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The conservation status of small cetaceans has significantly worsened since the 1980s, when the baiji was the only species of small cetacean listed as Endangered by IUCN. Now the baiji is almost certainly extinct and 13 other species, subspecies, or populations (hereafter units-to-conserve or units) of small cetaceans are listed as Critically Endangered (CR) on the IUCN Red List. Bycatch is the main threat to 11 of the CR units. Entanglement in gillnets contributed to the extinction of the baiji and is responsible for the imminent extinction of the vaquita. Unfortunately, there is no simple technical solution to the problem of bycatch of small cetaceans. If the 8 CR units with 100 or fewer remaining individuals are to be saved, conservation zones must be established where gillnets are eliminated and bans on their use are strictly enforced. Recent experience with the vaquita in Mexico demonstrates that enforcement of such conservation zones can be very difficult. Ineffective enforcement is also a problem for at least 4 of the other CR units. Time is very short and, unless major efforts are made now to address the bycatch problem, the prospects for CR small cetaceans and other at-risk aquatic megafauna are grim. The ultimate long-term solution to the bycatch problem is the development of efficient, inexpensive, alternative fishing gear that can replace gillnets without jeopardizing the livelihoods of fishermen. Good fishery governance and the direct involvement of fishing communities are also essential to the successful conservation of most threatened populations of small cetaceans.

Cortical bone development is characterised by initial formation of woven bone followed by deposition of lamellar bone on the woven scaffold. This occurs in normal bone formation as an integral obligate self-assembly pattern throughout all vertebrate groups, with specific temporal and spatial features. It also occurs in repair bone, modified by the biophysical/mechanical environment, and in pathological bone, modified by the specific disorder and its severity. Two spatially distinct osteoblast cell populations synthesise woven and lamellar bone: mesenchymal osteoblasts surround themselves circumferentially with collagen in a random array to form woven bone; surface osteoblasts align themselves in a linear array on the woven bone surface (or adjacent lamellar bone) to synthesise parallel-fibred lamellar bone. Four specific stages of woven bone formation are defined: stage I, early differentiation of pre-osteoblasts from undifferentiated mesenchymal cells; stage II, mesenchymal osteoblasts surrounding themselves in a 360° arc with randomly oriented matrix fibres; stage III, woven matrix acting as a scaffold on which surface osteoblasts begin to synthesise bone in parallel-fibred lamellar conformation; stage IV, progressive relative diminution of woven bone in the woven bone/lamellar bone complex. Stages II and IV are further subdivided (in a, b and c) by shifting cell area/matrix area and woven bone/lamellar bone relationships. The under-appreciated biological significance of woven bone is that it initiates formation de novo at sites of no previous bone. This information allows for targeted assessment of molecular-biophysical mechanisms underlying woven bone formation and their utilisation for initiating enhanced bone formation.

Most osteoporotic fractures occur at metaphyseal regions of long bones. The present study proposed a clinically relevant animal model that satisfied: i) induction of osteoporosis, ii) unilateral complete osteotomy at metaphysis, iii) internal fixation. 6 months old female Sprague-Dawley rats (n = 64) were randomly divided into the ovariectomised-metaphyseal osteotomy (OVX, n = 32) and metaphyseal osteotomy (SHAM, n = 32) groups. The metaphyseal-osteotomy model was created with a plate-fixation of the osteotomy and assessed by X-ray, micro-computed tomography, histomorphometry and mechanical testing at weeks 1, 3 and 6. X-ray results showed complete healing of metaphyseal osteotomy at week 6. Histology showed 3 stages of metaphyseal healing. Stage 1 was characterised by fibrous tissue, consisting of disorganised orientation of collagen fibres, and infiltration of immune cells. At stage 2, a transitional zone consisting of maturing fibrous tissue and differentiating mesenchymal cells with early trabecular bone formation and disorganised woven bone were observed. During stage 3, cortical bone ends unified and woven bone underwent transformation to lamellar bone. OVX group healing was significantly delayed when compared to SHAM samples. The study demonstrated that healing of osteoporotic osteotomy at the metaphyseal region was delayed in terms of radiography, histomorphometry and mechanical strength. These quantitative evaluations, along with histological features, may provide key references for future studies. The animal model may provide additional clinical relevance as most osteoporotic fracture in humans occurs at metaphyseal regions.

