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 28,634 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Studies have shown that over 50% of cardiovascular deaths occur before hospitalization. A major factor associated with survival in cases of out-of-hospital cardiac arrest is the time from cardiovascular collapse to the initiation of cardiopulmonary resuscitation (CPR) or "downtime." The purpose of this study was to determine whether blood lactate levels could be used to predict downtime in the canine cardiac arrest model. Femoral arterial and Swan-Ganz catheters were placed in 22 mongrel dogs, and ventricular fibrillation was electrically induced. The dogs remained in ventricular fibrillation without ventilation for 5, 10, 15, 30, or 60 minutes. After the predetermined fibrillation time, a left anterolateral thoracotomy was performed, and open-chest cardiac massage was begun. Arterial and mixed venous lactate levels were determined for every 5 minutes during 30 minutes of cardiopulmonary resuscitation. The correlation coefficient between the mixed venous and arterial lactate levels was 0.96 or greater during all stages of resuscitation. Peak serum lactate level increased linearly in relation to downtime. The increase in lactate level was not evident until after CPR was begun, and it remained at peak levels or decreased insignificantly, despite optimal open-chest CPR. Linear regression analysis revealed that 84% of the variability in serum lactate levels could be explained by downtime differences. In this model, blood lactate level is a reliable and objective measure of downtime and may be a useful indicator of the adequacy of CPR if levels decrease or remain stable. The clinical implications of this study lie with the use of blood lactate levels in the emergency department to guide the aggressiveness of resuscitative efforts.
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PMID:Lactic acidosis as a predictor of downtime during cardiopulmonary arrest in dogs. 397 Jul 67

A 19-year-old man died after the intake of ten tablets of Ecstasy containing 3,4-methyl-enedioxy-N-ethylamphetamine (MDEA) as the main active ingredient. According to an eyewitness the symptoms of intoxication were strong sweating, sudden aggressiveness followed by hallucinations, subsequent failure of motoric coordination, severe spasms of arms and back, complete depression of the respiratory system, unconsciousness, and collapse. Resuscitation by an emergency doctor failed. Major autopsy findings were severe vascular congestion of all internal organs, liquid post-mortem blood, numerous subpleural and subepicardial petechial haemorrhages. By GC/MS analysis, MDEA was found in large amounts in serum (12 mg/l in femoral vein, 22 mg/l in heart blood serum), urine (201 mg/l), brain (18 to 28 mg/l) and in other tissue samples. Scalp-hair was highly positive for MDEA (17 ng/mg). Besides MDEA and its metabolites only trace amounts of MDMA could be found in urine and blood; no other drugs were detected. It can be concluded that the cause of death was a monointoxication by overdosage of MDEA.
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PMID:Lethal monointoxication by overdosage of MDEA. 954 99

Airway evaluation is critical for surgical decision making. In patients with obstructive sleep apnea (OSA), a minimal evaluation should include a basic head and neck physical examination to evaluate for overt pathology. An upper airway examination will also provide insight into identifying patients with a higher risk of OSA. For patients who are evaluated for surgery, endoscopy combined with cephalometrics is the most accepted method of identifying patients with retroglossal collapse and obstruction. A new paradigm suggests that most patients have multilevel obstruction, so examination should be directed at assessing risk factors to direct the aggressiveness of surgical intervention.
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PMID:Predicting which patients will benefit from surgery for obstructive sleep apnea: the ENT exam. 1054 35

The centrosome is the major organelle responsible for the nucleation and organization of microtubules into arrays. Recent studies demonstrate that microtubules can nucleate outside the centrosome. The molecular mechanisms controlling acentrosomal microtubule nucleation are currently poorly defined, and the function of this type of microtubule regulation in tumor cell biology is particularly unclear. Since microtubule nucleation is initiated by the gamma-tubulin protein, we examined the regulation of gamma-tubulin in a panel of human breast tumor cell lines, ranging from non-tumorigenic to highly aggressive. We have identified a more dispersive subcellular localization of gamma-tubulin in aggressive breast cancer cell lines, while gamma-tubulin localization remains largely centrosomal in non-aggressive cell lines. Delocalization of gamma-tubulin occurs independently from changes in protein expression and is therefore regulated at the post-translational level. Subcellular fractionation revealed that tumor cell lines show an aberrantly increased release of gamma-tubulin into a soluble cytoplasmic fraction, with the most dramatic changes observed in tumor cell lines of greater aggressiveness. Extraction of soluble gamma-tubulin revealed acentrosomal incorporation of gamma-tubulin in cytoplasmic microtubules and along cell junctions. Moreover, acentrosomal delocalization of gamma-tubulin yielded resistance to colchicine-mediated microtubule collapse. These findings support a model where the solubility of gamma-tubulin can be altered through post-translational modification and provides a new mechanism for microtubule dysregulation in breast cancer. Gamma-tubulin that is delocalized from the centrosome can still clearly be incorporated into filaments, and defines a novel mechanism for tumor cells to develop resistance to microtubule-targeted chemotherapies.
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PMID:Delocalization of gamma-tubulin due to increased solubility in human breast cancer cell lines. 2000 67

