Abstract:
Recombinant human erythropoietin (EPO) has been in widespread clinical use for over 15 years. Initially employed for the treatment of anemia associated chronic renal failure, it has now been demonstrated to be effective in treating anemia in a variety of other clinical settings, including HIV, cancer, surgery, and most recently critical illness [1]. Over the past several years it has become apparent that EPO has actions other than 'just' stimulating bone marrow to produce mature erythrocytes. EPO is also a cytokine with important antiapoptotic activity [2]. In this latter role, EPO has been demonstrated to confer important tissue protection in preclinical and some clinical studies [3-6].In their excellent review in this issue of Critical Care, Coleman and Brines [7] provide a succinct discussion of the 'nonhematologic' actions of EPO in protecting tissues and raise the intriguing possibility of clinical use of EPO to 'protect' tissues in the critically ill. Apoptosis is important in the pathogenesis of many critical illnesses such as sepsis and multiorgan failure. Experimental studies have also suggested that blocking apoptosis may be of benefit. Therefore, if pharmacologic doses of EPO were administered to critically ill patients, would the antiapoptotic activity EPO result in improved clinical outcomes?Some data bearing on this question are currently available. Two prospective randomized clinical trials examined the efficacy of EPO administration in reducing red blood cell (RBC) transfusion in the critically ill [8,9]. Both studies demonstrated a significant reduction in the number of RBC transfusions with EPO administration; however, no clinical outcome benefits were observed to be associated with this reduction in RBC transfusion. It is important to note that these studies were only designed to look at RBC transfusion and were not powered to look at clinical outcome differences. On the other hand, even if a clinical outcome benefit were observed, it would be ver

Abstract:
Anemia is common in critically ill patients and appears early during their intensive care unit (ICU) course. By day 3 after ICU admission, almost 95% of patients are anemic [1-3]. The anemia in these critically ill patients persists throughout their ICU and hospital stay, with or without red blood cell (RBC) transfusion [3].Historically, the anemia observed in the critically ill resulted in a high number of RBC transfusions. Studies conducted a decade ago [4] revealed that 50% of all patients admitted to the ICU are transfused during their stay. In addition, 85% of patients with a prolonged ICU stay (> 1 week) received transfusions [5]. On average, these latter patients were transfused 9.5 RBC units during their ICU stay. These transfusions are not restricted to the early ICU course; rather, patients are transfused at a rate of 2–3 units per week.An observational study of 4892 patients admitted to ICUs in the USA throughout 2000 and 2001 [3] found that almost 50% of patients are still transfused. The results also showed that initial RBC transfusion tends to occur early in the ICU stay, with ongoing RBC transfusions throughout the ICU stay. The mean pretransfusion hemoglobin observed (i.e. the 'transfusion trigger') was 8.6 ± 1.7 g/dl – a value that is comparable to that described in earlier reports [4,5]. Interestingly, RBC transfusions were not restricted to the ICU; 13% of patients received on average almost 3 units after ICU discharge.A similar observational study of transfusion practice in ICUs was performed across Western Europe [6]. Data were collected for a maximum of 28 days on 3534 patients admitted to the ICU during a 2-week period in late 1999. Of these patients 37% received a mean of 4.8 RBC units while in the ICU and 12.7% of patients were transfused during the post-ICU period, for an overall transfusion rate of 42% during the 28-day study period. The mean pretransfusion hemoglobin level was 8.4 g/dl.The similarity in results between these two large obs

Abstract:
We present a search for the decay B+ -> tau+ nu using 288 inverse femtobarns of data collected at the Upsilon(4S) resonance with the BaBar detector at the SLAC PEP-II B-Factory. A sample of events with one reconstructed semileptonic B decay (B- -> D0 l- nu X) is selected, and in the recoil a search for the signal decay mode is performed. The tau is identified in four channels. We measure a branching fraction of BF(B+ -> tau+ nu) = (0.88+0.68 -0.67(stat.) +- 0.11(syst.)) x 10^{-4} and extract an upper limit on the branching fraction, at the 90% confdence level, of 1.8 x 10^{-4}.

Abstract:
There has been much success in describing the limiting spatial fluctuations of growth models in the Kardar-Parisi-Zhang (KPZ) universality class. A proper rescaling of time should introduce a non-trivial temporal dimension to these limiting fluctuations. In one-dimension, the KPZ class has the dynamical scaling exponent $z=3/2$, that means one should find a universal space-time limiting process under the scaling of time as $t\,T$, space like $t^{2/3} X$ and fluctuations like $t^{1/3}$ as $t\to\infty$. In this paper we provide evidence for this belief. We prove that under certain hypotheses, growth models display temporal slow decorrelation. That is to say that in the scalings above, the limiting spatial process for times $t\, T$ and $t\, T+t^{\nu}$ are identical, for any $\nu<1$. The hypotheses are known to be satisfied for certain last passage percolation models, the polynuclear growth model, and the totally / partially asymmetric simple exclusion process. Using slow decorrelation we may extend known fluctuation limit results to space-time regions where correlation functions are unknown. The approach we develop requires the minimal expected hypotheses for slow decorrelation to hold and provides a simple and intuitive proof which applied to a wide variety of models.

