Search PubMed⌕ Search

Biomedical subjects

J H Howell

Publications and source records attributed to J H Howell.

At least 19 recordsLinked to original sources
PubMed1992

Patient education.

Only recently has it been appreciated that the considerable morbidity of asthma can be reduced with tools readily available to every physician who treats children. The pharmacotherapeutic armamentarium has been strengthened by better understanding of the pathogenesis of asthma, the impact of inflammation, and the role of preventive therapy. The task remains to put this expanded knowledge to use to help a larger number of children with asthma and their families to diminish the impact that the disease has on their lives. Concomitant with increased understanding of the pathophysiology of asthma and the medications used to control the process has been a greater appreciation of the role of co-management or self-management. Several programs have been developed to help parents and children with asthma gain better control over the disease, thus decreasing morbidity and significantly improving quality of life. These programs are available to physicians and health care organizations, and it is strongly recommended that asthma education, both as a formal course and in the physician's office, be regularly incorporated into the care plan for every child with asthma.

Adolescent↗
PubMed1987

Sodium bicarbonate in the perinatal setting--revisited.

After more than 25 years of experience with sodium bicarbonate, the following conclusions may be in order: 1. It is not certain that the net effect of administration of this agent to patients with metabolic acidosis is positive, other than when given as replacement for renal or gastrointestinal bicarbonate losses. 2. Adequate oxygenation and ventilation must be ensured before it is given. 3. Profound fluctuations in blood pressure and cerebral blood flow, intracranial bleeds, and compromise of oxygen delivery to tissues all have been found to be possible adverse effects of sodium bicarbonate infusion. Because hyperosmolarity and sodium content are important factors, the commercially prepared solutions (0.9 or 1M) should be diluted 1:2 to 1:4 with water and given over not less than several minutes--if it is to be given at all. 4. Current recommendations for dose, dilution, and rate of administration, including those mentioned above, are largely arbitrary. If sodium bicarbonate were a newly proposed treatment for hypoxic metabolic acidosis, one would recommend that carefully conducted prospective laboratory and clinical trials be done before giving it to sick patients. As it is in widespread use, one can only reiterate that if it is to be given, it should be used with extreme caution.

Acidosis↗
PubMed1984

Biliary proteins. Unique inhibitors of cholesterol crystal nucleation in human gallbladder bile.

The onset time for cholesterol crystal nucleation of supersaturated normal human gallbladder biles is consistently prolonged when compared with biles from patients with cholesterol gallstone disease. Investigation of the factor(s) responsible for the suspended supersaturation (metastability) of normal human biles revealed that model bile solutions of cholesterol saturation index (CSI) and molar lipid composition identical to individual gallbladder bile specimens had much shorter crystal nucleation times, i.e., exhibited decreased metastability. Unsaturated normal biles, after supplementation with lecithin, cholesterol, and sodium taurocholate to a 'standard' supersaturated lipid composition, also demonstrated nucleation times three- to 15-fold longer than the comparable standard model bile. Total lipid extracts of normal biles, however, when similarly supplemented, did not differ in nucleation time from the control model solution. Gallbladder biles were fractionated by gel chromatography and the eluted fractions were pooled into two fractions. The fractions eluting in about the first 25% of the included volume when mixed with the supersaturated standard model bile induced a modest increase in nucleation time of approximately 1.5 times the control value. The fractions eluting in the second 25% of the included volume and which contained all of the bile lipids, were concentrated and supplemented with lipids to the standard composition. The nucleation times of these supplements were 3-10 times longer than the control nucleation times. Delipidated bile protein mixtures, purified by discontinuous sucrose gradient centrifugation, were recombined with purified lipids at the standard composition used previously. The nucleation times of these mixtures were significantly prolonged to the same extent as those associated with the second chromatographic fraction. These observations demonstrate that the delayed onset (inhibition) of cholesterol crystal nucleation observed in normal human gallbladder bile is produced by a factor(s) present in the biliary protein fraction.

Anticholesteremic Agents↗
PubMed1983

Hepatic microsomal activities of cholesterol 7 alpha-hydroxylase and 3-hydroxy-3-methylglutaryl-CoA reductase in the prairie dog. An animal model for cholesterol gallstone disease.

The prairie dog is a useful experimental animal model for studies of cholesterol gallstone pathogenesis. The unique susceptibility to rapid induction of gallstones solely by feeding of a 1.2% cholesterol diet in this species could result from low levels of hepatic cholesterol 7 alpha-hydroxylase. With optimal assay conditions in hepatic microsomes, a basal specific activity of about 25 pmol/min per g protein was found. Administration of diets containing 1.2% cholesterol or 5% cholestyramine caused hydroxylase levels to increase 60 and 250%, respectively. This response pattern is similar to that observed in other species under the same conditions, indicating that abnormally low basal or inappropriately unresponsive hydroxylase levels are not susceptibility factors unique to this model. With optimal assay conditions for hydroxymethylglutaryl-CoA reductase, a Km of 32.5 microM (S-HMG-CoA) and basal specific activities of between 60 and 175 pmol/min per mg protein were found. Following feeding of either sodium chenodeoxycholate or sodium cholate, in reasonable pharmacologic doses, no suppression of hydroxylase and reductase levels was found. These findings undermine the widely held view that the therapeutic effect of oral chenodeoxycholate in man for cholesterol gallstone dissolution is directly mediated by suppression of the activities of these enzymes.

