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We present a protocol for the biosensor Cell-Fit-HD4D. It enables long-term monitoring and correlation of single-cell fate with subcellular-deposited energy of ionizing radiation. Cell fate tracking using widefield time-lapse microscopy is uncoupled in time from confocal ion track imaging. Registration of both image acquisition steps allows precise ion track assignment to cells and correlation with cellular readouts. For complete details on the use and execution of this protocol, please refer to Niklas et al. (2022).

The possibility of band gap engineering (BGE) in RAlO3 (R = Y, La, Gd, Yb, Lu) perovskites in the context of trap depths of intrinsic point defects was investigated comprehensively using experimental and theoretical approaches. The optical band gap of the materials, E g, was determined via both the absorption measurements in the VUV spectral range and the spectra of recombination luminescence excitation by synchrotron radiation. The experimentally observed effect of E g reduction from ∼8.5 to ∼5.5 eV in RAlO3 perovskites with increasing R3+ ionic radius was confirmed by the DFT electronic structure calculations performed for RMIIIO3 crystals (R = Lu, Y, La; MIII = Al, Ga, In). The possibility of BGE was also proved by the analysis of thermally stimulated luminescence (TSL) measured above room temperature for the far-red emitting (Y/Gd/La)AlO3:Mn4+ phosphors, which confirmed decreasing of the trap depths in the cation sequence Y → Gd → La. Calculations of the trap depths performed within the super cell approach for a number of intrinsic point defects and their complexes allowed recognizing specific trapping centers that can be responsible for the observed TSL. In particular, the electron traps of 1.33 and 1.43 eV (in YAlO3) were considered to be formed by the energy level of oxygen vacancy (VO) with different arrangement of neighboring YAl and VY, while shallower electron traps of 0.9-1.0 eV were related to the energy level of YAl antisite complexes with neighboring VO or (VO + VY). The effect of the lowering of electron trap depths in RAlO3 was demonstrated for the VO-related level of the (YAl + VO + VY) complex defect for the particular case of La substituting Y.

Alcohol abuse and dependence remain significant public health issues, and yet the brain circuits that are involved in the rewarding effects of alcohol are poorly understood. One promising way to study the effects of alcohol on neural activity is to examine its effects on functional connectivity between brain areas involved in reward and other functions. Here, we compared the effects of two doses of alcohol (0.4 and 0.8 g/kg) to placebo on resting-state functional connectivity in brain circuits related to reward in 19 healthy young men without histories of alcohol problems. The higher, but not the lower, dose of alcohol, significantly increased connectivity from reward-related regions to sensory and motor cortex, and between seeds associated with cognitive control. Contrary to expectation, alcohol did not significantly change connectivity for the ventral striatum at either dose. These findings reveal unrecognized effects of alcohol on connectivity from reward-related regions to visual and sensory cortical areas.

Climatic warming can shift community composition driven by the colonization-extinction dynamics of species with different thermal preferences; but simultaneously, habitat fragmentation can mediate species' responses to warming. As this potential interactive effect has proven difficult to test empirically, we collected data on birds over 10 years of climate warming in a reservoir subtropical island system that was formed 65 years ago. We investigated how the mechanisms underlying climate-driven directional change in community composition were mediated by habitat fragmentation. We found thermophilization driven by increasing warm-adapted species and decreasing cold-adapted species in terms of trends in colonization rate, extinction rate, occupancy rate and population size. Critically, colonization rates of warm-adapted species increased faster temporally on smaller or less isolated islands; cold-adapted species generally were lost more quickly temporally on closer islands. This provides support for dispersal limitation and microclimate buffering as primary proxies by which habitat fragmentation mediates species range shift. Overall, this study advances our understanding of biodiversity responses to interacting global change drivers.

AbstractAlthough the kappa-opioid receptor (KOR) and its endogenous ligand, dynorphin, are believed to be involved in ethanol drinking, evidence on the direction of their effects has been mixed. The nucleus accumbens (NAc) shell densely expresses KORs, but previous studies have not found KOR activation to influence ethanol drinking. Using microinjections into the NAc shell of male and female Long-Evans rats that drank under the intermittent-access procedure, we found that the KOR agonist, U50,488, had no effect on ethanol drinking when injected into the middle NAc shell, but that it promoted intake in males and high-drinking females in the caudal NAc shell and high-drinking females in the rostral shell, and decreased intake in males and low-drinking females in the rostral shell. Conversely, injection of the KOR antagonist, nor-binaltorphimine, stimulated ethanol drinking in low-drinking females when injected into the rostral NAc shell and decreased drinking in high-drinking females when injected into the caudal NAc shell. These effects of KOR activity were substance-specific, as U50,488 did not affect sucrose intake. Using quantitative real-time PCR, we found that baseline gene expression of the KOR was higher in the rostral compared to caudal NAc shell, but that this was upregulated in the rostral shell with a history of ethanol drinking. Our findings have important clinical implications, demonstrating that KOR stimulation in the NAc shell can affect ethanol drinking, but that this depends on NAc subregion, subject sex, and ethanol intake level, and suggesting that this may be due to differences in KOR expression.

Primary amebic meningoencephalitis (PAM) is a necrotizing and hemorrhagic inflammation of the brain and meninges caused by Naegleria fowleri, a free-living thermophilic ameba of freshwater systems. PAM remains a neglected disease that disproportionately affects children in tropical and subtropical climates, with an estimated mortality rate of 95-98%. Due to anthropogenic climate change, the average temperature in the USA has increased by 0.72 to 1.06 °C in the last century, promoting the poleward spread of N. fowleri. PAM is often misdiagnosed as bacterial meningitis or viral encephalitis, which shortens the window for potentially life-saving treatment. Diagnosis relies on the patient's history of freshwater exposure and the physician's high index of suspicion, supported by cerebrospinal fluid studies. While no experimental trials have been conducted to assess the relative efficacy of treatment regimens, anti-amebic therapy with adjunctive neuroprotection is standard treatment in the USA. We performed a literature review and identified five patients from North America between 1962 and 2022 who survived PAM with various degrees of sequelae.