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The recognition of food images is of great significance for nutrition monitoring, food retrieval and food recommendation. However, the accuracy of recognition had not been high enough due to the complex background of food images and the characteristics of small inter-class differences and large intra-class differences. To solve these problems, this paper proposed a food image recognition method based on transfer learning and ensemble learning. Firstly, generic image features were extracted by using the convolutional neural network models (VGG19, ResNet50, MobileNet V2, AlexNet) pre-trained on the ImageNet dataset. Secondly, the 4 pre-trained models were transferred to the food image dataset for model fine-tuning. Finally, different basic learner combination strategies were adopted to establish the ensemble model and classify feature information. In this paper, several kinds of experiments were performed to compare the results of food image recognition between single models and ensemble models on food-11 dataset. The experimental results demonstrated that the accuracy of the ensemble model was the highest, reaching 96.88%, which was superior to any base learner. Therefore, the convolutional neural network model based on transfer learning and ensemble learning has strong learning ability and generalization ability, and it is feasible and practical to apply the method to food image recognition.

Amyloid-β (Aβ) accumulation in the brain is a pivotal event in the pathogenesis of Alzheimer’s disease (AD), and its clearance from the brain is impaired in sporadic AD. Previous studies suggest that approximately half of the Aβ produced in the brain is cleared by transport into the periphery. However, the mechanism and pathophysiological significance of peripheral Aβ clearance remain largely unknown. The kidney is thought to be responsible for Aβ clearance, but direct evidence is lacking. In this study, we investigated the impact of unilateral nephrectomy on the dynamic changes in Aβ in the blood and brain in both humans and animals and on behavioural deficits and AD pathologies in animals. Furthermore, the therapeutic effects of the diuretic furosemide on Aβ clearance via the kidney were assessed. We detected Aβ in the kidneys and urine of both humans and animals and found that the Aβ level in the blood of the renal artery was higher than that in the blood of the renal vein. Unilateral nephrectomy increased brain Aβ deposition; aggravated AD pathologies, including Tau hyperphosphorylation, glial activation, neuroinflammation, and neuronal loss; and aggravated cognitive deficits in APP/PS1 mice. In addition, chronic furosemide treatment reduced blood and brain Aβ levels and attenuated AD pathologies and cognitive deficits in APP/PS1 mice. Our findings demonstrate that the kidney physiologically clears Aβ from the blood, suggesting that facilitation of Aβ clearance via the kidney represents a novel potential therapeutic approach for AD.

Infections have been hypothesised to increase the risk for dementia; however, whether infections are potentially causative of dementia is unclear.2 In The Lancet Infectious Diseases, Pyry Sipilä and colleagues investigated whether hospital-treated infections increased the risk of different types of dementia.3 Associations between infectious diseases (consisting of bacterial, viral, parasitic, and fungal infections) and the subsequent incidence of dementias (comprising vascular dementia, Alzheimer's disease, frontotemporal dementia, Parkinson's disease dementia, and other or unspecified dementias) were assessed in three prospective cohorts consisting of 260 490 Finnish participants without incident dementia with a median follow-up of about 15·4 years (IQR 9·8–21·0) and then confirmed in another independent cohort of 485 708 individuals from the UK Biobank. [...]the findings were reliable in facilitating the understanding of the relationship between infectious diseases and dementia incidence. Patients with COVID-19 do present with mental and neurological symptoms at the acute stage of infection.6 Inflammatory cytokine storms occurring in patients with COVID-19 might cause long-lasting sequelae in the brain. [...]more attention should be given to the effects of COVID-19 on long-term cognitive decline later in life, including Alzheimer's disease and other dementias.

Deficits in the clearance of amyloid β-protein (Aβ) play a pivotal role in the pathogenesis of sporadic Alzheimer’s disease (AD). The roles of blood monocytes in the development of AD remain unclear. In this study, we sought to investigate the alterations in the Aβ phagocytosis function of peripheral monocytes during ageing and in AD patients. A total of 104 cognitively normal participants aged 22–89 years, 24 AD patients, 25 age- and sex-matched cognitively normal (CN) subjects, 15 Parkinson’s disease patients (PD), and 15 age- and sex-matched CN subjects were recruited. The Aβ uptake by blood monocytes was measured and its alteration during ageing and in AD patients were investigated. Aβ 1-42 uptake by monocytes decreased during ageing and further decreased in AD but not in PD patients. Aβ 1-42 uptake by monocytes was associated with Aβ 1-42 levels in the blood. Among the Aβ uptake-related receptors and enzymes, the expression of Toll-like receptor 2 (TLR2) was reduced in monocytes from AD patients. Our findings suggest that monocytes regulate the blood levels of Aβ and might be involved in the development of AD. The recovery of the Aβ uptake function by blood monocytes represents a potential therapeutic strategy for AD.

