTR) locus on human chromosome 11p15.5. By 'cross-match' haplotype analysis and linkage disequilibrium mapping, we have mapped the mutation IDDM2 to within the VNTR itself. Other polymorphisms were systematically excluded as primary disease determinants. Transmission of IDDM2 may be influenced by parent-of-origin phenomena. Although we show that the insulin gene is expressed biallelically in the adult pancreas, we present preliminary evidence that the level of transcription in vivo is correlated with allelic variation within the VNTR. Allelic variation at VNTRs may play an important general role in human disease.

Adult↗

Crosses of NOD mice with the related NON strain. A polygenic model for IDDM.

Chromosome locations of non-major histocompatibility complex (MHC) genes contributing to insulin-dependent diabetes mellitus (IDDM) in mice have been determined by outcrossing NOD mice to other inbred strains congenic for the NOD MHC haplotype (H2g7). At least nine non-MHC IDDM susceptibility genes (Idd) were previously identified at first backcross (BC1) after outcross of NOD to C57BL/10.H2g7 congenic mice (B10.H2g7). We investigated whether the same set of Idd loci segregated with IDDM susceptibility after outcross of NOD to NON.H2g7 congenic mice. Since the outcrosses to NON.H2g7 and B10.H2g7 were performed in the same vivarium, direct comparisons were made of the chromosomal locations and relative strengths of Idd alleles in diabetic progeny from the two different outcrosses. In comparison with the NOD x B10.H2g7 outcross, the NOD x NON.H2g7 outcross produced significantly higher IDDM frequencies in F1, F2, and BC1 generations. The high F2 diabetes frequency allowed evaluation of the effects of homozygous expression of both the susceptibility and the resistance allele at Idd loci. This analysis demonstrated that no single non-MHC Idd locus was essential for the onset of diabetes in this cross. After outcross to NON.H2g7, Idd4 (chromosome [Chr] 11), Idd5 (Chr 1), and Idd8 (Chr 14) did not segregate with IDDM in either the BC1 or the F2 generation. Diabetogenic NOD-derived alleles at Idd2 (Chr 9), Idd3 (Chr 3), and Idd10 (Chr 3) were segregating in the BC1. An NON-derived allele contributing to susceptibility on Chr 7 (Idd7) was also detected. Dominant traits, detectable only in the F2 cross, were encoded by Chr 4 (Idd9) and two newly mapped loci on Chr 13 (Idd14) and 5 (Idd15). A third dominant trait was encoded by Chr 6 (possibly Idd6), but here, in contrast to Idd9, Idd14, and Idd15, the NON allele was diabetogenic. Stepwise logistic regression analysis of the BC1 and F2 data confirmed that the ability to identify certainty of the non-MHC Idd loci was contingent on the extent of homozygosity for NOD background genes. This study shows that the diabetogenic phenotype can be achieved through the actions of variable combinations of MHC-unlinked genes and a diabetogenic MHC haplotype.

Animals↗

Low density lipoprotein receptor and 3-hydroxy-3-methylglutaryl coenzyme A reductase gene expression in human mononuclear leukocytes is regulated coordinately and parallels gene expression in human liver.

The liver plays a key regulatory role in cholesterol metabolism. Two proteins are central in this role; the LDL receptor and 3-hydroxy-3-methylglutaryl CoA reductase (HMG CoA reductase), the rate-limiting enzyme in cholesterol biosynthesis. In the current investigation, we have used a sensitive nonradioactive method to study the regulation of LDL receptor and HMG CoA reductase mRNA levels in liver biopsy samples and freshly isolated mononuclear leukocytes from 13 patients who underwent cholecystectomy for gallstones. mRNA copy numbers were determined by PCR amplification of reverse-transcribed RNA using synthetic RNA as an internal standard. Incorporation of digoxigenin-11-dUTP during amplification allowed direct detection and quantitation of mRNA levels by chemiluminescence. These experiments showed that the average number of LDL receptor mRNA molecules in liver (21 +/- 3 x 10(4)/micrograms of RNA) and mononuclear leukocytes (24 +/- 3 x 10(4)/micrograms of RNA) are indistinguishable, whereas the number of HMG CoA reductase molecules in liver (107 +/- 15 x 10(4)/micrograms of RNA) is smaller than that in mononuclear leukocytes (158 +/- 21 x 10(4)/micrograms of RNA, P < 0.05). These numbers correspond to an average of 1-6 copies of LDL receptor mRNA and 5-42 copies of HMG CoA reductase mRNA per cell. There was a significant correlation between the numbers of LDL receptor (P = 0.0005) and HMG CoA reductase (P = 0.003) mRNA molecules in liver and mononuclear leukocytes. Furthermore, the numbers of copies of HMG CoA reductase and LDL receptor mRNA were correlated with each other in both liver (P = 0.02) and mononuclear leukocytes (P = 0.01), consistent with coordinate regulation. These data demonstrate that the mechanisms which regulate mRNA levels in liver and mononuclear cells are similar and suggest that freshly isolated mononuclear cells can be used to predict HMG CoA reductase and LDL receptor mRNA levels in liver.

Adult↗

Measurement of mRNA by quantitative PCR with a nonradioactive label.

