It is well known that the polar magnetic field is at its maximum during solar minima, and that the behaviour during this time acts as a strong predictor of the strength of the following solar cycle. This relationship relies on the action of differential rotation (the Omega effect) on the poloidal field, which generates the toroidal flux observed in sunspots and active regions. We measure the helicity flux into both the northern and the southern hemispheres using a model that takes account of the Omega effect, which we apply to data sets covering a total of 60 years. We find that the helicity flux offers a strong prediction of solar activity up to five years in advance of the next solar cycle. We also hazard an early guess as to the strength of Solar Cycle 25, which we believe will be of similar amplitude and strength to Cycle 24.

Human genetic studies have provided substantial insight into the biological mechanisms governing ovarian ageing, yet previous approaches have been largely restricted to assessing common genetic variation. Here we report analyses of rare (MAF<0.1%) protein-coding variants in the exomes of 106,973 women from the UK Biobank study, implicating novel genes with effect sizes up to ~5 times larger than previously discovered in analyses of common variants. These include protein truncating variants in ZNF518A, which shorten reproductive lifespan by promoting both earlier age at natural menopause (ANM, 5.61 years [4.04-7.18], P=2*10-12) and later puberty timing in girls (age at menarche, 0.56 years [0.15-0.97], P=9.2*10-3). By integrating ChIP-Seq data, we demonstrate that common variants associated with ANM and menarche are enriched in the binding sites of ZNF518A. We also identify further links between ovarian ageing and cancer susceptibility, highlighting damaging germline variants in SAMHD1 that delay ANM and increase all-cause cancer risk in both males (OR=2.1 [1.7-2.6], P=4.7*10-13) and females (OR=1.61 [1.31-1.96], P=4*10-6). Finally, we demonstrate that genetic susceptibility to earlier ovarian ageing in women increases de novo mutation rate in their offspring. This provides direct evidence that female mutation rate is heritable and highlights an example of a mechanism for the maternal genome influencing child health.

Aims. We estimate the injection of relative magnetic helicity into the solar atmosphere by surface flux transport over 27 solar cycles (1700–2009). Methods. We determine the radial magnetic field evolution using two separate surface flux transport models: one driven by magnetogram inputs and another by statistical active region insertion guided by the sunspot number record. The injection of relative magnetic helicity is then computed from this radial magnetic field together with the known electric field in the flux transport models. Results. Neglecting flux emergence, solar rotation is the dominant contributor to the helicity injection. At high latitudes, the injection is always negative/positive in the northern/southern hemisphere, while at low latitudes the injection tends to have the opposite sign when integrated over the full solar cycle. The overall helicity injection in a given solar cycle depends on the balance between these two contributions. This net injected helicity correlates well with the end-of-cycle axial dipole moment.

Context. Magnetic helicity is approximately conserved in resistive MHD models. It quantifies the entanglement of the magnetic field within the plasma. The transport and removal of helicity is crucial in both the dynamo in the solar interior and active region evolution in the solar corona. This transport typically leads to highly inhomogeneous distributions of entanglement.Aims. There exists no consistent systematic means of decomposing helicity over varying spatial scales and in localised regions. Spectral helicity decompositions can be used in periodic domains and is fruitful for the analysis of homogeneous phenomena. This paper aims to develop methods for analysing the evolution of magnetic field topology in non-homogeneous systems. Methods. We apply a multiresolution wavelet decomposition to the magnetic field and demonstrate how it can be applied to various quantities associated with magnetic helicity, including the field line helicity. We use a geometrical definition of helicity which allows these quantities to be calculated for fields with arbitrary boundary conditions. Results. It is shown that the multiresolution decomposition of helicity has the crucial property of local additivity and demonstrate a general linear energy-topology conservation law which is a significant generalisation of the two point correlation decomposition used in the analysis of homogeneous turbulence and periodic fields. The localisation property of the wavelet representation is shown to characterise inhomogeneous distributions which a Fourier representation cannot. Using an analytic representation of a resistive braided field relaxation we demonstrate a clear correlation between the variations in energy at various length scales and the variations in helicity at the same spatial scales. Its application to helicity flows in a surface flux transport model show how various contributions to the global helicity input from active region field evolution and polar field development are naturally separated by this representation. Conclusions. The multiresolution wavelet decomposition can be used to analyse the evolution of helicity in magnetic fields in a manner which is consistently additive. This method has the advantage over more established spectral methods in that it clearly characterises the inhomogeneous nature of helicity flows where spectral methods cannot. Further its applicability in aperiodic models significantly increase the range of potential applications.

Premature ovarian insufficiency (POI) affects 1% of women and is a leading cause of infertility. It is often considered to be a monogenic disorder, with pathogenic variants in ~100 genes described in the literature. We sought to systematically evaluate the penetrance of variants in these genes using exome sequence data in 104,733 women from the UK Biobank, 2,231 (1.14%) of whom reported natural menopause under the age of 40. We found limited evidence to support any previously reported autosomal dominant effect. For nearly all heterozygous effects on previously reported POI genes we ruled out even modest penetrance, with 99.9% (13,699/13,708) of all protein truncating variants found in reproductively healthy women. We found evidence of haploinsufficiency effects in several genes, including TWNK (1.54 years earlier menopause, P=1.59*10 -6 ) and SOHLH2 (3.48 years earlier menopause, P=1.03*10 -4 ). Collectively our results suggest that for the vast majority of women, POI is not caused by autosomal dominant variants either in genes previously reported or currently evaluated in clinical diagnostic panels. Our findings, plus previous studies, suggest that the majority of POI cases are likely oligogenic or polygenic in nature, which has major implications for future clinical genetic studies, and genetic counselling for families affected by POI.