bluuebunny/crossref_metadata_2025_split huggingface dataset:
Measuring the influence of blood component infusion rate on recipient vital signs
Authors: Gehrie E. A. , Hendrickson J. E. , Tormey C. A. 
Published: July 2015

Background and ObjectivesOne of the challenges surrounding blood component administration is the determination of an appropriate rate of infusion. There are very few evidence‐based guidelines available to guide healthcare providers looking for a ‘standard’ infusion rate for red blood cells (RBCs), plasma or platelets (PLTs). Our objective was to determine the extent to which blood component infusion rates were associated with changes in transfusion recipient vital signs.Materials and MethodsWe retrospectively examined records of 3496 component infusions (RBCs, n = 2359; PLTs, n = 478; plasma, n = 659) over a 1‐year period at a 362‐bed multispecialty hospital. The following data were collected for each transfusion: blood product volume and infusion time, recipient pre‐ and post‐transfusion temperature, blood pressure and pulse rate, and hospital ward where transfusion occurred.ResultsPlasma (median 10·4 ml/min) was infused faster than PLTs (median 7·2 ml/min, P < 0·0001) or RBCs (median 2·3 ml/min, P < 0·0001). For all blood components, infusion rates varied based on the hospital unit performing the infusion. No association was found between relatively fast RBC, plasma or PLT infusion rates (>20 ml/min) and clinically significant reported changes in vital signs.ConclusionsThere does not appear to be a strong correlation between infusion rate and significant changes in recipient temperature, blood pressure or pulse rate. Based on these data, a reasonable rate for routine transfusion is 2–3 ml/min for RBCs and 7–10 ml/min for plasma and PLTs. Faster infusion rates (>20 ml/min) likely can be applied with close patient monitoring if there is a more urgent need for transfusion.
A national common massive transfusion protocol (MTP) is a feasible and advantageous option for centralized blood services and hospitals
Authors: Chay J. , Koh M. , Tan H. H. , Ng J. , Ng H. J. , Chia N. , Kuperan P. , Tan J. , Lew E. , Tan L. K. , Koh P. L. , Desouza K. A. , Bin Mohd Fathil S. , Kyaw P. M. , Ang A. L. 
Published: July 2015

BackgroundA common national MTP was jointly implemented in 2011 by the national blood service (Blood Services Group) and seven participating acute hospitals to provide rapid access to transfusion support for massively haemorrhaging patients treated in all acute care hospitals.MethodsThrough a systematic clinical workflow, blood components are transfused in a ratio of 1:1:1 (pRBC: whole blood‐derived platelets: FFP), together with cryoprecipitate for fibrinogen replacement. The composition of components for the MTP is fixed, although operational aspects of the MTP can be adapted by individual hospitals to suit local hospital workflow. The MTP could be activated in support of any patient with critical bleeding and at risk of massive transfusion, including trauma and non‐trauma general medical, surgical and obstetric patients.ResultsThere were 434 activations of the MTP from October 2011 to October 2013. Thirty‐nine per cent were for trauma patients, and 30% were for surgical patients with heavy intra‐operative bleeding, with 25% and 6% for patients with gastrointestinal bleeding and peri‐partum haemorrhage, respectively. Several hospitals reported reduction in mean time between request and arrival of blood. Mean transfusion ratio achieved was one red cell unit: 0·8 FFP units: 0·8 whole blood‐derived platelet units: 0·4 units of cryoprecipitate. Although cryoprecipitate usage more than doubled after introduction of MTP, there was no significant rise in overall red cells, platelet and FFP usage following implementation.ConclusionThis successful collaboration shows that shared transfusion protocols are feasible and potentially advantageous for hospitals sharing a central blood provider.
High rate of HIV infection in voluntary, first time, young male donors at HEMOAM, a reference blood bank in the Brazilian Amazon: 1992–2012 historical series
Authors: Viga‐Yurtsever S. , Fraiji N. , Lira E. , Stefani M. M. , Kiesslich D. 
Published: July 2015

