Time filter

Source Type

Mahin J.M.,Tehran University of Medical Sciences | Parivash D.,Infectious Disease Research Center | Madani A.H.,Infectious Disease Research Center | Madani A.H.,Hormozgan University of Medical Sciences | And 5 more authors.
American Journal of Infectious Diseases | Year: 2010

Problem statement: As number of Persons Living with HIV/AIDS (PLWAs) increases, caring for them is a new rising problem. The World Health Organization encourages caring these people at home. Patients themselves also prefer to stay at home than staying in hospital. Adequate knowledge and positive attitude are important factors in providing better care for a patient. Approach: This study was conducted to assess level of knowledge and describe attitudes existing between family members of PLWAs. A cross-sectional study was conducted on PLWAs to assess the basic level of knowledge and attitude regarding AIDS. One hundred family members of PLWAs were selected using simple random sampling. A three-part questionnaire was delivered to measure HIV/AIDS-related attitude and knowledge. Results: Mean score of participants were 10.69±2.05 of a maximum of 14 points in knowledge. Knowledge on some aspect of the disease was quite high in the study group; Mean score was 25.42±6.05 from a maximum of 40 points in attitude. Female gender, higher income and education level were associated with a greater level of knowledge. Parents in comparison with other relatives and persons older than 60 usually had lower level of knowledge. Patients with higher income or education level also had more positive attitude toward patient. Conclusion: The findings of the study suggest that the family members of patients living with AIDS have a satisfactory level of essential knowledge on HIV/AIDS. Most of them have good attitudes toward person with HIV/AIDS. However, there are some misconceptions about the routes of transmission that can be problems on the way of providing home-based care. © 2010 Science Publications.


News Article | December 6, 2016
Site: www.prweb.com

Symbios Technologies, Inc., a world-leading developer of dynamic aqueous plasma technology platforms, announced today that the company has engaged in a collaborative research partnership with Colorado State University (CSU) through a five-year Master Research and Development Agreement (MRDA) with the CSU Office of the Vice President for Research. This agreement is designed to further the commercialization of the company’s technology and the mission of CSU as a modern land-grant university. The MRDA outlines the working relationship between Symbios and CSU’s world-renowned programs in agriculture, engineering, veterinary medicine, biomedical sciences, chemistry, oncology, biology, and many other disciplines that have established CSU as an international academic and research leader. Through the MRDA, Symbios has sponsored research agreements, technology transfer, and joint intellectual property development via faculty collaborations and employment. Currently, Symbios is collaborating with CSU's Dr. Douglas Thamm, professor of Oncology and director of Clinical Research at the CSU Flint Animal Cancer Center. Dr. Thamm, a veterinary oncologist, is a consultant on Symbios' current National Institutes of Health (NIH) grant from the National Cancer Institute. In addition, Symbios engaged CSU graduate Jessica Joslin, who has a doctorate in physical chemistry, as a National Science Foundation (NSF) postdoctoral fellow. Joslin was subsequently hired as the company’s senior scientist and serves as the principal investigator on two NIH grants in collaboration with CSU. Through the partnership, Symbios has provided multiple internships to CSU engineering students; James McCall was recently hired as the company’s chemical & biological engineer. CSU also hosts Symbios as one of the companies in residence at the CSU Research Innovation Center at the Infectious Disease Research Center on the Foothills Campus, further facilitating contracts with multiple laboratories and manufacturing facilities on campus. “The Office of the Vice President for Research helps fulfill the land-grant mission of CSU by fostering and supporting the research enterprise, promoting scholarship and artistry, instilling a culture of integrity, and capitalizing on opportunities to address global challenges,” said Mark Wdowik, assistant vice president for Research & Industry Partnerships. “The collaboration with Symbios has resulted in a significant investment in CSU research. We anticipate many times that level of engagement, as well as possible licensing of CSU and jointly-developed technologies, as part of Symbios' ongoing collaborations with CSU faculty and students, centers and startup companies, and other private and public partners.” Justin Bzdek, Symbios president & CEO, said, “CSU has been an outstanding resource to help Symbios commercialize our groundbreaking plasma technology. This agreement will help facilitate further collaborative work with the CSU Flint Animal Cancer Center as well as other research faculty who can utilize our low-power, continuous flow plasma technology to develop applications to treat some of the most difficult to remediate industrial processes and wastewater and generate advanced chemotherapeutics and anti-infective products to reduce the global impact of deadly diseases.” Alan Rudolph, vice president for Research at CSU, also hailed this partnership. “Collaborative research relationships like the one with Symbios play a critical role in driving innovations from laboratories to the marketplace," he said. "As companies seek new product pipelines, more of them are turning to CSU, which is well-known for its core technical and research and development strengths, its ability to solve today’s complex problems across a broad range of industries, and its capabilities to provide independent, third-party assessments.” Symbios Technologies, Inc. is a world-leading developer of dynamic aqueous plasma technology platforms for water treatment, specialty manufacturing, and biotherapeutic applications. The company, working with its university, government, and industrial partners, is commercializing its disruptive advanced low-cost aqueous plasma oxidation technology, the Symbios Tubular Plasma Reactor™ (TPR4000™), to clean water, preserve the environment, and protect human health while improving production economics and sustainability. Symbios Technologies’ modular reactor is low in capital cost, able to replace existing energy-hungry or poor-performing advanced oxidation processes, while reducing or eliminating the use of biocides and/or chemical additives, thus improving the overall maintenance cost of water treatment systems. The TPR4000 also has the potential to generate less toxic chemotherapy drugs and safer anti-infectives to reduce the global impact of deadly diseases. For more information, go to http://www.symbiosplasma.com/. Founded in 1870 as the Colorado Agricultural College, Colorado State University is now among the nation's leading research universities. Located in Fort Collins, CSU currently enrolls more than 33,000 students, and has more than 1,800 faculty members working in eight colleges. Colorado State University is recognized as a premier research institution and routinely ranks as one of the top American universities without a medical school in research expenditures. In Fiscal Year 2016, CSU research expenditures totaled $332 million; this was the ninth consecutive year research expenditures at the university have topped $300 million. More information is available at http://www.colostate.edu. The IDRC provides a secure, state-of-the-art facility for university investigators, government scientists, and industry representatives to collaboratively research the basic biology, biochemistry, molecular biology, and epidemiology of bacteria and viruses that cause human and animal diseases. The Center provides a research environment for developing new scientific discoveries, vaccines, methods of diagnosis, and therapeutic agents for infectious agents. The CSU Research Innovation Center is a 72,000 sq. ft. research center that fosters private and public sector collaboration. The CSU Bioscience Business Incubator, located within the Research Innovation Center, is aligned with the mission of the University to provide a return on public investment in research by generating economic opportunities through new companies focused on problems or issues of public interest.


