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Methamphetamine (Meth) is a potent psychostimulant with well-established hepatotoxicity. Gut microbiota-derived short-chain fatty acids (SCFAs) have been reported to yield beneficial effects on the liver. In this study, we aim to further reveal the mechanisms of Meth-induced hepatic injuries and investigate the potential protective effects of SCFAs. Herein, mice were intraperitoneally injected with 15 mg/kg Meth to induce hepatic injuries. The composition of fecal microbiota and SCFAs was profiled using 16 S rRNA sequencing and Gas Chromatography/Mass Spectrometry (GC/MS) analysis, respectively. Subsequently, SCFAs supplementation was performed to evaluate the protective effects against hepatic injuries. Additionally, Sigma-1 receptor knockout (S1R-/-) mice and fluvoxamine (Flu), an agonist of S1R, were introduced to investigate the mechanisms underlying the protective effects of SCFAs. Our results showed that Meth activated S1R and induced hepatic autophagy, inflammation, and oxidative stress by stimulating the MAPK/ERK pathway. Meanwhile, Meth disrupted SCFAs product-related microbiota, leading to a reduction in fecal SCFAs (especially Acetic acid and Propanoic acid). Accompanied by the optimization of gut microbiota, SCFAs supplementation normalized S1R expression and ameliorated Meth-induced hepatic injuries by repressing the MAPK/ERK pathway. Effectively, S1R knockout repressed Meth-induced activation of the MAPK/ERK pathway and further ameliorated hepatic injuries. Finally, the overexpression of S1R stimulated the MAPK/ERK pathway and yielded comparable adverse phenotypes to Meth administration. These findings suggest that Meth-induced hepatic injuries relied on the activation of S1R, which could be alleviated by SCFAs supplementation. Our study confirms the crucial role of S1R in Meth-induced hepatic injuries for the first time and provides a potential preemptive therapy.

The superconducting radiofrequency electron linear accelerator of the Shanghai HIgh repetition rate XFEL aNd Extreme light facility (SHINE) will use 600 TESLA-style cavities with 1.3 GHz fundamental power couplers for continuous-wave operation. The first batch of 26 1.3 GHz coupler prototypes has been fabricated from three domestic manufacturers for qualification. Several key manufacturing processes have been developed and qualified, including high residual resistivity ratio copper plating, vacuum brazing of ceramic windows, electron beam welding, and titanium nitride coating. In addition, uniform quality control and inspection processes have been established to ensure the power couplers meet the requirements for the intended use in the SHINE project. All the 1.3 GHz coupler prototypes have been power conditioned with 14-kW traveling wave and 7-kW standing wave rf in continuous-wave mode. Even higher power levels have been demonstrated with 20-kW traveling wave and 10-kW standing wave rf, which indicates their robustness.

Antarctic krill (Euphausua superba) need to undergo freeze-drying to facilitate lipid extraction, but freeze-drying is time-consuming and energy-intensive, resulting in high processing costs. Microwave heating technology can reduce freeze-drying time and lower energy consumption costs. The objective of this study was to establish a drying kinetic model to help the microwave freeze-drying process by predicting krill drying time and evaluating the impact of the drying process on krill quality. The results showed that changing the microwave power did not alter the total energy requirement to complete drying when the sample weight was fixed. The total energy requirement for microwave drying increases with the sample weight. Comparing the three methods of freeze-drying (FD), microwave freeze-drying (MWFD), and hot-air drying at 55 °C (HAD) showed that they took 18, 0.67, and 16 h, respectively, to reach the drying endpoint for krill. Overall, HAD resulted in browning, shrinkage, and quality degradation of krill due to its high temperature and long duration. While the appearance and active ingredient contents of FD krill are slightly better than those of MWFD krill, FD requires a longer process and more energy. MWFD can reduce drying time by 20 times and energy consumption by 95% compared to FD. [ABSTRACT FROM AUTHOR]

Key Clinical Message: Adult intussusception necessitates early surgical intervention. We emphasis the significance of considering diffuse large B‐Cell lymphoma in differential diagnoses for adult intussusception, particularly in the colon, to ensure precise diagnosis and optimal management. [ABSTRACT FROM AUTHOR]

