Light therapy for seasonal affective disorder with blue narrow-band light-emitting diodes (LEDs)

Background: While light has proven an effective treatment for Seasonal Affective Disorder (SAD), an optimal wavelength combination has not been determined. Short wavelength light (blue) has demonstrated potency as a stimulus for acute melatonin suppression and circadian phase shifting. Methods: This study tested the efficacy of short wavelength light therapy for SAD. Blue light emitting diode (LED) units produced 468 nm light at 607 µW/cm2 (27 nm half-peak bandwidth); dim red LED units provided 654 nm at 34 µW/cm2 (21 nm half-peak bandwidth). Patients with major depression with a seasonal pattern, a score of ≥20 on the Structured Interview Guide for the Hamilton Depression Rating Scale-SAD version (SIGH-SAD) and normal sleeping patterns (routine bedtimes between 10:00 pm and midnight) received 45 minutes of morning light treatment daily for 3 weeks. Twenty-four patients completed treatment following random assignment of condition (blue vs. red light). The SIGH-SAD was administered weekly. Results: Mixed-effects analyses of covariance determined that the short wavelength light treatment decreased SIGH-SAD scores significantly more than the dimmer red light condition (F = 6.45, p = .019 for average over the post-treatment times). Conclusions: Narrow bandwidth blue light at 607 µW/cm2 outperforms dimmer red light in reversing symptoms of major depression with a seasonal pattern

Effects of the neurogranin variant rs12807809 on thalamocortical morphology in schizophrenia

10.1371/journal.pone.0085603PLoS ONE812-POLN

Primary Stroke Centers: Their Role and Impact on Acute Stroke Management

The management of acute ischemic stroke has been recognized as a significant medical problem. Stroke remains to be the third leading cause of death and the leading cause of long-term disability; 80% of all strokes are ischemic (a blood clot disrupts blood flow), and the rest are hemorrhagic (a blood vessel ruptures in the brain). Nearly 1 in 15 deaths in 2003 were the result of a stroke.1 Approximately 750,000 new strokes occur annually, of which 250,000 result in the deaths in the United States alone. The latest estimates for stroke costs total to about $30 billion in direct costs, and$20 billion are in indirect costs.2 If nothing is done about this disease, the annual incidence of strokes is expected to reach 1.1 million by the year 2015

Cardioembolic Stroke Secondary to Lambl\u27s Excrescence on the Aortic Valve: A Case Report.

We report a patient who presented with aphasia and was found to have an embolic cerebral infarction secondary to LE. LE is a rare source of cardioembolic stroke

Improving Resident Confidence and Efficiency During Stroke Alerts Through Simulation Training

Objectives Teach incoming neurology residents how to respond efficiently and appropriately to stroke alerts Improve the confidence level of residents during stroke alertshttps://jdc.jefferson.edu/patientsafetyposters/1084/thumbnail.jp

The Prevalence and Risk Factors of Acute Myocardial Infarction (AMI) After Acute Ischemic Stroke (AIS) in the United States

Objectives: To determine the prevalence and risk factors for, and the association with in-hospital mortality of, AMI after AIS, and to study the effect of intravenous recombinant tissue plasminogen activator (r-tPA) in this setting. We hypothesized that AMI would be associated with lower survival rate at hospital discharge but that intravenous r-tPA would be associated with lower risk of AMI

Pennsylvania comprehensive stroke center collaborative: Statement on the recently updated IV rt-PA prescriber information for acute ischemic stroke.

OBJECTIVE: Recently, the FDA guidelines regarding the eligibility of patients with acute ischemic stroke to receive IV rt-PA have been modified and are not in complete accord with the latest AHA/ASA guidelines. The resultant differences may result in discrepancies in patient selection for intravenous thrombolysis. METHODS: Several comprehensive stroke centers in the state of Pennsylvania have undertaken a collaborative effort to clarify and unify our own recommendations regarding how to reconcile these different guidelines. RESULTS: Seizure at onset of stroke, small previous strokes that are subacute or chronic, multilobar infarct involving more than one third of the middle cerebral artery territory on CT scan, hypoglycemia, minor or rapidly improving symptoms should not be considered as contraindications for intravenous thrombolysis. It is recommended to follow the AHA/ASA guidelines regarding blood pressure management and bleeding diathesis. Patients receiving factor Xa inhibitors and direct thrombin inhibitors within the preceding 48h should be excluded from receiving IV rt-PA. CT angiography is effective in identifying candidates for endovascular therapy. Consultation with and/or transfer to a comprehensive stroke center should be an option where indicated. Patients should receive IV rt-PA up to 4.5h after the onset of stroke. CONCLUSIONS: The process of identifying patients who will benefit the most from IV rt-PA is still evolving. Considering the rapidity with which patients need to be evaluated and treated, it remains imperative that systems of care adopt protocols to quickly gather the necessary data and have access to expert consultation as necessary to facilitate best practices

Transaldolase inhibition impairs mitochondrial respiration and induces a starvation-like longevity response in <i>Caenorhabditis elegans</i>

<div><p>Mitochondrial dysfunction can increase oxidative stress and extend lifespan in <i>Caenorhabditis elegans</i>. Homeostatic mechanisms exist to cope with disruptions to mitochondrial function that promote cellular health and organismal longevity. Previously, we determined that decreased expression of the cytosolic pentose phosphate pathway (PPP) enzyme transaldolase activates the mitochondrial unfolded protein response (UPR^mt) and extends lifespan. Here we report that transaldolase (<i>tald-1</i>) deficiency impairs mitochondrial function <i>in vivo</i>, as evidenced by altered mitochondrial morphology, decreased respiration, and increased cellular H₂O₂ levels. Lifespan extension from knockdown of <i>tald-1</i> is associated with an oxidative stress response involving p38 and c-Jun N-terminal kinase (JNK) MAPKs and a starvation-like response regulated by the transcription factor EB (TFEB) homolog HLH-30. The latter response promotes autophagy and increases expression of the flavin-containing monooxygenase 2 (<i>fmo-2</i>). We conclude that cytosolic redox established through the PPP is a key regulator of mitochondrial function and defines a new mechanism for mitochondrial regulation of longevity.</p></div