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Increased resistin in brain dead organ donors is associated with delayed graft function after kidney transplantation

Increased resistin in brain dead organ donors is associated with delayed graft function after kidney transplantation

The association between resistin and MCP-1 in the brain dead organ donors seems to indicate a causative relationship between these two and may suggest a role for resistin in the initiation of the inflammatory response after brain-death. Unlike MCP-1, resistin did not appear influenced by the steroid pretreatment, suggesting either a different mechanism (i.e., passive release instead of de- novo synthesis) or a more upstream position in the in- flammatory cascade that is not influenced by medication. The effect of steroid treatment on resistin and endocan- 1 is more difficult to assess since our data come from only one, rather late time-point. This hypothesis should be pref- erably studied at several time points before and after the intervention.

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Decision making on organ donation: the dilemmas of relatives of potential brain dead donors

Decision making on organ donation: the dilemmas of relatives of potential brain dead donors

The decision-making process was described by the rela- tives of potential brain dead donors, as complex, primarily because relatives had to make a decision on behalf of the deceased (surrogate decision). Three conditions contribut- ing to this complexity were mentioned: [1] the time limit to make the decision created a sense of urgency; [2] the consent for donation request was made immediately after the relative had heard that a beloved one had died or was expected to die of brain death, making it difficult to focus on the request, because relatives were grieving. Half of the participants (most relatives who refused consent for dona- tion = non-donor families) said that they were not compe- tent to decide in such a crisis. “The problem is that, often when the physician asks something, although you con- sciously hear the question, do you actually digest the infor- mation coming in? Because you are preoccupied by other things, you are dealing with grief or just….” (R03). [3] The decision had to be agreed upon by a group of relatives. Initial disagreement between relatives –which occurred within both groups – was always overcome; agreement between relatives was mentioned as conditio sine qua non by the participants of both groups.

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Circulating resistin levels are early and significantly increased in deceased brain dead organ donors, correlate with inflammatory cytokine response and remain unaffected by steroid treatment

Circulating resistin levels are early and significantly increased in deceased brain dead organ donors, correlate with inflammatory cytokine response and remain unaffected by steroid treatment

Introduction: Resistin is a pro-inflammatory adipokine that increases after brain injury (trauma, bleeding) and may initiate an inflammatory response. Resistin was found increased in deceased, brain dead organ donors (DBD) and correlated with delayed graft function after kidney transplantation. The kinetics of resistin during brain death (BD), its impact on the inflammatory response and the influence of several donor variables on resistin levels are still unknown. Methods: Resistin along with a panel of Th1/Th2 cytokines [interferon (IFN)-gamma, interleukin (IL)-1beta, IL-2, IL-6, IL-8, IL10, IL-12, IL-13 and tumor necrosis factor (TNF)] was analyzed in 36 DBDs after the diagnosis of BD and before organ procurement and in 12 living kidney donors (LD). The cytokine levels and resistin were analyzed in relation to donor parameters including cause of death, donors’ age and steroid treatment.

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Prednisolone has a positive effect on the kidney but not on the liver of brain dead rats: a potencial role in complement activation

Prednisolone has a positive effect on the kidney but not on the liver of brain dead rats: a potencial role in complement activation

Our study also demonstrated a reduction in HO-1 expression in the kidney following methylprednisolone pretreatment of BD rats. As has been shown by Terry et al. [46] HO-1 is up-regulated by inflammatory cytokines like IL-1α via protein kinase C and phospholipase A2 in endothelial cells. We hypothesize that prednisolone is down-regulating HO-1 in the kidney by reducing the expression of inflammatory cytokines. In contrast to the kidney, in the liver HO-1 expression was increased fol- lowing prednisolone pretreatment of the brain dead rat, even when the expression of inflammatory genes was decreased. We think that these results could be an indica- tion of the cellular stress during the brain death period.

