scholarly journals Combined pulmonary fibrosis and emphysema: an increasingly recognized condition

2014 ◽  
Vol 40 (3) ◽  
pp. 304-312 ◽  
Author(s):  
Olívia Meira Dias ◽  
Bruno Guedes Baldi ◽  
André Nathan Costa ◽  
Carlos Roberto Ribeiro Carvalho
Keyword(s):  
Pulmonary Fibrosis ◽  
Current Knowledge ◽  
Treatment Options ◽  
Lower Lobe ◽  
Published Data ◽  
Increased Risk ◽  
Pulmonary Arterial ◽  
Former Smokers ◽  
Severe Pulmonary Arterial Hypertension

Combined pulmonary fibrosis and emphysema (CPFE) has been increasingly recognized in the literature. Patients with CPFE are usually heavy smokers or former smokers with concomitant lower lobe fibrosis and upper lobe emphysema on chest HRCT scans. They commonly present with severe breathlessness and low DLCO, despite spirometry showing relatively preserved lung volumes. Moderate to severe pulmonary arterial hypertension is common in such patients, who are also at an increased risk of developing lung cancer. Unfortunately, there is currently no effective treatment for CPFE. In this review, we discuss the current knowledge of the pathogenesis, clinical characteristics, and prognostic factors of CPFE. Given that most of the published data on CPFE are based on retrospective analysis, more studies are needed in order to address the role of emphysema and its subtypes; the progression of fibrosis/emphysema and its correlation with inflammation; treatment options; and prognosis.

Combined pulmonary fibrosis and emphysema (CPFE)

2017 ◽  
Vol 5 (2) ◽  
pp. 122-125
Author(s):  
Rawshan Arra Khanam
Keyword(s):  
Pulmonary Fibrosis ◽  
Clinical Characteristics ◽  
Current Knowledge ◽  
Treatment Options ◽  
Lower Lobe ◽  
Diffusing Capacity ◽  
Lung Volumes ◽  
Function Test ◽  
History Of ◽  
Former Smokers

Combined pulmonary fibrosis and emphysema (CPFE) is rare but increasingly recognized condition characterized by simultaneous coexistence of both upper lobe predominant emphysema and diffuse pulmonary fibrosis mainly in lower lobe. Patients with CPFE are usually heavy smokers or former smokers. HRCT has a pivotal role in diagnosis. Pulmonary function test showed relatively preserved lung volumes and reduced diffusing capacity of the lung for carbon monoxide (DLCO). Development of pulmonary hypertension (PH) is largely attributed to morbidity in patients with CPFE which is the principal prognostic factor for this condition. However more studies are needed to establish natural history of the disease & treatment option. In this review, we will discuss the current knowledge of the pathogenesis, clinical characteristics, treatment options and prognostic factors of CPFE.Bangladesh Crit Care J September 2017; 5(2): 122-125

scholarly journals Role of PFKFB3 and PFKFB4 in Cancer: Genetic Basis, Impact on Disease Development/Progression, and Potential as Therapeutic Targets

Cancers ◽  
2021 ◽  
Vol 13 (4) ◽  
pp. 909
Author(s):  
Krzysztof Kotowski ◽  
Jakub Rosik ◽  
Filip Machaj ◽  
Stanisław Supplitt ◽  
Daniel Wiczew ◽  
...  
Keyword(s):  
Current Knowledge ◽  
Treatment Options ◽  
Protein Structures ◽  
New Drugs ◽  
Proliferating Cells ◽  
Cancer Tissues ◽  
The Impact ◽  
Rate Limiting ◽  
Synthesis And Degradation

