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Biomedical subjects

D M Wilson

Publications and source records attributed to D M Wilson.

At least 181 records · Page 10Linked to original sources
PubMed1991

Oxalate, silicon and vanadium in acquired cystic kidney disease.

We have investigated the importance of several clinical and laboratory parameters on the development of acquired cystic kidney disease (ACKD) as detected by ultrasonography in 19 patients who had received dialysis therapy for at least three years. We were particularly interested on the possible effect of the serum levels of oxalate and silicon, which can produce tubular obstruction, and that of vanadium, which can affect cell proliferation. The severity of ACKD increased with the duration of dialysis and was greater in men than in women. Positive correlations were observed between the grades of ACKD and the levels of hemoglobin, hematocrit, and parathyroid hormone, while there was a negative correlation between ACKD and serum ferritin levels. The serum levels of oxalate, silicon, and vanadium, pre- and postdialysis, were markedly and significantly higher than those in normal controls, but there was no significant correlation between these levels and the duration of dialysis therapy or severity of ACKD. The pre- and postdialysis levels of vanadium were not significantly different, while the levels of oxalate and silicon were significantly lower in the postdialysis samples. No significant correlations were detected between ACKD and age of the patients, blood pressure, protein catabolic rate, efficiency of dialysis index, or the serum levels of iron, sodium, potassium, calcium, phosphorus, aluminum, and beta 2-microglobulin.

Dialysis Solutions↗
PubMed1990

Plasma prorenin activity and complications in children with insulin-dependent diabetes mellitus.

BACKGROUND: Renin, secreted into the blood by the juxtaglomerular cells of the kidneys, is derived from a larger precursor, prorenin. Plasma prorenin activity is increased in patients with insulin-dependent (Type I) diabetes mellitus who have microvascular complications of their disease. We undertook this study to determine prospectively whether rising prorenin activity can predict the development of complications in young patients with Type I diabetes. METHODS AND RESULTS: Plasma prorenin was measured in 135 children and adolescents with Type I diabetes. The mean (+/- SE) plasma prorenin activity among the 32 patients over the age of 10 years who had had uncomplicated diabetes for 0.1 to 5 years was 8.43 +/- 0.58 ng of angiotensin I per liter.second, as compared with 7.06 +/- 0.32 in 37 control subjects of the same age (P less than 0.05). In the 9 patients older than 10 who had retinopathy or overt albuminuria, the mean plasma prorenin activity was 13.09 +/- 1.43 ng of angiotensin I per liter.second (P less than 0.0001). In 34 patients 10 years old or older with uncomplicated diabetes, 3 to 13 measurements of plasma prorenin activity were taken during a follow-up period of 6 to 39 months. Urinary albumin was determined at each visit, and the patients had regular retinal examinations. Only 1 of the 20 patients who had consistently normal plasma prorenin values had overt albuminuria (ratio of urinary albumin to creatinine, greater than 0.017) or retinopathy, whereas one or both of these complications appeared in 8 of the 14 who had at least one high prorenin value. The plasma prorenin value was significantly higher in these eight patients at least 18 months before a complication was found. CONCLUSIONS: Increased plasma prorenin activity identifies a group of young patients with diabetes who are at high risk for retinopathy or nephropathy.

Adolescent↗
PubMed1990

Malignant transformation of human fibroblasts by a transfected N-ras oncogene.

The only ras oncogene as yet identified in cells from human fibrosarcomas is N-ras, but the relationship between N-ras oncogene expression and the malignant state of these cell lines is not known. To determine if expression of an N-ras oncogene causes human cells to become malignant, we transfected the N-ras oncogene from human leukemia cell line 8402, cloned into a high expression vector pSV N-ras, into MSU-1.1 cells, a nontumorigenic, infinite life span fibroblast cell strain with a normal morphology and a stable near-diploid karyotype. The transformants formed distinct foci composed of morphologically transformed cells. Cells from such foci expressed higher than normal levels of N-ras protein, exhibited growth factor independence, and formed large colonies in soft agar at a high frequency. Injection of progeny of these focus-derived cells s.c. into athymic mice resulted in progressively growing, invasive malignant tumors (round cell, spindle cell, or giant cell sarcomas) which reached a diameter of 6 mm in 3 to 4 weeks. Injection of focus-derived or tumor-derived cells i.v. resulted in tumors in various organs of the mice. The focus-derived cell strain tested, as well as the majority of the cells derived from the tumor it produced, exhibited the same near-diploid karyotype as the parental MSU-1.1 cells. Cells transfected with an N-ras oncogene that was expressed at a normal level formed only a single, indistinct focus, and cells from that focus were not malignant.

Animals↗
PubMed1990

Bovine natural killer-like cell responses against cell lines expressing recombinant bovine herpesvirus type 1 glycoproteins.

