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Search Results: 1 - 10 of 195416 matches for " Stéphane G. Paquette "
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Influenza Transmission in the Mother-Infant Dyad Leads to Severe Disease, Mammary Gland Infection, and Pathogenesis by Regulating Host Responses
Stéphane G. Paquette,David Banner?,Stephen S. H. Huang?,Raquel Almansa?,Alberto Leon?,Luoling Xu?,Jessica Bartoszko?,David J. Kelvin?,Alyson A. Kelvin
PLOS Pathogens , 2015, DOI: 10.1371/journal.ppat.1005173
Abstract: Seasonal influenza viruses are typically restricted to the human upper respiratory tract whereas influenza viruses with greater pathogenic potential often also target extra-pulmonary organs. Infants, pregnant women, and breastfeeding mothers are highly susceptible to severe respiratory disease following influenza virus infection but the mechanisms of disease severity in the mother-infant dyad are poorly understood. Here we investigated 2009 H1N1 influenza virus infection and transmission in breastfeeding mothers and infants utilizing our developed infant-mother ferret influenza model. Infants acquired severe disease and mortality following infection. Transmission of the virus from infants to mother ferrets led to infection in the lungs and mother mortality. Live virus was also found in mammary gland tissue and expressed milk of the mothers which eventually led to milk cessation. Histopathology showed destruction of acini glandular architecture with the absence of milk. The virus was localized in mammary epithelial cells of positive glands. To understand the molecular mechanisms of mammary gland infection, we performed global transcript analysis which showed downregulation of milk production genes such as Prolactin and increased breast involution pathways indicated by a STAT5 to STAT3 signaling shift. Genes associated with cancer development were also significantly increased including JUN, FOS and M2 macrophage markers. Immune responses within the mammary gland were characterized by decreased lymphocyte-associated genes CD3e, IL2Ra, CD4 with IL1β upregulation. Direct inoculation of H1N1 into the mammary gland led to infant respiratory infection and infant mortality suggesting the influenza virus was able to replicate in mammary tissue and transmission is possible through breastfeeding. In vitro infection studies with human breast cells showed susceptibility to H1N1 virus infection. Together, we have shown that the host-pathogen interactions of influenza virus infection in the mother-infant dyad initiate immunological and oncogenic signaling cascades within the mammary gland. These findings suggest the mammary gland may have a greater role in infection and immunity than previously thought.
Inflammatory Cytokine Expression Is Associated with Chikungunya Virus Resolution and Symptom Severity
Alyson A. Kelvin ,David Banner,Giuliano Silvi,Maria Luisa Moro,Nadir Spataro,Paolo Gaibani,Francesca Cavrini,Anna Pierro,Giada Rossini,Mark J. Cameron,Jesus F. Bermejo-Martin,Stéphane G. Paquette,Luoling Xu,Ali Danesh,Amber Farooqui,Ilaria Borghetto,David J. Kelvin,Vittorio Sambri,Salvatore Rubino
PLOS Neglected Tropical Diseases , 2011, DOI: 10.1371/journal.pntd.0001279
Abstract: The Chikungunya virus infection zones have now quickly spread from Africa to parts of Asia, North America and Europe. Originally thought to trigger a disease of only mild symptoms, recently Chikungunya virus caused large-scale fatalities and widespread economic loss that was linked to recent virus genetic mutation and evolution. Due to the paucity of information on Chikungunya immunological progression, we investigated the serum levels of 13 cytokines/chemokines during the acute phase of Chikungunya disease and 6- and 12-month post-infection follow-up from patients of the Italian outbreak. We found that CXCL9/MIG, CCL2/MCP-1, IL-6 and CXCL10/IP-10 were significantly raised in the acute phase compared to follow-up samples. Furthermore, IL-1β, TNF-α, Il-12, IL-10, IFN-γ and IL-5 had low initial acute phase levels that significantly increased at later time points. Analysis of symptom severity showed association with CXCL9/MIG, CXCL10/IP-10 and IgG levels. These data give insight into Chikungunya disease establishment and subsequent convalescence, which is imperative to the treatment and containment of this quickly evolving and frequently re-emerging disease.
