Photocurrent-driven transient symmetry breaking in the Weyl semimetal TaAs.

Symmetry plays a central role in conventional and topological phases of matter, making the ability to optically drive symmetry changes a critical step in developing future technologies that rely on such control. Topological materials, like topological semimetals, are particularly sensitive to a breaking or restoring of time-reversal and crystalline symmetries, which affect both bulk and surface electronic states. While previous studies have focused on controlling symmetry via coupling to the crystal lattice, we demonstrate here an all-electronic mechanism based on photocurrent generation. Using second harmonic generation spectroscopy as a sensitive probe of symmetry changes, we observe an ultrafast breaking of time-reversal and spatial symmetries following femtosecond optical excitation in the prototypical type-I Weyl semimetal TaAs. Our results show that optically driven photocurrents can be tailored to explicitly break electronic symmetry in a generic fashion, opening up the possibility of driving phase transitions between symmetry-protected states on ultrafast timescales.

DAT isn't all that: cocaine reward and reinforcement require Toll-like receptor 4 signaling.

The initial reinforcing properties of drugs of abuse, such as cocaine, are largely attributed to their ability to activate the mesolimbic dopamine system. Resulting increases in extracellular dopamine in the nucleus accumbens (NAc) are traditionally thought to result from cocaine's ability to block dopamine transporters (DATs). Here we demonstrate that cocaine also interacts with the immunosurveillance receptor complex, Toll-like receptor 4 (TLR4), on microglial cells to initiate central innate immune signaling. Disruption of cocaine signaling at TLR4 suppresses cocaine-induced extracellular dopamine in the NAc, as well as cocaine conditioned place preference and cocaine self-administration. These results provide a novel understanding of the neurobiological mechanisms underlying cocaine reward/reinforcement that includes a critical role for central immune signaling, and offer a new target for medication development for cocaine abuse treatment.

Tunable anomalous Hall conductivity through volume-wise magnetic competition in a topological kagome magnet.

Magnetic topological phases of quantum matter are an emerging frontier in physics and material science. Along these lines, several kagome magnets have appeared as the most promising platforms. Here, we explore magnetic correlations in the kagome magnet Co3Sn2S2. Using muon spin-rotation, we present evidence for competing magnetic orders in the kagome lattice of this compound. Our results show that while the sample exhibits an out-of-plane ferromagnetic ground state, an in-plane antiferromagnetic state appears at temperatures above 90 K, eventually attaining a volume fraction of 80% around 170 K, before reaching a non-magnetic state. Strikingly, the reduction of the anomalous Hall conductivity (AHC) above 90 K linearly follows the disappearance of the volume fraction of the ferromagnetic state. We further show that the competition of these magnetic phases is tunable through applying either an external magnetic field or hydrostatic pressure. Our results taken together suggest the thermal and quantum tuning of Berry curvature induced AHC via external tuning of magnetic order.

The failure to survive of autogenous free grafts of whole gracilis muscles in dogs.

An experimental study was undertaken to define the limits in size (if any) of successful free autogenous grafts of skeletal muscle. In 8 dogs, 16 gracilis muscle grafts were transplanted to the contralateral hind limb. The left hind limb served as a control for the right side, which contained paralyzed muscle. Macroscopic, microscopic, and EMG analyses demonstrated a complete failure of the free muscle grafts to take and survive. We have shown that one can exceed the limitations to the size of a successful muscle graft. Perhaps future investigators will define exactly what the maximum viable size is.

Phenylbutazone kinetics and metabolite concentrations in the horse after five days of administration.

Phenylbutazone (PBZ) was administered (8.8 mg/kg of body weight) every 24 hours for 5 consecutive days, orally for the first 4 days and IV on day 5. The half-life (t 1/2) after this daily administration was 6.2 hours and the volume of distribution was 0.152 +/- 0.014 L/kg; the bioavailability after oral administration was 91.8 +/- 2.5%. The plasma concentration of PBZ at experimental hour (EH) 24 (24 hours after the 1st oral dose) was 1.7 +/- 0.39 micrograms/ml and increased to 4.2 +/- 0.29 micrograms/ml at EH 48 (24 hours after the 2nd oral dose). Values at EH 72, 96, and 120 (24 hours after administration of oral doses 3 and 4, and IV dose 5, respectively) were 4.8 +/- 0.62 micrograms/ml, 5.3 +/- 0.84 micrograms/ml, and 4.3 +/- 1.1 micrograms/ml, respectively. Significant increases (P less than 0.05) were measured between EH 24 and 48 with no changes during the subsequent 3 days. Changes in the urinary concentrations of PBZ were not seen over the 5-day dosing period. There were increases in the metabolites oxyphenbutazone and the alpha-alcohol during the 5-day dosing period. There was a delay in the appearance of alpha-alcohol in urine after oral and IV administration.

