Ligand-Engineered Structural and Physiochemical Properties of 1D Molybdenum-MOFs: A Seldom Explored System for Photocatalytic Applications.

As one of the seldom explored systems, molybdenum-based metal-organic frameworks (Mo-MOFs) with different ligands such as terephthalic acid (Mo-TA), 2-aminoterephthalic acid (Mo-ATA), benzenetricarboxylic acid (Mo-BTC), 2-methylimidazole (Mo-2MI), 2-bipyridine (Mo-2bpy), and 4-bipyridine (Mo-4bpy) were developed in this study. X-ray diffraction (XRD), Raman, and attenuated total reflectance-infrared (ATR-IR) analyses confirmed the ligand-dependent crystal structure of the Mo-MOFs along with the characteristic functional groups present in the respective systems. Interestingly, the morphology of all of these the developed Mo-MOFs was found to be a one-dimensional rod-like structure, which was attributed to the binding nature of the ligands onto the growing Mo-frameworks. Optical analysis indicated that all these Mo-MOFs exhibit ultraviolet (UV) light absorption properties with band gap energy in the range of 3.47-3.03 eV. Among the various Mo-MOFs developed, Mo-4bpy MOF degraded a maximum of ∼76 and 62% of malachite green and Congo red dyes, respectively, under sunlight irradiation. The observed improved photocatalytic efficiency of Mo-4bpy MOF was attributed to its appropriate band edge potential, confirmed by Mott-Schottky analysis, improved carrier lifetime (∼34.6 ns) estimated using the time-resolved photoluminescence (TRPL) spectrum, presence of elements with stable oxidation states in the system confirmed by X-ray photoelectron spectroscopy (XPS), improved charge transfer characteristics, and decreased recombination resistance, as confirmed by impedance and PL analyses, respectively. The degradation of Mo-4bpy MOFs mediated by superoxide (•O2-) and hydroxyl radicals (OH•) was further confirmed by scavenger studies. Cyclic studies performed for up to 5 cycles suggested that the degradation efficiency of the Mo-4bpy MOF was stable, attributed to its excellent structural, optical, and morphological features confirmed via postcharacterization of the recycled photocatalyst.

Inhibition of striatal dopamine release by the L-type calcium channel inhibitor isradipine co-varies with risk factors for Parkinson's.

Ca2+ entry into nigrostriatal dopamine (DA) neurons and axons via L-type voltage-gated Ca2+ channels (LTCCs) contributes, respectively, to pacemaker activity and DA release and has long been thought to contribute to vulnerability to degeneration in Parkinson's disease. LTCC function is greater in DA axons and neurons from substantia nigra pars compacta than from ventral tegmental area, but this is not explained by channel expression level. We tested the hypothesis that LTCC control of DA release is governed rather by local mechanisms, focussing on candidate biological factors known to operate differently between types of DA neurons and/or be associated with their differing vulnerability to parkinsonism, including biological sex, α-synuclein, DA transporters (DATs) and calbindin-D28k (Calb1). We detected evoked DA release ex vivo in mouse striatal slices using fast-scan cyclic voltammetry and assessed LTCC support of DA release by detecting the inhibition of DA release by the LTCC inhibitors isradipine or CP8. Using genetic knockouts or pharmacological manipulations, we identified that striatal LTCC support of DA release depended on multiple intersecting factors, in a regionally and sexually divergent manner. LTCC function was promoted by factors associated with Parkinsonian risk, including male sex, α-synuclein, DAT and a dorsolateral co-ordinate, but limited by factors associated with protection, that is, female sex, glucocerebrosidase activity, Calb1 and ventromedial co-ordinate. Together, these data show that LTCC function in DA axons and isradipine effect are locally governed and suggest they vary in a manner that in turn might impact on, or reflect, the cellular stress that leads to parkinsonian degeneration.

A new model of axon degeneration in the mouse optic nerve using repeat intraocular pressure challenge.

We characterize a new experimental model for inducing retinal ganglion cell (RGC) dysfunction and degeneration in mice. C57BL/6J mice were subjected to two acute periods of intraocular pressure (IOP) elevation (50 mmHg for 30 min) by cannulation of the anterior chamber. We used full-field electroretinography and visual evoked potentials (VEPs) to measure subsequent changes in retina and optic nerve function, and histochemical techniques to assess RGC survival and optic nerve structure. In 12 month old mice, a single IOP challenge caused loss and subsequent recovery of RGC function over the following 28 days with minimal cell death and no observed axonal damage. A second identical IOP challenge resulted in persistent RGC dysfunction and significant (36%) loss of RGC somas. This was accompanied by a 16.7% delay in the latency and a 27.6% decrease in the amplitude of the VEP. Severe axonal damage was seen histologically with enlargement of axons, myelin disruption, reduced axon density, and the presence of glial scarring. In contrast, younger 3 month old mice when exposed to a single or repeat IOP challenge showed quicker RGC functional recovery after a single challenge and full functional recovery after a repeat challenge with no detectable optic nerve dysfunction. These data demonstrate a highly reproducible and minimally invasive method for inducing RGC degeneration and axonal damage in mice. Resilience of the optic nerve to damage is highly dependent on animal age. The time-defined nature of functional versus structural loss seen in this model stands to facilitate investigation of neuroglial responses in the retina after IOP injury and the associated evaluation of neuroprotective treatment strategies. Further, the model may be used to investigate the impact of aging and the cellular switch between neurorecovery and neurodegeneration.

Morbidities in Neonates Delivered Electively at Early Term.

OBJECTIVE: To study the incidence of elective cesarean deliveries at term and to correlate their neonatal outcomes at different gestational ages (37(0/7)-40(6/7)). METHODS: Outcomes including the rate of NICU admissions, usage of ventilator/CPAP, and other morbidities were analysed and compared with the gestational age during the study period from January 2012 to April 2013. RESULTS: The incidences of elective deliveries at 37, 38, 39, and 40 weeks of gestation were 10.6, 29.7, 28, and 31.5 %, respectively. NICU admissions-RR 3.94 (95 % CI 1.92-8.09), respiratory distress-RR 5.255 (95 % CI 1.9-14.4), ventilatory usage, and hospitalization stay (P value < 0.05) were higher in neonates born at 37(0/7-6/7) versus 39(0/7-6/7) weeks (least morbidity group). CONCLUSION: Despite recommendations, more than one-third of term babies are delivered electively at <39 weeks. The fivefold augmented respiratory morbidity and fourfold increased NICU admissions in early term neonates, and the least morbidity in neonates delivered at 39 weeks emphasize the importance of restricting the non-emergent/elective deliveries to 39 weeks of gestation.