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We independently manipulated ITD and ILD cues in virtual acoustic space and found that sensitivity to ITD and ILD respectively shaped the directional sensitivity of ICC neurons to low- ( 3 kHz) stimuli, regardless of the neuron's CF. We also found evidence that high-CF neurons transmit information about both the fine-structure and envelope ITD of low-frequency sound. Our results indicate that at conversational sound levels, the majority of the cochleotopic map is engaged in transmitting directional information, even for sources with narrowband spectra.Traumatic brain injury (TBI) is one of the most prevalent forms of morbidity in veterans and service members with mild traumatic brain injury (mTBI) being the most common. The diagnosis of mTBI in veterans is difficult because of mixed etiologies, and high comorbidity with other disorders such as posttraumatic stress disorder (PTSD), depression and substance use. Advanced neuroimaging techniques such as magnetic resonance spectroscopy (MRS) may be useful in identifying neurochemical alterations in TBI, which may aid the development of new targets for therapeutic intervention. Veterans with (n=53) and without a history of TBI (n=26) underwent single-voxel proton (1H) magnetic resonance spectroscopy (MRS) at 3 Tesla in the anterior cingulate cortex (ACC) using a two-dimensional (2D) J-resolved point spectroscopy sequence in addition to completing a clinical battery. Increased mI/H2O was observed in the ACC of the TBI group than the non-TBI group, which may be reflective of astrogliosis. Furthermore, the mI/H2O showed a trend towards an inverse relationship with the global assessment of functioning (GAF) scores in the TBI group. Several metabolites in the ACC demonstrated significant associations with TBI variables including number of TBI with loss of consciousness (LOC) and time since most severe TBI, suggesting that changes in some metabolites may be potential diagnostic and prognostic indicators.Zinc oxide nanoparticles are well-known metal oxide nanoparticles having numbers of applications in the field of cosmetology, medicine, and chemistry. However, the number of reports has indicated its toxicity also such as hepatotoxicity, pulmonary toxicity, neurotoxicity, and immunotoxicity. Thus, in this article, we have analyzed the potential risks and benefits of zinc oxide nanoparticles. The data related to risks and benefits of zinc oxide nanoparticles have been extracted from PubMed (from January 2007 to August 2019). A total of 3,892 studies have been published during this period regarding zinc oxide nanoparticles. On the basis of inclusion and exclusion criteria, 277 studies have been included for the analysis of risks and benefits. Emerging reports have indicated both risks and benefits of zinc oxide nanoparticles in concentration- and time-dependent manner under in vitro and in vivo conditions through different mechanism of action. In conclusion, zinc oxide nanoparticles could play a beneficial role in the treatment of various diseases but safety of these particles at particular effective concentration should be thoroughly evaluated.PURPOSE Partial nephrectomy (PN) is prioritized over radical nephrectomy (RN) in patients with chronic-kidney-disease (CKD) whenever feasible. However, we hypothesized that some patients with severe-CKD might rapidly progress to end-stage-renal-disease (ESRD), in which case the morbidity that can be associated with PN would not be justified. MATERIALS/METHODS A retrospective review of all 62 patients with stage-IV CKD undergoing PN at our institution (1999-2015) was performed. Etoposide chemical structure We analyzed preoperative/intraoperative factors and postoperative outcomes. Survival-analyses evaluated factors associated with time-to-progression to ESRD, the primary end-point. RESULTS Median age was 67 years, 71% of patients were male, and 84% Caucasian. Comorbidities included hypertension (94%), cardiovascular-disease (53%) and diabetes (32%). Median preoperative-eGFR was 23ml/min/1.73m2; and 73% had an open approach. Benign pathology was found in 10 (16%) patients; only 23 (37%) and 7 (11%) patients had tumor grade 3/4 or pT3a disay be more appropriate, particularly when PN is high-complexity or when the patients is African-American or preoperative-GFR is less then 25ml/min/1.73m2.Stroke is a leading cause of death and disability worldwide with many people left with impaired motor function. Evidence from experimental animal models of stroke indicates that reducing motor cortex inhibition may facilitate neural plasticity and motor recovery. This study compared primary motor cortex (M1) inhibition measures over the first 12 weeks after stroke with a cohort of age-similar healthy controls. The excitation-inhibition ratio and gamma-aminobutyric acid (GABA) neurotransmission within M1 were assessed using magnetic resonance spectroscopy and threshold hunting paired-pulse transcranial magnetic stimulation respectively. Upper limb impairment and function were assessed with Fugl-Meyer Upper Extremity Scale and Action Research Arm Test. Patients with a functional corticospinal pathway had motor evoked potentials on the paretic side and exhibited better recovery from upper limb impairment and recovery of function than patients without a functional corticospinal pathway. Compared to age-similar controls, the neurochemical balance in terms of the excitation-inhibition ratio was greater within contralesional M1 in patients with a functional corticospinal pathway. There was evidence for elevated long-interval inhibition in both ipsilesional and contralesional M1 compared with controls. Short-interval inhibition measures differed between the first and second phases, with evidence for elevation of the former only in ipsilesional M1 and no evidence of disinhibition for the latter. Overall, findings from transcranial magnetic stimulation indicate an up-regulation of GABA-mediated tonic inhibition in M1 early after stroke. Therapeutic approaches that aim to normalize inhibitory tone during the sub-acute period warrants further investigation.Pancreatic cancer tends to be highly resistant to current therapy and remains one of the great challenges in biomedicine with very low 5-year survival rates. Here, we report that zalcitabine, an antiviral drug for human immunodeficiency virus infection, can suppress the growth of primary and immortalized human pancreatic cancer cells through the induction of ferroptosis, an iron-dependent form of regulated cell death. Mechanically, this effect relies on zalcitabine-induced mitochondrial DNA stress, which activates the STING1/TMEM173-mediated DNA sensing pathway, leading to macroautophagy/autophagy-dependent ferroptotic cell death via lipid peroxidation, but not a type I interferon response. Consequently, the genetic and pharmacological inactivation of the autophagy-dependent ferroptosis pathway diminishes the anticancer effects of zalcitabine in cell culture and animal models. Together, these findings not only provide a new approach for pancreatic cancer therapy but also increase our understanding of the interplay between autophagy and DNA damage response in shaping cell death.

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