Improving quality in a complex primary care system-An example of refugee care and literature review
by Kaitlin
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Rationale, aims and objectives: Implement quality improvement of traditional industries (QI) methodology for primary care is often inappropriate for primary care and its relationship with Macrosystem health has many features of a complex adaptive system (CAS), which is highly responsive to a bottom-up instead of top management -down approach. We report on a case study demonstration of improvements made in the Family Health Center (FHC) of the JPS Health Network in a patient population of refugees who describe the features of QI in the framework of the CAS as opposed to the traditional approach to QI.
Methods: We report the changes in the health system utilization with new refugees from FHC patients from 2016 to 2017. We reviewed the literature and summarize the relevant theoretical understanding of quality management in a complex adaptive system that applies to this case for example.
Results: Applying the principles of CAS in the FHC, the use of the Emergency Department and Urgent Care Center patients newly arrived refugees before their first clinic visit is reduced by more than half (total visits decreased from 31% -14% of patients IDPs). Our review of the literature shows that the top-down algorithmic QI traditional process that most often succeed in raising even more metrics-single disease, and improve physician fatigue and punish doctors who treat patients who are susceptible.
An increase in the CAS occurs when the front-line physicians identify care gaps and given the flexibility to learn and adjust itself to enable emerging treatment process, which was created from the bottom-up leadership that utilizes the interdependence and interaction that exists with the top level of the organization through intelligent cause and as a result of top-down. We give examples of early adapters who better to apply the principles of CAS change their QI efforts.
Conclusion: Increased Means in primary care are more likely to be achieved when the urge to apply changes to shift from top-down to bottom-up.
Improving quality in a complex primary care system-An example of refugee care and literature review
The international consensus guidelines for Risk Factors in Chronic pancreatitis. Recommendations of the working group for international consensus guidelines for chronic pancreatitis in collaboration with the International Association Pancreatology, the American Pancreatic Association, Japan Pancreas Society, and the European Pancreatic Club.
chronic pancreatitis (CP) is a complex inflammatory disease with severely impaired quality of life and permanent destruction of the pancreas. This article is part of an international consensus guidelines on CP and gift consensus on elevating risk factor for the international working group of 20 experts CP.An CP of the main pancreatic society (IAP, APA, JPS, and EPC) evaluated 14 statements resulting from the evidence on four questions considered most relevant clinically in CP.
The Grading Assessment, Development and Evaluation (GRADE) approach is used to evaluate the level Recommendation evidence provided by the report. To determine the degree of agreement, the working group as at 14 statement to the strength of the agreement, using a nine-point Likert scale for calculating Cronbach alpha reliability coefficient.Strong consensus and agreement obtained for the following statement :, smoke Alcohol and certain genetic changes are risk factors for CP , past history, family history, symptoms, and lifestyle factors, including alcohol intake and smoking history should be determined. Dose-dependent alcohol consumption raised the risk of CP to 4-fold.
Description: MAPK8IP1 encodes a regulator of the pancreatic beta-cell function. C-Jun-amino-terminal kinase-interacting protein 1 is highly similar to JIP-1, a mouse protein known to be a regulator of c-Jun amino-terminal kinase (Mapk8). C-Jun-amino-terminal kinase-interacting protein 1 has been shown to prevent MAPK8 mediated activation of transcription factors, and to decrease IL-1 beta and MAP kinase kinase 1 (MEKK1) induced apoptosis in pancreatic beta cells. This protein also functions as a DNA-binding transactivator of the glucose transporter GLUT2. RE1-silencing transcription factor (REST) is reported to repress the expression of this gene in insulin-secreting beta cells. This gene is found to be mutated in a type 2 diabetes family, and thus is thought to be a susceptibility gene for type 2 diabetes.
Description: MAPK8IP1 encodes a regulator of the pancreatic beta-cell function. C-Jun-amino-terminal kinase-interacting protein 1 is highly similar to JIP-1, a mouse protein known to be a regulator of c-Jun amino-terminal kinase (Mapk8). C-Jun-amino-terminal kinase-interacting protein 1 has been shown to prevent MAPK8 mediated activation of transcription factors, and to decrease IL-1 beta and MAP kinase kinase 1 (MEKK1) induced apoptosis in pancreatic beta cells. This protein also functions as a DNA-binding transactivator of the glucose transporter GLUT2. RE1-silencing transcription factor (REST) is reported to repress the expression of this gene in insulin-secreting beta cells. This gene is found to be mutated in a type 2 diabetes family, and thus is thought to be a susceptibility gene for type 2 diabetes.
