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Purpose Convolution operator-based neural networks have shown great success in medical image segmentation over the past decade. The U-shaped network with a codec structure is one of the most widely used models. Transformer, a technology used in natural language processing, can capture long-distance dependencies and has been applied in Vision Transformer to achieve state-of-the-art performance on image classification tasks. Recently, researchers have extended transformer to medical image segmentation tasks, resulting in good models. Methods This review comprises publications selected through a Web of Science search. We focused on papers published since 2018 that applied the transformer architecture to medical image segmentation. We conducted a systematic analysis of these studies and summarized the results. Results To better comprehend the benefits of convolutional neural networks and transformers, the construction of the codec and transformer modules is first explained. Second, the medical image segmentation model based on transformer is summarized. The typically used assessment markers for medical image segmentation tasks are then listed. Finally, a large number of medical segmentation datasets are described. Conclusion Even if there is a pure transformer model without any convolution operator, the sample size of medical picture segmentation still restricts the growth of the transformer, even though it can be relieved by a pretraining model. More often than not, researchers are still designing models using transformer and convolution operators.

We aimed to evaluate the effects of the COVID-19 lock down on lifestyle in China during the initial stage of the pandemic. A questionnaire was distributed to Chinese adults living in 31 provinces of China via the internet using a snowball sampling strategy. Information on 7-day physical activity recall, screen time, and emotional state were collected between January 24 and February 2, 2020. ANOVA, χ² test, and Spearman’s correlation coefficients were used for statistical analysis. 12,107 participants aged 18–80 years were included. During the initial phase of the COVID-19 outbreak, nearly 60% of Chinese adults had inadequate physical activity (95% CI 56.6%–58.3%), which was more than twice the global prevalence (27.5%, 25.0%–32.2%). Their mean screen time was more than 4 hours per day while staying at home (261.3 ± 189.8 min per day), and the longest screen time was found in young adults (305.6 ± 217.5 min per day). We found a positive and significant correlation between provincial proportions of confirmed COVID-19 cases and negative affect scores (r = 0.501, p = 0.004). Individuals with vigorous physical activity appeared to have a better emotional state and less screen time than those with light physical activity. During this nationwide lockdown, more than half of Chinese adults temporarily adopted a sedentary lifestyle with insufficient physical activity, more screen time, and poor emotional state, which may carry considerable health risks. Promotion of home-based self-exercise can potentially help improve health and wellness.

Cancer cells exhibit altered and usually increased metabolic processes to meet their high biogenetic demands 1 , 2 . Under these conditions, ammonia is concomitantly produced by the increased metabolic processing. However, it is unclear how tumour cells dispose of excess ammonia and what outcomes might be caused by the accumulation of ammonia. Here we report that the tumour suppressor p53, the most frequently mutated gene in human tumours, regulates ammonia metabolism by repressing the urea cycle. Through transcriptional downregulation of CPS1 , OTC and ARG1 , p53 suppresses ureagenesis and elimination of ammonia in vitro and in vivo, leading to the inhibition of tumour growth. Conversely, downregulation of these genes reciprocally activates p53 by MDM2-mediated mechanism(s). Furthermore, the accumulation of ammonia causes a significant decline in mRNA translation of the polyamine biosynthetic rate-limiting enzyme ODC, thereby inhibiting the biosynthesis of polyamine and cell proliferation. Together, these findings link p53 to ureagenesis and ammonia metabolism, and further reveal a role for ammonia in controlling polyamine biosynthesis and cell proliferation. p53 regulates the metabolism of ammonia by repressing genes of the urea cycle that function to eliminate excess ammonia.

