Probing analytical and numerical integrability: The curious case of (AdS5×S5)η(AdS_5\times S^5)_{\eta}

Motivated by recent studies related to integrability of string motion in various backgrounds via analytical and numerical procedures, we discuss these procedures for a well known integrable string background $(AdS_5\times S^5)_{\eta}$. We start by revisiting conclusions from earlier studies on string motion in $(\mathbb{R}\times S^3)_{\eta}$ and $(AdS_3)_{\eta}$ and then move on to more complex problems of $(\mathbb{R}\times S^5)_{\eta}$ and $(AdS_5)_{\eta}$. Discussing both analytically and numerically, we deduce that while $(AdS_5)_{\eta}$ strings do not encounter any irregular trajectories, string motion in the deformed five-sphere can indeed, quite surprisingly, run into chaotic trajectories. We discuss the implications of these results both on the procedures used and the background itself.Comment: 31 pages, 3 figures, references updated, analysis for Spiky strings in section (4.1) have been revised, version to appear in JHE

Fast spinning strings on η \eta deformed AdS5×S5 AdS_5 \times S^{5}

In this paper, considering the correspondence between spin chains and string sigma models, we explore the rotating string solutions over $\eta$ deformed $AdS_5 \times S^{5}$ in the so called fast spinning limit. In our analysis, we focus only on the bosonic part of the full superstring action and compute the relevant limits on both $(R \times S^{3})_{\eta}$ and $(R \times S^{5})_{\eta}$ models. The resulting system reveals that in the fast spinning limit, the sigma model on $\eta$ deformed $S^5$ could be $\textit{approximately}$ thought of as the continuum limit of anisotropic $SU(3)$ Heisenberg spin chain model. We compute the energy for a certain class of spinning strings in deformed $S^5$ and we show that this energy can be mapped to that of a similar spinning string in the purely imaginary $\beta$ deformed background.Comment: 30 pages; references updated; version to appear in JHE

From CFTs to theories with Bondi-Metzner-Sachs symmetries: Complexity and out-of-time-ordered correlators

We probe the contraction from $2d$ relativistic CFTs to theories with Bondi-Metzner-Sachs (BMS) symmetries, or equivalently Conformal Carroll symmetries, using diagnostics of quantum chaos. Starting from an Ultrarelativistic limit on a relativistic scalar field theory and following through at the quantum level using an oscillator representation of states, one can show the CFT$_2$ vacuum evolves smoothly into a BMS$_3$ vacuum in the form of a squeezed state. Computing circuit complexity of this transmutation using the covariance matrix approach shows clear divergences when the BMS point is hit or equivalently when the target state becomes a boundary state. We also find similar behaviour of the circuit complexity calculated from methods of information geometry. Furthermore, we discuss the hamiltonian evolution of the system and investigate Out-of-time-ordered correlators (OTOCs) and operator growth complexity, both of which turn out to scale polynomially with time at the BMS point.Comment: V3: To appear in PRD. Change of title has been implemented by the editors. It was simply titled "CFT to BMS: Complexity and OTOC" befor

Induction of Krüppel-Like Factor 4 Mediates Polymorphonuclear Neutrophil Activation in Streptococcus pneumoniae Infection

The recruitment and activation of polymorphonuclear neutrophils (PMNs) are of central importance for the elimination of pathogens in bacterial infections. We investigated the Streptococcus pneumoniae-dependent induction of the transcription factor Kruppel-like factor (KLF) 4 in PMNs as a potential regulator of PMN activation. We found that KLF4 expression is induced in human blood-derived PMNs in a time- and dose-dependent manner by wild-type S. pneumoniae and capsule knockout mutants. Unencapsulated knockout mutants induced stronger KLF4 expression than encapsulated wild types. The presence of autolysin LytA-competent (thus viable) pneumococci and LytA-mediated bacterial autolysis were required for KLF4 induction in human and murine PMNs. LyzMcre-mediated knockdown of KLF4 in murine blood-derived PMNs revealed that KLF4 influences pneumococci killing and increases the release of the proinflammatory cytokines tumor necrosis factor alpha and keratinocyte chemoattractant and decreases the release of the anti-inflammatory cytokine interleukin-10. Thus, S. pneumoniae induces KLF4 expression in PMNs, which contributes to PMN activation in S. pneumoniae infection