Retinoic acid‐induced 1 (RAI1) encodes a transcriptional regulator critical for brain development and function. RAI1 haploinsufficiency in humans causes a syndromic autism spectrum disorder known as Smith−Magenis syndrome (SMS). The neuroanatomical distribution of RAI1 has not been quantitatively analyzed during the development of the prefrontal cortex, a brain region critical for cognitive function and social behaviors and commonly implicated in autism spectrum disorders, including SMS. Here, we performed comparative analyses to uncover the evolutionarily convergent and divergent expression profiles of RAI1 in major cell types during prefrontal cortex maturation in common marmoset monkeys (Callithrix jacchus) and mice (Mus musculus). We found that while RAI1 in both species is enriched in neurons, the percentage of excitatory neurons that express RAI1 is higher in newborn mice than in newborn marmosets. By contrast, RAI1 shows similar neural distribution in adult marmosets and adult mice. In marmosets, RAI1 is expressed in several primate‐specific cell types, including intralaminar astrocytes and MEIS2‐expressing prefrontal GABAergic neurons. At the molecular level, we discovered that RAI1 forms a protein complex with transcription factor 20 (TCF20), PHD finger protein 14 (PHF14), and high mobility group 20A (HMG20A) in the marmoset brain. In vitro assays in human cells revealed that TCF20 regulates RAI1 protein abundance. This work demonstrates that RAI1 expression and protein interactions are largely conserved but with some unique expression in primate‐specific cells. The results also suggest that altered RAI1 abundance could contribute to disease features in disorders caused by TCF20 dosage imbalance. [ABSTRACT FROM AUTHOR]

Retinoic acid-induced 1 (RAI1) encodes a transcriptional regulator critical for brain development and function. RAI1 haploinsufficiency in humans causes a syndromic autism spectrum disorder known as Smith-Magenis syndrome (SMS). The neuroanatomical distribution of RAI1 has not been quantitatively analyzed during the development of the prefrontal cortex, a brain region critical for cognitive function and social behaviors and commonly implicated in autism spectrum disorders, including SMS. Here, we performed comparative analyses to uncover the evolutionarily convergent and divergent expression profiles of RAI1 in major cell types during prefrontal cortex maturation in common marmoset monkeys (Callithrix jacchus) and mice (Mus musculus). We found that while RAI1 in both species is enriched in neurons, the percentage of excitatory neurons that express RAI1 is higher in newborn mice than in newborn marmosets. By contrast, RAI1 shows similar neural distribution in adult marmosets and adult mice. In marmosets, RAI1 is expressed in several primate-specific cell types, including intralaminar astrocytes and MEIS2-expressing prefrontal GABAergic neurons. At the molecular level, we discovered that RAI1 forms a protein complex with transcription factor 20 (TCF20), PHD finger protein 14 (PHF14), and high mobility group 20A (HMG20A) in the marmoset brain. In vitro assays in human cells revealed that TCF20 regulates RAI1 protein abundance. This work demonstrates that RAI1 expression and protein interactions are largely conserved but with some unique expression in primate-specific cells. The results also suggest that altered RAI1 abundance could contribute to disease features in disorders caused by TCF20 dosage imbalance., (© 2024 The Authors. The Journal of Comparative Neurology published by Wiley Periodicals LLC.)

Hepatoid differentiation in pancreatic carcinoma is a rare phenomenon. It occurs either as a pure form or as a component with other subtypes. Herein, we report a 52-year-old man with an ampullary large cell neuroendocrine carcinoma presenting with obstructive jaundice for 2 months. A 0.5-cm nodule was found in the pancreatic head. Morphologically, the nodule was composed of exclusively hepatocytic tumor cells and sinusoids with dysplastic cytology and capsular invasion. The patient did not have a hepatic mass or ectopic normal liver tissue. This is the first reported case of ampullary large cell neuroendocrine carcinoma coinciding with a pancreatic hepatoid microcarcinoma. The clinicopathological features of pancreatic hepatoid carcinomas and their histogenesis are discussed.

Colonic duplication is a very rare congenital anomaly that is usually detected in infancy and early childhood. In the English literature, 6 cases of Y-shaped colonic duplication have been reported since 1953. We conducted a review of the reported cases, and we present a new case of a Y-shaped duplication of the sigmoid colon manifesting as long-term abdominal pain and constipation.