Ischemic diseases, the leading cause of disability and death, are caused by the stenosis or obstruction of arterioles/capillaries that is not compensated for by vessel dilatation or collateral circulation. Angiogenesis is a complex process leading to new blood vessel formation and is triggered by ischemic conditions. Adequate angiogenesis, as a compensatory mechanism in response to ischemia, may increase oxygen and nutrient supplies to tissues and protect their function. Therapeutic angiogenesis has been the most promising therapy for treating ischemic diseases. In recent years, stem cell transplantation has been recognized as a new technique with therapeutic angiogenic effects on ischemic diseases. Adipose-derived stem cells, characterized by their ease of acquisition, high yields, proliferative growth, and low immunogenicity, are an ideal cell source. In this review, the characterization of adipose-derived stem cells and the role of angiogenesis in ischemic attack are summarized. The angiogenic effects of adipose-derived stem cells are discussed from the perspectives of in-vitro, in-vivo, and clinical trial studies for the treatment of ischemic diseases, including ischemic cardiac, cerebral, and peripheral vascular diseases and wound healing. The microvesicles/exosomes released from adipose-derived stem cells are also presented as a novel therapeutic prospect for treating ischemic diseases.

Ischemic heart disease (IHD) is caused by the narrowing of arteries that work to provide blood, nutrients, and oxygen to the myocardial tissue. The worldwide epidemic of IHD urgently requires innovative treatments despite the significant advances in medical, interventional, and surgical therapies for this disease. Angiogenesis is a physiological and pathophysiological process that initiates vascular growth from pre-existing blood vessels in response to a lack of oxygen. This process occurs naturally over time and has encouraged researchers and clinicians to investigate the outcomes of accelerating or enhancing this angiogenic response as an alternative IHD therapy. Therapeutic angiogenesis has been shown to revascularize ischemic heart tissue, reduce the progression of tissue infarction, and evade the need for invasive surgical procedures or tissue/organ transplants. Several approaches, including the use of proteins, genes, stem/progenitor cells, and various combinations, have been employed to promote angiogenesis. While clinical trials for these approaches are ongoing, microvesicles and exosomes have recently been investigated as a cell-free approach to stimulate angiogenesis and may circumvent limitations of using viable cells. This review summarizes the approaches to accomplish therapeutic angiogenesis for IHD by highlighting the advances and challenges that addresses the applicability of a potential pro-angiogenic medicine.

Cisplatin (DDP) was reported to improve pathological complete response (pCR) rates in triple-negative breast cancer (TNBC) patients, however, the molecular mechanism still remains largely unknown. Emerging evidence suggested that some chemotherapeutic drugs played anti-tumor effects by inducing cell pyroptosis. Nevertheless, whether pyroptosis contributes to the DDP-induced anti-tumor effect in TNBC remains unexploited. In the present study, NLRP3/caspase-1/GSDMD pyroptosis pathway was involved in the DDP-induced anti-tumor effect of TNBC and , providing evidence that DDP might induce pyroptosis in TNBC. Moreover, DDP activated NLRP3/caspase-1/GSDMD pyroptosis pathway by up-regulating the long non-coding RNA (lncRNA) maternally expressed gene 3 (MEG3). Furthermore, knockdown of MEG3 not only partly abolished the activation effect of DDP on NLRP3/caspase-1/GSDMD pathway-mediated pyroptosis, but also reversed the suppression of DDP on tumor growth and metastasis ability and further confirming that MEG3 may partially mediate the pyroptotic signaling upon DDP treatment. Thus, our data uncovered a novel mechanism that DDP induced pyroptosis via activation of MEG3/NLRP3/caspase-1/GSDMD pathway in TNBC to exert anti-tumor effects, which may help to develop new strategies for the therapeutic interventions in TNBC.

