Retraction: Synthesis of Yttrium Superhydride Superconductor with a Transition Temperature up to 262 K by Catalytic Hydrogenation at High Pressures [Phys. Rev. Lett. 126, 117003 (2021)].

Retraction of DOI: 10.1103/PhysRevLett.126.117003.

Expression of Concern: Synthesis of Yttrium Superhydride Superconductor with a Transition Temperature up to 262 K by Catalytic Hydrogenation at High Pressures [Phys. Rev. Lett. 126, 117003 (2021)].

This corrects the article DOI: 10.1103/PhysRevLett.126.117003.

Synthesis of Yttrium Superhydride Superconductor with a Transition Temperature up to 262 K by Catalytic Hydrogenation at High Pressures.

The recent observation of room-temperature superconductivity will undoubtedly lead to a surge in the discovery of new, dense, hydrogen-rich materials. The rare earth metal superhydrides are predicted to have very high-T_{c} superconductivity that is tunable with changes in stoichiometry or doping. Here we report the synthesis of an yttrium superhydride that exhibits superconductivity at a critical temperature of 262 K at 182±8 GPa. A palladium thin film assists the synthesis by protecting the sputtered yttrium from oxidation and promoting subsequent hydrogenation. Phonon-mediated superconductivity is established by the observation of zero resistance, an isotope effect and the reduction of T_{c} under an external magnetic field. The upper critical magnetic field is 103 T at zero temperature.

Neural correlates of sleepiness induced by catecholamine depletion.

Although extensive indirect evidence exists to suggest that the central dopaminergic system plays a significant role in the modulation of arousal, the functional effect of the dopaminergic influence on the regulation of the sleep-wake cycle remains unclear. Thirteen healthy volunteers and 15 unmedicated subjects with a history of major depressive disorder underwent catecholamine depletion (CD) using oral alpha-methyl-para-tyrosine in a randomized, placebo-controlled, double-blind, crossover study. The main outcome measures in both sessions were sleepiness (Stanford-Sleepiness-Scale), cerebral glucose metabolism (positron emission tomography), and serum prolactin concentration. CD consistently induced clinically relevant sleepiness in both groups. The CD-induced prolactin increase significantly correlated with CD-induced sleepiness but not with CD-induced mood and anxiety symptoms. CD-induced sleepiness correlated with CD-induced increases in metabolism in the medial and orbital frontal cortex, bilateral superior temporal cortex, left insula, cingulate motor area and in the vicinity of the periaqueductal gray. This study suggests that the association between dopamine depletion and sleepiness is independent of the brain reward system and the risk for depression. The visceromotor system, the cingulate motor area, the periaqueductal gray and the caudal hypothalamus may mediate the impact of the dopaminergic system on regulation of wakefulness and sleep.

Screening for mild traumatic brain injury in the presence of psychiatric comorbidities.

OBJECTIVE: To determine whether or not a battery of neurobehavioral tests, the Brief Objective Neurobehavioral Detector (BOND), could detect mild traumatic brain injury (mTBI) among a group of psychiatric inpatients with numerous substance-related and medical comorbidities. The 16-item BOND is comprised of neurologic examination tasks and has been shown to correlate with radiologic and cognitive findings in previous studies. DESIGN: Masked comparison. SETTING: Inpatient psychiatric unit at the Veterans Affairs Medical Center in Washington, DC. PARTICIPANTS: Patients (N=51) sequentially admitted for suicidal ideation in the context of various psychiatric disorders. INTERVENTIONS: No intervention. MAIN OUTCOME MEASURE: BOND total and subtest scores. RESULTS: Forty-three patients were eligible and analyzed. Twenty-seven had sustained an mTBI in the distant past, and 16 had never sustained a traumatic brain injury (TBI) (non-TBI group). On average, the mTBI group demonstrated a significantly greater number of abnormal subtests on the BOND (mean, 7.22) than did the non-TBI group (mean, 4.50; P=.003). Although the BOND significantly correlated with the presence of mTBI, it did not correlate with any of the psychiatric, substance-related, or medical comorbidities. Multiple regressions indicated that the BOND total score was not explained by age, posttraumatic stress disorder diagnosis, or any combination of the psychiatric, substance-related, or medical comorbidities. High rates of sensitivity (70%) and specificity (69%) were found. CONCLUSIONS: The results of this pilot study suggest that the inexpensive, brief, and objective BOND instrument may be a useful screening tool for the detection of subtle neurologic brain abnormalities after mTBI, even in the presence of substantial comorbidities.

Reward processing after catecholamine depletion in unmedicated, remitted subjects with major depressive disorder.