PREVALENCE OF ANTI-HCV, HBSAG, HIV AMONG MULTI-TRANSFUSED THALASSEMIC INDIVIDUALS AND THEIR SOCIO-ECONOMIC BACKGROUND IN EASTERN INDIA

Objective: The objective was to study the serological prevalence of post-transfusion transmitted infections such as hepatitis C virus (HCV), hepatitisB virus (HBV), and HIV among multi-transfused thalassemic individuals of the Eastern India and the socio and financial difficulties faced by them.Methods: The study was carried out from January 2012 until December 2014 involving 1711 thalassemic major individuals. Blood serum wascollected from each patient to perform ELISA for the detection of HBV and HCV seroprevalence. HIV seropositivity along with their hematological andliver function parameters were obtained from the transfusion centers and the host institutions. Other socio-economic conditions were obtained bypredesigned proforma of the questionnaire.Results: 67.9% males and 32.1% females were present in our study population of which 75% were from rural area. The mean hemoglobin was foundto be lower, whereas mean ferritin, bilirubin, and liver enzymes were much higher than the normal range. Only a handful of 19.76% of the fathers ofthalassemic individuals had secondary education. 263 families (15.37%) were familiar with the chances of transfusion-transmitted infections (TTIs).The dominant TTI found within the population was HCV with 18.70% prevalence followed by HIV (3.74%) and HBV (3.33%). 82.93% of the affectedfamilies suffered poverty with a meager monthly income within Rs. 5000 fighting against high costs of transfusion and related treatments.Conclusion: Our study reflects the different socio-economic and psychological burdens faced by the thalassemia patients and their families. The highrate of TTIs highlights the need for stringent screening of blood or blood products before administration.Keywords: Thalassemia, Socio-economic, Transfusion-transmitted infections, Hepatitis C virus, Hepatitis B virus, HIV

Krueppel-Like Factor 4 Expression in Phagocytes Regulates Early Inflammatory Response and Disease Severity in Pneumococcal Pneumonia

The transcription factor Krueppel-like factor (KLF) 4 fosters the pro-inflammatory immune response in macrophages and polymorphonuclear neutrophils (PMNs) when stimulated with Streptococcus pneumoniae, the main causative pathogen of community-acquired pneumonia (CAP). Here, we investigated the impact of KLF4 expression in myeloid cells such as macrophages and PMNs on inflammatory response and disease severity in a pneumococcal pneumonia mouse model and in patients admitted to hospital with CAP. We found that mice with a myeloid-specific knockout of KLF4 mount an insufficient early immune response with reduced levels of pro-inflammatory cytokines and increased levels of the anti-inflammatory cytokine interleukin (IL) 10 in bronchoalveolar lavage fluid and plasma and an impaired bacterial clearance from the lungs 24 hours after infection with S. pneumoniae. This results in higher rates of bacteremia, increased lung tissue damage, more severe symptoms of infection and reduced survival. Higher KLF4 gene expression levels in the peripheral blood of patients with CAP at hospital admission correlate with a favourable clinical presentation (lower sequential organ failure assessment (SOFA) score), lower serum levels of IL-10 at admission, shorter hospital stay and lower mortality or requirement of intensive care unit treatment within 28 days after admission. Thus, KLF4 in myeloid cells such as macrophages and PMNs is an important regulator of the early proinflammatory immune response and, therefore, a potentially interesting target for therapeutic interventions in pneumococcal pneumonia