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Conjunctival microcirculatory blood flow is altered but not abolished in brain dead patients: a prospective observational study

Conjunctival microcirculatory blood flow is altered but not abolished in brain dead patients: a prospective observational study

These observations raise a number of questions. Is conjunctival/ocular blood flow fully dependent on ICA supply? And, if so, to what extent are the observed conjunctival microcirculatory alterations the result of reduced cerebral blood flow, as opposed to disruption of endothelial integrity during brain death? The fact that conjunctival microvascular blood flow is preserved to a large extend during absence of flow in the ICA may be in line with an alternative ocular blood supply. Schaser et al. [13] demonstrated that ICA clamping reduces capillary density and red blood cells velocity in the ipsi- lateral conjunctiva in carotid artery surgery patients. However, these authors also noticed that the conjunc- tival microcirculation by no means was halted to a standstill, which they explained by the development of a collateral compensatory circulation. However, in brain dead humans the acute timeline is unlikely to allow for neovascularisation. Alternatively, conjunctival vascular- isation is not fully ICA dependent. In retrospect we found evidence of preserved circulation via the OA in two out of three brain dead patients with lateral angio- graphic imaging. We were unable to evaluate ophthalmic circulation in other patients, since the routine position for cerebral pan-angiography is anterior-posterior. This position is not ideal for the detection of contrast filling of the OA. It is conceivable that parts of the external ca- rotid artery circulation contribute to the conjunctival microcirculation. We expect to perform lateral imaging during cerebral angiography in the future to clarify dif- ferent ocular blood supply routes in brain dead patients.

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Prospective Study of Evaluation of the Role of Vasopressin in the Management of Hypernatremia in Clinically Brain Dead Patients

Prospective Study of Evaluation of the Role of Vasopressin in the Management of Hypernatremia in Clinically Brain Dead Patients

They, hypothesized that low dose Vasopressin, infusion during organ recovery in critically ill children exerted a pressor effect, without major organ toxicity. Method: 34 VP-treated and 29 age-matched critically ill controls (C) 18 years were retrospectively reviewed during brain death evaluation and organ recovery. Vasopressin dose titrated clinically to urine output, with high variability. Pressor and inotrope management was titrated clinically to BP, cerebral perfusion and CVP in VP and C groups. Outcome measures include dose, type and number of, pressors and inotropes. Organ function was assessed at recovery and 48 h post-transplant.

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Interest of low dose hydrocortisone therapy during brain dead organ donor resuscitation: the CORTICOME study

Interest of low dose hydrocortisone therapy during brain dead organ donor resuscitation: the CORTICOME study

The ACTH stimulation test was performed in the 80 patients in the steroid group and in 41 patients in the control group; it revealed adrenal insufficiency in 94/121 brain-dead patients (78%). In the steroid group, the mean time before administration of hydrocortisone was 168 ± 130 minutes after brain death diagnosis. The mean quantity of hypotension episodes was comparable in control group and steroid group (1.2 ± 1.4 versus 1.0 ± 1.6, P = 0.18). The mean vascular filling volume per hour was similar in the two groups (179 ± 106 ml/h versus 219 ± 165 ml/h, P = 0.88). Although there were more pa- tients in the steroid group who received norepinephrine before brain death (80% versus 66%, P = 0.03), the mean dose of vasopressor administered after brain death was significantly lower than in the control group (1.18 ± 0.92 mg/h versus 1.49 ± 1.29 mg/h, P = 0.03), duration of vasopressor support use was shorter than in control group (874 minutes versus 1,160 minutes: P <0.0001) and norepinephrine weaning before aortic clamping was more frequent (33.8% versus 9.5%, P <0.0001) (Table 3). Using a survival approach, probability of norepinephrine weaning was significantly different between the two groups (P <0.0001) with a probability of weaning 4.67 Table 1 Delayed graft function (DGF) criteria

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The living dead and the dead living: contagion and complicity in contemporary universities

The living dead and the dead living: contagion and complicity in contemporary universities

