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Biomedical subjects

D L Morris

Publications and source records attributed to D L Morris.

At least 415 records · Page 23Linked to original sources
PubMed1978

Gallbladder disease and gallbladder cancer among American Indians in tricultural New Mexico.

Previous studies have reported high rates of gallbladder disease and gallbladder cancer among all American Indians. Data from the New Mexico Tumor Registry confirm these findings, specifically showing high rates for New Mexico's American Indians, as well as for the state's Spanish population. This review explores several risk factors, including parity, obesity, age, cholesterol level, and genetic factors. From the available evidence, genetic factors appear to be the most important, with parity a contributing factor.

Epidemiologic Methods↗
PubMed1977

Value of delayed hypersensitivity index in patients with malignancy.

A delayed hypersensitivity index can be obtained by standardized in vivo testing with available antigens. Recall antigens and DNCB to measure the afferent limb can be used to assess this important body function. The index is a valid indicator of cellular immunity, which is important as a dynamic indicator in many medical conditions and in treating patients with malignancy.

Candida↗
PubMed1975

The preparation of several new nylon tube-glucose oxidase derivatives and their incorporation into the "reagentless" automated analysis of glucose.

Nylon tube was activated by alkylation with dimethyl sulfate and used for the immobilization of glucose oxidase. Lysine, hexamethylene diamine and polyethylene imine were also attached to activated nylon tube, and these nylon tube-spacer derivatives were reactivated with either glutaraldehyde or ethyl adipimidate for the subsequent coupling of glucose oxidase. The activities of all of the different nylon tube-glucose oxidase derivatives were compared by their incorporation into standard Technicon automated analysis systems. Activities were measured either spectrophotometrically, by following the production of hydrogen peroxide using an acid/KI assay, or polarographically by following the decrease in the oxygen concentration using a flow-through oxygen electrode assembly. The activity and stability of all of the nylon tube-glucose oxidase derivatives was such that their use in the routine estimation of glucose levels was an attractive proposition.

Amines↗
PubMed1975

The preparation of nylon-tube-supported hexokinase and glucose 6-phosphate dehydrogenase and the use of the co-immobilized enzymes in the automated determination of glucose.

Triethyloxonium tetrafluoroborate was used to O-alkylate nylon-tube thus producing the imidate salt of the nylon which was further made to react with 1,6-diaminohexane. 2. Hexokinase (EC 2.7.1.1) and glucose 6-phosphate dehydrogenase (EC 1.1.1.49) were immobilized on the amino-substituted nylon tube through glutaraldeyde and bisimidates. 3. The effect of varying the conditions of O-alkylation and the amount of enzyme immobilized on the activity of nylon tube-hexokinase derivatives was determined. 4. The effect of varying the amount of enzyme immobilized on the activity of nylon-tube-glucose 6-phosphate dehydrogenase derivatives was determined. 5. The thermal stability of nylon-tube-hexokinase and nylon-tube-glucose 6-phosphate dehydrogenase derivatives was studied. 6. Different ratios of hexokinase and glucose 6-phosphate dehydrogenase were co-immobilized on nylon tube, and the rate of conversion of glucose into 6-phosphogluconolactone was compared with the individual activities of the immobilized enzymes. 7. Hexokinase and glucose 6-phosphate dehydrogenase co-immobilized on nylon tube were used in the automated analysis of glucose.

Alkylation↗
PubMedDate not supplied

Effect of hepatic artery chemotherapy on survival of patients with hepatic metastases from colorectal carcinoma treated with cryotherapy.

Thirty-eight patients with unresectable multiple liver metastases from colorectal carcinoma were treated with either hepatic artery chemotherapy (HAC) and cryotherapy (n = 27) or cryotherapy alone (n = 11). Follow-up survival data were summarized using Cox regression. Allowing for the effect of the pathology of the primary tumor and the preoperative carcinoembryonic antigen (CEA) level, those patients who did not receive HAC after cytoreduction were three times as likely to die as those given HAC (RR 3.3, 95%; CI 1.2-9.3). The estimated median survival of patients treated with cryotherapy alone was 245 days, whereas for those given more than 3 months of HAC plus cytoreduction therapy it was 570 days. It is recommended that all patients who receive cryotherapy for multiple liver metastases from colorectal rectal carcinoma be given subsequent hepatic artery chemotherapy.

Adult↗
PubMedDate not supplied

Thrombocytopenia after hepatic cryotherapy for colorectal metastases: correlates with hepatocellular injury.