Abdominal lipectomy as an office procedure.

Because of the increasing cost of hospitalization, many plastic surgeons have tried to make cosmetic surgery more affordable by performing procedures in the office operating room under local anesthesia and sedation. Standard abdominal lipectomy has classically been considered a procedure to be carried out in the hospital under general anesthesia. Following is the author's technique for performing the procedure under local anesthesia in the office setting.

Activation of adult rat CNS endothelial cells by opioid-induced toll-like receptor 4 (TLR4) signaling induces proinflammatory, biochemical, morphological, and behavioral sequelae.

CNS immune signaling contributes to deleterious opioid effects including hyperalgesia, tolerance, reward, and dependence/withdrawal. Such effects are mediated by opioid signaling at toll-like receptor 4 (TLR4), presumptively of glial origin. Whether CNS endothelial cells express TLR4 is controversial. If so, they would be well positioned for activation by blood-borne opioids, contributing to opioid-induced pro-inflammatory responses. These studies examined adult primary rat CNS endothelial cell responses to (-)-morphine or its mu opioid receptor (MOR)-inactive metabolite morphine-3-glucuronide (M3G), both known TLR4 agonists. We demonstrate that adult rat CNS endothelial cells express functional TLR4. M3G activated nuclear factor kappaB (NF-κB), increased tumor necrosis factor-α (TNFα) and cyclooxygenase-2 (COX2) mRNAs, and released prostaglandin E2 (PGE2) from these cells. (-)-Morphine-induced upregulation of TNFα mRNA and PGE2 release were unmasked by pre-treatment with nalmefene, a MOR antagonist without TLR4 activity (unlike CTAP, shown to have both MOR- and TLR4-activity), suggestive of an interplay between MOR and TLR4 co-activation by (-)-morphine. In support, MOR-dependent Protein Kinase A (PKA) opposed TLR4 signaling, as PKA inhibition (H-89) also unmasked (-)-morphine-induced TNFα and COX2 mRNA upregulation. Intrathecal injection of CNS endothelial cells, stimulated in vitro with M3G, produced TLR4-dependent tactile allodynia. Further, cortical suffusion with M3G in vivo induced TLR4-dependent vasodilation. Finally, endothelial cell TLR4 activation by lipopolysaccharide and/or M3G was blocked by the glial inhibitors AV1013 and propentofylline, demonstrating endothelial cells as a new target of such drugs. These data indicate that (-)-morphine and M3G can activate CNS endothelial cells via TLR4, inducing proinflammatory, biochemical, morphological, and behavioral sequelae. CNS endothelial cells may have previously unanticipated roles in opioid-induced effects, in phenomena blocked by presumptive glial inhibitors, as well as TLR4-mediated phenomena more broadly.

Bleeding peptic ulcer: surgical therapy.

The management of bleeding peptic ulcer disease varies with multiple clinical and endoscopic variables. For the patient with rapid hemorrhage and hemodynamic instability refractory to endoscopic control, operation clearly is indicated. For patients with a low probability of recurrent ulcer hemorrhage because of the absence of endoscopic stigmata or clinical predictors of further ulcer bleeding, nonoperative management with selective use of endoscopic hemostasis is appropriate. For the remaining patients with a moderate risk of recurrent ulcer hemorrhage, the clinician must use what is known of the clinical and endoscopic predictors of recurrent hemorrhage and arrive at a judgment regarding the selective use of endoscopic hemostasis and subsequent early operation. For elderly patients with a large duodenal or gastric ulcer who have experienced significant blood loss precipitating an episode of hypovolemic shock and who have endoscopic stigmata of ulcer hemorrhage, early elective operation after endoscopic hemostasis is the most judicious course. Surgery also is the wise choice for those patients in whom an initially successful attempt at endoscopic hemostasis fails and who rebleed while hospitalized. Recommendations for the surgical management of bleeding peptic ulcer disease include Immediate operation for (1) patients with rapidly exsanguinating ulcer hemorrhage and (2) patients with active bleeding and failure of endoscopic hemostasis to control the bleeding. Early elective operation after initial endoscopic hemostasis for (1) elderly patients with comorbid disease and/or hemodynamic instability who have active arterial ulcer hemorrhage (Forrest Ia) controlled with endoscopic hemostasis; (2) elderly patients with comorbid disease and/or hemodynamic instability who have a visible vessel in an ulcer crater (Forrest IIa) treated with endoscopic hemostasis: surgery is particularly advised in this circumstance for those with a positive arterial Doppler signal in the ulcer crater or a large posterior duodenal ulcer or a large lesser-curvature gastric ulcer; and (3) elderly patients with comorbid disease and/or hemodynamic instability who develop recurrent ulcer bleeding while hospitalized or with a total blood transfusion requirement exceeding 5 U.