ePoster Presentation
Biography
Dr Rashmi Sharma has completed her PhD in 2001 on the topic “Studies on certain Substances Antagonizing the action of Vitamin A during regeneration in anuran amphibians.†She has more than 17 years of teaching and research experience. She has published many papers in repute journals. She has attended more than 70 conferences both national and International. She is also doing post doctorate.
Abstract
Ajmer is located in the center of Rajasthan (INDIA) between 25 0 38 “ and 26 0 58 “ north Latitude and 73 0 54 “ and 75 0 22†east longitude covering a geographical area of about 8481sq km hemmed in all sides by Aravalli hills . About 7 miles from the city is Pushkar lake created by the touch of lord Brahma. The Dargah of khawaja Moinuddin chisti is holiest shrine next to Mecca in the world. Ajmer has hot dry summer and cold bracing winter. The winter extends from November to February and summer extends from March to June followed by rainy season till mid-September. The temperature varies from 2oC in winter and 49 0C in summer. The normal annual rainfall is 527.3mm. The seasons of viral diseases are March and September . In year 2015 more than 200 cases of Dengue (breakbone fever) were registered. Dengue is mosquito born tropical disease. Virus is +ssRNA enveloped. Symptoms include fever, headache, muscle pain, skin rash. It can be life threatening dengue hemorrhagic fever resulting in bleeding, low level blood platelets and plasma leakage. In dengue shock syndrome dangerously low B.P. occurs. In the present study cases of dengue were studied in Ajmer with reference to different age groups.
Biography
Gehan Saddik Abd El Hamid El Hadidy has completed her MD from Suez Canal University, Egypt. She is presently working as a Professor of Medical Microbiology and Immunology in Faculty of Medicine, Suez Canal University. She has published around 9 papers in reputed journals.
Abstract
Polymorphonuclear leukocyte (PMN) functions have been studied extensively in hemodialysis (HD) patients; however, results are contradictory and the mechanisms that modulate phagocytosis and oxidative burst are not completely understood. Hepatitis-C virus (HCV) is a frequent complication of HD that may be associated with disturbed PMN function; however, the impact of HCV infection on neutrophil oxidative burst function in HD patients is unknown. We investigated neutrophil oxidative burst function in 24 HD patients (15 HCV-positive and 9 HCV-negative patients) before and after dialysis. HCV-RNA was detected by RT-nested PCR while, quantitative measurement of oxidative burst function was assessed by flow cytometry. Neutrophil oxidized burst function was significantly diminished in HD patients as compared to controls (P=0.001, oxidized PMN (%); P=0.02 mean fluorescence intensity, MFI) and in pre-dialysis as compared to post-dialysis samples (oxidized PMNs (%): 60.5±3.2 vs. 72.1±3.9, P=0.02); (MFI: 352±42 vs. 500±50, P=0.03). Alteration in neutrophil oxidative burst function in the pre-dialysis samples was significant in HCV-positive patients as compared to HCV-negative patients (oxidized PMNs (%): 50±2.9 vs. 63±5.1, P=0.02); (MFI: 291±31 vs. 438±64, P=0.006). Marked reduction in E. coli induced burst in pre-dialysis samples compared to post-dialysis was found in HCV-positive when compared to HCV-negative patients (oxidized PMNs (%): 50±2.9 vs. 74.8±4.7, P=0.001), (MFI: 291±31 vs. 493±63, P=0.002). In conclusion, a possible role of concomitant HCV infection in alteration of neutrophil oxidative burst function is highly suggested.
Biography
Elvana Rista is presently completing her PhD from the University of Tirana, School of Medicine. She previously graduated with a bachelor and a master degree from the School of Medicine, at the same university. Elvana is now employed as a Nephrologist with Hygea Hospital in Tirana. Throughout her career, she has published about than 10 papers with health related professional magazines and has been serving these past five years, as a member of ERA-EDTA.
