London : And J. Balfour, and W. Creech, Edinburgh, 1791.

London : printed for A. Strahan and T. Cadell, London, 1794.

Edinburgh : printed for Thomas Nelson, 1820.

London : printed for A. Strahan, and T. Cadell jun. and W. Davies, (successors to Mr. Cadell,) in the Strand, 1797.

London : printed for A. Strahan, T. Cadell jun. and W. Davies, 1800.

London : And J. Balfour, and W. Creech, Edinburgh, 1805.

London : printed for A. Strahan, T. Cadell and W. Davies, 1803.

Manchester : printed by S. Russell, 1806.

London : J. Johnson, 1807.

London : F.C. and J. Rivington, 1813.

Dunbar : printed by and for G. Miller, 1817.

Newcastle : printed by K. Anderson, 1812.

London : J. & A. Churchill, 1877.

Detroit, Mich. : G.S. Davis, 1889.

London : J. & A. Churchill, 1887.

London : Philadelphia, 1889.

London : Taylor and Walton, 1841.

Bath : And sold by Underwood, London, 1825.

London : printed for J. Dodsley, 1782.

London : J. & A. Churchill, 1873.

London : J. Churchill, 1861.

Edinburgh : Young J. Pentland, 1901.

London : H. Renshaw, 1849.

The extent to which young adults' laboratory-confirmed sexually transmitted disease results and self-reported sexual behaviors are consistent has not been assessed in a nationally representative sample.

The primary purpose of this study was to determine whether young adults' reports of recent sexual behavior (presence of penile/vaginal sex in the previous 12 months) correspond with the presence of laboratory-confirmed nonviral STDs assessed by nucleic acid amplification testing. (Read the full article)

Rare diseases in childhood can be debilitating and require lifelong care. Since 1983, the Orphan Drug Act incentives have stimulated the development and significantly improved the availability of treatment products for patients with rare diseases.

We report an increasing pediatric orphan product designations and approvals from 2000 to 2009. The trend indicates that the Orphan Drug Act has continued to address this important unmet need. (Read the full article)

Childhood interstitial lung diseases occur in a variety of clinical contexts and are associated with high morbidity and mortality. Advances in the understanding of disease pathogenesis and use of standardized terminology have facilitated increased case ascertainment.

This study demonstrates that cases of newly described forms of childhood interstitial lung diseases likely occur at all children’s hospitals. With advances in genetic testing and recognition of imaging patterns, a significant portion of cases are identifiable with noninvasive evaluations. (Read the full article)

The Nigerian Civil Society Organisations have recommended modalities that would ensure citizens’ participation in the conduct of the proposed virtual public hearing on the controversial Infectious Diseases Bill.

The group said that public scrutiny of the bill can only be achieved through a broad-based engagements of stakeholders. 

In a statement jointly signed by 69 civil organisations on Thursday in Abuja, the groups stated that any legislative process that does not guarantee active and free participation of the people would fail and not be accepted.  

The statement noted that the proposed public hearing, which would be held via video conferencing be scheduled to hold between two to three days and representatives of organizations be allowed to make presentation for five-10 minutes.

The rights group also asked the lawmakers to provide information on the committee responsible for the coordination of the hearing.

According to the statement, "The committee responsible for organising these activities should conduct citizen outreach and share this information widely with the public through diverse media platforms. 

"This is critical to ensure broad awareness and participation and enhance legislative transparency" 

They said the virtual public hearing on the bill must be comprehensive, and conform with the dictates of the constitution. 

(MENAFN - EIN Presswire) Coronavirus - Africa: Commemorating Smallpox Eradication � a legacy of hope, for COVID-19 and other�diseases [To enable links... ......

(MENAFN - African Press Organization) [To enable links in your articles, contact MENAFN Click here ] [To enable links in your articles, contact MEN... ......

Download logo On 8 May 1980, the 33rd World Health Assembly officially declared: ‘The world and all its peoples have won freedom from smallpox.’ The declaration marked the end of a disease that had plagued humanity for at least 3 000 years, killing 300 million people in the 20th century alone. It was ended, thanks to a 10-year global effort, spearheaded by the World Health Organization, that involved thousands of health workers around the world to administer half a billion vaccinations to stamp out smallpox. The US$ 300m price-tag to eradicate smallpox saves the world well over US$ 1 billion every year since 1980. Speaking at a virtual event hosted at WHO-HQ, involving key...

