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Abstract •we report the case of a 36-year-old female patient who presented to our hospital with a diagnosis of cystitis glandularis manifesting as a vesicovaginal fistula. She underwent cystoscopic biopsy at a local hospital, but anti-inflammatory treatment was ineffective, and the patient was experiencing low urination frequency and urgency, as well as pain. The patient underwent laparoscopic repair of a cystoscopy-confirmed vesicovaginal fistula. After surgery, the patient experienced a paroxysm of Crohn’s disease with multiple small bowel fistulas and erosion of the external iliac vessels that ruptured to form an external iliac vessel small bowel fistula. The fistula was confirmed by surgical exploration, and the patient eventually died.

There are currently no studies exploring omicron infection and male sexual function and semen quality. Our aim was to estimate changes in sexual function and semen quality in men recovering from infection since the COVID-19 Omicron pandemic started in China in late 2022. We collected 1540 questionnaires and assessed male function before infection and acute phase after infection by using International Index of Erectile Function-5, Premature Ejaculation Diagnostic Tool, and Arizona Sexual Experience Scale. We also collected the before and after semen analysis results of 247 male patients. During the acute phase after infection, the proportion of erectile dysfunction was significantly higher than before infection, but ejaculatory function was not significantly altered; In addition, semen analysis showed significant difference in semen concentration, semen activity and PR a+b sperm forward movement after infection compared to pre-infection.: COVID-19 Omicron can affect erectile function as well as sexual experience in male patients in the acute phase. Decreased sexual function due to COVID-19 Omicron may be related to body temperature and anxiety during infection. [ABSTRACT FROM AUTHOR]

Aiming at the rich bifurcation and chaotic characteristics in the inverter with proportion integral derivative (PID) controller, the discrete iterative model of such an inverter was derived based on the stroboscopic mapping theory; the nonlinear evolution and the cause of instability in this inverter are analyzed. It was observed that the low‐frequency oscillation following instability was due to the Hopf bifurcation, which will decrease the power supplied quality by the inverter. To address the potential issue of the system instability caused by nonlinear behaviors, an improved exponential time‐delay feedback control scheme was proposed. The controlled object's output current first subtracted its own delay a period of time to form a difference term, which was subsequently fed into an exponential link to make difference with the constant 1. The resulting value was then fed into a proportional link to obtain the control term, which was applied to the PID controlled inverter in a feedback manner. Moreover, the range of the feedback proportional coefficient was solved via the Jury criterion. Finally, the effectiveness of this scheme was verified through the comparative simulations, demonstrating that this scheme can not only increase the stability domain for each parameter by more than 50% in the PID controlled inverter but also stabilize the quasi‐periodic behavior due to the low scale oscillation caused by the Hopf bifurcation at the switching frequency. [ABSTRACT FROM AUTHOR]

Cascaded H-bridge inverters, which belong to strongly nonlinear time-varying system with complex dynamics, have been widely used in high-voltage and high-power engineering fields. In this paper, a carrier phase-shifted sinusoidal pulse-width modulation cascaded H-bridge inverter is taken as an example with piecewise analysis to establish the discrete iterative mathematical model. Furthermore, the nonlinear dynamic behavior of this inverter system is investigated using folding diagrams, spectrum diagrams, bifurcation diagrams, Lyapunov exponents, etc. We find that this inverter can exhibit multiperiod bifurcation, tangential bifurcation and paroxysmal chaos within certain ranges of control coefficients and other circuit parameters, which will influence the system's stability seriously. On the basis of this discovery, the sinusoidal time-delay feedback control method is proposed. The difference between the load current of the controlled object and its own delay is used to form a feedback term, which is then fed into the sine function and proportional link to obtain the control term. Moreover, the Jacobian matrix of this feedback inverter system is derived, and the constraints on the feedback control coefficient are obtained based on the Jury criterion. Simulation results have verified the effectiveness of such a sinusoidal time-delay feedback control method, which can improve the stability and anti-interference of the system. The research can be used to provide some reference and guidance for the circuit design, debugging and control of cascaded H-bridge inverters. [ABSTRACT FROM AUTHOR]

Neurons are post‐mitotic cells, with microtubules playing crucial roles in axonal transport and growth. Kinesin family member 2c (KIF2C), a member of the Kinesin‐13 family, possesses the ability to depolymerize microtubules and is involved in remodelling the microtubule lattice. Myocyte enhancer factor 2c (MEF2C) was initially identified as a regulator of muscle differentiation but has recently been associated with neurological abnormalities such as severe cognitive impairment, stereotyping, epilepsy and brain malformations when mutated or deleted. However, further investigation is required to determine which target genes MEF2C acts upon to influence neuronal function as a transcription regulator. Our data demonstrate that knockdown of both Mef2c and Kif2c significantly impacts spinal motor neuron development and behaviour in zebrafish. Luciferase reporter assays and chromosome immunoprecipitation assays, along with down/upregulated expression analysis, revealed that MFE2C functions as a novel transcription regulator for the Kif2c gene. Additionally, the knockdown of either Mef2c or Kif2c expression in E18 cortical neurons substantially reduces the number of primary neurites and axonal branches during neuronal development in vitro without affecting neurite length. Finally, depletion of Kif2c eliminated the effects of overexpression of Mef2c on the neurite branching. Based on these findings, we provided novel evidence demonstrating that MEF2C regulates the transcription of the Kif2c gene thereby influencing the axonal branching. [ABSTRACT FROM AUTHOR]

Aim: Glucose‐dependent insulinotropic polypeptide (GIP) is a ligand of glucose‐dependent insulinotropic polypeptide receptor (GIPR) that plays an important role in the digestive system. In recent years, GIP has been regarded as a hormone‐like peptide to regulate the local metabolic environment. In this study, we investigated the antioxidant role of GIP on the neuron and explored the possible mechanism. Methods: Cell counting Kit‐8 (CCK‐8) was used to measure cell survival. TdT‐mediated dUTP Nick‐End Labeling (TUNEL) was used to detect apoptosis in vitro and in vivo. Reactive oxygen species (ROS) levels were probed with 2', 7'‐Dichloro dihydrofluorescein diacetate (DCFH‐DA), and glucose intake was detected with 2‐NBDG. Immunofluorescence staining and western blot were used to evaluate the protein level in cells and tissues. Hematoxylin‐eosin (HE) staining, immunofluorescence staining and tract‐tracing were used to observe the morphology of the injured spinal cord. Basso‐Beattie‐Bresnahan (BBB) assay was used to evaluate functional recovery after spinal cord injury. Results: GIP reduced the ROS level and protected cells from apoptosis in cultured neurons and injured spinal cord. GIP facilitated wound healing and functional recovery of the injured spinal cord. GIP significantly improved the glucose uptake of cultured neurons. Meanwhile, inhibition of glucose uptake significantly attenuated the antioxidant effect of GIP. GIP increased glucose transporter 3 (GLUT3) expression via up‐regulating the level of hypoxia‐inducible factor 1α (HIF‐1α) in an Akt‐dependent manner. Conclusion: GIP increases GLUT3 expression and promotes glucose intake in neurons, which exerts an antioxidant effect and protects neuronal cells from oxidative stress both in vitro and in vivo. [ABSTRACT FROM AUTHOR]