The murine retrovirus shuttle vector pZipNeo SV(X)1 was used to construct plasmids encoding the three major surface glycoproteins of bovine herpesvirus-1 (BHV-1). Each plasmid was transfected into D17, a canine osteosarcoma cell line sensitive to lysis by bovine NK-like cells when infected with BHV-1. After selection in G418 sulfate, cell lines expressing the recombinant gene products were sorted by flow microfluorimetry, radioimmunoprecipitated, and analyzed by SDS-PAGE for fidelity as compared to the native viral glycoproteins. Two of the three genetically engineered cell lines (gI and gIV) could successfully serve as targets to detect bovine NK-like cytolysis. These findings support and extend a previous study from our laboratory indicating a role for BHV-1 glycoproteins in the cytolytic response by bovine NK-like cells. Additionally, this study demonstrated that individual proteins are recognized by these effector cells, and that recombinant glycoproteins can direct cytolytic activity in the absence of host cell infection-associated proteins. This is the first known report of Ag directed cytotoxicity by bovine null (non-B, non-T) cells.

Animals↗
PubMed1990

Growth hormone response to growth hormone releasing hormone in depression and schizophrenia.

Growth hormone releasing hormone, a 44-amino acid peptide (GHRH-44), was administered (1 micrograms/kg i.v.) to 6 normal controls, 10 schizophrenic subjects, and 7 depressed subjects. A significantly lower growth hormone (GH) response was found in the schizophrenic and depressed groups. Two molecular forms of GH, 22K GH and 20K GH, were also measured but did not further differentiate the three groups of subjects.

Adult↗
PubMed1990

Laxative abuse as a cause for ammonium urate renal calculi.

Nine women with laxative abuse and predominantly ammonium urate renal calculi underwent metabolic studies to identify common chemical abnormalities and determine pathophysiology. The 24-hour urine studies demonstrated marked decreases in volume (902 cm.3), sodium (28 mEq.), citrate (116 mg.) and potassium (21 mEq.). A significant elevation in ammonium urate supersaturation was found compared to control subjects when studied by the computer model EQUIL 2. Of the patients 7 had 1 or more urine specimens positive for phenolphthalein. Gastrointestinal loss of fluid and electrolytes allowed for chronic extracellular volume depletion. Intracellular acidosis was present as judged by low urinary citrate and potassium. The fact that the ion product for ammonium urate is increased significantly compared to controls reflects the stated pathophysiological changes. Laxative abuse should be suspected whenever a woman has an ammonium urate renal calculus in sterile urine.

Adult↗
PubMed1990

Blood pressure in blacks. Twin studies in Barbados.

We have recently reported that there are significant genetic influences on the population variation in blood pressure in black twins in Los Angeles. The present cross-sectional study was undertaken to replicate these findings in a black twin population that lives in a different biosocial environment. We chose the Caribbean island nation of Barbados, where 96% of the population is black, the literacy rate is 99%, and the access to health care is guaranteed. The goals were 1) to test the feasibility of twin studies in blood pressure research in a developing country and 2) to estimate the relative contribution of genes and environment to blood pressure variability in blacks in the Caribbean. The names of 200 twin sets were obtained with the assistance of community resources including a twin club, by media advertisement, and by asking people at public blood pressure screenings if they knew any twins. By using these methods, we identified 200 sets of twins. Of these, 37.5% (75/200) met our criteria for study. Although 97% of the sets of twins (73/75) said they were willing to participate, only 69% (52/75) were able to be scheduled during the 1 week of the study when the full team of investigators was in Barbados. Of those scheduled, 83% (43/52) were examined. Examination included medical history, physical examination, recumbent blood pressure measurements by two observers, anthropometric measurements, 24-hour urine collections for sodium and potassium tests, and blood tests for zygosity.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1990

Efficacy of insulin-like growth factor I levels in predicting the response to provocative growth hormone testing.

Clinical testing of growth hormone (GH) sufficiency is a controversial area in endocrinology. Due to the episodic nature of endogenous GH secretion, diagnosis of GH deficiency has been defined as a failure to achieve normal GH levels in response to at least two stimuli. This testing is associated with significant patient morbidity and cost. We analyzed our experience over a 4-y period to determine whether clinical or biochemical variables could be used to predict the results of a specific GH testing procedure. Of 180 cases analyzed (67% male, mean age 8.89 +/- 4.39 y, range neonate-16 y), eight cases had incomplete GH testing results. Of the remaining 172, 19 were GH deficient (GH level less than 7 ng/mL). Younger age, higher body mass index and a greater degree of bone age delay were characteristic of the GH-deficient population; however, none of these variables alone was of diagnostic utility. Serum IGF-I level was below the normal range for 81% of the GH deficient and 47% of the GH-sufficient children; and was the only single variable that provided a reasonable between-group distinction. Discriminant analysis resulted in development of a new variable, based on IGF-I z scores, chronologic age, degree of bone age delay, and body mass index, which would have allowed exclusion of GH deficiency without provocative testing for 58% of the GH sufficient population, whereas permitting the diagnosis of GH deficiency for all GH-deficient subjects. Our data are dependent on the IGF-I assay method and the clinical definition for GH deficiency; therefore, the calculated predictive values are not applicable to all clinical populations.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1990