Shakeri F.,Islamic Azad University at Lahijan | Shojai A.,Islamic Azad University at Lahijan | Golalipour M.,Golestan University | Alang S.R.,Islamic Azad University at Lahijan | And 3 more authors.
International Journal of Microbiology | Year: 2010

Protein A of Staphylococcus aureus is a pathogenic factor whose encoding gene, spa, shows a variation in length in different strains. In this study the spa gene variation in S. aureus isolated from healthy carriers and patients was studied, We also compared this variation among MRSA with MSSA strains. 208 strains of Staphylococcus aureus which we were isolated from Gorgan, north of Iran were studied, 121 cases from patients and 87 cases from healthy carriers, 59 out of them were MRSA and 149 MSSA. Samples DNA were extracted and amplified by specific primer of spa gene. In 4 (3.8%) strains of them no spa gene was detected, and 10.6% had a dual band (1200 and 1400 bp). In strains with one band, the length of spa gene differed from 1150 to 1500 bp. The most prevalent length was 1350-1400 bp (37%). The frequencies of short spa bands (1150-1200 bp) in patients strains were significantly higher. In 4 (3.8%) strains of them no spa gene was detected, and 10.6% had a dual band (1200 and 1400 bp). In strains with one band, the length of spa gene differed from 1150 to 1500 bp. The most prevalent length was 1350-1400 bp (37%). The frequencies of short spa bands (1150-1200 bp) in patients strains were significantly higher. The spa gene length of 1350-1400 bp in MSSA was more than in MRSA strains (P< .05). The average length of spa in isolated strains from urinary tract infections was more than others. It is concluded that the length of spa gene depends either on resistance to Methicillin or the source of S. aureus isolation. Copyright © 2010 Fatemeh Shakeri et al.


Raymond F.,Infectious Disease Research Center | Boisvert S.,Infectious Disease Research Center | Roy G.,Infectious Disease Research Center | Ritt J.-F.,Infectious Disease Research Center | And 12 more authors.
Nucleic Acids Research | Year: 2012