Glycolysis is a crucial metabolic process in rapidly proliferating cells such as cancer cells. Phosphofructokinase-1 (PFK-1) is a key rate-limiting enzyme of glycolysis. Its efficiency is allosterically regulated by numerous substances occurring in the cytoplasm. However, the most potent regulator of PFK-1 is fructose-2,6-bisphosphate (F-2,6-BP), the level of which is strongly associated with 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase activity (PFK-2/FBPase-2, PFKFB). PFK-2/FBPase-2 is a bifunctional enzyme responsible for F-2,6-BP synthesis and degradation. Four isozymes of PFKFB (PFKFB1, PFKFB2, PFKFB3, and PFKFB4) have been identified. Alterations in the levels of all PFK-2/FBPase-2 isozymes have been reported in different diseases. However, most recent studies have focused on an increased expression of PFKFB3 and PFKFB4 in cancer tissues and their role in carcinogenesis. In this review, we summarize our current knowledge on all PFKFB genes and protein structures, and emphasize important differences between the isoenzymes, which likely affect their kinase/phosphatase activities. The main focus is on the latest reports in this field of cancer research, and in particular the impact of PFKFB3 and PFKFB4 on tumor progression, metastasis, angiogenesis, and autophagy. We also present the most recent achievements in the development of new drugs targeting these isozymes. Finally, we discuss potential combination therapies using PFKFB3 inhibitors, which may represent important future cancer treatment options.

scholarly journals CHEK2∗1100delC Mutation and Risk of Prostate Cancer

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Victoria Hale ◽  
Maren Weischer ◽  
Jong Y. Park
Keyword(s):  
Prostate Cancer ◽  
Current Knowledge ◽  
Prostate Cancer Screening ◽  
Critical Role ◽  
Prostate Cancer Risk ◽  
Conclusive Evidence ◽  
Increased Risk ◽  
History Of ◽  
Cancer Studies

Although the causes of prostate cancer are largely unknown, previous studies support the role of genetic factors in the development of prostate cancer.CHEK2plays a critical role in DNA replication by responding to double-stranded breaks. In this review, we provide an overview of the current knowledge of the role of a genetic variant, 1100delC, ofCHEK2on prostate cancer risk and discuss the implication for potential translation of this knowledge into clinical practice. Currently, twelve articles that discussedCHEK2∗1100delC and its association with prostate cancer were identified. Of the twelve prostate cancer studies, five studies had independent data to draw conclusive evidence from. The pooled results of OR and 95% CI were 1.98 (1.23–3.18) for unselected cases and 3.39 (1.78–6.47) for familial cases, indicating thatCHEK2∗1100delC mutation is associated with increased risk of prostate cancer. Screening for CHEK2∗1100delC should be considered in men with a familial history of prostate cancer.

scholarly journals Regulatory Immune Cells in Idiopathic Pulmonary Fibrosis: Friends or Foes?

2021 ◽  
Vol 12 ◽  
Author(s):  
Chiel van Geffen ◽  
Astrid Deißler ◽  
Markus Quante ◽  
Harald Renz ◽  
Dominik Hartl ◽  
...  
Keyword(s):  
Immune System ◽  
Idiopathic Pulmonary Fibrosis ◽  
Pulmonary Fibrosis ◽  
Immune Responses ◽  
Immune Cells ◽  
Current Knowledge ◽  
Suppressor Cells ◽  
Interstitial Lung Diseases ◽  
Stromal Stem Cells

The immune system is receiving increasing attention for interstitial lung diseases, as knowledge on its role in fibrosis development and response to therapies is expanding. Uncontrolled immune responses and unbalanced injury-inflammation-repair processes drive the initiation and progression of idiopathic pulmonary fibrosis. The regulatory immune system plays important roles in controlling pathogenic immune responses, regulating inflammation and modulating the transition of inflammation to fibrosis. This review aims to summarize and critically discuss the current knowledge on the potential role of regulatory immune cells, including mesenchymal stromal/stem cells, regulatory T cells, regulatory B cells, macrophages, dendritic cells and myeloid-derived suppressor cells in idiopathic pulmonary fibrosis. Furthermore, we review the emerging role of regulatory immune cells in anti-fibrotic therapy and lung transplantation. A comprehensive understanding of immune regulation could pave the way towards new therapeutic or preventive approaches in idiopathic pulmonary fibrosis.

scholarly journals The Infant Gut Microbiota and Risk of Asthma: The Effect of Maternal Nutrition during Pregnancy and Lactation

2020 ◽  
Vol 8 (8) ◽  
pp. 1119 ◽  
Author(s):  
Naser A. Alsharairi
Keyword(s):  
Gut Microbiota ◽  
Early Life ◽  
Nutrient Intake ◽  
Maternal Nutrition ◽  
Current Knowledge ◽  
Increased Risk ◽  
Dietary Nutrient ◽  
Pregnancy And Lactation ◽  
Gut Microbiota Composition

