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Prevalence of obesity among infants and children below 5 years of age is rising dramatically, and early childhood obesity is a forerunner of obesity and obesity-associated diseases in adulthood. Childhood obesity is hence one of the most serious public health challenges today. Here, we have identified a mother-to-child lipid signaling that protects from obesity. We have found that breast milk-specific lipid species, so-called alkylglycerol-type (AKG-type) ether lipids, which are absent from infant formula and adult-type diets, maintain beige adipose tissue (BeAT) in the infant and impede the transformation of BeAT into lipid-storing white adipose tissue (WAT). Breast milk AKGs are metabolized by adipose tissue macrophages (ATMs) to platelet-activating factor (PAF), which ultimately activates IL-6/STAT3 signaling in adipocytes and triggers BeAT development in the infant. Accordingly, lack of AKG intake in infancy leads to a premature loss of BeAT and increases fat accumulation. AKG signaling is specific for infants and is inactivated in adulthood. However, in obese adipose tissue, ATMs regain their ability to metabolize AKGs, which reduces obesity. In summary, AKGs are specific lipid signals of breast milk that are essential for healthy adipose tissue development.

The present study sought to identify gene networks that are hallmarks of the developing inguinal subcutaneous adipose tissue (iWAT) and the interscapular brown adipose tissue (BAT) in the mouse. RNA profiling revealed that the iWAT of postnatal (P) day 6 mice expressed thermogenic and lipid catabolism transcripts, along with the abundance of transcripts associated with the beige adipogenesis program. This was an unexpected finding, as thermogenic BAT was believed to be the only site of nonshivering thermogenesis in the young mouse. However, the transcriptional landscape of BAT in P6 mice suggests that it is still undergoing differentiation and maturation, and that the iWAT temporally adopts thermogenic and lipolytic potential. Moreover, P6 iWAT and adult (P56) BAT were similar in their expression of immune gene networks, but P6 iWAT was unique in the abundant expression of antimicrobial proteins and virus entry factors, including a possible receptor for SARS-CoV-2. In summary, postnatal iWAT development is associated with a metabolic shift from thermogenesis and lipolysis towards fat storage. However, transcripts of beige-inducing signal pathways including β-adrenergic receptors and interleukin-4 signaling were underrepresented in young iWAT, suggesting that the signals for thermogenic fat differentiation may be different in early postnatal life and in adulthood.

The quantity and activation state of adipose tissue macrophages (ATMs) impact the development of obesity-induced metabolic diseases. Appetite-controlling hormones play key roles in obesity; however, our understanding of their effects on ATMs is limited. Here, we have shown that human and mouse ATMs express NPFFR2, a receptor for the appetite-reducing neuropeptide FF (NPFF), and that NPFFR2 expression is upregulated by IL-4, an M2-polarizing cytokine. Plasma levels of NPFF decreased in obese patients and high-fat diet-fed mice and increased following caloric restriction. NPFF promoted M2 activation and increased the proliferation of murine and human ATMs. Both M2 activation and increased ATM proliferation were abolished in NPFFR2-deficient ATMs. Mechanistically, the effects of NPFF involved the suppression of E3 ubiquitin ligase RNF128 expression, resulting in enhanced stability of phosphorylated STAT6 and increased transcription of the M2 macrophage-associated genes IL-4 receptor α (Il4ra), arginase 1 (Arg1), IL-10 (Il10), and alkylglycerol monooxygenase (Agmo). NPFF induced ATM proliferation concomitantly with the increase in N-Myc downstream-regulated gene 2 (Ndrg2) expression and suppressed the transcription of Ifi200 cell-cycle inhibitor family members and MAF bZIP transcription factor B (Mafb), a negative regulator of macrophage proliferation. NPFF thus plays an important role in supporting healthy adipose tissue via the maintenance of metabolically beneficial ATMs.