Objective: Mortality in sepsis is believed to be associated with exaggerated inflammatory responses, but recent evidence suggests that poor outcome is associated with reduced inflammation. To test this hypothesis, we measured several inflammatory markers to determine whether any of them or any combinations are associated with mortality or organ dysfunction.Design: Clinical study.Setting: School of medicine.Patients: Thirty-five patients with severe sepsis.Interventions: Markers of endothelial, platelet, and leukocyte activation were measured on days 1, 2, and 3 after enrollment. The markers were a) endothelial microparticles (EMPs) and their conjugates with monocytes (EMP/MONO); b) platelet microparticles (PMPs) and platelet activation marker CD62P; c) platelet-leukocyte conjugates (PLT/LEU) and leukocyte activation marker CD11b; and d) intracellular nitric oxide in leukocytes.Measurements and Main Results: The 28-day mortality rate was 51% (18 of 35). Significant differences between survivors and nonsurvivors on day 1 were found in PLT/LEU (p = .001), CD11b (p = 0.02), and EMP/MONO (p = .02) groups. Using logistic regression to assess if these markers predict mortality on day 1, we found that PLT/LEU had the best predictive value among the markers used (area under receiver operating characteristics curve = 0.82). All markers of cell activation and inflammation were significantly higher among survivors on days 2 and 3, except nitric oxide, which was lower. This marker showed significant negative correlation with the Sequential Organ Failure Assessment score throughout the study.Conclusions: Our data support the hypothesis that early increased, not decreased, inflammatory response as measured by our markers is associated with improved survival rate. A high negative correlation was found between some of these markers and Sequential Organ Failure Assessment score. [ABSTRACT FROM AUTHOR]

Limited resources and increasing environmental concerns have prompted calls to identify the critical questions that most need to be answered to advance conservation, thereby providing an agenda for scientific research priorities. Cetaceans are often keystone indicator species but also high profile, charismatic flagship taxa that capture public and media attention as well as political interest. A dedicated workshop was held at the conference of the Society for Marine Mammalogy (December 2013, New Zealand) to identify where lack of data was hindering cetacean conservation and which questions need to be addressed most urgently. This paper summarizes 15 themes and component questions prioritized during the workshop. We hope this list will encourage cetacean conservation-orientated research and help agencies and policy makers to prioritize funding and future activities. This will ultimately remove some of the current obstacles to science-based cetacean conservation.

The population of humpback dolphins Sousa chinensis that resides in the eastern Taiwan Strait (ETS) is geographically and genetically isolated from populations inhabiting the coastal waters of mainland China and appears to be facing unsustainable levels of human threats. Using VORTEX 9.99b, we modeled the viability of this Critically Endangered population under the present conditions as well as under realistic additional threat scenarios. We examined 6 different levels of bycatch mortality, 3 scenarios of habitat loss/degradation, and scenarios in which these threats were experienced together. Under the baseline (present) scenario, the population exhibited a decreasing growth rate and was predicted to be smaller than the initial population size in more than 76% of all model runs. In all scenarios with additional threats, the proportion of model runs in which population size was smaller than the initial size varied from 77.1 to 92.6%. Over the short term, fisheries-related mortality appears to have a more obvious impact on the population’s trajectory than habitat loss/degradation. Even minimal increases in mortality from the current baseline levels will increase the probability of extinction of this population. Due to the fragile situation of ETS humpback dolphins, mitigation actions to reduce the current threats to this population are needed immediately.

