Objective: This study aims to investigate may moesin deficiency resulted in neurodevelopmental abnormalities caused by negative impact on synaptic signaling ultimately leading to synaptic structure and plasticity. Methods: Behavioral assessments measured neurodevelopment (surface righting, negative geotaxis, cliff avoidance), anxiety (open field test, elevated plus maze test), and memory (passive avoidance test, Y-maze test) in moesin-knockout mice (KO) compared to wild-type mice (WT). Whole exome sequencing (WES) of brain (KO vs. WT) and analysis of synaptic proteins were performed to determine the disruption of signal pathways downstream of moesin. Risperidone, a therapeutic agent, was utilized to reverse the neurodevelopmental aberrance in moesin KO. Results: Moesin-KO pups exhibited decrease in the surface righting ability on postnatal day 7 (p<0.05) and increase in time spent in the closed arms (p<0.01), showing increased anxiety-like behavior. WES revealed mutations in pathway aberration in neuron projection, actin filament-based processes, and neuronal migration in KO. Decreased cell viability (p<0.001) and expression of soluble NSF adapter protein 25 (SNAP25) (p<0.001) and postsynaptic density protein 95 (PSD95) (p<0.01) was observed in days in vitro 7 neurons. Downregulation of synaptic proteins, and altered phosphorylation levels of Synapsin I, mammalian uncoordinated 18 (MUNC18), extracellular signal-regulated kinase (ERK), and cAMP response element-binding protein (CREB) was observed in KO cortex and hippocampus. Risperidone reversed the memory impairment in the passive avoidance test and the spontaneous alternation percentage in the Y maze test. Risperidone also restored the reduced expression of PSD95 (p<0.01) and the phosphorylation of Synapsin at Ser605 (p<0.05) and Ser549 (p<0.001) in the cortex of moesin-KO. Conclusion Moesin deficiency leads to neurodevelopmental delay and memory decline, which may be caused through altered regulation in synaptic proteins and function.

Purpose: The associated factors for hypertensive retinopathy (HTR) are rarely investigated. This study aimed to identify the associated factors for HTR using a systematic review. Methods: The review included cross-sectional, case-controlled, and cohort studies on HTR risk factors published in Korean and English with full texts available from PubMed, Embase, CINAHL, Web of Science, and Korean databases. Methodological quality was assessed using the Joanna Briggs Institute (JBI) checklist. Results: Eleven studies were finally selected, and three studies including patients with hypertension without diabetes mellitus, older age, male sex, alcohol consumption, the duration of hypertension, hyperglycemia, dyslipidemia, microalbuminuria, high creatinine levels, chronic kidney disease, and cardiovascular changes were identified as factors associated with HTR. Conversely, in the remaining eight studies, younger age, non-smoking status, and renal function indicators (albuminuria, high creatinine levels, chronic kidney disease, and uric acid) were identified as associated factors. Conclusions Regardless of the inclusion of patients with diabetes mellitus, impaired kidney functions were determined as significant factors associated with retinopathy in patients with HTR. However, considering a limited number of evidence and lack of evidence to confirm causality, we recommend further research on renal function and HTR.