Background and ObjectivesThere are significant regional differences in the Brazilian AIDS epidemic, which expands in the Amazonas State/north, while it is stable in the epicentre/southeast. This study evaluated incidence of HIV infection (1992–2012) at a main public blood bank in the Brazilian Amazon (Hematology and Hemotherapy Foundation from Amazonas State/HEMOAM, Manaus).MethodsRetrospective analysis of institutional‐computerized data set (SPSS version 13; P < 0·05).ResultsAmong 762 378 consecutive blood donations performed by 687 080 donors, replacement donations (56·8%), repeat donors (65·3%) and males (80·4%) prevailed. Among them, 685 confirmed cases of HIV infection with significantly higher frequency in: voluntary donations (0·14% vs. 0·08% replacement), first‐time donors (0·17% vs. 0·06% repeat) and males (0·11% vs. 0·07% females). Around 80% had 21–40 years. Overtime HIV positivity raised both in younger (16–20 years; P = 0·005) and older individuals (51–65 years; P = 0·03).ConclusionHigher rate of HIV in voluntary, first time, young males may orient recruitment of lower risk donors, especially in the Brazilian Amazon where AIDS incidence and mortality are rising.
Characterisation of Avena fatua populations with resistance to multiple herbicides
Authors: Keith B K , Lehnhoff E A , Burns E E , Menalled F D , Dyer W E 
Published: July 2015

SummaryAvena fatua (wild oat) populations with resistance (R) to one or more herbicides have been described in numerous cropping systems worldwide. We previously reported that the R3 and R4 wild oat populations from Montana, USA, were resistant to four herbicides representing three different modes of action: tralkoxydim [acetyl‐CoA carboxylase (ACCase] inhibitor), imazamethabenz and flucarbazone [acetolactate synthase (ALS) inhibitors] and difenzoquat (growth inhibitor). We now quantify resistance levels of these populations to triallate [very long chain fatty acid (VLCFA) biosynthesis inhibitor], pinoxaden (ACCase inhibitor) and paraquat (photosystem I inhibitor). Glasshouse dose–response experiments showed that, compared with the means of two susceptible (S) populations, the R3 and R4 populations were 17.5‐ and 18.1‐fold more resistant to triallate, 3.6‐ and 3.7‐fold more resistant to pinoxaden, respectively, and 3.2‐fold (R3) more resistant to paraquat. Pre‐treatment of R plants with the cytochrome P450 inhibitor malathion partially reversed the resistance phenotype for flucarbazone (both populations), imazamethabenz (R4), difenzoquat (R4) and pinoxaden (R3), but not for tralkoxydim, fenoxaprop‐P‐ethyl or triallate. Target site point mutations known to confer resistance to ALS or ACCase inhibitors were not detected via DNA sequencing and allele‐specific PCR assays in R plants, suggesting the involvement of non‐target site resistance mechanism(s) for these herbicides. Together, our results complete the initial characterisation of wild oat populations that are resistant to seven (R3) or six (R4) herbicides from five or four mode of action families respectively.
Microclimate is an independent risk factor for the development of intraoperatively acquired pressure ulcers in the park‐bench position: A prospective observational study
Authors: Yoshimura Mine , Nakagami Gojiro , Iizaka Shinji , Yoshida Mikako , Uehata Yoko , Kohno Michihiro , Kasuya Yusuke , Mae Tomoko , Yamasaki Takashi , Sanada Hiromi 
Published: July 2015

ABSTRACTPreventing pressure ulcers is important in patients undergoing procedures in the park‐bench position. We hypothesized that the microclimate around the skin is a significant risk factor for developing pressure ulcers. This research continuously assessed factors of the microclimate in terms of skin temperature and perspiration as well as the interface pressure in order to determine whether the microclimate is an independent risk factor for the development of park‐bench position‐related pressure ulcers (PBP‐PUs). A prospective observational study was conducted among patients undergoing elective surgery in the park‐bench position at a general hospital in the metropolitan area of Japan between April and November 2014. Factors of the microclimate, including skin temperature and perspiration, in addition to the interface pressure were continuously measured throughout surgery. Twenty‐nine patients were analyzed (mean age 44.4 ± 13.2 years, male 44.8%). Of these 29 patients, seven (24.1%) developed Category I PBP‐PUs. The change in skin temperature from baseline to the end of surgery (2.7 ± 0.3 °C vs. 1.9 ± 0.8 °C) and the average peak pressure (119.1 ± 36.8 mmHg vs. 94.5 ± 23.1 mmHg) were significantly higher in the patients with PBP‐PUs than in those without PBP‐PUs. There were no significant differences in the amount of perspiration between the two groups. A hierarchical logistic regression analysis showed that the change in skin temperature was significantly related to the development of PBP‐PUs (unit = 0.1 °C: odds ratio 1.44, 95% confidential interval 1.09–2.33) when adjusted for the average peak pressure and length of surgery. Our results suggest that a change in skin temperature toward a higher value is an independent risk factor for the development of PBP‐PUs. Proper intraoperative management of skin temperature may therefore be a promising candidate as a preventive method against PBP‐PU development.
Evidence‐based chronic ulcer care and lower limb outcomes among Pacific Northwest veterans
Authors: Karavan Mahsa , Olerud John , Bouldin Erin , Taylor Leslie , Reiber Gayle E. 
Published: July 2015