Biological and fisheries data were analysed to assess the impact of fisheries mortality on a Critically Endangered subpopulation of 30% of the ETS Sousa subpopulation exhibited injuries caused by fishing gear. Three individuals were photographed with fishing gear attached to their bodies, and 1 dolphin was found dead with fresh injuries caused by fishing gear. To ensure recovery of ETS Sousa, mortality due to human causes should be reduced to

Abstract Objectives This review summarizes recent developments in platelet biology relevant to neuroinflammatory disorders. Multiple sclerosis (MS) is taken as the "Poster Child" of these disorders but the implications are wide. The role of platelets in inflammation is well appreciated in the cardiovascular and cancer research communities but appears to be relatively neglected in neurological research. Organization After a brief introduction to platelets, topics covered include the matrix metalloproteinases, platelet chemokines, cytokines and growth factors, the recent finding of platelet PPAR receptors and Toll-like receptors, complement, bioactive lipids, and other agents/functions likely to be relevant in neuroinflammatory diseases. Each section cites literature linking the topic to areas of active research in MS or other disorders, including especially Alzheimer's disease. Conclusion The final section summarizes evidence of platelet involvement in MS. The general conclusion is that platelets may be key players in MS and related disorders, and warrant more attention in neurological research.

Abstract Objectives This is a critical review of anti-phospholipid antibodies (aPL). Most prior reviews focus on the aPL syndrome (APS), a thrombotic condition often marked by neurological disturbance. We bring to attention recent evidence that aPL may be equally relevant to non-thrombotic autoimmune conditions, notably, multiple sclerosis and ITP. Organization After a brief history, the recent proliferation of aPL target antigens is reviewed. The implication is that many more exist. Theories of aPL in thrombosis are then reviewed, concluding that all have merit but that aPL may have more diverse pathological consequences than now recognized. Next, conflicting results are explained by methodological differences. The lupus anticoagulant (LA) is then discussed. LA is the best predictor of thrombosis, but why this is true is not settled. Finally, aPL in non-thrombotic disorders is reviewed. Conclusion The current paradigm of aPL holds that they are important in thrombosis, but they may have much wider clinical significance, possibly of special interest in neurology.

Abstract Objective A fatality in one multiple sclerosis (MS) patient due to acute idiopathic thrombocytopenic purpura (ITP) and a near fatality in another stimulated our interest in platelet function abnormalities in MS. Previously, we presented evidence of platelet activation in a small cohort of treatment-naive MS patients. Methods In this report, 92 normal controls and 33 stable, untreated MS patients were studied. Platelet counts, measures of platelet activation [plasma platelet microparticles (PMP), P-selectin expression (CD62p), circulating platelet microaggragtes (PAg)], as well as platelet-associated IgG/IgM, were carried out. In addition, plasma protein S activity was measured. Results Compared to controls, PMP were significantly elevated in MS (p < 0.001) and CD62p expression was also markedly elevated (p < 0.001). Both are markers of platelet activation. Platelet-associated IgM, but not IgG, was marginally elevated in MS (p = 0.01). Protein S in MS patients did not differ significantly from normal values. Conclusion Platelets are significantly activated in MS patients. The mechanisms underlying this activation and its significance to MS are unknown. Additional study of platelet activation and function in MS patients is warranted.

