Hydatid disease is still endemic in several regions worldwide and is caused in most cases by the larval form of two species of the tapeworm Echinococcus: E. granulosus and E. multilocularis. Bone involvement is rare (0.2-4%), affecting the spine in almost half of the cases. The disease is usually silent until a complication (e.g. paraplegia or pathologic fracture) occurs. Many cases are diagnosed intraoperatively. Pre-operative diagnosis is based on radiological findings and serological assays, which lack high sensitivity and specificity. A high index of suspicion is necessary for the diagnosis, especially in patients that live in or travel to sheep-raising areas where hydatid disease is endemic. The treatment of choice is surgical, following the principles of a locally malignant lesion. Chemotherapy (albendazole alone or in combination with praziquantel) is used as an adjuvant treatment or when surgery is not possible. The prognosis is often poor, especially in the spine: most patients do not recover neurologically, the mortality and complication rate is high and many cases recur, as it is often impossible to radically excise the pathologic tissue.

Background: KIT is a transmembrane tyrosine kinase receptor, expressed in high amounts in various normal cells. In addition, c-kit mutation or activation is a major pathogenetic event in certain tumours (such as gastrointestinal stromal tumours). There are only limited data in the literature on the expression of KIT in normal and neoplastic renal tissues. Aims: To investigate KIT expression in normal and neoplastic renal tissues. Methods: KIT expression was evaluated by means of immunohistochemistry in paraffin wax embedded sections from 67 tissue samples. Results: Eight of eight fetal kidneys, and 10 of 10 normal adult kidneys revealed cytoplasmic staining of renal tubules. The three cases of renal dysplasia studied expressed KIT in their normal and aberrant tubules. Two of 13 conventional renal cell carcinomas (RCCs), two of seven papillary type RCCs, four of seven chromophobe type RCCs, none of six nephroblastomas, seven of seven oncocytomas, two of two mesoblastic nephromas, and two of four angiomyolipomas were positive. Conclusion: KIT is expressed in normal fetal and adult renal tubules, and in a subset of renal tumours. The expression of KIT in these renal tumours may prove to have diagnostic relevance and/or therapeutic implications.

Following a myocardial infarction (MI), the immune system helps to repair ischaemic damage and restore tissue integrity, but excessive inflammation has been implicated in adverse cardiac remodelling and development towards heart failure (HF). Pre-clinical studies suggest that timely resolution of inflammation may help prevent HF development and progression. Therapeutic attempts to prevent excessive post-MI inflammation in patients have included pharmacological interventions ranging from broad immunosuppression to immunomodulatory approaches targeting specific cell types or factors with the aim to maintain beneficial aspects of the early post-MI immune response. These include the blockade of early initiators of inflammation including reactive oxygen species and complement, inhibition of mast cell degranulation and leucocyte infiltration, blockade of inflammatory cytokines, and inhibition of adaptive B and T-lymphocytes. Herein, we provide a systematic review on post-MI immunomodulation trials and a meta-analysis of studies targeting the inflammatory cytokine Interleukin-1. Despite an enormous effort into a significant number of clinical trials on a variety of targets, a striking heterogeneity in study population, timing and type of treatment, and highly variable endpoints limits the possibility for meaningful meta-analyses. To conclude, we highlight critical considerations for future studies including (i) the therapeutic window of opportunity, (ii) immunological effects of routine post-MI medication, (iii) stratification of the highly diverse post-MI patient population, (iv) the potential benefits of combining immunomodulatory with regenerative therapies, and at last (v) the potential side effects of immunotherapies.

Background In the era of the current COVID-19 health crisis, the aim of the present study was to explore population behavior as regards the visits in the Εmergency Cardiology department (ECD) of a tertiary General Hospital that does not hospitalize SARS-CoV-2 infected patients Methods and results Daily number of visits at the EDC and admissions to Cardiology Wards and Intensive Care Unit of a tertiary General Hospital, in Athens, Greece, were retrieved from hospital's database (January 1st-April 30th 2018, 2019 and 2020). A highly significant reduction in the visits at ECD of the hospital during March and April 2020 was observed as compared with January and February of the same year (p for linear trend < •001); in particular the number of visits was 41.1% lower in March 2020 and 32.7% lower in April 2020, as compared to January 2020. As the number of confirmed COVID-19 cases throughout the country increased (i.e., from February 26th to April 2nd) the number of visits at ECD decreased (p = 0.01), whereas, the opposite was observed in the period afterwards (p = 0.01).The number of acute Myocardial infarctions (MI) cases in March 2020 was the lowest compared to the entire three year period (p < 0•001); however, the number of acute MI cases in April 2020 was doubled as compared to March 2020, but still was lower than the preceding years (p < 0•001). Conclusions It is hard to explain the mystery of the "missing" emergency hospital visits. However, if this decline in cardiovascular disease related hospital visits is "true", it is something that needs to be rigorously studied, to learn how to keep these rates down.