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Ischemic cerebrovascular disease (ICVD) is a major cause of mortality and disability worldwide and is often caused by atherosclerosis. As a systemic disease, atherosclerosis usually affects multiple vascular beds, mainly including cerebral, coronary, and peripheral arteries. Therefore, ICVD is easily complicated by lower-extremity peripheral arterial disease (PAD). ICVD patients with PAD have more serious symptoms and a worse prognosis, however, neurologists might neglect the evaluation and management of the coexistent PAD, and there is still a lack of consensuses about the diagnosis and treatment for such patients. By summarizing relevant research progresses, this review showed that duplex ultrasound had more advantages in the early screening and evaluation of PAD in ICVD patients among multiple methods to diagnose PAD. Furthermore, the current evidence seems to support that single-drug antiplatelet can be used as the basic treatment, and new antithrombotic strategies, such as ticagrelor only or aspirin combined with low-dose rivaroxaban are expected to further reduce the incidence of stroke for ICVD patients with PAD. More effective treatments would be explored by large-scale trials to guide the clinical management to prevent secondary stroke for such patients.

\"Luke Him Sau/Lu Qianshou (1904-1991) is best known internationally and in China as the architect of the iconic Bank of China Headquarters in Shanghai. One of the first Chinese students to be trained at the Architectural Association in London in the late 1920s, Luke's long, prolific and highly successful career in China and Hong Kong offers unique insights into an extraordinary period of Chinese political turbulence that scuppered the professional prospects and historical recognition of so many of his colleagues. Global interest in China has risen exponentially in recent times, creating an appetite for the country's history and culture. This book satiates this by providing a highly engaging and visual account of China's 20th-century architecture through the lens of one of the country's most distinguished yet overlooked designers. It features over 250 new colour photographs by Edward Denison of Luke's buildings and original archive material\"--Provided by publisher.

Age‐associated obesity and muscle atrophy (sarcopenia) are intimately connected and are reciprocally regulated by adipose tissue and skeletal muscle dysfunction. During ageing, adipose inflammation leads to the redistribution of fat to the intra‐abdominal area (visceral fat) and fatty infiltrations in skeletal muscles, resulting in decreased overall strength and functionality. Lipids and their derivatives accumulate both within and between muscle cells, inducing mitochondrial dysfunction, disturbing β‐oxidation of fatty acids, and enhancing reactive oxygen species (ROS) production, leading to lipotoxicity and insulin resistance, as well as enhanced secretion of some pro‐inflammatory cytokines. In turn, these muscle‐secreted cytokines may exacerbate adipose tissue atrophy, support chronic low‐grade inflammation, and establish a vicious cycle of local hyperlipidaemia, insulin resistance, and inflammation that spreads systemically, thus promoting the development of sarcopenic obesity (SO). We call this the metabaging cycle. Patients with SO show an increased risk of systemic insulin resistance, systemic inflammation, associated chronic diseases, and the subsequent progression to full‐blown sarcopenia and even cachexia. Meanwhile in many cardiometabolic diseases, the ostensibly protective effect of obesity in extremely elderly subjects, also known as the ‘obesity paradox’, could possibly be explained by our theory that many elderly subjects with normal body mass index might actually harbour SO to various degrees, before it progresses to full‐blown severe sarcopenia. Our review outlines current knowledge concerning the possible chain of causation between sarcopenia and obesity, proposes a solution to the obesity paradox, and the role of fat mass in ageing.

ObjectivesTo utilize a deep learning model for automatic detection of abnormalities in chest CT images from COVID-19 patients and compare its quantitative determination performance with radiological residents.MethodsA deep learning algorithm consisted of lesion detection, segmentation, and location was trained and validated in 14,435 participants with chest CT images and definite pathogen diagnosis. The algorithm was tested in a non-overlapping dataset of 96 confirmed COVID-19 patients in three hospitals across China during the outbreak. Quantitative detection performance of the model was compared with three radiological residents with two experienced radiologists’ reading reports as reference standard by assessing the accuracy, sensitivity, specificity, and F1 score.ResultsOf 96 patients, 88 had pneumonia lesions on CT images and 8 had no abnormities on CT images. For per-patient basis, the algorithm showed superior sensitivity of 1.00 (95% confidence interval (CI) 0.95, 1.00) and F1 score of 0.97 in detecting lesions from CT images of COVID-19 pneumonia patients. While for per-lung lobe basis, the algorithm achieved a sensitivity of 0.96 (95% CI 0.94, 0.98) and a slightly inferior F1 score of 0.86. The median volume of lesions calculated by algorithm was 40.10 cm3. An average running speed of 20.3 s ± 5.8 per case demonstrated the algorithm was much faster than the residents in assessing CT images (all p < 0.017). The deep learning algorithm can also assist radiologists make quicker diagnosis (all p < 0.0001) with superior diagnostic performance.ConclusionsThe algorithm showed excellent performance in detecting COVID-19 pneumonia on chest CT images compared with resident radiologists.Key Points• The higher sensitivity of deep learning model in detecting COVID-19 pneumonia were found compared with radiological residents on a per-lobe and per-patient basis.• The deep learning model improves diagnosis efficiency by shortening processing time.• The deep learning model can automatically calculate the volume of the lesions and whole lung.