Abstract Background The presence of antiphospholipid antibodies (APLA) in multiple sclerosis (MS) patients has been reported frequently but no clear relationship between APLA and the clinical and neuroimaging features of MS have heretofore been shown. We assessed the clinical and neuroimaging features of MS patients with plasma APLA. Methods A consecutive cohort of 24 subjects with relapsing-remitting (RR) MS were studied of whom 7 were in remission (Rem) and 17 in exacerbation (Exc). All subjects were examined and underwent MRI of brain. Patients' plasma was tested by standard ELISA for the presence of both IgM and IgG antibodies using a panel of 6 targets: cardiolipin (CL), β2 glycoprotein I (β2GPI), Factor VII/VIIa (FVIIa), phosphatidylcholine (PC), phosphatidylserine (PS) and phosphatidylethanolamine (PE). Results In exacerbation up to 80% of MS subjects had elevated titers of IgM antibodies directed against the above antigens. However, in remission, less than half of MS patients had elevated titers of IgM antibodies against one or more of the above antigens. This difference was significant, p < 0.01, for all 6 target antigens. Interestingly, none of the MS patients had elevated plasma titers of IgG against any of the target antigens tested. Correlation analysis between MRI enhancing lesions and plasma levels of APLA revealed high correlation for aPC, aPS and aFVIIa (p ≤ 0.0065), a trend for aPE and aCL (p = 0.056), and no correlation for aβ2GP1. The strongest correlation was for aFVIIa, p = 0.0002. Conclusion The findings of this preliminary study show that increased APLA IgM is associated with exacerbations of MS. Currently, the significance of this association in pathogenesis of MS remains unknown. However, systematic longitudinal studies to measure APLA in larger cohorts of patients with relapsing-remitting MS, particularly before and after treatment with immunomodulatory agents, are needed to confirm these preliminary findings.

Abstract Background A correlation between plasma CD31+ endothelial microparticles (CD31+EMP) levels and clinical, as well as brain MRI activity, in multiple sclerosis (MS) patients has been previously reported. However, the effect(s) of treatment with interferon-β1a (IFN-β1a) on plasma levels of CD31+EMP has not been assessed. In a prospective study, we measured plasma CD31+EMP levels in 30 patients with relapsing-remitting MS. Methods Using flow cytometry, in a blinded study, we measured plasma CD31+EMP in 30 consecutive patients with relapsing-remitting MS (RRMS) prior to and 4, 12, 24 and 52 weeks after initiation of intramuscular therapy with interferon-β1a (IFN-β1a), 30 micrograms weekly. At each visit, clinical examination was performed and expanded disability status scale (EDSS) scores were assessed. Results Plasma levels of CD31+EMP were significantly reduced from 24 through 52 weeks following initiation of treatment with IFN-β1a. Conclusion Our data suggest that serial measurement of plasma CD31+EMP levels may be used as a surrogate marker of response to therapy with INF-β1a. In addition, the decline in plasma levels of CD31+EMP further supports the concept that IFN-β1a exerts stabilizing effect on the cerebral endothelial cells in pathogenesis of MS.

Objectives: This review summarizes recent developments in platelet biology relevant to neuroinflammatory disorders. Multiple sclerosis (MS) is taken as the "Poster Child" of these disorders but the implications are wide. The role of platelets in inflammation is well appreciated in the cardiovascular and cancer research communities but appears to be relatively neglected in neurological research.Organization: After a brief introduction to platelets, topics covered include the matrix metalloproteinases, platelet chemokines, cytokines and growth factors, the recent finding of platelet PPAR receptors and Toll-like receptors, complement, bioactive lipids, and other agents/functions likely to be relevant in neuroinflammatory diseases. Each section cites literature linking the topic to areas of active research in MS or other disorders, including especially Alzheimer's disease.Conclusion: The final section summarizes evidence of platelet involvement in MS. The general conclusion is that platelets may be key players in MS and related disorders, and warrant more attention in neurological research. [ABSTRACT FROM AUTHOR]

Objectives: This is a critical review of anti-phospholipid antibodies (aPL). Most prior reviews focus on the aPL syndrome (APS), a thrombotic condition often marked by neurological disturbance. We bring to attention recent evidence that aPL may be equally relevant to non-thrombotic autoimmune conditions, notably, multiple sclerosis and ITP.Organization: After a brief history, the recent proliferation of aPL target antigens is reviewed. The implication is that many more exist. Theories of aPL in thrombosis are then reviewed, concluding that all have merit but that aPL may have more diverse pathological consequences than now recognized. Next, conflicting results are explained by methodological differences. The lupus anticoagulant (LA) is then discussed. LA is the best predictor of thrombosis, but why this is true is not settled. Finally, aPL in non-thrombotic disorders is reviewed.Conclusion: The current paradigm of aPL holds that they are important in thrombosis, but they may have much wider clinical significance, possibly of special interest in neurology. [ABSTRACT FROM AUTHOR]

