The effect of hydrogen etching on 6H-SiC studied by temperature-dependent current-voltage and atomic force microscopy

6H–SiC was etched with hydrogen at temperatures between 1000 and 1450°C. The etchedSi-terminated face for the 6H‐SiC wafer was investigated by atomic force microscopy and temperature-dependent current–voltage (I–V–T)measurements. Mechanical polishing damage was effectively removed by hydrogen etching at temperatures above 1250°C. Atomic force microscopy images revealed that very good surface morphology, atomic layer flatness, and large and large step width were achieved. Schottky diode characteristics were investigated in detail by current–voltage and temperature-dependent current–voltage measurements, and the results showed a transition from defect assisted tunneling to thermionic emission as the annealingtemperature was increased from 1250 to 1450°C

Effect of n+-GaN subcontact layer on 4H–SiC high-power photoconductive switch

High-power photoconductive semiconductor switching devices were fabricated on 4H–SiC. In order to prevent current crowding, reduce the contact resistance, and avoid contact degradation, a highly n-doped GaN subcontact layer was inserted between the contact metal and the high resistivity SiC bulk. This method led to a two orders of magnitude reduction in the on-state resistance and, similarly, the photocurrent efficiency was increased by two orders of magnitude with the GaN subcontact layer following the initial high current operation. Both dry etching and wet etching were used to remove the GaN subcontact layer in the channel area. Wet etching was found to be more suitable than dry etching

Backilluminated ultraviolet photodetector based on GaN/AlGaN multiple quantum wells

The operation of backilluminated ultraviolet (UV)photodetector based on GaN/Al0.27Ga0.73Nmultiple quantum wells(MQWs) is reported. The MQW structure was deposited on a 1-μm-thick Al0.35Ga0.65Nbuffer layer which was epitaxied on a sapphire substrate. Coplanar Ohmic contacts were made on the top side of the MQW structure. By illuminating the Ohmic contact positions from the backside of the detector, a flat and narrow band spectral response is achieved in the UV wavelength range from 297 nm to 352 nm. The electron-heavy hole absorption in the MQW region produces the sharp long-wavelength cutoff at 352 nm and the band-to-band absorption of the Al0.35Ga0.65Nbuffer layer introduces the sharp short-wavelength cutoff at 297 nm. The polarization-induced electric fields result in a redshift of the long-wavelength cutoff. The response time is measured to be RC limited and determined to be 5 μs at a 50 Ω load

Backilluminated GaN/AlGaN heterojunction ultraviolet photodetector with high internal gain

We report on a backilluminated GaN/Al0.18Ga0.82Nheterojunction ultraviolet (UV)photodetector with high internal gain based on metal-semiconductor-metal structures. A narrow band pass spectral response between 365 and 343 nm was achieved. When operating in dc mode, the responsivity reaches up to the order of 102 A/W under weak UVillumination, which is due to enormous internal gain up to 103. The linear dependence of photocurrent on bias and its square root dependence on optical power are found and explained by a trapping and recombination model. The high photocurrent gain is attributed to trapping and recombination centers with an acceptor character induced by dislocations in GaN

To respond or not to respond - a personal perspective of intestinal tolerance

For many years, the intestine was one of the poor relations of the immunology world, being a realm inhabited mostly by specialists and those interested in unusual phenomena. However, this has changed dramatically in recent years with the realization of how important the microbiota is in shaping immune function throughout the body, and almost every major immunology institution now includes the intestine as an area of interest. One of the most important aspects of the intestinal immune system is how it discriminates carefully between harmless and harmful antigens, in particular, its ability to generate active tolerance to materials such as commensal bacteria and food proteins. This phenomenon has been recognized for more than 100 years, and it is essential for preventing inflammatory disease in the intestine, but its basis remains enigmatic. Here, I discuss the progress that has been made in understanding oral tolerance during my 40 years in the field and highlight the topics that will be the focus of future research

Low-level regulatory T-cell activity is essential for functional type-2 effector immunity to expel gastrointestinal helminths

Helminth infection is frequently associated with the expansion of regulatory T cells (Tregs) and suppression of immune responses to bystander antigens. We show that infection of mice with the chronic gastrointestinal helminth Heligmosomoides polygyrus drives rapid polyclonal expansion of Foxp3(+)Helios(+)CD4(+) thymic (t)Tregs in the lamina propria and mesenteric lymph nodes while Foxp3(+)Helios(-)CD4(+) peripheral (p)Treg expand more slowly. Notably, in partially resistant BALB/c mice parasite survival positively correlates with Foxp3(+)Helios(+)CD4(+) tTreg numbers. Boosting of Foxp3(+)Helios(+)CD4(+) tTreg populations by administration of recombinant interleukin-2 (rIL-2):anti-IL-2 (IL-2C) complex increased worm persistence by diminishing type-2 responsiveness in vivo, including suppression of alternatively activated macrophage and granulomatous responses at the sites of infection. IL-2C also increased innate lymphoid cell (ILC) numbers, indicating that Treg functions dominate over ILC effects in this setting. Surprisingly, complete removal of Tregs in transgenic Foxp3-DTR mice also resulted in increased worm burdens, with "immunological chaos" evident in high levels of the pro-inflammatory cytokines IL-6 and interferon-γ. In contrast, worm clearance could be induced by anti-CD25 antibody-mediated partial depletion of early Treg, alongside increased T helper type 2 responses and without incurring pathology. These findings highlight the overarching importance of the early Treg response to infection and the non-linear association between inflammation and the prevailing Treg frequency

