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- A Curious Case of Cardiomyopathy: The Limbic - Heart Connection. [JOURNAL ARTICLE]
- Chest 2014 Oct 1; 146(4_MeetingAbstracts):97A.
Cardiovascular Student/Resident Case Report Posters IISESSION TYPE: Medical Student/Resident Case ReportPRESENTED ON: Tuesday, October 28, 2014 at 01:30 PM - 02:30 PMINTRODUCTION: Excessive stimulation of the cortical limbic system is associated with hyperactivity of the catecholamine circuits which can result in cardiac involvement. Hyperactivity of the catecholamine circuits can be precipitated by substance abuse, such as cannabis. Neurogenic cardiomyopathy is an uncommon presentation of cannabis and it can lead to misdiagnosis.CASE PRESENTATION: A 60-year-old male brought to the ED after persistent retrograde memory loss of 4 days duration. He had a remote tobacco history, did not consume alcohol recently but consumed cannabis 5 days prior. He had no known drug allergy. On examination, he was afebrile, blood pressure was 132/84 mm Hg, and heart rate was 86/minute. Physical examination was unremarkable except for impaired 3 minute recall test. The results of routine biochemical tests were satisfactory. Serial cardiac biomarkers were mildly elevated. UDS was positive for cannabis only. An EKG showed NSR with deep T-wave inversions in anterior leads. TTE revealed severe anterior wall hypokinesia with estimated EF 30-35%. A head CT scan was unremarkable. Head MRI revealed patchy contrast enhancement in the left limbic region without mass effect or evidence of acute infarct, suggestive of limbic encephalitis. An EEG showed no evidence of seizure activity. Heart catheterization showed non obstructive coronary disease and apical ballooning. Further evaluation including viral serology and CSF analysis (chemistry, cell count, viral PCR panel, microbial cultures and cytology) were all unremarkable. A malignancy work up including whole body CT scan, para-neoplastic antibodies and a vasculitis panel were all negativeDISCUSSION: After excluding viral and autoimmune disorders, many patients with limbic encephalitis have CSF, EEG or MRI abnormalities, and rarely, myocardial compromise. Our patient's cardiac abnormalities included EKG changes, mild elevation of cardiac biomarkers and transient LV dysfunction. A diagnosis of neurogenic stunned myocardium as a manifestation of cannabis induced limbic encephalitis was established. Mini-Mental Status examination towards the end of the hospitalization was noted with deficits in recalls and date abilities. Follow up showed a significant resolution of his EKG, TTE and memory deficit with complete cannabis abstinenceCONCLUSIONS: Over activity of the sympathetic limb is the common phenomenon that associates the major cardiac pathologies seen in neurological insults. It is thus conceivable that overstimulation of catecholamine circuits in the limbic system due to cannabis ingestion could manifest as neurogenic heart disease. Providers should be aware of an uncommon presentation of cannabis ingestion.Reference #1: Machado, S., A. N. Pinto, and S. R. Irani. 2012. "What should You Know about Limbic Encephalitis? 70 (10): 817-822.Reference #2: Hagan, I. G. and K. Burney. 2007."Radiology of Recreational Drug Abuse.Radiographics: A Review Publication of Radiological Society of North America,Inc 27(4)919-940.DISCLOSURE: The following authors have nothing to disclose: Ahmed Abuzaid, Gale Etherton, Amjad KabachNo Product/Research Disclosure Information.
- Purpura Fulminans: An Unexpected Manifestation of Janus Kinase Inhibition. [JOURNAL ARTICLE]
- Chest 2014 Oct 1; 146(4_MeetingAbstracts):266A.
