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.

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.

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.

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.

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.

OBJECTIVE: To investigate the clinical effect of electroacupuncture (EA) in preventing chemotherapy-induced peripheral neuropathy (CIPN). METHODS: Fifty-two patients with breast cancer in the regimen of taxane-assisted/neoadjuvant chemotherapy, were randomly divided into an EA group (26 cases, 3 cases dropped out) and a usual care (UC) group (26 cases, 1 case dropped out). In the UC group, on the basis of standard chemotherapy regimen, the routine nursing was administered. In the EA group, on the intervention as the UC group, EA was added, the acupoints included Yintang (GV 24⁺), Baxie (EX-UE 9, the second one), Waiguan (TE 5), Hegu (LI 4), Quchi (LI 11), Zusanli (ST 36), Yinlingquan (SP 9), Sanyinjiao (SP 6), Taixi (KI 3), Taichong (LR 3), Xuanzhong (GB 39) and Bafeng (EX-LE 10, the fourth one). Electric stimulation was attached to Taichong (LR 3) and Sanyinjiao (SP 6) on the same side, with disperse-dense wave and the frequency of 2 Hz/10 Hz, for 30 min. EA started one day before the first cycle of chemotherapy, twice weekly in the first two weeks and once weekly in the rest weeks of chemotherapy. The duration of the intervention with EA was 12 weeks. The incidence of CIPN was compared in week 24 of the trial between the two groups. At the baseline and in week 12 and 24 of the trial, the score of EORTC QLQ-CIPN20 (European Organization for Research and Treatment of Cancer on chemotherapy-induced peripheral nerve toxicity quality of life questionnaire 20), the score of TCM syndrome scale and the score of EORTC QLQ-C30 (European Organization for Research and Treatment of Cancer on quality of life scale) were observed in the two groups. At the baseline and in week 12 of the trial, the sensory nerve conduction velocity (SCV) and the motor nerve conduction velocity (MCV) was detected. RESULTS: In week 24 of the trial, the incidence of CIPN was 17.4% (4/23) in the EA group, lower than that (72.0%, 18/25) in the UC group (P<0.001). The incidence of high-grade CIPN was 0% (0/23) in the EA group, lower than that (28.0%, 7/25) in the UC group (P<0.05). In week 12 and 24 of the trial, the scores for the sensory nerve symptom of EORTC QLQ-CIPN20 and the total scores were higher when compared with the baseline in the UC group (P<0.001, P<0.05, P<0.01). In week 24 of the trial, the score for the sensory nerve symptom of EORTC QLQ-CIPN20 in the EA group was lower than that of the UC group (P<0.05). In week 12 of the trial, SCV of the right superficial peroneal nerve was reduced when compared with the baseline in the UC group (P<0.05), and SCV of the left median nerve and the right superficial peroneal nerve was higher in the EA group when compared with the UC group (P<0.05, P<0.01). In week 12 and 24 of the trial, the scores for the secondary symptoms of TCM scale were decreased in the EA group compared with the baseline (P<0.05), and the scores for the primary and secondary symptoms, as well as the total scores of TCM scale were all higher than those of the baseline in the UC group (P<0.01, P<0.001, P<0.05). In week 12 of the trial, the scores for the primary and secondary symptoms, as well as the total score of TCM scale in the EA group were lower than those of the UC group (P<0.05, P<0.01). In week 24 of the trial, the score for the secondary symptoms and the total score of TCM scale in the EA group were lower than those of the UC group (P<0.05). In week 12 of the trial, the scores for fatigue, pain, nausea and vomiting in EORTC QLQ-C30 were increased in comparison with the baseline in the UC group (P<0.05, P<0.01); in week 24 of the trial, the score of the general health in EORTC QLQ-C30 was elevated when compared with the baseline in the EA group (P<0.001), and the scores for nausea and vomiting, loss of appetite were decreased in comparison with the baseline (P<0.01). In week 12 of the trial, the score of the general health in EORTC QLQ-C30 in the EA group was higher compared with the UC group (P<0.01), and the scores for pain, nausea and vomiting were lower (P<0.01, P<0.05). In week 24 of the trial, the score of the general health in EORTC QLQ-C30 was higher in the EA group compared with the UC group (P<0.001), and the score for loss of appetite was lower (P<0.05). CONCLUSION Electroacupuncture reduces the incidence and severity of CIPN, ameliorates nerve conduction velocity and improves the quality of life of the patients.
Humans ; Electroacupuncture ; Female ; Peripheral Nervous System Diseases/prevention & control* ; Middle Aged ; Adult ; Breast Neoplasms/therapy* ; Antineoplastic Agents/adverse effects* ; Aged

