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The continuous flow of new research articles on MDR-TB diagnosis, treatment, prevention and rehabilitation requires frequent update of existing guidelines. This review is aimed at providing clinicians and public health staff with an updated and easy-to-consult document arising from consensus of Global Tuberculosis Network (GTN) experts.The core published documents and guidelines have been reviewed, including the recently published MDR-TB WHO rapid advice and ATS/CDC/ERS/IDSA guidelines.After a rapid review of epidemiology and risk factors, the clinical priorities on MDR-TB diagnosis (including whole genome sequencing and drug-susceptibility testing interpretations) and treatment (treatment design and management, TB in children) are discussed. Furthermore, the review comprehensively describes the latest information on contact tracing and LTBI management in MDR-TB contacts, while providing guidance on post-treatment functional evaluation and rehabilitation of TB sequelae, infection control and other public health priorities. Keywords: MDR-TB, XDR-TB, Diagnosis, Treatment, Prevention, Rehabilitation of sequelae

BackgroundThe achievement of recovery is related to the notion of developing personal potential and restoring a legitimate social role, even against the backdrop of mental illness limitations. It is still difficult to fully understand this highly subjective and dynamic process. Therefore, in order to test the recovery process, specific tools, still only marginally used in our country, are needed.AimsThe Italian Study on Recovery is the first study aimed at confirming the validity of the Italian version of the Recovery Assessment Scale (RAS), an instrument developed with the goal of detecting recovery among patients.MethodThis multicentric research involved several Mental Health Services from various parts of Italy. The first phase of the study consisted in the administration of the Italian translation of RAS, previously used in a pilot study conducted in 2009. RAS was administered to 219 patients diagnosed with psychosis, whose mental disorder lasted for at least 5 years.ResultsFindings supported the good psychometric properties of the Italian version of RAS, demonstrating its capability of identifying patients matching the “in recovery” operational criteria.ConclusionsIn consideration of the results highlighting the good psychometric properties of RAS, the present study may contribute to the diffusion of instruments to be included in Mental Health Service planning in the Italian context, in order to start a recovery-oriented transformation.

Long noncoding RNAs (lncRNAs) play major roles in regulating gene expression in mammals, but are poorly understood in ischemic stroke. Using a mouse model of transient focal ischemia, we applied RNA-seq to evaluate for the first time the unbiased, genome-wide expression of lncRNAs as a function of reperfusion time in the cerebral cortex. Focal ischemia was induced in adult male C57BL/6 mice followed by reperfusion for 6, 12 or 24h. Total RNA from ipsilateral cortices was used for Illumina sequencing and reads were mapped to the mouse reference genome (GRCm38). Annotated and novel transcript isoforms were identified and differential expression between the groups was estimated. We observed that the baseline expression of lncRNAs in the healthy cortex was low, but many were highly altered after stroke. Very few of these altered lncRNAs were previously annotated. A total of 259 lncRNA isoforms at 6h, 378 isoforms at 12h, and 217 isoforms at 24h of reperfusion were differentially expressed versus sham controls. Of these, 213, 322 and 171 isoforms at 6, 12 and 24h of reperfusion, respectively, were novel lncRNAs. Reperfusion time-point-specific analyses revealed that the lncRNAs reached peak expression levels at 6h of reperfusion. Positional analysis of ischemia-responsive lncRNAs with respect to ischemia-responsive protein-coding genes identified potential gene-regulatory relationships. Overall, this work shows that transient focal ischemia induces widespread changes in the expression of lncRNAs in the mouse cortex with distinct reperfusion time-point-dependent expression characteristics that may underlie progression of the ischemic pathophysiology. The detection of hundreds of novel ischemia-responsive lncRNAs marks the discovery of new disease-related genomic regions in the adult cortex and may help identify novel opportunities for therapeutic targeting.

Tuberculosis (TB) remains one of the leading causes of morbidity and mortality worldwide and pulmonary TB (PTB) is the main variant responsible for fueling transmission of the infection. Effective treatment of drug-susceptible (DS) TB is crucial to avoid the emergence of Mycobacterium tuberculosis-resistant strains. In this narrative review, through a fictional suggestive case of DS PTB, we guide the reader in a step-by-step commentary to provide an updated review of current evidence in the management of TB, from diagnosis to post-treatment follow-up. World Health Organization and Centre for Diseases Control (CDC) guidelines for TB, as well as the updated literature, were used to support this manuscript. [ABSTRACT FROM AUTHOR]

Purpose Transient global ischemia arising in human due to cardiac arrest causes selective, delayed neuronal death in hippocampal CA1 and cognitive impairment. Growth arrest and DNA-damage-inducible protein 45 beta (Gadd45b) is a wellknown molecule in both DNA damage-related pathogenesis and therapies. Emerging evidence suggests that Gadd45b is an anti-apoptotic factor in nonneuronal cells and is an intrinsic neuroprotective molecule in neurons. However, the mechanism of Gadd45b pathway is not fully examined in neurodegeneration associated with global ischemia. Methods Rats were subjected to transient global ischemia by the 4-vessel occlusion or sham operation. The animals were sacrificed at 24 hours, 48 hours, and 7 days after ischemia. The hippocampal CA1 was microdissected and processed to examine mRNA and protein level. To assess neuronal death, tissue sections were cut and processed for Fluoro-Jade and Nissl staining. Results Here we show that ischemic insults increase abundance of Gadd45b and brain-derived neurotrophic factor, a known target of Gadd45 mediated demethylation, in selectively-vulnerable hippocampal CA1 neurons. We further show that knockdown of Gadd45b increases abundance of a pro-apoptotic Bcl-2 family member Bax while decreasing the antiapoptotic protein Bcl-2, which together promote neuronal death. Conclusions These findings document a protective role of Gadd45b against neuronal insults associated with global ischemia and identify Gadd45b as a potential therapeutic target for the amelioration of hippocampal neurodegeneration.