Barrier Tissue Macrophages: Functional Adaptation to Environmental Challenges

Macrophages are found throughout the body, where they have crucial roles in tissue development, homeostasis and remodeling, as well as being sentinels of the innate immune system that can contribute to protective immunity and inflammation. Barrier tissues, such as the intestine, lung, skin and liver, are exposed constantly to the outside world, which places special demands on resident cell populations such as macrophages. Here we review the mounting evidence that although macrophages in different barrier tissues may be derived from distinct progenitors, their highly specific properties are shaped by the local environment, which allows them to adapt precisely to the needs of their anatomical niche. We discuss the properties of macrophages in steady-state barrier tissues, outline the factors that shape their differentiation and behavior and describe how macrophages change during protective immunity and inflammation

Global, regional, and national burden of disorders affecting the nervous system, 1990–2021: a systematic analysis for the Global Burden of Disease Study 2021

BackgroundDisorders affecting the nervous system are diverse and include neurodevelopmental disorders, late-life neurodegeneration, and newly emergent conditions, such as cognitive impairment following COVID-19. Previous publications from the Global Burden of Disease, Injuries, and Risk Factor Study estimated the burden of 15 neurological conditions in 2015 and 2016, but these analyses did not include neurodevelopmental disorders, as defined by the International Classification of Diseases (ICD)-11, or a subset of cases of congenital, neonatal, and infectious conditions that cause neurological damage. Here, we estimate nervous system health loss caused by 37 unique conditions and their associated risk factors globally, regionally, and nationally from 1990 to 2021.MethodsWe estimated mortality, prevalence, years lived with disability (YLDs), years of life lost (YLLs), and disability-adjusted life-years (DALYs), with corresponding 95% uncertainty intervals (UIs), by age and sex in 204 countries and territories, from 1990 to 2021. We included morbidity and deaths due to neurological conditions, for which health loss is directly due to damage to the CNS or peripheral nervous system. We also isolated neurological health loss from conditions for which nervous system morbidity is a consequence, but not the primary feature, including a subset of congenital conditions (ie, chromosomal anomalies and congenital birth defects), neonatal conditions (ie, jaundice, preterm birth, and sepsis), infectious diseases (ie, COVID-19, cystic echinococcosis, malaria, syphilis, and Zika virus disease), and diabetic neuropathy. By conducting a sequela-level analysis of the health outcomes for these conditions, only cases where nervous system damage occurred were included, and YLDs were recalculated to isolate the non-fatal burden directly attributable to nervous system health loss. A comorbidity correction was used to calculate total prevalence of all conditions that affect the nervous system combined.FindingsGlobally, the 37 conditions affecting the nervous system were collectively ranked as the leading group cause of DALYs in 2021 (443 million, 95% UI 378–521), affecting 3·40 billion (3·20–3·62) individuals (43·1%, 40·5–45·9 of the global population); global DALY counts attributed to these conditions increased by 18·2% (8·7–26·7) between 1990 and 2021. Age-standardised rates of deaths per 100 000 people attributed to these conditions decreased from 1990 to 2021 by 33·6% (27·6–38·8), and age-standardised rates of DALYs attributed to these conditions decreased by 27·0% (21·5–32·4). Age-standardised prevalence was almost stable, with a change of 1·5% (0·7–2·4). The ten conditions with the highest age-standardised DALYs in 2021 were stroke, neonatal encephalopathy, migraine, Alzheimer's disease and other dementias, diabetic neuropathy, meningitis, epilepsy, neurological complications due to preterm birth, autism spectrum disorder, and nervous system cancer.InterpretationAs the leading cause of overall disease burden in the world, with increasing global DALY counts, effective prevention, treatment, and rehabilitation strategies for disorders affecting the nervous system are needed

Cellular senescence links aging and diabetes in cardiovascular disease.

Aging is a powerful independent risk factor for cardiovascular diseases such as atherosclerosis and heart failure. Concomitant diabetes mellitus strongly reinforces this effect of aging on cardiovascular disease. Cellular senescence is a fundamental mechanism of aging and appears to play a crucial role in the onset and prognosis of cardiovascular disease in the context of both aging and diabetes. Senescent cells are in a state of cell cycle arrest but remain metabolically active by secreting inflammatory factors. This senescence-associated secretory phenotype is a trigger of chronic inflammation, oxidative stress, and decreased nitric oxide bioavailability. A complex interplay between these three mechanisms results in age- and diabetes-associated cardiovascular damage. In this review, we summarize current knowledge on cellular senescence and its secretory phenotype, which might be the missing link between aging and diabetes contributing to cardiovascular disease.info:eu-repo/semantics/publishe