Codenseness and openness with respect to an interior operator

Working in an arbitrary category endowed with a fixed (E, M) -factorization system such that M is a fixed class of monomorphisms, we first define and study a concept of codense morphisms with respect to a given categorical interior operator i. Some basic properties of these morphisms are discussed. In particular, it is shown that i-codenseness is preserved under both images and dual images under morphisms in M and E, respectively. We then introduce and investigate a notion of quasi-open morphisms with respect to i. Notably, we obtain a characterization of quasi i-open morphisms in terms of i-codense subobjects. Furthermore, we prove that these morphisms are a generalization of the i-open morphisms that are introduced by Castellini. We show that every morphism which is both i-codense and quasi i-open is actually i-open. Examples in topology and algebra are also provided

Quasi-uniform structures determined by closure operators

We demonstrate a one-to-one correspondence between idempotent closure operators and the so-called saturated quasi-uniform structures on a category C. Not only this result allows to obtain a categorical counterpart P of the Császár-Pervin quasi-uniformity P, that we characterize as a transitive quasi-uniformity compatible with an idempotent interior operator, but also permits to describe those topogenous orders that are induced by a transitive quasi-uniformity on C. The categorical counterpart P⁎ of P−1 is characterized as a transitive quasi-uniformity compatible with an idempotent closure operator. When applied to other categories outside topology P allows, among other things, to generate a family of idempotent closure operators on Grp, the category of groups and group homomorphisms, determined by the normal closure

Diabetes, Obesity, and Hypertension May Enhance Associations between Air Pollution and Markers of Systemic Inflammation

Airborne particulate matter (PM) may lead to increased cardiac risk through an inflammatory pathway. Therefore, we investigated associations between ambient PM and markers of systemic inflammation among repeated measures from 44 senior citizens (≥ 60 years of age) and examined susceptibility by conditions linked to chronic inflammation. Mixed models were used to identify associations between concentrations of fine PM [aerodynamic diameter ≤ 2.5 μm (PM(2.5))] averaged over 1–7 days and measures of C-reactive protein (CRP), interleukin-6 (IL-6), and white blood cells (WBCs). Effect modification was investigated for diabetes, obesity, hypertension, and elevated mean inflammatory markers. We found positive associations between longer moving averages of PM(2.5) and WBCs across all participants, with a 5.5% [95% confidence interval (CI), 0.10 to 11%] increase per interquartile increase (5.4 μg/m(3)) of PM(2.5) averaged over the previous week. PM(2.5) and CRP also exhibited positive associations among all individuals for averages longer than 1 day, with the largest associations for persons with diabetes, obesity, and hypertension. For example, an interquartile increase in the 5-day mean PM(2.5) (6.1 μg/m(3)) was associated with a 14% increase in CRP (95% CI, −5.4 to 37%) for all individuals and an 81% (95% CI, 21 to 172%) increase for persons with diabetes, obesity, and hypertension. Persons with diabetes, obesity, and hypertension also exhibited positive associations between PM(2.5) and IL-6. Individuals with elevated mean inflammatory markers exhibited enhanced associations with CRP, IL-6, and WBCs. We found modest positive associations between PM(2.5) and indicators of systemic inflammation, with larger associations suggested for individuals with diabetes, obesity, hypertension, and elevated mean inflammatory markers

CD24 Expression Identifies Teratogen-Sensitive Fetal Neural Stem Cell Subpopulations: Evidence from Developmental Ethanol Exposure and Orthotopic Cell Transfer Models

Ethanol is a potent teratogen. Its adverse neural effects are partly mediated by disrupting fetal neurogenesis. The teratogenic process is poorly understood, and vulnerable neurogenic stages have not been identified. Identifying these is a prerequisite for therapeutic interventions to mitigate effects of teratogen exposures.We used flow cytometry and qRT-PCR to screen fetal mouse-derived neurosphere cultures for ethanol-sensitive neural stem cell (NSC) subpopulations, to study NSC renewal and differentiation. The identity of vulnerable NSC populations was validated in vivo, using a maternal ethanol exposure model. Finally, the effect of ethanol exposure on the ability of vulnerable NSC subpopulations to integrate into the fetal neurogenic environment was assessed following ultrasound guided, adoptive transfer.Ethanol decreased NSC mRNAs for c-kit, Musashi-1and GFAP. The CD24(+) NSC population, specifically the CD24(+)CD15(+) double-positive subpopulation, was selectively decreased by ethanol. Maternal ethanol exposure also resulted in decreased fetal forebrain CD24 expression. Ethanol pre-exposed CD24(+) cells exhibited increased proliferation, and deficits in cell-autonomous and cue-directed neuronal differentiation, and following orthotopic transplantation into naïve fetuses, were unable to integrate into neurogenic niches. CD24(depleted) cells retained neurosphere regeneration capacity, but following ethanol exposure, generated increased numbers of CD24(+) cells relative to controls.Neuronal lineage committed CD24(+) cells exhibit specific vulnerability, and ethanol exposure persistently impairs this population's cell-autonomous differentiation capacity. CD24(+) cells may additionally serve as quorum sensors within neurogenic niches; their loss, leading to compensatory NSC activation, perhaps depleting renewal capacity. These data collectively advance a mechanistic hypothesis for teratogenesis leading to microencephaly