ABSTRACTEvidence‐based ulcer care guidelines detail optimal components of care for treatment of ulcers of different etiologies. We investigated the impact of providing specific evidence‐based ulcer treatment components on healing outcomes for lower limb ulcers (LLU) among veterans in the Pacific Northwest. Components of evidence‐based ulcer care for venous, arterial, diabetic foot ulcers/neuropathic ulcers were abstracted from medical records. The outcome was ulcer healing. Our analysis assessed the relationship between evidence‐based ulcer care by etiology, components of care provided, and healing, while accounting for veteran characteristics. A minority of veterans in all three ulcer‐etiology groups received the recommended components of evidence‐based care in at least 80% of visits. The likelihood of healing improved when assessment for edema and infection were performed on at least 80% of visits (hazard ratio [HR] = 3.20, p = 0.009 and HR = 3.54, p = 0.006, respectively) in patients with venous ulcers. There was no significant association between frequency of care components provided and healing among patients with arterial ulcers. Among patients with diabetic/neuropathic ulcers, the chance of healing increased 2.5‐fold when debridement was performed at 80% of visits (p = 0.03), and doubled when ischemia was assessed at the first visit (p = 0.045). Veterans in the Pacific Northwest did not uniformly receive evidence‐based ulcer care. Not all evidence‐based ulcer care components were significantly associated with healing. At a minimum, clinicians need to address components of ulcer care associated with improved ulcer healing.
Severe hypoxia and malnutrition collectively contribute to scar fibroblast inhibition and cell apoptosis
Authors: Lynam Emily C. , Xie Yan , Dawson Rebecca , Mcgovern Jacqui , Upton Zee , Wang XiQiao 
Published: July 2015

ABSTRACTThis study aims to investigate whether severe hypoxia and malnutrition in scar tissue play key roles to induce hypertrophic scar regression. And scar‐derived fibroblasts were treated with moderate/severe hypoxia and malnutrition to model condition of proliferative and regressive scar (5%O2+5%FCS and 0.5%O2 + 0.5%FCS), and normoxia with well nutrition as control (10%O2 + 10%FCS). Our results demonstrated that severe hypoxia and malnutrition resulted in significantly reduced cell viability and collagen production, as well as HIF‐1, VEGF, TGF‐β1, and Bcl‐2 protein expression when compared with control, and cell apoptosis occurred. Therefore, the severe hypoxia and malnutrition in scar tissue contribute to fibroblast inhibition and cell apoptosis, which is correlated with scar regression.
Early graft failure of GalTKO pig organs in baboons is reduced by expression of a human complement pathway‐regulatory protein
Authors: Azimzadeh Agnes M. , Kelishadi Sean S. , Ezzelarab Mohamed B. , Singh Avneesh K. , Stoddard Tiffany , Iwase Hayato , Zhang Tianshu , Burdorf Lars , Sievert Evelyn , Avon Chris , Cheng Xiangfei , Ayares David , Horvath Keith A. , Corcoran Philip C. , Mohiuddin Muhammad M. , Barth Rolf N. , Cooper David K. C. , Pierson Richard N. 
Published: July 2015

AbstractWe describe the incidence of early graft failure (EGF, defined as loss of function from any cause within 3 days after transplant) in a large cohort of GalTKO pig organs transplanted into baboons in three centers, and the effect of additional expression of a human complement pathway‐regulatory protein, CD46 or CD55 (GalTKO.hCPRP). Baboon recipients of life‐supporting GalTKO kidney (n = 7) or heterotopic heart (n = 14) grafts received either no immunosuppression (n = 4), or one of several partial or full immunosuppressive regimens (n = 17). Fourteen additional baboons received a GalTKO.hCPRP kidney (n = 5) or heart (n = 9) and similar treatment regimens. Immunologic, pathologic, and coagulation parameters were measured at frequent intervals. EGF of GalTKO organs occurred in 9/21 baboons (43%). hCPRP expression reduced the GalTKO EGF incidence to 7% (1/14; P < 0.01 vs. GalTKO alone). At 30 mins, complement deposits were more intense in organs in which EGF developed (P < 0.005). The intensity of peri‐transplant platelet activation (as β‐thromboglobulin release) correlated with EGF, as did the cumulative coagulation score (P < 0.01). We conclude that (i) the transgenic expression of a hCPRP on the vascular endothelium of a GalTKO pig reduces the incidence of EGF and reduces complement deposition, (ii) complement deposition and platelet activation correlate with early GalTKO organ failure, and (iii) the expression of a hCPRP reduces EGF but does not prevent systemic coagulation activation. Additional strategies will be required to control coagulation activation.
Biogeography of Australasian flightless weevils (Curculionidae, Celeuthetini) suggests permeability of Lydekker's and Wallace's Lines
Authors: Toussaint Emmanuel F. A. , Tänzler Rene , Rahmadi Cahyo , Balke Michael , Riedel Alexander 
Published: July 2015