The Leishmania tarentolae Parrot-TarII strain genome sequence was resolved to an average 16-fold mean coverage by next-generation DNA sequencing technologies. This is the first non-pathogenic to humans kinetoplastid protozoan genome to be described thus providing an opportunity for comparison with the completed genomes of pathogenic Leishmania species. A high synteny was observed between all sequenced Leishmania species. A limited number of chromosomal regions diverged between L. tarentolae and L. infantum, while remaining syntenic to L. major. Globally, >90 of the L. tarentolae gene content was shared with the other Leishmania species. We identified 95 predicted coding sequences unique to L. tarentolae and 250 genes that were absent from L. tarentolae. Interestingly, many of the latter genes were expressed in the intracellular amastigote stage of pathogenic species. In addition, genes coding for products involved in antioxidant defence or participating in vesicular-mediated protein transport were underrepresented in L. tarentolae. In contrast to other Leishmania genomes, two gene families were expanded in L. tarentolae, namely the zinc metallo-peptidase surface glycoprotein GP63 and the promastigote surface antigen PSA31C. Overall, L. tarentolae's gene content appears better adapted to the promastigote insect stage rather than the amastigote mammalian stage. © 2011 The Author(s).


Nam G.,Korea Institute of Science and Technology | Kim Y.S.,Infectious disease Research Center | Choi K.I.,Korea Institute of Science and Technology
Bioorganic and Medicinal Chemistry Letters | Year: 2010

A novel series of 9-O-arylpropenyloxime ketolide was synthesized and evaluated for their antibacterial activity. This series of ketolide exhibited potent activity against clinically isolated gram-positive strains including Staphylococcus pneumoniae and Straptococcus Pyogenes. © 2010.


Andreani G.,Infectious Disease Research Center
Journal of visualized experiments : JoVE | Year: 2012

Plasmodium falciparum, the causative agent of the deadliest form of malaria, and human immunodeficiency virus type-1 (HIV-1) are among the most important health problems worldwide, being responsible for a total of 4 million deaths annually. Due to their extensive overlap in developing regions, especially Sub-Saharan Africa, co-infections with malaria and HIV-1 are common, but the interplay between the two diseases is poorly understood. Epidemiological reports have suggested that malarial infection transiently enhances HIV-1 replication and increases HIV-1 viral load in co-infected individuals. Because this viremia stays high for several weeks after treatment with antimalarials, this phenomenon could have an impact on disease progression and transmission. The cellular immunological mechanisms behind these observations have been studied only scarcely. The few in vitro studies investigating the impact of malaria on HIV-1 have demonstrated that exposure to soluble malarial antigens can increase HIV-1 infection and reactivation in immune cells. However, these studies used whole cell extracts of P. falciparum schizont stage parasites and peripheral blood mononuclear cells (PBMC), making it hard to decipher which malarial component(s) was responsible for the observed effects and what the target host cells were. Recent work has demonstrated that exposure of immature monocyte-derived dendritic cells to the malarial pigment hemozoin increased their ability to transfer HIV-1 to CD4+ T cells, but that it decreased HIV-1 infection of macrophages(8). To shed light on this complex process, a systematic analysis of the interactions between the malaria parasite and HIV-1 in different relevant human primary cell populations is critically needed. Several techniques for investigating the impact of HIV-1 on the phagocytosis of micro-organisms and the effect of such pathogens on HIV-1 replication have been described. We here present a method to investigate the effects of P. falciparum-infected erythrocytes on the replication of HIV-1 in human primary monocyte-derived macrophages. The impact of parasite exposure on HIV-1 transcriptional/translational events is monitored by using single cycle pseudotyped viruses in which a luciferase reporter gene has replaced the Env gene while the effect on the quantity of virus released by the infected macrophages is determined by measuring the HIV-1 capsid protein p24 by ELISA in cell supernatants.


Andreani G.,Infectious Disease Research Center | Gagnon D.,Infectious Disease Research Center | Lodge R.,Infectious Disease Research Center | Tremblay M.J.,Infectious Disease Research Center | Richard D.,Infectious Disease Research Center
Journal of Visualized Experiments | Year: 2012

