Risks of small-for-gestational-age births in immigrants: A nationwide epidemiological study in Sweden.

Aim: To examine if there is an association between country of birth in parents and small-for-gestational-age (defined as a birthweight of more than two standard deviations (SDs) below the mean) in first singletons births. Methods: In this follow-up study, national population and healthcare registers were used to identify small-for-gestational-age births in all first singleton births in Sweden between 1 January 1982 and 31 December 2006. Odds ratios, standardised with regard to maternal age at birth, period of birth, marital status, family income, geographical region, employment, maternal height, and smoking history, were estimated by maternal and paternal country of birth. Singletons with both parents born in Sweden were used as reference group. Results: There were 1,060,467 records for first singletons births over the study period, of whom 3.5% were small-for-gestational-age. The rate was higher in newborns with non-Swedish born than in those with Swedish born mothers (4.1 and 3.3%, respectively). Immigrants from Southern European countries, Africa, and Asia had higher risks of small-for-gestational-age in than those in the reference group, and the risks were even higher in compatriot parents. CONCLUSIONS: Country of birth affected the risk of small-for-gestational-age. Maternity care should pay a special attention to pregnancies in certain population groups

Immigrants and Preterm Births: A Nationwide Epidemiological Study in Sweden.

To examine, nationwide, if there is an association between country of birth in mothers and preterm birth and to study whether any such association remains in second-generation immigrant women. In this follow-up study, a nationwide research database located at Lund University, Sweden, was used to identify all preterm born singletons in Sweden between January 1, 1982, and December 31, 2006. Incidence ratios were standardized with regard to maternal age at birth, marital status, geographical region, body height, and smoking history as well as period of birth, family income, and gender of the infant. Singletons of mothers born in Sweden were used as the reference group. There were 2,192,843 records for singletons over the study period, of whom 4.9 % were preterm births and 0.8 % were very preterm births. Increased risk of preterm birth was observed for mothers from Austria, Yugoslavia, Romania, Central Europe, and Asia. Increased risk of very preterm birth was observed for mothers from Eastern Europe, Central Europe, Africa, and Asia; these increased risk disappeared, however, in the second-generation female immigrants. Country of birth in mothers affected the risk of preterm birth; maternity care should pay special attention to women from certain population groups

Subsequent Risks of Parkinson Disease in Patients with Autoimmune and Related Disorders: A Nationwide Epidemiological Study from Sweden.

Objectives: To investigate associations between autoimmune disorders and Parkinson disease (PD), and to study whether the risk is associated with follow-up time and age. Methods: Standardized incidence ratios (SIRs) were calculated for PD in patients with autoimmune disorders by comparing them to subjects without autoimmune disorders. Results: Among 310,522 patients with a total of 33 conditions of autoimmune disorders, 932 patients developed subsequent PD, giving an overall SIR of 1.33 and 1.19 for PD diagnosed later than 1 year after follow-up. Six types of autoimmune disorders showed an increased risk. These conditions included: amyotrophic lateral sclerosis, Graves's disease/hyperthyroidism, Hashimoto's disease/hypothyroidism, multiple sclerosis, pernicious anemia, and polymyalgia rheumatica. The risks depended on the age at hospitalization for PD. Conclusions: A 33% overall excess risk of PD was noted among patients with an autoimmune disorder; the risk was increased during the first 10 years of follow-up after hospitalization of autoimmune disorders

Towards a reduced phase space quantization in loop quantum cosmology with an inflationary potential