The inference of transcriptional networks that regulate transitions into physiological or pathological cellular states remains a central challenge in systems biology. A mesenchymal phenotype is the hallmark of tumour aggressiveness in human malignant glioma, but the regulatory programs responsible for implementing the associated molecular signature are largely unknown. Here we show that reverse-engineering and an unbiased interrogation of a glioma-specific regulatory network reveal the transcriptional module that activates expression of mesenchymal genes in malignant glioma. Two transcription factors (C/EBPbeta and STAT3) emerge as synergistic initiators and master regulators of mesenchymal transformation. Ectopic co-expression of C/EBPbeta and STAT3 reprograms neural stem cells along the aberrant mesenchymal lineage, whereas elimination of the two factors in glioma cells leads to collapse of the mesenchymal signature and reduces tumour aggressiveness. In human glioma, expression of C/EBPbeta and STAT3 correlates with mesenchymal differentiation and predicts poor clinical outcome. These results show that the activation of a small regulatory module is necessary and sufficient to initiate and maintain an aberrant phenotypic state in cancer cells.
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PMID:The transcriptional network for mesenchymal transformation of brain tumours. 2003 75

Hyaluronan (HA) has many functions in the extracellular milieu of normal and diseased tissues. Disease-associated HA accumulation has been shown to predict a worsened prognosis in cancer patients, with tumors having a high-extracellular HA content (HA-high) being more aggressive than their HA-low counterparts. HA-high tumor aggressiveness is derived from the specialized biomechanical and molecular properties of the HA-based assembly of HA binding proteins and the growth-promoting factors that accumulate in it. Biophysical characteristics of an HA-high tumor microenvironment include high tumor interstitial pressure, compression of tumor vasculature, and resulting tumor hypoxia. Within the tumor cell membrane, HA receptors, primarily CD44 and RHAMM, anchor the HA-high extracellular network. HA-CD44 association on the tumor cell surface enhances receptor tyrosine kinase activity to drive tumor progression and treatment resistance. Together, malignant cells in this HA-high matrix may evolve dependency on it for growth. This yields the hypothesis that depleting HA in HA-high tumors may be associated with a therapeutic benefit. A pegylated form of recombinant human hyaluronidase PH20 (PEGPH20) has been deployed as a potential cancer therapeutic in HA-high tumors. PEGPH20 can collapse this matrix by degrading the HA-assembled tumor extracellular framework, leading to tumor growth inhibition, preferentially in HA-high tumors. Enzymatic depletion of HA by PEGPH20 results in re-expansion of the tumor vasculature, reduction in tumor hypoxia, and increased penetration of therapeutic molecules into the tumor. Finally, HA-depletion results in reduced signaling via CD44/RHAMM. Taken together, HA-depletion strategies accomplish their antitumor effects by multiple mechanisms that include targeting both biophysical and molecular signaling pathways. Ongoing clinical trials are examining the potential of PEGPH20 in combination with partner therapeutics in several cancers.
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PMID:Breaching the Castle Walls: Hyaluronan Depletion as a Therapeutic Approach to Cancer Therapy. 2638 Feb 22

