BACKGROUND AND PURPOSE: As amide proton transfer imaging is sensitive to protein content and intracellular pH, it has been widely used in the nervous system, including brain tumors and stroke. This work aimed to measure the lactate content and amide proton transfer values in the basal ganglia of a neonatal piglet hypoxic-ischemic brain injury model by using MR spectroscopy and amide proton transfer imaging. MATERIALS AND METHODS: From 58 healthy neonatal piglets (3–5 days after birth; weight, 1–1.5 kg) selected initially, 9 piglets remained in the control group and 43 piglets, in the hypoxic-ischemic brain injury group. Single-section amide proton transfer imaging was performed at the coronal level of the basal ganglia. Amide proton transfer values of the bilateral basal ganglia were measured in all piglets. The ROI of MR spectroscopy imaging was the right basal ganglia, and the postprocessing was completed with LCModel software. RESULTS: After hypoxic-ischemic insult, the amide proton transfer values immediately decreased, and at 0–2 hours, they remained at their lowest level. Thereafter, they gradually increased and finally exceeded those of the control group at 48–72 hours. After hypoxic-ischemic insult, the lactate content increased immediately, was maximal at 2–6 hours, and then gradually decreased to the level of the control group. The amide proton transfer values were negatively correlated with lactate content (r = −0.79, P < .05). CONCLUSIONS: This observation suggests that after hypoxic-ischemic insult, the recovery of pH was faster than that of lactate homeostasis.

BACKGROUND AND PURPOSE: The neonatal brain has active energy metabolism, and glucose oxidation is the major energy source of brain tissue. Lactate is produced by astrocytes and released to neurons. In the central nervous system, lactate is transported between neurons and astrocytes via the astrocyte-neuron lactate shuttle. The aim of this study was to investigate the regulatory mechanisms of energy metabolism in neurons and astrocytes in the basal ganglia of a neonatal hypoxic-ischemic brain injury piglet model. MATERIALS AND METHODS: A total of 35 healthy piglets (3–5 days of age; 1.0–1.5 kg) were assigned to a control group (n = 5) or a hypoxic-ischemic model group (n = 30). The hypoxic-ischemic model group was further divided into 6 groups according to the ¹H-MR spectroscopy and PET/CT scan times after hypoxia-ischemia (0–2, 2–6, 6–12, 12–24, 24–48, and 48–72 hours; n = 5/group). ¹H-MR spectroscopy data were processed with LCModel software. Maximum standard uptake values refer to the maximum standard uptake values for glucose (or FDG). The maximum standard uptake values of the basal ganglia–to-occipital cortex ratio were analyzed. The expression levels of glucose transporters and monocarboxylate transporters were detected by immunohistochemical analysis. RESULTS: Lactate levels decreased after an initial increase, with the maximal level occurring around 2–6 hours following hypoxia-ischemia. After hypoxia-ischemia, the maximum standard uptake values of the basal ganglia and basal ganglia/occipital cortex initially increased then decreased, with the maximum occurring at approximately 6–12 hours. The lactate and glucose uptake (basal ganglia/occipital cortex maximum standard uptake values) levels were positively correlated. The expression levels of glucose transporter-1 and glucose transporter-3 were positively correlated with the basal ganglia/occipital cortex. The expression levels of monocarboxylic acid transporter-2 and monocarboxylic acid transporter-4 were positively correlated with lactate content. CONCLUSIONS: The results indicate that lactate and glucose transporters have a synergistic effect on the energy metabolism of neurons and astrocytes following hypoxic-ischemic reperfusion brain injury.

