Burning mouth syndrome: pathogenic and therapeutic

Summary Burning mouth syndrome (BMS) is a chronic pain condition characterized by pain, burning sensations and dryness within an oral mucosa, without any clinical changes of the latter. It occurs approximately seven times more frequently in women, mostly in perimenopausal age. The psychiatric aspect of BMS is significant: the most frequent co-morbidities are depression and anxiety disorders, and a number of psychotropic drugs play an essential role in its treatment. In the present review, the most important pathogenic and treatment concepts of BMS have been discussed. The BMS may be similar to neuropathic pain and has some related pathogenic elements with fibromyalgia and the restless leg syndrome. In primary BMS, the features of presynaptic dysfunction of dopaminergic neurons and deficiency of endogenous dopamine levels have been demonstrated. Other neurotransmitters such as serotonin, noradrenaline, histamine as well as hormonal and inflammatory factors may also play a role in the pathogenesis of BMS. In the pharmacological treatment of BMS a variety of drugs have been used including benzodiazepines, anticonvulsants, antidepressants and atypical antipsychotic drugs. In the final part of the paper, the possibility of using atypical antipsychotic drug, olanzapine, in the treatment of BMS has been discussed. In the context of the recent studies on this topic, a case of female patient with the BMS lasting more than ten years has been mentioned, in whom the treatment with olanzapine brought about a rapid and significant reduction of symptoms. The probable mechanism of the therapeutic effect of olanzapine in BMS can include its effect on dopaminergic receptors and probably also on histaminergic, noradrenergic and serotonergic ones. Key words: burning mouth syndrome, dopaminergic system, olanzapine Burning mouth syndrome (BMS) is a chronic pain syndrome which affects oral mucous membrane. It is characterized by burning sensations, pain, pinching or numbness within oral mucosa, accompanied by dryness, paresthesia, dysgeusia or hypersensitivity to some food

Two years after pandemic influenza A/2009/H1N1: What have we learned?

The world had been anticipating another influenza pandemic since the last one in 1968. The pandemic influenza A H1N1 2009 virus (A/2009/H1N1) finally arrived, causing the first pandemic influenza of the new millennium, which has affected over 214 countries and caused over 18,449 deaths. Because of the persistent threat from the A/H5N1 virus since 1997 and the outbreak of the severe acute respiratory syndrome (SARS) coronavirus in 2003, medical and scientific communities have been more prepared in mindset and infrastructure. This preparedness has allowed for rapid and effective research on the epidemiological, clinical, pathological, immunological, virological, and other basic scientific aspects of the disease, with impacts on its control. A PubMed search using the keywords "pandemic influenza virus H1N1 2009" yielded over 2,500 publications, which markedly exceeded the number published on previous pandemics. Only representative works with relevance to clinical microbiology and infectious diseases are reviewed in this article. A significant increase in the understanding of this virus and the disease within such a short amount of time has allowed for the timely development of diagnostic tests, treatments, and preventive measures. These findings could prove useful for future randomized controlled clinical trials and the epidemiological control of future pandemics. © 2012, American Society for Microbiology. All Rights Reserved.link_to_subscribed_fulltex

Multiple independent variants at the TERT locus are associated with telomere length and risks of breast and ovarian cancer

<p>TERT-locus SNPs and leukocyte telomere measures are reportedly associated with risks of multiple cancers. Using the Illumina custom genotyping array iCOG, we analyzed similar to 480 SNPs at the TERT locus in breast (n = 103,991), ovarian (n = 39,774) and BRCA1 mutation carrier (n = 11,705) cancer cases and controls. Leukocyte telomere measurements were also available for 53,724 participants. Most associations cluster into three independent peaks. The minor allele at the peak 1 SNP rs2736108 associates with longer telomeres (P = 5.8 x 10(-7)), lower risks for estrogen receptor (ER)-negative (P = 1.0 x 10(-8)) and BRCA1 mutation carrier (P = 1.1 x 10(-5)) breast cancers and altered promoter assay signal. The minor allele at the peak 2 SNP rs7705526 associates with longer telomeres (P = 2.3 x 10(-14)), higher risk of low-malignant-potential ovarian cancer (P = 1.3 x 10(-15)) and greater promoter activity. The minor alleles at the peak 3 SNPs rs10069690 and rs2242652 increase ER-negative (P = 1.2 x 10(-12)) and BRCA1 mutation carrier (P = 1.6 x 10-14) breast and invasive ovarian (P = 1.3 x 10(-11)) cancer risks but not via altered telomere length. The cancer risk alleles of rs2242652 and rs10069690, respectively, increase silencing and generate a truncated TERT splice variant.</p>

Guidelines for the use and interpretation of assays for monitoring autophagy (4th edition)

In 2008, we published the first set of guidelines for standardizing research in autophagy. Since then, this topic has received increasing attention, and many scientists have entered the field. Our knowledge base and relevant new technologies have also been expanding. Thus, it is important to formulate on a regular basis updated guidelines for monitoring autophagy in different organisms. Despite numerous reviews, there continues to be confusion regarding acceptable methods to evaluate autophagy, especially in multicellular eukaryotes. Here, we present a set of guidelines for investigators to select and interpret methods to examine autophagy and related processes, and for reviewers to provide realistic and reasonable critiques of reports that are focused on these processes. These guidelines are not meant to be a dogmatic set of rules, because the appropriateness of any assay largely depends on the question being asked and the system being used. Moreover, no individual assay is perfect for every situation, calling for the use of multiple techniques to properly monitor autophagy in each experimental setting. Finally, several core components of the autophagy machinery have been implicated in distinct autophagic processes (canonical and noncanonical autophagy), implying that genetic approaches to block autophagy should rely on targeting two or more autophagy-related genes that ideally participate in distinct steps of the pathway. Along similar lines, because multiple proteins involved in autophagy also regulate other cellular pathways including apoptosis, not all of them can be used as a specific marker for bona fide autophagic responses. Here, we critically discuss current methods of assessing autophagy and the information they can, or cannot, provide. Our ultimate goal is to encourage intellectual and technical innovation in the field