In present epidemiological and economic conditions tuberculosis suspects should be hospitalized to specialized tuberculosis hospitals only after they are carefully examined for cancer of the lungs and lingering pneumonia. For this an obligatory diagnostic minimum should be introduced.
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Injury
January 2025
Professor of Orthopedics - Section Head Trauma & Orthopaedic Surgery, School of Medicine University of Leeds, UK.
The term "fragility fractures of the pelvis" refers to the disruptions of the pelvic ring that are caused by low energy injuries (such as low-level falls or falls from the standing position) in the elderly population (age over 65 years) in the absence of metastatic bone disease. These fractures are increasing in numbers, due to the aging population, particularly in the developed countries, causing significant morbidity and mortality [1]. Although some fracture patterns are stable enough requiring only conservative treatment, other fracture types can cause significant pelvic instability, demanding a more insistent management protocol.
View Article and Find Full Text PDFObstet Gynecol
January 2025
Medical Practice Evaluation Center, the Division of Infectious Disease, and the Division of Maternal Fetal Medicine, Massachusetts General Hospital, Boston, Massachusetts; the Department of Pediatrics, Centre Hospitalier Universitaire Sainte-Justine, University of Montreal, Montreal, Quebec, Canada; and the Department of Obstetrics and Gynecology, Weill Cornell Medicine, New York, New York.
The purpose of this review is to serve as an update on congenital cytomegalovirus (CMV) evaluation and management for obstetrician-gynecologists and to provide a framework for counseling birthing people at risk for or diagnosed with a primary CMV infection or reactivation or reinfection during pregnancy. A DNA virus, CMV is the most common congenital viral infection and the most common cause of nongenetic childhood hearing loss in the United States. The risk of congenital CMV infection from transplacental viral transfer depends on the gestational age at the time of maternal infection and whether the infection is primary or nonprimary.
View Article and Find Full Text PDFEnviron Health Perspect
January 2025
Division of Experimental Medicine, Department of Medicine, McGill University, Montréal, Canada.
Background: Millions worldwide are exposed to elevated levels of arsenic that significantly increase their risk of developing atherosclerosis, a pathology primarily driven by immune cells. While the impact of arsenic on immune cell populations in atherosclerotic plaques has been broadly characterized, cellular heterogeneity is a substantial barrier to in-depth examinations of the cellular dynamics for varying immune cell populations.
Objectives: This study aimed to conduct single-cell multi-omics profiling of atherosclerotic plaques in apolipoprotein E knockout () mice to elucidate transcriptomic and epigenetic changes in immune cells induced by arsenic exposure.
J Med Chem
January 2025
Guangdong Key Laboratory of Animal Conservation and Resource Utilization, Guangdong Public Laboratory of Wild Animal Conservation and Utilization, Institute of Zoology, Guangdong Academy of Sciences, Guangzhou, Guangdong 510260, China.
Pulmonary inflammation is the main cause of lung injury. Phosphodiesterase 4 (PDE4) is a promising anti-inflammatory target for the treatment of respiratory diseases. Herein, we designed and synthesized 43 compounds in two novel series of benzimidazole derivatives as PDE4 inhibitors.
View Article and Find Full Text PDFScience
January 2025
Center for Pulmonary Vascular Biology and Medicine, Pittsburgh, Heart, Lung, and Blood Vascular Medicine Institute, University of Pittsburgh, Pittsburgh, PA, USA.
Vascular inflammation regulates endothelial pathophenotypes, particularly in pulmonary arterial hypertension (PAH). Dysregulated lysosomal activity and cholesterol metabolism activate pathogenic inflammation, but their relevance to PAH is unclear. Nuclear receptor coactivator 7 () deficiency in endothelium produced an oxysterol and bile acid signature through lysosomal dysregulation, promoting endothelial pathophenotypes.
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