Insulin-like growth factor binding proteins in human breast cancer cells: relationship to hIGFBP-2 and hIGFBP-3.

Human breast cancer cells (HBCC) secrete at least four different forms of IGFBPs. We have previously demonstrated that hIGFBP-1 is a minor component of IGFBPs secreted by Hs578T cells and is absent in CM from MCF-7 cells. In our present report, we describe the immunological and structural relationship of HBCC IGFBPs to hIGFBP-2 and hIGFBP-3. Analysis of conditioned media (CM) from Hs578T by Western ligand blotting revealed three IGFBPs of apparent Mr = 38K, 28K, and 24K; CM from MCF-7 revealed only two IGFBPs, of apparent Mr = 31K and 24K. Immunoprecipitation studies with polyclonal antibodies raised against hIGFBP-2 and hIGFBP-3 demonstrated that the 38K IGFBP in Hs578T CM is immunologically related to hIGFBP-3, while the 31K IGFBP in MCF-7 cells is related to the hIGFBP-2. Analysis by Northern blot demonstrated that MCF-7 cells contained mRNA for hIGFBP-2, while Hs578T cells contained the mRNA characteristic of the hIGFBP-3. The identity of the 24K IGFBP remains unknown, and may represent a distinct IGFBP. Of note, assay of CM following removal of BPs by acid chromatography demonstrated no detectable IGF-I or -II. The role of these IGFBPs in HBCC is of interest in view of the potential modulation of IGF actions by these proteins.

Blotting, Western↗
PubMed1990

Clinical and laboratory evaluation of renal stone patients.

The management of renal lithiasis is a life-long proposition for most patients. Stone diseases are difficult for both patients and physicians to monitor and treat appropriately. The long-term management of metabolically active patients requires close association with a physician who is prepared to monitor stone formation, appropriate risk factors, and the progress of those risk factors over an extended time. Although this is a large economic commitment, it has been calculated that failure to carry out this responsibility is an even larger economic burden for patients and society. With aggressive risk factor management and follow-up, 95% of patients can become metabolically inactive. The long-term management of these patients, still evolving, is going to continue to require some assessment of the presence or absence of stones. The analysis of risk factors and the assessment of therapeutic maneuvers should continue to improve. It is possible that some specific index of risk factors for these patients will become readily available. Unfortunately, the efficacy of the ones currently available have not been clearly established.

Acetazolamide↗
PubMed1990

Malignant transformation of human fibroblasts by oncogene transfection or carcinogen treatment.

Exposure to chemical carcinogens or radiation is considered to cause most human cancer, but human cells in culture have not been successfully transformed to malignancy by such agents. Malignant transformation is a multi-step process and one explanation for the failure to induce such transformation of human cells in culture could be inability to recognize the phenotypes of carcinogen-treated cells that have undergone intermediate changes, so that these cells can be isolated and exposed a second time to cause further changes. To identify possible intermediates, we transfected diploid human fibroblasts with oncogenes known to be active in cells derived from fibrosarcomas and determined the phenotypes produced. H- or N-ras oncogenes flanked by suitable enhancer and promoter sequences caused the cells to exhibit several characteristics of malignant cells, but not to acquire an infinite life span or form tumors. Transfection of these oncogenes in the same constructions, or a viral K-ras oncogene, into an infinite life span, near-diploid, non-tumorigenic cell strain developed in this laboratory (MSU-1.1 cells) resulted in distinct foci of morphologically-altered, anchorage independent, and growth factor independent cells that formed progressively-growing, invasive malignant sarcomas in athymic mice and expressed the p21s of the transfected ras genes. Transfection of two other infinite life span human cell lines with the H-ras oncogene in the same construction also yielded malignant cells. Recently, we succeeded in inducing the malignant state in MSU-1.1 cells using carcinogen identified that are one step removed from malignant transformation, others that are two-steps removed, etc. Furthermore, we know what new phenotypes these cells need to express to be malignantly transformed and which oncogenes can make such a change. If, as suggested above, proto-oncogenes are the cellular targets for carcinogen attack, it should be possible, by carcinogen treatment to bring about the malignant state. We have recently succeeded in achieving just such transformation by exposing MSU-1.1 cells to chemical carcinogens.