We explore a reduced phase space quantization of loop quantum cosmology (LQC) for a spatially flat FLRW universe filled with reference fields and an inflaton field in a Starobinsky inflationary potential. We consider three separate cases in which the reference fields are taken to be the Gaussian dust, the Brown-Kucha\v{r} dust, and massless Klein-Gordon scalar reference fields respectively. This is a "two-fluid" model in which reference fields act as global clocks providing a physical time in an inflationary spacetime, and allow bypassing various technical hurdles in conventional quantum cosmological models. The reduced phase space is obtained in terms of the Dirac observables of the gravitational as well as the inflaton degrees of freedom. The physical Hamiltonians of the two dust models take the same form but turn out to be quite different from that of the Klein-Gordon reference field which reflects an aspect of the multiple choice problem of time. Loop quantization is implemented using the so-called $\bar \mu$ scheme and the Schr\"{o}dinger equations involving the physical Hamiltonian operators generating the evolution in the physical time in the dust and massless Klein-Gordon models are obtained. These turn out to be quantum difference equations with same non-singular structure as for other models in LQC. We study some phenomenological implications of the quantization using the effective dynamics resulting from the reduced phase space quantization including the resolution of the big bang singularity via a quantum bounce, and effects of the different reference fields on e-foldings in both the pre-inflationary and the slow-roll inflationary phases. We find that different clocks, even when starting with a small but same energy density, can leave tiny but different imprints on the inflationary dynamics. (abridged)Comment: Revised shorter version with no change in results. Figures updated. References added. To appear in Phys. Rev.

Nonsingular quantum gravitational dynamics of an Lemaitre-Tolman-Bondi dust shell model: The role of quantization prescriptions

We study some consequences of the loop quantization of the outermost dust shell in the LemaitreTolman-Bondi spacetime with a homogeneous dust density using different quantization strategies motivated by loop quantum gravity. Prior work has dealt with loop quantizing this model by employing holonomies and the triads, following the procedure in standard loop quantum cosmology. In this work we compare this quantization with the one in which holonomies and gauge-covariant fluxes are used. While both of the quantization schemes resolve the central singularity, they lead to different mass gaps at which a trapped surface forms. This trapped surface which is matched to an exterior generalized Vaidya spacetime disappears when the density of the dust cloud is in the Planck regime. We find that the quantization based on holonomies and gauge-covariant fluxes generically results in an asymmetric evolution of the dust shell in which the Vaidya mass associated with the white hole as seen by an external observer is 2/pi of the one for the black hole. This effective difference in masses results from difference in the classical limits in preand postbounce regimes in the two quantizations. This distinctive feature rules out formation of any blackhole-white-hole twins in presence of gauge-covariant flux modifications, which is in contrast to the quantization using holonomies and triads where the gravitational collapse always leads to black hole-white hole twins. Another striking difference lies in the fact that for the quantization based on holonomies and gauge-covariant fluxes there can be situations in which during a nonsingular collapse only a black hole forms without a white hole

Parental poverty and occupation as risk factors for pediatric sleep-disordered breathing.

Previous studies have found associations between pediatric sleep-disordered breathing (SDB) and socioeconomic status (SES), as well as a neighborhood-related disadvantage. This study analyzes the association among familial SES, parental occupation, and SDB in Swedish offspring

Effect of Continuous Capacity Rising Performed by FeS/Fe₃C/C Composite Electrodes for Lithium‐Ion Batteries

FeS‐based composites are sustainable conversion electrode materials for lithium‐ion batteries, combining features like low cost, environmental friendliness, and high capacities. However, they suffer from fast capacity decay and low electron conductivity. Herein, novel insights into a surprising phenomenon of this material are provided. A FeS/Fe3C/C nanocomposite synthesized by a facile hydrothermal method is compared with pure FeS. When applied as anode materials for lithium‐ion batteries, these two types of materials show different capacity evolution upon cycling. Surprisingly, the composite delivers a continuous increase in capacity instead of the expected capacity fading. This unique behavior is triggered by a catalyzing effect of Fe3C nanoparticles. The Fe3C phase is a beneficial byproduct of the synthesis and was not intentionally obtained. To further understand the effect of interconnected carbon balls on FeS‐based electrodes, complementary analytic techniques are used. Ex situ X‐ray radiation diffraction and ex situ scanning electron microscopy are employed to track phase fraction and morphology structure. In addition, the electrochemical kinetics and resistance are evaluated by cyclic voltammetry and electrochemical impedance spectroscopy. These results reveal that the interconnected carbon balls have a profound influence on the properties of FeS‐based electrodes resulting in an increased electrode conductivity, reduced particle size, and maintenance of the structure integrity

