Probing negatively charged and neutral excitons in MoS2/hBN and hBN/MoS2/hBN van der Waals heterostructures.

High-quality van der Waals heterostructures assembled from hBN-encapsulated monolayer transition metal dichalcogenides enable observations of subtle optical and spin-valley properties whose identification was beyond the reach of structures exfoliated directly on standard SiO2/Si substrates. Here, we describe different van der Waals heterostructures based on uncapped single-layer MoS2 stacked onto hBN layers of different thicknesses and hBN-encapsulated monolayers. Depending on the doping level, they reveal the fine structure of excitonic complexes, i.e. neutral and charged excitons. In the emission spectra of a particular MoS2/hBN heterostructure without an hBN cap we resolve two trion peaks, T1 and T2, energetically split by about 10 meV, resembling the pair of singlet and triplet trion peaks (T S and T T ) in tungsten-based materials. The existence of these trion features suggests that monolayer MoS2 has a dark excitonic ground state, despite having a 'bright' single-particle arrangement of spin-polarized conduction bands. In addition, we show that the effective excitonic g-factor significantly depends on the electron concentration and reaches the lowest value of -2.47 for hBN-encapsulated structures, which reveals a nearly neutral doping regime. In the uncapped MoS2 structures, the excitonic g-factor varies from -1.15 to -1.39 depending on the thickness of the bottom hBN layer and decreases as a function of rising temperature.

Pseudosubarachnoid haemorrhage in subdural haematoma.

Two patients with large bilateral subdural haematomas with patterns of non-enhanced brain computed tomography (CT) falsely suggesting coexistent subarachnoid haemorrhage are presented. The CT images showed marked effacement of the basal cisterns with hyperdense signal along the tentorium, sylvian fissure, and the perimesencephalic cisterns. In both cases, the suspicion of subarachnoid haemorrhage led to the performance of angiographic studies to rule out vascular lesions. Thus, recognition of this radiological feature is important to avoid unnecessary testing and treatment delay.

Immunological effects of amphotericin B and liposomal amphotericin B on splenocytes from immune-normal and immune-compromised mice.

The immunological effects of amphotericin B and liposomal amphotericin B were studied in vitro by measuring B- and T-lymphocyte proliferation on splenocytes from immune-normal, cyclosporine-compromised, and cyclophosphamide-compromised mice. Cellular viability of cells from immune-normal mice was also evaluated. The concentrations used (0, 0.5, 1, 2, 4, 8, and 16 micrograms/ml) encompassed clinically relevant doses. Amphotericin B consistently reduced the abilities of B cells and T cells to proliferate, especially when administered at higher than clinically relevant doses. Direct cytotoxicity probably played only a minor role, since viability studies showed that, compared with its liposomal analog, amphotericin B reduced the number of viable cells by no more than 10%. Clinically relevant doses of liposomal amphotericin B (A. S. Janoff, L. T. Boni, M. C. Popescu, S. R. Minchey, P. R. Cullis, T. D. Madden, T. Tarashi, S. M. Gruner, E. Shyamsunder, M. W. Tate, R. Mendelsohn, and D. Bonner, Proc. Natl. Acad. Sci. USA 85:6122-6126, 1988; R. Mehta, G. Lopez-Berestein, R. Hopfer, K. Mills, and R. L. Juliano, Biochim. Biophys. Acta 770:230-234, 1984) did not inhibit any of the immune parameters examined. Liposomes may, therefore, be a useful means of delivering more drug to a host infected with a fungal organism without further compromising the patient's already suppressed immune system.