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Integrative Single-Cell Transcriptomic Evaluation associated with Man Fetal Thymocyte Development.
Brain tumors are hard to treat with the currently available therapy. The major obstacle in the treatment of brain tumors is the lack of therapeutic strategies capable to penetrate the blood-brain barrier (BBB). The BBB is an endothelial interface that separates the brain from the circulatory blood system and prevents the exposure of the central nervous system (CNS) to circulating toxins and potentially harmful compounds. Unfortunately, the BBB prevents also the penetration of therapeutic compounds into the brain. We present here a drug-delivery liposomal carrier, conjugated to a peptide inserted in the liposomal membrane, which is putatively recognized by BBB transporters. The peptide is a short sequence of 5 amino acids (RERMS) present in the amyloid precursor protein (APP). This APP-targeted liposomal system was designed specifically for transporting compounds with anti-cancer activity via the BBB into the brain in an effective manner. This drug-delivery liposomal carrier loaded with the anti-cancer compounds temozolomide (TMZ), curcumin, and doxorubicin crossed the BBB in an in vitro model as well as in vivo (mice model). In the in vitro model, the targeted liposomes crossed the BBB model fourfold higher than the non-targeted liposomes. Labeled targeted liposomes penetrated the brain in vivo 35% more than non-targeted liposomes. Treatment of mice that underwent intracranial injection of human U87 glioblastoma, with the targeted liposomes loaded with the three tested anti-cancer agents, delayed the tumor growth and prolonged the mice survival in a range of 45% -70%. It appears that the targeted liposomal drug-delivery system enables better therapeutic efficacy in a SCID mouse model of glioblastoma compared to the corresponding non-targeted liposomes and the free compounds.In this document, we outline the challenges faced by patients and clinicians in heart failure, specifically centered around the needed coordination of care among the various subspecialties within cardiovascular medicine. We call for a more organized and collaborative effort among clinicians in primary care, general cardiology, electrophysiology, interventional cardiology, cardiothoracic surgery, cardiac imaging, and heart failure-all caring for mutual patients. Care is contextualized within the framework of two phases a cardiomyopathy phase and an advanced heart failure phase, each of which lends to different considerations in therapy. Ultimately multidisciplinary coordinated care within cardiovascular medicine may lead to greater patient and clinician satisfaction as well as improved outcomes, but this remains to be investigated.Ghrelin, a small peptide hormone (28 aa), secreted mainly by X/A-like cells of gastric mucosa, is also locally produced in cardiomyocytes. Being an orexigenic factor (appetite stimulant), it promotes release of growth hormone (GH) and exerts diverse physiological functions, viz. regulation of energy balance, glucose, and/or fat metabolism for body weight maintenance. Interestingly, administration of exogenous ghrelin significantly improves cardiac functions in CVD patients as well as experimental animal models of heart failure. Ghrelin ameliorates pathophysiological condition of the heart in myocardial infarction, cardiac hypertrophy, fibrosis, cachexia, and ischemia reperfusion injury. This peptide also exerts significant impact at the level of vasculature leading to lowering high blood pressure and reversal of endothelial dysfunction and atherosclerosis. However, the molecular mechanism of actions elucidating the healing effects of ghrelin on the cardiovascular system is still a matter of conjecture. Some experimental data indicate its beneficial effects via complex cellular cross talks between autonomic nervous system and cardiovascular cells, some other suggest more direct receptor-mediated molecular actions via autophagy or ionotropic regulation and interfering with apoptotic and inflammatory pathways of cardiomyocytes and vascular endothelial cells. Here, in this review, we summarise available recent data to encourage more research to find the missing links of unknown ghrelin receptor-mediated pathways as we see ghrelin as a future novel therapy in cardiovascular protection.Sarcoidosis is a systemic granulomatous disease with a high prevalence of cardiac involvement in autopsic studies. Cardiac sarcoidosis is associated with increased cardiovascular morbidity and mortality. Endomyocardial biopsy is a specific technique, but unfortunately not sensitive enough. Non-invasive cardiac imaging has an important role in the evaluation of patients with suspected or confirmed cardiac sarcoidosis. Echocardiography remains the first choice imaging technique because of its availability and low cost. However, this method could not provide tissue characterization or evaluation of disease activity level. 18F-fluorodeoxyglucose (FDG) positron emission tomography (PET) has essential role in diagnosis and monitoring of patients with suspected or confirmed cardiac sarcoidosis. Tanespimycin in vitro Nevertheless, more recently it has been shown that cardiac magnetic resonance (CMR) might provide useful information about cardiac sarcoidosis. Hybrid imaging approach that includes PET-CMR and PET-CT is particularly interesting for diagnosis, assessment of activity and follow-up in these patients. Diagnostic algorithm in sarcoidosis patients should include clinical data, hybrid imaging and biopsy. Use of different CMR sequences such as cine imaging, late gadolinium enhancement, T1 and T2 mapping, as well as strain imaging, may significantly contribute to diagnosis and monitoring of patients with cardiac sarcoidosis. However, validation of these techniques and particularly T1 and T2 mapping in sarcoidosis patients in large studies is necessary. This review aimed to summarize current knowledge about clinical usefulness of CMR in patients with cardiac sarcoidosis.Growth differentiation factor 11 (GDF11 or bone morphogenetic protein 11, BMP11) belongs to the transforming growth factor-β superfamily and is closely related to other family member-myostatin (also known as GDF8). GDF11 was firstly identified in 2004 due to its ability to rejuvenate the function of multiple organs in old mice. However, in the past few years, the heralded rejuvenating effects of GDF11 have been seriously questioned by many studies that do not support the idea that restoring levels of GDF11 in aging improves overall organ structure and function. Moreover, with increasing controversies, several other studies described the involvement of GDF11 in fibrotic processes in various organ setups. This review paper focuses on the GDF11 and its pro- or anti-fibrotic actions in major organs and tissues, with the goal to summarize our knowledge on its emerging role in regulating the progression of fibrosis in different pathological conditions, and to guide upcoming research efforts.
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