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J D Wagner

Publications and source records attributed to J D Wagner.

107 records · Page 6Linked to original sources
PubMed1989

1-p-chlorophenyl-4,4-dimethyl-5-diethylamino-1-penten-3-one hydrobromide, a sulfhydryl-specific compound which reacts irreversibly with protein thiols but reversibly with small molecular weight thiols.

1-p-Chlorophenyl-4,4-dimethyl-5-diethylamino-1-penten-3-one hydrobromide (CDDP) has been shown to react selectively with small molecular weight and protein thiols. The reaction of this compound with thiols can be monitored directly owing to the large decrease (approximately 21,000 M-1 cm-1 at 310 nm) in extinction coefficient subsequent to thiol addition. CDDP reacted stoichiometrically with large molecular weight (greater than 11,000) protein thiols. However, with small molecular weight thiols (less than 500) the reaction was less than stoichiometric, indicating a significant degree of back-reaction. The forward and reverse rate constants have been estimated. The fact that the reaction is reversible enables CDDP to be used for the direct monitoring of the oxidation of small molecular weight thiols.

Chlorobenzenes↗
PubMed1988

Gluten-sensitive enteropathy in a cynomolgus monkey.

A malabsorption syndrome was observed in a cynomolgus macaque. Clinical signs included weight loss despite increased appetite, and diarrhea, characterized by an increased volume of soft, tan, malodorous feces. Clinicopathologic findings included hypoalbuminemia, generalized dilation of bowel loops with a prolonged transit time, steatorrhea and markedly diminished absorption of D-xylose. Biopsies of the duodenum and jejunum had total villous atrophy, crypt hyperplasia and a plasmacytic-lymphocytic infiltrate of the lamina propria. The monkey's diet was changed to a semi-synthetic diet containing no grain products. Subsequently, stool characteristics, body weight and intestinal villous morphology returned to normal. This response to removal of grain products from the diet suggests a syndrome similar to gluten-sensitivity enteropathy in human beings.

Animals↗
PubMed1986

Effect of systemic acid-base disorders on ileal intracellular pH and ion transport.

We previously reported that changes in ileal net Na absorption correlated with arterial pH, changes in net HCO3 secretion correlated with the plasma HCO3 concentration, and changes in net Cl absorption correlated with arterial CO2 partial pressure (PCO2) during the systemic acid-base disorders. To determine whether changes in intracellular pH (pHi) and HCO3 concentration [( HCO3]i) mediated these effects, we measured pHi and calculated [HCO3]i in the distal ileal mucosa of anesthetized, mechanically ventilated Sprague-Dawley rats using 5,5-[14C]dimethyloxazolidine-2,4,-dione and [3H]inulin. Rats were studied during normocapnia, acute respiratory acidosis, and alkalosis, and uncompensated and pH-compensated acute metabolic acidosis and alkalosis. When animals in all groups were considered, mucosal pHi was not altered, but there were strong correlations between mucosal [HCO3]i and both arterial PCO2 (r = 0.97) and [HCO3] (r = 0.61). When we considered the rates of ileal electrolyte transport that characterized these acid-base disorders [A. N. Charney and L.P. Haskell, Am. J. Physiol. 245 (Gastrointest. Liver Physiol. 8): G230-G235, 1983], we found strong correlations between mucosal [HCO3]i and both net Cl absorption (r = 0.88) and net HCO3 secretion (r = 0.82). These findings suggest that the systemic acid-base disorders do not affect ileal mucosal pHi but do alter mucosal [HCO3]i as a consequence of altered arterial PCO2 and [HCO3]. The effects of these disorders on ileal net Cl absorption and HCO3 secretion may be mediated by changes in [HCO3]i. Arterial pH does not appear to alter ileal Na absorption through changes in the mucosal acid-base milieu.

Acid-Base Imbalance↗
PubMed1986

Functional role of carbonic anhydrase in intestinal electrolyte transport.