Critical Care Case Report Posters IIISESSION TYPE: Affiliate Case Report PosterPRESENTED ON: Tuesday, October 28, 2014 at 01:30 PM - 02:30 PMINTRODUCTION: Janus kinase inhibitors are increasingly being used for rheumatoid arthritis. We highlight a case of immune modulation induced by tofacitinib resulting in severe sepsis and purpura fulminans.CASE PRESENTATION: A 64 year old Caucasian lady with rheumatoid arthritis was admitted with septic shock and suprapubic tenderness after a 1 day prodrome of fever and malaise. A review of home medications revealed that she was started on tofacitinib two weeks ago for refractory rheumatoid arthritis. Empiric treatment included piperacillin/tazobactam and ciprofloxacin. Cultures were positive for E.coli in urine but no bacteremia. She required hemodynamic support with vasopressors and mechanical ventilation for two days. In the next 24 hours, she developed petechiae on the hands and feet (Fig 1) which progressed to the lower extremities from the mid-calf down, as well as several fingers on the hands. A punch biopsy from the right calf confirmed purpura fulminans. Subsequently she recovered from her critical illness and required multiple finger and toe amputations.DISCUSSION: Purpura fulminans is a hematologic emergency, usually associated with gram positive septicemia. It rapidly progresses to peripheral gangrene which often requires amputation, and is associated with high mortality. This patient represents a unique case of purpura fulminans caused by an E. coli UTI, while being treated with tofacitinib for rheumatoid arthritis. Tofacitinib is a Janus kinase (JAK) inhibitor that has a high affinity for JAK3, resulting in a marked reduction in NK cells, memory CD8+ T cells, and multiple interleukins essential for immunoregulatory function2. Serious bacterial infections were the most common significant adverse event and cause of death reported in long term studies of tofacitinib use3. However our case is the first report of severe sepsis leading to purpura fulminans induced by tofacitinib.We theorize that tofacitinib (JAK inhibitor) played an etiological role in this presentation and want to alert clinicians to the possibility of unusual and severe infections in the setting of JAK inhibitors. Reference #1: Scott, LJ. "Tofacitinib: A Review of its Use in Adult Patients with Rheumatoid Arthritis." Drugs. 2013. 73:857-874Reference #2: Salgado, E, et al, "Safety profile of protein kinase inhibitors in rheumatoid arthritis: systematic review and meta-analysis." Ann Rheum Dis. 2013 April 18DISCLOSURE: The following authors have nothing to disclose: Naomi Mathew, Christopher Henry, Manaf Zaizafoun, Shekhar GhamandeNo Product/Research Disclosure Information.
- A Case of West Nile Poliomyelitis. [JOURNAL ARTICLE]
- Chest 2014 Oct 1; 146(4_MeetingAbstracts):150A.
Infectious Disease Global Case ReportsSESSION TYPE: Global Case ReportPRESENTED ON: Tuesday, October 28, 2014 at 01:30 PM - 02:30 PMINTRODUCTION: Acute flaccid paralysis has a wide array of differentials ranging from infectious or noninfectious etiologies and requires a thorough history, physical examination, and radiological assessment. We present a case of an elderly woman with fevers and acute flaccid paralysis found to be West Nile Poliomyelitis.CASE PRESENTATION: 80 year-old woman with history of coronary artery disease status post bypass and pacemaker, hypertension, diabetes mellitus, and chronic kidney disease initially presented with weakness, fatigue, and failure to thrive. She was found to have a urinary tract infection, admitted and started on intravenous antibiotic treatment. Over the course of the next few days, she developed persistent high grade fevers associated with vomiting, decline in mental status, respiratory distress and hypoxia. She was transferred to the intensive care unit for further management, and required intubation and mechanical ventilation. Her antibiotic regimen was broadened to cover for possible aspiration pneumonia versus meningitis. Neurologic exam revealed flaccid paralysis involving the right upper and right lower extremities and hypoactive deep tendon reflexes. Computed tomography (CT) scan of the brain did not demonstrate any acute intracranial abnormalities, and MRI was not done given pacemaker in situ. Lumbar puncture was performed and cerebrospinal fluid (CSF) results were equivocal, with no evidence of bacterial meningitis or herpes simplex virus encephalitis, and cultures all remained