Abstract:
Seven hundred and forty feeding tubes were inserted during the study period. In 14 cases (2%), the feeding tube was inserted into the tracheopulmonary system. Five patients (0.7%) suffered a major complication, including two (0.3%) who died from complications directly related to the feeding tube placement. All patients had altered consciousness and 13 of the 14 had endotracheal tubes in place. Malposition of the feeding tube was not predictable from clinical signs and auscultation, but was detectable by chest roentgenogram.Inadvertent insertion of enteral feeding tubes into the tracheopulmonary system during placement is associated with significant morbidity and mortality. Clinical signs at the time of insertion are not useful in identifying feeding tubes which are malpositioned. In the ICU patient, a chest roentgenogram is required after all feeding tube insertions prior to the initiation of enteral feeding. In the high-risk patient, alternatives to blind feeding tube insertion should be considered.Enteral feeding is now generally recognized as the preferred method for providing nutritional support to critically ill patients. When compared to parenteral nutrition, enteral feeding is considered to be both safer and associated with improved outcome [1]. Over the last two decades narrow-bore enteral feeding tubes have gained widespread acceptance as the preferred device for providing enteral nutrition. They were introduced in response to problems associated with the stiffer larger-bore tubes [2, 3]. The narrow-bore tubes are softer, made from silastic, and generally provide for greater patient comfort and fewer erosive complications than occur with the larger type. Most tubes of this type have a removable steel stylet, which makes them stiffer and allows for easier passage. A particular advantage of enteral feeding is the avoidance of the risk associated with placement of a central venous catheter [4, 5]. However, the use of feeding tubes is not without its own compli

Abstract:
In a prospective design, we identified and recorded the mortality ratio, percentage of unanticipated deaths, length of stay in the intensive care unit (ICU), and survival time of 147 patients transferred directly from other hospitals and 178 transferred from the wards within a rural tertiary-care hospital.The two groups did not differ significantly in the characteristics measured. Differences in access to tertiary critical care in this rural region did not affect survival or length of stay after admission to this tertiary ICU. The odds ratio (1.14; 95% confidence interval 0.72-1.83) for mortality associated with transfer from a rural community hospital was not statistically significant.Patients at community hospitals in this area who develop need for tertiary critical care are just as likely to survive as patients who develop ICU needs on the wards of this rural tertiary-care hospital, despite different accessibility to tertiary intensive-care services.Some hospitalized medical and surgical patients develop the need for critical-care resources that are available only at tertiary hospitals. Differences in accessibility to tertiary intensive care exist among hospitals within a rural region. For example, some patients are admitted from rural community hospitals that do not provide the same access to critical-care resources as is available to patients in the wards of tertiary hospitals. Therefore, the location of care (rural community hospital versus tertiary care center) before admission to a tertiary intensive care unit (ICU) may affect outcome.Determining whether accessibility is associated with outcome is important for understanding the role of regionalization when providing critical care to a rural population. Currently there is little direct evidence to support regionalization of adult medical and surgical critical-care services [1]. If accessibility proves to be a determinant of outcome, then development of a regional critical-care program might be beneficial. If

Abstract:
We compute the one-point probability distribution for the stationary KPZ equation (i.e. initial data H(0,X)=B(X), for B(X) a two-sided standard Brownian motion) and show that as time T goes to infinity, the fluctuations of the height function H(T,X) grow like T^{1/3} and converge to those previously encountered in the study of the stationary totally asymmetric simple exclusion process, polynuclear growth model and last passage percolation. The starting point for this work is our derivation of a Fredholm determinant formula for Macdonald processes which degenerates to a corresponding formula for Whittaker processes. We relate this to a polymer model which mixes the semi-discrete and log-gamma random polymers. A special case of this model has a limit to the KPZ equation with initial data given by a two-sided Brownian motion with drift beta to the left of the origin and b to the right of the origin. The Fredholm determinant has a limit for beta>b, and the case where beta=b (corresponding to the stationary initial data) follows from an analytic continuation argument.

Abstract:
We introduce the strict-weak polymer model, and show the KPZ universality of the free energy fluctuation of this model for a certain range of parameters. Our proof relies on the observation that the discrete time geometric q-TASEP model, studied earlier by A. Borodin and I. Corwin, scales to this polymer model in the limit q->1. This allows us to exploit the exact results for geometric q-TASEP to derive a Fredholm determinant formula for the strict-weak polymer, and in turn perform rigorous asymptotic analysis to show KPZ scaling and GUE Tracy-Widom limit for the free energy fluctuations. We also derive moments formulae for the polymer partition function directly by Bethe ansatz, and identify the limit of the free energy using a stationary version of the polymer model.

Abstract:
We consider the totally asymmetric simple exclusion process (TASEP) with two-sided Bernoulli initial condition, i.e., with left density rho_- and right density rho_+. We consider the associated height function, whose discrete gradient is given by the particle occurrences. Macroscopically one has a deterministic limit shape with a shock or a rarefaction fan depending on the values of rho_{+/-}. We characterize the large time scaling limit of the fluctuations as a function of the densities rho_{+/-} and of the different macroscopic regions. Moreover, using a slow decorrelation phenomena, the results are extended from fixed time to the whole space-time, except along the some directions (the characteristic solutions of the related Burgers equation) where the problem is still open. On the way to proving the results for TASEP, we obtain the limit processes for the fluctuations in a class of corner growth processes with external sources, of equivalently for the last passage time in a directed percolation model with two-sided boundary conditions. Additionally, we provide analogous results for eigenvalues of perturbed complex Wishart (sample covariance) matrices.

Abstract:
The purpose of this article is to describe the two approaches to compute exact formulas (which are amenable to asymptotic analysis) for the probability distribution of the current of particles past a given site in the asymmetric simple exclusion process (ASEP) with step initial data. The first approach is via a variant of the coordinate Bethe ansatz and was developed in work of Tracy and Widom in 2008-2009, while the second approach is via a rigorous version of the replica trick and was developed in work of Borodin, Sasamoto and the author in 2012.