Long-term variation in the Sun's activity caused by magnetic Rossby waves in the tachocline

Long-term records of sunspot number and concentrations of cosmogenic radionuclides (10Be and 14C) on the Earth reveal the variation of the Sun's magnetic activity over hundreds and thousands of years. We identify several clear periods in sunspot, 10Be, and 14C data as 1000, 500, 350, 200 and 100 years. We found that the periods of the first five spherical harmonics of the slow magnetic Rossby mode in the presence of a steady toroidal magnetic field of 1200-1300 G in the lower tachocline are in perfect agreement with the time scales of observed variations. The steady toroidal magnetic field can be generated in the lower tachocline either due to the steady dynamo magnetic field for low magnetic diffusivity or due to the action of the latitudinal differential rotation on the weak poloidal primordial magnetic field, which penetrates from the radiative interior. The slow magnetic Rossby waves lead to variations of the steady toroidal magnetic field in the lower tachocline, which modulate the dynamo magnetic field and consequently the solar cycle strength. This result constitutes a key point for long-term prediction of the cycle strength. According to our model, the next deep minimum in solar activity is expected during the first half of this century.Comment: 4 pages, 4 figures, accepted in ApJ

არამკაფიო ანალიზის ერთი მეთოდის შესახებ მიწისძვრის პარამეტრების შეფასების ამოცანაში

ნაშრომის ძირითადი ამოცანა მდგომარეობს მათემატიკური მოდელის აგებასა და მიწისძვრის პარამეტრების განსაზღვრასთან დაკავშირებით გადაწყვეტილების მისაღებად რეკომენდაციების ფორმულირებაში. პირველად მონაცემთა წინასწარი ანალიზის დროს დადგენილია, რომ მათი ბუნება არის კომბინირებული ანუ ალბათურ-შესაძლებოთი. ამიტომ მათი დამუშავებისთვის შერჩეულია სპეციალური არამკაფიო ანალიზის მეთოდი-ბმულობათა ანალიზი

Association between seropositivity for cytomegalovirus (CMV) and CD4+ cytotoxic T cells expansions in patients with B-cell Chronic Lymphocyte Leukaemia (B-CLL) and healthy controls

B cell chronic lymphocytic leukaemia (B-CLL) is characterized by the clonal expansion of CD5+CD19+CD23+ B cells. During the course of B-CLL, the expansion of neoplastic clone is accompanied by a disbalance between CD4+/CD8+ T cells and by deficiency of T cell function. We have previously shown an expansion of CD4+ perforin (PF)+ cytotoxic T cells (cytT) with undefined specificity in patients with B-CLL. It has been demonstrated by others that the expansion of CD4+PF+ T cells in control individuals is often associated with chronic viral infections. Taking into consideration that B-CLL patients are immunocompromised, with frequent viral infections, we investigated the role of CD4+PF+ cytotoxic T cells in immune responses to one of the most common chronic viral infections - human cytomegalovirus (hCMV). We studied an association of cytT cell frequencies with the chronic CMV infection in 32 B-CLL patients and 18 age-matched healthy controls. Peripheral blood mononuclear cells (PBMCs) were immunostained with anti-CD4~PerCP monoclonal antibodies (mAb), fixed, permeabilised and immunostained with anti-PF~FITC mAb. Cells were fixed and analyzed by flow cytometry. Serum samples were routinely tested for anti-IgG antibodies to CMV. Here we show that CD4+PF+ T cell expansions appeared to be strongly associated with CMV seropositivity in healthy individuals, and, particularly, in B-CLL patients. The immunocompromised status of the majority of B-CLL patients may facilitate expansion of this unusual population of cytotoxic cells to combat reactivation of a chronic CMV infection

CRISPR Interference-Based Platform for Multimodal Genetic Screens in Human iPSC-Derived Neurons

CRISPR/Cas9-based functional genomics have transformed our ability to elucidate mammalian cell biology. However, most previous CRISPR-based screens were conducted in cancer cell lines rather than healthy, differentiated cells. Here, we describe a CRISPR interference (CRISPRi)-based platform for genetic screens in human neurons derived from induced pluripotent stem cells (iPSCs). We demonstrate robust and durable knockdown of endogenous genes in such neurons and present results from three complementary genetic screens. First, a survival-based screen revealed neuron-specific essential genes and genes that improved neuronal survival upon knockdown. Second, a screen with a single-cell transcriptomic readout uncovered several examples of genes whose knockdown had strikingly cell-type-specific consequences. Third, a longitudinal imaging screen detected distinct consequences of gene knockdown on neuronal morphology. Our results highlight the power of unbiased genetic screens in iPSC-derived differentiated cell types and provide a platform for systematic interrogation of normal and disease states of neurons. VIDEO ABSTRACT