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A bstract We propose a novel modular anomaly equation for the unflavored Schur index in the N = 4 SU( N ) super-Yang-Mills theory. The vanishing conditions overdetermine the modular ambiguity ansatz from the equation, thus together they are sufficient to recursively compute the exact Schur indices for all SU( N ) gauge groups. Using the representations as MacMahon’s generalized sum-of-divisors functions and Jacobi forms, we then prove our proposal as well as elucidate a general formula conjectured by Pan and Peelaers.

A bstract Göttsche-Nakajima-Yoshioka K-theoretic blowup equations characterize the Nekrasov partition function of five dimensional N = 1 supersymmetric gauge theories compactified on a circle, which via geometric engineering correspond to the refined topological string theory on SU( N ) geometries. In this paper, we study the K-theoretic blowup equations for general local Calabi-Yau threefolds. We find that both vanishing and unity blowup equations exist for the partition function of refined topological string, and the crucial ingredients are the r fields introduced in our previous paper. These blowup equations are in fact the functional equations for the partition function and each of them results in infinite identities among the refined free energies. Evidences show that they can be used to determine the full refined BPS invariants of local Calabi-Yau threefolds. This serves an independent and sometimes more powerful way to compute the partition function other than the refined topological vertex in the A-model and the refined holomorphic anomaly equations in the B-model. We study the modular properties of the blowup equations and provide a procedure to determine all the vanishing and unity r fields from the polynomial part of refined topological string at large radius point. We also find that certain form of blowup equations exist at generic loci of the moduli space.

Growing evidence has implicated that myelin deficits and neuroinflammation are the coexisted pathological features that contribute to the mood swing and cognitive decline in major depressive disorder (MDD) and multiple sclerosis (MS). Therefore, attenuation of neuroinflammation and reduction of demyelination became newly emerging treatment strategies for the mood and cognitive symptoms. Antidepressant venlafaxine has been used in depression and anxiety through its multiple neuroprotective effects. However, it is unclear whether venlafaxine can improve myelin integrity and alter inflammation status in the brain. By using a well-established cuprizone-induced acute mouse model of demyelination, we investigated the protective effects of venlafaxine on these facets. The cuprizone-fed animals exhibited cognitive impairment and mood disturbances together with myelin loss and prominent neuroinflammation in the brain. Our present study showed that a high dose of venlafaxine alleviated the loss of myelin and oligodendrocytes (OLs), mitigated depression-like behaviors, and improved cognitive function in cuprizone-fed animals. Data from the present study also showed that venlafaxine reduced microglia-mediated inflammation in the brains of cuprizone-fed animals. These findings suggest that venlafaxine may exert its therapeutic effects facilitating myelin integrity and controlling neuroinflammation, which may provide extra benefits to MS patients with depression and anxiety beyond the symptom management.

Mesenchymal stem cells （MSCs） are progenitors of con- nective tissues, which have emerged as important tools for tissue engineering due to their differentiation potential along various cell types. In recent years, accumulating evidence has suggested that the regulation of mitochon- dria dynamics and function is essential for successful dif- ferentiation of MSCs. In this paper, we review and provide an integrated view on the role of mitochondria in MSC dif- ferentiation. The mitochondria are maintained at a relatively low activity level in MSCs, and upon induction, mtDNA copy number, protein levels of respiratory enzymes, the oxygen consumption rate, mRNA levels of mitochondrial biogene- sis-associated genes, and intracellular ATP content are increased. The regulated level of mitochondrial ROS is found not only to influence differentiation but also to con- tribute to the direction determination of differentiation. Understanding the roles of mitochondrial dynamics during MSC differentiation will facilitate the optimization of differ- entiation protocols by adjusting biochemical properties, such as energy production or the redox status of stem cells, and ultimately, benefit the development of new pharmacologic strategies in regenerative medicine.

Mitochondria are essential organelles for cellular metabolism and physiology in eukaryotic cells. Human mitochondria have their own genome (mtDNA), which is maternally inherited with 37 genes, encoding 13 polypeptides for oxidative phosphorylation, and 22 tRNAs and 2 rRNAs for translation. mtDNA mutations are associated with a wide spectrum of degenerative and neuromuscular diseases. However, the pathophysiology of mitochondrial diseases, especially for threshold effect and tissue specificity, is not well understood and there is no effective treatment for these disorders. Especially, the lack of appropriate cell and animal disease models has been significant obstacles for deep elucidating the pathophysiology of maternally transmitted diseases and developing the effective therapy approach. The use of human induced pluripotent stem cells (iPSCs) derived from patients to obtain terminally differentiated specific lineages such as inner ear hair cells is a revolutionary approach to deeply understand pathogenic mechanisms and develop the therapeutic interventions of mitochondrial disorders. Here, we review the recent advances in patients-derived iPSCs as ex vivo models for mitochondrial diseases. Those patients-derived iPSCs have been differentiated into specific targeting cells such as retinal ganglion cells and eventually organoid for the disease modeling. These disease models have advanced our understanding of the pathophysiology of maternally inherited diseases and stepped toward therapeutic interventions for these diseases.

