Value of Extended Warming in Patients Undergoing Elective Surgery

Perioperative temperature management is imperative for positive surgical outcomes. This study assessed the clinical and wellbeing benefits of extending normothermia by using a portable warming gown. A total of 94 patients undergoing elective surgery were enrolled. They were randomized pre-operatively to either a portable warming gown or the standard warming procedure. The warming gown stayed with patients from pre-op to operating room to postrecovery room discharge. Core temperature was tracked throughout the study. Patients also provided responses to a satisfaction and comfort status survey. The change in average core temperature did not differ significantly between groups (P = 0.23). A nonsignificant 48% relative decrease in hypothermic events was observed for the extended warming group (P = 0.12). Patients receiving the warming gown were more likely to report always having their temperature controlled (P = 0.04) and significantly less likely to request additional blankets for comfort (P = 0.006). Clinical outcomes and satisfaction were improved for patients with extended warming.Key words: Perioperative warming, Hypothermia, Warming gown, Patient warming unitIntra-operative management of core temperature has been shown to reduce postoperative complications including infections, risk of blood transfusions, and length of hospital stay.¹ Core temperature at induction has been demonstrated to be a significant risk for development of perioperative hypothermia.² Research findings in support of avoiding hypothermia (core temperature <36°) during surgery and the impact of lower temperature on patient recovery is well documented.^3,4 These include increased bleeding during surgery, increased infection rates, increased length of stay, as well as, ultimately, a higher mortality rate.^1,5,6Perioperative normothermia has also been shown to reduce postoperative complications.³ Most recently it has been suggested that active warming commencing preoperatively is more effective in achieving normothermic admission temperatures to postanesthesia recovery than warming commenced intra-operatively.⁴ That complications are reduced with preoperative warming is well established. These findings further suggest that extended warming significantly reduces rates of hypothermia over the standard warming just during surgery and at this time, no study has been performed.This study was conducted with three objectives in mind. The first objective was to compare rates of hypothermia (core temp < 36°) recorded intra-operatively in both a standard warming procedure group and an extended perioperative warming group. The second objective was to examine the association between normothermia extension and well-being. The third objective was to describe the costs of extended warming (peri-operative warming gown) and compare it to the standard warming procedure.     

Effects of coronary artery bypass grafting on left ventricular function assessed by multiple gated ventricular scintigraphy.

The effect of coronary artery bypass grafting on global left ventricular ejection fraction and regional contraction was studied in 56 consecutive patients with chronic stable angina pectoris by means of multiple gated ventricular scintigraphy at rest and during dynamic supine exercise before and six weeks after myocardial revascularisation. Before operation, exercise induced a significant fall in ejection fraction and regional wall motion score. Six weeks after operation 52 patients were symptomless. Resting ejection fraction and regional wall motion score were unchanged but during exercise ejection fraction increased significantly, and the previous exercise induced regional wall motion abnormalities were abolished. All four patients with persisting angina showed the same pattern as before operation, with a fall in left ventricular ejection fraction and regional wall motion score during exercise. Multiple gated ventricular scintigraphy affords a safe, objective, reproducible, and non-invasive means of assessing serial ventricular function at rest and during exercise in patients with ischaemic heart disease. The technique confirms that coronary bypass surgery abolishes exercise induced abnormalities of left ventricular function, but has no influence on resting function.     

Crystal structure of a central stalk subunit C and reversible association/dissociation of vacuole-type ATPase

The vacuole-type ATPases (V-ATPases) exist in various intracellular compartments of eukaryotic cells to regulate physiological processes by controlling the acidic environment. The crystal structure of the subunit C of Thermus thermophilus V-ATPase, homologous to eukaryotic subunit d of V-ATPases, has been determined at 1.95-A resolution and located into the holoenzyme complex structure obtained by single particle analysis as suggested by the results of subunit cross-linking experiments. The result shows that V-ATPase is substantially longer than the related F-type ATPase, due to the insertion of subunit C between the V(1) (soluble) and the V(o) (membrane bound) domains. Subunit C, attached to the V(o) domain, seems to have a socket like function in attaching the central-stalk subunits of the V(1) domain. This architecture seems essential for the reversible association/dissociation of the V(1) and the V(o) domains, unique for V-ATPase activity regulation.     

The role of Raf-1 kinase inhibitor protein in the regulation of pancreatic beta cell proliferation in mice

Aims/hypothesis

Manoeuvres aimed at increasing beta cell mass have been proposed as regenerative medicine strategies for diabetes treatment. Raf-1 kinase inhibitor protein 1 (RKIP1) is a common regulatory node of the mitogen-activated protein kinase (MAPK) and nuclear factor κB (NF-κB) pathways and therefore may be involved in regulation of beta cell homeostasis. The aim of this study was to investigate the involvement of RKIP1 in the control of beta cell mass and function.

Methods

Rkip1 (also known as Pebp1) knockout (Rkip1 ^?/?) mice were characterised in terms of pancreatic and glucose homeostasis, including morphological and functional analysis. Glucose tolerance and insulin sensitivity were examined, followed by assessment of glucose-induced insulin secretion in isolated islets and beta cell mass quantification through morphometry. Further characterisation included determination of endocrine and exocrine proliferation, apoptosis, MAPK activation and whole genome gene expression assays. Capacity to reverse a diabetic phenotype was assessed in adult Rkip1 ^?/? mice after streptozotocin treatment.

Results

Rkip1 ^?/? mice exhibit a moderately larger pancreas and increased beta cell mass and pancreatic insulin content, which correlate with an overall improvement in whole body glucose tolerance. This phenotype is established in young postnatal stages and involves enhanced cellular proliferation without significant alterations in cell death. Importantly, adult Rkip1 ^?/? mice exhibit rapid reversal of streptozotocin-induced diabetes compared with control mice.

Conclusions/interpretation

These data implicate RKIP1 in the regulation of pancreatic growth and beta cell expansion, thus revealing RKIP1 as a potential pharmacological target to promote beta cell regeneration.     

STING manifests self DNA-dependent inflammatory disease

Inflammatory autoimmune diseases such as systemic lupus erythematosus (SLE) and polyarthritis are characterized by chronic cytokine overproduction, suggesting that the stimulation of host innate immune responses, speculatively by persistent infection or self nucleic acids, plays a role in the manifestation of these disorders. Mice lacking DNase II die during embryonic development through comparable inflammatory disease because phagocytosed DNA from apoptotic cells cannot be adequately digested and intracellular host DNA sensor pathways are engaged, resulting in the production of a variety of cytokines including type I IFN. The cellular sensor pathway(s) responsible for triggering DNA-mediated inflammation aggravated autoimmune disease remains to be determined. However, we report here that Stimulator of IFN Genes (STING) is responsible for inflammation-related embryonic death in DNase II defective mice initiated by self DNA. DNase II-dependent embryonic lethality was rescued by loss of STING function, and polyarthritis completely prevented because cytosolic DNA failed to robustly trigger cytokine production through STING-controlled signaling pathways. Our data provides significant molecular insight into the causes of DNA-mediated inflammatory disorders and affords a target that could plausibly be therapeutically controlled to help prevent such diseases.