Childhood obesity is a serious public health crisis and a critical factor that determines future obesity prevalence. Signals affecting adipocyte development in early postnatal life have a strong potential to trigger childhood obesity; however, these signals are still poorly understood. We show here that mitochondrial (mt)RNA efflux stimulates transcription of nuclear-encoded genes for mitobiogenesis and thermogenesis in adipocytes of young mice and human infants. While cytosolic mtRNA is a potential trigger of the interferon (IFN) response, young adipocytes lack such a response to cytosolic mtRNA due to the suppression of IFN regulatory factor (IRF)7 expression by vitamin D receptor signalling. Adult and obese adipocytes, however, strongly express IRF7 and mount an IFN response to cytosolic mtRNA. In turn, suppressing IRF7 expression in adult adipocytes restores mtRNA-induced mitobiogenesis and thermogenesis and eventually mitigates obesity. Retrograde mitochondrion-to-nucleus signalling by mtRNA is thus a mechanism to evoke thermogenic potential during early adipocyte development and to protect against obesity. Hoang et al. show that mitochondrial RNA in young beige adipocytes triggers mitobiogenesis and thermogenesis, while an interferon response is avoided through vitamin D-mediated suppression of IRF7 expression.

Background and objectives: Obesity is an epidemic, noncommunicable, metabolic disease which can develop early in life, leading to a rapid and dramatic increase in the global prevalence of obesity-associated diseases. To avoid obesity, we have to understand the developing adipose tissue at the level of its molecular mechanisms and genomics.Hypothesis and aims: Gene expression changes and immune-metabolic mechanisms of the obese adipose tissue in adulthood are well studied, however we know much less about these in the developing adipose tissue. In this thesis we aimed to identify unique and defining transcriptional landscape and morphology of the adipose tissue in the early postnatal life. Furthermore, since fat catabolism is greater in early life than in adulthood, we hypothesize that adipocytes in the developing fat household a high amount of mitochondria to fulfil the demand of fat metabolism. It is plausible to assume that the extensive mitochondrial network may require a suppression of the immune response elicited by mitochondrial contents. Therefore, we searched for immune regulators, signals and mechanisms which favour mitochondrial network expansion.Results: We found that during postnatal development, infant fat depots contained beige adipocytes. We show that these adipocytes perform thermogenesis and develop independently from the brown adipose tissue (BAT). Thermogenic adipocytes in the early postnatal life expand their mitochondrial network by suppressing the innate immune recognition of mitochondrial DNA and RNA (mtDNA and mtRNA). This was achieved through a suppressed interferon (IFN) regulatory factor 7 (IRF7) expression. A unique mtRNA-driven signal mechanism triggers the mitobiogenesis and beige adipogenesis. The role of mtRNA is restricted to infant adipocytes, since adult adipocytes respond with an IFN burst after mtRNA exposure. Obesity increased IRF7 expression, leading to IFN response towards mitochondria, eventually impairing the mitochondrial network. Vit-D3 allows IFN-free, mtRNA-mediated mitobiogenesis in diet-induced obese adult mice which ultimately reduce obesity development.Summary and impact: This thesis showed that (i) beige adipocytes could be identified in the developing fat, and that (ii) maintaining these adipocytes´ mitochondria is key for the lipid catabolism and beige adipogenesis. These finding have impact on the adipose tissue field because it may add a 3rd adipocyte type which is present during infancy and has to be reestablishing in adulthood to potentially reduce obesity.

The quantity and activation state of adipose tissue macrophages (ATMs) impact the development of obesity-induced metabolic diseases. Appetite-controlling hormones play key roles in obesity; however, our understanding of their effects on ATMs is limited. Here, we have shown that human and mouse ATMs express NPFFR2, a receptor forthe appetite-reducing neuropeptide FF (NPFF), and that NPFFR2 expression is upregulated by IL-4, an M2-polarizing cytokine. Plasma levels of NPFF decreased in obese patients and high-fat diet-fed mice and increased following caloric restriction. NPFF promoted M2 activation and increased the proliferation of murine and human ATMs. Both M2 activation and increased ATM proliferation were abolished in NPFFR2-deficient ATMs. Mechanistically, the effects of NPFF involved the suppression of E3 ubiquitin ligase RNF128 expression, resulting in enhanced stability of phosphorylated STAT6 and increased transcription of the M2 macrophage-associated genes IL-4 receptor [alpha](lI/4ra), arginase 1 Arg1), IL-10 (lI10), and alkylglycerol monooxygenase (Agmo). NPFF induced ATM proliferation concomitantly with the increase in N-Myc downstream-regulated gene 2 (Ndrg2) expression and suppressed the transcription of Ifi200 cell-cycle inhibitor family members and MAF bZIP transcription factor B (Mafb), a negative regulator of macrophage proliferation. NPFF thus plays an important role in supporting healthy adipose tissue via the maintenance of metabolically beneficial ATMs.

