The impact of anger on intertemporal decision-making in individuals with internet addiction: an fNIRS study.

Intertemporal decision-making is the choice between an immediate smaller reward (SS) and a delayed larger reward (LL). Intertemporal decision-making depends on the interaction of the cognitive and emotional systems, and the latter is particularly vital. According to the Appraisal Tendency Frame (ATF) theory, anger influences intertemporal decision-making by increasing an individual's sense of certainty and control. This study examined whether anger affects intertemporal decision-making in individuals with internet addiction (IA) in this manner and investigated its neural mechanisms. Nineteen individuals with IA and 20 healthy controls were recruited. All subjects performed the Monetary choice task under anger and neutral emotions while functional near-infrared spectroscopy (fNIRS) equipment simultaneously recorded the hemodynamics in the prefrontal cortex (PFC). Individuals with IA showed a more considerable delay discount and lower brain activations in the orbitofrontal cortex (OFC) and left dorsolateral prefrontal cortex (L-dlPFC) compared to HC. Moreover, individuals with IA made more LL choices in the angry condition than in the neutral emotion, yet there was no difference in HC. The brain activation in L-dlPFC of individuals with IA tends to increase in the angry condition compared to the neutral condition. These findings revealed that impairment of intertemporal decision-making in individuals with individuals with IA might be related to the dysfunction of OFC and L-dlPFC. Our work also provided initial footing for the applicability of the appraisal tendency frame theory to individuals with IA, and L-dlPFC might play a role in the effects of anger on intertemporal decision-making.

Reprogramming human urine cells into intestinal organoids with long-term expansion ability and barrier function.

Generation of intestinal organoids from human somatic cells by reprogramming would enable intestinal regeneration, disease modeling, and drug screening in a personalized pattern. Here, we report a direct reprogramming protocol for the generation of human urine cells induced intestinal organoids (U-iIOs) under a defined medium. U-iIOs expressed multiple intestinal specific genes and showed resembling gene expression profiles to primary small intestines. U-iIOs can be stably long-term expanded and further differentiated into more mature intestinal lineage cells with high expression of metallothionein and cytochrome P450 (CYP450) genes. These specific molecular features of U-iIOs differ from human pluripotent stem cells derived intestinal organoids (P-iIOs) and intestinal immortalized cell lines. Furthermore, U-iIOs exhibit intestinal barriers indicated by blocking FITC-dextran permeation and uptaking of the specific substrate rhodamine 123. Our study provides a novel platform for patient-specific intestinal organoid generation, which may lead to precision treatment of intestinal diseases and facilitate drug discovery.

Emodin attenuates hypoxic-ischemic brain damage by inhibiting neuronal apoptosis in neonatal mice.

Neonatal hypoxic-ischemic brain damage (HIBD) can lead to mortality and severe neurological dysfunction. Emodin is a natural anthraquinone derivative that is easy to obtain and has good neuroprotective effects. This study aimed to investigate the neuroprotective effect of emodin on neonatal mouse HIBD. The modified Rice-Vannucci method was used to induce HIBD in mouse pups. Eighty postnatal 7-day (P7) C57BL/6 neonatal mice were randomly divided into the sham group (sham), vehicle group (vehicle), and emodin group (emodin). TTC staining and whole-brain morphology were used to evaluate the infarct volume and morphology of the brain tissue. The condition of the neurons was observed through Nissl staining, HE staining, FJC staining, immunofluorescence and Western blot for NeuN, IBA-1, and GFAP. The physiological status of the mice was evaluated using weight measurements. The neural function of the mice was assessed using the negative geotaxis test, righting reflex test, and grip test. TUNEL staining was used to detect apoptosis in brain cells. Finally, Western blot and immunofluorescence were used to detect the expression levels of apoptosis-related proteins, such as P53, cleaved caspase-3, Bax and Bcl-2, in the brain. Experiments have shown that emodin can reduce the cerebral infarct volume, brain oedema, neuronal apoptosis, and degeneration and improve the reconstruction of brain tissue morphology, neuronal morphology, physiological conditions, and neural function. Additionally, emodin inhibited the expression of proapoptotic proteins such as P53, Bax and cleaved caspase-3 and promoted the expression of the antiapoptotic protein Bcl-2. Emodin attenuates HIBD by inhibiting neuronal apoptosis in neonatal mice.

Neural mechanisms of intertemporal and risky decision-making in individuals with internet use disorder: A perspective from directed functional connectivity.

Background and aims: The intertemporal and risk decision-making impairments are vital cognitive mechanisms in internet use disorder (IUD). However, the underlying neural mechanisms for these two decision-making dysfunctions in individuals with IUD remain unclear. Methods: This study employed Functional Near-Infrared Spectroscopy (fNIRS) to record changes in blood oxygen concentration in the prefrontal cortex of individuals with IUD during intertemporal and risk decision-making tasks. Results: The findings revealed that the intertemporal decision-making deficits in IUD group were primarily associated with reduced activation in the left dorsolateral prefrontal cortex (dlPFC) and orbitofrontal cortex (OFC) and FC from the left dlPFC to the right dlPFC. On the other hand, risk decision-making impairments were linked to decreased OFC activation and weakened functional connectivity from the left dlPFC to the right dlPFC and OFC. Discussions and Conslusions: These results suggested that while there were common neural mechanisms underlying intertemporal and risk decision-making impairments in individuals with IUD, specific neural foundations existed for each type of dysfunction.