A bstract We give evidence that the all genus amplitudes of topological string theory on compact elliptically fibered Calabi-Yau manifolds can be written in terms of meromorphic Jacobi forms whose weight grows linearly and whose index grows quadratically with the base degree. The denominators of these forms have a simple universal form with the property that the poles of the meromorphic form lie only at torsion points. The modular parameter corresponds to the fibre class while the rôle of the string coupling is played by the elliptic parameter. As a consequence the topological string amplitudes are modular and quasi periodic in the string coupling. This leads to very strong all genus results on these geometries, which are checked against results from curve counting. The structure can be viewed as an indication that an N = 2 analog of the reciprocal of the Igusa cusp form exists that might govern the topological string theory on these Calabi-Yau manifolds completely.

Insulator defect detection is of great significance to compromise the stability of the power transmission line. The state-of-the-art object detection network, YOLOv5, has been widely used in insulator and defect detection. However, the YOLOv5 network has limitations such as poor detection rate and high computational loads in detecting small insulator defects. To solve these problems, we proposed a light-weight network for insulator and defect detection. In this network, we introduced the Ghost module into the YOLOv5 backbone and neck to reduce the parameters and model size to enhance the performance of unmanned aerial vehicles (UAVs). Besides, we added small object detection anchors and layers for small defect detection. In addition, we optimized the backbone of YOLOv5 by applying convolutional block attention modules (CBAM) to focus on critical information for insulator and defect detection and suppress uncritical information. The experiment result shows the mean average precision (mAP) is set to 0.5, and the mAP is set from 0.5 to 0.95 of our model and can reach 99.4% and 91.7%; the parameters and model size were reduced to 3,807,372 and 8.79 M, which can be easily deployed to embedded devices such as UAVs. Moreover, the speed of detection can reach 10.9 ms/image, which can meet the real-time detection requirement.

Background Emerging research has reported that circular RNAs (circRNAs) play important roles in cardiac cell death after myocardial ischemia and reperfusion (I/R). Ferroptosis, a new form of cell death discovered in recent years, has been proven to participate in the regulation of myocardial I/R. This study used circRNA sequencing to explore the key circRNA in the regulation of cardiac ferroptosis after I/R and study the mechanisms of potential circRNA function. Methods We performed circRNA sequencing to explore circRNAs differentially expressed after myocardial I/R. We used quantitative polymerase chain reactions to determine the circRNA expression in different tissues and detect the circRNA subcellular localization in the cardiomyocyte. Gain- and loss-of-function experiments were aimed to examine the function of circRNAs in cardiomyocyte ferroptosis and cardiac tissue damage after myocardial I/R. RNA pull-down was applied to explore proteins interacting with circRNA. Results Here, we identified a ferroptosis-associated circRNA (FEACR) that has an underlying regulatory role in cardiomyocyte ferroptosis. FEACR overexpression suppressed I/R-induced myocardial infarction and ameliorated cardiac function. FEACR inhibition induces ferroptosis in cardiomyocytes and FEACR overexpression inhibits hypoxia and reoxygenation-induced ferroptosis. Mechanistically, FEACR directly bound to nicotinamide phosphoribosyltransferase (NAMPT) and enhanced the protein stability of NAMPT, which increased NAMPT-dependent Sirtuin1 (Sirt1) expression, which promoted the transcriptional activity of forkhead box protein O1 (FOXO1) by reducing FOXO1 acetylation levels. FOXO1 further upregulated the transcription of ferritin heavy chain 1 ( Fth1 ), a ferroptosis suppressor, which resulted in the inhibition of cardiomyocyte ferroptosis. Conclusions Our finding reveals that the circRNA FEACR-mediated NAMPT-Sirt1-FOXO1-FTH1 signaling axis participates in the regulation of cardiomyocyte ferroptosis and protects the heart function against I/R injury. Thus, FEACR and its downstream factors could be novel targets for alleviating ferroptosis-related myocardial injury in ischemic heart diseases.

A bstract We study the unflavored Schur indices in the N = 4 super-Yang-Mills theory for the B n , C n , D n , G 2 gauge groups. We explore two methods, namely the character expansion method and the Fermi gas method, to efficiently compute the q -series expansion of the Schur indices to some high orders. Using the available data and the modular properties, we are able to fix the exact formulas for the general gauge groups up to some high ranks and discover some interesting new features. We also identify some empirical modular anomaly equations, but unlike the case of A n groups, they are quite complicated and not sufficiently useful to fix exact formulas for gauge groups of arbitrary rank.