Influence of hole-drilling diameter on aluminum alloy residual stress measurement

A hole-drilling method and finite element (FEM) numerical simulation are used to estimate the residual stress of aluminum alloy welding joints. In order to study the influence of hole diameter on measurement accuracy, a group of experiments are conducted. Experiment results show that the measuring error can be the minimal when the drilling hole diameter is 4 mm. Residual stress of 2219-T87 aluminum alloy welding joints under this optimal hole diameter are obtained. The distribution of the residual stress from the welding seam to the outward is first tensile stress and then compressive stress. And the maximum residual stress is 123.2 MPa

ATG16L1 and pathogenesis of urinary tract infections

Autophagy is generally considered to be antipathogenic. The autophagy gene ATG16L1 has a commonly occurring mutation associated with Crohn disease (CD) and intestinal cell abnormalities. Mice hypomorphic for ATG16L1 (ATG16L1(HM)) recreate specific features of CD. Our recent study shows that the same ATG16L1(HM) mice that are susceptible to intestinal inflammatory disease are protected from urinary tract infections (UTI), a common and important human disease primarily caused by uropathogenic E. coli (UPEC). UPEC colonize the bladder and exhibit both luminal and intra-epithelial stages. The host responds by recruiting innate immune cells and shedding infected epithelial cells to clear infection. Despite these countermeasures, UPEC can persist within the bladder epithelium as membrane-enclosed quiescent intracellular reservoirs (QIRs) that can seed recurrent UTI. The mechanisms of persistence remain unknown. In this study, we show that ATG16L1 deficiency protects the host against acute UTI and UPEC latency. ATG16L1(HM) mice clear urinary bacterial loads more rapidly and thoroughly due to ATG16L1-deficient innate immune components. Furthermore, ATG16L1(HM) mice exhibit superficial urothelial cell-autonomous architectural aberrations that also result in significantly reduced QIR numbers. Our findings reveal a host-protective effect of ATG16L1 deficiency in vivo against a common pathogen

Analysis of risk factors for recurrence in infertile endometrial cancer patients after in vitro fertilization treatment

PurposeTo investigate the oncologic outcomes of patients with early-stage endometrioid endometrial cancer (EEC) treated with in vitro fertilization/intracytoplasmic sperm injection (IVF/ICSI) following fertility-sparing treatment (FST).MethodsA total of 62 patients who underwent IVF/ICSI treatment in a single fertility center between June 2010 and December 2021 after conservative treatment for early-stage EEC were assigned to a recurrence group and a non-recurrence group. Their clinical characteristics and disease outcomes were retrospectively evaluated.ResultsThe 62 women with complete remission (CR) after FST for EEC underwent 103 IVF cycles, resulting in 41 fresh embryo transfers (ETs) and 70 frozen–thawed transfers; 27 (43.55%) achieved clinical pregnancies, and 20 (32.26%) gave birth to a total of 23 live neonates. Additionally, nine patients had live births from natural pregnancies after IVF failure, bringing the cumulative live birth rate to 46.77% (29/62). After a median follow-up period of 53.88 months (range 20.2–127.5 months), 17 patients (27.42%) experienced recurrence within 2.8 to 57.9 months after the first controlled ovarian stimulation (COS). The probability of relapse at 1, 2, and 3 years after the initiation of COS was 14.52% (9/62), 21% (13/62), and 25.81% (16/62), respectively. Factors such as the time to CR, the time to IVF, the frequency of COS, maintenance treatment before IVF, and histology type were not found to significantly affect recurrence (p = 0.079, 0.182, 0.093, 0.267, and 0.41, respectively). Live births (hazard ratio (HR): 0.28, 95% CI: 0.082–0.962, p = 0.043) and the protocol of letrozole plus gonadotropin-releasing hormone (GnRH) antagonist/agonist used during IVF (HR: 0.1, 95% CI: 0.011–0.882, p = 0.038) were identified as independent favorable factors for recurrence.ConclusionsLive birth was associated with decreased recurrence of EEC. Reducing estrogen levels during COS may serve to mitigate the risk of endometrial cancer recurrence

Effects of Time Delay and Noise on Asymptotic Stability in Human Quiet Standing Model

A human quiet standing stability is discussed in this paper. The model under consideration is proposed to be a delayed differential equation (DDE) with multiplicative white noise perturbation. The method of the center manifold is generalized to reduce a delayed differential equation to a two-dimensional ordinary differential equation, to study delay-induced instability or Hopf bifurcation. Then, the stochastic average method is employed to obtain the Itô equation. Thus, the top Lyapunov exponent is calculated and the necessary and sufficient condition of the asymptotic stability in views of probability one is obtained. The results show that the exponent is related to not only the strength of noise but also the delay, namely, the reaction speed of brain. The effect of the strength of noise on the human quiet standing losing stability is weak for a small delay. With the delay increasing, such effect becomes stronger and stronger. A small change in the strength of noise may destabilize the quiet standing for a large delay. It implies that a person with slow reaction is easy to lose the stability of his/her quiet standing

Some Properties of Furuta Type Inequalities and Applications

This work is to consider Furuta type inequalities and their applications. Firstly, some Furuta type inequalities under A≥B≥0 are obtained via Loewner-Heinz inequality; as an application, a proof of Furuta inequality is given without using the invertibility of operators. Secondly, we show a unified satellite theorem of grand Furuta inequality which is an extension of the results by Fujii et al. At the end, a kind of Riccati type operator equation is discussed via Furuta type inequalities

Estrogenic modulation of uropathogenic Escherichia coli infection pathogenesis in a murine menopause model

Recurrent urinary tract infections (UTIs), primarily caused by uropathogenic Escherichia coli (UPEC), annually affect over 13 million patients in the United States. Menopausal women are disproportionally susceptible, suggesting estrogen deficiency is a significant risk factor for chronic and recurrent UTI. How estrogen status governs susceptibility to UTIs remains unknown, and whether hormone therapy protects against UTIs remains controversial. Here, we used a mouse model of surgical menopause by ovariectomy and demonstrate a protective role for estrogen in UTI pathogenesis. We found that ovariectomized mice had significantly higher bacteriuria, a more robust inflammatory response, and increased production of the proinflammatory cytokine interleukin-6 (IL-6) upon UPEC infection compared to sham-operated controls. We further show that response of the urothelial stem cell niche to infection, normally activated to restore homeostasis after infection, was aberrant in ovariectomized mice with defective superficial urothelial cell differentiation. Finally, UPEC-infected ovariectomized mice showed a significant increase in quiescent intracellular bacterial reservoirs, which reside in the urothelium and can seed recurrent infections. Importantly, this and other ovariectomy-induced outcomes of UTI were reversible upon estrogen supplementation. Together, our findings establish ovariectomized mice as a model for UTIs in menopausal women and pinpoint specific events during course of infection that are most susceptible to estrogen deficiency. These findings have profound implications for the understanding of the role of estrogen and estrogen therapy in bladder health and pathogen defense mechanisms and open the door for prophylaxis for menopausal women with recurrent UTIs