Description: MAPK8IP1 encodes a regulator of the pancreatic beta-cell function. C-Jun-amino-terminal kinase-interacting protein 1 is highly similar to JIP-1, a mouse protein known to be a regulator of c-Jun amino-terminal kinase (Mapk8). C-Jun-amino-terminal kinase-interacting protein 1 has been shown to prevent MAPK8 mediated activation of transcription factors, and to decrease IL-1 beta and MAP kinase kinase 1 (MEKK1) induced apoptosis in pancreatic beta cells. This protein also functions as a DNA-binding transactivator of the glucose transporter GLUT2. RE1-silencing transcription factor (REST) is reported to repress the expression of this gene in insulin-secreting beta cells. This gene is found to be mutated in a type 2 diabetes family, and thus is thought to be a susceptibility gene for type 2 diabetes.
Description: A polyclonal antibody for detection of JIP-1 phospho Thr103) from Human, Mouse, Rat. This JIP-1 phospho Thr103) antibody is for WB, IHC-P, IF, ELISA. It is affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogenand is unconjugated. The antibody is produced in rabbit by using as an immunogen synthesized peptide derived from human JIP-1 around the phosphorylation site of T103
Description: A polyclonal antibody for detection of JIP-1 phospho Thr103) from Human, Mouse, Rat. This JIP-1 phospho Thr103) antibody is for WB, IHC-P, IF, ELISA. It is affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogenand is unconjugated. The antibody is produced in rabbit by using as an immunogen synthesized peptide derived from human JIP-1 around the phosphorylation site of T103
Description: A polyclonal antibody for detection of JIP-1 phospho Thr103) from Human, Mouse, Rat. This JIP-1 phospho Thr103) antibody is for WB, IHC-P, IF, ELISA. It is affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogenand is unconjugated. The antibody is produced in rabbit by using as an immunogen synthesized peptide derived from human JIP-1 around the phosphorylation site of T103
Description: This gene encodes a regulator of the pancreatic beta-cell function. It is highly similar to JIP-1, a mouse protein known to be a regulator of c-Jun amino-terminal kinase (Mapk8). This protein has been shown to prevent MAPK8 mediated activation of transcription factors, and to decrease IL-1 beta and MAP kinase kinase 1 (MEKK1) induced apoptosis in pancreatic beta cells. This protein also functions as a DNA-binding transactivator of the glucose transporter GLUT2. RE1-silencing transcription factor (REST) is reported to repress the expression of this gene in insulin-secreting beta cells. This gene is found to be mutated in a type 2 diabetes family, and thus is thought to be a susceptibility gene for type 2 diabetes.
Description: This gene encodes a regulator of the pancreatic beta-cell function. It is highly similar to JIP-1, a mouse protein known to be a regulator of c-Jun amino-terminal kinase (Mapk8). This protein has been shown to prevent MAPK8 mediated activation of transcription factors, and to decrease IL-1 beta and MAP kinase kinase 1 (MEKK1) induced apoptosis in pancreatic beta cells. This protein also functions as a DNA-binding transactivator of the glucose transporter GLUT2. RE1-silencing transcription factor (REST) is reported to repress the expression of this gene in insulin-secreting beta cells. This gene is found to be mutated in a type 2 diabetes family, and thus is thought to be a susceptibility gene for type 2 diabetes.
Description: This gene encodes a regulator of the pancreatic beta-cell function. It is highly similar to JIP-1, a mouse protein known to be a regulator of c-Jun amino-terminal kinase (Mapk8). This protein has been shown to prevent MAPK8 mediated activation of transcription factors, and to decrease IL-1 beta and MAP kinase kinase 1 (MEKK1) induced apoptosis in pancreatic beta cells. This protein also functions as a DNA-binding transactivator of the glucose transporter GLUT2. RE1-silencing transcription factor (REST) is reported to repress the expression of this gene in insulin-secreting beta cells. This gene is found to be mutated in a type 2 diabetes family, and thus is thought to be a susceptibility gene for type 2 diabetes.
