coli strains carrying mcr-1 harbored bla TEM gene encoding extended spectrum beta lactamase. Antibiotic assay results revealed all 13 E. coli strains carrying mcr-1 to be multi-drug resistant (MDR), including to colistin. The minimum inhibitory concentration (MIC) for colistin ranged from 2 to 6 μg/ml. DNA sequencing confirmed homogeneity of the nucleotide sequence for mcr-1, but the E. coli strains were heterogenous, as confirmed by pulsed-field gel electrophoresis suggesting horizontal transmission of colistin resistance in Bangladesh. Conclusion Widespread dissemination of E. coli strains carrying mcr-1 encoding resistance to colistin in the present study is alarming as this is the last resort drug for the treatment of infections caused by MDR gram-negative bacteria resistant to almost all drugs used commonly. © The Author(s) 2020.Background The role of human polyomaviruses (HPyVs) in epithelial tumors such as head and neck carcinomas (HNSCCs) including oral and oropharyngeal carcinomas has not been established. In this study, we evaluated for the first time the presence of Merkel cell polyomavirus (MCPyV), BK human polyomavirus (BKPyV), and JC human polyomavirus (JCPyV) in HNSCCs from Chilean subjects. Methods One hundred and twenty HNSCCs were analyzed for the presence of MCPyV, BKPyV and JCPyV using real-time polymerase chain reaction procedures. In addition, 54 oral brushes from age- and sex-paired subjects were analyzed. Results Of the total of 120 HNSCCs, 15 were positive for MCPyV (12.5%). Only one case was positive for BKPyV (0.8%) and none for JCPyV (0%). In subjects without cancer, only one case (1.8%) resulted positive for MCPyV and none for JCPyV and BKPyV. MCPyV was associated with HNSCCs (p = 0.0239; OR = 7.571; 95% CI 1.192-81.46). No association was found between age (p = 0.1996), gender (p = 0.7111) or differentiation status (p > 0.9999) and MCPyV presence in HNSCCs. Conclusions MCPyVs were detected in HNSCCs from Chilean patients and were not detected in oral brushes from patients without cancer. More studies are warranted for defining an etiological role and clinical/molecular consequences of these viruses in HNSCCs. © The Author(s). 2020.Metazoan animals are characterized by restricted phenotypic heterogeneity (i.e. morphological disparity) of organisms within various species, a feature that contrasts sharply with intra-species morphological diversity observed in the plant kingdom. Robust emergence of morphogenic blueprint in metazoan animals reflects restricted autonomy of individual cells in adoption of fate outcomes such as differentiation. Fates of individual cells are linked to and influenced by fates of neighboring cells at the population level. Such coupling is a common property of all self-organising systems and propels emergence of order from simple interactions between individual cells without supervision by external directing forces. As a consequence of coupling, expected functional relationship between the constituent cells of an organ system is robustly established concurrent with multiple rounds of cell division during morphogenesis. Notably, the molecular regulation of multicellular coupling during morphogenic self-organisation remains largely unexplored. Here, we review the existing literature on multicellular self-organisation with particular emphasis on recent discovery that β-catenin is the key coupling factor that programs emergence of multi-cellular self-organisation by regulating synchronised cycling of individual cells. © The Author(s) 2020.Introduction There are no currently approved treatments for choroideremia, an X-linked progressive inherited retinal degeneration that leads to blindness by middle age. Several treatment options are being explored, but with major advances in adeno-associated vector (AAV) gene replacement therapy that has reached phase III clinical trials. Areas covered In this review we discuss new insights into the clinical phenotyping and genetic testing of choroideremia patients, that aid disease characterisation, progression and patient inclusion into clinical trials. Recent advances in in-vitro studies have resulted in the development of functional assays that can be used to confirm the diagnosis in challenging cases and to quantify vector potency for use in clinical trials. We review the progress in current gene therapy trials and some considerations towards gene therapy approval for the treatment of choroideremia. Lastly, we discuss developments in alternative therapies including optogenetics. Expert Commentary AAV gene replacement therapy is the most promising treatment strategy for choroideremia, that has developed exponentially over the last few years with a phase III clinical trial now underway. Optogenetics is a promising alternative strategy that might be applicable in late stages of degeneration.Background Children with hypothyroidism typically present with delayed growth and development, but on rare occasions can present with signs of precocious puberty. This presentation is called Van Wyk-Grumbach syndrome. Van Wyk-Grumbach syndrome has seldom been described in patients with trisomy 21. Case presentation We present the case of a 4-year-old girl with trisomy 21, who recently moved to the United States from Guyana, and presented to the emergency room with recurrent vaginal bleeding. She was eventually diagnosed with hypothyroidism and Van Wyk-Grumbach syndrome. She was noted to have Tanner I breasts and pubic hair. A pelvic ultrasound was performed, which showed a simple cyst in the right adnexa. Subsequent laboratory evaluation revealed a thyroid stimulating hormone (TSH) of > 150 mIU/ml along with low free thyroxine of 0.3 ng/dl, suggesting longstanding untreated hypothyroidism. Estradiol and alpha-fetoprotein (AFP) levels were elevated. Bone age was delayed. The patient was diagnosed with Van Wyk-Grumbach syndrome and was started on levothyroxine therapy with subsequent resolution of vaginal bleeding. Estradiol and AFP both normalized after initiating levothyroxine therapy. Conclusion This case emphasizes the importance of recognizing the presence of precocious puberty, delayed bone age and ovarian cyst as a manifestation of primary hypothyroidism. In addition, it highlights the need for thyroid function screening in patients with Trisomy 21. Tumor markers may be elevated in Van Wyk-Grumbach syndrome with subsequent normalization after treatment. selleck kinase inhibitor © The Author(s). 2020.