Publications by authors named "Butrous G"

Leveraging the potential of virtual platforms in the post-COVID-19 era, the Infection and Pulmonary Vascular Diseases Consortium (iPVDc), with the support of the Pulmonary Vascular Research Institute (PVRI), launched a globally accessible educational program to highlight top-notch research on inflammation and infectious diseases affecting the lung vasculature. This innovative virtual series has already successfully brought together distinguished investigators across five continents - Asia, Europe, South and North America, and Africa. Moreover, these open global forums have contributed to a comprehensive understanding of the complex interplay among immunology, inflammation, infection, and cardiopulmonary health, especially concerning pulmonary hypertension and related pulmonary disorders.

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The microbiota refers to a plethora of microorganisms with a gene pool of approximately three million, which inhabits the human gastrointestinal tract or gut. The latter, not only promotes the transport of nutrients, ions, and fluids from the lumen to the internal environment but is linked with the development of diseases including coronary artery disease, heart failure, and lung diseases. The exact mechanism of how the microbiota achieves crosstalk between itself and distant organs/tissues is not clear, but factors released to other organs may play a role, like inflammatory and genetic factors, and now we highlight melatonin as a novel mediator of the gut-lung crosstalk.

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The Coronavirus Disease 2019 (COVID-19) caused by Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) and its sublineages pose a new challenge to healthcare systems worldwide due to its ability to efficiently spread in immunized populations and its resistance to currently available therapies. COVID-19, although targeting primarily the respiratory system, is also now well established that later affects every organ in the body. Most importantly, despite the available therapy and vaccine-elicited protection, the long-term consequences of viral infection in breakthrough and asymptomatic individuals are areas of concern.

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COVID-19 infection primarily targets the lungs, which in severe cases progresses to cytokine storm, acute respiratory distress syndrome, multiorgan dysfunction, and shock. Survivors are now presenting evidence of cardiopulmonary sequelae such as persistent right ventricular dysfunction, chronic thrombosis, lung fibrosis, and pulmonary hypertension. This review will summarize the current knowledge on long-term cardiopulmonary sequelae of COVID-19 and provide a framework for approaching the diagnosis and management of these entities.

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HIV and Schistosoma infections have been individually associated with pulmonary vascular disease. Co-infection with these pathogens is very common in tropical areas, with an estimate of six million people co-infected worldwide. However, the effects of HIV and Schistosoma co-exposure on the pulmonary vasculature and its impact on the development of pulmonary vascular disease are largely unknown.

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Article Synopsis
  • SARS-CoV-2 primarily affects the lungs, causing severe hypoxia that can lead to death, especially in critical cases of COVID-19.
  • The disease shows significant variability in severity, recovery rates, and ongoing complications affecting multiple organs, including the lungs.
  • Understanding the dynamics of SARS-CoV-2 and the role of the pulmonary vascular system is vital for managing both acute and long-term effects of COVID-19, including the risk of chronic pulmonary hypertension.
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December 1, 2021, is "World AIDS Day," reminding us that HIV infection is still widespread and that many of its long-term effects can be deadly. One of these complications is its effect on the pulmonary vascular beds, leading to an increase in the pulmonary pressure, causing the clinical manifestation of "pulmonary hypertension." Unfortunately, we are still far from fully understanding the prevalence, mechanics, and pathobiology of "HIV pulmonary hypertension," especially in Africa and other developing countries where HIV is still common.

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A wide variety of infectious diseases are major contributors to the causation of pulmonary vascular disease and, consequently, pulmonary hypertension, especially in the developing world. Schistosomiasis and human immunodeficiency virus are the most common infections that are known to contribute to pulmonary hypertension worldwide. The resultant inflammation and immunologic milieu caused by infection are the main pathologic processes affecting the pulmonary vasculature.

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Background Inflammation underlies many forms of pulmonary hypertension (PH), including that resulting from Schistosoma infection, a major cause of PH worldwide. Schistosomiasis-associated PH is proximately triggered by embolization of parasite eggs into the lungs, resulting in localized type 2 inflammation. However, the role of CD4 T cells in this disease is not well defined.

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Schistosomiasis is the most common parasitic disease associated with pulmonary hypertension. It induces remodelling via complex inflammatory processes, which eventually produce the clinical manifestation of pulmonary hypertension. The pulmonary hypertension shows clinical signs and symptoms that are not distinguishable from other forms of pulmonary arterial hypertension.

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Human immunodeficiency virus (HIV) infection is an established risk factor for pulmonary arterial hypertension (PAH); however, the pathogenesis of HIV-related PAH remains unclear. Since K channel dysfunction is a common marker in most forms of PAH, our aim was to analyze whether the expression of HIV proteins is associated with impairment of K channel function in the pulmonary vascular bed. HIV transgenic mice (Tg26) expressing seven of the nine HIV viral proteins and wild-type (WT) mice were used.

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Schistosomiasis (bilharzia) is a neglected parasitic disease caused by trematode flatworms of the genus which affects over 240 million people worldwide. It is characterized by the formation of inflammatory granulomas around deposited parasite eggs. Recent studies have revealed that immune and inflammatory responses play a crucial role in pathogenesis of schistosomiasis.

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Pulmonary hypertension (PH) is characterized by elevated pulmonary arterial pressure, which leads to right ventricular (RV) hypertrophy and failure. The pathophysiological mechanisms of PH remain unclear but oxidative stress is believed to contribute to RV dysfunction. Melatonin is a powerful antioxidant and is cardioprotective against ischemia-reperfusion injury and hypertension.

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The extent to which pulmonary arterial hypertension (PAH) experts share common practice patterns that are in alignment with published expert consensus recommendations is unknown. Our objective was to characterize the clinical management strategies used by an international cohort of self-identified PAH experts. A 32-item questionnaire composed mainly of rank order or Likert scale questions was distributed via the Internet (August 5, 2013, through January 20, 2014) to four international pulmonary vascular disease organizations.

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Schistosomiasis is caused by infection with the parasite Schistosoma, which is a flat-worm or fluke. The dominant species are Schistosoma mansoni, Schistosoma japonicum, and Schistosoma haematobium. Schistosomiasis is the third most common parasitic disease in the world after malaria and amoebiasis.

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The Saudi Association for Pulmonary Hypertension (previously called Saudi Advisory Group for Pulmonary Hypertension) has published the first Saudi Guidelines on Diagnosis and Treatment of Pulmonary Arterial Hypertension back in 2008.[1] That guideline was very detailed and extensive and reviewed most aspects of pulmonary hypertension (PH). One of the disadvantages of such detailed guidelines is the difficulty that some of the readers who just want to get a quick guidance or looking for a specific piece of information might face.

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