TxProbe: Discovering Bitcoin’s Network Topology Using Orphan Transactions

Bitcoin relies on a peer-to-peer overlay network to broadcast transactions and blocks. From the viewpoint of network measurement, we would like to observe this topology so we can characterize its performance, fairness and robustness. However, this is difficult because Bitcoin is deliberately designed to hide its topology from onlookers. Knowledge of the topology is not in itself a vulnerability, although it could conceivably help an attacker performing targeted eclipse attacks or to deanonymize transaction senders. In this paper we present TxProbe, a novel technique for reconstructing the Bitcoin network topology. TxProbe makes use of peculiarities in how Bitcoin processes out of order, or “orphaned” transactions. We conducted experiments on Bitcoin testnet that suggest our technique reconstructs topology with precision and recall surpassing 90%. We also used TxProbe to take a snapshot of the Bitcoin testnet in just a few hours. TxProbe may be useful for future measurement campaigns of Bitcoin or other cryptocurrency networks

Bartter- and Gitelman-like syndromes: salt-losing tubulopathies with loop or DCT defects

Salt-losing tubulopathies with secondary hyperaldosteronism (SLT) comprise a set of well-defined inherited tubular disorders. Two segments along the distal nephron are primarily involved in the pathogenesis of SLTs: the thick ascending limb of Henle’s loop, and the distal convoluted tubule (DCT). The functions of these pre- and postmacula densa segments are quite distinct, and this has a major impact on the clinical presentation of loop and DCT disorders – the Bartter- and Gitelman-like syndromes. Defects in the water-impermeable thick ascending limb, with its greater salt reabsorption capacity, lead to major salt and water losses similar to the effect of loop diuretics. In contrast, defects in the DCT, with its minor capacity of salt reabsorption and its crucial role in fine-tuning of urinary calcium and magnesium excretion, provoke more chronic solute imbalances similar to the effects of chronic treatment with thiazides. The most severe disorder is a combination of a loop and DCT disorder similar to the enhanced diuretic effect of a co-medication of loop diuretics with thiazides. Besides salt and water supplementation, prostaglandin E2-synthase inhibition is the most effective therapeutic option in polyuric loop disorders (e.g., pure furosemide and mixed furosemide–amiloride type), especially in preterm infants with severe volume depletion. In DCT disorders (e.g., pure thiazide and mixed thiazide–furosemide type), renin–angiotensin–aldosterone system (RAAS) blockers might be indicated after salt, potassium, and magnesium supplementation are deemed insufficient. It appears that in most patients with SLT, a combination of solute supplementation with some drug treatment (e.g., indomethacin) is needed for a lifetime

Bīografīi kompozitorov s IV-XX vi͡ek s portretami /

"Knigi i zhurnaly"--leaf preceding p. 709."Russkai͡a muzyka" (signed: Semen Kruglikov) : xxi p. preceding p. 417.Mode of access: Internet

Gitelman's syndrome: towards genotype-phenotype correlations?

Contains fulltext : 51735.pdf (publisher's version ) (Closed access)Gitelman's syndrome (GS) is a salt-losing tubulopathy characterized by hypokalemic alkalosis with hypomagnesemia and hypocalciuria. The disease is associated with inactivating mutations in the SLC12A3 gene that codes for the thiazide-sensitive Na+-Cl- cotransporter (NCCT) that is expressed in the apical membrane of the cells lining the distal convoluted tubule (DCT). GS is relatively frequent, and more than 100 mutations scattered through SLC12A3 have been identified thus far. Although the disease is recessively inherited, up to 40% of patients are found to carry only a single mutation, instead of being compound heterozygous or homozygous. The phenotype of GS is highly heterogeneous in terms of age at presentation, and nature/severity of the biochemical abnormalities and clinical manifestations. This phenotypical heterogeneity is observed not only between all patients harbouring SLC12A3 mutations but also among family members or patients with identical mutations. In this review, we discuss the potential explanations for the failure to identify mutant alleles in SLC12A3, as well as the different mechanisms that can account for the inter- and intra-familial phenotype variability in GS, including genetic heterogeneity, position and nature of the mutations, functional consequences, compensatory mechanisms, and modifying genes