negative. Eventually, viral encephalitis screening of the CSF returned positive for west nile virus immunoglobulin M antibodies. She was treated with supportive care, requiring tracheostomy placement and ultimately discharged to a nursing home.DISCUSSION: West Nile virus is a mosquito-borne flavivirus that is known the affect the two extremities of age, the young and the elderly. It is also more commonly seen in seen in HIV positive, organ transplant, and pregnant patients. The mode of transmission is mainly by the Culex species of mosquitos. Other documented modes of transmission include transplantation of infected organs, vertical transmission via intrauterine route, and via human milk. Most infections are asymptomatic or subclinical with patients reporting headaches, myalgias, arthralgias or gastrointestinal symptoms. Neuroinvasive disease occurs in less than 1% of infections and may present as meningitis, encephalitis or acute flaccid paralysis. Long term outcomes of West Nile encephalitis have shown morbidity and mortality rates of up to 20% with lasting implications. Patients may have movement disorders and extrapyramidal involvement for months to years. West Nile encephalitis with acute flaccid paralysis is known as West Nile Poliomyelitis, as in our patient. Mortality has been noted to be greater that 50%. Treatment is supportive only, and focuses more on prevention of disease.In conclusion, West Nile encephalitis is an important clinical entity in the differential of acute onset of asymmetric flaccid paralysis. It holds a high morbidity and mortality rate and no specific curative treatment. It also has long term psychiatric effects, notably anxiety, memory loss, and chronic fatigue which should be concurrently addressed with other general supportive measures.Reference #1: Sejvar, J. et al. Neurologic manifestations and outcome of West Nile Virus Infection. JAMA, 2003 July 23; 290(4):511-5Reference #2: Jeha LE, et al. West Nile virus infection: a new acute paralytic illness. Neurology 2003 July8;61(1): 55-9Reference #3: Hughes, J. et al. The Long-term Outcomes of Human West Nile Infections. Emerging infections. 2007:44 (June 15)DISCLOSURE: The following authors have nothing to disclose: George Juan, Ruchi Bansal, Ivan Wong, Saleem ShahzadNo Product/Research Disclosure Information.
- Boosting Long-Term Memory via Wakeful Rest: Intentional Rehearsal Is Not Necessary, Consolidation Is Sufficient. [JOURNAL ARTICLE]
- PLoS One 2014; 9(10):e109542.
People perform better on tests of delayed free recall if learning is followed immediately by a short wakeful rest than by a short period of sensory stimulation. Animal and human work suggests that wakeful resting provides optimal conditions for the consolidation of recently acquired memories. However, an alternative account cannot be ruled out, namely that wakeful resting provides optimal conditions for intentional rehearsal of recently acquired memories, thus driving superior memory. Here we utilised non-recallable words to examine whether wakeful rest boosts long-term memory, even when new memories could not be rehearsed intentionally during the wakeful rest delay. The probing of non-recallable words requires a recognition paradigm. Therefore, we first established, via Experiment 1, that the rest-induced boost in memory observed via free recall can be replicated in a recognition paradigm, using concrete nouns. In Experiment 2, participants heard 30 non-recallable non-words, presented as 'foreign names in a bridge club abroad' and then either rested wakefully or played a visual spot-the-difference game for 10 minutes. Retention was probed via recognition at two time points, 15 minutes and 7 days after presentation. As in Experiment 1, wakeful rest boosted recognition significantly, and this boost was maintained for at least 7 days. Our results indicate that the enhancement of memory via wakeful rest is not dependent upon intentional rehearsal of learned material during the rest period. We thus conclude that consolidation is sufficient for this rest-induced memory boost to emerge. We propose that wakeful resting allows for superior memory consolidation, resulting in stronger and/or more veridical representations of experienced events which can be detected via tests of free recall and recognition.
- Prenatal choline supplementation ameliorates the long-term neurobehavioral effects of fetal-neonatal iron deficiency in rats. [Journal Article]
- J Nutr 2014 Nov; 144(11):1858-65.