Spontaneous intracerebral hemorrhage (sICH) is a disabling stroke sub-type, and tobacco use is a prominent risk factor for sICH. We showed that chronic nicotine exposure enhances bleeding post-sICH. Reduction of hematoma growth is a promising effective therapy for sICH in smoking subjects. Red-blood-cell-derived microparticles (RMPs) are hemostatic agents that limit hematoma expansion following sICH in naïve rats. Considering the importance of testing the efficacy of experimental drugs in animal models with a risk factor for a disease, we tested RMP efficacy and the therapeutic time window in limiting hematoma growth post-sICH in rats exposed to nicotine. Young rats were chronically treated with nicotine using osmotic pumps. sICH was induced in rats using an injection of collagenase in the right striatum. Vehicle/RMPs were administered intravenously. Hematoma volume and neurological impairment were quantified ≈24 h after sICH. Hematoma volumes in male and female nicotine-exposed rats that were treated with RMPs at 2 h post-sICH were significantly lower by 26 and 31% when compared to their respective control groups. RMP therapy was able to limit hematoma volume when administered up to 4.5 h post-sICH in animals of both sexes. Therefore, RMPs may limit hematoma growth in sICH patients exposed to tobacco use.

Background: Spontaneous intracerebral hemorrhage (sICH) is the deadliest stroke subtype with no effective therapies. Limiting hematoma expansion is a promising therapeutic approach. Red blood cell-derived microparticles (RMPs) are novel hemostatic agents. Therefore, we studied the potential of RMPs in limiting hematoma growth and improving outcomes post-sICH., Methods: sICH was induced in rats by intrastriatal injection of collagenase. RMPs were prepared from human RBCs by high-pressure extrusion. Behavioral and hematoma/lesion volume assessment were done post-sICH. The optimal dose, dosing regimen, and therapeutic time window of RMP therapy required to limit hematoma growth post-sICH were determined. We also evaluated the effect of RMPs on long-term behavioral and histopathologic outcomes post-sICH., Results: RMP treatment limited hematoma growth following sICH. Hematoma volume (mm 3 ) for vehicle- and RMP- (2.66×10 10 particles/kg) treated group was 143±8 and 86±4, respectively. The optimal RMP dosing regimen that limits hematoma expansion was identified. RMPs limit hematoma volume when administered up to 4.5-hour post-sICH. Hematoma volume in the 4.5-hour post-sICH RMP treatment group was lower by 24% when compared with the control group. RMP treatment also improved long-term histopathologic and behavioral outcomes post-sICH., Conclusions: Our results demonstrate that RMP therapy limits hematoma growth and improves outcomes post-sICH in a rodent model. Therefore, RMPs have the potential to limit hematoma growth in sICH patients.

Background: Uncontrollable bleeding is a major cause of mortality and morbidity worldwide. Effective hemostatic agents are urgently needed. Red cell microparticles (RMPs) are a highly promising hemostatic agent. This study evaluated the safety profile of RMPs preliminary to clinical trial., Methods and Results: RMPs were prepared from type O+ human red blood cell by high-pressure extrusion. Male rats were treated with RMPs either a 1 × bolus, or 4 × or 20 × administered over 60 minutes. The vehicle-treated group was used as a control. Effects on physiological parameters were evaluated; namely, blood pressure, body and head temperature, hematocrit, and blood gases. We did not observe any adverse effects of RMPs on these physiological parameters. In addition, brain, heart, and lungs of rats treated with 4 × dose (bolus followed by infusion over 60 minutes) or vehicle were examined histologically for signs of thrombosis or other indications of toxicity. No thrombosis or indications of toxicity in brain, heart, or lungs were observed. Studies revealed that RMPs were distributed mainly in liver, spleen, and lymph nodes, and were potentially excreted through the kidneys., Conclusions: Our study indicates that RMP administration appears not to have any negative impact on the parameters studied and did not produce thrombosis in heart, brain, and lungs. However, more detailed long-term studies confirming the safety of RMP as a hemostatic agent are warranted.

