Financial Diversification and Sudden Stops

Recent literature on sudden stops analyses the sharp and varied capital account reversals experienced by many emerging market economies. This paper claims that more information can be extracted from the behavior of gross capital flows than from their net results. It emphasizes the fact that, while one economy’s sudden stop can reveal exclusion from the international financial markets, another can be making adjustments to its investment portfolio causing a sudden start, and both produce the same net effect on the capital account. We present a simple model that rationalizes this empirical fact and its relationship with the economy’s financial diversification.

An inhibitor of HIV-1 protease modulates constitutive eIF2α dephosphorylation to trigger a specific integrated stress response.

Inhibitors of the HIV aspartyl protease [HIV protease inhibitors (HIV-PIs)] are the cornerstone of treatment for HIV. Beyond their well-defined antiretroviral activity, these drugs have additional effects that modulate cell viability and homeostasis. However, little is known about the virus-independent pathways engaged by these molecules. Here we show that the HIV-PI Nelfinavir decreases translation rates and promotes a transcriptional program characteristic of the integrated stress response (ISR). Mice treated with Nelfinavir display hallmarks of this stress response in the liver, including α subunit of translation initiation factor 2 (eIF2α) phosphorylation, activating transcription factor-4 (ATF4) induction, and increased expression of known downstream targets. Mechanistically, Nelfinavir-mediated ISR bypassed direct activation of the eIF2α stress kinases and instead relied on the inhibition of the constitutive eIF2α dephosphorylation and down-regulation of the phophatase cofactor CReP (Constitutive Repressor of eIF2α Phosphorylation; also known as PPP1R15B). These findings demonstrate that the modulation of eIF2α-specific phosphatase cofactor activity can be a rheostat of cellular homeostasis that initiates a functional ISR and suggest that the HIV-PIs could be repositioned as therapeutics in human diseases to modulate translation rates and stress responses

Can we predict development of impulsive-compulsive behaviours in Parkinson's disease?

OBJECTIVE: To determine clinical and structural imaging predictors of impulsive-compulsive behaviour (ICB) in de novo Parkinson's disease (PD). METHODS: From a cohort of 1116 subjects from the Parkinson's Progression Marker Initiative database, we created a subcohort of 42 de novo PD without ICB at baseline with available 3T MRI and who developed ICB during follow-up. PD-ICB were matched for age, gender and disease duration to 42 patients with PD without ICB over follow-up (PD-no-ICB) and 42 healthy controls (HCs). Baseline demographic and clinical predictors of ICB were analysed. For the longitudinal neuroimaging analysis, we selected 27 patients with PD-ICB with available neuroimaging after ICB onset, who were matched with 32 PD-no-ICB and 35 HCs. Baseline and longitudinal structural differences were compared using voxel-based morphometry and voxel-based quantification. RESULTS: People who went on to develop ICB had more severe anxiety, worse autonomic and global cognitive functions and were more likely to have rapid eye movement sleep behaviour disorder. Logistic regression confirmed that worse autonomic and cognitive functions were predictors of ICB. We could not find any morphological feature on baseline MRI that predicted later onset of ICB. When comparing PD groups at follow-up, a small region of increased atrophy in the anterior limb of the left internal capsule adjacent to the head of the left caudate nucleus was found in PD-ICB, but not surviving correction for multiple comparisons. CONCLUSIONS: Worse autonomic and cognitive functions predict development of ICB at the time of PD diagnosis. Structural imaging fails to identify morphological features associated with the development of ICB

Quantifiers for randomness of chaotic pseudo random number generators

We deal with randomness quantifiers and concentrate on their ability to discern the hallmark of chaos in time series used in connection with pseudo-random number generators (PRNGs). Workers in the field are motivated to use chaotic maps for generating PRNGs because of the simplicity of their implementation. Although there exist very efficient general-purpose benchmarks for testing PRNGs, we feel that the analysis provided here sheds additional didactic light on the importance of the main statistical characteristics of a chaotic map, namely (i) its invariant measure and (ii) the mixing constant. This is of help in answering two questions that arise in applications: (i) which is the best PRNG among the available ones? and (ii) if a given PRNG turns out not to be good enough and a randomization procedure must still be applied to it, which is the best applicable randomization procedure? Our answer provides a comparative analysis of several quantifiers advanced in the extant literature.Instituto de Física La Plat

A global fit to determine the pseudoscalar mixing angle and the gluonium content of the eta' meson

