ObjectiveFew data exist regarding physician attitudes and implementation of family-centred rounds (FCR) in cardiovascular care. This study aimed to assess knowledge and attitudes among cardiologists ...and cardiology fellows regarding barriers and benefits of FCRs.MethodsAn electronic, web-based questionnaire was nationally distributed to cardiology fellows and attending cardiologists.ResultsIn total, 118 subjects were surveyed, comprising cardiologists (n=64, 54%) and cardiology fellows (n=54, 46%). Overall, 61% of providers reported participating in FCRs and 64% felt family participation on rounds benefits the patient. Both fellows and cardiologists agreed that family rounds eased family anxiety (fellows, 63%; cardiologists, 56%; p=0.53), improved communication between the medical team and the patient and family (fellows, 78%; cardiologists, 61%; p=0.18) and improved patient safety (fellows, 59%; cardiologists, 47%; p=0.43). Attitudes regarding enhancement of trainee education were similar (fellows, 69%; cardiologists, 55%; p=0.19). Fellows and cardiologists felt that family increased the duration of rounds (fellows, 78%; cardiologists, 80%; p=0.18) and led to less efficient rounds (fellows, 54%; cardiologists, 58%; p=0.27).ConclusionThe majority of cardiologists and fellows believed that FCRs benefited families, communication and patient safety, but led to reduced efficiency and longer duration of rounds.
Abstract Purpose This study had 2 objectives: (1) to quantify the metabolic response to physical cooling in febrile patients with systemic inflammatory response syndrome (SIRS) and (2) to provide ...proof for the hypothesis that the efficiency of external cooling and the subsequent shivering response are influenced by site and temperature of surface cooling pads. Methods To quantify shivering thermogenesis during surface cooling for fever, we monitored oxygen consumption (VO2 ) in 6 febrile patients with SIRS during conventional cooling with cooling blankets and ice packs. To begin to determine how location and temperature of surface cooling influence shivering, we compared 5 cooling protocols for inducing mild hypothermia in 6 healthy volunteers. Results In the patients with SIRS, core temperature decreased 0.67°C per hour, all patients shivered, VO2 increased 57.6%, and blood pressure increased 15% during cooling. In healthy subjects, cooling with the 10°C vest was most comfortable and removed heat most efficiently without shivering or VO2 increase. Cooling with combined vest and thigh pads stimulated the most shivering and highest VO2 and increased core temperature. Reducing vest temperature from 10°C to 5°C failed to increase heat removal secondary to cutaneous vasoconstriction. Capsaicin, an agonist for the transient receptor potential cation channel subfamily V member 1 (TRPV1) warm-sensing channels, partially reversed this effect in 5 subjects. Conclusions Our results identify the hazards of surface cooling in febrile critically ill patients and support the concept that optimization of cooling pad temperature and position may improve cooling efficiency and reduce shivering.
Fever commonly occurs in acute lung injury (ALI) and ALI occurs in 25% of victims of heat stroke. We have shown in mouse models of ALI that exposure to febrile-range hyperthermia (FRH), 39.5°C, ...increases non-cardiogenic pulmonary oedema. In this study we studied the direct effects of FRH on endothelial barrier integrity using human microvascular endothelial cells (HMVEC-Ls). We analysed the effect of exposure to culture temperatures between 38.5° and 41°C with and without tumour necrosis factor-α (TNF-α) up to 250 U/mL for 6-24 h. We found that exposure to 2.5-250 U/mL TNF-α increased HMVEC-L permeability by 4.1-15.8-fold at 37°C. Exposure to 39.5°C alone caused variable, modest, lot-specific increases in HMVEC-L permeability, however raising culture temperature to 39.5°C in the presence of TNF-α increased permeability an additional 1.6-4.5-fold compared with cells incubated with the same TNF-α concentration at 37°C. Permeability occurred without measurable cytotoxicity and was reversible upon removal of TNF-α and reduction in temperature to 37°C. Exposure to 39.5°C or TNF-α each stimulated rapid activation of p38 and ERK but the effects were not additive. Treatment with inhibitors of ERK (U0126) or p38 (SB203580) each reduced TNF-α-induced permeability in 39.5°C monolayers to levels in 37°C cells, but did not alter TNF-α-induced permeability in the 37°C cells. These results demonstrate that FRH directly increases paracellular pathway opening through a process that requires ERK and p38 MAPKs. A better understanding of this mechanism may provide new understanding about how fever may contribute to the pathogenesis of ALI and provide new therapeutic targets to improve clinical outcomes.
Celotno besedilo
Dostopno za:
DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
Purpose: Chronic heat exposure in mice has cellular and physiological effects that improve thermal tolerance 1, but also modifies innate immune responses with potential adverse consequences 2. While ...male and female mice are known to respond differently to acute exposure to severe hyperthermia, sex-based differences in responses to chronic moderate heat exposure have not been reported. The major objective of this study was to compare the tolerance of male and female mice for chronic heat exposure.
Materials and methods: We used a mouse model of 5-day moderate heat exposure (ambient temperature ∼37°C) to compare the physiological and cellular heat shock response in male and female mice. Core temperature, heart rate, and activity were monitored telemetrically and heat shock protein levels were measured in brain and lung by western blotting.
