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.

The purpose of this study was to enrich the genomic information and provide a basis for further development and utilization of Polygonatum kingianum. The fresh rhizome of P. kingianum was used as the experimental material, and the full-length transcriptome was sequenced by PacBio Sequel platform. The final measured polymerase reads were 1 120 485, with a total of 77.73 GB of data. In NR database, 41 864 homologous sequence alignments were aligned to 5 species; 40 506 were annotated in the KOG database and classified into 26 categories based on their functionality; 69 060 GO annotated 32 functional groups divided into 3 categories: cellular components, molecular functions, and biological processes; 45 779 annotations were added to 145 metabolic pathways in the KEGG database. Among them, there are 127 identified transcripts related to polysaccharide synthesis in the glycolysis/gluconeogenesis metabolic pathway, 144 in the starch and sucrose metabolic pathway, 85 in the amino acid sugar and nucleotide sugar metabolic pathway, and 69 in the fructose and mannose metabolic pathway. In addition, 1 781 transcription factors were detected, distributed in 37 transcription factor families; 180 293 SSR loci were detected, among which single base repeats accounted for the most, accounting for 30.48% of all base repeats, and at least five base repeats, accounting for only 0.14% of single base repeats. The results of this study provide important data supporting for enriching the genomic information of P. kingianum and exploring its effective biosynthetic pathway.

In this study, the pharmacodynamic substance basis of the therapeutic activity of different origin sources of the Tibetan medicinal herb Zha xun was evaluated, and the protective effect of the Zha xun, from Habahe county of Altay region, Xinjiang Uygur Autonomous Region; Gilgit region, Pakistan; Lhozhag county of Lhozhag city, Tibet Autonomous Region; Lhorong county of Chamdo city, Tibet Autonomous Region; and Jiulong county of Ganzi Tibetan Autonomous Prefecture, Sichuan Province, on 0.2% carbon tetrachloride (CCl₄)-induced acute liver injury in ICR mice was evaluated. The results showed that different sources of Zha xun significantly reduced serum alanine aminotransferase (ALT), aspartate aminotransferase (AST), lactate dehydrogenase (LDH) in the CCl₄-induced acute oxidative liver injury model, improved liver histopathological damage. Among them, Zha xun from Habahe County, Altay Region, Xinjiang Uygur Autonomous Region; Gilgit Region, Pakistan; and Lhorong County, Chamdo City, Tibet Autonomous Region significantly reduced the malondialdehyde (MDA) content in liver tissues (P < 0.05), increased the glutathione (GSH) content (P < 0.01), improved the oxidative stress in liver tissues. The preliminary evaluation of the hepatoprotective activity of Zha xun from different origins was carried out using the model of HepG2 cell injury induced by acetaminophen (APAP). The results showed that Zha xun from different origins could significantly inhibit APAP-induced hepatocellular injury and improve the survival rate of hepatocytes. The present study demonstrated that the different origins of Zha xun had definite hepatoprotective activities in vivo and ex vivo, among which, Zha xun from Lhorong County, Chamdo City, Tibet Autonomous Region, had stronger hepatoprotective activities. The animals used in this experiment and the related dispositions were in accordance with the requirements of animal welfare, and the experiment was approved by the Committee of Laboratory Animal Management and Use of the Institute of Pharmaceutical Sciences of the Chinese Academy of Medical Sciences (approval No. 00004024) before the experiment was carried out.

Objective To explore the myopia control effect of orthokeratology(OK)lenses and build a prediction model of myopia control effect based on random forest and Logistic regression,so as to provide a basis for further impro-ving adolescent vision.Methods A total of 289 patients who wore OK lenses after seeing an ophthalmologist in Shiji-azhuang People's Hospital from January to June 2019 were selected as the OK lens group,and a total of 289 patients who wore framed glasses during the same period were selected as the framed glass group.After 2 and 4 years of wearing,the in-crease in axial length(AL)of the patients was observed.The patients were divided into a well-controlled myopia group and a poorly-controlled myopia group according to the changes in AL of the eyes after wearing OK lenses for 4 years.The fac-tors influencing the myopia control effect were analyzed based on random forest and Logistic regression,and a nomogram prediction model was constructed.The performance of the model was evaluated using the receiver operating characteristic(ROC)curve,calibration curve,and decision curve analysis(DCA).Results After 2 and 4 years,the diopter increase and AL increase of patients wearing OK lenses were lower than those of patients wearing framed glasses(all P＜0.001).There were no significant changes in corneal endothelial cell parameters and central corneal thickness at the thinnest point before,2 years and 4 years after wearing between the two groups(all P＞0.05).The random forest model showed that basic AL,daily wear time,correct eye health behavior,pupil diameter,daily outdoor activity time,homework time after school,and daily sleep time were the top 7 variables in importance ranking.Logistic regression analysis showed that home-work time after school was a risk factor for poor myopia control in OK lens wearers,while basic AL,pupil diameter,daily wear time,correct eye health behavior,daily outdoor activity time,and daily sleep time were protective factors for myopia control.The ROC curve,calibration curve,and DCA suggested that the nomogram prediction model constructed based on random forest and Logistic regression analysis had good accuracy,consistency and clinical effectiveness.Conclusion OK lens shows good myopia control effect,has little effect on corneal endothelial cells and corneal thickness,and demon-strates high safety.Homework time after school,basic AL,pupil diameter,daily wear time,correct eye health behavior,daily outdoor activity time,and daily sleep time are influencing factors of myopia control.Strengthening the construction of a prediction model is helpful in identifying high-risk groups with poor myopia control and guiding clinical interventions in time.

