7 research outputs found
Staphylococcal Cassette Chromosome mec and Panton-Valentine Leukocidin Characterization of Methicillin-Resistant Staphylococcus Aureus Clones
Staphylococcal cassette chromosome mec (SCCmec) types and Panton-Valentine leukocidin (PVL) gene carriage were compared among suspected community-associated methicillin-resistant Staphylococcus aureus MRSA (CA-MRSA) and health care-associated MRSA (HA-MRSA) isolates. CA-MRSA isolates carried the SCCmec type IV complex, and most were PVL positive. The HA-MRSA isolates carried the SCCmec type II complex and did not harbor the PVL genes
Comparison of DNA Pyrosequencing with Alternative Methods for Identification of Mycobacteriaâ–¿
Identification of mycobacterial clinical isolates by pyrosequencing within the hypervariable A region of the 16S rRNA gene was compared to other identification methods. For >90% of isolates, these identifications correlated to the level of complex or species. For identification of many mycobacteria, pyrosequencing offers an inexpensive alternative to traditional sequencing
Staphylococcal Cassette Chromosome mec and Panton-Valentine Leukocidin Characterization of Methicillin-Resistant Staphylococcus aureus Clones
Staphylococcal cassette chromosome mec (SCCmec) types and Panton-Valentine leukocidin (PVL) gene carriage were compared among suspected community-associated methicillin-resistant Staphylococcus aureus MRSA (CA-MRSA) and health care-associated MRSA (HA-MRSA) isolates. CA-MRSA isolates carried the SCCmec type IV complex, and most were PVL positive. The HA-MRSA isolates carried the SCCmec type II complex and did not harbor the PVL genes
Identification of Transcription Start Sites and Preferential Expression of Select CB2 Transcripts in Mouse and Human B Lymphocytes
Familial hypercholesterolaemia: a global call to arms
Familial Hypercholesterolaemia (FH) is the commonest autosomal
co-dominantly inherited condition affecting man. It is caused
by mutation in one of three genes, encoding the low-density lipoprotein
(LDL) receptor, or the gene for apolipoprotein B (which is
the major protein component of the LDL particle), or in the gene
coding for PCSK9 (which is involved in the degradation of the LDLreceptor
during its cellular recycling). These mutations result in
impaired LDL metabolism, leading to life-long elevations in LDLcholesterol
(LDL-C) and development of premature atherosclerotic
cardiovascular disease (ASCVD) [1e3]. If left untreated, the
relative risk of premature coronary artery disease is significantly
higher in heterozygous patients than unaffected individuals, with
most untreated homozygotes developing ASCVD before the age of
20 and generally not surviving past 30 years [2e5]. Although early
detection and treatment with statins and other LDL-C lowering
therapies can improve survival, FH remains widely underdiagnosed
and undertreated, thereby representing a major global public
health challenge
Overview of the current status of familial hypercholesterolaemia care in over 60 countries - The EAS Familial Hypercholesterolaemia Studies Collaboration (FHSC)
Background and aims: Management of familial hypercholesterolaemia (FH) may vary across different settings due to factors related to population characteristics, practice, resources and/or policies. We conducted a survey among the worldwide network of EAS FHSC Lead Investigators to provide an overview of FH status in different countries. Methods: Lead Investigators from countries formally involved in the EAS FHSC by mid-May 2018 were invited to provide a brief report on FH status in their countries, including available information, programmes, initiatives, and management. Results: 63 countries provided reports. Data on FH prevalence are lacking in most countries. Where available, data tend to align with recent estimates, suggesting a higher frequency than that traditionally considered. Low rates of FH detection are reported across all regions. National registries and education programmes to improve FH awareness/knowledge are a recognised priority, but funding is often lacking. In most countries, diagnosis primarily relies on the Dutch Lipid Clinics Network criteria. Although available in many countries, genetic testing is not widely implemented (frequent cost issues). There are only a few national official government programmes for FH. Under-treatment is an issue. FH therapy is not universally reimbursed. PCSK9-inhibitors are available in 3c2/3 countries. Lipoprotein-apheresis is offered in 3c60% countries, although access is limited. Conclusions: FH is a recognised public health concern. Management varies widely across countries, with overall suboptimal identification and under-treatment. Efforts and initiatives to improve FH knowledge and management are underway, including development of national registries, but support, particularly from health authorities, and better funding are greatly needed