A toy model of the five-dimensional universe with the cosmological constant

A value of the cosmological constant in a toy model of the five-dimensional universe is calculated in such a manner that it remains in agreement with both astronomical observations and the quantum field theory concerning the zero-point fluctuations of the vacuum. The (negative) cosmological constant is equal to the inverse of the Planck length squared, which means that in the toy model the vanishing of the observed value of the cosmological constant is a consequence of the existence of an energy cutoff exactly at the level of the Planck scale. In turn, a model for both a virtual and a real particle-antiparticle pair is proposed which describes properly some energetic properties of both the vacuum fluctuations and created particles, as well as it allows one to calculate the discrete "bare" values of an elementary-particle mass, electric charge and intrinsic angular momentum (spin) at the energy cutoff. The relationships between the discussed model and some phenomena such as the Zitterbewegung and the Unruh-Davies effect are briefly analyzed, too. The proposed model also allows one to derive the Lorentz transformation and the Maxwell equations while considering the properties of the vacuum filled with the sea of virtual particles and their antiparticles. Finally, the existence of a finite value of the vacuum-energy density resulting from the toy model leads us to the formulation of dimensionless Einstein field equations which can be derived from the Lagrangian with a dimensionless (naively renormalized) coupling constant.Comment: 52 pages, 1 figure; a post-final, rewritten version with a number of new remarks and conclusion

Macrophage-derived human resistin is induced in multiple helminth infections and promotes inflammatory monocytes and increased parasite burden.

Parasitic helminth infections can be associated with lifelong morbidity such as immune-mediated organ failure. A better understanding of the host immune response to helminths could provide new avenues to promote parasite clearance and/or alleviate infection-associated morbidity. Murine resistin-like molecules (RELM) exhibit pleiotropic functions following helminth infection including modulating the host immune response; however, the relevance of human RELM proteins in helminth infection is unknown. To examine the function of human resistin (hResistin), we utilized transgenic mice expressing the human resistin gene (hRetnTg+). Following infection with the helminth Nippostrongylus brasiliensis (Nb), hResistin expression was significantly upregulated in infected tissue. Compared to control hRetnTg- mice, hRetnTg+ mice suffered from exacerbated Nb-induced inflammation characterized by weight loss and increased infiltration of inflammatory monocytes in the lung, along with elevated Nb egg burdens and delayed parasite expulsion. Genome-wide transcriptional profiling of the infected tissue revealed that hResistin promoted expression of proinflammatory cytokines and genes downstream of toll-like receptor signaling. Moreover, hResistin preferentially bound lung monocytes, and exogenous treatment of mice with recombinant hResistin promoted monocyte recruitment and proinflammatory cytokine expression. In human studies, increased serum resistin was associated with higher parasite load in individuals infected with soil-transmitted helminths or filarial nematode Wuchereria bancrofti, and was positively correlated with proinflammatory cytokines. Together, these studies identify human resistin as a detrimental factor induced by multiple helminth infections, where it promotes proinflammatory cytokines and impedes parasite clearance. Targeting the resistin/proinflammatory cytokine immune axis may provide new diagnostic or treatment strategies for helminth infection and associated immune-mediated pathology

Occupational asthma caused by cobalt chloride in a diamond polisher after cessation of occupational exposure: a case report

Objectives: The inspiration of cobalt containing dust leads to various respiratory symptoms, including asthma and interstitial lung disease. Occupational asthma caused by cobalt chloride has been diagnosed in a 35-year-old patient, who worked as a diamond polishing disc former. The patient presented a 2-year history of dyspnea, cough and symptoms of rhinitis. Materials and Methods: The patient underwent a medical history interview, skin prick tests with common and occupational allergens (cobalt and nickel chloride), and pulmonary function testing both before and after the nasal provocation with 0.05% cobalt chloride. Additionally, the authors analyzed morphological and biochemical changes before and after the specific nasal challenge test. Cell proliferation analysis was also carried out. Results: Skin prick tests (SPTs) with common environmental allergens were found to be negative, while SPTs with cobalt chloride were positive for all applied solutions. The provocation with cobalt chloride caused a significant increase in the proportion of eosinophils, basophils and albumin during the late allergic reaction. The positive lymphocyte transformation caused by cobalt was also observed. Conclusions: Cobalt salts may induce occupational asthma. The mechanism of this asthma may be IgE-mediated. The cobalt-sensitized lymphocytes may play an important role in this disease