Research has amply demonstrated that early life dysbiosis of the gut microbiota influences the propensity to develop asthma. The influence of maternal nutrition on infant gut microbiota is therefore of growing interest. However, a handful of prospective studies have examined the role of maternal dietary patterns during pregnancy in influencing the infant gut microbiota but did not assess whether this resulted in an increased risk of asthma later in life. The mechanisms involved in the process are also, thus far, poorly documented. There have also been few studies examining the effect of maternal dietary nutrient intake during lactation on the milk microbiota, the effect on the infant gut microbiota and, furthermore, the consequences for asthma development remain largely unknown. Therefore, the specific aim of this mini review is summarizing the current knowledge regarding the effect of maternal nutrition during pregnancy and lactation on the infant gut microbiota composition, and whether it has implications for asthma development.

scholarly journals Endocrine Risk Factors of Endometrial Cancer: Polycystic Ovary Syndrome, Oral Contraceptives, Infertility, Tamoxifen

Cancers ◽  
2020 ◽  
Vol 12 (7) ◽  
pp. 1766 ◽  
Author(s):  
Atanas Ignatov ◽  
Olaf Ortmann
Keyword(s):  
Endometrial Cancer ◽  
Polycystic Ovary Syndrome ◽  
Oral Contraceptives ◽  
Polycystic Ovary ◽  
Gynecologic Cancer ◽  
Age At Menarche ◽  
Published Data ◽  
Ovary Syndrome ◽  
Increased Risk

Endometrial cancer is the most common gynecologic cancer and is predominantly endocrine-related. The role of unopposed estrogen in the development of endometrial cancer has been investigated in numerous studies. Different reproductive factors such as younger age at menarche, late age at menopause, infertility, nulliparity, age of birth of the first child, and long-term use of unopposed estrogens during hormone replacement therapy have been associated with an increased risk of endometrial cancer. In contrast, there is a growing body of evidence for a protective role of oral contraceptives. Most of the published data on the association between infertility and polycystic ovary syndrome are inconclusive, whereas the effect of tamoxifen on the risk of endometrial cancer has been well established. With this review, we aim to summarize the evidence on the association between infertility, polycystic ovary syndrome, oral contraceptives, and tamoxifen and the development of endometrial cancer.

Role for Chemokines in the Vasculopathy Associated with Sickle Cell Dsease and Pulmonary Hypertension

Blood ◽  
2008 ◽  
Vol 112 (11) ◽  
pp. 4804-4804 ◽  
Author(s):  
Anitaben Tailor ◽  
Gregory J. Kato
Keyword(s):  
Sickle Cell ◽  
Vascular Inflammation ◽  
Inverse Correlation ◽  
Inflammatory Protein ◽  
Potential Marker ◽  
Increased Risk ◽  
High Prevalence ◽  
Pulmonary Arterial

Abstract Sickle cell disease (SCD) is a hemolytic disorder characterized by transient vaso-occlusive crisis (VOC). Moreover, there is a high prevalence of SCD-associated pulmonary arterial hypertension (PAH), indicated by a tricuspid regurgitant jet velocity (TRV) ≥ 2.5 m/sec, leading to increased risk for early mortality. Monocytes have been proposed as pivotal cells in vascular inflammation in animal models of SCD. Preliminary studies in our group have shown a potential role for monocyte chemokines in the vasculopathy of SCD. The objective of this study is to investigate the role of two chemokines: regulated upon activation, normal T cell expressed and secreted (RANTES) and macrophage inflammatory protein-1β (MIP-1β) in SCD and SCD-associated PAH. Plasma samples were collected from patients with SCD at steady state and from healthy African-American control subjects. Plasma levels of RANTES and MIP-1β were measured using an enzyme immunoassay system. Patients with SCD exhibited significantly higher levels of both MIP-1β (median 465.3 vs. 398.5 pg/ml, p<0.0001) and RANTES (median 47774 vs. 17445pg/ml, p<0.0004) than healthy controls. Further characterization of SCD patients with or without PAH demonstrated that whereas MIP-1β exhibited no correlation with PAH, RANTES demonstrated an inverse correlation with PAH (r= −0.25, p<0.03) with significance achieved in patients that exhibited severe PAH (TRV> 2.9, p<0.05). These findings suggest that both chemokines, RANTES and MIP-1β, are associated with the vasculopathy of SCD, and whereas MIP-1β does not appear to be associated with SCD-associated PAH, RANTES levels are inversely correlated to the severity of PAH. RANTES merits further investigation as a potential marker in PAH, and for a possible role in its progression.

