The Boltzmann distribution of electrons poses a fundamental barrier to lowering energy dissipation in conventional electronics, often termed as Boltzmann Tyranny. Negative capacitance in ferroelectric materials, which stems from the stored energy of a phase transition, could provide a solution, but a direct measurement of negative capacitance has so far been elusive. Here, we report the observation of negative capacitance in a thin, epitaxial ferroelectric film. When a voltage pulse is applied, the voltage across the ferroelectric capacitor is found to be decreasing with time--in exactly the opposite direction to which voltage for a regular capacitor should change. Analysis of this 'inductance'-like behaviour from a capacitor presents an unprecedented insight into the intrinsic energy profile of the ferroelectric material and could pave the way for completely new applications.

The introduction of advanced techniques and technology in radiotherapy has greatly improved our ability to deliver highly conformal tumor doses while minimizing the dose to adjacent organs at risk. Despite these tremendous improvements, there remains a general concern about doses to normal tissues that are not the target of the radiation treatment; any "nontarget" radiation should be minimized as it offers no therapeutic benefit. As patients live longer after treatment, there is increased opportunity for late effects including second cancers and cardiac toxicity to manifest. Complicating the management of these issues, there are unique challenges with measuring, calculating, reducing, and reporting nontarget doses that many medical physicists may have limited experience with. Treatment planning systems become dramatically inaccurate outside the treatment field, necessitating a measurement or some other means of assessing the dose. However, measurements are challenging because outside the treatment field, the radiation energy spectrum, dose rate, and general shape of the dose distribution (particularly the percent depth dose) are very different and often require special consideration. Neutron dosimetry is also particularly challenging, and common errors in methodology can easily manifest as errors of several orders of magnitude. Task Group 158 was, therefore, formed to provide guidance for physicists in terms of assessing and managing nontarget doses. In particular, the report: (a) highlights major concerns with nontarget radiation; (b) provides a rough estimate of doses associated with different treatment approaches in clinical practice; (c) discusses the uses of dosimeters for measuring photon, electron, and neutron doses; (d) discusses the use of calculation techniques for dosimetric evaluations; (e) highlights techniques that may be considered for reducing nontarget doses; (f) discusses dose reporting; and (g) makes recommendations for both clinical and research practice.

Stroke is a leading cause of mortality and severe long-term disability worldwide. Development of effective treatment or new therapeutic strategies for ischemic stroke patients is therefore crucial. Ischemic stroke promotes neurogenesis by several growth factors including FGF-2, IGF-1, BDNF, VEGF and chemokines including SDF-1, MCP-1. Stroke-induced angiogenesis is similarly regulated by many factors most notably, eNOS and CSE, VEGF/VEGFR2, and Ang-1/Tie2. Important findings in the last decade have revealed that neurogenesis is not the stand-alone consideration in the fight for full functional recovery from stroke. Angiogenesis has been also shown to be critical in improving post-stroke neurological functional recovery. More than that, recent evidence has shown a highly possible interplay or dependence between stroke-induced neurogenesis and angiogenesis. Moving forward, elucidating the underlying mechanisms of this coupling between stroke-induced neurogenesis and angiogenesis will be of great importance, which will provide the basis for neurorestorative therapy.

Among age-related diseases, cardiovascular and cerebrovascular diseases are major causes of death. Vascular dysfunction is a key characteristic of these diseases wherein age is an independent and essential risk factor. The present work will review morphological alterations of aging vessels in-depth, which includes the discussion of age-related microvessel loss and changes to vasculature involving the capillary basement membrane, intima, media, and adventitia as well as the accompanying vascular dysfunctions arising from these alterations.

Novel coronavirus disease 2019 (COVID-19) is a highly infectious, rapidly spreading viral disease with an alarming case fatality rate up to 5%. The risk factors for severe presentations are concentrated in patients with chronic kidney disease, particularly patients with end-stage renal disease (ESRD) who are dialysis dependent. We report the first US case of a 56-year-old nondiabetic male with ESRD secondary to IgA nephropathy undergoing thrice-weekly maintenance hemodialysis for 3 years, who developed COVID-19 infection. He has hypertension controlled with angiotensin receptor blocker losartan 100 mg/day and coronary artery disease status-post stent placement. During the first 5 days of his febrile disease, he presented to an urgent care, 3 emergency rooms, 1 cardiology clinic, and 2 dialysis centers in California and Utah. During this interval, he reported nausea, vomiting, diarrhea, and low-grade fevers but was not suspected of COVID-19 infection until he developed respiratory symptoms and was admitted to the hospital. Imaging studies upon admission were consistent with bilateral interstitial pneumonia. He was placed in droplet-eye precautions while awaiting COVID-19 test results. Within the first 24 h, he deteriorated quickly and developed acute respiratory distress syndrome (ARDS), requiring intubation and increasing respiratory support. Losartan was withheld due to hypotension and septic shock. COVID-19 was reported positive on hospital day 3. He remained in critical condition being treated with hydroxychloroquine and tocilizumab in addition to the standard medical management for septic shock and ARDS. Our case is unique in its atypical initial presentation and highlights the importance of early testing.

ObjectivesTo compare health-related quality of life (HRQoL) before and after treatment with etanercept in patients with moderate to severe rheumatoid arthritis (RA), psoriatic arthritis (PsA) and psoriasis using spydergram representations. Methods Data from randomised, controlled trials of etanercept in patients with RA, PsA and psoriasis were analysed. HRQoL was assessed by the medical outcomes survey short form 36 (SF-36) physical (PCS) and mental (MCS) component summary and domain scores. Baseline comparisons with age and gender-matched norms and treatment-associated changes in domain scores were quantifi ed using spydergrams and the health utility SF-6D measure.

Cancer patients undergoing radiation treatment are exposed to high doses to the target (tumour), intermediate doses to adjacent tissues and low doses from scattered radiation to all parts of the body. In the case of proton therapy, secondary neutrons generated in the accelerator head and inside the patient reach many areas in the patient body. Due to the improved efficacy of management of cancer patients, the number of long term survivors post-radiation treatment is increasing substantially. This results in concern about the risk of radiation-induced cancer appearing at late post-treatment times. This paper presents a case study to determine the effective dose from secondary neutrons in patients undergoing proton treatment. A whole-body patient model, VIP-Man, was employed as the patient model. The geometry dataset generated from studies made on VIP-Man was implemented into the GEANT4 Monte Carlo code. Two proton treatment plans for tumours in the lung and paranasal sinus were simulated. The organ doses and ICRP-60 radiation and tissue weighting factors were used to calculate the effective dose. Results show whole body effective doses for the two proton plans of 0.162 Sv and 0.0266 Sv, respectively, to which the major contributor is due to neutrons from the proton treatment nozzle. There is a substantial difference among organs depending on the treatment site.

Reactive gliosis and glial scar formation have been evidenced in the animal model of ischemic stroke, but not in human ischemic brain. Here, we have found that GFAP, ED1 and chondroitin sulphate proteoglycans (CSPG) expression were significantly increased in the cortical peri-infarct regions after ischemic stroke, compared with adjacent normal tissues and control subjects. Double immunolabeling showed that GFAP-positive reactive astrocytes in the peri-infarct region expressed CSPG, but showed no overlap with ED1-positive activated microglia. Our findings suggest that reactive gliosis and glial scar formation as seen in animal models of stroke are reflective of what occurs in the human brain after an ischemic injury.