Electrical stimulation (ES) is proposed as a therapeutic solution for managing chronic wounds. However, its widespread clinical adoption is limited by the requirement of additional extracorporeal devices to power ES‐based wound dressings. In this study, a novel sandwich‐structured photovoltaic microcurrent hydrogel dressing (PMH dressing) is designed for treating diabetic wounds. This innovative dressing comprises flexible organic photovoltaic (OPV) cells, a flexible micro–electro–mechanical systems (MEMS) electrode, and a multifunctional hydrogel serving as an electrode–tissue interface. The PMH dressing is engineered to administer ES, mimicking the physiological injury current occurring naturally in wounds when exposed to light; thus, facilitating wound healing. In vitro experiments are performed to validate the PMH dressing's exceptional biocompatibility and robust antibacterial properties. In vivo experiments and proteomic analysis reveal that the proposed PMH dressing significantly accelerates the healing of infected diabetic wounds by enhancing extracellular matrix regeneration, eliminating bacteria, regulating inflammatory responses, and modulating vascular functions. Therefore, the PMH dressing is a potent, versatile, and effective solution for diabetic wound care, paving the way for advancements in wireless ES wound dressings. A sandwich‐structured photovoltaic microcurrent hydrogel dressing (PMH dressing) for chronic bacteria‐infected diabetic wounds is developed. PMH dressing generates a biomimetic current under indoor light, which is delivered to the wound through the hydrogel interface. PMH dressing significantly enhances the healing of infected diabetic wounds through improved extracellular matrix regeneration, bacterial clearance, and regulation of inflammatory responses and vascular functions.

Patients with ischemic cerebrovascular disease (ICVD) frequently develop concomitant peripheral artery disease (PAD) or renal artery stenosis (RAS), and multiterritorial atherosclerotic patients usually have a worse prognosis. We aimed to evaluate the status of peripheral atherosclerosis (AS) and cervicocephalic AS (CAS) in ICVD patients with AS, their correlation, and related risk factors contributing to coexisting cervicocephalic-peripheral AS (CPAS). Based on the severity and extent of AS evaluated by computed tomography angiography and ultrasound, the degree of AS was triple categorized to assess the correlation between CAS and PAD/RAS. CAS and PAD/RAS were defined as the most severe stenosis being ≥ 50% luminal diameter in cervicocephalic or lower limb arteries, and a peak systolic velocity at the turbulent site being ≥ 180 cm/s in the renal artery. Among 403 patients with symptom onset within 30 days, CAS, PAD, and RAS occurrence rates were 68.7%, 25.3%, and 9.9%, respectively. PAD was independently associated with the degree of extracranial and intracranial CAS ( p  = 0.042, OR = 1.428, 95% CI 1.014–2.012; p  = 0.002, OR = 1.680, 95% CI 1.206–2.339), while RAS was independently associated with the degree of extracranial CAS ( p  = 0.001, OR = 2.880, 95% CI 1.556–5.329). Independent CPAS risk factors included an ischemic stroke history ( p  = 0.033), increased age ( p  < 0.01), as well as elevated fibrinogen ( p  = 0.021) and D-dimer levels ( p  = 0.019). In conclusion, the occurrence rates of RAS and PAD in ICVD patients with AS is relatively high, and with the severity of RAS or PAD increase, the severity of CAS also increase. Strengthening the evaluation of peripheral AS and controlling elevated fibrinogen might be crucial for preventing and delaying the progression of multiterritorial AS in ICVD patients with AS, thereby improving risk stratification and promoting more effective prevention and treatment strategies.