Gestational iron deficiency in humans and rodents produces long-term deficits in cognitive and socioemotional function and alters expression of plasticity genes in the hippocampus that persist despite iron treatment. Prenatal choline supplementation improves cognitive function in other rodent models of developmental insults.The objective of this study was to determine whether prenatal choline supplementation prevents the long-term effects of fetal-neonatal iron deficiency on cognitive and social behaviors and hippocampal gene expression.Pregnant rat dams were administered an iron-deficient (2-6 g/kg iron) or iron-sufficient (IS) (200 g/kg iron) diet from embryonic day (E) 3 to postnatal day (P) 7 with or without choline supplementation (5 g/kg choline chloride, E11-18). Novel object recognition (NOR) in the test vs. acquisition phase, social approach (SA), and hippocampal mRNA expression were compared at P65 in 4 male adult offspring groups: formerly iron deficient (FID), FID with choline supplementation (FID-C), IS, and IS with choline supplementation.Relative to the intact NOR in IS rats (acquisition: 47.9%, test: 60.2%, P < 0.005), FID adult rats had impaired recognition memory at the 6-h delay (acquisition: 51.4%, test: 55.1%, NS), accompanied by a 15% reduction in hippocampal expression of brain-derived neurotrophic factor (Bdnf) (P < 0.05) and myelin basic protein (Mbp) (P < 0.05). Prenatal choline supplementation in FID rats restored NOR (acquisition: 48.8%, test: 64.4%, P < 0.0005) and increased hippocampal gene expression (FID-C vs. FID group: Bdnf, Mbp, P < 0.01). SA was also reduced in FID rats (P < 0.05 vs. IS rats) but was only marginally improved by prenatal choline supplementation.Deficits in recognition memory, but not social behavior, resulting from gestational iron deficiency are attenuated by prenatal choline supplementation, potentially through preservation of hippocampal Bdnf and Mbp expression. Prenatal choline supplementation may be a promising adjunct treatment for fetal-neonatal iron deficiency.
- Colivelin ameliorates amyloid β peptide-induced impairments in spatial memory, synaptic plasticity and calcium homeostasis in rats. [JOURNAL ARTICLE]
- Hippocampus 2014 Oct 20.
Amyloid β peptide (Aβ) has been thought to be neurotoxic and responsible for the impairment of learning and memory in Alzheimer's disease (AD). Humanin (HN), a 24 amino acid polypeptide firstly identified from the unaffected occipital lobe of an AD patient, is believed to be neuroprotective against the AD-related neurotoxicity. In this study, we investigated the neuroprotective effects of Colivelin (CLN), a novel HN derivative, against Aβ by using behavioral test, in vivo electrophysiological recording, and intracellular calcium imaging. Our results showed that intrahippocampal injection of CLN (0.2 nmol) effectively prevented Aβ25-35 (4nmol)-induced deficits in spatial learning and memory of rats in Morris water maze test; the suppression of in vivo hippocampal long term potentiation (LTP) by Aβ25-35 was nearly completely prevented by CLN; in addition, CLN pretreatment also effectively inhibited Aβ25-35-induced calcium overload in primary cultured hippocampal neurons. These results indicate that CLN has significant neuroprotective properties against Aβ, and CLN may holds great promise for the treatment and prevention of AD. © 2014 Wiley Periodicals, Inc.
- Characteristics of Memory B Cells Elicited by a Highly Efficacious HPV Vaccine in Subjects with No Pre-existing Immunity. [JOURNAL ARTICLE]
- PLoS Pathog 2014 Oct; 10(10):e1004461.