The Indo‐Australian region was formed by the collision of the Australian and Asian plates, and its fauna largely reflects this dual origin. Lydekker's and Wallace's Lines represent biogeographic transition boundaries between biotas although their permeability through geological times was rarely assessed. Here, we explore the evolutionary history of flightless weevils of the tribe Celeuthetini in this geologically highly complex region. We generated a DNA sequence data set of 2236 bp comprising two nuclear and two mitochondrial markers for 62 species of the Indo‐Australian tribe Celeuthetini. We used Bayesian Inference and Maximum Likelihood to reconstruct the first molecular phylogeny of the group. Based on this phylogenetic tree, we employed the program BioGeoBEARS to infer the biogeographical history of Celeuthetini in the region. The group's radiation begun east of Wallace's Line, probably during the mid‐Eocene. We unveil multiple transgressions of Lydekker's and Wallace's Lines mostly during the Miocene with a significant role of founder‐event speciation. The phylogeny of Celeuthetini is geographically highly structured with the first lineages occurring in New Guinea and the Moluccas, and a deep divergence between two clades largely confined to Sulawesi and their respective sister clades of the Lesser Sunda Islands. Wallace's Line was crossed once from Sulawesi and three times from the Lesser Sunda Islands to Java whilst Lydekker's Line was crossed once from New Guinea to the Moluccas. Although this beetle group shows extensive local diversification with little dispersal, the biogeographical demarcations of the Australasian region appear to have been rather porous barriers to dispersal.
Peripheral chemoreceptors determine the respiratory sensitivity of central chemoreceptors to CO2: role of carotid body CO2
Authors: Smith Curtis. A. , Blain Grégory M. , Henderson Kathleen S. , Dempsey Jerome A. 
Published: July 2015

Key Points
The influence of specific carotid body (CB) normoxic hypocapnia, hypercapnia and normocapnia on the ventilatory sensitivity of central chemoreceptors to systemic hypercapnia was assessed in seven awake dogs with extracorporeal perfusion of the vascularly isolated CB.
Chemosensitivity in this preparation was similar to that in the intact animal.
Separation of CB circulation from that of the brain was confirmed.
When the isolated CB was hypercapnic vs. hypocapnic and when the isolated CB was normocapnic vs. hypocapnic, the group mean central CO2 response slopes of minute ventilation () (P ≤ 0.01) and mean inspiratory flow rate (VT/TI) (P ≤ 0.05) increased significantly. Tidal volume (VT), breathing frequency (fb)and rate of rise of diaphragm EMG were increased in 6 of 7 dogs but did not achieve statistical significance.
We propose that hyperaddition is the dominant form of chemoreceptor interaction under conditions of quiet wakefulness in intact animals and over a wide range of CB and .
AbstractWe asked if the type of carotid body (CB) chemoreceptor stimulus influenced the ventilatory gain of the central chemoreceptors to CO2. The effect of CB normoxic hypocapnia, normocapnia and hypercapnia (carotid body ≈ 22, 41 and 68 mmHg, respectively) on the ventilatory CO2 sensitivity of central chemoreceptors was studied in seven awake dogs with vascularly‐isolated and extracorporeally‐perfused CBs. Chemosensitivity with one CB was similar to that in intact dogs. In four CB‐denervated dogs, absence of hyper‐/hypoventilatory responses to CB perfusion with of 19–75 mmHg confirmed separation of the perfused CB circulation from the brain. The group mean central CO2 response slopes were increased 303% for minute ventilation ()(P ≤ 0.01) and 251% for mean inspiratory flow rate (VT/TI) (P ≤ 0.05) when the CB was hypercapnic vs. hypocapnic; central CO2 response slopes for tidal volume (VT), breathing frequency (fb) and rate of rise of the diaphragm EMG increased in 6 of 7 animals but the group mean changes did not reach statistical significance. Group mean central CO2 response slopes were also increased 237% for (P ≤ 0.01) and 249% for VT/TI(P ≤ 0.05) when the CB was normocapnic vs. hypocapnic, but no significant differences in any of the central ventilatory response indices were found between CB normocapnia and hypercapnia. These hyperadditive effects of CB hyper‐/hypocapnia agree with previous findings using CB hyper‐/hypoxia.We propose that hyperaddition is the dominant form of chemoreceptor interaction in quiet wakefulness when the chemosensory control system is intact, response gains physiological, and carotid body chemoreceptors are driven by a wide range of O2 and/or CO2.
Acid‐sensing ion channel 1a drives AMPA receptor plasticity following ischaemia and acidosis in hippocampal CA1 neurons
Authors: Quintana Patrice , Soto David , Poirot Olivier , Zonouzi Marzieh , Kellenberger Stephan , Muller Dominique , Chrast Roman , Cull‐Candy Stuart G. 
Published: July 2015