Postoperative thrombocytopenia following hepatic cryotherapy has been well documented and shown to be significantly greater than in control patients who had an identical incision or major laparotomy. Serum aspartate transaminase (AST) levels have been used as a reliable indicator of hepatocellular destruction. This study reviews 65 consecutive hepatic cryotherapy operations. We have excluded all patients who had repeat cryotherapy to lesions (n = 6), all who had a colonic or hepatic resection procedure (n = 7), all who had tumors other than colorectal metastases (n = 5), patients with inadequate data (n = 9), and those who were asplenic (n = 2). Of the remaining 36 patients, 14 were treated with a single freeze/thaw cycle, 12 were treated with a double freeze/thaw cycle, and 10 were treated with mixed single and double freezes. The most common platelet nadir was day 3 (n = 21) followed by day 2 (n = 11), with the remaining platelet nadirs being day 1 or 4 (n = 4). The percentage fall in platelet count was found to correlate with the rise in day 1 AST level (r2 = 0.74, least squares linear regression). The double freeze/thaw cycle patients had a significantly greater fall in platelet count (p = 0.01, Mann-Whitney two sample test). Another institution has reported three deaths due to multiple problems, including coagulopathy in patients treated with double freeze/thaw cycle cryotherapy.(ABSTRACT TRUNCATED AT 250 WORDS)

Colorectal Neoplasms↗
PubMedDate not supplied

Interactions of human NKG2D with its ligands MICA, MICB, and homologs of the mouse RAE-1 protein family.

NKG2D is an activating receptor that is expressed on most natural killer (NK) cells, CD8 alphabeta T cells, and gammadelta T cells. Among its ligands is the distant major histocompatibility complex class I homolog MICA, which has no function in antigen presentation but is induced by cellular stress. To extend previous functional evidence, the NKG2D-MICA interaction was studied in isolation. NKG2D homodimers formed stable complexes with monomeric MICA in solution, demonstrating that no other components were required to facilitate this interaction. MICA glycosylation was not essential but enhanced complex formation. Soluble NKG2D also bound to cell surface MICB, which has structural and functional properties similar to those of MICA. Moreover, NKG2D stably interacted with surface molecules encoded by three newly identified cDNA sequences (N2DL-1, -2, and -3), which are identical to the human ULBP proteins and may represent homologs of the mouse retinoic acid-early inducible family of NKG2D ligands. Because of the substantial sequence divergence among these molecules, these results indicated promiscuous modes of receptor binding. Comparison of allelic variants of MICA revealed large differences in NKG2D binding that were associated with a single amino acid substitution at position 129 in the alpha2 domain. Varying affinities of MICA alleles for NKG2D may affect thresholds of NK-cell triggering and T-cell modulation.

Amino Acid Sequence↗
PubMedDate not supplied

Echinococcus granulosus: in vitro maintenance of whole cysts and the assessment of the effects of albendazole sulphoxide and praziquantel on the germinal layer.

Small entire cysts of Echinococcus granulosus of human and animal origin were cultured in vitro in the presence or absence of albendazole sulphoxide (1000 micrograms/litre) or praziquantel (500 micrograms/litre) for 10 or 11 d, and subsequently passaged into the peritoneal cavity of gerbils to assess viability by continued cyst growth. Viability was reduced in the presence of albendazole sulphoxide, and disintegration of the germinal layer immediately after culture was demonstrated at the ultrastructural level. Praziquantel had no apparent effect on cyst growth.

Albendazole↗
PubMedDate not supplied

Elucidation of cellular targets responsible for tetrachlorodibenzo-p-dioxin (TCDD)-induced suppression of antibody responses: II. The role of the T-lymphocyte.

Various immunological assays have been applied by our laboratory in an attempt to assess the role of the T-cell in the TCDD-induced suppression of the antibody response by murine B6C3F1 splenic lymphocytes. Animals were treated in vivo (via gavage) with 1.0 microgram/kg TCDD in corn oil for 5 days before in vitro analysis of splenocyte immunocompetence and T-cell function. To study the effects on T-helper cell function, alterations in the proliferative responses of T-cells following TCDD exposure were investigated. Results show no significant difference in [3H]thymidine uptake between vehicle- and TCDD-treated whole splenocytes 24 h after in vitro stimulation with the T-cell mitogen Con A. This is consistent with the finding that IL-2 production at either 24 or 48 h after Con A stimulation of TCDD-treated lymphocytes was not significantly different from that of vehicle-treated controls. The possibility of the induction of a suppressor T-cell by TCDD was also investigated. Titration of T-cells from TCDD-treated mice into naive splenocyte cultures did not suppress the humoral response to either a T-dependent (SRBC) or a T-independent (DNP-Ficoll) antigen. In contrast, titration of cells stimulated in vitro with Con A for 48 h (a positive control for the induction of a suppressor T-cell) inhibited humoral responses of naive cells to both types of antigen. Likewise, T-cells plus macrophages from TCDD-treated mice did not suppress the in vitro humoral responsiveness of naive B-cells plus macrophages to a T-independent antigen (DNP-Ficoll). These results would indicate that an alteration in T-cell function following TCDD exposure does not play a role in the suppression of the antibody response elicited by antigen stimulation of murine B6C3F1 splenocytes.

