The cell envelope stress response mediated by the LiaFSR Lm three-component system of Listeria monocytogenes is controlled via the phosphatase activity of the bifunctional histidine kinase LiaS Lm

A 62-year-old previously healthy man was diagnosed with a deep vein thrombosis, a suspicious nevus, and macrocytic anemia. Otherwise, his hematogram and coagulation indices were normal. His vitamin B 12 level was 52 pg/mL (reference 211-911 pg/mL), iron level was 58 mcg/dL (reference 59-158 mcg/dL), and folate level was normal. His nevus pathology revealed an in situ melanoma. Assuming his anemia and hypercoagulable state were related to newfound melanoma, and given his lack of neurologic complaints, his physician regarded the vitamin B 12 level as incidental and asymptomatic. He went home on anticoagulation and iron supplementation.He returned 1 month later, still anemic, with unrelated small-bowel obstruction. He underwent emergent lysis of adhesions without bowel resection, receiving 30 minutes of inhaled nitrous oxide (N 2 O) during anesthesia. Postoperatively, he recovered physically, but developed dysgusia and anorexia, and was discharged home on hospital day 5.Two months later, he again returned, now unable to walk. Shortly after surgery, he developed numbness and burning in his feet, which quickly ascended to his knees. The patient had progressive difficulties with balance and falls, requiring a walker, then becoming nonambulatory. His daughter also observed progressive confusion, requiring assistance with all activities of daily living.His general medical and cranial nerve examinations were unremarkable. Mental status examination was notable for bradyphrenia, disorientation to time, and mild naming difficulties. His strength was decreased in distal arms and throughout his legs to 4/5. Reflexes were absent throughout and there was no Babinski sign. He demonstrated patchy loss of pinprick and temperature sensation throughout, with vibratory and joint position sense absent to his elbows and hips in respective limbs. He had pseudoathetosis and sensory ataxia in both arms and trunk. His hemoglobin was 8 g/dL, and mean corpuscular volume was 106 femtoliters. Vitamin B 12 was undetectable, homocysteine was 221 mmol/L (reference #15 mmol/L), and methylmalonic acid (MMA) was 107 nmol/mL (reference #0.4 nmol/mL). Intrinsic factor antibodies were present, but not parietal cell antibodies. The remainder of his neuropathy laboratory evaluation was normal, including studies for diabetes, thyroid, syphilis, and paraproteinemia. MRI of the spinal cord

FAHA: We thank Drs. Hart and Eikelboom 1 for their insightful commentary in Neurology ® Clinical Practice regarding the American Academy of Neurology (AAN) evidence-based guideline update on atrial fibrillation (AF). 2 Both authors have extensively researched stroke prevention in patients with AF 3 and we respect their views. The Commentary states, "atrial fibrillation patients with prior ischemic stroke or TIA benefit the most from anticoagulation and should receive anticoagulation, if it can be given safely." We could not agree more. The AAN guideline development process yields a Level B recommendation when clinicians "should" provide a therapy; a Level A recommendation is limited to situations when clinicians "must" provide a therapy. As the Commentary authors have implied, there are circumstances when anticoagulation cannot be safely given, and the guideline panel determined that clinical judgment was paramount in the final decision. Thus, a Level B was applied, which remains a strong recommendation. Cognizant of the AAN's global reach, we included a recommendation to consider the administration of triflusal (a generic product available in developing countries) with lowintensity acenocoumarol in patients with AF at intermediate stroke risk and higher bleeding risk (Level B). 4 In many developing countries, new oral anticoagulants may not be available or affordable, and this evidence-based recommendation fills the gap.