9 research outputs found

    An unusual case of tuberculous parotitis

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    Background: Tuberculosis (TB) of the parotid gland is exceedingly rare, even in areas of high disease burden. We report a case of isolated tuberculosis (TB) of the parotid gland. Methods: 25-year-old Puerto Rican female, who was born and raised in the United States, presented with a 3-month of history of recurrent left parotid gland swelling and pain. She had three attempts of fine needle aspirations (FNA), which were non-diagnostic. She was treated for a 3-month duration of antibiotics without much success. She did not have any constitutional symptoms, personal history of immunosuppression or prior exposure to TB. On CT and MRI, there appeared to be a fairly well-circumscribed mass in the deep lobe of left parotid. Because various FNA were unsuccessful in identifying the etiology of the mass, the decision was made to perform a deep lobe parotidectomy. Results: Histopathology revealed a large necrotizing granuloma with fibrous wall and numerous histiocytes. Based on these findings, she had a PPD and quantiferon gold test, both of which were positive. A chest X-ray was negative, thus demonstrating that she had latent TB. Conclusion: We believe this is one of the first reported cases of tuberculous parotitis in the United States. Clinicians should be aware of this rare entity and may consider ordering a PPD test in those patients who have failed treatment or yielding a diagnosis

    Sociability Deficits and Altered Amygdala Circuits in Mice Lacking Pcdh10, an Autism Associated Gene

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    BackgroundBehavioral symptoms in individuals with autism spectrum disorder (ASD) have been attributed to abnormal neuronal connectivity, but the molecular bases of these behavioral and brain phenotypes are largely unknown. Human genetic studies have implicated PCDH10, a member of the δ2 subfamily of nonclustered protocadherin genes, in ASD. PCDH10 expression is enriched in the basolateral amygdala, a brain region implicated in the social deficits of ASD. Previous reports indicate that Pcdh10 plays a role in axon outgrowth and glutamatergic synapse elimination, but its roles in social behaviors and amygdala neuronal connectivity are unknown. We hypothesized that haploinsufficiency of Pcdh10 would reduce social approach behavior and alter the structure and function of amygdala circuits.MethodsMice lacking one copy of Pcdh10 (Pcdh10+/–) and wild-type littermates were assessed for social approach and other behaviors. The lateral/basolateral amygdala was assessed for dendritic spine number and morphology, and amygdala circuit function was studied using voltage-sensitive dye imaging. Expression of Pcdh10 and N-methyl-D-aspartate receptor (NMDAR) subunits was assessed in postsynaptic density fractions of the amygdala.ResultsMale Pcdh10+/– mice have reduced social approach behavior, as well as impaired gamma synchronization, abnormal spine morphology, and reduced levels of NMDAR subunits in the amygdala. Social approach deficits in Pcdh10+/– male mice were rescued with acute treatment with the NMDAR partial agonist d-cycloserine.ConclusionsOur studies reveal that male Pcdh10+/– mice have synaptic and behavioral deficits, and establish Pcdh10+/– mice as a novel genetic model for investigating neural circuitry and behavioral changes relevant to ASD

    Comparative risk of major congenital malformations with eight different antiepileptic drugs: a prospective cohort study of the EURAP registry

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    Background: Evidence for the comparative teratogenic risk of antiepileptic drugs is insufficient, particularly in relation to the dosage used. Therefore, we aimed to compare the occurrence of major congenital malformations following prenatal exposure to the eight most commonly used antiepileptic drugs in monotherapy. Methods: We did a longitudinal, prospective cohort study based on the EURAP international registry. We included data from pregnancies in women who were exposed to antiepileptic drug monotherapy at conception, prospectively identified from 42 countries contributing to EURAP. Follow-up data were obtained after each trimester, at birth, and 1 year after birth. The primary objective was to compare the risk of major congenital malformations assessed at 1 year after birth in offspring exposed prenatally to one of eight commonly used antiepileptic drugs (carbamazepine, lamotrigine, levetiracetam, oxcarbazepine, phenobarbital, phenytoin, topiramate, and valproate) and, whenever a dose dependency was identified, to compare the risks at different dose ranges. Logistic regression was used to make direct comparisons between treatments after adjustment for potential confounders and prognostic factors. Findings: Between June 20, 1999, and May 20, 2016, 7555 prospective pregnancies met the eligibility criteria. Of those eligible, 7355 pregnancies were exposed to one of the eight antiepileptic drugs for which the prevalence of major congenital malformations was 142 (10·3%) of 1381 pregnancies for valproate, 19 (6·5%) of 294 for phenobarbital, eight (6·4%) of 125 for phenytoin, 107 (5·5%) of 1957 for carbamazepine, six (3·9%) of 152 for topiramate, ten (3·0%) of 333 for oxcarbazepine, 74 (2·9%) of 2514 for lamotrigine, and 17 (2·8%) of 599 for levetiracetam. The prevalence of major congenital malformations increased with the dose at time of conception for carbamazepine (p=0·0140), lamotrigine (p=0·0145), phenobarbital (p=0·0390), and valproate (

    WTO must ban harmful fisheries subsidies

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    Sustainably managed wild fisheries support food and nutritional security, livelihoods, and cultures (1). Harmful fisheries subsidies—government payments that incentivize overcapacity and lead to overfishing—undermine these benefits yet are increasing globally (2). World Trade Organization (WTO) members have a unique opportunity at their ministerial meeting in November to reach an agreement that eliminates harmful subsidies (3). We—a group of scientists spanning 46 countries and 6 continents—urge the WTO to make this commitment..

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