Interleukin-6 Is a Potential Biomarker for Severe Pandemic H1N1 Influenza A Infection
Stéphane G. Paquette, David Banner, Zhen Zhao, Yuan Fang, Stephen S. H. Huang, Alberto J. Le?n, Derek C. K. Ng, Raquel Almansa, Ignacio Martin-Loeches, Paula Ramirez, Lorenzo Socias, Ana Loza, Jesus Blanco, Paola Sansonetti, Jordi Rello, David Andaluz, Bianche Shum, Salvatore Rubino, Raul Ortiz de Lejarazu, Dat Tran, Giovanni Delogu, Giovanni Fadda, Sigmund Krajden, Barry B. Rubin, Jesús F. Bermejo-Martin, Alyson A. Kelvin, David J. Kelvin
PLOS ONE , 2012, DOI: 10.1371/journal.pone.0038214
Abstract: Pandemic H1N1 influenza A (H1N1pdm) is currently a dominant circulating influenza strain worldwide. Severe cases of H1N1pdm infection are characterized by prolonged activation of the immune response, yet the specific role of inflammatory mediators in disease is poorly understood. The inflammatory cytokine IL-6 has been implicated in both seasonal and severe pandemic H1N1 influenza A (H1N1pdm) infection. Here, we investigated the role of IL-6 in severe H1N1pdm infection. We found IL-6 to be an important feature of the host response in both humans and mice infected with H1N1pdm. Elevated levels of IL-6 were associated with severe disease in patients hospitalized with H1N1pdm infection. Notably, serum IL-6 levels associated strongly with the requirement of critical care admission and were predictive of fatal outcome. In C57BL/6J, BALB/cJ, and B6129SF2/J mice, infection with A/Mexico/4108/2009 (H1N1pdm) consistently triggered severe disease and increased IL-6 levels in both lung and serum. Furthermore, in our lethal C57BL/6J mouse model of H1N1pdm infection, global gene expression analysis indicated a pronounced IL-6 associated inflammatory response. Subsequently, we examined disease and outcome in IL-6 deficient mice infected with H1N1pdm. No significant differences in survival, weight loss, viral load, or pathology were observed between IL-6 deficient and wild-type mice following infection. Taken together, our findings suggest IL-6 may be a potential disease severity biomarker, but may not be a suitable therapeutic target in cases of severe H1N1pdm infection due to our mouse data.
Diethyl 2-amino-5-[(E)-(1-methyl-1H-pyrrol-2-yl)methylideneamino]thiophene-3,4-dicarboxylate
Stéphane Dufresne,W. G. Skene
Acta Crystallographica Section E , 2010, DOI: 10.1107/s1600536810046775
Abstract: The structure of the title compound, C16H19N3O4S, shows the planes described by the thiophene and the pyrroles are twisted by 17.06 (4)°. Additionally, the structure shows the azomethine bond adopts the E configuration, while the pyrrole is disordered as a heterocycle flip [occupancy ratio 0.729 (5):0.271 (5)]. The three-dimensional network is well packed and involves N–H...O hydrogen bonding and π–π stacking [centroid–centroid distance = 4.294 (8) ].
Diethyl 2-amino-5-[(E)-(furan-2-ylmethylidene)amino]thiophene-3,4-dicarboxylate
Stéphane Dufresne,W. G. Skene
Acta Crystallographica Section E , 2010, DOI: 10.1107/s1600536810043746
Abstract: In the crystal structure of the title compound, C15H16N2O5S, the azomethine adopts the E configuration. The two heterocyclic rings adopt an antiperiplanar orientation. The mean planes of the thiophene and furan rings are twisted by 2.51 (4)°. The crystal structure exhibits intermolecular N—H...O hydrogen bonding. π–π stacking is also observed, the centroid-to-centroid distance being 3.770 (4) .
Diethyl 2,5-bis[(1E)-(1H-pyrrol-2-ylmethylidene)amino]thiophene-3,4-dicarboxylate
Stéphane Dufresne,W. G. Skene
Acta Crystallographica Section E , 2011, DOI: 10.1107/s1600536811031576
Abstract: In the crystal structure of the title compound, C20H20N4O4S, the azomethine group adopt E conformations. The pyrrole units are twisted by 10.31 (4) and 18.90 (5)° with respect to the central thiophene ring. The three-dimensional network is close packed and involves N—H...O, N—H...N, C—H...N and C—H...O hydrogen bonding.