The recent emergence of the zombie in popular culture has led critics to argue that we are experiencing a ‘zombie renaissance’ (Bishop 2009). Indeed, the proliferation of zombies on media screens led one journalist to enthuse, ‘zombies are so hot right now’ (TvFix n.d.). Scientists have recently discovered a new species of fungus in the Amazon ‘that turns ants into zombies’ (Osborne 2011), universities now offer courses on zombies (The Telegraph 2010) and a group of mathematicians hypothesised that the only pandemic capable of wiping out the human race are zombies (Lenon 2009). As the latter events indicate, zombies and their kin have now begun to invade the academy. Felicity Wood describes academics as the zombies of audit culture (2010: 237) who become enchanted by the occult qualities of corporate managerialism ‘purported to bestow efficiency, economic prosperity and success’ (227). Nick Couldry and Angela McRobbie describe ‘the idea’ of the university as dead (2010: 1), Henry Giroux claims that it is ‘hardly breathing’ (2009: 691) and Mary Evans finds that Higher Education has become infected with a ‘horrible psychic reality’ (2004: 32) which has produced a ‘nightmare world’ (34) full of ‘dead bodies’ (42) with creatures ‘from the depths of hell’ (46).

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Defaming the Dead

Defaming the Dead

And what about the exquisite care the U.S. military takes in repairing the corpses of dead soldiers? This too happens on  an industrial scale, with numbers illustrating the grisly ramifications of being on a more or less permanent war foot- ing: over sixty mortuary workers working in a building of sev- enty-two thousand square feet. But once cargo jets bring back the corpses, every step is suffused with respect for these dead individuals. White-gloved men in uniform transfer the in- coming coffins to white vans, which bring them back to the mortuary. Watch your tax dollars at work: morticians embalm the body, wash it, shampoo the hair, wire together broken bones, repair damaged tissue with stitches and suitably col- ored wax, even try to get the facial wrinkles right: “ ‘It has to look normal, like someone who is sleeping,’ said Petty Officer First Class Jennifer Howell, a Navy liaison with a mortician’s license.” Not a single loose thread on the uniforms they’ll be dressed in and every medal accurate, even if the coffin will remain resolutely shut in the funeral ceremony. 34

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To be or not to be a (dead) father

To be or not to be a (dead) father

What is less often remembered is that the father who introduces the child to the law is the dead father. Lacan reminds us this insight of Freud’s has been overlooked: ‘to the question, “what is a father” Freud replies “It is the dead Father”, but no one hears him.’ 22 What does it mean the father is the dead father and how can a dead figure usher in the law? It is important here to recall Lacan’s reliance on Hegel’s insight that signifiers, the names of things, kill the things themselves: as Hegel puts it, ‘The first act by which Adam established his lordship over the animals is this, that he gave them a name, ie, he nullified them as beings on their own account.’ 23 Following Hegel, Lacan insists ‘the word is the murder of the thing’. 24 The father, just like Hegel’s ‘thing’ is dead because it is not the father the person but the father as func- tion that institutes the law; once the function is performed, the father, like the thing killed by the word, becomes the dead father. Not only is this father dead but further, as conduit of the law, he is himself subject to the law: ‘The father must be the author of the law, yet he cannot vouch for it any more than anyone else can, because he, too, must submit to the bar which makes him, insofar as he is the real father, a cas- trated father.’ 25 The upshot for this good father, Lacan admits, ‘is a remarkably diffi- cult one; to a certain extent he is an insecure figure’. 26

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Remembering the Dead

Remembering the Dead

After the Victorian obsession with death and mourning, ostentatious gravestones and funeral memorials, macabre mourning jewellery containing the hair of the deceased and even more macabre family photographs taken with the dead, the backlash to this came in the form of reactions akin to Wilson’s quoted above. Cemeteries became spaces of consistency, headstones “simple and dignified” (Wilson, quoted in Rugg 219). Funeral rites were abridged, the dead were tidied away. As Freud remarked, summarising attitudes to death during the post-Victorian years prior to the First World War: “We showed an unmistakeable tendency to put death on one side, to eliminate it from life. We tried to hush it up.” (Quoted in Ramazani 11).