Licensed human papillomavirus (HPV) vaccines provide near complete protection against the types of HPV that most commonly cause anogenital and oropharyngeal cancers (HPV 16 and 18) when administered to individuals naive to these types. These vaccines, like most other prophylactic vaccines, appear to protect by generating antibodies. However, almost nothing is known about the immunological memory that forms following HPV vaccination, which is required for long-term immunity. Here, we have identified and isolated HPV 16-specific memory B cells from female adolescents and young women who received the quadrivalent HPV vaccine in the absence of pre-existing immunity, using fluorescently conjugated HPV 16 pseudoviruses to label antigen receptors on the surface of memory B cells. Antibodies cloned and expressed from these singly sorted HPV 16-pseudovirus labeled memory B cells were predominantly IgG (>IgA>IgM), utilized diverse variable genes, and potently neutralized HPV 16 pseudoviruses in vitro despite possessing only average levels of somatic mutation. These findings suggest that the quadrivalent HPV vaccine provides an excellent model for studying the development of B cell memory; and, in the context of what is known about memory B cells elicited by influenza vaccination/infection, HIV-1 infection, or tetanus toxoid vaccination, indicates that extensive somatic hypermutation is not required to achieve potent vaccine-specific neutralizing antibody responses.
- Long-term effectiveness of combined cognitive-behavioral and neuropsychological intervention in a case of multiple sclerosis. [JOURNAL ARTICLE]
- Neurocase 2014 Oct 20.:1-8.
This study examines the long-term effectiveness of a combined cognitive-behavioral and neuropsychological intervention in a woman of 19 years old with multiple sclerosis, by evaluating functional neuroimaging, neuropsychological and psychometric testing. The results showed a partial improvement in some brain areas and brain inflammatory activity. There was an increase in attention, verbal memory, and nonverbal executive functioning as well as in the emotional state at posttest and one-year follow-up. This study indicates the need for including components of both cognitive-behavioral therapy and neuropsychological rehabilitation based on an individualized and tailored plan in standard treatments for multiple sclerosis. Future studies should further develop these contributions.
- The yeast galactose network as a quantitative model for cellular memory. [JOURNAL ARTICLE]
- Mol Biosyst 2014 Oct 20.
Recent experiments have revealed surprising behavior in the yeast galactose (GAL) pathway, one of the preeminent systems for studying gene regulation. Under certain circumstances, yeast cells display memory of their prior nutrient environments. We distinguish two kinds of cellular memory discovered by quantitative investigations of the GAL network and present a conceptual framework for interpreting new experiments and current ideas on GAL memory. Reinduction memory occurs when cells respond transcriptionally to one environment, shut down the response during several generations in a second environment, then respond faster and with less cell-to-cell variation when returned to the first environment. Persistent memory describes a long-term, arguably stable response in which cells adopt a bimodal or unimodal distribution of induction levels depending on their preceding environment. Deep knowledge of how the yeast GAL pathway responds to different sugar environments has enabled rapid progress in uncovering the mechanisms behind GAL memory, which include cytoplasmic inheritance of inducer proteins and positive feedback loops among regulatory genes. This network of genes, long used to study gene regulation, is now emerging as a model system for cellular memory.
- Diffusion tensor imaging in Alzheimer's disease: insights into the limbic-diencephalic network and methodological considerations. [Journal Article, Review]
- Front Aging Neurosci 2014.:266.
Glucose hypometabolism and gray matter atrophy are well known consequences of Alzheimer's disease (AD). Studies using these measures have shown that the earliest clinical stages, in which memory impairment is a relatively isolated feature, are associated with degeneration in an apparently remote group of areas-mesial temporal lobe (MTL), diencephalic structures such as anterior thalamus and mammillary bodies, and posterior cingulate. These sites are thought to be strongly anatomically inter-connected via a limbic-diencephalic network. Diffusion tensor imaging or DTI-an imaging technique capable of probing white matter tissue microstructure-has recently confirmed degeneration of the white matter connections of the limbic-diencephalic network in AD by way of an unbiased analysis strategy known as tract-based spatial statistics (TBSS). The present review contextualizes the relevance of these findings, in which the fornix is likely to play a fundamental role in linking MTL and diencephalon. An interesting by-product of this work has been in showing that alterations in diffusion behavior are complex in AD-while early studies tended to focus on fractional anisotropy, recent work has highlighted that this measure is not the most sensitive to early changes. Finally, this review will discuss in detail several technical aspects of DTI both in terms of image acquisition and TBSS analysis as both of these factors have important implications to ensure reliable observations are made that inform understanding of neurodegenerative diseases.