Most of the existing chest X-ray datasets include labels from a list of findings without specifying their locations on the radiographs. This limits the development of machine learning algorithms for the detection and localization of chest abnormalities. In this work, we describe a dataset of more than 100,000 chest X-ray scans that were retrospectively collected from two major hospitals in Vietnam. Out of this raw data, we release 18,000 images that were manually annotated by a total of 17 experienced radiologists with 22 local labels of rectangles surrounding abnormalities and 6 global labels of suspected diseases. The released dataset is divided into a training set of 15,000 and a test set of 3,000. Each scan in the training set was independently labeled by 3 radiologists, while each scan in the test set was labeled by the consensus of 5 radiologists. We designed and built a labeling platform for DICOM images to facilitate these annotation procedures. All images are made publicly available in DICOM format along with the labels of both the training set and the test set. Measurement(s) diseases and abnormal findings from chest X-ray scans Technology Type(s) AI is used to detect diseases and abnormal findings Sample Characteristic - Location Vietnam

Biomass, one of the renewable resources, is expected to play an important role in the world’s energy future. In Asia, rice straw is an abundant agricultural surplus because rice is one of the leading staple food crops in the region. Often, rice straw is burned directly in the field via uncontrolled combustion methods that emit large amounts of short-lived air pollutants, greenhouse gases, and other pollutants. In Vietnam, the energy and environment protection sectors are facing great challenges because of rapid urbanisation and industrialisation. A national strategic choice is to exploit renewable energy, including biomass-derived energy, to achieve energy security and CO 2 emission reduction. This study investigates the potential of rice straw as an energy source for power plants at a local scale in Vietnam using data derived from satellite Sentinel-1 images. The results show that Vietnam can produce 2,565 MW from rice straw, for which 24 out of 63 provinces have a potential capacity higher than 30 MW, and the Kien Giang province has the highest capacity (245 MW). The study also analyses limitations and obstacles overcoming which can promote the biomass energy sector in the country.

Electrical impedance tomography (EIT)–guided positive end-expiratory pressure (PEEP) titration may optimize ventilation and reduce ventilator-induced lung injury in acute respiratory distress syndrome (ARDS). We compared EIT-guided PEEP with low PEEP/FiO₂ strategy in patients with moderate-to-severe ARDS. In this randomized controlled trial, 108 patients with PaO₂/FiO₂ below 200 mmHg were allocated to EIT-guided PEEP after a recruitment maneuver (n = 56) or low PEEP/FiO₂ strategy (n = 52). Patients in the EIT group underwent PEEP titration guided by the intersection point between alveolar overdistension and collapse during a decremental PEEP trial. Primary outcomes were oxygenation (PaO₂/FiO₂) and static compliance. Secondary outcomes included mortality, ventilator-free days, ICU stay, barotrauma, rescue therapies, and sequential organ failure assessment (SOFA) score changes. On day 1, oxygenation was higher with EIT (mean PaO₂/FiO₂ 180 vs. 159 mmHg; p = 0.036). Static compliance was greater at both day 1 (26 vs. 23 mL/cmH₂O; p = 0.016) and day 2 (27 vs. 24 mL/cmH₂O; p = 0.029). Driving pressure was lower with EIT at day 1 (16 vs. 17 cmH₂O; p < 0.001) and day 2 (15 vs. 17 cmH₂O; p = 0.005). SOFA scores improved more in the EIT group (day 1: − 1 vs. 0, p = 0.013; day 2: − 1 vs. − 0.5, p = 0.015). Twenty-eight–day mortality was lower with EIT (29 vs. 44%), although not statistically significant (p = 0.090). ICU stay, ventilation duration, barotrauma, ECMO use, and rescue therapies were similar. Benefits were most pronounced in patients with severe ARDS. EIT-guided PEEP improved oxygenation, lung mechanics, and reduced organ dysfunction in moderate-to-severe ARDS, particularly in severe cases. It showed a trend toward reduced mortality and may serve as a practical bedside tool for lung-protective ventilation. Larger multicenter trials are needed to confirm its clinical benefits. Trial registration: ClinicalTrials, NCT06733168. Registered on 13/12/2024, https://clinicaltrials.gov/study/NCT06733168 .