The objective of this study was to investigate the effects of diets supplemented with sodium stearoyl-2-lactylate (SSL), polyglycerol fatty acid ester (PGFE), and combined emulsifiers (0.02% SSL and 0.08% PGFE) on growth performance, nutrient digestibility and plasma lipid profiles in weaned piglets and to further evaluate the possible effects of feeding exogenous emulsifiers on digestive enzyme activities and liver bile acid (BA) metabolism. Twenty-eight barrows (age at 35 days, Duroc × Landrace × Yorkshire) with an initial body weight (BW) of 10.13±0.16 kg were randomly assigned to four dietary treatment groups (7 pigs/treatment). Dietary treatment groups included 1) basal diet (CTR); 2) basal diet with 0.1% SSL (SSL); 3) basal diet with 0.1% PGFE (PGFE); and 4) basal diet with 0.08% PGFE+0.02% SSL (PG-SL). SSL diet increased average daily gain (ADG) and average daily feed intake (ADFI) of piglets during d 0-17 (P < 0.05) compared with the CTR treatment. Piglets fed emulsifier diets experienced a significant improvement in the digestibility of nutrients (dry matter, crude protein, ether extract, energy, calcium and phosphorus) during the first 17 days (P < 0.05). The level of low-density lipoprotein cholesterol (LDL-C) was lower in the PGFE and PG-SL treatment groups than in the CTR treatment group (P < 0.05). Feeding emulsifier diets increased the lipase activity of the pancreas when compared with the CTR diet (P < 0.05). Moreover, the emulsifier diets significantly increased the mRNA expression of FXR (P < 0.05) and decreased the mRNA expression of CYP27A1 (P < 0.05) in the liver. In conclusion, the addition of emulsifiers improved nutrient digestibility and increased the mRNA expression of FXR BA receptors while inhibiting the mRNA expression of BA biosynthesis by CYP27A1 in weanling piglets.

Purpose.This study aims to evaluate the process of brain development in neonates using combined amide proton transfer (APT) imaging and conventional magnetization transfer (MT) imaging.Materials and Methods.Case data were reviewed for all patients hospitalized in our institution’s neonatal ward. Patients underwent APT and MT imaging (a single protocol) immediately following the routine MR examination. Single-slice APT/MT axial imaging was performed at the level of the basal ganglia. APT and MT ratio (MTR) measurements were performed in multiple brain regions of interest (ROIs). Data was statistically analyzed in order to assess for significant differences between the different regions of the brain or correlation with patient gestational age.Results.A total of 38 neonates were included in the study, with ages ranging from 27 to 41 weeks’ corrected gestational age. There were statistically significant differences in both APT and MTR measurements between the frontal lobes, basal ganglia, and occipital lobes (APT: frontal lobe versus occipital lobeP=0.031and other groupsP=0.00; MTR: frontal lobe versus occipital lobeP=0.034and other groupsP=0.00). Furthermore, APT and MTR in above brain regions exhibited positive linear correlations with patient gestational age.Conclusions.APT/MT imaging can provide valuable information about the process of the neonatal brain development at the molecular level.

JOURNAL/nrgr/04.03/01300535-202310000-00035/figure1/v/2026-05-25T160659Z/r/image-tiff Maintaining glutamate homeostasis after hypoxic ischemia is important for synaptic function and neural cell activity, and regulation of glutamate transport between astrocyte and neuron is one of the important modalities for reducing glutamate accumulation. However, further research is needed to investigate the dynamic changes in and molecular mechanisms of glutamate transport and the effects of glutamate transport on synapses. The aim of this study was to investigate the regulatory mechanisms underlying Notch pathway mediation of glutamate transport and synaptic plasticity. In this study, Yorkshire neonatal pigs (male, age 3 days, weight 1.0–1.5 kg, n = 48) were randomly divided into control (sham surgery group) and five hypoxic ischemia subgroups, according to different recovery time, which were then further subdivided into subgroups treated with dimethyl sulfoxide or a Notch pathway inhibitor (N-[N-(3, 5-difluorophenacetyl-l-alanyl)]-S-phenylglycine t-butyl ester). Once the model was established, immunohistochemistry, immunofluorescence staining, and western blot analyses of Notch pathway-related proteins, synaptophysin, and glutamate transporter were performed. Moreover, synapse microstructure was observed by transmission electron microscopy. At the early stage (6–12 hours after hypoxic ischemia) of hypoxic ischemic injury, expression of glutamate transporter excitatory amino acid transporter-2 and synaptophysin was downregulated, the number of synaptic vesicles was reduced, and synaptic swelling was observed; at 12–24 hours after hypoxic ischemia, the Notch pathway was activated, excitatory amino acid transporter-2 and synaptophysin expression was increased, and the number of synaptic vesicles was slightly increased. Excitatory amino acid transporter-2 and synaptophysin expression decreased after treatment with the Notch pathway inhibitor. This suggests that glutamate transport in astrocytes-neurons after hypoxic ischemic injury is regulated by the Notch pathway and affects vesicle release and synaptic plasticity through the expression of synaptophysin.