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J Stubbs

Publications and source records attributed to J Stubbs.

At least 37 records · Page 2Linked to original sources
PubMed1993

The Edinburgh Postnatal Depression Scale: validation for an Australian sample.

One hundred and three post-partum women completed the Edinburgh Postnatal Depression Scale (EPDS) and were interviewed using the Diagnostic Interview Schedule. A cut-off score of 12.5 on the Edinburgh Postnatal Depression Scale identified all nine women who reached criteria for major depression. At this threshold the sensitivity (the percentage of true "cases" identified) of the EPDS was 100%, its specificity (the percentage of true "non-cases" identified as such) 95.7% and its positive predictive value (the percentage of all those tested as positive who were correctly identified as such) 69.2%. Although this study supported the validity of the EPDS, a replication of this study on a larger sample is suggested.

Adult↗
PubMed1992

Studies of Muc-1 mucin expression and polarity in the mouse mammary gland demonstrate developmental regulation of Muc-1 glycosylation and establish the hormonal basis for mRNA expression.

Muc-1 is a major mucin glycoprotein expressed on the surface of mammary epithelial cells. It has attracted considerable attention as it is expressed in an aberrant form on many breast tumor cells. Here we describe studies using a recently obtained cDNA probe of Muc-1 expression during lactogenic development in the mouse. Northern blot analysis demonstrated that Muc-1 is expressed at all stages of lactogenic development but its levels are increased very significantly during mid-pregnancy and into lactation. The basis of this was examined using CID-9 mammary epithelial cell cultures. It was found that in the presence of insulin Muc-1 mRNA levels were increased by both hydrocortisone and prolactin, with the combination of the three hormones supporting maximum expression. Muc-1 mRNA levels were also modulated by culturing cells on a basement-membrane-like extracellular matrix that promoted mRNA levels 5- to 10-fold above levels in cells cultured on plastic tissue culture dishes. Immunocytochemical studies using monoclonal antibodies to carbohydrate epitopes on Muc-1 demonstrated that while Muc-1 was found at all developmental stages, it became increasingly sialylated during the course of pregnancy and into lactation. Additionally, we found that while Muc-1 is tightly polarized to the apical surface of the epithelium of lactating and pregnant mice it exhibited a less-polarized distribution on a small proportion of ductal cells in virgin mice. We conclude that the expression of Muc-1 is regulated at several different levels and by a number of different factors. We speculate that this may reflect different functional roles for Muc-1 at different stages of mammary development.

Animals↗
PubMed1984

Adhesive multiplicity in the interaction of embryonic fibroblasts and myoblasts with extracellular matrices.

Neff et al. (1982, J. Cell Biol., 95:654-666) have described a monoclonal antibody, CSAT, directed against a cell surface antigen that participates in the adhesion of skeletal muscle to extracellular matrices. We used the same antibody to compare and parse the determinants of adhesion and morphology on myogenic and fibrogenic cells. We report here that the antigen is present on skeletal and cardiac muscle and on tendon, skeletal, dermal, and cardiac fibroblasts; however, its contribution to their morphology and adhesion is different. The antibody produces large alterations in the morphology and adhesion of skeletal myoblasts and tendon fibroblasts; in contrast, its effects on the cardiac fibroblasts are not readily detected. The effects of CSAT on the other cell types, i.e., dermal and skeletal fibroblasts, cardiac muscle, 5-bromodeoxyuridine-treated skeletal muscle, lie between these extremes. The effects of CSAT on the skeletal myoblasts depends on the calcium concentration in the growth medium and on the culture age. We interpret these differential responses to CSAT as revealing differences in the adhesion of the various cells to extracellular matrices. This interpretation is supported by parallel studies using quantitative assays of cell-matrix adhesion. The likely origin of these adhesive differences is the progressive display of different kinds of adhesion-related molecules and their organizational complexes on increasingly adhesive cells. The antigen to which CSAT is directed is present on all of the above cells and thus appears to be a lowest common denominator of their adhesion to extracellular matrices.

Animals↗
PubMed1983

The effect of cardiac denervation and beta-blockade on control of cardiac output in exercising dogs.

Normal and cardiac denervated dogs, with an electromagnetic aortic flowprobe implanted at least 14 days before the experiments, ran at different speeds on a 25% graded treadmill. The experiments were carried out before and after blockade of betareceptors in the heart by PO administration of 125 mg X kg-1 practolol per day. Changes in stroke volume, heart rate, and cardiac output were measured. After beta-adrenergic blockade, only two of the seven dogs with denervated hearts were prepared to run at a limited number of speeds. Time constants of the cardiac output changes at the onset of exercise were significantly different (P less than 0.001) for the normal (11.5 +/- 0.7 s, mean +/- SEM) and the denervated dogs (29.5 +/- 1.1 s), but in normal dogs did not change with practolol (11.8 +/- 0.8 s). The steady state relationship between cardiac output (CO) and work per unit time performed on the treadmill (P) was for normal dogs: CO = 156 + 1.55P, for normal dogs after practolol treatment: CO = 156 + 0.43P (slope significantly different, P less than 0.05), and for dogs with denervated hearts: CO = 121 + 2.06P (not significantly different from normal dogs). It was concluded that changes in the venous or arterial system alone are not sufficient to increase cardiac output appreciably during exercise. The magnitude of the cardiac output increase depends more on the presence of intact beta-receptors than on the presence of intact cardiac nerves.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1981

The role of the cardiac nerves in regulation of sodium excretion in conscious dogs.