Advantages of grass-legume mixture for improvement of crop growth and reducing potential nitrogen loss in a boreal climate

Peer reviewe

The effect of glutamine absence on the viability of endothelial cells with mTOR knockdown genes

BACKGROUND: Endothelial cells line the inner vessels of all organ systems. Endothelial cells share many similarities with cancer cells from their preference for glucose consumption even in the presence of oxygen availability (Warburg effect) to their incredibly fast proliferation through the mTOR pathway. Both cell types also rely heavily on glutamine, in addition to glucose, to maintain their metabolic activities. Glutamine is the most abundant free amino acid in the body, making it readily available to both endothelial and tumor cells as a source of carbons for the synthesis of biomass. Due to these overlapping similarities, there has become an interest in understanding how mutations of cells can allow them to survive in the absence of glutamine. A greater understanding of the mechanism of action from down regulation of specific genes can lead to many clinical applications. OBJECTIVE: To understand if down regulation of specific mTOR genes can affect the viability and proliferation of endothelial cells in glutamine deficient and glutamine supplemented media, respectively. METHODS: siRNA transfection was used as a secondary method to knock down specific genes in endothelial cell lines (ECFC and HUVEC). QPCR was used to validate knockdown efficiency. Cell progression was documented both visually and through cell counting over a long period of time. Cells were placed in both glutamine deficient and glutamine supplemented media to monitor mTOR activity and viability. RESULTS: Of all the genes tested, endothelial cells with CS, SLC7A11, WDR59, and WDR24 knockdowns were shown to have greater viability in glutamine deficient media than the controls. They were also shown to have suppressed proliferative behavior in complete media. CONCLUSIONS: Despite initial CRISPR screening results, not all of the knockdown genes selected from the list were able to survive in glutamine deficient conditions. However, we were able to show that knockdown of CS and SLC7A11 demonstrate similar viability in endothelial cells as previously published studies in cancer cells in glutamine deficient media. Interestingly, both GATOR2 complex genes (WDR59 and WDR24), which act as positive and negative regulators of the mTORC1 pathway via amino acid sensing, were able to survive without glutamine. Future studies could be done to understand the mechanisms behind their survival.2020-07-03T00:00:00

MDM2 prevents spontaneous tubular epithelial cell death and acute kidney injury

Murine double minute-2 (MDM2) is an E3-ubiquitin ligase and the main negative regulator of tumor suppressor gene p53. MDM2 has also a non-redundant function as a modulator of NF-kB signaling. As such it promotes proliferation and inflammation. MDM2 is highly expressed in the unchallenged tubular epithelial cells and we hypothesized that MDM2 is necessary for their survival and homeostasis. MDM2 knockdown by siRNA or by genetic depletion resulted in demise of tubular cells in vitro. This phenotype was completely rescued by concomitant knockdown of p53, thus suggesting p53 dependency. In vivo experiments in the zebrafish model demonstrated that the tubulus cells of the larvae undergo cell death after the knockdown of mdm2. Doxycycline-induced deletion of MDM2 in tubular cell-specific MDM2-knockout mice Pax8rtTa-cre; MDM2f/f caused acute kidney injury with increased plasma creatinine and blood urea nitrogen and sharp decline of glomerular filtration rate. Histological analysis showed massive swelling of renal tubular cells and later their loss and extensive tubular dilation, markedly in proximal tubules. Ultrastructural changes of tubular epithelial cells included swelling of the cytoplasm and mitochondria with the loss of cristae and their transformation in the vacuoles. The pathological phenotype of the tubular cell-specific MDM2-knockout mouse model was completely rescued by co-deletion of p53. Tubular epithelium compensates only partially for the cell loss caused by MDM2 depletion by proliferation of surviving tubular cells, with incomplete MDM2 deletion, but rather mesenchymal healing occurs. We conclude that MDM2 is a non-redundant survival factor for proximal tubular cells by protecting them from spontaneous p53 overexpression-related cell death