Objective: This study aims to investigate may moesin deficiency resulted in neurodevelopmental abnormalities caused by negative impact on synaptic signaling ultimately leading to synaptic structure and plasticity. Methods: Behavioral assessments measured neurodevelopment (surface righting, negative geotaxis, cliff avoidance), anxiety (open field test, elevated plus maze test), and memory (passive avoidance test, Y-maze test) in moesin-knockout mice (KO) compared to wild-type mice (WT). Whole exome sequencing (WES) of brain (KO vs. WT) and analysis of synaptic proteins were performed to determine the disruption of signal pathways downstream of moesin. Risperidone, a therapeutic agent, was utilized to reverse the neurodevelopmental aberrance in moesin KO. Results: Moesin-KO pups exhibited decrease in the surface righting ability on postnatal day 7 (p<0.05) and increase in time spent in the closed arms (p<0.01), showing increased anxiety-like behavior. WES revealed mutations in pathway aberration in neuron projection, actin filament-based processes, and neuronal migration in KO. Decreased cell viability (p<0.001) and expression of soluble NSF adapter protein 25 (SNAP25) (p<0.001) and postsynaptic density protein 95 (PSD95) (p<0.01) was observed in days in vitro 7 neurons. Downregulation of synaptic proteins, and altered phosphorylation levels of Synapsin I, mammalian uncoordinated 18 (MUNC18), extracellular signal-regulated kinase (ERK), and cAMP response element-binding protein (CREB) was observed in KO cortex and hippocampus. Risperidone reversed the memory impairment in the passive avoidance test and the spontaneous alternation percentage in the Y maze test. Risperidone also restored the reduced expression of PSD95 (p<0.01) and the phosphorylation of Synapsin at Ser605 (p<0.05) and Ser549 (p<0.001) in the cortex of moesin-KO. Conclusion Moesin deficiency leads to neurodevelopmental delay and memory decline, which may be caused through altered regulation in synaptic proteins and function.

Purpose: The associated factors for hypertensive retinopathy (HTR) are rarely investigated. This study aimed to identify the associated factors for HTR using a systematic review. Methods: The review included cross-sectional, case-controlled, and cohort studies on HTR risk factors published in Korean and English with full texts available from PubMed, Embase, CINAHL, Web of Science, and Korean databases. Methodological quality was assessed using the Joanna Briggs Institute (JBI) checklist. Results: Eleven studies were finally selected, and three studies including patients with hypertension without diabetes mellitus, older age, male sex, alcohol consumption, the duration of hypertension, hyperglycemia, dyslipidemia, microalbuminuria, high creatinine levels, chronic kidney disease, and cardiovascular changes were identified as factors associated with HTR. Conversely, in the remaining eight studies, younger age, non-smoking status, and renal function indicators (albuminuria, high creatinine levels, chronic kidney disease, and uric acid) were identified as associated factors. Conclusions Regardless of the inclusion of patients with diabetes mellitus, impaired kidney functions were determined as significant factors associated with retinopathy in patients with HTR. However, considering a limited number of evidence and lack of evidence to confirm causality, we recommend further research on renal function and HTR.

Objective: This study aims to investigate may moesin deficiency resulted in neurodevelopmental abnormalities caused by negative impact on synaptic signaling ultimately leading to synaptic structure and plasticity. Methods: Behavioral assessments measured neurodevelopment (surface righting, negative geotaxis, cliff avoidance), anxiety (open field test, elevated plus maze test), and memory (passive avoidance test, Y-maze test) in moesin-knockout mice (KO) compared to wild-type mice (WT). Whole exome sequencing (WES) of brain (KO vs. WT) and analysis of synaptic proteins were performed to determine the disruption of signal pathways downstream of moesin. Risperidone, a therapeutic agent, was utilized to reverse the neurodevelopmental aberrance in moesin KO. Results: Moesin-KO pups exhibited decrease in the surface righting ability on postnatal day 7 (p<0.05) and increase in time spent in the closed arms (p<0.01), showing increased anxiety-like behavior. WES revealed mutations in pathway aberration in neuron projection, actin filament-based processes, and neuronal migration in KO. Decreased cell viability (p<0.001) and expression of soluble NSF adapter protein 25 (SNAP25) (p<0.001) and postsynaptic density protein 95 (PSD95) (p<0.01) was observed in days in vitro 7 neurons. Downregulation of synaptic proteins, and altered phosphorylation levels of Synapsin I, mammalian uncoordinated 18 (MUNC18), extracellular signal-regulated kinase (ERK), and cAMP response element-binding protein (CREB) was observed in KO cortex and hippocampus. Risperidone reversed the memory impairment in the passive avoidance test and the spontaneous alternation percentage in the Y maze test. Risperidone also restored the reduced expression of PSD95 (p<0.01) and the phosphorylation of Synapsin at Ser605 (p<0.05) and Ser549 (p<0.001) in the cortex of moesin-KO. Conclusion Moesin deficiency leads to neurodevelopmental delay and memory decline, which may be caused through altered regulation in synaptic proteins and function.