More than 250,000 people have died in this pandemic, but untold indirect losses lie ahead as other health services risk being neglected.

[WHO] Geneva -On 8 May 1980, the 33rd World Health Assembly officially declared: 'The world and all its peoples have won freedom from smallpox.'

Ocean Outbreak unveils the little-known diseases wreaking havoc in the seas and the book does a first-rate job of inspiring readers at the same time

The remains of three slaves found in Mexico contain the earliest signs of the hepatitis B virus and yaws bacteria in the Americas, suggesting transatlantic slavery introduced these diseases

Lipid rafts are highly ordered regions of the plasma membrane that are enriched in cholesterol and sphingolipids and play important roles in many cells. In hematopoietic stem and progenitor cells (HSPCs), lipid rafts house receptors critical for normal hematopoiesis. Lipid rafts also can bind and sequester kinases that induce negative feedback pathways to limit proliferative cytokine receptor cycling back to the cell membrane. Modulation of lipid rafts occurs through an array of mechanisms, with optimal cholesterol efflux one of the major regulators. As such, cholesterol homeostasis also regulates hematopoiesis. Increased lipid raft content, which occurs in response to changes in cholesterol efflux in the membrane, can result in prolonged receptor occupancy in the cell membrane and enhanced signaling. In addition, certain diseases, like diabetes, may contribute to lipid raft formation and affect cholesterol retention in rafts. In this review, we explore the role of lipid raft-related mechanisms in hematopoiesis and CVD (specifically, atherosclerosis) and discuss how defective cholesterol efflux pathways in HSPCs contribute to expansion of lipid rafts, thereby promoting myelopoiesis and thrombopoiesis. We also discuss the utility of cholesterol acceptors in contributing to lipid raft regulation and disruption, and highlight the potential to manipulate these pathways for therapeutic gain in CVD as well as other disorders with aberrant hematopoiesis.

Lipid rafts are small, dynamic membrane areas characterized by the clustering of selected membrane lipids as the result of the spontaneous separation of glycolipids, sphingolipids, and cholesterol in a liquid-ordered phase. The exact dynamics underlying phase separation of membrane lipids in the complex biological membranes are still not fully understood. Nevertheless, alterations in the membrane lipid composition affect the lateral organization of molecules belonging to lipid rafts. Neural lipid rafts are found in brain cells, including neurons, astrocytes, and microglia, and are characterized by a high enrichment of specific lipids depending on the cell type. These lipid rafts seem to organize and determine the function of multiprotein complexes involved in several aspects of signal transduction, thus regulating the homeostasis of the brain. The progressive decline of brain performance along with physiological aging is at least in part associated with alterations in the composition and structure of neural lipid rafts. In addition, neurodegenerative conditions, such as lysosomal storage disorders, multiple sclerosis, and Parkinson’s, Huntington’s, and Alzheimer’s diseases, are frequently characterized by dysregulated lipid metabolism, which in turn affects the structure of lipid rafts. Several events underlying the pathogenesis of these diseases appear to depend on the altered composition of lipid rafts. Thus, the structure and function of lipid rafts play a central role in the pathogenesis of many common neurodegenerative diseases.

ABSTRACT

Coinfections shape immunity and influence the development of inflammatory diseases, resulting in detrimental or beneficial outcome. Coinfections with concurrent Plasmodium species can alter malaria clinical evolution, and malaria infection itself can modulate autoimmune reactions. Yet, the underlying mechanisms remain ill defined. Here, we demonstrate that the protective effects of some rodent malaria strains on T cell-mediated inflammatory pathologies are due to an RNA virus cohosted in malaria-parasitized blood. We show that live and extracts of blood parasitized by Plasmodium berghei K173 or Plasmodium yoelii 17X YM, protect against P. berghei ANKA-induced experimental cerebral malaria (ECM) and myelin oligodendrocyte glycoprotein (MOG)/complete Freund’s adjuvant (CFA)-induced experimental autoimmune encephalomyelitis (EAE), and that protection is associated with a strong type I interferon (IFN-I) signature. We detected the presence of the RNA virus lactate dehydrogenase-elevating virus (LDV) in the protective Plasmodium stabilates and we established that LDV infection alone was necessary and sufficient to recapitulate the protective effects on ECM and EAE. In ECM, protection resulted from an IFN-I-mediated reduction in the abundance of splenic conventional dendritic cell and impairment of their ability to produce interleukin (IL)-12p70, leading to a decrease in pathogenic CD4⁺ Th1 responses. In EAE, LDV infection induced IFN-I-mediated abrogation of IL-23, thereby preventing the differentiation of granulocyte-macrophage colony-stimulating factor (GM-CSF)-producing encephalitogenic CD4⁺ T cells. Our work identifies a virus cohosted in several Plasmodium stabilates across the community and deciphers its major consequences on the host immune system. More generally, our data emphasize the importance of considering contemporaneous infections for the understanding of malaria-associated and autoimmune diseases.

