Early diagnosis and timely initiation of treatment of cancer patients may improve survival and quality of life. Various measures of delay can be made during diagnosis and treatment initiation. Most of the studies were...Early diagnosis and timely initiation of treatment of cancer patients may improve survival and quality of life. Various measures of delay can be made during diagnosis and treatment initiation. Most of the studies were based on single type of cancer with different definitions and measurements of delay in diagnosis and treatment. Thus, it has been difficult to synthesize results and generalize to other types of cancer. The study proposes to measure total duration between onsets of symptom to start of treatment into three components, namely primary, secondary and tertiary delays. Primary delay is defined as onset of symptoms to contacting the first medical person, secondary delay is from first medical contact to confirmed diagnosis, and tertiary delay is from confirmed diagnosis to treatment initiation. The aim of this study is to determine factors associated with primary, secondary and tertiary delays in cancer patients. This study was planned as a cross-sectional study. Data was collected from patients admitted to the surgical wards of Department of Surgical Oncology, Institute Rotary Cancer Hospital, New Delhi during 2006-2007. Gamma regression and quantile regressions at 25th, 50th and 75th percentile of each of the delays were used to determine related factors. A total of 403 patients were included in the analysis. The median tertiary delay was found almost two folds (59;Interquartile range: 26 - 101 days) than the primary and secondary delays. Extremity cancer patients had longest primary, secondary and tertiary delays. Shortest primary, secondary and tertiary delays were observed for gastrointestinal cancer, breast and genitourinary cancer respectively. There is an urgent need and scope to reduce delay at each level primary, secondary and tertiary delay. Intervention studies are needed through information, education and communication/screening programs to reduce the diagnostic and treatment delays in cancer patients.展开更多
The liver injury leads to an inflammatory response, which causes the activation of hepatic stellate cells (HSCs) that further secrete ECM proteins and play an important role in liver fibrosis. Moreover, the inflammato...The liver injury leads to an inflammatory response, which causes the activation of hepatic stellate cells (HSCs) that further secrete ECM proteins and play an important role in liver fibrosis. Moreover, the inflammatory response is a driving force for fibrogenesis, which is triggered by many types of injuries. Exaggerated inflammatory immune responses are mediated by cytoplasmic protein complexes known as inflammasomes, which are involved in many chronic liver diseases. Inflammasomes are pattern recognition receptors (PRRs) that can sense any microbial motifs known as pathogen-associated molecular patterns (PAMPs), and host- or environmental-derived stress signals known as damage-associated molecular patterns (DAMPs). The inflammasomes cause caspase-mediated proteolytic cleavage of pro-IL-1β and pro-IL-18 into active IL-1β and IL-18. In this review, we provide a comprehensive summary of the important roles of NLRP3 inflammasome in the pathogenesis of liver fibrosis with an emphasis on several direct and indirect pathways responsible for the NLRP3 inflammasome-mediated HSCs activation and fibrogenesis. In addition, we discuss the general pharmacological and genetics strategies for the inhibition of NLRP3 inflammasome activation and its downstream signaling with examples of emerging pharmacotherapeutics, targeting the NLRP3 inflammasome signaling as well as a possible way to develop effective and safer NLRP3 inflammasome inhibitors.展开更多
文摘Early diagnosis and timely initiation of treatment of cancer patients may improve survival and quality of life. Various measures of delay can be made during diagnosis and treatment initiation. Most of the studies were based on single type of cancer with different definitions and measurements of delay in diagnosis and treatment. Thus, it has been difficult to synthesize results and generalize to other types of cancer. The study proposes to measure total duration between onsets of symptom to start of treatment into three components, namely primary, secondary and tertiary delays. Primary delay is defined as onset of symptoms to contacting the first medical person, secondary delay is from first medical contact to confirmed diagnosis, and tertiary delay is from confirmed diagnosis to treatment initiation. The aim of this study is to determine factors associated with primary, secondary and tertiary delays in cancer patients. This study was planned as a cross-sectional study. Data was collected from patients admitted to the surgical wards of Department of Surgical Oncology, Institute Rotary Cancer Hospital, New Delhi during 2006-2007. Gamma regression and quantile regressions at 25th, 50th and 75th percentile of each of the delays were used to determine related factors. A total of 403 patients were included in the analysis. The median tertiary delay was found almost two folds (59;Interquartile range: 26 - 101 days) than the primary and secondary delays. Extremity cancer patients had longest primary, secondary and tertiary delays. Shortest primary, secondary and tertiary delays were observed for gastrointestinal cancer, breast and genitourinary cancer respectively. There is an urgent need and scope to reduce delay at each level primary, secondary and tertiary delay. Intervention studies are needed through information, education and communication/screening programs to reduce the diagnostic and treatment delays in cancer patients.
文摘The liver injury leads to an inflammatory response, which causes the activation of hepatic stellate cells (HSCs) that further secrete ECM proteins and play an important role in liver fibrosis. Moreover, the inflammatory response is a driving force for fibrogenesis, which is triggered by many types of injuries. Exaggerated inflammatory immune responses are mediated by cytoplasmic protein complexes known as inflammasomes, which are involved in many chronic liver diseases. Inflammasomes are pattern recognition receptors (PRRs) that can sense any microbial motifs known as pathogen-associated molecular patterns (PAMPs), and host- or environmental-derived stress signals known as damage-associated molecular patterns (DAMPs). The inflammasomes cause caspase-mediated proteolytic cleavage of pro-IL-1β and pro-IL-18 into active IL-1β and IL-18. In this review, we provide a comprehensive summary of the important roles of NLRP3 inflammasome in the pathogenesis of liver fibrosis with an emphasis on several direct and indirect pathways responsible for the NLRP3 inflammasome-mediated HSCs activation and fibrogenesis. In addition, we discuss the general pharmacological and genetics strategies for the inhibition of NLRP3 inflammasome activation and its downstream signaling with examples of emerging pharmacotherapeutics, targeting the NLRP3 inflammasome signaling as well as a possible way to develop effective and safer NLRP3 inflammasome inhibitors.
