Observation of photon-photon thermodynamic processes under negative optical temperature conditions.

Statistical mechanics demands that the temperature of a system is positive provided that its internal energy has no upper bound. Yet if this condition is not met, it is possible to attain negative temperatures for which higher-order energy states are thermodynamically favored. Although negative temperatures have been reported in spin and Bose-Hubbard settings as well as in quantum fluids, the observation of thermodynamic processes in this regime has thus far remained elusive. Here, we demonstrate isentropic expansion-compression and Joule expansion for negative optical temperatures, enabled by purely nonlinear photon-photon interactions in a thermodynamic microcanonical photonic system. Our photonic approach provides a platform for exploring new all-optical thermal engines and could have ramifications in other bosonic systems beyond optics, such as cold atoms and optomechanics.

Effects of clarithromycin, azithromycin and rifampicin on terbutaline-induced sweating in foals.

BACKGROUND: Erythromycin (ERY) induces anhidrosis in foals. Azithromycin (AZI) and clarithromycin (CLA), often combined with rifampicin (RIF), are commonly used to treat Rhodococcus equi infections, but effects on sweating have not been investigated. OBJECTIVE: To determine the effects of AZI, CLA and RIF on sweat responses in normal foals. STUDY DESIGN: Each experiment was a blinded, duplicated, six foal × three period counterbalanced within subjects design (12 foals/experiment). METHODS: Antimicrobials were given orally for 5 days. In Experiment 1, ERY, AZI and CLA were given. In Experiment 2, ERY, RIF and ERY/RIF combination were used. Quantitative intradermal terbutaline sweat tests were performed daily for 3 days before and 1, 2, 5, 9, 24, and 39 days after treatment. Data were analysed by repeated measures analysis of variance procedures. Significance was P≤0.05. RESULTS: In Experiment 1, all macrolides suppressed sweating although CLA and AZI were less potent than ERY. In Experiment 2, significant sweat suppression occurred in foals given ERY with or without RIF, but there was no effect of RIF alone. Rifampicin reduced sweat suppression by ERY on Day 1 of treatment but not thereafter. MAIN LIMITATIONS: Because ERY blood concentrations were not measured, effects of RIF on ERY-induced anhidrosis could not definitively be ascribed to altered ERY bioavailability. CONCLUSIONS: All macrolides commonly used to treat R. equi pneumonia, i.e. ERY, AZI and CLA, induce anhidrosis in foals. The potent anti-sudorific effect of ERY is delayed, but not substantially affected by concurrent RIF administration.

Effect of TNF-α production inhibitors on the production of pro-inflammatory cytokines by peripheral blood mononuclear cells from HTLV-1-infected individuals

Human T lymphotropic virus type 1 (HTLV-1) is the causal agent of myelopathy/tropical spastic paraparesis (HAM/TSP), a disease mediated by the immune response. HTLV-1 induces a spontaneous proliferation and production of pro-inflammatory cytokines by T cells, and increasing interferon-γ (IFN-γ) and tumor necrosis factor-α (TNF-α) levels are potentially involved in tissue damage in diseases related to HTLV-1. This exaggerated immune response is also due to an inability of the natural regulatory mechanisms to down-modulate the immune response in this group of patients. TNF-α inhibitors reduce inflammation and have been shown to improve chronic inflammatory diseases in clinical trials. The aim of this study was to evaluate the ability of pentoxifylline, forskolin, rolipram, and thalidomide to decrease in vitro production of TNF-α and IFN-γ in cells of HTLV-1-infected subjects. Participants of the study included 19 patients with HAM/TSP (mean age, 53 ± 11; male:female ratio, 1:1) and 18 HTLV-1 carriers (mean age, 47 ± 11; male:female ratio, 1:2.6). Cytokines were determined by ELISA in supernatants of mononuclear cell cultures. Pentoxifylline inhibited TNF-α and IFN-γ synthesis with the minimum dose used (50 µM). The results with forskolin were similar to those observed with pentoxifylline. The doses of rolipram used were 0.01-1 µM and the best inhibition of TNF-α production was achieved with 1 µM and for IFN-γ production it was 0.01 µM. The minimum dose of thalidomide used (1 µM) inhibited TNF-α production but thalidomide did not inhibit IFN-γ production even when the maximum dose (50 µM) was used. All drugs had an in vitro inhibitory effect on TNF-α production and, with the exception of thalidomide, all of them also decreased IFN-γ production.

Effect of TNF-α production inhibitors on the production of pro-inflammatory cytokines by peripheral blood mononuclear cells from HTLV-1-infected individuals.

