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D Howell

Publications and source records attributed to D Howell.

At least 37 records · Page 2Linked to original sources
PubMed1997

Successful treatment of post-cholecystectomy bile leaks using nasobiliary tube drainage and sphincterotomy.

OBJECTIVE: Bile leaks are known complications of cholecystectomy. The combination of sphincterotomy and nasobiliary tube (NBT) drainage is effective for the immediate decompression of bile ducts and provides access for follow-up cholangiography. Our objective was to study, retrospectively, 19 patients who had undergone treatment for bile leaks with this combination between October 1991 and December 1995. METHODS: Nineteen patients (15 F, 4 M) ages 23-83 yr (mean 50 yr) presented with bile leaks secondary to open cholecystectomy (n = 1) and laparoscopic cholecystectomy (n = 18). All patients had sphincterotomy and NBT placement. Symptoms, findings at ERCP, and outcome were reviewed. RESULTS: Patients presented from 0 to 150 days after cholecystectomy (median = 2) with pain (n = 17), fever (n = 8), bile leakage in a surgical drain (n = 4), elevated liver tests (n = 8), and nausea and vomiting (n = 4). Fourteen patients had diagnostic imaging before endoscopic management. ERCP findings included cystic stump leak (n = 12), including one with a colocutaneous biliary fistula, gallbladder fossa leak (n = 3), right hepatic branch leak (n = 1), or no leak (n = 3). Three patients had choledocholithiasis. NBT drainage was used for a mean of 3.9 days (range 1-12 days). Fourteen patients had radiographic evidence of leak closure. One patient ultimately required surgical correction for a chronic colocutaneous biliary fistula. There were no early or late endoscopic complications. CONCLUSIONS: Endoscopic management with nasobiliary drainage and sphincterotomy is effective for acute uncomplicated bile leaks but may not be adequate for chronic fistulas. The advantages over endoprostheses include access for subsequent cholangiography, improved biliary decompression, and catheter removal without further endoscopy.

Adult↗
PubMed1994

Evaluation of new monoclonal antibody-based latex agglutination test for detection of cryptococcal polysaccharide antigen in serum and cerebrospinal fluid.

We evaluated the performance of CRYPTO-LEX (Trinity Laboratories, Inc., Raleigh, N. C.), a new mouse immunoglobulin M monoclonal antibody latex agglutination reagent which reacts with the capsular polysaccharide of the four serogroups of Cryptococcus neoformans. This test was compared with CALAS (Meridian Diagnostics, Cincinnati, Ohio) for the ability to detect cryptococcal antigen in serum and cerebrospinal fluid (CSF). A total of 580 clinical specimens (327 serum and 253 CSF samples), primarily from human immunodeficiency virus-infected patients, were tested in this study. Sixty-seven specimens (44 serum and 23 CSF samples) were positive for cryptococcal antigen with both tests, and 511 (282 serum and 229 CSF samples) were negative. The two latex reagents agreed for 326 of 327 serum specimens (44 positives and 282 negatives). One serum specimen with a titer of 1:2 was CALAS positive but CRYPTO-LEX negative. The titer correlation coefficient for the two tests was 0.884 when two highly discordant serum specimens were eliminated from analysis of the data. The two latex tests agreed for 252 of 253 CSF specimens (23 positives and 229 negatives). One specimen with a titer of 1:2 was positive with CALAS and negative by CRYPTO-LEX. The correlation coefficient of the two tests for CSF titers was 0.886. The sensitivity and specificity of CRYPTO-LEX were 97 and 100%, respectively, with a 99.6% correlation with CALAS. These data show that the performance of CRYPTO-LEX is comparable to that of CALAS for detection of cryptococcal antigen in serum and CSF.

Animals↗
PubMed1993

Induction of immune-mediated glomerulonephritis in normal mice immunized with bacterial DNA.

Normal mice immunized with bacterial DNA produce high titers of anti-DNA antibodies and represent a new model for autoantibody production in systemic lupus erythematosus. To determine whether DNA immunization can also provoke clinical manifestations of lupus, the occurrence of nephritis in immunized mice was assessed and correlated with levels of anti-DNA as well as antibodies to glomerular antigens. BALB/c mice immunized with Escherichia coli single-stranded DNA in complexes with methylated bovine serum albumin in adjuvant showed increased proteinuria compared to control mice immunized with mBSA alone. Furthermore, DNA immunized mice had significantly greater glomerular proliferative changes and immunoglobulin deposition than control mice. In an in vitro assay, sera from DNA immunized mice exhibited greater binding to glomerular antigens than sera from control mice. Compared to sera, renal eluates from DNA-immunized mice were enriched for anti-DNA and glomerular binding activity. These data indicate that immunization of normal mice with E. coli DNA induces an immune-mediated proliferative glomerulonephritis that is likely secondary to the renal deposition of anti-DNA antibodies.