This report describes the development of a method to measure mRNA in small samples of human tissue by the polymerase chain reaction with a nonradioactive label. In this method RNA is reverse-transcribed in the presence of a control RNA, and subsequently amplified by the polymerase chain reaction during which a nonradioactive label (digoxigenin-11-dUTP) is incorporated. Gel blotting and immunological detection of digoxigenin followed by a chemiluminescent reaction provide an intense signal on film. This allows the detection and quantitation of 3-hydroxy-3-methylglutaryl (HMG) CoA reductase mRNA in 12 ng of RNA. We demonstrate that this is a sensitive and reproducible method, and that quantitation is linear with respect to the amount of mRNA present. The application of this method to the measurement of low density lipoprotein receptor and 3-hydroxy-3-methylglutaryl coenzyme A reductase mRNA levels in circulating peripheral blood mononuclear cells and human liver biopsy samples is discussed. The use of chemiluminescent reagents instead of radioactive labels allows this procedure to be performed safely in laboratories not equipped for radioactivity.

Base Sequence↗

Markers of chronic alcohol ingestion in patients with nonalcoholic steatohepatitis: an aid to diagnosis.

We report here the use of the biochemical marker desialylated transferrin to aid in the diagnosis of nonalcoholic steatohepatitis. Conventional biochemical tests used for the detection of chronic alcohol consumption fail to differentiate nonalcoholic steatohepatitis patients from alcoholic subjects. In addition, even in those alcoholic subjects with alcoholic liver disease in whom biopsy has been performed, it is impossible to differentiate these two disease states on the basis of morphological examination alone. In this study we have examined two new markers of excessive alcohol intake, desialylated transferrin and mitochondrial AST in subjects with nonalcoholic steatohepatitis and in patients consuming excessive amounts of alcohol. All nonalcoholic steatohepatitis patients consumed minimal or no alcohol and were diagnosed by morphological criteria based on liver biopsy specimens. Alcoholic subjects were consuming in excess of 80 gm/day ethanol, often with clinical evidence of overt alcoholism. Control subjects included both healthy controls and patient controls with liver diseases unrelated to alcohol. The ratio of desialylated transferrin/total transferrin was elevated only in patients who consumed excessive amounts of alcohol, whereas the ratio of mitochondrial AST to total AST (mitochondrial AST/total AST) was not significantly different between alcoholic subjects and patients with nonalcoholic steatohepatitis. The sensitivity and specificity for the ratio desialylated transferrin/total transferrin was 81% and 98%, respectively, whereas the sensitivity for the mitochondrial AST/total AST ratio was 92%; the specificity was only 50%, indicating that there were a large number of false-positives. All the conventional markers were less sensitive and less specific than the ratio desialylated transferrin/total transferrin.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

The natural history of nonalcoholic steatohepatitis: a follow-up study of forty-two patients for up to 21 years.

Forty-two patients with nonalcoholic steatohepatitis were followed for a median of 4.5 yr (range = 1.5 to 21.5 yr). Except for two patients with lipodystrophy, all were obese; 35 of 42 were women, 26 of 32 were hyperlipidemic and 15 were hyperglycemic. Upper abdominal pain was the most common reason for presentation. Initial liver biopsy specimens showed the presence of macrovesicular fatty infiltration, lobular (acinar) inflammation, apoptosis, Mallory bodies (in four cases) and fibrosis (in 18 cases). Cirrhosis was present at initial diagnosis in one subject and in another two subjects liver biopsy showed marked fibrosis with disturbed architecture. Serial liver biopsy specimens revealed minimal or no apparent progression of the disorder in most of the patients, in keeping with their benign clinical course. However, one patient showed progression from fibrosis to cirrhosis during the 5-yr observation period, and in the patients with extensive fibrosis the liver disease evolved from one of active inflammation to one of inactive cirrhosis without fat or inflammation. The patient with cirrhosis later died of hepatocellular carcinoma. The severity or type of hepatic change did not correlate with the degree of obesity, hyperlipidemia or hyperglycemia. However, in individual patients, poorly controlled diabetes and rapid weight loss preceded the onset of steatohepatitis. We conclude that nonalcoholic steatohepatitis is a cause of hepatic inflammation histologically resembling that of alcohol-induced liver disease but usually slowly progressive and of low-grade severity. However, the disorder may ultimately result in cirrhosis. Nonalcoholic steatohepatitis should be distinguished from alcoholic steatohepatitis and recognized as a further cause of "cryptogenic cirrhosis."

Adolescent↗

Improvement in chronic hepatocerebral degeneration following liver transplantation.

Chronic progressive hepatocerebral degeneration with spastic paraparesis, dementia, dysarthria, ataxia, tremor, and neuropsychiatric symptoms follows long-standing portal-systemic shunting, is associated with structural changes in the central nervous system, and does not respond to conventional therapy for hepatic encephalopathy. A case of advanced chronic liver disease with severe, progressive hepatocerebral degeneration after 23 yr of portal-systemic shunting is reported in whom there was significant objective improvement in intellectual function and in the chronic neurological signs 3 mo after orthotopic liver transplantation and further improvement 12 mo after transplantation.

Adult↗

Lupus anticoagulant.

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Adrenal Gland Diseases↗

Steatohepatitis associated with limb lipodystrophy.

Two patients who presented with steatohepatitis had acquired partial lipodystrophy. This association has not previously been well documented. A common pathophysiological mechanism in lipodystrophy, obesity-associated nonalcoholic steatohepatitis, and alcoholic liver disease is possible.

Adolescent↗