Key points
The hippocampal CA1 region is highly vulnerable to ischaemic stroke. Two forms of AMPA receptor (AMPAR) plasticity – an anoxic form of long‐term potentiation and a delayed increase in Ca2+‐permeable (CP) AMPARs – contribute to this susceptibility by increasing excitotoxicity.
In CA1, the acid‐sensing ion channel 1a (ASIC1a) is known to facilitate LTP and contribute to ischaemic acidotoxicity.
We have examined the role of ASIC1a in AMPAR ischaemic plasticity in organotypic hippocampal slice cultures exposed to oxygen glucose deprivation (a model of ischaemic stroke), and in hippocampal pyramidal neuron cultures exposed to acidosis.
We find that ASIC1a activation promotes both forms of AMPAR plasticity and that neuroprotection, by inhibiting ASIC1a, circumvents any further benefit of blocking CP‐AMPARs.
Our observations establish a new interaction between acidotoxicity and excitotoxicity, and provide insight into the role of ASIC1a and CP‐AMPARs in neurodegeneration. Specifically, we propose that ASIC1a activation drives certain post‐ischaemic forms of CP‐AMPAR plasticity.
AbstractThe CA1 region of the hippocampus is particularly vulnerable to ischaemic damage. While NMDA receptors play a major role in excitotoxicity, it is thought to be exacerbated in this region by two forms of post‐ischaemic AMPA receptor (AMPAR) plasticity – namely, anoxic long‐term potentiation (a‐LTP), and a delayed increase in the prevalence of Ca2+‐permeable GluA2‐lacking AMPARs (CP‐AMPARs). The acid‐sensing ion channel 1a (ASIC1a), which is expressed in CA1 pyramidal neurons, is also known to contribute to post‐ischaemic neuronal death and to physiologically induced LTP. This raises the question does ASIC1a activation drive the post‐ischaemic forms of AMPAR plasticity in CA1 pyramidal neurons? We have tested this by examining organotypic hippocampal slice cultures (OHSCs) exposed to oxygen glucose deprivation (OGD), and dissociated cultures of hippocampal pyramidal neurons (HPNs) exposed to low pH (acidosis). We find that both a‐LTP and the delayed increase in the prevalence of CP‐AMPARs are dependent on ASIC1a activation during ischaemia. Indeed, acidosis alone is sufficient to induce the increase in CP‐AMPARs. We also find that inhibition of ASIC1a channels circumvents any potential neuroprotective benefit arising from block of CP‐AMPARs. By demonstrating that ASIC1a activation contributes to post‐ischaemic AMPAR plasticity, our results identify a functional interaction between acidotoxicity and excitotoxicity in hippocampal CA1 cells, and provide insight into the role of ASIC1a and CP‐AMPARs as potential drug targets for neuroprotection. We thus propose that ASIC1a activation can drive certain forms of CP‐AMPAR plasticity, and that inhibiting ASIC1a affords neuroprotection.
Cardioprotection in ischaemia–reperfusion injury: novel mechanisms and clinical translation
Authors: Altamirano Francisco , Wang Zhao V. , Hill Joseph A. 
Published: July 2015

AbstractIn recent decades, robust successes have been achieved in conquering the acutely lethal manifestations of heart disease. Nevertheless, the prevalence of heart disease, especially heart failure, continues to rise. Among the precipitating aetiologies, ischaemic disease is a leading cause of heart failure. In the context of ischaemia, the myocardium is deprived of oxygen and nutrients, which elicits a cascade of events that provokes cell death. This ischaemic insult is typically coupled with reperfusion, either spontaneous or therapeutically imposed, wherein blood supply is restored to the previously ischaemic tissue. While this intervention limits ischaemic injury, it triggers a new cascade of events that is also harmful, viz. reperfusion injury. In recent years, novel insights have emerged regarding mechanisms of ischaemia–reperfusion injury, and some hold promise as targets of therapeutic relevance. Here, we review a select number of these pathways, focusing on recent discoveries and highlighting prospects for therapeutic manipulation for clinical benefit.