Impact of the myeloid Krüppel-like factor 4 during pneumococcal pneumonia

Bakterielle Pneumonien sind weltweit eine der häufigsten Todesursachen und S. pneumoniae ist das häufigste klinische Isolat. Neutrophile Granulozyten gehören zur Klasse der myeloiden Zellen und sind eine wichtige Komponente der angeborenen Immunität gegen bakterielle Infektionen. Krüppel-like factor 4 (KLF4) spielt dabei nicht nur eine Rolle in der Differenzierung der Zellen des Immunsystems, sondern auch während der Infektion bei der Vermittlung inflammatorischer Signale in unterschiedlichen Zelltypen. Diese Studie zeigt zum ersten Mal in vivo, dass myeloides KLF4 Einfluss auf den Krankheitsverlauf hat und die mit einer bakteriellen Pneumonie einhergehende Entzündungsreaktion reguliert. Die hier aufgeführten Ergebnisse demonstrieren, dass der Transkriptionsfaktor KLF4 während einer Pneumokokken Pneumonie in humanen und murinen neutrophilen Granulozyten induziert wird. Diese Induktion ist Zeit- und Dosisabhängig. Außerdem wird die Expression von myeloidem KLF4 durch die Autolyse von S. pneumoniae reguliert, aber nicht über Toll-like Rezeptor 2 (TLR2), TLR4 oder TLR9 vermittelt. Studien in einem Maus-Pneumonie Modell zeigen, dass myeloides KLF4 einen proinflammatorischen Phänotyp bewirkt. Mäuse mit einem KLF4 knockout (KLF4-/-) in myeloiden Zellen haben im Vergleich zu Wildtyp (KLF4+/+) Mäusen eine höhere Bakterienlast in Lunge, Blut und Milz. Obwohl die Produktion proinflammatorischer Zytokine (wie TNF-α, IL-1β und KC) in BALF und Plasma von KLF4-/- Mäusen geringer war, gab es keine Unterschiede bei der Zellrekrutierung in der BALF von KLF4-/- und KLF4+/+ Mäusen. Allerdings war die Zellrekrutierung im Blut der KLF4-/- Mäuse geringer als bei den KLF4+/+ Mäusen. Außerdem wurde eine erhöhte vaskuläre Permeabilität verbunden mit perivaskulären Ödemen und Pleuritis bei KLF4-/- Mäusen während der S. pneumoniae-induzierten Infektion beobachtet. Diese Mäuse erreichten auch eher die humanen Endpunkte als die vergleichbaren KLF4+/+ Mäuse.Bacterial pneumonia is one of the leading causes of death worldwide. Streptococcus pneumoniae is the most frequently isolated pathogen from clinical pneumonia samples. Neutrophils belong to the class of myeloid cells and forms an important component of this innate immune system against bacterial infections. Krüppel-like factor 4 (KLF4) has been reported to not only play a role in differentiation of cells of the immune system but also in mediating inflammatory signals in different kinds of host cells during infection. This study shows myeloid KLF4 has an impact on pneumococcal pneumonia outcome and regulates the inflammation associated with bacterial pneumonia in vivo in mice. The results presented in the work show that the transcription factor KLF4 is induced in human and mice neutrophils during pneumococcal pneumonia. The induction of KLF4 is time and dose dependent. Additionally, the expression of myeloid KLF4 is regulated by the autolysis of S. pneumoniae but is not mediated via Toll-like receptor (TLR) 2, TLR4 or TLR9. Studies using a mouse pneumonia model showed that myeloid KLF4 exhibits a pro-inflammatory phenotype. Mice with KLF4 knockout (KO) or KLF4-/- in myeloid cells had higher bacterial load in their lungs, blood and spleen in comparison to wildtype (WT) or KLF4+/+ mice. Although there was less pro-inflammatory cytokine (such as TNF-α, IL-1β and KC) production in the broncho-alveolar lavage fluid (BALF) and plasma of KLF4-/- mice yet there no differences in cell recruitment in the BALF of the KLF4-/- and KLF4+/+ mice. There was however less cell recruitment in the blood of KLF4-/- mice in comparison to KLF4+/+ mice. Additionally, an increased vascular permeability associated with perivascular edema and pleuritis was seen during Streptococcus pneumoniae-induced infection in KLF4-/- mice, which also reached earlier the human endpoints than the KLF4+/+ mice