ABSTRACT
As of October 21, 2022, a total of 27,884 monkeypox cases (confirmed and probable) have been reported in the United States.§ Gay, bisexual, and other men who have sex with men have constituted a majority of cases, and persons with HIV infection and those from racial and ethnic minority groups have been disproportionately affected (1,2). During previous monkeypox outbreaks, severe manifestations of disease and poor outcomes have been reported among persons with HIV infection, particularly those with AIDS (3-5). This report summarizes findings from CDC clinical consultations provided for 57 patients aged ≥18 years who were hospitalized with severe manifestations of monkeypox¶ during August 10-October 10, 2022, and highlights three clinically representative cases. Overall, 47 (82%) patients had HIV infection, four (9%) of whom were receiving antiretroviral therapy (ART) before monkeypox diagnosis. Most patients were male (95%) and 68% were non-Hispanic Black (Black). Overall, 17 (30%) patients received intensive care unit (ICU)-level care, and 12 (21%) have died. As of this report, monkeypox was a cause of death or contributing factor in five of these deaths; six deaths remain under investigation to determine whether monkeypox was a causal or contributing factor; and in one death, monkeypox was not a cause or contributing factor.** Health care providers and public health professionals should be aware that severe morbidity and mortality associated with monkeypox have been observed during the current outbreak in the United States (6,7), particularly among highly immunocompromised persons. Providers should test all sexually active patients with suspected monkeypox for HIV at the time of monkeypox testing unless a patient is already known to have HIV infection. Providers should consider early commencement and extended duration of monkeypox-directed therapy in highly immunocompromised patients with suspected or laboratory-diagnosed monkeypox.§§ Engaging all persons with HIV in sustained care remains a critical public health priority.
Subject(s)
HIV Infections , Mpox (monkeypox) , Sexual and Gender Minorities , United States/epidemiology , Humans , Male , Adolescent , Adult , Female , HIV Infections/diagnosis , Homosexuality, Male , Ethnicity , Population Surveillance , Minority Groups , Mpox (monkeypox)/epidemiologyABSTRACT
Epithelioid trophoblastic tumor (ETT) is a rare neoplasm derived from chorionic intermediate trophoblast cells, representing less than 2% of all gestational trophoblastic neoplasms. Classically, ETT presents as a uterine mass in women of reproductive age following a term pregnancy. The time from pregnancy to tumor development varies from months to several years. ETT most often arises in the endometrium, followed by the cervix. Extrauterine ETT are extremely infrequent, with few cases reported in the literature. We report a case of a 41-year-old woman, with history of three term pregnancies who presented with abdominal pain and elevated beta human chorionic gonadotropin (ß-hCG) level, ten years after her last pregnancy. Imaging reported a 3.5â cm adnexal mass, suspicious for ectopic pregnancy. Hysterectomy and mass resection revealed a 4.7â cm, tan-yellow, necrotic mass adjacent to the broad ligament. Histologic evaluation in conjunction with immunohistochemical stains revealed a tumor consistent with ETT. No connection to the endometrium was found grossly or microscopically. DNA fingerprinting analysis revealed the tumor to have two copies of paternal alleles, as seen in molar gestations. One of the primary differential diagnoses for ETT is squamous cell carcinoma due to similar morphologic features. In challenging cases, genetic analysis demonstrating paternally derived genes can establish the diagnosis. In this report, we discuss the challenges in the diagnosis of extrauterine ETT, due to its rarity and highly variable presentation, given that appropriate diagnosis is critical for correct patient management.
Subject(s)
Gestational Trophoblastic Disease , Pregnancy, Ectopic , Trophoblastic Neoplasms , Uterine Neoplasms , Pregnancy , Humans , Female , Adult , Uterine Neoplasms/pathology , Gestational Trophoblastic Disease/pathology , Chorionic Gonadotropin, beta Subunit, Human , Diagnosis, Differential , Trophoblastic Neoplasms/diagnosis , Epithelioid Cells/pathologyABSTRACT
In this paper, we analyze the existence of the environmental Kuznets curve as reported by Kuznets (Am Econ Rev 5:1-28, 1955) by using the methodology proposed by Kejriwal and Perron (J Econ 146:59-73, 2008, J Bus Econ Stat 28:503-522, 2010) and applying Jaunky's (Energy Policy 39(3):1228-1240, 2011) specification using quarterly data from 1973:1 to 2015:2. We also allow different behaviors across time and identify it by economic sectors. Our results show the existence of the environmental Kuznets curve (EKC) in the USA only when we allow for structural breaks. Interestingly, the industrial sector shows a different pattern than do other economic sectors; with the beginning of the economic crisis, it appears to have abandoned the objective of the environmental stabilization found until then.
Subject(s)
Carbon Dioxide/analysis , Environment , Industry , United StatesABSTRACT
Los pacientes con Trastorno por déficit de atención e hiperactividad (TDAH) presentan una elevada prevalencia de trastorno por consumo de sustancias (TCS), a la vez que los sujetos con TCS presentan con mayor frecuencia de la esperada un diagnóstico comórbido con TDAH, dificultando la clínica, evolución, pronóstico y por tanto el abordaje terapéutico. En el presente trabajo se pretende explorar la relación entre el TDAH y los TCS, fundamentalmente desde el punto de vista neurobiológico, mostrando factores y sustratos cerebrales comunes, genes implicados, precipitantes de ambas manifestaciones, así como la relación con la neurobiología de los circuitos de recompensa. La alta comorbilidad del TDAH con los TCS, indica tal como evidencian estudios de neuroimagen, estudios genéticos y estudios de experimentación, algunos sustratos neurobiológicos subyacentes compartidos, si bien sobre todo parece existir una influencia a nivel genético que se traduciría en alteraciones neuroquímicas, neuroanatómicas y neurofisiológicas comunes. Conociendo estos sustratos se podrá aumentar la comprensión de la patología dual en un futuro y ayudar en el diagnóstico y tratamiento de la enfermedad (AU)
Patients with attention deficit hyperactivity disorder (ADHD) have a high prevalence of substance use disorder (SUD), and likewise individuals with SUD show more commonly than expected a comorbid diagnosis of ADHD, thus presenting a more complex symptom presentation, clinical outcome and overall prognosis, as well a more difficult management. In the present paper, it is aimed to explore the evidence on the relationship between ADHD and SUDs, focusing on the neurobiological basis, discussing common brain factors and substrates, genes involved, shared precipitating factors to both disorders, as well as the neurobiology of the reinforcement pathway. The elevated comorbidity of SUD with ADHD, indicates, as shown in neuroimaging, genetic and experimental studies, the presence of some shared underlying neurobiological substrates. In particular, there appears to exist a strong genetic influence that may underlie a series of common neurochemical, neuroanatomical and neurophysiological alterations. A better understanding of these substrates would be of great help to an improved learning of this dual diagnosis in a future and help in its diagnosis and treatment (AU)