This study aimed to elucidate the clinical characteristics of patients diagnosed with toxoplasmosis in Korea. We collected and analyzed the specific research data of 5,917 patients from the Health Insurance Review and Assessment (HIRA; 2007–2020) and 533 electronic medical records (EMRs; 2003–2021) of Korean patients. The HIRA data showed that toxoplasmosis is an endemic disease that occurs constantly in Korea, with a large proportion of patients complaining of ocular symptoms. Of the 533 patients for whom EMR data were available, 54.6% were diagnosed with toxoplasmosis; ocular toxoplasmosis (35.7%), congenital toxoplasmosis (4.7%), cerebral toxoplasmosis (4.1%), pulmonary toxoplasmosis (0.4%), and toxoplasma hepatitis (0.6%), in order of frequency. In ocular cases, 54.4% of the patients had diverse ocular pathologies. Toxoplasmosis in Korea is characterized by a high frequency of ocular symptoms, most patients are adults, and 51.8% of patients with seropositivity were positive for IgG, suggesting prior infection. This study highlights that patients with ocular symptoms are included in the major diagnosis group for acquired toxoplasmosis in Korea.

This study aimed to elucidate the clinical characteristics of patients diagnosed with toxoplasmosis in Korea. We collected and analyzed the specific research data of 5,917 patients from the Health Insurance Review and Assessment (HIRA; 2007–2020) and 533 electronic medical records (EMRs; 2003–2021) of Korean patients. The HIRA data showed that toxoplasmosis is an endemic disease that occurs constantly in Korea, with a large proportion of patients complaining of ocular symptoms. Of the 533 patients for whom EMR data were available, 54.6% were diagnosed with toxoplasmosis; ocular toxoplasmosis (35.7%), congenital toxoplasmosis (4.7%), cerebral toxoplasmosis (4.1%), pulmonary toxoplasmosis (0.4%), and toxoplasma hepatitis (0.6%), in order of frequency. In ocular cases, 54.4% of the patients had diverse ocular pathologies. Toxoplasmosis in Korea is characterized by a high frequency of ocular symptoms, most patients are adults, and 51.8% of patients with seropositivity were positive for IgG, suggesting prior infection. This study highlights that patients with ocular symptoms are included in the major diagnosis group for acquired toxoplasmosis in Korea.

This study aimed to elucidate the clinical characteristics of patients diagnosed with toxoplasmosis in Korea. We collected and analyzed the specific research data of 5,917 patients from the Health Insurance Review and Assessment (HIRA; 2007–2020) and 533 electronic medical records (EMRs; 2003–2021) of Korean patients. The HIRA data showed that toxoplasmosis is an endemic disease that occurs constantly in Korea, with a large proportion of patients complaining of ocular symptoms. Of the 533 patients for whom EMR data were available, 54.6% were diagnosed with toxoplasmosis; ocular toxoplasmosis (35.7%), congenital toxoplasmosis (4.7%), cerebral toxoplasmosis (4.1%), pulmonary toxoplasmosis (0.4%), and toxoplasma hepatitis (0.6%), in order of frequency. In ocular cases, 54.4% of the patients had diverse ocular pathologies. Toxoplasmosis in Korea is characterized by a high frequency of ocular symptoms, most patients are adults, and 51.8% of patients with seropositivity were positive for IgG, suggesting prior infection. This study highlights that patients with ocular symptoms are included in the major diagnosis group for acquired toxoplasmosis in Korea.

This study aimed to elucidate the clinical characteristics of patients diagnosed with toxoplasmosis in Korea. We collected and analyzed the specific research data of 5,917 patients from the Health Insurance Review and Assessment (HIRA; 2007–2020) and 533 electronic medical records (EMRs; 2003–2021) of Korean patients. The HIRA data showed that toxoplasmosis is an endemic disease that occurs constantly in Korea, with a large proportion of patients complaining of ocular symptoms. Of the 533 patients for whom EMR data were available, 54.6% were diagnosed with toxoplasmosis; ocular toxoplasmosis (35.7%), congenital toxoplasmosis (4.7%), cerebral toxoplasmosis (4.1%), pulmonary toxoplasmosis (0.4%), and toxoplasma hepatitis (0.6%), in order of frequency. In ocular cases, 54.4% of the patients had diverse ocular pathologies. Toxoplasmosis in Korea is characterized by a high frequency of ocular symptoms, most patients are adults, and 51.8% of patients with seropositivity were positive for IgG, suggesting prior infection. This study highlights that patients with ocular symptoms are included in the major diagnosis group for acquired toxoplasmosis in Korea.