As a contribution to a better understanding of cavitation erosion mechanisms, a compressible inviscid finite volume flow solver with barotropic homogeneous liquid-vapor mixture cavitation model is applied to ultrasonic horn set-ups with and without stationary specimen, that exhibit attached cavitation at the horn tip. Void collapses and shock waves, which are closely related to cavitation erosion, are resolved. The computational results are compared to hydrophone, shadowgraphy and erosion test data. At the horn tip, vapor volume and topology, subharmonic oscillation frequency as well as the amplitude of propagating pressure waves are in good agreement with experimental data. For the evaluation of flow aggressiveness and the assessment of erosion sensitive wall zones, statistical analyses of wall loads and of the multiplicity of distinct collapses in wall-adjacent flow regions are applied to the horn tip and the stationary specimen. An a posteriori projection of load collectives, i.e. cumulative collapse rate vs. collapse pressure, onto a reference grid eliminates the grid dependency effectively for attached cavitation at the horn tip, whereas a significant grid dependency remains at the stationary specimen. The load collectives show an exponential decrease towards higher collapse pressures. Erosion sensitive wall zones are well predicted for both, horn tip and stationary specimen, and load profiles are in good qualitative agreement with measured topography profiles of eroded duplex stainless steel samples after long-term runs. For the considered amplitude and gap width according to ASTM G32-10 standard, the analysis of load collectives reveals that the distinctive erosive ring shape at the horn tip can be attributed to frequent breakdown and re-development of a small portion of the tip-attached cavity. This partial breakdown of the attached cavity repeats at each driving cycle and is associated with relatively moderate collapse peak pressures, whereas the stationary specimen is rather unfrequently stressed at the end of each subharmonic oscillation cycle by the violent collapse of the complete cavity.
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PMID:Numerical 3D flow simulation of ultrasonic horns with attached cavitation structures and assessment of flow aggressiveness and cavitation erosion sensitive wall zones. 2696 85

A suicide bomb blast in 2013 at a distant city of Pakistan killed 84 and wounded more than 150 people. Some patients were transferred to our tertiary care hospital because of extreme load on medical services there. This patient arrived at the Aga Khan Hospital, 2 days after the bomb blast injury and underwent an orthopedic procedure. Next day, he developed sudden tachypnea, desaturation, and circulatory collapse. After initial cardiopulmonary resuscitation, he was immediately transferred to surgical intensive care unit. Based on history, echocardiography findings and patient parameters, a clinical diagnosis of massive pulmonary embolism was made and immediate thrombolytic therapy with alteplase was started. The immediate improvement in hemodynamic status was evident following 2 hours of alteplase infusion. This case also highlights the aggressiveness of resuscitation, decision making in initiating thrombolytic therapy on clinical grounds, importance of deep venous thrombosis prophylaxis, and exhaustion of health resources due to blast related mass destruction.
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PMID:Bomb Blast and Its Consequences: Successful Intensive Care Management of Massive Pulmonary Embolsim. 2737 30

Perturbation of normal behaviors in honey bee colonies by any external factor can immediately reduce the colony's capacity for brood rearing, which can eventually lead to colony collapse. To investigate the effects of brood-rearing suppression on the biology of honey bee workers, gene-set enrichment analysis of the transcriptomes of worker bees with or without suppressed brood rearing was performed. When brood rearing was suppressed, pathways associated with both protein degradation and synthesis were simultaneously over-represented in both nurses and foragers, and their overall pathway representation profiles resembled those of normal foragers and nurses, respectively. Thus, obstruction of normal labor induced over-representation in pathways related with reshaping of worker bee physiology, suggesting that transition of labor is physiologically reversible. In addition, some genes associated with the regulation of neuronal excitability, cellular and nutritional stress and aggressiveness were over-expressed under brood rearing suppression perhaps to manage in-hive stress under unfavorable conditions.
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PMID:Pathway profiles based on gene-set enrichment analysis in the honey bee Apis mellifera under brood rearing-suppressed conditions. 2880 79

The causal agent of bacterial wilt, Ralstonia solanacearum, is a soilborne pathogen that invades plants through their roots, traversing many tissue layers until it reaches the xylem, where it multiplies and causes plant collapse. The effects of R. solanacearum infection are devastating, and no effective approach to fight the disease is so far available. The early steps of infection, essential for colonization, as well as the early plant defense responses remain mostly unknown. Here, we have set up a simple, in vitro Arabidopsis thaliana-R. solanacearum pathosystem that has allowed us to identify three clear root phenotypes specifically associated to the early stages of infection: root-growth inhibition, root-hair formation, and root-tip cell death. Using this method, we have been able to differentiate, on Arabidopsis plants, the phenotypes caused by mutants in the key bacterial virulence regulators hrpB and hrpG, which remained indistinguishable using the classical soil-drench inoculation pathogenicity assays. In addition, we have revealed the previously unknown involvement of auxins in the root rearrangements caused by R. solanacearum infection. Our system provides an easy-to-use, high-throughput tool to study R. solanacearum aggressiveness. Furthermore, the observed phenotypes may allow the identification of bacterial virulence determinants and could even be used to screen for novel forms of early plant resistance to bacterial wilt.
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PMID:Type III Secretion-Dependent and -Independent Phenotypes Caused by Ralstonia solanacearum in Arabidopsis Roots. 2884 Jul 86


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