Alexander & Margaret Stewart Trust

Health care systems continue to experience the sequential aftermath of the COVID-19 pandemic, with major care access, quality, safety, financial sustainability, and workforce considerations. Yet, academic-clinical partnership opportunities exist for transformational change, even when efforts to respond to a pandemic seem insurmountable. A nursing partnership between an academic health center nursing school and university health system provided short- and long-term support for the nursing workforce shortage during a COVID-19 surge. An academic-clinical integration framework guided planning, clinical support activities, outcomes achieved, technology innovations, and shared lessons associated with these efforts. The COVID-19 surge response steps included a call to action, preparation for surge support by the academic and clinical partners, and a team approach for clinical service delivery by faculty, students, and staff. Through the 6-week COVID-19 surge response, more than 10 000 hours of hospital nurse staffing were provided by nursing school faculty and students; over 770 worked shifts that provided approximately 30% of the full surge hospital supplemental staffing and approximately 46 000 vaccine encounters. Well-established academic-clinical nursing partnerships allow for quick pivots in the rapidly changing COVID-19 environment that can enhance nursing clinical proficiency and competency, augment clinically immersive learning, and reinforce analytics to measure health outcomes, lower costs, improve access, quality, safety, and workforce conditions.

Making major treatment decisions with life-altering consequences is a significant challenge faced by parents of children with cancer. The unique experience of parents is not well represented in the growing literature on cancer treatment decision making (TDM). The objective of this study was to describe the process of parents making major treatment decisions for their children with cancer. Using grounded theory methods, we interviewed 15 parents of 13 children with cancer facing major treatment decisions. Parents' determination to make the right decision was both a demanding responsibility and a natural extension of the parental role. Everything parents encountered and undertook during the TDM process was in the service of making the right decision for their child. All parents expressed conviction that they had made the right decision, but conviction was tempered by doubts triggered by the pervasive uncertainty of the childhood cancer experience. Parents described limited TDM participation by extended family members and the affected children themselves, asserting their primary responsibility to act as their child's surrogate in partnership with the child's medical team. Making the right decision for one's child under challenging conditions is an extension of the parental obligation to act in the child's best interest and a responsibility that parents claim as their own. The findings from this study can serve as the foundation for future studies to refine the conceptualization of TDM in childhood cancer, which will in turn ground the development and evaluation of interventions to support parents in their critical TDM role.

Cost allocation issues have befuddled management around the world for over a century. And, because of “informational asymmetries” and agency conflicts between operating management and headquarters, there is no clear theoretical solution to the problem. Nevertheless, there are good reasons for allocating costs. If properly structured, transfer‐pricing schemes can serve the same purpose as a market price. By communicating useful information about the relative scarcity of resources within an organization, they can serve to balance supply and demand for the product or service being priced.Unfortunately, most transfer‐pricing approaches, like Activity Based Costing, attempt to solve the problem by refining standard cost measures. In contrast to ABC, this article begins by recognizing that efforts to develop more precise cost allocations are bound to be frustrated by the information and incentive problems noted above. And in place of more precisely formulated measures of cost, the author proposes a process of negotiation between two parties to an exchange—a process that is reinforced by a performance measurement system that gives both parties incentives to reveal their “reservation” prices for the good or service in question. For transfers involving multiple users of a given service or products, the author recommends a transfer auction process that is also designed to make would‐be users reveal their assessments of value.

ABSTRACT A new approach to assessing the on-bottom stability of jack-up rigs during preloading is presented. A leaning Instability IS described, which may appear similar to a punch through, but is associated with soil stiffness and rig flexure. Suggestions for avoiding this instability are given. INTRODUCTION Jack-up foundation failures during preloading are generally associated with a so-called "punch through". When a strong soil layer overlies a weak layer punch through may occur. The typical example is a sand layer, or sand lens, above a weak clay. If spud can load exceeds the bearing capacity of the sand layer, the spud can will penetrate into the weaker layer. This may happen suddenly and penetration into the weaker layer may be deep. Buoyancy support on the hull may eventually prevent further spud can penetration. In soft uniform soils, where bearing capacity increases continuously With depth, punch through failures are not expected. However, there have been foundation failures in such conditions, which appear to be punch through, but cannot be explained geotechnical by the normal punch through model. Ingram & Dutt (Reference 1) describe such an event in the Gulf of Mexico in 1982. This paper describes a new method for calculating elevated stability of jack-ups during preload where spud can loads are steadily increased. It shows how unstable leaning, leading to rapid leg penetration, can occur in soft soils where punch through cannot be the failure mechanism. For the purposes of this paper, the term rapid leg penetration is used to describe leg penetration rates which are faster than the rig's jacking rate. This typically means 1.5 feet per minute. As will become evident in the paper, the speed at which events take place is a critical factor. STABILITY REQUIREMENTS Stability requirements (Operations Elevated) for Mobile Offshore. Drilling units are normally addressed by classification societies along with governmental regulatory bodies. These requirements vary from being quite extensive as pertains to Environmental Forces, Soil Particulars, Overturning moments, Air Gaps and various Safety Factors, to being Just a general statement in regards to these variables. The U.S. Coast Guard (USCG) and the American Bureau of Shipping (ABS) make a general statement in regards to operations. Elevated/Stability On Bottom. The ABS, in their publication Rules for Building and Classing Mobile Offshore Drilling Units, Section 3' Part 3.13 state : Units Resting on the Sea Bed "Units which are to rest on the sea bed are to have sufficient positive downward gravity loadings on the support footings or mat to withstand the overturning moment of the combined environmental forces from any direction. Realistic variable loads are to be considered." Underwriter-approved Marine Surveyors can provide Location Approvals for Mobile Offshore Drilling Units Operations Elevated. ' It is standard in the industry that these location approvals be based on compliance with the approved Rig Operations Manual.