Results: Adult CD-1 female mice maintained a 1.2°C lower core temperature (38.31 ± 0.64 versus 39.51 ± 0.72°C; p = 0.002), experienced less weight loss (1.54 ± 0.45 versus 4.54 ± 1.97 g; p = 0.0007), and had improved survival (16/16 survived versus 13/21, p < 0.006) than male mice of the same age. After 5 days of moderate heat exposure Hsp72 levels in brain and lung increased 2.1-fold (p = 0.007) and 5-fold (p = 0.048) in male mice compared with 1.3- (p = 0.054) and 1.5-fold (p = 0.134) in female mice.
Conclusions: This study reveals previously unknown and potentially important differences between male and female mice in physiological and cellular responses to chronic heat exposure, which had consequences for survival. Future studies may identify biomarkers of differential heat tolerance and treatments to improve heat tolerance in humans.
Celotno besedilo
Dostopno za:
DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
The heat shock (HS) response is an important cytoprotective response comprising the expression of heat shock proteins (HSPs) and orchestrated by the heat/stress-induced transcription factor, heat ...shock factor-1 (HSF-1). Previous studies suggest that the activation threshold and magnitude of the HS response may be modified by treatment with arachidonic acid (AA). We analyzed the effect of exogenous AA and its metabolites, PGE
2, LTD
4, and 15-HETE on HSF-1-dependent gene expression in A549 human respiratory epithelial-like cells. When added at 1
μM, PGE
2 much more than LTD
4, but not 15-HETE increased activity of a synthetic HSF-1-dependent reporter after HS exposure (42
°C for 2
h), but had no effect in the absence of HS. Exposing A549 cells to HS stimulated the release of PGE
2 and treatment with the cyclooxygenase inhibitor, ibuprofen, reduced HS-induced HSF-1-dependent transcription. PGE
2 increased HS-induced HSP72 mRNA and protein expression but EMSA and Western blot analysis failed to show an effect on HSF-1 DNA binding activity or post-translational modification. In summary, we showed that HS stimulates the generation of PGE
2, which augments the generation of HSPs. The clinical consequences of this pathway have yet to be determined.
Fever commonly occurs in acute lung injury (ALI) and ALI occurs in 25% of victims of heat stroke. We have shown in mouse models of ALI that exposure to febrile-range hyperthermia (FRH), 39.5°C, ...increases non-cardiogenic pulmonary oedema. In this study we studied the direct effects of FRH on endothelial barrier integrity using human microvascular endothelial cells (HMVEC-Ls). We analysed the effect of exposure to culture temperatures between 38.5° and 41°C with and without tumour necrosis factor- (TNF- ) up to 250 U/mL for 6-24 h. We found that exposure to 2.5-250 U/mL TNF- increased HMVEC-L permeability by 4.1-15.8-fold at 37°C. Exposure to 39.5°C alone caused variable, modest, lot-specific increases in HMVEC-L permeability, however raising culture temperature to 39.5°C in the presence of TNF- increased permeability an additional 1.6-4.5-fold compared with cells incubated with the same TNF- concentration at 37°C. Permeability occurred without measurable cytotoxicity and was reversible upon removal of TNF- and reduction in temperature to 37°C. Exposure to 39.5°C or TNF- each stimulated rapid activation of p38 and ERK but the effects were not additive. Treatment with inhibitors of ERK (U0126) or p38 (SB203580) each reduced TNF- -induced permeability in 39.5°C monolayers to levels in 37°C cells, but did not alter TNF- -induced permeability in the 37°C cells. These results demonstrate that FRH directly increases paracellular pathway opening through a process that requires ERK and p38 MAPKs. A better understanding of this mechanism may provide new understanding about how fever may contribute to the pathogenesis of ALI and provide new therapeutic targets to improve clinical outcomes.
Celotno besedilo
Dostopno za:
DOBA, IZUM, KILJ, NUK, PILJ, PNG, SAZU, SIK, UILJ, UKNU, UL, UM, UPUK
Earlier studies have shown that the stress‐activated transcription factor, heat shock factor‐1 (HSF1), modified expression of certain non‐HSP genes including cytokine and chemokine genes. An analysis ...of human and mouse CXC chemokine genes showed that 28 of the 29 genes had multiple putative heat shock response elements (HSEs) present in their promoters. To determine whether these potential HSEs were functional, we analyzed HSF1 recruitment and expression of 5 human CXC chemokine genes (CXCL‐1, 2, 3, 5 and 8) in heat shocked human lung epithelial‐like A549 cells. Chromatin immunoprecipitation (ChIP) analysis showed that HSF1 was recruited to all but one of these genes (CXCL‐3) and heat shock caused a significant increase in recruitment of HSF1 to one or multiple HSEs present in the promoters of CXCL‐1, 2, 5 and 8 genes. However, the effect of HS exposure on expression of these genes showed a variable gene‐specific effect. For example, CXCL8 expression was markedly enhanced (p<0.05) but CXCL5 expression was significantly repressed (p<0.05) in heat shocked A549 cells. In contrast, expression of CXCL1 and CXCL2, despite HSF1 recruitment to their promoters, was not affected by HS exposure. Our results indicate that some, if not all, putative HSEs present in the CXC chemokine gene promoters are functional and recruit HSF1 in vivo but the effects on gene expression are variable and gene specific.
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