Using supramolecular machinery to engineer directional charge propagation in photoelectrochemical devices.

Molecular photoelectrochemical devices are hampered by electron-hole recombination after photoinduced electron transfer, causing losses in power conversion efficiency. Inspired by natural photosynthesis, we demonstrate the use of supramolecular machinery as a strategy to inhibit recombination through an organization of molecular components that enables unbinding of the final electron acceptor upon reduction. We show that preorganization of a macrocyclic electron acceptor to a dye yields a pseudorotaxane that undergoes a fast (completed within ~50 ps) 'ring-launching' event upon electron transfer from the dye to the macrocycle, releasing the anionic macrocycle and thus reducing charge recombination. Implementing this system into p-type dye-sensitized solar cells yielded a 16-fold and 5-fold increase in power conversion efficiency compared to devices based on the two control dyes that are unable to facilitate pseudorotaxane formation. The active repulsion of the anionic macrocycle with concomitant reformation of a neutral pseudorotaxane complex circumvents recombination at both the semiconductor-electrolyte and semiconductor-dye interfaces, enabling a threefold enhancement in hole lifetime.

Facilitators & barriers and practices of early mobilization in critically ill burn patients: A survey.

BACKGROUND: Early mobilization (EM) of intensive care (IC) patients is important but complex with facilitators and barriers. Compared to general IC patients, burn IC patients are more hyper-metabolic. They have extensive wounds, lengthy wound dressing changes, and repeated surgeries that may affect possibilities of EM. This study aimed to identify facilitators and barriers of EM in burn IC patients among all disciplines involved. Additionally, we assessed EM practices, i.e. when are which patients considered suitable for EM. METHODS: A survey was sent to 139 professionals involved in EM of burn IC patients (discipline groups: Intensivists, medical doctors, registered nurses, therapists). RESULTS: Response rate was 57 %. The majority found EM very important, yet different definitions were chosen. Perceived barriers mainly concerned patient-level factors, most frequently hemodynamic instability and excessive sedation followed by skin graft surgery, fatigue, and pain management. Most frequent barriers at the provider-level were limited staffing, safety concerns, and conflicting perceptions about the suitability of EM. At the institutional-level, we found no high barriers. Interdisciplinary variation on perceived barriers, when to initiate it, and permitted maximal activity were ascertained. CONCLUSION: Skin grafts and pain management were barriers of EM specific for burn care. Opinions on frequency, dosage and duration of EM varied widely. Improving interdisciplinary communication is key.

Attachment style classification and posttraumatic stress disorder in former prisoners of war.

Adult attachment style and post-traumatic stress disorder (PTSD) symptomatology were investigated in 107 former prisoner of war veterans. Those with secure attachment styles scored significantly lower on measures of PTSD than did those with insecure styles, and attachment style was a stronger predictor of PTSD symptom intensity than was trauma severity. The suggested association between attachment style and PTSD's development and persistence are discussed in relation to research and clinical practice.

SAG: a Schwann cell membrane glycoprotein.

We report on characterization of a 170,000 Da glycoprotein found exclusively in the PNS. We refer to this protein as the Schwann cell membrane glycoprotein (SAG). SAG contains the HNK-1 carbohydrate, which is considered by some to be a marker of adhesion molecules. Its N-terminal sequence is not similar to previously known polypeptide sequences. SAG is found exclusively in the PNS, is present in rat sciatic nerve prior to myelination, and is in both myelinating and nonmyelinating Schwann cells. Tumors of Schwann cell lineage express SAG where axons are present (neurofibromas) but do not in the absence of axons (schwannomas). Schwannoma cells in culture do not express SAG even when exposed to forskolin, an activator of adenylate cyclase. However, schwannoma cells grown in the presence of a neuronal cell line (PC12) express SAG.

Experimental allergic neuritis in the SJL/J mouse: dysfunction of peripheral nerve without clinical signs.

Experimental allergic neuritis (EAN) was studied in the SJL/J mouse and compared to EAN in the Lewis rat. The Lewis rat developed hind limb weakness and weight loss while the SJL/J mouse had no discernible clinical abnormalities. The SJL/J mouse, however, suffered subclinical damage to peripheral nerve (PN) myelin. Both species reproducibly developed electrophysiologic dysfunction of PN and histopathology confined to the peripheral nervous system (PNS). Understanding of autoimmune demyelination in the central nervous system was greatly enhanced by the development of experimental allergic encephalomyelitis in the SJL/J mouse. We believe that EAN in the SJL/J mouse could lead to a similar increase in our understanding of autoimmune demyelination in the PNS.

Circulating autoantibodies to the 200,000-dalton protein of neurofilaments in the serum of healthy individuals.

There is substantial evidence that human serum contains antibodies to many autoantigens. For example, all healthy people have autoantibodies (immunoglobulin M) to some undefined brain antigens. In this study immunoblots and immunohistochemical staining were used to detect antibodies to neural tissues in serum samples from 200 healthy people and 200 patients with various neurological diseases. Ninety-nine percent of the 400 subjects had serum immunoglobulin M and 95 percent had immunoglobulin G that bound to a 200-kilodalton protein in homogenates of neural tissues. In most cases there were no antibodies to anything else in the homogenates. The 200-kilodalton protein was the heaviest of the neurofilament triplet proteins. These observations do not support a role for antibodies to the 200-kilodalton protein of neurofilaments in the pathogenesis of neurological diseases.