A daily body temperature rhythm (BTR) is critical for the maintenance of homeostasis in mammals. While mammals use internal energy to regulate body temperature, ectotherms typically regulate body temperature behaviorally [1]. Some ectotherms maintain homeostasis via a daily temperature preference rhythm (TPR) [2], but the underlying mechanisms are largely unknown. Here, we show that Drosophila exhibit a daily circadian clock dependent TPR that resembles mammalian BTR. Pacemaker neurons critical for locomotor activity are not necessary for TPR; instead, the dorsal neuron 2s (DN2s), whose function was previously unknown, is sufficient. This indicates that TPR, like BTR, is controlled independently from locomotor activity. Therefore, the mechanisms controlling temperature fluctuations in fly TPR and mammalian BTR may share parallel features. Taken together, our results reveal the existence of a novel DN2- based circadian neural circuit that specifically regulates TPR; thus, understanding the mechanisms of TPR will shed new light on the function and neural control of circadian rhythms.

The major complication associated with protein replacement therapy currently used in the treatment of hemophilia B (HB) is the development of antibodies to the infused human Factor IX (hF.IX). We hypothesized that vector-mediated expression of hF.IX, either at a prenatal stage or early in life may lead to tolerance to hF.IX and long-term transgene expression. Fetal, neonatal, and adult F.IX-deficient mice were injected with AAV-1-hF.IX, and the hF.IX levels as well as antibodies to hF.IX in the circulation were assayed. In utero injection followed by postnatal re-administration of adeno-associated virus 1 (AAV-1) vector achieved persistent expression of hF.IX in all animals, with no cellular or humoral immune response to F.IX. Similar results were seen after initial injection in neonatal mice followed by re-administration, whereas all mice injected at the adult stage developed antibodies to hF.IX. In contrast, after administration of AAV-2-hF.IX in the neonatal period, antibodies to hF.IX were formed in all the injected animals. We conclude that in utero or neonatal-stage injection of AAV-1-hF.IX can lead to long-term expression and absence of immune response. The differences in immune response between the AAV-1 and AAV-2 groups suggests that tolerance may be related to differences in bio-distribution, timing of expression, and/or the initial levels of hF.IX expression. This supports the concept of a narrow "window of opportunity" for tolerance induction.

Supplementation of selenium (Se) is a common practice in the poultry industry via sodium selenite (SS) and selenium yeast (SY), while the effects of nano-selenium (NS) on laying hens are poorly known. This study aimed to compare the effects of NS, SS, and SY on productivity; selenium (Se) deposition in eggs; and antioxidant capacity in laying hens. A total of 288 30-week-old Brown Hy-line laying hens were randomly assigned into four dietary treatments, which included corn-soybean meal basal diet (Con) without Se sources and basal diets supplemented with 0.3 mg Se/kg as SS, SY, or NS, respectively. The results exhibited that Se-supplemented treatments achieved greater egg production, egg weight, and daily egg mass, also better feed conversion ratio than Con group (p < 0.05). Se supplementation significant increased egg Se concentration and decreased the egg Se deposition efficiency (p < 0.05), while SY or NS supplementation had higher Se deposition efficiency than SS group at 35 days (p < 0.05). Moreover, serum glutathione peroxidase (GSH-Px) activity increased in SS or NS group compared to Con group (p < 0.05). The glutathione peroxidase 4 (GPX-4) mRNA levels in liver were significantly higher (p < 0.05) in SS or SY group than in NS group, and mRNA levels of the methionine (Met) metabolism gene glycine N-methyltranserfase (GNMT) were markedly upregulated (p < 0.05) in SY group compared to SS or NS group. Taken together, the results revealed Se from SY is deposited into eggs more efficiently than Se from NS or SS, probably via enhancing the route of Met metabolism. Meanwhile, it might be concluded that SS or SY supplementation directly regulated GSH-Px activity via enhancing GPx4 level, whereas NS via GPx1, thus affecting body oxidation and development.

Nucleotide plays an important role in the regulation of cellular energy and protein homeostasis. The objective of the current study was to investigate the cumulative effects of maternal supplementation with nucleotides in the form of uridine (UR) on fatty acids and amino acids constituents of neonatal piglets. A total of 52 pregnant sows with similar parity were assigned randomly and equally into the control (CON) group (fed a basal diet) or UR group (fed a basal diet with 150g/t UR). The experiment started on d 85 of gestation and ended on the day of delivery. The reproductive performance was recorded, and placenta, blood and liver samples of neonatal piglets were collected before consuming colostrum during farrowing. Results showed that supplementing with UR in sow’ diet significantly decreased the birth mortality of pigs (P = 0.05). In addition, maternal dietary UR supplementation increased serum total cholesterol (CHOL), high-density lipoprotein (HDL) and low-density lipoprotein (LDL) of neonatal piglets (P < 0.05). Moreover, the amino acid profile of serum and liver of neonatal piglets was affected by the addition of UR in sows’ diets (P<0.05). Furthermore, an up-regulation of mRNA expression of energy metabolism-related genes, including fatty acid elongase 5 (ELOVL5), fatty acid desaturase 1 (FADS1), hormone-sensitive lipase (HSL) and cholesterol- 7a-hydroxylase (CYP7a1), was observed in the liver of neonates from the UR group. Additionally, a decrease in placental gene expression of excitatory amino acid transporters 2 (EAAT2), excitatory amino acid transporters 3 (EAAT3), neutral AA transporter 1(LAT1) in UR group was concurrently observed (P<0.05), and higher protein expression of phosphorylated protein kinase B (P-AKT), raptor, peroxisome proliferator activated receptor α (PPARα) and PPARγ in placenta from UR group was also observed, (P<0.05). Together, these results showed that maternal UR supplementation could regulate the nutrients transport of placenta, largely in response to an alteration of mTORC1-PPARs signaling, thus regulating the nutrition metabolism of neonatal piglets, and improving reproductive performance.