Human T lymphotropic virus type 1 (HTLV-1) is the causal agent of myelopathy/tropical spastic paraparesis (HAM/TSP), a disease mediated by the immune response. HTLV-1 induces a spontaneous proliferation and production of pro-inflammatory cytokines by T cells, and increasing interferon-γ (IFN-γ) and tumor necrosis factor-α (TNF-α) levels are potentially involved in tissue damage in diseases related to HTLV-1. This exaggerated immune response is also due to an inability of the natural regulatory mechanisms to down-modulate the immune response in this group of patients. TNF-α inhibitors reduce inflammation and have been shown to improve chronic inflammatory diseases in clinical trials. The aim of this study was to evaluate the ability of pentoxifylline, forskolin, rolipram, and thalidomide to decrease in vitro production of TNF-α and IFN-γ in cells of HTLV-1-infected subjects. Participants of the study included 19 patients with HAM/TSP (mean age, 53 ± 11; male:female ratio, 1:1) and 18 HTLV-1 carriers (mean age, 47 ± 11; male:female ratio, 1:2.6). Cytokines were determined by ELISA in supernatants of mononuclear cell cultures. Pentoxifylline inhibited TNF-α and IFN-γ synthesis with the minimum dose used (50 µM). The results with forskolin were similar to those observed with pentoxifylline. The doses of rolipram used were 0.01-1 µM and the best inhibition of TNF-α production was achieved with 1 µM and for IFN-γ production it was 0.01 µM. The minimum dose of thalidomide used (1 µM) inhibited TNF-α production but thalidomide did not inhibit IFN-γ production even when the maximum dose (50 µM) was used. All drugs had an in vitro inhibitory effect on TNF-α production and, with the exception of thalidomide, all of them also decreased IFN-γ production.

[Salivary and lacrymal gland disorders and HTLV-1 infection]. / Atteinte des glandes salivaires et lacrymales et infection par le HTLV-1.

INTRODUCTION: The frequency and severity of salivary and lacrymal gland human T-cell lymphotropic virus type 1 (HTLV-1) infection were assessed in HTLV-1 plus patients, presenting with neurological deficit (tropical spastic paraparesis/HTLV-1 associated myelopathy [TSP/HAM]) or not. The mechanism of this deficit was investigated. MATERIAL AND METHODS: A case-control study was made from April 2002 to December 2005, in an area strongly endemic for HTLV-1. The patients were classified in three groups: group 1 with 16 patients presenting with TSP/HAM; group 2 with 67 HTLV-1 carriers and group 3 with 29 healthy volunteers. The dry syndrome was investigated by history taking and by oral and ophthalmological clinical examination. Immunological and biological screening for rhumatoid factors, antinuclear antibodies, and antibodies against soluble nuclear antigens (SSA, SSB). Peripheral blood was separated by density gradient and mononuclear cells were recovered to dose interferon-gamma and tumor necrosis factor-alpha. Patients in the three groups were assessed for salivary flow by stimulated weighing using Saxon's test. A Chi-2 test, a variance analysis (Anova), and the Spearman rank correlation test were used for the statistical analysis. RESULTS: The dry syndrome was mild and more common in group 1 patients (75%). In group 2, 22% of the patients presented with functional signs of buccal mucosa dryness comparable to those observed in group 1. No correlation was found between salivary flow and screened pro-inflammatory cytokines. DISCUSSION: Our results show that hyposialia is an important part of the disease induced by HTLV-1, even in virus carriers without neurological deficit. Its mechanism seems different than that of the Gougerot-Sjögren syndrome.

Levels of serum chemokines discriminate clinical myelopathy associated with human T lymphotropic virus type 1 (HTLV-1)/tropical spastic paraparesis (HAM/TSP) disease from HTLV-1 carrier state.

Approximately 5% of people infected with human T lymphotropic virus type 1 (HTLV-1) develop clinical myelopathy or tropical spastic paraparesis (HAM/TSP) that is associated with high-levels of Th1 cytokines, interferon (IFN)-gamma and tumour necrosis factor (TNF)-alpha. Chemokines are known to induce cytokine secretion and direct the trafficking of immune cells to sites of disease. The present study measured serum chemokines correlated with autonomously released IFN-gamma in cell cultures. HTLV-1 infection was defined by enzyme-linked immunosorbent assay (ELISA) and confirmed by Western blot. Subjects included HTLV-1 carriers (n = 56), patients with HAM/TSP (n = 31) and healthy HTLV-1 seronegative volunteer controls (n = 20). Serum chemokines and IFN-gamma autonomously released by mononuclear cells in culture were quantified by ELISA. Compared to HTLV-1 carriers, serum chemokines in HAM/TSP patients showed significantly increased levels of CXCL9 and CXCL10, significantly diminished levels of CCL2 and similar amounts of CCL11 and CCL24. In contrast, CCL11 and CCL24 were significantly lower in serum of HAM/TSP patients than either control. IFN-gamma was positively correlated with CXCL9 and CXCL10 when HAM/TSP and HTLV-1 carriers were used as a combined group. However, despite a large proportion of HTLV-1 carriers having high IFN-gamma levels, these chemokines were not increased in carriers. This study showed that high levels of CXCL9 and CXCL10 in the systemic circulation and low serum CCL2 levels are features of HAM/TSP. HTLV-1 infection and Tax and/or additional viral encoded factor-mediated pathological processes triggering T cell activation with autogenous IFN-gamma release are probably involved in regulating chemokine release.