HSF1 promotes endometriosis development and glycolysis by up-regulating PFKFB3 expression

Background Endometriosis is a chronic hormonal inflammatory disease characterized by the presence of endometrial tissue outside the uterus. Endometriosis often causes infertility, which brings physical and mental pain to patients and their families. Methods We examined the functions of heat shock factor 1 (HSF1) in endometriosis development through cell count assay, cell-scratch assay and clone formation experiments. We used quantitative real-time PCR (qRT-PCR) and Western blot (WB) to detect HSF1 expression. Glucose and lactate levels were determined using a glucose (GO) assay kit and a lactate assay kit. Furthermore, we used a HSF1 inhibitor-KRIBB11 to establish a mouse model of endometriosis. Results Our data demonstrated that HSF1 promoted endometriosis development. Interestingly, HSF1 enhanced glycolysis via up-regulating PFKFB3 expression in endometriosis cells, which was a key glycolysis enzyme. Consistently, the HSF1 inhibitor KRIBB11 could abrogate endometriosis progression in vivo and in vitro. Conclusions Findings indicate that HSF1 plays an important role in endometriosis development, which might become a new target for the treatment of endometriosis. Electronic supplementary material Supplementary data are available.

HSF1 promotes endometriosis development and glycolysis by up-regulating PFKFB3 expression

Background Endometriosis is a chronic hormonal inflammatory disease characterized by the presence of endometrial tissue outside the uterus. Endometriosis often causes infertility, which affects the body and mind of patients and their families.Methods We examined the functions of heat shock factor 1 (HSF1) in endometriosis development through cell count, scratch and clone formation experiments. We used quantitative real-time PCR (qRT-PCR) and Western blot (WB) to detect the functions of HSF1 in endometriosis cells. Glucose and lactate levels were determined using a glucose (GO) assay kit and a lactate assay kit. Furthermore, we established a mouse model of endometriosis by using a HSF1 inhibitor-KRIBB11.Results Our study demonstrated that HSF1 was highly expressed in endometriosis, and promoted endometriosis development. Interestingly, we found that HSF1 promoted glycolysis in endometriosis cells. Further, HSF1 enhanced glycolysis by up-regulating PFKFB3 in endometriosis cells, which was a key enzyme in glucose metabolism. Moreover, the HSF1 inhibitor KRIBB11 could abrogate endometriosis progression in vivo and in vitro.Conclusions Findings indicate that HSF1 plays an important role in the development of endometriosis, which might become a new target for the treatment of endometriosis and provide a new idea for the clinical treatment of endometriosis.Electronic supplementary material Supplementary data are available.

Correction to: Pore Network Modeling of the Effects of Viscosity Ratio and Pressure Gradient on Steady-State Incompressible Two-Phase Flow in Porous Media

In the original publication of the article, the Electronic Supplementary Material was missed.

Correction to: Processing and Analyzing Multiple Genomes Alignments with MafFilter

Chapter 2, “Processing and Analyzing Multiple Genomes Alignments with MafFilter,” was previously published without including the Electronic Supplementary Material. This has now been included in the revised version of this book.

Long-term clinical outcome of two revision strategies for failed total disc replacements

Purpose To compare the long-term clinical results and complications of two revision strategies for patients with failed total disc replacements (TDRs). Methods In 19 patients, the TDR was removed and the intervertebral defect was filled with a femoral head bone strut graft. In addition, instrumented posterolateral fusion was performed (removal group). In 36 patients, only a posterolateral instrumented fusion was performed (fusion group). Visual Analogue Scale (VAS) for pain and Oswestry Disability Index (ODI) were completed pre- and post-revision surgery. Intra- and post-operative complications of both revision strategies were assessed. Results The median follow-up was 12.3 years (range 5.3–24.3). In both the removal and fusion groups, a similar (p = 0.515 and p = 0419, respectively) but significant decrease in VAS (p = 0.001 and p = 0.001, respectively) and ODI score (p = 0.033 and p = 0.013, respectively) at post-revision surgery compared to pre-revision surgery was seen. A clinically relevant improvement in VAS and ODI score was found in 62.5% and 43.8% in the removal group and in 43.5% and 39.1% in the fusion group (p = 0.242 and p = 0.773, respectively). Removal of the TDR was associated with substantial intra-operative complications such as major vessel bleeding and ureter lesion. The percentage of late re-operations for complications such as pseudarthrosis were comparable for both revision strategies. Conclusions Revision of a failed TDR is clinically beneficial in about half of the patients. No clear benefits for additional TDR removal as compared to posterolateral instrumented fusion alone could be identified. In particular, when considering the substantial risks and complications, great caution is warranted with removal of the TDR. Graphic abstract These slides can be retrieved under Electronic Supplementary Material.

Four-dimensional Fano quiver flag zero loci

Quiver flag zero loci are subvarieties of quiver flag varieties cut out by sections of representation theoretic vector bundles. We prove the Abelian/non-Abelian correspondence in this context: this allows us to compute genus zero Gromov–Witten invariants of quiver flag zero loci. We determine the ample cone of a quiver flag variety, and disprove a conjecture of Craw. In the appendices (which can be found in the electronic supplementary material), which are joint work with Tom Coates and Alexander Kasprzyk, we use these results to find four-dimensional Fano manifolds that occur as quiver flag zero loci in ambient spaces of dimension up to 8, and compute their quantum periods. In this way, we find at least 141 new four-dimensional Fano manifolds.

A restatement of the natural science evidence base concerning neonicotinoid insecticides and insect pollinators

There is evidence that in Europe and North America many species of pollinators are in decline, both in abundance and distribution. Although there is a long list of potential causes of this decline, there is concern that neonicotinoid insecticides, in particular through their use as seed treatments are, at least in part, responsible. This paper describes a project that set out to summarize the natural science evidence base relevant to neonicotinoid insecticides and insect pollinators in as policy-neutral terms as possible. A series of evidence statements are listed and categorized according to the nature of the underlying information. The evidence summary forms the appendix to this paper and an annotated bibliography is provided in the electronic supplementary material.

A stab in the dark: chick killing by brood parasitic honeyguides

The most virulent avian brood parasites obligately kill host young soon after hatching, thus ensuring their monopoly of host parental care. While the host eviction behaviour of cuckoos (Cuculidae) is well documented, the host killing behaviour of honeyguide (Indicatoridae) chicks has been witnessed only once, 60 years ago, and never in situ in host nests. Here, we report from the Afrotropical greater honeyguide the first detailed observations of honeyguides killing host chicks with their specially adapted bill hooks, based on repeated video recordings (available in the electronic supplementary material). Adult greater honeyguides puncture host eggs when they lay their own, but in about half of host nests at least one host egg survived, precipitating chick killing by the honeyguide hatchling. Hosts always hatched after honeyguide chicks, and were killed within hours. Despite being blind and in total darkness, honeyguides attacked host young with sustained biting, grasping and shaking motions. Attack time of 1–5 min was sufficient to cause host death, which took from 9 min to over 7 h from first attack. Honeyguides also bit unhatched eggs and human hands, but only rarely bit the host parents feeding them.