MicroRNAs as potential biomarkers for diagnosis of attention deficit hyperactivity disorder

Inappropriate levels of hyperactivity,impulsivity,and inattention characterize attention deficit hyperactivity disorder,a common childhood-onset neuropsychiatric disorder.The cognitive function and learning ability of children with attention deficit hyperactivity disorder are affected,and these symptoms may persist to adulthood if they are not treated.The diagnosis of attention deficit hyperactivity disorder is only based on symptoms and objective tests for attention deficit hyperactivity disorder are missing.Treatments for attention deficit hyperactivity disorder in children include medications,behavior therapy,counseling,and education services which can relieve many of the symptoms of attention deficit hyperactivity disorder but cannot cure it.There is a need for a molecular biomarker to distinguish attention deficit hyperactivity disorder from healthy subjects and other neurological conditions,which would allow for an earlier and more accurate diagnosis and appropriate treatment to be initiated.Abnormal expression of microRNAs is connected to brain development and disease and could provide novel biomarkers for the diagnosis and prognosis of attention deficit hyperactivity disorder.The recent studies reviewed had performed microRNA profiling in whole blood,white blood cells,blood plasma,and blood serum of children with attention deficit hyperactivity disorder.A large number of microRNAs were dysregulated when compared to healthy controls and with some overlap between individual studies.From the studies that had included a validation set of patients and controls,potential candidate biomarkers for attention deficit hyperactivity disorder in children could be miR-140-3p,let-7g-5p,-30e-5p,-223-3p,-142-5p,-486-5p,-151a-3p,-151a-5p,and-126-5p in total white blood cells,and miR-4516,-6090,-4763-3p,-4281,-4466,-101-3p,-130a-3p,-138-5p,-195-5p,and-106b-5p in blood serum.Further studies are warranted with children and adults with attention deficit hyperactivity disorder,and consideration should be given to utilizing rat models of attention deficit hyperactivity disorder.Animal studies could be used to confirm microRNA findings in human patients and to test the effects of targeting specific microRNAs on disease progression and behavior.

A carbon dot-based total green and self-recoverable solid-state electrochemical cell fully utilizing H_(2)O_(2)redox couple

Electrochemical cell can overcome the inherent intermittence of the renewable energy sources,thus showing great potentials in applications ranging from elec-trical energy storage to future smart grid.However,the current electrochemical cells could not achieve the“total green”feature by fully utilizing the clean and abundant O_(2)/H_(2)O redox couples due to the enormous overpotentials for both oxygen reduction reaction(ORR)and oxygen release reaction(OER).Herein,we report a“total green”electrochemical composite film cell based on carbon dots(CDots),which can realize both ORR and OER in the acid environment.The in-air voltage generation(0.95 V,with a maximum power of 5.3μW)relies on the multiple-electron-transfer redox chemical reaction between the two active components inside the composite film,that is,ORR/OER of CDots and the redox reaction of polyaniline(PANI)on the electrode and the resulting proton concentration gradient.Interestingly,the cell can be self-recovered at low load,recharged by adding H_(2)O_(2),or electrocharged at high load.We anticipate that current study may open up new opportunities for designing and developing total-green energy storage and conversion systems for diverse applications.

Pure Total Flavonoids from Citrus paradisi Macfad InduceLeukemia Cell Apoptosis In Vitro

Objective： To investigate the potential effect of pure total flavonoids from Citrus paradisi Macfad peel（PTFC） on the proliferation and apoptosis of human myeloid leukemia cells Kasumi-1, HL-60 and K562, and the underlying mechanisms. Methods： PTFC was extracted from Citrus paradisi Macfad peel and was identified by high performance liquid chromatography. The effect of PTFC on the proliferation and apoptosis of leukemia cells were determined by 3-（4,5-dimethylthiazol-2-yl）-2,5-diphenyltetrazolium bromide, fluorescent microscopy and flow cytometry, respectively. The effect of PTFC on the expression levels of apoptosis-related regulators was determined by Western blot assay. Results： Treatment with PTFC inhibited leukemia cell proliferation in a dose-and time-dependent manner and triggered Kasumi-1 cell apoptosis. Treatment with PTFC significantly increased the levels of activated poly adenosine diphosphate-ribosepolymerase and caspase-3/-9, but reduced the levels of Mcl-1 expression in Kasumi-1 cells. However, PTFC did not obviously induce HL-60 cell apoptosis. Conclusion： PTFC inhibited leukemia cell proliferation and induced their apoptosis by modulating apoptosisrelated regulator expression in leukemia cells in vitro.