Blister-based-laser-induced-forward-transfer: a non-contact, dry laser-based transfer method for nanomaterials.

We show that blister-based-laser-induced forward-transfer can be used to cleanly desorb and transfer nano- and micro-scale particles between substrates without exposing the particles to the laser radiation or to any chemical treatment that could damage the intrinsic electronic and optical properties of the materials. The technique uses laser pulses to induce the rapid formation of a blister on a thin metal layer deposited on glass via ablation at the metal/glass interface. Femtosecond laser pulses are advantageous for forming beams of molecules or small nanoparticles with well-defined velocity and narrow angular distributions. Both fs and ns laser pulses can be used to cleanly transfer larger nanoparticles including relatively fragile monolayer 2D transition metal dichalcogenide crystals and for direct transfer of nanoparticles from chemical vapour deposition growth substrates, although the mechanisms for inducing blister formation are different.

Defining sepsis on the wards: results of a multi-centre point-prevalence study comparing two sepsis definitions.

Our aim was to prospectively determine the predictive capabilities of SEPSIS-1 and SEPSIS-3 definitions in the emergency departments and general wards. Patients with National Early Warning Score (NEWS) of 3 or above and suspected or proven infection were enrolled over a 24-h period in 13 Welsh hospitals. The primary outcome measure was mortality within 30 days. Out of the 5422 patients screened, 431 fulfilled inclusion criteria and 380 (88%) were recruited. Using the SEPSIS-1 definition, 212 patients had sepsis. When using the SEPSIS-3 definitions with Sequential Organ Failure Assessment (SOFA) score ≥ 2, there were 272 septic patients, whereas with quickSOFA score ≥ 2, 50 patients were identified. For the prediction of primary outcome, SEPSIS-1 criteria had a sensitivity (95%CI) of 65% (54-75%) and specificity of 47% (41-53%); SEPSIS-3 criteria had a sensitivity of 86% (76-92%) and specificity of 32% (27-38%). SEPSIS-3 and SEPSIS-1 definitions were associated with a hazard ratio (95%CI) 2.7 (1.5-5.6) and 1.6 (1.3-2.5), respectively. Scoring system discrimination evaluated by receiver operating characteristic curves was highest for Sequential Organ Failure Assessment score (0.69 (95%CI 0.63-0.76)), followed by NEWS (0.58 (0.51-0.66)) (p < 0.001). Systemic inflammatory response syndrome criteria (0.55 (0.49-0.61)) and quickSOFA score (0.56 (0.49-0.64)) could not predict outcome. The SEPSIS-3 definition identified patients with the highest risk. Sequential Organ Failure Assessment score and NEWS were better predictors of poor outcome. The Sequential Organ Failure Assessment score appeared to be the best tool for identifying patients with high risk of death and sepsis-induced organ dysfunction.

Co-infection and synergy of human immunodeficiency virus-1 and herpes simplex virus-1.

The human immunodeficiency virus (HIV-1) uses the CD4 molecule, expressed by T helper cells and activated macrophages, as a receptor for entry into host cells. In tissues co-infected with herpes simplex type 1 (HSV-1), HIV-1 virions were observed to infect keratinocytes, which, because they lack the CD4 molecule, are normally incapable of being infected by HIV-1. Although a number of other viruses have been reported to enhance HIV-1 viral transcription in vitro, this is the first in-vivo report to our knowledge of reciprocal enhancement of viral replication associated with co-infection of keratinocytes and macrophages by HIV-1 and HSV-1 in patients with AIDS and non-genital herpes simplex lesions. The virions in the co-infected cells were larger, morphologically atypical, and appear to be hybrids; most contain the HIV-1 envelope necessary for infectivity. The increased viral load and the proximity of the virions to the cutaneous surface may lead to increased risk of transcutaneous transmission of both viruses. These findings point to the need for incorporation of suppressive treatment for herpes simplex in the treatment of AIDS.

Expression of the L-fucose moiety on epidermal keratinocytes in psoriasis induced by the Koebner phenomenon: a sequential study.

The expression of Ulex europaeus agglutinin (UEA I) binding sites on cell-surface glycoproteins has been used as a marker for terminal differentiation. Increased number of UEA I binding sites of L-fucose specificity have been demonstrated in psoriatic epidermis. The results of lectin-binding studies in a series of biopsies taken sequentially (0 min, 5 min, 24 h, 7 days and 8 weeks) after tape-stripping of uninvolved skin in 12 psoriatic patients (three of whom were taking diltiazem, a calcium blocker at the time of the study) and six controls are presented. UEA I binding sites, which were expressed on the granular layer and upper layers of the stratum spinosum of pre-tape stripped uninvolved skin in psoriatic individuals, were progressively more numerous, with the expression of the L-fucose moiety on the lower stratum spinosum keratinocytes in the 7-day post-tape-stripping biopsies and 8-week biopsies, correlating with a moderate and marked increase in the proliferative index, respectively. In the Koebner-negative and non-psoriatic individuals who failed to develop psoriasis after tape-stripping, the UEA I binding sites were not expressed on keratinocytes of the lower stratum spinosum in any of the biopsies, although a mild increase in the proliferative index was noted in the 7-day biopsies. Our data suggest that the increased commitment of keratinocytes to terminally differentiate may be involved in the psoriatic process.(ABSTRACT TRUNCATED AT 250 WORDS)

An electron microscopic study of the epidermal infiltrate in recurrent herpes simplex.

Host immunity has been suspected of playing a role in recurrent herpes simplex. In this preliminary ultrastructural study of two patients with acute herpetic eruption, it was noted that the keratinocytes exhibiting the most severe damage are those adjacent to large granular lymphocytes. In contrast, many keratinocytes filled with viral particles of herpes simplex show little or no signs of keratinocyte damage. These observations suggest that in recurrent herpes simplex the epidermal damage may be due, at least in part, to cell-mediated host immunity as well as to the viral infection.