BACKGROUND: We investigated whether performance on a reward processing task differs between fully remitted patients with major depressive disorder (MDD) and healthy control subjects after catecholamine depletion. METHODS: Seventeen unmedicated subjects with remitted MDD (RMDD) and 13 healthy control subjects underwent catecholamine depletion with oral alpha-methyl-para-tyrosine (AMPT) in a randomized, placebo-controlled, double-blind crossover study. The main outcome measure was the reaction time on the monetary incentive delay (MID) task. RESULTS: A diagnosis x drug interaction was evident (p = .001), which was attributable to an increase in reaction time across all incentive levels after AMPT in RMDD subjects (p = .001) but no significant AMPT effect on reaction time in control subjects (p = .17). There was no drug x diagnosis interaction on control tasks involving working memory or attention. In the RMDD sample the AMPT-induced depressive symptoms correlated with AMPT-induced changes in reaction time at all incentive levels of the MID task (r values = .58-.82, p < .002). CONCLUSIONS: Under catecholamine depletion the RMDD subjects were robustly differentiated from control subjects by development of performance deficits on a reward processing task. These performance deficits correlated directly with the return of depressive symptoms after AMPT administration. The sensitivity of central reward processing systems to reductions in brain catecholamine levels thus seems to represent a trait-like marker in MDD.

Neural response to catecholamine depletion in unmedicated subjects with major depressive disorder in remission and healthy subjects.

CONTEXT: The pathophysiologic mechanism of major depressive disorder (MDD) has been consistently associated with altered catecholaminergic function, especially with decreased dopamine neurotransmission, by various sources of largely indirect evidence. An instructive paradigm for more directly investigating the relationship between catecholaminergic function and depression has involved the mood response to experimental catecholamine depletion (CD). OBJECTIVES: To determine whether catecholaminergic dysfunction represents a trait abnormality in MDD and to identify brain circuitry abnormalities involved in the pathophysiologic mechanism of MDD. DESIGN: Randomized, double-blind, placebo-controlled, crossover, single-site experimental trial. SETTING: Psychiatric outpatient clinic. PARTICIPANTS: Fifteen unmedicated subjects with MDD in full remission (hereinafter referred to as RMDD subjects) and 13 healthy controls. INTERVENTION: Induction of CD by oral administration of alpha-methylparatyrosine. Sham depletion used identical capsules containing hydrous lactose. MAIN OUTCOME MEASURES: Quantitative positron emission tomography of regional cerebral glucose utilization to study the neural effects of CD and sham depletion. Behavioral assessments included the Montgomery-Asberg Depression Rating Scale and the Snaith-Hamilton Pleasure Scale (anhedonia). RESULTS: Depressive and anhedonic symptoms increased during CD to a greater extent in RMDD subjects than in controls. In both groups, CD increased metabolism in the anteroventral striatum and decreased metabolism in the orbital gyri. In a limbic-cortical-striatal-pallidal-thalamic network previously implicated in MDD, composed of the ventromedial frontal polar cortex, midcingulate and subgenual anterior cingulate cortex, temporopolar cortex, ventral striatum, and thalamus, metabolism increased in RMDD subjects but decreased or remained unchanged in controls. Metabolic changes induced by CD in the left ventromedial frontal polar cortex correlated positively with depressive symptoms, whereas changes in the anteroventral striatum were correlated with anhedonic symptoms. CONCLUSIONS: This study provides direct evidence for catecholaminergic dysfunction as a trait abnormality in MDD. It demonstrates that depressive and anhedonic symptoms as a result of decreased catecholaminergic neurotransmission are related to elevated activity within the limbic-cortical-striatal-pallidal-thalamic circuitry.

Reduced prefrontal glutamate/glutamine and gamma-aminobutyric acid levels in major depression determined using proton magnetic resonance spectroscopy.

CONTEXT: Increasing evidence indicates that major depressive disorder (MDD) is associated with altered function of the major excitatory and inhibitory neurotransmitters glutamate and gamma-aminobutyric acid (GABA), respectively. A recently developed magnetic resonance spectroscopy method allows for reliable measurement of glutamate/glutamine (Glx) and GABA concentrations in prefrontal brain regions that have been implicated in the pathophysiologic mechanisms of MDD by studies using other neuroimaging and postmortem techniques. OBJECTIVE: To measure Glx and GABA levels in 2 regions of the prefrontal brain tissue in unmedicated adults with MDD. DESIGN: Cross-sectional study for association. SETTING: Psychiatric outpatient clinic. PARTICIPANTS: Twenty unmedicated, depressed patients with MDD and 20 age- and sex-matched controls. Intervention Participants underwent scanning using a 3-T whole-body scanner with a transmit-receive head coil, providing a homogeneous radiofrequency field and the capability of obtaining spectroscopic measurements in a dorsomedial/dorsal anterolateral prefrontal region of interest (ROI) and a ventromedial prefrontal ROI. MAIN OUTCOME MEASURES: Glx and GABA levels derived from magnetic resonance spectroscopy signals. RESULTS: Depressed patients had reduced Glx levels in both ROIs. The GABA levels were reduced in the dorsomedial/dorsal anterolateral prefrontal ROI. Levels of GABA and Glx were positively correlated in both ROIs. CONCLUSIONS: For the first time, GABA and Glx concentrations were compared between unmedicated depressed adults and controls in prefrontal ROIs. The abnormal reductions in Glx and GABA concentrations found in the MDD sample were compatible with findings from postmortem histopathologic studies, indicating that glial cell density is reduced in the same areas in MDD.