Vaginal progesterone for prevention of preterm birth in asymptomatic high-risk women with a normal cervical length: a systematic review and meta-analysis.

Objective: To determine whether vaginal progesterone reduces spontaneous preterm birth (sPTB) before 37 weeks in asymptomatic high-risk women with a singleton pregnancy and normal mid-gestation cervical length.Study design: Databases were searched (from inception to December 2020) with the search terms "progesterone" and "premature birth" or "preterm birth". Studies were screened and included if they assessed vaginal progesterone compared to placebo in women with normal cervical length. Data were pooled and synthesized in a meta-analysis using a random effects model.Data sources: MEDLINE and Embase databases.Study synthesis: Following PRISMA screening guidelines, data from 1127 women across three studies were available for synthesis. All studies had low risk of bias and were of high quality. The primary outcome was sPTB <37 weeks, with secondary outcomes of sPTB <34 weeks. Vaginal progesterone did not significantly reduce sPTB before 37 weeks, or before 34 weeks with a relative risk (RR) of 0.76 (95% CI 0.37-1.55, p = .45) and 0.51 (95% CI 0.12-2.13, p = .35), respectively.Conclusions: Vaginal progesterone does not decrease the risk of sPTB in high-risk singleton pregnancies with a normal mid-gestation cervical length.

Interfacial Symmetry Control of Emergent Ferromagnetism at the Nanoscale.

The emergence of complex new ground states at interfaces has been identified as one of the most promising routes to highly tunable nanoscale materials. Despite recent progress, isolating and controlling the underlying mechanisms behind these emergent properties remains among the most challenging materials physics problems to date. In particular, generating ferromagnetism localized at the interface of two nonferromagnetic materials is of fundamental and technological interest. Moreover, the ability to turn the ferromagnetism on and off would shed light on the origin of such emergent phenomena and is promising for spintronic applications. We demonstrate that ferromagnetism confined within one unit cell at the interface of CaRuO3 and CaMnO3 can be switched on and off by changing the symmetry of the oxygen octahedra connectivity at the boundary. Interfaces that are symmetry-matched across the boundary exhibit interfacial CaMnO3 ferromagnetism while the ferromagnetism at symmetry-mismatched interfaces is suppressed. We attribute the suppression of ferromagnetic order to a reduction in charge transfer at symmetry-mismatched interfaces, where frustrated bonding weakens the orbital overlap. Thus, interfacial symmetry is a new route to control emergent ferromagnetism in materials such as CaMnO3 that exhibit antiferromagnetism in bulk form.

Electric Field Control of Interfacial Ferromagnetism in CaMnO_{3}/CaRuO_{3} Heterostructures.

New mechanisms for achieving direct electric field control of ferromagnetism are highly desirable in the development of functional magnetic interfaces. To that end, we have probed the electric field dependence of the emergent ferromagnetic layer at CaRuO_{3}/CaMnO_{3} interfaces in bilayers fabricated on SrTiO_{3}. Using polarized neutron reflectometry, we are able to detect the ferromagnetic signal arising from a single atomic monolayer of CaMnO_{3}, manifested as a spin asymmetry in the reflectivity. We find that the application of an electric field of 600 kV/m across the bilayer induces a significant increase in this spin asymmetry. Modeling of the reflectivity suggests that this increase corresponds to a transition from canted antiferromagnetism to full ferromagnetic alignment of the Mn^{4+} ions at the interface. This increase from 1 µ_{B} to 2.5-3.0 µ_{B} per Mn is indicative of a strong magnetoelectric coupling effect, and such direct electric field control of the magnetization at an interface has significant potential for spintronic applications.

Iron intoxication in a dog consequent to the ingestion of oxygen absorber sachets in pet treat packaging.

Oxygen absorbers are commonly used in packages of dried or dehydrated foods (e.g., beef jerky, dried fruit) to prolong shelf life and protect food from discoloration and decomposition. They usually contain reduced iron as the active ingredient although this is rarely stated on the external packaging. Although reduced iron typically has minimal oral bioavailability, such products are potential sources of iron poisoning in companion animals and children. We present a case of canine ingestion of an oxygen absorber from a bag of dog treats that resulted in iron intoxication necessitating chelation therapy. A 7-month-old female Jack Russell terrier presented for evaluation of vomiting and melena 8-12 h after ingesting 1-2 oxygen absorber sachets from a package of dog treats. Serum iron concentration and ALT were elevated. The dog was treated with deferoxamine and supportive care. Clinical signs resolved 14 h following treatment, but the ALT remained elevated at the 3-month recheck. The ingestion of reduced iron in humans has been reported to cause mild elevation of serum iron concentration with minimal clinical effects. To our knowledge, no cases of iron intoxication following the ingestion of oxygen absorbers have been reported. The lack of ingredient information on the packaging prompted analysis of contents of oxygen absorber sachets. Results indicate the contents contained 50-70% total iron. This case demonstrates that iron intoxication can occur following the ingestion of such products. Human and veterinary medical personnel need to be aware of this effect and monitor serum iron concentrations as chelation may be necessary.

IRS-2 pathways integrate female reproduction and energy homeostasis.

Severe dietary restriction, catabolic states and even short-term caloric deprivation impair fertility in mammals. Likewise, obesity is associated with infertile conditions such as polycystic ovary syndrome. The reproductive status of lower organisms such as Caenorhabditis elegans is also modulated by availability of nutrients. Thus, fertility requires the integration of reproductive and metabolic signals. Here we show that deletion of insulin receptor substrate-2 (IRS-2), a component of the insulin/insulin-like growth factor-1 signalling cascade, causes female infertility. Mice lacking IRS-2 have small, anovulatory ovaries with reduced numbers of follicles. Plasma concentrations of luteinizing hormone, prolactin and sex steroids are low in these animals. Pituitaries are decreased in size and contain reduced numbers of gonadotrophs. Females lacking IRS-2 have increased food intake and obesity, despite elevated levels of leptin. Our findings indicate that insulin, together with leptin and other neuropeptides, may modulate hypothalamic control of appetite and reproductive endocrinology. Coupled with findings on the role of insulin-signalling pathways in the regulation of fertility, metabolism and longevity in C. elegans and Drosophila, we have identified an evolutionarily conserved mechanism in mammals that regulates both reproduction and energy homeostasis.

Irs-2 coordinates Igf-1 receptor-mediated beta-cell development and peripheral insulin signalling.

Insulin receptor substrates (Irs proteins) mediate the pleiotropic effects of insulin and Igf-1 (insulin-like growth factor-1), including regulation of glucose homeostasis and cell growth and survival. We intercrossed mice heterozygous for two null alleles (Irs1+/- and Irs2+/-) and investigated growth and glucose metabolism in mice with viable genotypes. Our experiments revealed that Irs-1 and Irs-2 are critical for embryonic and post-natal growth, with Irs-1 having the predominant role. By contrast, both Irs-1 and Irs-2 function in peripheral carbohydrate metabolism, but Irs-2 has the major role in beta-cell development and compensation for peripheral insulin resistance. To establish a role for the Igf-1 receptor in beta-cells, we intercrossed mice heterozygous for null alleles of Igf1r and Irs2. Our results reveal that Igf-1 receptors promote beta-cell development and survival through the Irs-2 signalling pathway. Thus, Irs-2 integrates the effects of insulin in peripheral target tissues with Igf-1 in pancreatic beta-cells to maintain glucose homeostasis.