We update the values of the eta-eta' mixing angle and of the eta' gluonium content by fitting our measurement R_phi = BR(phi to eta' gamma)/ BR(phi to eta gamma) together with several vector meson radiative decays to pseudoscalars (V to P gamma), pseudoscalar mesons radiative decays to vectors (P to V gamma) and the eta' to gamma gamma, pi^0 to gamma gamma widths. From the fit we extract a gluonium fraction of Z^2_G = 0.12 +- 0.04, the pseudoscalar mixing angle psi_P = (40.4 +- 0.6) degree and the phi-omega mixing angle psi_V = (3.32 +- 0.09) degree. Z^2_G and psi_P are fairly consistent with those previously published. We also evaluate the impact on the eta' gluonium content determination of future experimental improvements of the eta' branching ratios and decay width.Comment: 13 pages, 7 figures to submit to JHE

Thromboelastographic profiles as a tool for thrombotic risk in digestive tract cancer

Background: Quantification of the magnitude of thrombotic risk associated with malignancy and with anti-cancer therapy is indispensable to use anticoagulant drugs which selectively interfere with haemostatic mechanisms protecting patients from venous thromboembolism (VTE) and probably from tumor progression. However, none of activation coagulation markers has any predictive value for the occurrence of the thrombotic events in one individual patient. Current clotting methods can’t reveal the overall dynamic clot formation; in contrast thromboelastographic methods specifically assess overall coagulation kinetics and its strength in whole blood. Aim: Objective of study was to evaluate if the activation of coagulation as eventually revealed by ROTEM® thromboelastometry could assess an hypercoagulable state in surgical neoplastic patients. Patients and Methods: Fifty consecutive patients with carcinoma of the digestive tract in preoperative period (23 M, 27 F aging 61.5 (45–79 years) and 147 healthy subjects (71 M, 76 F) were studied. A recent thromboelastometric method based on thrombelastography after Hartert was employed. Measurements were performed on ROTEM Coagulation Analyzer. The continuous coagulation data from 50 min course were transformed into dynamic velocity profiles of WB clot formation. Results: Standard parameters (CT, CFT, MCF) of cancer patients were similar to controls. CT (in cancer patients): females 50 s (38.3–58.7), males 50 s (42–71.2) vs 51 s (42–59), p = 0.1210 / 53 s (42–74.8), p = 0.1975 (in controls). CFT (in cancer patients): females 72 s (32- 92.4), males 80 s (50.2- 128.7) vs 78 s (62–100), p = 0.0128 / 80 s (59–124.4), p = 0.9384 (in controls). MCF (in cancer patients): females 70 mm (59.9–82.5), males 63 mm (56–73.7) vs 69 mm (59–95.8), p = 0.9911 / 69 mm (53.6–90), p = 0.0135 (in controls). Females showed a higher MaxVel when compared to males. The MaxVel was increased in cancer patients: females 19 mm /100 s (14.3–49.5) males 18 mm / 100 s (11–27) vs 15 mm 100 s (11.8–22), p < 0.001 / 13 mm / 100 s (10–21.8), p < 0.001 in controls .The t-MaxVel was shortened in cancer patients: females 65 s (48.6–112.8), males 81 s (50.1–135.9) vs 115 s (56.8–166), p <0.001 / 115 s (59.8–180.8), p = 0.0002 in controls. The AUC was increased in cancer patients: females 6451 mm 100 (5511–8148), males 5984 mm 100 (5119-6899) vs 5778 mm 100 (4998–6655), p < 0.001 / 5662 mm 100 (4704–6385), p = 0.0105. Conclusion: Unlike other assays measuring variations in a single component during coagulation, the thrombelastographic method records a profile of real-time continuous WB clot formation, and may provide extensive informations on haemostasis in neoplastic patients before surgery.Предпосылки исследования количественная оценка риска тромбоза, связанного со злокачественными заболеваниями и противоопухолевой терапией, обязательно включает в себя применение средств-антикоагулянтов, защищающих больного от развития венозной тромбоэмболии (VTE)и возможно п рогрессии заболевания . Тем не менее ни один из маркеров ак- тивации коагуляции не имеет прогностической ценности с точки зрения возможности возникновения тромбоза у каждого отдельно взятого пациента. Современные мето ды оценки свертывания крови не отража ют образование тромба винамике ; наоборот, метод тромбо эластографии дает возможность специфически оценить кинетику свертывания крови целом . Цель: определить, в какой мере активность коагуляции, определяемой методом тромбоэ ластометрии, отражает состояние гиперсвертываемости крови у больных онкологического профиля после хирургического вмешательства. Пациенты и м ды: обследованы 50 больных раком пищ еваритель ного тракта в дооп ерационный п ериод (27 женщин, 23 му жчины, средний возраст 61,5 года (45–79 лет) и 147 здоровых доноров (71 мужчина, 76 женщин). Применяли метод тромбоэластометрии , основанный на тромбоэластографии Гартерта, с использованием анализатора коагуляциифирмыROTEM. Текущие д анные о свертывании за 50 мин измерений представили в виде динамичных профилей вязкости при образовании сгустка крови. Результаты: стандартные параметры (перио д коагуляции (CT), перио д образования сгу стка (CFT), максимал ь ная п лот- ность сгустка (MCF)) больных онкологического п рофиля близки к контроль ным . CT у больных онкологического п рофиля составлял: у женщин — 50 с (38,3–58,7), у му жчин 50 (42–71,2) vs 51 (42–59), p = 0,1210/53 ( 42–74,8 ), p = 0,1975 в контрольной группе . CFT у таких пациентов составлял : у женщин — 72 ( 32–92,4 м жчин – 80 с (50,2–128,7) vs 78 (62–100), p = 0,0128 80 (59–124,4), p = 0,9384 в контрол ьной группе . MCF у больных онкологического п составлял: у женщин — 70 мм (59,9–82,5), у мужчин — 63 мм (56–73,7) vs 69 мм (59–95,8), p = 0,9911 / 69 мм (53,6–90), p = 0,0135 в контрол ьной группе. У женщинпоказатели вязкости крови MaxVel были выше, чем у му жчин . Показатели MaxVel повышены у таких пациентов : у женщин — 19 мм/100 с (14,3–49,5) у му жчин — 18 мм/100 (11–27 ) vs 15 мм / 100 (11,8–22), p < 0,001 / 13 мм / 100 с (10–21,8), p <0,001 в контрол ьной группе. ь t-MaxVel понижен у больных онкологического профиля: у женщин – 65 с (48,6–112,8) , у мужчин – 81 с (50,1–135,9) vs 115 с (56,8–166), p < 0,001 / 115 с (59,8–180,8), p = 0,0002 в контрольной группе. Показатель AUC у повышен у женщин — 6451 мм 100 (5511–8148), у мужчин — 5984 мм 100 (5119–6899) vs 5778 мм 100 (4998–6655), p < 0,001 / 5662 мм 100 (4704–6385), p = 0.0105. Выводы в отличие от других мето дов, измеря ющих вариации отдельных комп онентов системы крови, метод тромбо эластографии отражает текущийп рофиль образования сгу сткав режиме реаль ного времени является информативным споссобом оценки состояния гемостаза у онкологических больных