Animals↗
PubMed1992

Interferon-alpha-dependent and -independent participation of accessory cells in natural killer cell-mediated lysis of HSV-1-infected fibroblasts.

Human natural killer (NK) cells require an HLA-DR+ accessory cell (AC) population to lyse herpes simplex virus-type 1 (HSV-1)-infected fibroblasts (HSV-Fs) but not K562 target cells. It has been postulated that ACs may function by producing interferon-alpha (IFN-alpha), which stimulates NK cells. Using a sequential enrichment protocol, ACs were found to coenrich with the interferon-producing cells (IPCs). Treatment of the ACs with a protein synthesis inhibitor, emetine, inhibited both their IFN production and AC function, results that support a central role for IFN in AC activity. In contrast, when the arginine analogue canavanine was added to NK assays, no IFN-alpha was produced and NK(HSV-Fs) activity was only partially inhibited. Consistent with IFN-independent AC function, treatment with either polyclonal sheep or bovine anti-IFN-alpha neutralized all the IFN-alpha produced during the NK assays but caused either no or partial reduction of NK(HSV-Fs) activity, respectively. However, when limiting numbers of ACs were used, the bovine antiserum neutralized both IFN-alpha and NK(HSV-Fs) activity. We further found that HLA-DR+ cells are required for cell clustering, suggesting a role for cell contact. Finally, fixation of activated ACs prevented the accessory function. Together, these results demonstrate that ACs can provide help to NK cells in both IFN-alpha-dependent and -independent manners.

Animals↗
PubMed1976

Enzyme release after myocardial infarction: comparison of serial serum alpha-hydroxybutyrate dehydrogenase with creatine phosphokinase levels.

Serial measurements on serum creatine phosphokinase (CPK) and alpha-hydroxybutyrate dehydrogenase (HBD) activity were made in 17 patients with acute myocardial infarction. Activities of both enzymes were measured 4-hourly from less than 12 h after the onset of chest pain until CPK activity had returned to near-normal levels. Blood was then sampled twice daily for a further 4--6 days in order to follow the decline in HBD activity. Degradation rates (KD) were calculated for both enzymes, and individual figures for KD were used in order to estimate the total cumulative release of each enzyme. We found a significant correlation between the duration (r = 0.66, P less than 0.01) and magnitude (r = 0.67, P less than 0.01) of release of the 2 enzymes, comparing different patients with one another. Duration od HBD release was 11 h greater than the duration of CPK release in 9 of the 17 patients who were suffering from cardiac failure (t = 0.01, P less than 0.02). Degradation rate (KD) for HBD was on average about one quarter of that for CPK, but there was no significant correlation between KD for the 2 enzymes. KD did not appear to be reduced in patients with cardiac failure. We conclude that the release patterns of CPK and HBD after myocardial infarction are similar, and this strengthens the case for acceptance of total enzyme release as a valid index of myocardial infarct size.

Adult↗
PubMed1976

Proteolytic enzymes in human cartilage: the pathogenesis of osteoarthritis.

It is evident that human articular cartilage possesses, in addition to multiple forms of cathepsin D, multiple forms of other acid cathepsins, and, most important, a family of at least four closely related neutral protease enzyme forms, all of which degrade proteoglycan. In addition, caseinase and histonase activities are present. The search for these enzymes in human cartilage ahs been presented in some detail in order to give an idea of some of the problems faced in such research, as well as the hypotheses and hopes that flow from it and prepare the ground for further research. The actual role of proteolytic enzymes in the physiologic and pathologic condition of cartilage remains to be determined. It is hoped that these enzymes, especially the neutral protease forms, will be sufficiently purified to enable preparation of antibodies to them. This will help to clarify what controls their release from the chondrocytes and where they function in the cartilage. Meanwhile, it seems appropriate to study the neutral protease forms and their role in initiating the degradation of proteoglycan in the early stages of osteoarthritis. The chief role of cathepsin D and the new acid cathepsins is most likely in intracellular digestion. One may hypothesize a three-step sequence of the degradation of the matrix proteoglycan: (1) initial extracellular attack by the neutral matrix, (2) endocytosis of the fragments by the cells, and (3) completion of their degradation within the lysosomal digestive system of the cell. The initial degradation of the matrix proteoglycan would facilitate the entrance of other degrading enzymes from the synovium to aid in total destruction of the cartilage. While awaiting knowledge of the primary events that trigger the development of osteoarthritis, enzymatic research offers the real hope of finding a way to control the enzymatic degradation of proteoglycan occurring in the early stages of the disease. Research into the nature of these degrading enzymes will lead to the development of therapeutically suitable inhibitors.

Cartilage↗
PubMed1975

Ruth Campbell.

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Child Psychiatry↗