Panel: Shared Governance and Collective Bargaining: The Line Between Protecting Shared Governance Through Collective Bargaining: Models Used by AAUP Chapters

For over five decades following its founding in 1915, the American Association of University Professors (AAUP) carried out its mission outside of the realm of collective bargaining. The organization formulated policy on a constantly evolving range of issues of concern to higher education, and worked to have those policies adopted by individual institutions and state public higher education systems. The mechanisms employed were a combination of: encouraging faculty to use their participation in shared governance to work towards policy adoption; interacting directly—including in the initial formulation of policy pronouncements and in joint endorsements—with organizations representing the interests of administrators and trustees; and carrying out visible “enforcement” activities (primarily investigations leading to censure and sanction.

Protecting Academic Freedom Through Collective Bargaining: An AAUP Perspective

AAUP’s turn to collective bargaining grew out of a more expansive view of unionization than is typical for American labor unions. The mission of the AAUP incorporates addressing economic matters, as does the purpose of unions generally. But the AAUP adopted collective bargaining as a means of protecting and expanding the professional interests of the profession. This paper surveys the various approaches that AAUP chapters have used to accomplish the safeguarding and expansion of academic freedom

Panel: Shared Governance and Collective Bargaining: The Line Between Protecting Shared Governance Through Collective Bargaining: Models Used by AAUP Chapters

For over five decades following its founding in 1915, the American Association of University Professors (AAUP) carried out its mission outside of the realm of collective bargaining. The organization formulated policy on a constantly evolving range of issues of concern to higher education, and worked to have those policies adopted by individual institutions and state public higher education systems. The mechanisms employed were a combination of: encouraging faculty to use their participation in shared governance to work towards policy adoption; interacting directly—including in the initial formulation of policy pronouncements and in joint endorsements—with organizations representing the interests of administrators and trustees; and carrying out visible “enforcement” activities (primarily investigations leading to censure and sanction.

Association Between Blood Pressure and Adverse Renal Events in Type 1 Diabetes.

ObjectiveTo compare different blood pressure (BP) levels in their association with the risk of renal outcomes in type 1 diabetes and to determine whether an intensive glycemic control strategy modifies this association.Research design and methodsWe included 1,441 participants with type 1 diabetes between the ages of 13 and 39 years who had previously been randomized to receive intensive versus conventional glycemic control in the Diabetes Control and Complications Trial (DCCT). The exposures of interest were time-updated systolic BP (SBP) and diastolic BP (DBP) categories. Outcomes included macroalbuminuria (>300 mg/24 h) or stage III chronic kidney disease (CKD) (sustained estimated glomerular filtration rate <60 mL/min/1.73 m2).ResultsDuring a median follow-up time of 24 years, there were 84 cases of stage III CKD and 169 cases of macroalbuminuria. In adjusted models, SBP in the <120 mmHg range was associated with a 0.59 times higher risk of macroalbuminuria (95% CI 0.37-0.95) and a 0.32 times higher risk of stage III CKD (95% CI 0.14-0.75) compared with SBPs between 130 and 140 mmHg. DBP in the <70 mmHg range were associated with a 0.73 times higher risk of macroalbuminuria (95% CI 0.44-1.18) and a 0.47 times higher risk of stage III CKD (95% CI 0.21-1.05) compared with DBPs between 80 and 90 mmHg. No interaction was noted between BP and prior DCCT-assigned glycemic control strategy (all P > 0.05).ConclusionsA lower BP (<120/70 mmHg) was associated with a substantially lower risk of adverse renal outcomes, regardless of the prior assigned glycemic control strategy. Interventional trials may be useful to help determine whether the currently recommended BP target of 140/90 mmHg may be too high for optimal renal protection in type 1 diabetes

Insulin-dependent diabetic sibling pairs are concordant for sodium-hydrogen antiport activity11See Editorial by Giancarlo Viberti, p. 2526.