AIM2 inflammasome is activated by pharmacological disruption of nuclear envelope integrity.

Inflammasomes are critical sensors that convey cellular stress and pathogen presence to the immune system by activating inflammatory caspases and cytokines such as IL-1β. The nature of endogenous stress signals that activate inflammasomes remains unclear. Here we show that an inhibitor of the HIV aspartyl protease, Nelfinavir, triggers inflammasome formation and elicits an IL-1R-dependent inflammation in mice. We found that Nelfinavir impaired the maturation of lamin A, a structural component of the nuclear envelope, thereby promoting the release of DNA in the cytosol. Moreover, deficiency of the cytosolic DNA-sensor AIM2 impaired Nelfinavir-mediated inflammasome activation. These findings identify a pharmacologic activator of inflammasome and demonstrate the role of AIM2 in detecting endogenous DNA release upon perturbation of nuclear envelope integrity

Precise measurements of the eta and the neutral kaon meson masses with the KLOE detector

We present precise measurements of the eta and K0 masses using the processes phi to eta gamma, eta to gamma gamma and phi to Ks Kl, Ks to pi+ pi-. The K0 mass measurement, M_K=497.583 +/- 0.005 (stat) +/- 0.020 (syst) MeV, is in acceptable agreement with the previous measurements but is more accurate. We find m(eta) = 547.874 +/- 0.007 (stat) +/- 0.031 (syst) MeV. Our value is the most accurate to date and is in agreement with two recent measurements based on eta decays, but is inconsistent, by about 10 sigma, with a measurement of comparable precision based on eta production at threshold.Comment: 15 pages, 8 figures Submitted to Physics Letters