We have previously shown that topical brain application of kallikrein, an enzyme which converts kininogen to bradykinin, induces rabbit pial arteriole dilation. The purpose of the present investigation was to utilize a newly developed competitive kinin receptor antagonist to test the hypothesis that kallikrein-induced dilation was due to the conversion of brain kininogen to vasoactive kinins. As in our previous study, we measured rabbit pial arteriole diameter with a microscope using the closed cranial window technique. The kinin antagonist (6 microM) reduced the dose-dependent dilation produced by bradykinin and blocked the dilation induced by kallikrein. In addition, the kinin antagonist was specific since it did not alter the cerebral arteriole dilation produced by adenosine, acetylcholine, or vasoactive intestinal polypeptide. These experiments provide further evidence for a possible role of the endogenous brain kallikrein-kinin system in the modulation of the cerebral circulation and provide the necessary pharmacologic foundation for future use of this antagonist in testing the role of kinins in the normal or altered cerebral circulation.

Calcium antagonists may be of significant benefit in the pharmacotherapy of cerebral ischemia, possibly by improving postischemic cerebral blood flow (CBF). This study evaluated the effects of the calcium antagonist nimodipine on CBF in a newborn beagle pup model of perinatal asphyxia lasting 5 minutes. Immediately after the asphyxial episode, nimodipine (2 micrograms/kg/min) or saline was infused for 10 minutes, following which [14C]iodoantipyrine determinations of CBF were performed. In noninsulted pups, nimodipine caused both significant decreases in CBF to cortical and deep gray structures as well as a decrease in mean arterial blood pressure (MABP) (p less than 0.05). In insulted pups, nimodipine similarly decreased MABP (p less than 0.001) and CBF to cortical and deep gray matter regions. Nimodipine appeared to have no effect on arterial blood gases and EEG tracings in either insulted or noninsulted pups. Although nimodipine may be shown to improve neurologic outcome in asphyxiated newborn infants, the limits of this study do not show the mechanism to be that of improving CBF.

Neural crest cells are known to contribute to the normal architecture of the heart and aortic arch arteries. Ablation of neural crest cells over somites 1 to 3 in the chick embryo prevents conotruncal septation and results in persistent truncus arteriosus. To determine whether a deficiency of cardiac neural crest cells produces hemodynamic changes prior to the development of identifiable structural defects in the heart, we measured dorsal aortic blood velocity and vitelline artery blood pressure in lesioned and control embryos at a period of cardiac morphogenesis prior to septal formation. The internal diameter of the dorsal aorta at the level of the sinus venosus and the internal diameter of the aortic arch arteries at their midpoints were measured in embryos at Stage 18 of development using a filar micrometer eyepiece and a dissecting microscope. Embryos with neural crest lesions had significantly greater dorsal aortic blood flow velocity than control embryos. In addition, embryos lacking cardiac neural crest had significantly lower systolic and diastolic blood pressures than control embryos. There was no difference in heart rate, dorsal aortic diameter or internal diameter of the aortic arch arteries between lesioned and control embryos. Scanning electron micrographs revealed no gross morphological differences in cardiac looping or conotruncal wall development between lesioned and control embryos; however, embryos with cardiac neural crest ablations developed markedly hypoplastic 4th pharyngeal arches. This data suggests that hemodynamic changes precede the onset of structural heart defects in embryos with cardiac neural crest ablations.

Assessment of the severity of aortic stenosis remains a commonly encountered clinical problem. Noninvasive evaluation has to date not proven sufficiently accurate in most cases to permit clinical decision making in the individual patient. Therefore, cardiac catheterization and measurement of the valve area with use of the Gorlin equation remains the standard approach in patients with suspected aortic stenosis. Doppler ultrasound allows direct measurement of blood velocity in cardiac chambers. This technique was used to study 16 patients with suspected aortic stenosis after cardiac catheterization. Aortic valve area (AVA) was calculated with the equation AVA = CO/(SEP X mean velocity), where CO is cardiac output measured by thermodilution and SEP is the systolic ejection period derived from the Doppler tracings. The resulting value was compared with valve area calculated from cardiac catheterization data and an excellent correlation was noted (r = .99). This study demonstrates that Doppler ultrasound can be used to accurately measure aortic valve area without the need for left heart catheterization.