Abstract
Background: Hemorrhagic Fever with Renal Syndrome (HFRS) has a high mortality and is considered a serious life-threatening condition. Early diagnosis and treatment is critical to successful management.rnCASE REPORT: Two brothers, 32 and 35 years old respectively, who worked together as shepherds, were admitted at the emergency room several days after mouse bite with the following clinical picture: The first one, had a 5-day history of flu-like symptoms i.e. high fever, headache, malaise associated with abdominal pain, vomiting, cutaneous and mucosal hemorrhage (epistaxis, hematochezia, petechiae), oliguria, and hypotension. The second one was admitted 6 days after his brother with a 3-day history of fever, headache, malaise, myalgia, arthralgia, petechiae, conjuctival and pharyngeal congestion. Both cases had no prior medical history. They lived in northeast of Albania, an endemic area for HFRS.rnSerological assay- (ELISA) detected positive IgM and IgG Anti hantavirus. Virus serotype, detected by the real time one step reverse transcriptase polymerase chain reaction (RT-PCR) was DOBRAVA on both patients. This confirmed the diagnosis of HFRS.rnManagement: The first patient was oliguric since presentation. Dialysis treatment was started on the fourth hospitalization day. He died on the seventh day (during the oliguric phase).rnThe second patient had gradual decrease of urine output. It was < 0.3 ml/kg for 24 hours on the fifth day of hospitalization. Dialysis treatment was started on the sixth-day. He received four sessions on consecutive days. He developed poliuria on the tenth day, which lasted for eight days. The patient was successfully treated.rnConclusion: Physician should be alert for the possibility of HFRS in patients with acute kidney injury, thrombocytopenia and hemorrhagic signs, notably in endemic regions. These patients should be referred to specialized centers as soon as possible for early diagnosis and treatment since delayed treatment increases mortality. Intensive monitoring, supportive care and appropriately timed dialysis for oliguria, uremia, and electrolyte disturbances are extremely important to survival.rn
Biography
Ivana has completed her PhD in Biophysics at the age of 26 years from University of South Bohemia in Czech Republic and postdoctoral studies from Vienna University in Austria as well as La Jolla Institute for Allergy and Immunology in California. She has a junior project leader position at the Biomedical Research Center at the Slovak Academy of Sciences and she is proudly using a status of Marie Curie Fellow. She has 11 publications and more than 70 citations in reputed journals.
Abstract
The majority of biological events involve the action of one macromolecule on another, thus triggering a series of recognition, signaling and modification events. The details of such macromolecular interactions are critical to our understanding of biological function and bestow greater knowledge than the three-dimensional structures of single macromolecules. Although substantial progress has been made in macromolecular docking, it still remains difficult to predict the mode of interaction between macromolecules even when the structures of the interacting partners are known. Natural killer (NK) cells express multiple activating receptors that, upon engagement, result in the rapid release of cytolytic and antiviral effectors required for host defense, notably against herpes viruses (β-herpesvirus cytomegalovirus, CMV). The host is protected from the powerful inflammatory mediators produced by NK cells through the action of inhibitory receptors. It was shown that the UL144 mimic of herpesvirus entry mediator (HVEM, TNFRSF14) from the CMV, binds exclusively to B and T lymphocyte attenuator (BTLA) but not to CD160, resulting in inhibition of IL-2-mediated activation of NK cells. HVEM and the two Ig-superfamily member receptors that bind HVEM, CD160 and BTLA, are all expressed on NK cells. Here, we report on the molecular characterization and preliminary crystallographic analysis of CD160 and HVEM and therefore CD160-HVEM complex formation. CD160 is a 27 kDa glycoprotein which was initially identified with the monoclonal antibody BY55. Its expression is tightly associated with peripheral blood NK cells and CD8 T lymphocytes with cytolytic effector activity. The cDNA sequence of CD160 predicts a cysteine-rich, glycosylphosphatidylinositol-(GPI)-anchored protein of 181 amino acids with a single Ig-like domain weakly homologous to KIR2DL4 molecule. It was found that HVEM preferentially engages CD160 trimer to costimulate activation, while a viral ortholog of HVEM specifically binds to BTLA to suppress this signaling. CD160 antigen is a protein that in humans is encoded by the CD160 gene. We have found that CD160 is expressed at the cell surface as a tightly disulfide-linked multimer. The homology model of atomic structure of CD160 antigen domain shows cysteine-rich region that was found to be responsible for CD160 tight-timer formation even under reduced conditions. The crystallization of multimeric CD160-HVEM complex was accessed by advanced macromolecular crystallization methods while non-reducing conditions. CD160 trimer forms stable complex with HVEM, while monomeric form refused to binds its cognate ligand. Taken together, regulation of CD160 bidirectional binding may represent a common mechanism of immune regulation targeted by multiple pathogens, which by extension is a potential target for therapeutic manipulation. IN is Marie Curie Fellow financed by Programme SASPRO, co-funded by European Union and the Slovak Academy of Sciences. The authors gratefully acknowledge the contribution of the Slovak Research and Development Agency under the project APVV-14-0839 and the contribution of the Scientific Grant Agency of the Slovak Republic under the grant 2/0103/15.