scholarly journals Myeloid Fbxw7 Prevents Pulmonary Fibrosis by Suppressing TGF-β Production

2022 ◽  
Vol 12 ◽  
Author(s):  
Jia He ◽  
Yue Du ◽  
Gaopeng Li ◽  
Peng Xiao ◽  
Xingzheng Sun ◽  
...  
Keyword(s):  
Pulmonary Fibrosis ◽  
Mononuclear Cells ◽  
Transforming Growth Factor ◽  
Treatment Options ◽  
Myeloid Cell ◽  
Transforming Growth Factor Β ◽  
Peripheral Blood Mononuclear ◽  
Regulation Mechanisms ◽  
Insight Into

Idiopathic pulmonary fibrosis (IPF) is a group of chronic interstitial pulmonary diseases characterized by an inexorable decline in lung function with limited treatment options. The abnormal expression of transforming growth factor-β (TGF-β) in profibrotic macrophages is linked to severe pulmonary fibrosis, but the regulation mechanisms of TGF-β expression are incompletely understood. We found that decreased expression of E3 ubiquitin ligase Fbxw7 in peripheral blood mononuclear cells (PBMCs) was significantly related to the severity of pulmonary fibrosis in IPF patients. Fbxw7 is identified to be a crucial suppressing factor for pulmonary fibrosis development and progression in a mouse model induced by intratracheal bleomycin treatment. Myeloid cell-specific Fbxw7 deletion increases pulmonary monocyte-macrophages accumulation in lung tissue, and eventually promotes bleomycin-induced collagen deposition and progressive pulmonary fibrosis. Notably, the expression of TGF-β in profibrotic macrophages was significantly upregulated in myeloid cell-specific Fbxw7 deletion mice after bleomycin treatment. C-Jun has long been regarded as a critical transcription factor of Tgfb1, we clarified that Fbxw7 inhibits the expression of TGF-β in profibrotic macrophages by interacting with c-Jun and mediating its K48-linked ubiquitination and degradation. These findings provide insight into the role of Fbxw7 in the regulation of macrophages during the pathogenesis of pulmonary fibrosis.

scholarly journals The Role of Nutrients in Reducing the Risk for Noncommunicable Diseases during Aging

Nutrients ◽  
2019 ◽  
Vol 11 (1) ◽  
pp. 85 ◽  
Author(s):  
Maaike J. Bruins ◽  
Peter Van Dael ◽  
Manfred Eggersdorfer
Keyword(s):  
Nutrient Intake ◽  
Healthy Aging ◽  
Current Knowledge ◽  
Aging Population ◽  
Noncommunicable Diseases ◽  
Nutrient Intakes ◽  
Nutrition Programs ◽  
Increased Risk ◽  
Essential Nutrient

An increasing aging population worldwide accounts for a growing share of noncommunicable diseases (NCDs) of the overall social and economic burden. Dietary and nutritional approaches are of paramount importance in the management of NCDs. As a result, nutrition programs are increasingly integrated into public health policies. At present, programs aimed at reducing the burden of NCDs have focused mostly on the excess of unhealthy nutrient intakes whereas the importance of optimizing adequate essential and semi-essential nutrient intakes and nutrient-rich diets has received less attention. Surveys indicate that nutrient intakes of the aging population are insufficient to optimally support healthy aging. Vitamin and mineral deficiencies in older adults are related to increased risk of NCDs including fatigue, cardiovascular disease, and cognitive and neuromuscular function impairments. Reviewed literature demonstrates that improving intake for certain nutrients may be important in reducing progress of NCDs such as musculoskeletal disorders, dementia, loss of vision, and cardiometabolic diseases during aging. Current knowledge concerning improving individual nutrient intakes to reduce progression of chronic disease is still emerging with varying effect sizes and levels of evidence. Most pronounced benefits of nutrients were found in participants who had low nutrient intake or status at baseline or who had increased genetic and metabolic needs for that nutrient. Authorities should implement ways to optimize essential nutrient intake as an integral part of their strategies to address NCDs.

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