Dispensaries in Massachusetts, Particularly in Boston

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Tourniquetless Total Knee Arthroplasty With Modern Perioperative Protocols Decreases Pain and Opioid Consumption in Women

Background This study examined whether a modern total knee arthroplasty (TKA) protocol without a tourniquet results in less patient-reported pain and in-hospital opioid consumption compared to TKA with a tourniquet. Methods A retrospective study of 203 primary unilateral cemented TKAs consecutively performed with or without tourniquet was performed. Identical perioperative pain and blood loss protocols were used in all cases. In tourniquetless TKAs, the tourniquet was not inflated at any time, and sterile CO2 gas compression maximized cement interdigitation. Results After exclusions for scientific confounds, 184 TKAs (93 with tourniquet; 91 tourniquetless) were analyzed. Controlling for multiple covariates, females with a tourniquet reported significantly more pain (P = .002) and opioid consumption (P < .001) the first 24 hours after surgery compared to females without a tourniquet. There were no differences in pain (P = .192) or amount of opioids consumed (P = .203) among males with and without a tourniquet. Tourniquet use resulted in a significant reduction in blood loss for both females (P ≤ .040) and males (P ≤ .020), although the total blood savings of approximately 200 mL is of unknown clinical significance. Conclusion Avoiding tourniquet use during TKA for females may be a relatively risk-free adjunct to minimize opioid consumption during hospitalization. Further study is warranted to elucidate the factors accounting for different outcomes in females and males

Preparing for the initial observations of the Targeted Search and the Sky Survey systems

During this period, the SETI project prepared for the initial observations with both the Targeted Search and Sky Survey systems. I am nominally a member of the Targeted Search team, but participated actively in both parts of the project. My activities were concentrated primarily in three areas: coordination with Arecibo Observatory in preparation for the initial observations on October 12, 1992; development of a design concept for confirming observations; and participation (at JPL) in a design review of the rf system

Alpha1 -adrenergic stimulation selectively enhances endothelium-mediated vasodilation in rat cremaster arteries.

We have systematically investigated how vascular smooth muscle α1 -adrenoceptor activation impacts endothelium-mediated vasodilation in isolated, myogenically active, rat cremaster muscle 1A arteries. Cannulated cremaster arteries were pressurized intraluminally to 70&nbsp;mmHg to induce myogenic tone, and exposed to vasoactive agents via bath superfusion at 34°C. Smooth muscle membrane potential was measured via sharp microelectrode recordings in pressurized, myogenic arteries. The α1 -adrenergic agonist phenylephrine (25-100&nbsp;nmol/L) produced further constriction of myogenic arteries, but did not alter the vasorelaxant responses to acetylcholine (0.3&nbsp;μmol/L), SKA-31 (an activator of endothelial Ca2+ -dependent K+ channels) (3&nbsp;μmol/L) or sodium nitroprusside (10&nbsp;μmol/L). Exposure to 0.25-1&nbsp;μmol/L phenylephrine or 1&nbsp;μmol/L norepinephrine generated more robust constrictions, and also enhanced the vasodilations evoked by acetylcholine and SKA-31, but not by sodium nitroprusside. In contrast, the thromboxane receptor agonist U46619 (250&nbsp;nmol/L) dampened responses to all three vasodilators. Phenylephrine exposure depolarized myogenic arteries, and mimicking this effect with 4-aminopyridine (1&nbsp;mmol/L) was sufficient to augment the SKA-31-evoked vasodilation. Inhibition of L-type Ca2+ channels by 1&nbsp;μmol/L nifedipine decreased myogenic tone, phenylephrine-induced constriction and prevented α1 -adrenergic enhancement of endothelium-evoked vasodilation; these latter deficits were overcome by exposure to 3 and 10&nbsp;μmol/L phenylephrine. Mechanistically, augmentation of ACh-evoked dilation by phenylephrine was dampened by eNOS inhibition and abolished by blockade of endothelial KCa channels. Collectively, these data suggest that increasing α1 -adrenoceptor activation beyond a threshold level augments endothelium-evoked vasodilation, likely by triggering transcellular signaling between smooth muscle and the endothelium. Physiologically, this negative feedback process may serve as a "brake" to limit the extent of vasoconstriction in the skeletal microcirculation evoked by the elevated sympathetic tone

The Phases and Faces of the Duke Lacrosse Controversy: A Conversation James E. Coleman, Jr.

This panel took place at the 2008 Annual Meeting of the Southeastern Association of Law Schools ( SEALS ) in July 2008 in West Palm Beach, Florid