Relative fat mass (RFM) is a novel indicator for measuring body fat. This cross-section study aims to explore the association between RFM and periodontitis and to investigate possible effect modifiers in U.S. adults based on the National Health and Nutrition Examination Survey 2009–2014. The category of periodontitis was defined by the CDC/AAP. Mean clinical attachment loss and mean pocket probing depth (PPD) were calculated. The RFM formula is: 64 − (20 × height/WC) + (12 × sex), with sex coded as 1 for female and 0 for male. Natural cubic spline and weighted multivariable regression analyses were conducted to investigate the relationship between RFM and periodontal status. Subgroup and interaction analyses were also employed to assess the moderating roles of age, gender, and race. A total of 10,307 participants were included in our study. Compared to the lowest quartiles, individuals in the highest quartiles of RFM levels were more likely to have moderate/severe periodontitis (OR Q4vs1  = 1.64, 95% CI 1.30–2.06) and had a higher mean PPD (β Q4vs1  = 0.15, 95% CI 0.09–0.22). This association was particularly stronger in populations under the age of 60, with significant interactions. Taken together, RFM is positively associated with periodontitis, particularly in those under 60 years old.

Long non-coding RNA (lncRNA) maternally expressed gene 3 (MEG3) has been demonstrated as an important regulator in diverse human cancers. However, its function and regulatory mechanism in ischemic stroke remains largely unknown. Here, we report that MEG3 is physically associated with microRNA-21 (miR-21), while miR-21 is downregulated following ischemia in the ischemic core in vitro and in vivo , which is opposite to MEG3. Besides, overexpression of miR-21 protects oxygen–glucose deprivation and reoxygenation (OGD/R)-induced apoptotic cell death. Furthermore, MEG3 functions as a competing endogenous RNAs (ceRNAs) and competes with programmed cell death 4 (PDCD4) mRNA for directly binding to miR-21, which mediates ischemic neuronal death. Knockdown of MEG3 protects against ischemic damage and improves overall neurological functions in vivo . Thus, our data uncovers a novel mechanism of lncRNA MEG3 as a ceRNA by targeting miR-21/PDCD4 signaling pathway in regulating ischemic neuronal death, which may help develop new strategies for the therapeutic interventions in cerebral ischemic stroke.

Tumor drug resistance presents a growing challenge in medical practice, particularly during anti-cancer therapies, where the emergence of drug-resistant cancer cells significantly complicates clinical treatment. In recent years, three-dimensional (3D) tumor culture technology, which more effectively simulates the in vivo physiological environment, has gained increasing attention in tumor drug resistance research and clinical applications. By mimicking the in vivo cellular microenvironment, 3D tumor culture technology not only recapitulates cell-cell interactions but also more faithfully reproduces the biological effects of therapeutic agents. Consequently, 3D tumor culture technology is emerging as a crucial tool in biomedical and clinical research. We summarize the benefits of 3D culture models and organoid technology, explore their application in the realm of drug resistance, drug screening, and personalized therapy, and discuss their potential application prospects and challenges in clinical transformation, with the aim of providing insights for optimizing cancer treatment strategies and advancing precision therapy.

Enhancing corrosion resistance is essential for developing efficient electrocatalysts for acidic oxygen evolution reaction (OER). Herein, we report the strategic manipulation of the local compressive strain to reinforce the anti-corrosion properties of the non-precious Co 3 O 4 support. The incorporation of Ru single atoms, larger in atomic size than Co, into the Co 3 O 4 lattice (Ru-Co 3 O 4 ), triggers localized strain compression and lattice distortion on the Co-O lattice. A comprehensive exploration of the correlation between this specific local compressive strain and electrocatalytic performance is conducted through experimental and theoretical analyses. The presence of the localized strain in Ru-Co 3 O 4 is confirmed by operando X-ray absorption studies and supported by quantum calculations. This local strain, presented in a shortened Co-O bond length, enhances the anti-corrosion properties of Co 3 O 4 by suppressing metal dissolutions. Consequently, Ru-Co 3 O 4 shows satisfactory stability, maintaining OER for over 400 hours at 30 mA cm −2 with minimal decay. This study demonstrates the potential of the local strain effect in fortifying catalyst stability for acidic OER and beyond. Enhancing corrosion resistance is crucial for efficient electrocatalysts in the acidic oxygen evolution reaction. Here, the authors report the strategic manipulation of local compressive strain to improve the anti-corrosion properties of Co3O4, demonstrating stability for over 400 hours at 30 mA cm -2 .