Hadronisation at LEP

An overview of recent results from LEP concerning the hadronisation process is presented. Emphasis is placed on the $b$-quark. The first presented analysis is the measurement of the $b$-quark fragmentation function. It includes a new, hadronic-model independent method to extract the x-dependence of the non-perturbative QCD component from the measured fragmentation function. This is followed by the results of two analyses on, respectively, production rates of b-excited states and branching fractions of b-quarks to neutral and charged b-hadrons. Multiplicity in the final state is also discussed concerning the difference in multiplicities between b and light quark initiated events, and total multiplicities in three jet events. Finally, recent measurements of \omega and \eta meson production rates are given.Comment: Talk given at XXXVIII Rencontres de Moriond, March 23rd - 29th, 200

Distributed Structure: Joint Expurgation for the Multiple-Access Channel

In this work we show how an improved lower bound to the error exponent of the memoryless multiple-access (MAC) channel is attained via the use of linear codes, thus demonstrating that structure can be beneficial even in cases where there is no capacity gain. We show that if the MAC channel is modulo-additive, then any error probability, and hence any error exponent, achievable by a linear code for the corresponding single-user channel, is also achievable for the MAC channel. Specifically, for an alphabet of prime cardinality, where linear codes achieve the best known exponents in the single-user setting and the optimal exponent above the critical rate, this performance carries over to the MAC setting. At least at low rates, where expurgation is needed, our approach strictly improves performance over previous results, where expurgation was used at most for one of the users. Even when the MAC channel is not additive, it may be transformed into such a channel. While the transformation is lossy, we show that the distributed structure gain in some "nearly additive" cases outweighs the loss, and thus the error exponent can improve upon the best known error exponent for these cases as well. Finally we apply a similar approach to the Gaussian MAC channel. We obtain an improvement over the best known achievable exponent, given by Gallager, for certain rate pairs, using lattice codes which satisfy a nesting condition.Comment: Submitted to the IEEE Trans. Info. Theor

Finite-State Channels with Feedback and State Known at the Encoder

We consider finite state channels (FSCs) with feedback and state information known causally at the encoder. This setting is quite general and includes: a memoryless channel with i.i.d. state (the Shannon strategy), Markovian states that include look-ahead (LA) access to the state and energy harvesting. We characterize the feedback capacity of the general setting as the directed information between auxiliary random variables with memory to the channel outputs. We also propose two methods for computing the feedback capacity: (i) formulating an infinite-horizon average-reward dynamic program; and (ii) a single-letter lower bound based on auxiliary directed graphs called $Q$-graphs. We demonstrate our computation methods on several examples. In the first example, we introduce a channel with LA and derive a closed-form, analytic lower bound on its feedback capacity. Furthermore, we show that the mentioned methods achieve the feedback capacity of known unifilar FSCs such as the trapdoor channel, the Ising channel and the input-constrained erasure channel. Finally, we analyze the feedback capacity of a channel whose state is stochastically dependent on the input.Comment: 39 pages, 10 figures. The material in this paper was presented in part at the 56th Annual Allerton Conference on Communication, Control, and Computing, Monticello, IL, USA, October 2018, and at the IEEE International Symposium on Information Theory, Los Angeles, CA, USA, June 202

On the tightness of Marton's regions for semi-additive broadcast channels

We study cost constrained side-information channels, where the cost function depends on a state which is known only to the encoder. In the additive noise case, we bound the capacity loss due to not knowing the cost state at the decoder and show that it is small under various assumptions, and goes to zero in the limit of weak noise. This model plays an important role in the (non-degraded) broadcast channel. In the semi-additive noise case, we bound the gap between the best known single letter achievable region and the true capacity region, using tools developed for the first problem. In the limit of weak noise, we show that the bounds coincide, thus we get the complete characterization of the capacity region

The role of anion gap normalization time in the management of pediatric diabetic ketoacidosis

IntroductionOur aims were to determine whether anion gap normalization time (AGNT) correlates with risk factors related to the severity of diabetic ketoacidosis (DKA) in children, and to characterize AGNT as a criterion for DKA resolution in children admitted with moderate or severe disease.MethodsA ten-year retrospective cohort study of children admitted to the intensive care unit with DKA. We used a survival analysis approach to determine changes in serum glucose, bicarbonate, pH, and anion gap following admission. Using multivariate analysis, we examined associations between patients' demographic and laboratory characteristics with delayed normalization of the anion gap.ResultsA total of 95 patients were analyzed. The median AGNT was 8 h. Delayed AGNT (>8 h) correlated with pH < 7.1 and serum glucose >500 mg/dL. In multivariate analysis, glucose >500 mg/dL was associated with an increased risk for delayed AGNT, by 3.41 fold. Each 25 mg/dL elevation in glucose was associated with a 10% increment in risk for delayed AGNT. Median AGNT preceded median PICU discharge by 15 h (8 vs. 23 h).DiscussionAGNT represents a return to normal glucose-based physiology and an improvement in dehydration. The correlation observed between delayed AGNT and markers of DKA severity supports the usefulness of AGNT for assessing DKA recovery

MTADV 5-MER peptide suppresses chronic inflammations as well as autoimmune pathologies and unveils a new potential target-Serum Amyloid A.

Despite the existence of potent anti-inflammatory biological drugs e.g., anti-TNF and anti IL-6 receptor antibodies, for treating chronic inflammatory and autoimmune diseases, these are costly and not specific. Cheaper oral available drugs remain an unmet need. Expression of the acute phase protein Serum Amyloid A (SAA) is dependent on release of pro-inflammatory cytokines IL-1, IL-6 and TNF-α during inflammation. Conversely, SAA induces pro-inflammatory cytokine secretion, including Th17, leading to a pathogenic vicious cycle and chronic inflammation. 5- MER peptide (5-MP) MTADV (methionine-threonine-alanine-aspartic acid-valine), also called Amilo-5MER, was originally derived from a sequence of a pro-inflammatory CD44 variant isolated from synovial fluid of a Rheumatoid Arthritis (RA) patient. This human peptide displays an efficient anti-inflammatory effects to ameliorate pathology and clinical symptoms in mouse models of RA, Inflammatory Bowel Disease (IBD) and Multiple Sclerosis (MS). Bioinformatics and qRT-PCR revealed that 5-MP, administrated to encephalomyelytic mice, up-regulates genes contributing to chronic inflammation resistance. Mass spectrometry of proteins that were pulled down from an RA synovial cell extract with biotinylated 5-MP, showed that it binds SAA. 5-MP disrupted SAA assembly, which is correlated with its pro-inflammatory activity. The peptide MTADV (but not scrambled TMVAD) significantly inhibited the release of pro-inflammatory cytokines IL-6 and IL-1β from SAA-activated human fibroblasts, THP-1 monocytes and peripheral blood mononuclear cells. 5-MP suppresses the pro-inflammatory IL-6 release from SAA-activated cells, but not from non-activated cells. 5-MP could not display therapeutic activity in rats, which are SAA deficient, but does inhibit inflammations in animal models of IBD and MS, both are SAA-dependent, as shown by others in SAA knockout mice. In conclusion, 5-MP suppresses chronic inflammation in animal models of RA, IBD and MS, which are SAA-dependent, but not in animal models, which are SAA-independent