Clinical tracking of chimeric antigen receptor (CAR) T cells in vivo by positron emission tomography (PET) imaging is an area of intense interest. But the long-lived positron emitter-labeled CAR T cells stay in the liver and spleen for days or even weeks. Thus, the excessive absorbed effective dose becomes a major biosafety issue leading it difficult for clinical translation. In this study we used ⁶⁸Ga, a commercially available short-lived positron emitter, to label CAR T cells for noninvasive cell tracking in vivo. CAR T cells could be tracked in vivo by ⁶⁸Ga-PET imaging for at least 6 h. We showed a significant correlation between the distribution of ⁸⁹Zr and ⁶⁸Ga-labeled CAR T cells in the same tissues (lungs, liver, and spleen). The distribution and homing behavior of CAR T cells at the early period is highly correlated with the long-term fate of CAR T cells in vivo. And the effective absorbed dose of ⁶⁸Ga-labeled CAR T cells is only one twenty-fourth of ⁸⁹Zr-labeled CAR T cells, which was safe for clinical translation. We conclude the feasibility of ⁶⁸Ga instead of ⁸⁹Zr directly labeling CAR T cells for noninvasive tracking of the cells in vivo at an early stage based on PET imaging. This method provides a potential solution to the emerging need for safe and practical PET tracer for cell tracking clinically.

Primary coenzyme Q10 deficiency-6 (COQ10D6), as a rare autosomal recessive disease caused by COQ6 mutations, is characterized by progressive infantile-onset nephrotic syndrome resulting in end-stage renal failure and sensorineural hearing loss. Here, we report two Chinese siblings with COQ10D6 who primarily presented with severe metabolic acidosis, proteinuria, hypoalbuminemia, growth retardation, and muscle hypotonia and died in early infancy. Using whole-exome sequencing and Sanger sequencing, we identified two rare recessive nonsense mutations in the COQ6 gene segregating with disease in affected family members: c.249C > G (p.Tyr83Ter) and c.1381C > T (p.Gln461Ter), resulting in two truncated protein products. Both mutations are located in a highly conserved area and are predicted to be pathogenic. Indeed, the death of our patients in early infancy indicates the pathogenicity of the p.Tyr83Ter and p.Gln461Ter variants and highlights the significance of the two variants for COQ6 enzyme function, which is necessary for the biosynthesis of coenzyme Q10. In conclusion, we discovered a novel compound heterozygous pathogenic variant of the COQ6 gene as a cause of severe COQ10D6 in the two siblings. Based on the clinical history and genetic characteristics of the patients, our cases expand the genotypic spectrum of COQ10D6 and highlight the heterogeneity and severity of clinical features associated with COQ6 mutations. For patients with clinical manifestations suggestive of COQ10D6, early testing for COQ6 mutations is beneficial for disease diagnosis and therapeutic interventions as well as disease prevention in future generations.

Background: Childhood obesity is a worldwide critical health concern. We aimed to clarify whether eating behaviours increased the risk of childhood obesity.Methods: We recruited 2,049 pre-school children aged 3–6 years between 1 December 2021 and 31 January 2022 in Taizhou, China. Children's weight status was classified according to the International Obesity Task Force criteria, and their eating behaviours were evaluated using the Children's Eating Behaviour Questionnaire. Correlation analyses, linear regressions, and one-way ANCOVA. were performed to analyse the association between children's eating behaviours and weight status.Results: In ‘Food Avoidant' subscales, the scores of satiety responsiveness (P < 0.001) and slowness in eating (P = 0.001) were negatively associated with body mass index z score among pre-school children of both sexes. In ‘Food Approach’ subscales, the score of enjoyment of food was positively associated with body mass index z score in both boys (P = 0.007) and girls (P = 0.035), but the association of scores of food responsiveness with body mass index z score was found only in girls (P = 0.001).Conclusion: Our results supported that pre-school children with low scores in ‘Food Avoidant’ subscales and high scores in ‘Food Approach’ scales were more likely to become obese.

Objective: To evaluate the effects of antenatal corticosteroids (ACS) on blood glucose fluctuations in late-preterm neonates.Methods: A retrospective study was performed on 236 neonates with gestational age of 34⁺⁰ to 36⁺⁶ weeks who were admitted to the neonatology department of a tertiary general hospital in China's Zhejiang Province between April 2020 and February 2022. The neonates were divided into three groups: complete course, partial course, and control. Primary outcome was the neonatal blood glucose levels within the first 48 h of life.Results: 134 (56.8%) newborns were exposed to a complete course of ACS, 56 (23.7%) had a to a partial course of ACS, and 46 (19.5%) had no exposure to ACS. The patients in the complete course group had the highest proportion of neonatal hypoglycemia (16.4% vs. 3.6% and 6.5%).The patients exposed to a complete course of dexamethasone had significantly lower blood glucose levels within 12 h of birth than the control group, although no significant differences were observed after 24 h. Differences in blood glucose levels were more significant among male infants, although blood glucose curves of the male and female infants remained close to the overall trend.Conclusions: Blood glucose levels in late-preterm neonates may decrease after ACS administration, especially after exposure to a complete course. The effects are more pronounced in the first 12 h of life, with males being more severely affected; however, the effects on blood glucose levels were not significant 24 h after birth. This can provide a reference for future clinical studies.