Conscious, chronically instrumented dogs, maintained on a high sodium intake, were used to investigate whether surgical cardiac denervation impairs the natriuresis associated with left atrial pressure increase produced in three ways: during an increase in left atrial pressure by means of a reversible mitral stenosis (protocol 1); after an i.v. saline load (1.0 ml 0.9% saline min-1 . kg-1 over 60 min) (protocol 2); after an oral saline load (14.5 mmol Na . kg-1 given with the food as isotonic solution) (protocol 3). During a reversible mitral stenosis, in intact dogs, urine volume and sodium excretion increased markedly (from 34--145 microliters . min-1 . kg-1 and from 3--12 mumol . min-1 . kg-1); mean arterial pressure increased by an average of 2 kPa (15 mm Hg) and heart rate by 53 b/min; plasma renin activity fell from 0.37--0.21 ng AI . ml-1 . h-1 . Cardiac denervation eliminated these effects of left atrial distension except for a small increase in heart rate (12 b/min). This indicates that the natriuresis and diuresis during left atrial distension resulted from stimulation of receptors located in the left atrium. In contrast, during protocol 2 and 3, the same amounts of sodium and water were excreted in the cardiac denervated dogs as compared to the intact dogs. A comparable decrease in plasma renin activity also was observed. -- Apparently the presence of the cardiac nerves is not a prerequisite for maintenance of sodium and water homeostasis.

Animals↗
PubMed1980

Inhibition of glycolysis in the denervated dog heart.

We measured glucose metabolism in five dogs before and 3 weeks after cardiac denervation; after this time myocardial norepinephrine is depleted. The discharge by the myocardium, of 14CO2 from infused 14C-D-glucose (U), decreased following denervation (P = 0.05). The ratio of 14CO2 to total CO2 production, which measured the proportion of glucose to total substrate oxidized, also decreased following denervation (P = 0.05). The inhibition of glucose oxidation by denervation was not due to an increase in arterial lactate concentration. There was an associated increase in myocardial content of fructose-6-phosphate in an additional seven dogs (P < 0.01). We postulate that myocardial tissue norepinephrine is one of the controllers of the activity of phosphofructokinase.

Animals↗
PubMed1977

The effect of an increase in aortic pressure upon the inotropic state of cat and dog left ventricles.

1. The effect of increased aortic pressure on the inotropic state of the left ventricle was studied in isolated cat hearts, perfused with bovine red cells in Tyrode solution, ejecting into a hydraulic model with the same input impedance as that of the cat aorta.2. Inotropic state was assessed at a controlled left ventricular end-diastolic pressure by interpolating single isovolumic beats by means of an occluder in the aortic cannula.3. When such isovolumic beats during periods of raised aortic pressure were compared with those during control periods, the difference in peak isovolumic pressure ranged from -0.3 to +0.5 kPa indicating differences in inotropic state which were small and inconsistent in direction.4. The maximum rate of rise of left ventricular pressure (dP/dt(max).) of ejecting beats was little affected by a rise of aortic pressure and the direction of changes was inconsistent.5. The effect of increased aortic pressure was studied in intact dogs after cardiac denervation; left ventricular end-diastolic pressure was uncontrolled and therefore rose to a higher steady level.6. No consistent change of dP/dt(max). was found during the period of increased aortic pressure.7. All flow and pressure variables remained steady during the period of increased aortic pressure after the higher level of left ventricular end-diastolic pressure had been established.8. These results demonstrate that neither the positive inotropic effect nor the negative inotropic effect of increased load dominates in these preparations. This may be the result of a balance between the two effects, or they may be of unimportant magnitude under physiological conditions.

Animals↗
PubMed1973

Studies on beta-galactoside transport in a Proteus mirabilis merodiploid carrying an Escherichia coli lactose operon.

Merodiploid derivatives bearing an F-linked lac operon (i(+), o(+), z(+), y(+), a(+)) from Escherichia coli were prepared from a Proteus mirabilis strain unable to utilize lactose and from a lac deletion strain of E. coli. A suitable growth medium was found in which the episomal element in the P. mirabilis derivative was sufficiently stable to allow induction of the episome-borne lac operon and thus to permit a comparison of the activities and properties of E. coli lac products in the intracellular environments of P. mirabilis and E. coli. In both derivatives the episomal lac operon was shown to be repressed in the absence of inducer. Kinetics of induction with gratuitous inducer (isopropyl-1-thio-beta-d-galactoside) were similar for both beta-galactosidase activity (beta-d-galactoside galactohydrolase, EC 3.4.1.23) and beta-galactoside transport activity in both derivatives, although the ratio of galactoside transport to beta-galactosidase activity was approximately 1.6-fold higher in the E. coli derivative. Comparison of beta-galactosidase and M-protein (lac y gene product)-specific activities indicated coordinate expression of the induced lac operon in both derivatives. Quantitatively, the maximal beta-galactosidase specific activity was two or three times higher for the E. coli derivative. A significant sodium azide inhibition (65% inhibition by 10 mM sodium azide) of lactose permease-mediated transport of o-nitrophenyl-beta-galactoside from an outside region of high concentration to an inside region of very low concentration ("downhill transport") was observed for the P. mirabilis derivative. Identical conditions for the E. coli derivative yielded only about 15% inhibition. Active transport of thiomethyl-beta-galactoside was similar for both derivatives, the major difference being that active transport was more sensitive to azide poisoning in the P. mirabilis derivative. Preliminary examination of the thiomethyl-beta-galactoside derivatives following active transport did not demonstrate the accumulation of a phosphorylated product in either strain but did reveal an unidentified derivative present in the P. mirabilis merodiploid extract which was not detectable in the E. coli merodiploid.

Azides↗