Animals↗
PubMedDate not supplied

Effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on humoral immunity: I. Similarities to Staphylococcus aureus Cowan Strain I (SAC) in the in vitro T-dependent antibody response.

We have determined that suppression of the in vitro T-dependent humoral immune response by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) is dependent on the type and concentration of serum used in the culture media. Only five out of 23 commercial lots of serum (screened at both 5 and 10%) could support a suppression in the presence of 30 nM TCDD, with the remaining lots demonstrating an apparent 'protective-like' effect against the TCDD exposure. When log dose response curves were established with TCDD (0.3, 3.0, and 30 nM) in media containing each of the serum lots supporting a suppression (at both 5 and 10%), we determined that only three lots could support a full dose-responsive suppression. Subsequently, in a comparison study between the effects of TCDD and the polyclonal B-cell activator Staphylococcus aureus Cowan Strain I (SAC) on the in vitro T-dependent humoral immune response, we have found that SAC suppresses the antibody response to SRBC and demonstrates the same serum dependency for this effect as was previously noted for TCDD. Under serum-free culturing conditions, TCDD (30 nM) caused a 15-fold increase in the AFC response to SRBCs over controls, suggesting that direct addition of TCDD to whole splenocyte cultures in the absence of serum-derived growth factors results in an increase in B-cell activation. Likewise, under serum-free conditions, SAC dose-dependently increased the AFC response over media controls, and at doses which achieved the same degree of suppression of the humoral response aa TCDD. Taken together, these studies suggest that TCDD has actions that are similar to a T cell independent polyclonal B cell activator such as SAC, and selectively acts on the B cell to suppress the T-dependent humoral immune response by a mechanism which is unique to this series of compounds. This effect however, is only detectable under appropriate serum-supported (or serum-deficient) culture conditions as described.

Animals↗
PubMedDate not supplied

Effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on humoral immunity: II. B cell activation.

Previous reports have indicated similarities in the actions of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) and the polyclonal B cell activator Staphylococcus aureus Cowan Strain I (SAC) on the in vitro T-dependent antibody response to SRBC. This finding has suggested that B cell activation is likely to be an important component in the direct effects of TCDD on lymphocyte function. In the current investigation, various techniques were employed to determine whether TCDD could cause the activation of splenic-derived dense resting B cells in the absence of antigen and to determine if the modulatory effect of serum-derived growth factors is the result of a direct action on the B lymphocyte. TCDD (30 and 60 nM) caused an increase in proliferation of dense resting B cells at both 72 and 96 h following addition. This action of TCDD was demonstrated to possess a serum dependency that was based on the lot of serum in which the cells were cultured. Under similar conditions, TCDD (30 nM) stimulated an increase in total IgM secretion as measured on day 7 of culture. A similar profile of activity was observed in vivo, where splenic-derived dense resting B cells from animals treated with 1 microgram/kg TCDD for 5 days, but unsensitized to SRBC, demonstrated a 10-fold increase in proliferation on day 3 of culture which likewise occurred in a serum dependent manner. In addition, we observed that mice treated with 1 microgram/kg TCDD for 5 days and sensitized with SRBCs, sustained a complete loss in their splenic-derived dense B cell populations (day 4 after sensitization). The loss of this B cell population is indicative of a movement of these cells into a blastogenic state of activation and is not observed in matched corn oil-treated controls. These findings support our previous observations and give evidence that TCDD is capable of causing the direct activation of resting B cells. This activation is dependent on the type of serum present during in vitro culture and appears to be intensified in the presence of antigen in vivo.

Animals↗
PubMedDate not supplied

Direct effects of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) on responses to lipopolysaccharide (LPS) by isolated murine B-cells.

Previous results from this laboratory have indicated that the B-cell is the primary cell target responsible for the suppression of humoral immunity by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD). While other laboratories have confirmed that the B-cell is affected, there is not a clear understanding of TCDD's relative effects on B-cell proliferation and differentiation. In the present study, we isolated B-cells from whole spleen cell suspensions from female B6C3F1 mice and further separated them according to density on a percoll density step gradient. Cell cycle analysis by propidium iodide indicated that both high (i.e., 1.092-1.079 density interface) and low (i.e., 1.079-1.070 density interface) density B-cells were predominantly cells in the G0/G1 phase of the cell cycle. Based on acridine orange staining, low-density B-cells exhibited slightly higher RNA levels than high-density B-cells indicating they are an "activated" population of cells, probably somewhere in G1A. Confirmation of these results was the observation that the high density, small, resting B-cells had negligible background proliferation and immunoglobulin secretion, while the low density, larger, activated B-cells had marked background proliferative and antibody responses. Direct addition of TCDD (0.3-30.0 nM) produced a significant, dose-related and comparable suppression of both parameters in the low density B-cells. Similar results were obtained when low density B-cells were stimulated with LPS and exposed to TCDD. In contrast, neither the proliferation nor the antibody response by high density B-cells stimulated with LPS were affected by TCDD.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