Neurocysticercosis (NCC), a helminth infection of the brain, is a major cause of seizures. The mediators responsible for seizures in NCC are unknown, and their management remains controversial. Substance P (SP) is a neuropeptide produced by neurons, endothelial cells and immunocytes. The current studies examined the hypothesis that SP mediates seizures in NCC. We demonstrated by immunostaining that 5 of 5 brain biopsies from NCC patients contained substance P (SP)-positive (+) cells adjacent to but not distant from degenerating worms; no SP+ cells were detected in uninfected brains. In a rodent model of NCC, seizures were induced after intrahippocampal injection of SP alone or after injection of extracts of cysticercosis granuloma obtained from infected wild type (WT), but not from infected SP precursor-deficient mice. Seizure activity correlated with SP levels within WT granuloma extracts and was prevented by intrahippocampal pre-injection of SP receptor antagonist. Furthermore, extracts of granulomas from WT mice caused seizures when injected into the hippocampus of WT mice, but not when injected into SP receptor (NK1R) deficient mice. These findings indicate that SP causes seizures in NCC, and, suggests that seizures in NCC in humans may be prevented and/or treated with SP-receptor antagonists.

Viral-myocarditis is an important cause of heart failure for which no specific treatment is available. We previously showed the neuropeptide substance P (SP) is associated with the pathogenesis of murine myocarditis caused by encephalomyocarditis virus (EMCV). The current studies determined if pharmacological inhibition of SP-signaling via its high affinity receptor, NK1R and downstream G-protein, Ras homolog gene family, member-A (RhoA), will be beneficial in viral-myocarditis. Aprepitant (1.2 mg/kg), a SP-receptor antagonist, or fasudil (10 mg/kg), a RhoA inhibitor, or saline control was administered daily to mice orally for 3 days, prior to, or 5 days following, intraperitoneal infection with and without 50 PFU of EMCV, following which disease assessment studies, including echocardiogram and cardiac Doppler were performed in day 14 after infection. Pretreatment and posttreatment with aprepitant significantly reduced mortality, heart and cardiomyocyte size, and cardiac viral RNA levels (P < 0.05 all, ANOVA). Only aprepitant pretreatment improved heart functions; it significantly decreased end systolic diameter, improved fractional shortening, and increased peak aortic flow velocity (P < 0.05 all, ANOVA). Pre- or posttreatment with fasudil did not significantly impact disease manifestations. These findings indicate that SP contributes to cardiac-remodeling and dysfunction following ECMV infection via its high affinity receptor, but not through the Rho-A pathway. These studies suggest that SP-receptor antagonism may be a novel therapeutic-option for patients with viral-myocarditis.

Cysticercosis is an infection of tissues with the larval cysts of the cestode, Taenia   solium. While live parasites elicit little or no inflammation, dying parasites initiate a granulomatous reaction presenting as painful muscle nodules or seizures when cysts are located in the brain. We previously showed in the T. crassiceps murine model of cysticercosis that substance P (SP), a neuropeptide, was detected in early granulomas and was responsible for promoting granuloma formation, while somatostatin (SOM), another neuropeptide and immunomodulatory hormone, was detected in late granulomas; SOM's contribution to granuloma formation was not examined. In the current studies, we used somatostatin knockout (SOM−/−) mice to examine the hypothesis that SOM downmodulates granulomatous inflammation in cysticercosis, thereby promoting parasite growth. Our results demonstrated that parasite burden was reduced 5.9-fold in SOM−/− mice compared to WT mice (P < 0.05). This reduction in parasite burden in SOM−/− mice was accompanied by a 95% increase in size of their granulomas (P < 0.05), which contained a 1.5-fold increase in levels of IFN-γ and a 26-fold decrease in levels of IL-1β (P < 0.05 for both) compared to granulomas from WT mice. Thus, SOM regulates both parasite burden and granulomatous inflammation perhaps through modulating granuloma production of IFN-γ and IL-1β.

Kounis syndrome consists of angina pectoris or myocardial infarction that is triggered by the release of inflammatory mediators in the setting of an allergic reaction. We present the case of a 61-year-old man who presented to the emergency department with anaphylaxis after being stung by >100 bees. During resuscitation, he subsequently developed ST elevation myocardial infarction.A cute coronary syndrome is a common disease process seen in the emergency department. Many physiologic stressors can precipitate its acute presentation. Kounis syndrome, also referred to as "allergic angina," is a rare but increasingly reported cause of acute coronary syndrome. It can be induced by any anaphylactic reaction and thus must be on a diff erential diagnosis for anyone with chest pain or symptoms of acute coronary syndrome who presents with the surrounding setting of an anaphylactic reaction. Th is syndrome requires a high degree of clinical suspicion and can be easily overlooked given the dramatic presentation of anaphylaxis. CASE REPORTA 61-year-old white man with no documented coronary artery disease but known congestive heart failure (cause uncertain), type II diabetes, tobacco abuse, hypertension, and hyperlipidemia presented to the emergency department via ambulance after having multiple bee stings while riding on his tractor. Th e patient received diphenhydramine en route for reported dyspnea and arrived in the exam room with diaphoresis, dyspnea, and innumerable bee stings located mainly on his head, face, and arms. He also presented with a large urticarial rash on his back, with >100 bee stingers remaining in his skin ( Figure 1 ) . Th e patient was given 0.3 mg of 1:1000 intramuscular epinephrine in addition to 125 mg intravenous methylprednisolone for anaphylaxis and showed initial improvement.Two hours after initial evaluation, he began clutching his chest and reported sudden onset of new 10/10 stabbing leftsided chest pain. Th e initial electrocardiogram ( Figure 2a ) revealed sinus tachycardia with a right bundle branch block and frequent ventricular premature complexes and fusion beats, as well as intermittent ventricular bigeminy. Repeat electrocardiogram in the setting of chest pain ( Figure 2b ) disclosed ST elevation in leads II, III, aVF, and V4 to V6. Th e cardiac catheterization revealed thrombus in the distal right coronary artery, mid left anterior descending artery, and fi rst diagonal of the distal left anterior descending artery. Immediate percutaneous coronary intervention was performed with successful thrombectomy and placement of bare metal stents in the distal right coronary artery and mid left anterior descending artery.Th e patient was transferred to the cardiac intensive care unit, where an echocardiogram revealed severe global left ventricular hypokinesis with an ejection fraction of 25%. Dual antiplatelet therapy, optimal medical therapy, and a life vest were provided.

In the paper titled "Somatostatin Negatively Regulates Parasite Burden and Granulomatous Responses in Cysticercosis" there was an error in the Discussion and Bibliography section. The changes made to the references section are as follows.