Strigolactones inhibit auxin feedback on PIN-dependent auxin transport canalization

Directional transport of the phytohormone auxin is a versatile, plant-specific mechanism regulating many aspects of plant development. The recently identified plant hormones, strigolactones (SLs), are implicated in many plant traits; among others, they modify the phenotypic output of PIN-FORMED (PIN) auxin transporters for fine-tuning of growth and developmental responses. Here, we show in pea and Arabidopsis that SLs target processes dependent on the canalization of auxin flow, which involves auxin feedback on PIN subcellular distribution. D14 receptor- and MAX2 F-box-mediated SL signaling inhibits the formation of auxin-conducting channels after wounding or from artificial auxin sources, during vasculature de novo formation and regeneration. At the cellular level, SLs interfere with auxin effects on PIN polar targeting, constitutive PIN trafficking as well as clathrin-mediated endocytosis. Our results identify a non-transcriptional mechanism of SL action, uncoupling auxin feedback on PIN polarity and trafficking, thereby regulating vascular tissue formation and regeneration

Activating Killer Immunoglobulin Receptors and HLA-C: A successful combination providing HIV-1 control

Several studies demonstrated a relevant role of polymorphisms located within the HLA-B and -C loci and the Killer Immunoglobulin Receptors (KIRs) 3DL1 and 3DS1 in controlling HIV-1 replication. KIRs are regulatory receptors expressed at the surface of NK and CD8+ T-cells that specifically bind HLA-A and -B alleles belonging to the Bw4 supratype and all the -C alleles expressing the C1 or C2 supratype. We here disclose a novel signature associated with the Elite Controller but not with the long-term nonprogressor status concerning 2DS activating KIRs and HLA-C2 alleles insensitive to miRNA148a regulation. Overall, our findings support a crucial role of NK cells in the control of HIV-1 viremia

National support to public health research: a survey of European ministries

Background: Within SPHERE (Strengthening Public Health Research in Europe), a collaborative study funded by the European Commission, we have assessed the support for public health research at ministry level in European countries. Methods: We surveyed the health and science ministries in 25 EU countries and 3 EEA countries, using a broad definition of public-health research at population level. We made over 600 phone calls and emails to identify respondents and to gain answers. We gained formal replies from 42 out of 56 ministries (73% response) in 25 countries. There were 22 completed questionnaires (from 25 ministries), 6 short answers and 11 contacts declaring that their ministries were not responsible for public health research, while in 14 ministries (both ministries in three countries) no suitable ministry contact could be found. Results: In most European countries, ministries of health, or their devolved agencies, were regarded as the leading organizations. Most ministries were able to specify thematic areas for public-health research (from three to thirty), and others ministries referred to policy documents, health plans or public-health plans to define research priorities. Ministries and their agencies led on decisions for financial support of public-health research, with less involvement of other external organisations compared with the process of identifying priorities. However, the actual funds available for public health were not easily identifiable. Most ministries relied on general academic means for dissemination of results of public-health research, while ministries get information on the use of public-health research usually through informal means. Ministries made suggestions for strengthening public-health research through initiatives of their own countries and of the European Union: as well as more resources, improving coordination was most frequently suggested. Conclusion: There is no common approach to support for public-health research across Europe, and significant gaps in organisation and funding. Health ministries and national agencies value exchange between researchers and policy-makers, civil society organizations, and academic and public authorities, and the application of public-health research results. There would be benefits from better processes of priority setting and improved coordination for research, at regional, national and European levels