Among infertile women with the polycystic ovary syndrome, frozen-embryo transfer was associated with a higher rate of live birth, a lower risk of the ovarian hyperstimulation syndrome, and a higher risk of preeclampsia after the first transfer than was fresh-embryo transfer. (Funded by the National Basic Research Program of China and others; ClinicalTrials.gov number, NCT01841528.).

Stable aqueous solutions of ZnO@polymer core-shell nanoparticles with tunable photoluminescence are prepared through a simple sol-gel route. The copolymer shell has many hydrophilic external groups and a hydrophobic internal layer which connects ZnO cores through covalent bonds. The optimal samples show quantum yield above 50% and stable emission for months. These samples with their concentrations of below 0.2 mg/mL are nontoxic to human cells. After uptake of these ZnO@polymer nanoparticles, the luminescent cells have enough life under UV light for microscopic imaging.

No abstract

A bright idea: Mg/ZnO nanoparticles that exhibit bright, stable photoluminescence both in colloidal dispersions and in the solid state are formed by doping Mg(II) ions into ZnO nanoparticles by sonochemical synthesis. The changes in their band gaps and luminescence properties rely on the defect concentrations inside the ZnO nanoparticles; these concentrations are determined by the Mg/Zn molar ratios (see picture).

This study indicates that inhaled formaldehyde starts to negatively affect learning and memory at a middle concentration of formaldehyde without interference of other indoor air pollutants. Oxidative damage, and the alteration of NMDA receptor expression, which were induced by formaldehyde inhalation, may be the possible mechanism for gaseous formaldehyde-induced neurotoxicity.

ObjectiveFormaldehyde, a ubiquitous environmental pollutant has been classified as a human leukemogen. However, toxicity of formaldehyde in bone marrow, the target site of leukemia induction, is still poorly understood.Methodology/Principal FindingsTo investigate bone marrow toxicity (bone marrow pathology, hematotoxicity) and underlying mechanisms (oxidative stress, inflammation, apoptosis) in formaldehyde-exposed mice. Male Balb/c mice were exposed to formaldehyde (0, 0.5, and 3.0 mg/m3) by nose-only inhalation for 8 hours/day, over a two week period designed to simulate a factory work schedule, with an exposure-free “weekend” on days 6 and 7, and were sacrificed on the morning of day 13. Counts of white blood cells, red blood cells and lymphocytes were significantly (p<0.05) decreased at 0.5 mg/m3 (43%, 7%, and 39%, respectively) and 3.0 mg/m3 (52%, 27%, and 43%, respectively) formaldehyde exposure, while platelet counts were significantly increased by 109% (0.5 mg/m3) and 67% (3.0 mg/m3). Biomarkers of oxidative stress (reactive oxygen species, glutathione depletion, cytochrome P450 1A1 and glutathione s-transferase theta 1 expression), inflammation (nuclear factor kappa-B, tomour necrosis factor alpha, interleukin-1 beta), and apoptosis (activity of cysteine-aspartic acid protease 3) in bone marrow tissues were induced at one or both formaldehyde doses mentioned above.Conclusions/SignificanceExposure of mice to formaldehyde by inhalation induced bone marrow toxicity, and that oxidative stress, inflammation and the consequential apoptosis jointly constitute potential mechanisms of such induced toxicity.

Recent studies show that formaldehyde participates in DNA demethylation/methylation cycle. Emerging evidence identifies that neuronal activity induces global DNA demethylation and re-methylation; and DNA methylation is a critical step for memory formation. These data suggest that endogenous formaldehyde may intrinsically link learning-responsive DNA methylation status and memory formation. Here, we report that during spatial memory formation process, spatial training induces an initial global DNA demethylation and subsequent re-methylation associated with hippocampal formaldehyde elevation then decline to baseline level in Sprague Dawley rats. Scavenging this elevated formaldehyde by formaldehyde-degrading enzyme (FDH), or enhancing DNA demethylation by a DNA demethylating agent, both led to spatial memory deficits by blocking DNA re-methylation in rats. Furthermore, we found that the normal adult rats intrahippocampally injected with excess formaldehyde can imitate the aged-related spatial memory deficits and global DNA methylation decline. These findings indicate that aging-associated excess formaldheyde contributes to cognitive decline during aging.

Pepsin in saliva has moderate value in the diagnosis of LPR. The cutoff value used could affect the diagnostic value. Therefore, further investigations are required to find the optimal method to detect salivary pepsin in diagnosing LPR.