Animals↗
PubMed1990

Distribution of aflatoxins in tissues of growing pigs fed an aflatoxin-contaminated diet amended with a high affinity aluminosilicate sorbent.

The effect of hydrated sodium calcium aluminosilicate (HSCAS) added to the diet of swine fed an aflatoxin-contaminated diet on tissue aflatoxin levels was investigated. Pigs were fed control (less than 10 ng/g B1 + B2), contaminated (500-600 ng/g B1 + B2), and contaminated +0.5% HSCAS diets. Tissues analyzed for the presence of aflatoxin B1, B2, and M1 residues included liver, muscle, kidney, and adipose. Addition of HSCAS to the contaminated diet significantly reduced the amount of M1 in liver, kidney, and muscle tissue. Aflatoxin B1 was not reduced in liver or kidney, but was decreased in muscle.

Aflatoxins↗
PubMed1989

Sodium/proton antiport is required for growth of Escherichia coli at alkaline pH.

Evidence is presented indicating that Escherichia coli requires the Na+/H+ antiporter and external sodium (or lithium) ion to grow at high pH. Cells were grown in plastic tubes containing medium with a very low Na+ content (5-15 microM). Normal cells grew at pH 7 or 8 with or without added Na+, but at pH 8.5 external Na was required for growth. A mutant with low antiporter activity failed to grow at pH 8.5 with or without Na+. On the other hand, another mutant with elevated antiporter activity grew at a higher pH than normal (pH 9) in the presence of added Na+ or Li+. Amiloride, an inhibitor of the antiporter, prevented cells from growing at pH 8.5 (plus Na+), although it had no effect on growth in media of lower pH values.

Amiloride↗
PubMed1989

Somatic and intellectual development in a patient with 47,XX,psu dic(X)(p11.2) chromosome constitution.

An unusual form of X chromosome aneuploidy, 47,XX,psu dic(X)(p11.2), was found during an evaluation for short stature of a prepubertal girl. Unlike 45,X, 47,XXX, 48,XXXX, and 49,XXXXX females, this patient is phenotypically normal except for her short stature, which appears to be unrelated to her chromosome abnormality. X chromosome inactivation studies disclosed inactivation (late replication) of one normal X and the abnormal X chromosome in all cells examined from this patient. Therefore, she is disomic for early-replicating distal Xp loci, found in inactivated X chromosomes, and thought to remain active after lyonization. These data suggest that the presence of three or more copies of the early-replicating, active Xp loci may be responsible for the cognitive deficits and other phenotypic abnormalities seen in and other phenotypic abnormalities seen in polysomy X females.

Aneuploidy↗
PubMed1989

Effects of elevated serum insulinlike growth factor-II on growth hormone and insulinlike growth factor-I mRNA and secretion.

The insulinlike growth factors (IGF) appear to exert feedback control over their own production. In an effort to determine the physiologic mechanisms for this feedback modulation, we utilized a previously developed in vivo model in which rIGF-II secreting tumor cells are transplanted into immunodeficient rats to form IGF-II secreting tumors. The tumor-bearing rat have serum IGF-II concentrations sevenfold greater than those in controls (119 +/- 16 ng/mL [mean +/- SE] v 17 +/- 2 ng/mL, P less than .0001). Serum IGF-I concentrations were reduced among the tumor-bearing rats (438 +/- 42 ng/mL v 606 +/- 32 ng/mL, P = .002) and were negatively correlated with IGF-II concentrations (r = -.47, P = .025), suggesting that IGF-II suppressed the secretion of IGF-I. Increased serum IGF-II concentrations, however, did not affect basal growth hormone concentrations (tumor-bearing, 44 +/- 12 ng/mL; control 33 +/- 6 ng/mL, P = 0.96). The GH response to GH releasing factor was likewise similar in both groups. Moreover, pituitary GH mRNA level were not different in the two groups, suggesting that IGF-II does not have a significant effect on GH secretion in this in vivo model. There was no association between serum glucose and serum IGF-I or IGF-II concentrations. To examine the effect of IGF-II on IGF-I production from the liver, we measured IGF-I mRNA levels in a subset of animals. Despite these differences in serum IGF-I concentrations, the tumor-bearing rats did not have significantly lower liver IGF-I mRNA levels.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1989

Clinical and laboratory approaches for evaluation of nephrolithiasis.

A medical history and laboratory investigation of patients with recurrent stones serve as the cornerstone for preventive and therapeutic treatment. Identifiable risk factors can be discovered in 90 per cent of the patients. More sophisticated analyses of urinary supersaturation can be helpful in resistant cases.

Calcium↗