Plasmodium falciparum, the causative agent of the deadliest form of malaria, and human immunodeficiency virus type-1 (HIV-1) are among the most important health problems worldwide, being responsible for a total of 4 million deaths annually 1. Due to their extensive overlap in developing regions, especially Sub-Saharan Africa, co-infections with malaria and HIV-1 are common, but the interplay between the two diseases is poorly understood. Epidemiological reports have suggested that malarial infection transiently enhances HIV-1 replication and increases HIV-1 viral load in co-infected individuals 2,3. Because this viremia stays high for several weeks after treatment with antimalarials, this phenomenon could have an impact on disease progression and transmission. The cellular immunological mechanisms behind these observations have been studied only scarcely. The few in vitro studies investigating the impact of malaria on HIV-1 have demonstrated that exposure to soluble malarial antigens can increase HIV-1 infection and reactivation in immune cells. However, these studies used whole cell extracts of P. falciparum schizont stage parasites and peripheral blood mononuclear cells (PBMC), making it hard to decipher which malarial component(s) was responsible for the observed effects and what the target host cells were 4,5. Recent work has demonstrated that exposure of immature monocyte-derived dendritic cells to the malarial pigment hemozoin increased their ability to transfer HIV-1 to CD4+ T cells 6,7, but that it decreased HIV-1 infection of macrophages 8. To shed light on this complex process, a systematic analysis of the interactions between the malaria parasite and HIV-1 in different relevant human primary cell populations is critically needed. Several techniques for investigating the impact of HIV-1 on the phagocytosis of micro-organisms and the effect of such pathogens on HIV-1 replication have been described. We here present a method to investigate the effects of P. falciparum-infected erythrocytes on the replication of HIV-1 in human primary monocyte-derived macrophages. The impact of parasite exposure on HIV-1 transcriptional/translational events is monitored by using single cycle pseudotyped viruses in which a luciferase reporter gene has replaced the Env gene while the effect on the quantity of virus released by the infected macrophages is determined by measuring the HIV-1 capsid protein p24 by ELISA in cell supernatants. © 2012 Creative Commons Attribution-NonCommercial License.


PubMed | Infectious Disease Research Center
Type: Journal Article | Journal: Nucleic acids research | Year: 2012

The Leishmania tarentolae Parrot-TarII strain genome sequence was resolved to an average 16-fold mean coverage by next-generation DNA sequencing technologies. This is the first non-pathogenic to humans kinetoplastid protozoan genome to be described thus providing an opportunity for comparison with the completed genomes of pathogenic Leishmania species. A high synteny was observed between all sequenced Leishmania species. A limited number of chromosomal regions diverged between L. tarentolae and L. infantum, while remaining syntenic to L. major. Globally, >90% of the L. tarentolae gene content was shared with the other Leishmania species. We identified 95 predicted coding sequences unique to L. tarentolae and 250 genes that were absent from L. tarentolae. Interestingly, many of the latter genes were expressed in the intracellular amastigote stage of pathogenic species. In addition, genes coding for products involved in antioxidant defence or participating in vesicular-mediated protein transport were underrepresented in L. tarentolae. In contrast to other Leishmania genomes, two gene families were expanded in L. tarentolae, namely the zinc metallo-peptidase surface glycoprotein GP63 and the promastigote surface antigen PSA31C. Overall, L. tarentolaes gene content appears better adapted to the promastigote insect stage rather than the amastigote mammalian stage.


PubMed | Infectious Disease Research Center
Type: | Journal: Journal of visualized experiments : JoVE | Year: 2012

Plasmodium falciparum, the causative agent of the deadliest form of malaria, and human immunodeficiency virus type-1 (HIV-1) are among the most important health problems worldwide, being responsible for a total of 4 million deaths annually. Due to their extensive overlap in developing regions, especially Sub-Saharan Africa, co-infections with malaria and HIV-1 are common, but the interplay between the two diseases is poorly understood. Epidemiological reports have suggested that malarial infection transiently enhances HIV-1 replication and increases HIV-1 viral load in co-infected individuals. Because this viremia stays high for several weeks after treatment with antimalarials, this phenomenon could have an impact on disease progression and transmission. The cellular immunological mechanisms behind these observations have been studied only scarcely. The few in vitro studies investigating the impact of malaria on HIV-1 have demonstrated that exposure to soluble malarial antigens can increase HIV-1 infection and reactivation in immune cells. However, these studies used whole cell extracts of P. falciparum schizont stage parasites and peripheral blood mononuclear cells (PBMC), making it hard to decipher which malarial component(s) was responsible for the observed effects and what the target host cells were. Recent work has demonstrated that exposure of immature monocyte-derived dendritic cells to the malarial pigment hemozoin increased their ability to transfer HIV-1 to CD4+ T cells, but that it decreased HIV-1 infection of macrophages(8). To shed light on this complex process, a systematic analysis of the interactions between the malaria parasite and HIV-1 in different relevant human primary cell populations is critically needed. Several techniques for investigating the impact of HIV-1 on the phagocytosis of micro-organisms and the effect of such pathogens on HIV-1 replication have been described. We here present a method to investigate the effects of P. falciparum-infected erythrocytes on the replication of HIV-1 in human primary monocyte-derived macrophages. The impact of parasite exposure on HIV-1 transcriptional/translational events is monitored by using single cycle pseudotyped viruses in which a luciferase reporter gene has replaced the Env gene while the effect on the quantity of virus released by the infected macrophages is determined by measuring the HIV-1 capsid protein p24 by ELISA in cell supernatants.

Loading Infectious Disease Research Center collaborators
Loading Infectious Disease Research Center collaborators