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Defaming the Dead

Defaming the Dead

Now consider a consortium action flowing out of an alleged underlying libel, though with no dead parties to be found. In the early twentieth century, newspapers across the country assiduously reported on the doings of Mrs. Everett Garrison of Newark, New Jersey. “One of the most attractive and prominent social leaders in Newark and north Jersey society,” she disappeared sometime around 1903 – just a few days after one Elliot A. Archer, a family and business friend of the Garrisons, abandoned his wife and two young children and fled: he must have known a local bank was about to discover some seventy or eighty thousand dollars in forged receipts. Everett himself moved to Manhattan, wouldn’t talk about his wife, and tried to make a new life for himself. In 1908 Mrs. Garrison turned up in Seattle, a leading socialite there too, ostensibly married to Archer, now going by the name Archie Carter. A New Jersey detective, sent to arrest Archer for those forgeries, identified her. (Washington’s governor refused to extradite Archer to New Jersey. Mrs. Garrison-cum-Carter had led his inaugural ball with him.) In “another amazing tangle,” she sued

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Voice of the Dead

Voice of the Dead

NUTRIAS (large rat-like rodents) BAA like little sheep from inside of small, rusty cages as OLD JAZZ MUSIC (similar to the music from Harlan's Grandmother's house) mixed with a CHOPPING SOUND emanates throughout the old slaughterhouse. Nox, wearing the moon mask on the back of his head, hums along with the MUSIC playing from a radio on a table where he chops a dead nutria into pieces with a cleaver.

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Jack is Dead

Jack is Dead

Yes, it’s a new musical about the life and death of Jack Cody called Catch A Falling Star. Clever don’t you think? The title was my idea. We start rehearsals next month in Toronto for a short run. Do a run around the New York critics. I’ve hired that English guy who wins all the awards to write the book, Sir Somebody or Another. Limey bastard was not cheap either, let me tell you. But this could pay off big, real big. I’ve already begun negotiating the film rights. Cody may be worth as much dead as alive if I pull this off. Jerry better cough up the theater I want. That schmuck owes me. This entire industry owes me. I, I mean, what would the world have been like without Jack Cody?

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The optimal hormonal replacement modality selection for multiple organ procurement from brain-dead organ donors

The optimal hormonal replacement modality selection for multiple organ procurement from brain-dead organ donors

Hormonal replacement therapy has been widely used to increase organ procurement from human brain-dead donors. To date, there has been no conclusive research indicating the optimal hormonal combinations for procurement of a specific type of organ or of multiple organs. In the present study, we proposed a two-step approach using generalized linear mod- els (GLM) or GLMM, and multiple comparison procedures. Using Tukey’s MCA, Dunnett–Hsu’s MCC, and Hsu’s MCB, we analyzed data from 40,124 brain-dead potential donors (in which definitive hormonal replacement therapy was docu- mented) with the aim of identifying the optimal therapy for both individual and multiple organ procurement.

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CT Perfusion for Confirmation of Brain Death

CT Perfusion for Confirmation of Brain Death

Instead of 2-phase CTA, all patients underwent a 9.6-cm-coverage brain CTP protocol (80 kV, 200 mAs, 128 ⫻ 0.6 mm collimation, 9.6-cm scan volume in the z-axis by using an adaptive spiral scan- ning technique [“shuttle mode”], CT dose index of 189.64 mGy), with 18 scans every 1.67 seconds (inflow phase) followed by 4 scans every 3.47 seconds (outflow phase), resulting in a total scan- ning time of 40.17 seconds on the 128-section dual-energy CT scanner (Sensation Definition; Siemens Healthcare, Erlangen, Germany). A total of 40 mL of nonionic iodinated contrast media (iopamidol, Isovue-370; Bracco Diagnostic, Vaughan, Ontario, Canada) was injected at a rate of 5 mL/s, followed by a saline flush of 40-mL sodium chloride at 5 mL/s and a start delay of 5 seconds. Two sets of axial images with a section thickness of 1.5 mm for the CTA analysis and 5 mm for the perfusion analysis were reconstructed without overlap and sent to the PACS. Sagittal and coronal multiplanar and maximum-intensity-projection images from the CTA data were reconstructed and sent to the PACS.