Purpose: The associated factors for hypertensive retinopathy (HTR) are rarely investigated. This study aimed to identify the associated factors for HTR using a systematic review. Methods: The review included cross-sectional, case-controlled, and cohort studies on HTR risk factors published in Korean and English with full texts available from PubMed, Embase, CINAHL, Web of Science, and Korean databases. Methodological quality was assessed using the Joanna Briggs Institute (JBI) checklist. Results: Eleven studies were finally selected, and three studies including patients with hypertension without diabetes mellitus, older age, male sex, alcohol consumption, the duration of hypertension, hyperglycemia, dyslipidemia, microalbuminuria, high creatinine levels, chronic kidney disease, and cardiovascular changes were identified as factors associated with HTR. Conversely, in the remaining eight studies, younger age, non-smoking status, and renal function indicators (albuminuria, high creatinine levels, chronic kidney disease, and uric acid) were identified as associated factors. Conclusions Regardless of the inclusion of patients with diabetes mellitus, impaired kidney functions were determined as significant factors associated with retinopathy in patients with HTR. However, considering a limited number of evidence and lack of evidence to confirm causality, we recommend further research on renal function and HTR.

Objective: This study aims to investigate may moesin deficiency resulted in neurodevelopmental abnormalities caused by negative impact on synaptic signaling ultimately leading to synaptic structure and plasticity. Methods: Behavioral assessments measured neurodevelopment (surface righting, negative geotaxis, cliff avoidance), anxiety (open field test, elevated plus maze test), and memory (passive avoidance test, Y-maze test) in moesin-knockout mice (KO) compared to wild-type mice (WT). Whole exome sequencing (WES) of brain (KO vs. WT) and analysis of synaptic proteins were performed to determine the disruption of signal pathways downstream of moesin. Risperidone, a therapeutic agent, was utilized to reverse the neurodevelopmental aberrance in moesin KO. Results: Moesin-KO pups exhibited decrease in the surface righting ability on postnatal day 7 (p<0.05) and increase in time spent in the closed arms (p<0.01), showing increased anxiety-like behavior. WES revealed mutations in pathway aberration in neuron projection, actin filament-based processes, and neuronal migration in KO. Decreased cell viability (p<0.001) and expression of soluble NSF adapter protein 25 (SNAP25) (p<0.001) and postsynaptic density protein 95 (PSD95) (p<0.01) was observed in days in vitro 7 neurons. Downregulation of synaptic proteins, and altered phosphorylation levels of Synapsin I, mammalian uncoordinated 18 (MUNC18), extracellular signal-regulated kinase (ERK), and cAMP response element-binding protein (CREB) was observed in KO cortex and hippocampus. Risperidone reversed the memory impairment in the passive avoidance test and the spontaneous alternation percentage in the Y maze test. Risperidone also restored the reduced expression of PSD95 (p<0.01) and the phosphorylation of Synapsin at Ser605 (p<0.05) and Ser549 (p<0.001) in the cortex of moesin-KO. Conclusion Moesin deficiency leads to neurodevelopmental delay and memory decline, which may be caused through altered regulation in synaptic proteins and function.