We examined the role of carbonic anhydrase activity in intestinal transport by measuring the effect of systemic pH and PCO2 on electrolyte transport in the presence and absence of luminal acetazolamide. Adult Sprague-Dawley rats were anesthetized, and ileal and colonic segments were perfused with Ringer solution that was acetazolamide-free or that contained 0.1 mM sodium acetazolamide. Consecutive states of acute respiratory alkalosis and acidosis were created by changing the inspired CO2 from 0% (room air) to 8% CO2. In the ileum, acetazolamide perfusion did not affect the increment in net sodium and chloride absorption caused by a reduction in systemic pH. Mucosal carbonic anhydrase activity in this segment was measurable, although very low. In both the ascending and descending colon, acetazolamide perfusion reduced the increment in net sodium absorption caused by an increase in systemic PCO2. In addition, acetazolamide increased the chloride absorptive response to PCO2 in the ascending colon but did not affect the chloride response at all in the descending colon. Colonic mucosal carbonic anhydrase exhibited a proximal-to-distal gradient of activity: levels in the ascending colon were severalfold greater than in the descending colon. These findings suggest a functional role for carbonic anhydrase in mediating the colonic but not the ileal absorptive response to changes in systemic acid-base balance.

Acetazolamide↗
PubMed1985

Effect of systemic acid-base disorders on colonic intracellular pH and ion transport.

We have previously reported that changes in colonic net Na and Cl absorption correlate with arterial CO2 partial pressure (PCO2) and that changes in colonic net Cl absorption and HCO3 secretion correlate with the plasma HCO3 concentration during the systemic acid-base disorders. To determine whether changes in intracellular pH (pHi) and HCO3 concentration [( HCO3]i) mediate these effects, we measured pHi and calculated [HCO3] in the distal colonic mucosa of anesthetized, mechanically ventilated Sprague-Dawley rats using 5,5-[14C]dimethyloxazolidine-2,4-dione and [3H]inulin. Rats were studied during normocapnia, acute respiratory acidosis and alkalosis, and uncompensated and pH-compensated acute metabolic acidosis and alkalosis. When animals in all groups were considered, there were strong correlations between mucosal pHi and both arterial PCO2 (r = -0.76) and pH (r = 0.82) and between mucosal [HCO3]i and both arterial PCO2 (r = 0.98) and HCO3 concentration (r = 0.77). When we considered the rates of colonic electrolyte transport that characterized these acid-base disorders [A. N. Charney and L. P. Haskell. Am. J. Physiol. 246 (Gastrointest. Liver Physiol. 9): G159-G165, 1984], we found strong correlations between mucosal pHi and net Na absorption (r = -0.86) and between mucosal [HCO3]i and both net Cl absorption (r = 0.98) and net HCO3 secretion (r = 0.83). These findings suggest that the systemic acid-base disorders cause changes in colonic mucosal pHi and [HCO3]i as a consequence of altered arterial PCO2 and HCO3 concentration. In addition, the effects of these disorders on colonic electrolyte transport may be mediated by changes in mucosal pHi and [HCO3]i.

Acid-Base Imbalance↗
PubMed1982

Glucagon and the Ca2+-linked hormones angiotensin II, norepinephrine, and vasopressin stimulate the phosphorylation of distinct substrates in intact hepatocytes.

Recent studies have demonstrated that angiotensin II, catecholamines, and vasopressin can stimulate the phosphorylation of hepatic cytosolic proteins via a Ca2+-linked cyclic AMP-independent mechanism. The present study used high resolution, two-dimensional gel electrophoresis to determine if the proteins phosphorylated in response to the Ca2+-linked hormones were distinct from those affected by glucagon acting via the cyclic AMP-dependent pathway. Intact hepatocytes labeled with [32P]PO4(3-) were stimulated with glucagon, angiotensin II, l-norepinephrine, and vasopressin and over 100 phosphorylated proteins resolved by two-dimensional electrophoresis and autoradiography. Six important enzymes known to be regulated through covalent modification were positively identified, including phosphorylase, phosphofructokinase, pyruvate kinase, fructose-6-phosphate, 2-kinase, phenylalanine hydroxylase, and fructose-1,6-bisphosphatase. Computer analysis of the autoradiograms from control and hormone-treated cells demonstrated that glucagon increased the phosphorylation state of 12 phosphoproteins and reduced the phosphorylation of one protein with a Mr = 21,000 and a pI = 5.9. The Ca2+-linked hormones stimulated the phosphorylation of 7 phosphoproteins and also reduced the phosphorylation state of the 21,000-dalton protein. Angiotensin II, l-norepinephrine, and vasopressin had equivalent effects on protein phosphorylation. There were six protein substrates uniquely affected by glucagon and one phosphoprotein uniquely stimulated by the Ca2+-linked hormones. Seven substrates were affected by stimulation of the cell with either glucagon or the Ca2+-linked hormones. These results demonstrate that, while there is overlap in the substrates affected by glucagon and the Ca2+-linked hormones, each pathway is able to affect the phosphorylation of unique substrates. This finding suggests that the two types of hormones may have some distinct effects on hepatic function.U

Angiotensin II↗
PubMed1978

[Serum alpha 1-fetoprotein and extrahepatic digestive cancers. Apropos of 4 further cases].