It was reported that either orexigenic neuropeptide galanin or anorexigenic hormone leptin caught benefit insulin sensitivity through increasing the translocation of glucose transporter 4 (GLUT4) in patients with diabetes. To date, it is unknown whether galanin can potentiate the effect of leptin on alleviation of insulin resistance. Therefore, in the current study we sought to assess the combined effect of central leptin and galanin on insulin resistance in the adipose tissues of type 2 diabetic rats. Galanin and leptin were injected into the intracerebroventricle of the diabetic rats, respectively, or cooperatively once a day for 2 weeks. Then, several indexes of insulin resistance were examined. The results showed that glucose infusion rates in the hyperinsulinaemic‐euglycaemic clamp test, plasma adiponectin content and GLUT4 translocation, as well as Akt phosphorylation in fat cells, were higher, not GLUT4 protein and GLUT4 mRNA expression, but HOMA index was lower in the galanin + leptin group than either one of them. Furthermore, treatment with MK‐2206, an Akt inhibitor, blocked the combined effects of galanin + leptin on alleviation of insulin resistance. These results suggest that galanin can improve the leptin‐induced mitigative effects on insulin resistance in the fat cells, and those provided new insights into the potential tactics for prevention and remedy of insulin resistance.

Amyloid-beta (Aβ) plays a pivotal role in the pathogenesis of Alzheimer’s disease (AD). The physiological capacity of peripheral tissues and organs in clearing brain-derived Aβ and its therapeutic potential for AD remains largely unknown. Here, we measured blood Aβ levels in different locations of the circulation in humans and mice, and used a parabiosis model to investigate the effect of peripheral Aβ catabolism on AD pathogenesis. We found that blood Aβ levels in the inferior/posterior vena cava were lower than that in the superior vena cava in both humans and mice. In addition, injected 125 I labeled Aβ40 was located mostly in the liver, kidney, gastrointestinal tract, and skin but very little in the brain; suggesting that Aβ derived from the brain can be cleared in the periphery. Parabiosis before and after Aβ deposition in the brain significantly reduced brain Aβ burden without alterations in the expression of amyloid precursor protein, Aβ generating and degrading enzymes, Aβ transport receptors, and AD-type pathologies including hyperphosphorylated tau, neuroinflammation, as well as neuronal degeneration and loss in the brains of parabiotic AD mice. Our study revealed that the peripheral system is potent in clearing brain Aβ and preventing AD pathogenesis. The present work suggests that peripheral Aβ clearance is a valid therapeutic approach for AD, and implies that deficits in the Aβ clearance in the periphery might also contribute to AD pathogenesis.

Keywords: Alzheimer's disease, Blood exchange, A[beta] clearance, Systemic factors

Alzheimer's disease (AD) is a neurodegenerative disease that involves multiple systems in the body. Numerous recent studies have revealed bidirectional crosstalk between the brain and bone, but the interaction between bone and brain in AD remains unclear. In this review, we summarize human studies of the association between bone and brain and provide an overview of their interactions and the underlying mechanisms in AD. We review the effects of AD on bone from the aspects of AD pathogenic proteins, AD risk genes, neurohormones, neuropeptides, neurotransmitters, brain‐derived extracellular vesicles (EVs), and the autonomic nervous system. Correspondingly, we elucidate the underlying mechanisms of the involvement of bone in the pathogenesis of AD, including bone‐derived hormones, bone marrow‐derived cells, bone‐derived EVs, and inflammation. On the basis of the crosstalk between bone and the brain, we propose potential strategies for the management of AD with the hope of offering novel perspectives on its prevention and treatment. Highlights The pathogenesis of AD, along with its consequent changes in the brain, may involve disturbing bone homeostasis. Degenerative bone disorders may influence the progression of AD through a series of pathophysiological mechanisms. Therefore, relevant bone intervention strategies may be beneficial for the comprehensive management of AD.

Alzheimer’s disease (AD), the most common type of dementia, is becoming a major challenge for global health and social care. However, the current understanding of AD pathogenesis is limited, and no early diagnosis and disease-modifying therapy are currently available. During the past year, significant progress has been made in clinical research on the diagnosis, prevention, and treatment of AD. In this review, we summarize the latest achievements, including diagnostic biomarkers, polygenic hazard score, amyloid and tau PET imaging, clinical trials targeting amyloid-beta (Aβ), tau, and neurotransmitters, early intervention, and primary prevention and systemic intervention approaches, and provide novel perspectives for further efforts to understand and cure the disease.

Building operational energy consumption accounts for a significant share of global energy consumption, and it is crucial to promote renewable energy self-sufficiency and operational optimization for zero-carbon buildings. However, scheduling strategies relying on day-ahead forecasts have limitations, and ignoring the ambiguity of short-term source-load forecasts is prone to the risk of scheduling failures. To address this issue, this study proposes an intraday optimization method for zero-carbon buildings under the source-load fuzzy space, which innovatively constructs a fuzzy chance constraint model of Photovoltaic (PV) output and load demand, enforces energy self-sufficiency as a constraint, and establishes a multi-objective optimization framework with thermal comfort as the main objective and power adjustment balance as the sub-objective, so as to quantify the decision risk through intraday energy optimization. Experiments show that the proposed method quantifies the decision-maker’s risk preference through fuzzy opportunity constraints, balances conservatism and aggressive strategies, and improves thermal comfort while safeguarding energy independence, providing a risk-controllable scheduling paradigm for the decarbonized operation of buildings.