Animals↗
PubMed1979

Selectivity of the micro-leukocyte adherence inhibition assay in pancreatic cancer.

A modified leukocyte adherence inhibition assay was performed on white blood cells from patients with ductal pancreatic cancer, other malignancies, benign gastrointestinal diseases including pancreatitis, and healthy controls, using four different ductal pancreatic cancer membrane preparations and similar preparations from gastric and colorectal cancers. A mean adherence index of less than or equal to 0.2 was evidence that the leukocytes "recognized" the antigen(s). In 9 of 10 patients with localized pancreatic cancer, 13 of 15 leukocyte populations "recognized" the pancreatic cancer antigen(s) and not other tested antigen(s). Leukocytes from only 11 of 18 patients (17 of 29 assays) with metastatic pancreatic cancer "recognized" the pancreatic tumor antigen (and no other antigen). The inability to recognize the pancreatic tumor antigen(s) was not related to nutritional, biochemical or therapeutic status of the patient, but was related to the demonstration of a response to skin test antigens. In contrast, 3 of 35 leukocyte populations in 2 of 31 patients with malignancies other than pancreatic, 1 of 28 with benign gastrointestinal disease, and one of 38 healthy control populations "recognized" the antigen. The LAI is worthy of further study in the differential diagnosis of pancreatic cancer.

Adenocarcinoma↗
PubMed1979

Correlations between the leukocyte adherence inhibition microassay and in vivo tests of transplantation resistance.

The leukocyte adherence inhibition (LAI) microassay detects tumor-associated antigen(s). Extracts of colon carcinoma (MCA-38 and B16 melanoma tumors, both syngeneic to the C57BL/6J mice) are recognized only by peritoneal cells from mice bearing the corresponding tumor. To ascertain whether this in vitro antigenic recognition correlates with the ability of the host to recognize and reject a tumor in vivo, serial LAI microassays were performed synchronously with experiments designed to test the ability of mice bearing tumors to reject live secondary tumor challenges. Concomitant tumor immunity was present in the MCA-38 tumor-bearing mice on 3 occasions from 5 to 15 days from primary inoculation. In the B16 system, concomitant immunity was present on one occasion 10 days after primary inoculation. These results in turn were paralleled with the specific in vitro recognition of tumor antigens as detected by the LAI microassays. Loss of immunity in the "eclipse" phase of tumor development, as detected by concomitant tumor immunity, was paralleled by nonreactivity of the indicator cells in the LAI microassay.

Adenocarcinoma↗
PubMed1979

Cellular and humoral factors involved in the mechanism of the micro-leukocyte adherence inhibition reaction.

To study the cellular basis for specific antigen-induced leukocyte adherence inhibition, enriched populations of B-cells, T-cells, and monocytes were prepared by a two-stage adherence separation procedure from spleen cells of normal C57BL/6J mice and mice bearing progressively growing MCA-38 tumors. The reactor cell undergoing specific antigen-induced adherence inhibition was identified as a monocyte (esterase positive, did not respond to mitogens, and did not bear Thy 1.2 antigen or surface immunoglobulin). Furthermore, an enriched population of MCA-38-sensitized B-cells could program normal monocytes to undergo specific antigen-induced adherence inhibition. In contrast, enriched populations of MCA-38-sensitized T-cells could not program normal nylon wool-adherent cells to undergo antigen-specific adherence inhibition. Programming of normal monocytes by MCA-38-sensitized B-cells occurs through a soluble mediator and not by direct cell contact. The soluble mediator appears to be immunoglobulin in nature and induced both adherence inhibition and the inhibition of adherence. Thus, in this murine tumor model, leukocyte adherence inhibition appears to be due to programming of monocytes by a secretory product of specifically sensitized B-cells.

Adenocarcinoma↗
PubMed1979

Demonstration of the microtest version of the leukocyte adherence inhibition assay.

This paper gives a detailed description of the microtest leukocyte adherence inhibition technique, as well as the results obtained with blood specimens coded by impartial observers. Three coded blood specimens from patients with colon cancer, pancreatic cancer, and melanoma were tested against crude membrane preparations of pancreatic and colon adenocarcinoma tumors. No tissue type-specific reactivity was observed. The inability to demonstrate specific reactivity was due to extensive variability observed within each test. The extensive variability resulted from time constraints of the workshop that necessitated deviations from the normal procedure.

Adenocarcinoma↗
PubMed1979

Isolation of T-cells, B-cells and macrophages by a two-stage adherence procedure.

This communication describes a method to obtain enriched populations of T-cells, B-cells and macrophages. Spleen cells were initially fractionated on nylon wool columns. The nylon wool adherent fraction was removed by mechanical agitation and further separated on the basis of adherence to a coated-plastic surface in the presence of autologous serum. The tissue flask adherent population was removed with the aid of a rubber policeman. The nylon wool non-adherent and the tissue flask non-adherent and adherent fractions were characterized for the presence of cell surface markers, size, and functional activity and were identified as T-cells, B-cells and macrophages, respectively. The two-stage adherence procedure is simple to perform and does not require sophisticated equipment or expensive reagents.

Animals↗