Diethyl 2-[(1-methyl-1H-pyrrol-2-yl)methyleneamino]-5-(2-thienylmethyleneamino)thiophene-3,4-dicarboxylate
Stéphane Dufresne,W. G. Skene
Acta Crystallographica Section E , 2008, DOI: 10.1107/s160053680800799x
Abstract: Both imine bonds of the title compound, C21H21N3O4S2, were found to be in the E configuration. The terminal pyrrole and thiophene rings are twisted by 2.5 (3) and 2.3 (2)°, respectively, from the mean plane of the central thiophene to which they are attached. The structure is disordered by exchange of the terminal heterocyclic rings; the site occupancy factors are ca 0.8 and 0.2. The crystal packing involves some π–π stacking [3.449 (4) between pyrrole and terminal thiophene rings].
Diethyl 2,5-bis[(E)-2-furylmethyleneamino]thiophene-3,4-dicarboxylate
Stéphane Dufresne,W. G. Skene
Acta Crystallographica Section E , 2008, DOI: 10.1107/s1600536808006612
Abstract: The title compound, C20H18N2O6S, crystallizes as two independent molecules that are disposed about a pseudo-inversion center (1/2, 1/4, 1/8). The mean planes of the two terminal furyl rings are twisted with respect to the central thiophene ring by 7.33 (4) and 21.74 (5)° in one molecule, and by 6.91 (4) and 39.80 (6)° in the other.
Metabolic and cardiovascular improvements after biliopancreatic diversion in a severely obese patient
Philippe Woods, Carmen Paquette, Julie Martin, Jean-Gaston Dumesnil, Picard Marceau, Simon Marceau, Simon Biron, Frédéric Hould, Odette Lescelleur, Stéphane Lebel, Paul Poirier
Cardiovascular Diabetology , 2004, DOI: 10.1186/1475-2840-3-5
Abstract: A 56-year-old man with severe clinical obesity underwent a biliopancreatic diversion with a duodenal switch after unsuccessful treatment with weight loss pharmacotherapy. He had diabetes, hypertension and sleep apnea syndrome and was on three medications for hypertension and two hypoglycemic agents in addition to > 200 insulin units daily. Eleven months after the surgery, he had lost 40% of his body weight. The lipid profile showed great improvement and the hypertension and diabetes were more easily controlled with no more insulin needed. The pseudonormalized pattern of left ventricular diastolic function improved and ventricular walls showed decreased thickness.Biliopancreatic diversion may bring metabolic and cardiovascular benefits in severely obese patients from a cardiovascular perspective.A 56-year-old man was referred for biliopancreatic diversion with a duodenal switch (BPD-DS) for intractable complications associated with morbid obesity. He had been unable to lose weight with orlistat 120 mg three times a day for three months. The patient had diabetes mellitus for twenty years associated with hypertension, "mal perforant" and hepatic steatosis. He had all features of the metabolic syndrome and was treated for sleep apnea with a nocturnal continuous positive airway pressure device (C-PAP). His body mass index (BMI) at the time of the surgery was 48.7 kg/m2, weighting 157.7 kg.The patient's blood tests showed normal electrolytes and a creatinine of 110 μmol/L. The hemoglobin level was 134 g/L, white blood cell and platelet counts were normal. The glycated hemoglobin was 7.1% (normal range 4.4–6.5%) with fasting glucose values ranging from 7 to 11 mmol/L. A 24-hour blood pressure monitoring was normal under medication. His total cholesterol was 4.41 mmol/L, the triglyceride level was 1.74 mmol/L with LDL-cholesterol and HDL-cholesterol levels of 2.63 and 0.99 mmol/L respectively. The total cholesterol/HDL ratio was 4.45. Rest and exercise electrocardiograms we
Pricing and Hedging in Stochastic Volatility Regime Switching Models  [PDF]
Stéphane Goutte
Journal of Mathematical Finance (JMF) , 2013, DOI: 10.4236/jmf.2013.31006
Abstract:

We consider general regime switching stochastic volatility models where both the asset and the volatility dynamics depend on the values of a Markov jump process. Due to the stochastic volatility and the Markov regime switching, this financial market is thus incomplete and perfect pricing and hedging of options are not possible. Thus, we are interested in finding formulae to solve the problem of pricing and hedging options in this framework. For this, we use the local risk minimization approach to obtain pricing and hedging formulae based on solving a system of partial differential equations. Then we get also formulae to price volatility and variance swap options on these general regime switching stochastic volatility models.

 

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