Circulating cell-derived microparticles (MPs) exhibit procoagulant activity and have been investigated for a possible role in some human pathologies. However, their potential role in hemostasis has been neglected and often denied. This review brings to attention a specific body of direct clinical evidence supporting an important but distinctive role of MPs in hemostasis. Evidence for a role of MPs in hemostasis includes: (1) two congenital bleeding disorders attributed to impaired release of MPs; (2) two recent studies of trauma patients relating naturally elevated endogenous MPs at admission to reduced transfusion requirements and better outcomes; (3) a study of coronary surgery patients showing that elevated MP before surgery reduces transfusion requirements during surgery; and (4) a clinical study of patients with immune thrombocytopenia demonstrating that those with high circulating MP have reduced bleeding compared to patients with similar platelet counts but lower MP levels. Mechanisms involving potentiating the contact factor pathway are thought to play a key role and are probably synergistic with polyphosphate released from activated platelets at sites of endothelial injury. Hemostatic defect of patients with deficient MP-mediated coagulation resembles deficiency of FXI (hemophilia C), distinct from hemophilia A or B, so can be termed type C hemostasis. A better understanding of this proposed hemostatic pathway may lead to improved methods for controlling excessive bleeding in surgery, trauma, and other clinical settings., Competing Interests: Dr. Jy reports grants from RxMP Therapeutics, Inc., during the conduct of the study, as well as owning 5% equity of RxMP Therapeutics; grants from Wallace H Coulter Foundation, outside the submitted work. In addition, Dr. Jy has a patent, US patent #8,105,632, licensed to RxMP Therapeutics, and a second patent, US Patent #9,155,764, also licensed to RxMP Therapeutics. Dr. Ahn reports grants from RxMP Therapeutics, Inc, during the conduct of the study, as well as owning 10% equity of RxMP Therapeutics; grants from Wallace H. Coulter Foundation, outside the submitted work. In addition, Dr. Ahn has a patent, US Patent #8,105,632, licensed to RxMP Therapeutics, and a second patent, US Patent #9,155,764, also licensed to RxMP Therapeutics. Mr. Horstman reports having a patent, US Patent #8,105,632, licensed to RxMP Therapeutics, and a second patent, US Patent #9,155,764, also licensed to RxMP Therapeutics. Mr. McCauley has nothing to disclose., (Thieme Medical Publishers 333 Seventh Avenue, New York, NY 10001, USA.)

Red blood cell microparticles (RMPs) is a high potency hemostatic agent, which may serve as a viable therapeutic approach. They generate thrombin in vitro and effective in arresting bleeding in animal bleeding models. However, prior to ascertaining the clinical efficacy of RMPs, detailed preclinical evaluation is necessary. Therefore, we aimed to characterize RMPs, ascertain their stability, and determine their pharmacokinetics in rats. RMPs were prepared from human RBCs by a high-pressure extrusion method. Pharmacokinetic parameters were computed from groups receiving various RMPs dosing regimens. Volume of distribution, elimination rate constant, and clearance for RMPs were also assessed. Major portion of prepared microparticles were RMPs and a very small portion of particles were from platelets and leukocytes. RMPs were stable when stored at 5 and -20°C for at least 12 months. In vivo half-life was found to vary for each paradigm, but in general, was less than 2 min for most of the paradigms evaluated. Our results demonstrate that RMPs are stable during prolonged storage and have a short half-life. Therefore, the clinical use of RMPs as a hemostatic agent, within a tailored treatment paradigm, may be advantageous in achieving prolonged systemic therapeutic benefit without provoking any thrombotic complications.