Early embryonic arrest and fragmentation (EEAF) is a common phenomenon leading to female infertility, but the genetic determinants remain largely unknown. The Moloney sarcoma oncogene ( MOS ) encodes a serine/threonine kinase that activates the ERK signaling cascade during oocyte maturation in vertebrates. Here, we identified four rare variants of MOS in three infertile female individuals with EEAF that followed a recessive inheritance pattern. These MOS variants encoded proteins that resulted in decreased phosphorylated ERK1/2 level in cells and oocytes, and displayed attenuated rescuing effects on cortical F‐actin assembly. Using oocyte‐specific Erk1/2 knockout mice, we verified that MOS‐ERK signal pathway inactivation in oocytes caused EEAF as human. The RNA sequencing data revealed that maternal mRNA clearance was disrupted in human mature oocytes either with MOS homozygous variant or with U0126 treatment, especially genes relative to mitochondrial function. Mitochondrial dysfunction was observed in oocytes with ERK1/2 deficiency or inactivation. In conclusion, this study not only uncovers biallelic MOS variants causes EEAF but also demonstrates that MOS‐ERK signaling pathway drives human oocyte cytoplasmic maturation to prevent EEAF. SYNOPSIS Biallelic variants in MOS gene cause recurrent early embryonic arrest and fragmentation (EEAF) and female infertility. MOS variants impair activation of MOS‐ERK signal cascade, prevent substantial maternal mRNAs decay and hamper embryonic development both in human and mice. Four rare variants in MOS gene were identified in three Chinese infertile females displaying EEAF followed recessive inheritance pattern. Mutant MOS proteins failed to activate ERK1/2 cascade, and Erk1/2 ‐deficient mice also exhibited EEAF, confirming the human diagnostic. MOS‐ERK1/2 signal cascade is required for maternal mRNA clearance during human oocyte maturation, especially of transcripts relative to mitochondrial function. Inactivation of human or mouse MOS‐ERK1/2 signal cascade caused mitochondrial dysfunction in mature oocytes. Graphical Abstract Biallelic variants in MOS gene cause recurrent early embryonic arrest and fragmentation (EEAF) and female infertility. MOS variants impair activation of MOS‐ERK signal cascade, prevent substantial maternal mRNAs decay and hamper embryonic development both in human and mice.

Some scholars have shown that metal nanoparticles have excellent antibacterial properties and can be used as a new type of antibacterial agent. In recent years, with the in-depth research on nanomaterials, its applications in the medical field have gradually increased. The oral cavity has a unique anatomical structure, and for oral infections, the current clinically commonly used treatment measures are oral or topical antibiotics. However, due to bacterial resistance and the special structure of dental plaque, the effect of antibiotics is not ideal. Metal and metal oxide nanoparticles have become the research hotspot of new antibacterial materials due to their small particles, large specific surface area, physical, mechanical, and chemical properties, and antibacterial properties. This article describes the antibacterial effect, antibacterial mechanism, biological toxicity, and application progress of metal nanomaterials in the oral cavity.

PINK1-Parkin mediated mitophagy, a selective form of autophagy, represents one of the most important mechanisms in mitochondrial quality control (MQC) via the clearance of damaged mitochondria. Although it is well known that the conjugation of mammalian ATG8s (mATG8s) to phosphatidylethanolamine (PE) is a key step in autophagy, its role in mitophagy remains controversial. In this study, we clarify the role of the mATG8-conjugation system in mitophagy by generating knockouts of the mATG8-conjugation machinery. Unexpectedly, we show that mitochondria could still be cleared in the absence of the mATG8-conjugation system, in a process independent of lysosomal degradation. Instead, mitochondria are cleared via extracellular release through a secretory autophagy pathway, in a process we define as Autophagic Secretion of Mitochondria (ASM). Functionally, increased ASM promotes the activation of the innate immune cGAS-STING pathway in recipient cells. Overall, this study reveals ASM as a mechanism in MQC when the cellular mATG8-conjugation machinery is dysfunctional and highlights the critical role of mATG8 lipidation in suppressing inflammatory responses. The mechanisms underlying mitochondrial quality control are not fully understood. Here the authors identify a switch from degradative to secretory autophagy in the absence of the mATG8-conjugation system, termed Autophagic Secretion of Mitochondria.