Purpose: The associated factors for hypertensive retinopathy (HTR) are rarely investigated. This study aimed to identify the associated factors for HTR using a systematic review. Methods: The review included cross-sectional, case-controlled, and cohort studies on HTR risk factors published in Korean and English with full texts available from PubMed, Embase, CINAHL, Web of Science, and Korean databases. Methodological quality was assessed using the Joanna Briggs Institute (JBI) checklist. Results: Eleven studies were finally selected, and three studies including patients with hypertension without diabetes mellitus, older age, male sex, alcohol consumption, the duration of hypertension, hyperglycemia, dyslipidemia, microalbuminuria, high creatinine levels, chronic kidney disease, and cardiovascular changes were identified as factors associated with HTR. Conversely, in the remaining eight studies, younger age, non-smoking status, and renal function indicators (albuminuria, high creatinine levels, chronic kidney disease, and uric acid) were identified as associated factors. Conclusions Regardless of the inclusion of patients with diabetes mellitus, impaired kidney functions were determined as significant factors associated with retinopathy in patients with HTR. However, considering a limited number of evidence and lack of evidence to confirm causality, we recommend further research on renal function and HTR.

Objective: This study aims to investigate may moesin deficiency resulted in neurodevelopmental abnormalities caused by negative impact on synaptic signaling ultimately leading to synaptic structure and plasticity. Methods: Behavioral assessments measured neurodevelopment (surface righting, negative geotaxis, cliff avoidance), anxiety (open field test, elevated plus maze test), and memory (passive avoidance test, Y-maze test) in moesin-knockout mice (KO) compared to wild-type mice (WT). Whole exome sequencing (WES) of brain (KO vs. WT) and analysis of synaptic proteins were performed to determine the disruption of signal pathways downstream of moesin. Risperidone, a therapeutic agent, was utilized to reverse the neurodevelopmental aberrance in moesin KO. Results: Moesin-KO pups exhibited decrease in the surface righting ability on postnatal day 7 (p<0.05) and increase in time spent in the closed arms (p<0.01), showing increased anxiety-like behavior. WES revealed mutations in pathway aberration in neuron projection, actin filament-based processes, and neuronal migration in KO. Decreased cell viability (p<0.001) and expression of soluble NSF adapter protein 25 (SNAP25) (p<0.001) and postsynaptic density protein 95 (PSD95) (p<0.01) was observed in days in vitro 7 neurons. Downregulation of synaptic proteins, and altered phosphorylation levels of Synapsin I, mammalian uncoordinated 18 (MUNC18), extracellular signal-regulated kinase (ERK), and cAMP response element-binding protein (CREB) was observed in KO cortex and hippocampus. Risperidone reversed the memory impairment in the passive avoidance test and the spontaneous alternation percentage in the Y maze test. Risperidone also restored the reduced expression of PSD95 (p<0.01) and the phosphorylation of Synapsin at Ser605 (p<0.05) and Ser549 (p<0.001) in the cortex of moesin-KO. Conclusion Moesin deficiency leads to neurodevelopmental delay and memory decline, which may be caused through altered regulation in synaptic proteins and function.

Purpose: The associated factors for hypertensive retinopathy (HTR) are rarely investigated. This study aimed to identify the associated factors for HTR using a systematic review. Methods: The review included cross-sectional, case-controlled, and cohort studies on HTR risk factors published in Korean and English with full texts available from PubMed, Embase, CINAHL, Web of Science, and Korean databases. Methodological quality was assessed using the Joanna Briggs Institute (JBI) checklist. Results: Eleven studies were finally selected, and three studies including patients with hypertension without diabetes mellitus, older age, male sex, alcohol consumption, the duration of hypertension, hyperglycemia, dyslipidemia, microalbuminuria, high creatinine levels, chronic kidney disease, and cardiovascular changes were identified as factors associated with HTR. Conversely, in the remaining eight studies, younger age, non-smoking status, and renal function indicators (albuminuria, high creatinine levels, chronic kidney disease, and uric acid) were identified as associated factors. Conclusions Regardless of the inclusion of patients with diabetes mellitus, impaired kidney functions were determined as significant factors associated with retinopathy in patients with HTR. However, considering a limited number of evidence and lack of evidence to confirm causality, we recommend further research on renal function and HTR.