Human-to-Human Transmission of Monkeypox Virus, United Kingdom, October 2018.

In September 2018, monkeypox virus was transmitted from a patient to a healthcare worker in the United Kingdom. Transmission was probably through contact with contaminated bedding. Infection control precautions for contacts (vaccination, daily monitoring, staying home from work) were implemented. Of 134 potential contacts, 4 became ill; all patients survived.

Periodic ultraviolet-C illumination for marine sensor antifouling.

Ultraviolet light has intriguing potential as a marine antifoulant, targeting almost any species and applicable to almost any surface, while not accumulating in the environment. This study field-tested the effects of periodic ultraviolet-C illumination on marine macrofouling. Across four experiments, several UV illumination duty cycles were tested against controls with no illumination. Duty cycles between 1:2 (time with UV:total time per cycle) and 1:20 were all similarly effective, inhibiting almost all macrofouling at three different temperate Northeast Pacific and Northwest Atlantic sites. Susceptible taxa included barnacles, bryozoans, tunicates (colonial and solitary), and, to a slightly lesser extent, mussels. Duty cycles of 1:30 and 1:60 reduced but did not eliminate biofouling. Measurements of ultraviolet illumination on oceanographic sensors showed similar results. The results suggest further investigation of ultraviolet light as an antifoulant for marine sensors, including susceptibility of other taxa, optimizing illumination patterns, and exploring the potential for evolved resistance.

Two cases of monkeypox imported to the United Kingdom, September 2018.

In early September 2018, two cases of monkeypox were reported in the United Kingdom (UK), diagnosed on 7 September in Cornwall (South West England) and 11 September in Blackpool (North West England). The cases were epidemiologically unconnected and had recently travelled to the UK from Nigeria, where monkeypox is currently circulating. We describe the epidemiology and the public health response for the first diagnosed cases outside the African continent since 2003.

Primary collared uncemented total hip arthroplasties in the elderly: a safe and reliable treatment option.

The age of patients undergoing primary Total Hip Arthroplasty (THA) remains fairly constant despite an increasingly elderly population, possibly owing to concern over postoperative complications. This study evaluated 90-day outcomes in patients over 80, undergoing uncemented collared primary THA for osteoarthritis in a high volume unit. Data were recorded from 153 consecutive patients. There were 0.65% mortality rate and 1.3% major systemic complication rate. American Society of Anesthesiologist (ASA) grade was an independent predictor of inpatient complications. Mean preoperative and 90-day postoperative Oxford Hip Score was 24 and 46 respectively. No radiological evidence of femoral stem migration was seen. Our cohort shows low morbidity and mortality rates. ASA not age helps predict inpatient complications. Uncemented collared femoral prosthesis resulted in excellent functional and radiological outcomes.

Death receptor-induced apoptosis reveals a novel interplay between the chromosomal passenger complex and CENP-C during interphase.

Despite the fact that the chromosomal passenger complex is well known to regulate kinetochore behavior in mitosis, no functional link has yet been established between the complex and kinetochore structure. In addition, remarkably little is known about how the complex targets to centromeres. Here, in a study of caspase-8 activation during death receptor-induced apoptosis in MCF-7 cells, we have found that cleaved caspase-8 rapidly translocates to the nucleus and that this translocation is correlated with loss of the centromere protein (CENP)-C, resulting in extensive disruption of centromeres. Caspase-8 activates cytoplasmic caspase-7, which is likely to be the primary caspase responsible for cleavage of CENP-C and INCENP, a key chromosomal passenger protein. Caspase-mediated cleavage of CENP-C and INCENP results in their mislocalization and the subsequent mislocalization of Aurora B kinase. Our results demonstrate that the chromosomal passenger complex is displaced from centromeres as a result of caspase activation. Furthermore, mutation of the primary caspase cleavage sites of INCENP and CENP-C and expression of noncleavable CENP-C or INCENP prevent the mislocalization of the passenger complex after caspase activation. Our studies provide the first evidence for a functional interplay between the passenger complex and CENP-C.

Enhanced Fas-associated death domain recruitment by histone deacetylase inhibitors is critical for the sensitization of chronic lymphocytic leukemia cells to TRAIL-induced apoptosis.

Chronic lymphocytic leukemia (CLL) is an incurable disease characterized by failure of mature lymphocytes to undergo apoptosis. CLL cells are inherently resistant to tumor necrosis factor-related apoptosis-inducing ligand (TRAIL). Pretreatment with histone deacetylase inhibitors (HDACi) sensitizes CLL cells to TRAIL-mediated apoptosis primarily via TRAIL-R1 and offers a novel approach for the therapy of CLL and other malignancies. Depsipeptide (romidepsin), a HDACi, did not enhance TRAIL binding to TRAIL-R1, TRAIL-R1 aggregation, or internalization of TRAIL-R1, but it enhanced Fas-associated death domain protein (FADD) recruitment to TRAIL-R1 in the death-inducing signaling complex. Cotreatment with phorbol 12-myristate 13-acetate (PMA), a protein kinase C (PKC) activator, dramatically inhibited the HDACi-mediated increase in FADD recruitment and sensitization to TRAIL-induced apoptosis and both of these were reversed by PKC inhibitors. Thus, enhanced FADD recruitment is a critical step in HDACi-mediated sensitization of CLL cells to TRAIL-induced apoptosis and this step is differentially affected by HDACi and phorbol 12-myristate 13-acetate. Using biotinylated TRAIL and streptactin-tagged TRAIL, we have identified several novel TRAIL receptor interacting proteins, including PKCbeta, lymphocyte-specific protease-1, Lyn, and Syk. These molecules may play an as yet unappreciated role in TRAIL signaling in CLL cells and inhibition of one or more of these kinases/phosphatases may provide a novel target to overcome TRAIL resistance.