The authors report four new cases of primary digestive carcinoma other than hepatoma with alpha 1 feto-protein in the serum (greater than 200 ng/ml). Two were carcinoma of the colon without liver metastases. The remaining two were also colonic carcinoma but with liver metastases. In the first cases, alpha 1 feto-protein disappear after surgical procedure. In spite of the rareness of primary digestive carcinoma with presence of alpha 1 feto-protein noted until now, these cases require reconsideration of the idea that AFP is specific for hepatoma.

Aged↗
PubMedDate not supplied

Naturally occurring and experimental diabetes in cynomolgus monkeys: a comparison of carbohydrate and lipid metabolism and islet pathology.

Diabetes is a major health problem of increasing incidence in the United States. Diabetes research has been limited by lack of availability of good animal models, particularly for the study of comorbidities associated with diabetes. We investigated the use of cynomolgus monkeys as an animal model of both type 1 and type 2 diabetes and compared these naturally occurring diseases with streptozotocin-induced diabetes. Both type 1 diabetics and streptozotocin-induced diabetics present with sudden onset of hyperglycemia and are ketosis prone without exogenous insulin. Type 2 diabetics can have a very long period of moderate hyperglycemia and hypertriglyceridemia and only require exogenous insulin therapy if pancreatic islet reserves are depleted. Type 2 diabetes is preceded by a relatively long period of insulin resistance that is associated with obesity and dyslipidemia. As insulin resistance progresses, islet size and insulin content increases initially. However, with sustained periods of insulin resistance, islet amyloid polypeptide (IAPP) is deposited in islets and can replace normal islet architecture, resulting in an insulin-deficient state. Appearance of IAPP also occurs in human type 2 diabetics but not in conventional rodent models. Unlike type 2 diabetes, neither type 1 nor streptozotocin-induced diabetes is associated with IAPP. Rather, islets can appear normal histologically, but have decreased insulin secretion and immunostaining. Further, the amount of insulin present in the islet is correlated with plasma insulin levels following glucose challenge. Studies are ongoing to determine the pathogenic changes associated with the progression of diabetes and to find novel drug treatments for diabetics.

Animals↗
PubMedDate not supplied

A comparative study of homeless, previously homeless, and never homeless school-aged children's health.

The purpose of this cross-sectional study was to compare the mental health, physical health, and healthcare practices of homeless, previously homeless, and never homeless poor school-aged children. The sample was comprised of 134 children who ranged in age from 8 to 12 years. The children participated in health assessments and completed two psychometric tests: the Children's Depression Inventory (CDI) (Kovacs, 1985) and the Revised Children's Manifest Anxiety Scale (RCMAS) (Reynolds & Richmond, 1985). Their mothers completed the Child Behavior Problem Checklist (CBCL) (Achenbach, 1991) and participated in an interview. The homeless (n = 67), previously homeless (n = 30), and never homeless children (n = 37) were similar in regard to their health assessment findings, reported health problems, healthcare practices, and CBCL scores. The proportions of homeless and previously homeless children with CDI scores in the clinical range were significantly greater than the never homeless poor children. The homeless children had significantly higher anxiety scores than the previously homeless and never homeless children. All three groups of children were at risk for physical and mental health problems; however, the findings suggest that school-aged children who experience homelessness may be at greater risk for depression and anxiety than never homeless poor children.

Case-Control Studies↗
PubMedDate not supplied

The experience of homeless female-headed families.

Eighty-five percent of homeless families are headed by single women who are extremely vulnerable and at risk for poor physical, emotional, and social health. The purpose of this naturalistic inquiry was to describe the experiences of 16 women in homeless female-headed families. These women participated in tape-recorded interviews. The themes that emerged from the interviews were a loss of freedom, a sense of being different, feeling down, maternal survival, and living under pressure. Being homeless was compared to a nightmare in which one does not know what will happen or where one will be from day to day. Implications for nursing practice and research are discussed.

Adaptation, Psychological↗