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Spatial Temporal Quantitative Global Energy Differences between the Living and Dead Human Brain

Spatial Temporal Quantitative Global Energy Differences between the Living and Dead Human Brain

The second analysis involved correlating time-independent, band-specific PDs ob- tained over left and right hemispheric homologous areas. Living and Non-Living brain data obtained at different times (T1 and T2) were extracted for contralateral pairs of channels and needle-electrodes. Data were normalized by z-transformation and spectral analysed. Power profiles for contralateral pairs of channels (Living) and needle-elec- trodes (Non-Living) were correlated within typical QEEG frequency bands ( i.e . delta, theta, alpha, beta1, beta2, and gamma) as well as low- and high-frequency case-cont- rolled (n = 254) band ranges ( i.e . 1.5 Hz - 10 Hz and 31.5 Hz - 40Hz). We reasoned that strong correlations would indicate time-independent PD profile parity for contralateral pairs. This is an implicit measure of PD stability between hemispheric homologues over time. Alternatively, any reliable strong correlation between time-independent PD pro- files for contralateral pairs could be considered as an indicator of high signal redun- dancy for the paired structures being directly probed or over which QEEG channels were positioned.

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A Cloud based Virtual Brain Connectivity with EEG Sensor using Internet of Things (IoT)

A Cloud based Virtual Brain Connectivity with EEG Sensor using Internet of Things (IoT)

In this paper, we described a cloud-based system for performing large-scale brain connectivity analysis. We demonstrated that our approach can achieve fast data query and extraction for analytics and visualization. There are many avenues for future work. First, we would like to enhance the web GUI by making it more interactive and user friendly. Further, we intend to scale up to process much larger datasets (terabytes and above) with the goal of one day being able to perform such analysis on the human brain. We are also exploring the use of a polystore database such as BigDAWG as a data. Here we are using logid for every user, through that they are accessing their data. In future, thumb impression for every user can be added instead of logid. With this logid, misuse of data is possible. And this great kit can be converted into a chip and can insert either internally or externally. For autism people and illness people this can be inserted internally. And also, every person can use this in day to day life and can definitely escape from accidental health issues and also from forgeries being done without the particular person’s knowledge.

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Original Article Clinical, histopathological and genetic studies in a case of fatal familial insomnia with review of the literature

Original Article Clinical, histopathological and genetic studies in a case of fatal familial insomnia with review of the literature

Indeed, severe thalamic neuronal loss and glio- sis are characteristically seen in postmortem studies of FFI, usually without concomitant spongiform change, expect in very advanced stages of the disease. The most seriously affected thalamic nuclei are the anteroventral, mediodorsal nuclei, and the pulvinar [12]. Morphometric investigations have shown a 90% loss of neurons in association nuclei and in motor nuclei and a 60% loss in limbic- paralimbic, intralaminar, and reticular nuclei. Atrophy of the inferior olive with neuronal loss and gliosis is also commonly observed. In this study, the pathological results were consistent with these changes. The immunohistochemical staining of brain tissue could exclude inflamma- tory disease and vascular disease. Taupathy, which is sometimes seen in prion diseases with amyloidosis, has thus far not been reported in patients with FFI.

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Clinical and ethical perspectives on brain death

Clinical and ethical perspectives on brain death

the pathophysiology of brain death, in which sequential dysfunction due to anoxic injury moves in a rostral–caudal direction ending at the lower brainstem, these tests, prima facie, make logical sense, because they all test brainstem function. Unresponsiveness to pain or other stimuli primar- ily tests the reticular activating system originating at the pontomedullary junction; cranial nerve reflexes originate in a variety of nuclei throughout the brainstem; and the apnea test challenges medullary respiratory drive centers by increasing carbon dioxide in the blood. Furthermore, the cardinal fea- tures of unresponsiveness, brainstem areflexia, and apnea, in the absence of confounds and the presence of a known cause of coma, are the core elements of accepted diagnostic tests around the world, 1 even for brainstem death, since they test

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