Description: A polyclonal antibody for detection of JIP-2 from Human, Mouse, Rat. This JIP-2 antibody is for WB, IHC-P, IF, ELISA. It is affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogenand is unconjugated. The antibody is produced in rabbit by using as an immunogen synthesized peptide derived from the C-terminal region of human JIP-2 at AA rangle: 550-630
Description: A polyclonal antibody for detection of JIP-2 from Human, Mouse, Rat. This JIP-2 antibody is for WB, IHC-P, IF, ELISA. It is affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogenand is unconjugated. The antibody is produced in rabbit by using as an immunogen synthesized peptide derived from the C-terminal region of human JIP-2 at AA rangle: 550-630
Description: A polyclonal antibody for detection of JIP-2 from Human, Mouse, Rat. This JIP-2 antibody is for WB, IHC-P, IF, ELISA. It is affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogenand is unconjugated. The antibody is produced in rabbit by using as an immunogen synthesized peptide derived from the C-terminal region of human JIP-2 at AA rangle: 550-630
Description: A polyclonal antibody for detection of JIP-3 from Human, Mouse. This JIP-3 antibody is for WB, IHC-P, IF, ELISA. It is affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogenand is unconjugated. The antibody is produced in rabbit by using as an immunogen synthesized peptide derived from the Internal region of human JIP-3 at AA range: 590-670
Description: A polyclonal antibody for detection of JIP-3 from Human, Mouse. This JIP-3 antibody is for WB, IHC-P, IF, ELISA. It is affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogenand is unconjugated. The antibody is produced in rabbit by using as an immunogen synthesized peptide derived from the Internal region of human JIP-3 at AA range: 590-670
Description: A polyclonal antibody for detection of JIP-3 from Human, Mouse. This JIP-3 antibody is for WB, IHC-P, IF, ELISA. It is affinity-purified from rabbit antiserum by affinity-chromatography using epitope-specific immunogenand is unconjugated. The antibody is produced in rabbit by using as an immunogen synthesized peptide derived from the Internal region of human JIP-3 at AA range: 590-670
Description: The mitogen-activated protein kinase 8 interacting protein 2 encoded by MAPK8IP2 is closely related to MAPK8IP1/IB1/JIP-1, a scaffold protein that is involved in the c-Jun amino-terminal kinase signaling pathway. This protein is expressed in brain and pancreatic cells. It has been shown to interact with, and regulate the activity of MAPK8/JNK1, and MAP2K7/MKK7 kinases. This protein thus is thought to function as a regulator of signal transduction by protein kinase cascade in brain and pancreatic beta-cells.
Description: The mitogen-activated protein kinase 8 interacting protein 2 encoded by MAPK8IP2 is closely related to MAPK8IP1/IB1/JIP-1, a scaffold protein that is involved in the c-Jun amino-terminal kinase signaling pathway. This protein is expressed in brain and pancreatic cells. It has been shown to interact with, and regulate the activity of MAPK8/JNK1, and MAP2K7/MKK7 kinases. This protein thus is thought to function as a regulator of signal transduction by protein kinase cascade in brain and pancreatic beta-cells.
Description: The mitogen-activated protein kinase 8 interacting protein 2 encoded by MAPK8IP2 is closely related to MAPK8IP1/IB1/JIP-1, a scaffold protein that is involved in the c-Jun amino-terminal kinase signaling pathway. This protein is expressed in brain and pancreatic cells. It has been shown to interact with, and regulate the activity of MAPK8/JNK1, and MAP2K7/MKK7 kinases. This protein thus is thought to function as a regulator of signal transduction by protein kinase cascade in brain and pancreatic beta-cells.
Description: C-Jun-amino-terminal kinase-interacting protein 3 encoded by MAPK8IP3 shares similarity with the product of Drosophila syd gene, required for the functional interaction of kinesin I with axonal cargo. Studies of the similar gene in mouse suggested that this protein may interact with, and regulate the activity of numerous protein kinases of the JNK signaling pathway, and thus function as a scaffold protein in neuronal cells. The C. elegans counterpart of this gene is found to regulate synaptic vesicle transport possibly by integrating JNK signaling and kinesin-1 transport. Several alternatively spliced transcript variants of this gene have been described, but the full-length nature of some of these variants has not been determined.
Description: C-Jun-amino-terminal kinase-interacting protein 3 encoded by MAPK8IP3 shares similarity with the product of Drosophila syd gene, required for the functional interaction of kinesin I with axonal cargo. Studies of the similar gene in mouse suggested that this protein may interact with, and regulate the activity of numerous protein kinases of the JNK signaling pathway, and thus function as a scaffold protein in neuronal cells. The C. elegans counterpart of this gene is found to regulate synaptic vesicle transport possibly by integrating JNK signaling and kinesin-1 transport. Several alternatively spliced transcript variants of this gene have been described, but the full-length nature of some of these variants has not been determined.
Description: C-Jun-amino-terminal kinase-interacting protein 3 encoded by MAPK8IP3 shares similarity with the product of Drosophila syd gene, required for the functional interaction of kinesin I with axonal cargo. Studies of the similar gene in mouse suggested that this protein may interact with, and regulate the activity of numerous protein kinases of the JNK signaling pathway, and thus function as a scaffold protein in neuronal cells. The C. elegans counterpart of this gene is found to regulate synaptic vesicle transport possibly by integrating JNK signaling and kinesin-1 transport. Several alternatively spliced transcript variants of this gene have been described, but the full-length nature of some of these variants has not been determined.
Description: Boster Bio Anti-Phospho-JIP-1 (T103) MAPK8IP1 Antibody catalog # A05068T103. Tested in ELISA, IF, IHC, WB applications. This antibody reacts with Human, Mouse, Rat.
Never smokers, even smoked less than a pack of cigarettes per day, have an increased risk for CP, compared with never smokers.Both genetic and environmental factors can markedly increase the risk of CP. Therefore, health-promoting lifestyle education and in certain cases the genetic counseling should be used to reduce the occurrence of CP.