IMPORTANCE Any infection modifies the host immune status, potentially ameliorating or aggravating the pathophysiology of a simultaneous inflammatory condition. In the course of investigating how malaria infection modulates the severity of contemporaneous inflammatory diseases, we identified a nonpathogenic mouse virus in stabilates of two widely used rodent parasite lines: Plasmodium berghei K173 and Plasmodium yoelii 17X YM. We established that the protective effects of these Plasmodium lines on cerebral malaria and multiple sclerosis are exclusively due to this virus. The virus induces a massive type I interferon (IFN-I) response and causes quantitative and qualitative defects in the ability of dendritic cells to promote pathogenic T cell responses. Beyond revealing a possible confounding factor in rodent malaria models, our work uncovers some bases by which a seemingly innocuous viral (co)infection profoundly changes the immunopathophysiology of inflammatory diseases.

The number of onsite clinical microbiology laboratories in hospitals is decreasing, likely related to the business model for laboratory consolidation and labor shortages, and this impacts a variety of clinical practices, including that of banking isolates for clinical or epidemiologic purposes. To determine the impact of these trends, infectious disease (ID) physicians were surveyed regarding their perceptions of offsite services. Clinical microbiology practices for retention of clinical isolates for future use were also determined. Surveys were sent to members of the Infectious Diseases Society of America’s (IDSA) Emerging Infections Network (EIN). The EIN is a sentinel network of ID physicians who care for adult and/or pediatric patients in North America and who are members of IDSA. The response rate was 763 (45%) of 1,680 potential respondents. Five hundred forty (81%) respondents reported interacting with the clinical microbiology laboratory. Eighty-six percent of respondents thought an onsite laboratory very important for timely diagnostic reporting and ongoing communication with the clinical microbiologist. Thirty-five percent practiced in institutions where the core microbiology laboratory has been moved offsite, and an additional 7% (n = 38) reported that movement of core laboratory functions offsite was being considered. The respondents reported that only 24% of laboratories banked all isolates, with the majority saving isolates for less than 30 days. Based on these results, the trend toward centralized core laboratories negatively impacts the practice of ID physicians, potentially delays effective implementation of prompt and targeted care for patients with serious infections, and similarly adversely impacts infection control epidemiologic investigations.

Technologies allowing genetic sequencing of the human microbiome are opening new realms to discovery. The host microbiota substantially impacts immune responses both in immune-mediated inflammatory diseases (IMIDs) and in tumors affecting tissues beyond skin and mucosae. However, a mechanistic link between host microbiota and cancer or IMIDs has not been well established. Here, we propose T helper 17 (T_H17) lymphocytes as the connecting factor between host microbiota and rheumatoid or psoriatic arthritides, multiple sclerosis, breast or ovarian cancer, and multiple myeloma. We theorize that similar mechanisms favor the expansion of gut-borne T_H17 cells and their deployment at the site of inflammation in extraborder IMIDs and tumors, where T_H17 cells are driving forces. Thus, from a pathogenic standpoint, tumors may share mechanistic routes with IMIDs. A review of similarities and divergences in microbiota-T_H17 cell interactions in IMIDs and cancer sheds light on previously ignored pathways in either one of the two groups of pathologies and identifies novel therapeutic avenues.

OBJECTIVE

There is a controversy over the association between obesity and end-stage renal disease (ESRD) in people with or without type 2 diabetes; therefore, we examined the effect of BMI on the risk of ESRD according to glycemic status in the Korean population.