Objective:To explore the application of 3D visualisation technology combined with perforator flap transfer in reconstruction of soft tissue defects in traumatic hand and foot injury and explore the clinical outcomes.Methods:Between January 2021 and February 2023, a retrospective analysis was conducted in the Department of Emergency of the Affiliated Hospital of Jiangsu University and the Department of Sports Medical of Wuxi No. 9 People's Hospital, on the data of 12 patients (13 flaps) who received surgery of 3D visualisation technology combined with perforator flap transfer for soft tissue defects left by traumatic hand and foot injuries. The patients were 7 males and 5 females aged 45 [36.5, 55.8] years old. Nine patients had the defects in hand and 3 in foot, with 3 in the left and 9 in the right. The sizes of defects ranged from 8.0 cm×6.0 cm to 18.0 cm×17.0 cm. The time from injury to surgery was 13.5 [8.3, 20.8] days. Preoperative CTA scans of donor and recipient sites were performed, and the imaging data were processed for 3D image reconstruction and visualisation. A total of 13 flaps were designed and harvested, including 10 free anterolateral thigh perforator flaps (ALTPFs) and 3 pedicled perforator flaps of fibular artery containing fibular nerve nutrient vessel chains. The flap sizes ranged from 9.0 cm×6.0 cm to 20.0 cm×15.0 cm. Five of the donor sites were directly closed by suture and 8 by skin grafting. Monthly outpatient follow-ups were conducted for the first 3 months after surgery, and then the follow-up reviews were conducted through visits of outpatient clinic or reviewed via WeChat interviews. Information about the outcomes of the transferred flaps, complications and function recovery were recorded on all patients.Results:All 13 flaps were successfully harvested and transferred with the assistance of 3D visualisation technology. Preoperative location of perforator vessels was accurate and flap design was reasonable. The 3D visualisation provided an effective guidance for surgical manipulation. Twelve flaps survived completely after surgery. One flap that had partial necrosis healed after skin grafting. All patients were included in more than 6 months of postoperative follow-up, with a mean follow-up duration of 8.1 months±1.7 months. All flaps had good colour and texture. Four flaps that had swollen appearance received secondary thinning surgery with satisfactory outcomes. The recovery of 9 patients with hand injury was evaluated according to the Blood Circulation Elauation of Severed Finger Replantation Evaluation Standard of Upper Limb Functional of Hand Surgery of Chinese Medical Association. At the final follow-up, the blood supply of flaps was excellent in 11 flaps and good in 2 flaps. Hand function was excellent in 2 hands, good in 4 hands and poor in 3 hands. Scores of American Orthopedic Foot and Ankle Societ(AOFAS) ankle-hindfoot was used for foot function evaluation and all 3 patients were in excellent. Of the postoperative complications, due to a haematoma beneath the flap, a local infection and a delayed fracture healing were occurred in 3 patients separately.Conclusion:The 3D visualisation technology assisted perforator flap transfer can achieve high-quality reconstruction of defects in hand and foot through precise preoperative flap design and simulated surgical incision, therefore it provides a better treatment outcomes for patients.

Numerous studies have indicated that organic fertilizers (OFer) might contain heavy metals (HMs) that present health risks to organic farmers (OFar). This study compared the concentrations of six HMs (Zn, Ni, Cd, Cu, Pb, Cr) in the blood of two distinct groups of farmers: 30 OFar from a designated organic area in eastern Taiwan, and 74 conventional farmers (CFar) from neighboring non-organic designated regions. The findings revealed that the OFar exhibited higher levels of Zn (1202.70 ± 188.74 μg/L), Cr (0.20 ± 0.09 μg/L), and Ni (2.14 ± 1.48 μg/L) in their blood compared to the CFar (988.40 ± 163.16 μg/L, 0.18 ± 0.15 μg/L, and 0.77 ± 1.23 μg/L), respectively. The disparities in Zn, Cr, and Ni levels were measured at 214.3 μg/L, 0.02 μg/L, and 1.37 μg/L, respectively. Furthermore, among the OFar, those who utilized green manures (GM) displayed significantly elevated blood levels of Zn (1279.93 ± 156.30 μg/L), Cr (0.24 ± 0.11 μg/L), and Ni (1.94 ± 1.38 μg/L) compared to individuals who exclusively employed chemical fertilizers (CFer) (975.42 ± 165.35 μg/L, 0.19 ± 0.16 μg/L, and 0.74 ± 1.20 μg/L), respectively. The differences in Zn, Cr, and Ni levels were measured at 304.51 μg/L, 0.05 μg/L, and 1.20 μg/L, respectively. As a result, OFar should be careful in choosing OFer and avoid those that may have heavy metal contamination.