Insulin-dependent diabetic sibling pairs are concordant for sodium-hydrogen antiport activity.BackgroundRecent findings of enhanced Na+/H+ antiport activity in cultured fibroblasts and immortalized lymphoblasts from type 1 diabetic patients with nephropathy support the view that a phenotypic or genotypic factor(s) underlies nephropathy risk. This study evaluated the kinetic properties of Na+/H+ antiporter in cultured fibroblasts from families with two siblings affected by type 1 (insulin-dependent) diabetes.MethodsSeventeen diabetic sibling pairs were studied. The age was 38 ± 10years (mean ± sd) in probands, the first to develop diabetes, and 39 ± 7 in siblings; the duration of diabetes was, by definition, longer in probands (24 ± 12 vs. 17 ± 8years in siblings). Na+/H+ antiport activity was determined using a microfluorometric technique with the pH sensitive dye 2′,7′-bis(2-carboxyethyl)-5(6)-carboxyfluorescein in skin fibroblasts cultured for at least six passages.ResultsThere were no significant differences between probands and siblings for the following parameters: glycated hemoglobin, 8.3 ± 0.8% in probands and 8.6 ± 1.4% in siblings; creatinine clearance, 103 ± 24 ml/min/1.73m2 in probands and 103 ± 25 in siblings; albumin excretion rate, 6.8 (1 to 860) μg/min (median and range) in probands and 4.9 (2 to 1334) in siblings. Intracellular pH and buffering capacity were superimposable in the sibling pairs. The Vmax for the antiport was 39.2 ± 14.7mmol/liter cell/min in probands and 40.3 ± 17.6 in siblings. The internal pH for half-maximal activation (Km) and Hill coefficient was also similar in probands and siblings. There were correlations between probands and siblings in values for intracellular pH (r = 0.51, P < 0.04), Vmax (r = 0.84, P < 0.0001), and buffering capacity (r = 0.53, P < 0.03). Glycated hemoglobin values over five years were not significantly correlated in the sibling pairs (r = 0.3, P > 0.1). Vmax was related with the albumin excretion rate (r = +0.49, P = 0.005) and glycated hemoglobin (r = +0.41, P = 0.017) in the total cohort of sibling pairs. However, multiple regression analysis, using Vmax as the dependent variable, found no correlations between any of the subjects’ clinical and demographic variables.ConclusionsFamilial concordance for Na+/H+ antiport activity in long-term cultured skin fibroblasts from type 1 diabetic siblings suggests that at least some of the in vitro phenotypical characteristics of these cells are likely to be genetically determined and to be, at least in part, independent of in vivo metabolic control

Studies of renal autoregulation in pancreatectomized and streptozotocin diabetic rats

Studies of renal autoregulation in pancreatectomized and streptozotocin diabetic rats. We studied renal autoregulation in pancreatectomized Munich-Wistar diabetic rats and in their sham-operated controls. In a second experiment we studied renal autoregulation in untreated and insulin treated streptozotocin diabetic Munich-Wistar rats and their nondiabetic controls. In the first experiment the diabetic rats had higher baseline renal blood flows (RBF). There was a fall in renal vascular resistance (RVR) and sustained RBF in both diabetic and control rats as renal perfusion pressures (RPP) was reduced from 130 and 110mm Hg. As RPP was reduced from 110 and 80mm Hg, there was no significant change in RVR in control rats and RBF began to fall. Below RPP of 80mm Hg RVR rose and RBF fell sharply in these rats. In contrast, there was a progressive fall in RVR as RPP was lowered to 60mm Hg in the diabetic rats and, thus, RBF was much better sustained in these animals. In the second experiment the plasma glucose level was 502 ± 52 mg/dl (X ± SD) in the untreated diabetic rats and only modestly reduced to 411 ± 49 mg/dl in the insulin treated animals. Untreated streptozotocin diabetic rats had moderately reduced and insulin-treated diabetic rats had mildly reduced baseline RVR and RBF. However, in these animals as in the pancreatectomized rats the increases in RVR noted in control rats at subautoregulatory RPPs were not seen. Thus, regardless of whether baseline RBFs were increased or decreased, diabetic rats sustained RBF at markedly reduced RPPs far more efficiently than did nondiabetic rats. The pathogenesis of these abnormalities in diabetic rats was not learned in these studies. However, it is likely that further study of autoregulation in diabetic rats could uncover factors influencing renal vascular tone which would be helpful in understanding the renal hemodynamic perturbations which may attend this experimental model