Background: Genetic variants in the RASGRP2 gene encoding calcium and diacylglycerol-regulated guanine nucleotide exchange factor I (CalDAG-GEFI) represent a new inherited bleeding disorder linked to major defects of platelet aggregation and activation of αIIbβ3 integrin. They are of major interest as CalDAG-GEFI is receiving attention as a potential target for antiplatelet therapy for prevention and treatment of cardiovascular disorders including arterial thrombosis and atherosclerosis., Objectives: To better understand the phenotypical and clinical profiles of patients with CalDAG-GEFI deficiency., Patients: We report a five-generation family with a novel truncating CalDAG-GEFI mutation detailing clinical management and phenotypic variability., Results: Patients IV.6 & IV.4 manifested with episodes of serious mucocutanous bleeding or bleeding after surgery not responding to platelet transfusion but responding well to recombinant Factor VIIa infusions. Their blood counts and coagulation parameters were normal but platelet aggregation to ADP and collagen was defective. Further work-up confirmed normal levels of αIIb and β3 in their platelets but decreased αIIbβ3 function. DNA analysis by whole exome sequencing within the BRIDGE-BPD consortium (Cambridge, UK), allowed us to highlight a homozygous c.1490delT predicted to give rise to a p.F497Sfs*22 truncating mutation near to the C-terminal domain of CalDAG-GEFI. Sanger sequencing confirmed that both patients were homozygous for the c.1490delT and 3 out of 4 close family members were heterozygous., Conclusions: A long-term prospective study is warranted for full clinical exploration of CalDAG-GEFI to understand the bleeding phenotyes and their management.

Difficult and failed intubations account for the major causes of morbidity and mortality in current anesthetic practice. Several devices including McGrath Series 3 videolaryngoscope are available which may facilitate tracheal intubation by improving view of the larynx compared with Macintosh blade laryngoscopy. But no studies demonstrate whether McGrath Series 3 performs better than Macintosh laryngoscope in normal airway intubations by inexperienced anesthetists so far. We therefore designed this randomized controlled study to compare McGrath with Macintosh in routine tracheal intubation performed by inexperienced anesthetists.In total, 180 adult patients with normal-appearing airways requiring orotracheal intubation for elective surgery were randomly allocated to be intubated by 9 inexperienced anesthetists with McGrath or Macintosh. The primary outcome was time to intubation. Ease of intubation was assessed by a 5-point ordinal scale. Intubation attempts/failures, best laryngoscopy view using the Cormack-Lehane grade, associated complications and hemodynamic changes during intubation were recorded.We found that there was no significant difference between McGrath and Macintosh in the median time to intubation (P = 0.46); the Cormack-Lehane views attained using McGrath were superior (P < 0.001); the difference of ease of intubation was statistically significant (P = 0.01). No serious trauma occurred in both groups. And there was statistically significant difference in the systolic blood pressure changes between 2 groups (P < 0.05).We demonstrated that in orotracheal intubation in patients with normal airway by inexperienced anesthetists, McGrath compared with the Macintosh allows superior glottis views, greater ease of intubation, less complications, and hemodynamic changes with noninferior intubation time. And it remained a potential selection for inexperienced anesthetists in uncomplicated intubation.

To evaluate the effects of preoperative highly sensitive C-reactive protein (Hs-CRP) in serum on the prognostic outcomes of patients with hepatocellular carcinoma (HCC) following hepatic resection in Chinese samples.From January 2004 to December 2008, a total of 624 consecutive HCC patients who underwent hepatic resection were incorporated. Serum levels of Hs-CRP were tested at preoperation via a collection of venous blood samples. Survival analyses adopted the univariate and multivariate analyses.In our study, among the 624 screened HCC patients, 516 patients were eventually incorporated and completed follow-up. Positive correlations were found regarding preoperative serum Hs-CRP level and tumor size, Child-Pugh class, or tumor stage (all P < 0.0001). Patients with recurrence outcomes and nonsurvivors had increased Hs-CRP levels at preoperation (both P < 0.0001). When compared to the Hs-CRP-normal group, the overall survival (OS) and recurrence-free survival rates were evidently decreased in the Hs-CRP-elevated group. Further, preoperative serum Hs-CRP level might be having possible prediction effect regarding survival and recurrence of HCC patients after hepatic section in the multivariate analysis.Preoperative increased serum Hs-CRP level was an independent prognostic indicator in patients with HCC following hepatic resection in Chinese samples., Competing Interests: The authors have no conflicts of interest to disclose.

Objectives: Improved understanding of presurgical risk factors for transfusions will lead to reduction in their number and related complications. The goal of this study is to identify these factors in coronary artery bypass graft (CABG) surgery., Methods: Presented herein are results of analyses of data from an ongoing study of transfusion in CABG surgery. Of 122 patients, 81 received transfusion (Tx) and 41 did not (NoTx). In addition to routine tests, presurgical levels of microparticles from platelets (PMPs), red cells (RMPs), and other lineages were assayed., Results: The Tx and NoTx groups were similar with respect to most presurgical variables but differed in distribution of gender, blood type, diabetes prevalence, activated partial thromboplastin time (aPTT), hemoglobin (HGB), and microparticle levels. Stepwise multiple logistic regression was used to evaluate presurgical variables and to develop a model to assess risk factors for transfusion. CD41(+) PMP and CD235(+) RMP levels were found to be the main risk factors for transfusion. The Model's discriminating ability was assessed using receiver operating characteristic curve analysis, which showed that the area under the model curve (± standard error) was 0.86 ± 0.04 (95% confidence interval, 0.77-0.94). According to the model, patients with higher presurgical levels of circulating CD41(+) PMP, CD235a(+) RMP, and HGB, as well as a shorter aPTT, are less likely to receive transfusion(s)., Conclusions: Presurgical levels of CD41(+) PMPs and CD235a(+) RMPs are the main risk factors for transfusion in CABG, followed by HGB and aPTT., (Copyright © 2015 The American Association for Thoracic Surgery. Published by Elsevier Inc. All rights reserved.)

Among circulating cell-derived microparticles, those derived from red cells (RMP) have been least well investigated. To exploit potential haemostatic benefit of RMP, we developed a method of producing them in quantity, and here report on their haemostatic properties. High-pressure extrusion of washed RBC was employed to generate RMP. RMP were identified and enumerated by flow cytometry. Their size distribution was assessed by Doppler electrophoretic light scattering analysis (DELSA). Interaction with platelets was studied by platelet aggregometry, and shear-dependent adhesion by Diamed IMPACT-R. Thrombin generation and tissue factor (TF) expression was also measured. The effect of RMP on blood samples of patients with bleeding disorders was investigated ex vivo by thromboelastography (TEG). Haemostatic efficacy in vivo was assessed by measuring reduction of blood loss and bleeding time in rats and rabbits. RMP have mean diameter of 0.45 µm and 50% of them exhibit annexin V binding, a proxy for procoagulant phospholipids (PL). No TF could be detected by flow cytometry. At saturating concentrations of MPs, RMP generated thrombin robustly but after longer delay compared to PMP and EMP. RMP enhanced platelet adhesion and aggregation induced by low-dose ADP or AA. In TEG study, RMP corrected or improved haemostatic defects in blood of patients with platelet and coagulation disorders. RMP reduced bleeding time and blood loss in thrombocytopenic rabbits (busulfan-treated) and in Plavix-treated rats. In conclusion, RMP has broad haemostatic activity, enhancing both primary (platelet) and secondary (coagulation) haemostasis, suggesting potential use as haemostatic agent for treatment of bleeding.