By analyzing the connotation of "kenang （窠囊）" and its relationship with adenoid hypertrophy （AH） in children， this paper suggests that kenang plays a significant role in the development process of pediatric AH， from the initial accumulation of phlegm-dampness in the early stage， to the binding of phlegm and stasis in the middle stage， and finally the healthy qi deficiency with phlegm stagnation in the late stage， and may also serve as a key entry point for the diagnosis and treatment. From the perspective of "kenang"， and in combination with the core pathogenesis of pediatric AH characterized by lung heat and phlegm stasis， this paper proposes that the key therapeutic principles include clearing heat to resolve phlegm， activating blood to remove stasis， and reducing swelling to dissipate nodules. A staged treatment strategy based on the self-formulated Bizhi Formula （鼻窒方） with modifications is used. In the early stage of the disease， the treatment should be soothing the wind and relieving the exterior， resolving phlegm and dredging the orifices to prevent the initial knot of kenang， for which Bizhi Formula and Cangerzi Powder （苍耳子散） with modifications can be used. In the middle stage， the treatment should be dissolving phlegm and expelling stasis， dispersing knots and unblocking orifices to break down the establishment of kenang， and Bizhi Formula combined with Haizao Yuhu Decoction （海藻玉壶汤） with modifications is suggested. In the late stage， the treatment emphasizes reinforcing healthy qi and consolidating the root， resolving phlegm and dredging collaterals in order to prevent recurrence of kenang， and the suggested prescription is modified Bizhi Formula combined with Shenling Baizhu Powder （参苓白术散）.

By analyzing the connotation of "kenang （窠囊）" and its relationship with adenoid hypertrophy （AH） in children， this paper suggests that kenang plays a significant role in the development process of pediatric AH， from the initial accumulation of phlegm-dampness in the early stage， to the binding of phlegm and stasis in the middle stage， and finally the healthy qi deficiency with phlegm stagnation in the late stage， and may also serve as a key entry point for the diagnosis and treatment. From the perspective of "kenang"， and in combination with the core pathogenesis of pediatric AH characterized by lung heat and phlegm stasis， this paper proposes that the key therapeutic principles include clearing heat to resolve phlegm， activating blood to remove stasis， and reducing swelling to dissipate nodules. A staged treatment strategy based on the self-formulated Bizhi Formula （鼻窒方） with modifications is used. In the early stage of the disease， the treatment should be soothing the wind and relieving the exterior， resolving phlegm and dredging the orifices to prevent the initial knot of kenang， for which Bizhi Formula and Cangerzi Powder （苍耳子散） with modifications can be used. In the middle stage， the treatment should be dissolving phlegm and expelling stasis， dispersing knots and unblocking orifices to break down the establishment of kenang， and Bizhi Formula combined with Haizao Yuhu Decoction （海藻玉壶汤） with modifications is suggested. In the late stage， the treatment emphasizes reinforcing healthy qi and consolidating the root， resolving phlegm and dredging collaterals in order to prevent recurrence of kenang， and the suggested prescription is modified Bizhi Formula combined with Shenling Baizhu Powder （参苓白术散）.

Objective To investigate the correlation between skeletal muscle mass index(ASMI)and islet β cell reserve function in patients with newly diagnosed type 2 diabetes mellitus(T2DM).Methods A total of 100 patients with newly diagnosed T2DM were included in this study.All the patients were admitted to the Department of Endocrinology in the First People's Hospital of Yinchuan between June 2022 and November 2023.They were divided into two groups according to their skeletal muscle mass index(ASMI):patients with T2DM accompanied by sarcopenia(Sar,n=50)group,and patients with simple T2DM(T2DM,n=50)group.Additionally,a control(NC)group consisting of 50 healthy participants was selected.Fasting C-peptide levels,liver and kidney function,blood lipid profiles,and other indicators were assessed in all the individuals.The correlation between ASMI and other indicators was analyzed,and the influencing factors for ASMI and T2DM combined with sarcopenia were analyzed respectively.Results The levels of HbA1c,FPG,and TG were higher,while FC-P and Scr levels were lower in the T2DM group and Sar group compared with the NC group(P<0.05).FPG was higher,while ASMI,FC-P,BMI were lower in the Sar group than in the T2DM group(P<0.05).Spearman correlation analysis revealed a negative correlation between ASMI and FPG and HbA1c(P<0.05),whereas a positive correlation was observed with BMI,ALT,Scr,SUA and FC-P(P<0.05).Multiple linear regression analysis indicated that BMI,HbA1c and FC-P were influencing factors for ASMI(P<0.05).Furthermore,logistic regression analysis demonstrated that BMI,HbA1c,FC-P were influencing factors for T2DM with sarcopenia(P<0.05).Conclusions The level of ASMI may be related to the reserve function of islet β cells.

Objective To investigate the correlation between skeletal muscle mass index(ASMI)and islet β cell reserve function in patients with newly diagnosed type 2 diabetes mellitus(T2DM).Methods A total of 100 patients with newly diagnosed T2DM were included in this study.All the patients were admitted to the Department of Endocrinology in the First People's Hospital of Yinchuan between June 2022 and November 2023.They were divided into two groups according to their skeletal muscle mass index(ASMI):patients with T2DM accompanied by sarcopenia(Sar,n=50)group,and patients with simple T2DM(T2DM,n=50)group.Additionally,a control(NC)group consisting of 50 healthy participants was selected.Fasting C-peptide levels,liver and kidney function,blood lipid profiles,and other indicators were assessed in all the individuals.The correlation between ASMI and other indicators was analyzed,and the influencing factors for ASMI and T2DM combined with sarcopenia were analyzed respectively.Results The levels of HbA1c,FPG,and TG were higher,while FC-P and Scr levels were lower in the T2DM group and Sar group compared with the NC group(P<0.05).FPG was higher,while ASMI,FC-P,BMI were lower in the Sar group than in the T2DM group(P<0.05).Spearman correlation analysis revealed a negative correlation between ASMI and FPG and HbA1c(P<0.05),whereas a positive correlation was observed with BMI,ALT,Scr,SUA and FC-P(P<0.05).Multiple linear regression analysis indicated that BMI,HbA1c and FC-P were influencing factors for ASMI(P<0.05).Furthermore,logistic regression analysis demonstrated that BMI,HbA1c,FC-P were influencing factors for T2DM with sarcopenia(P<0.05).Conclusions The level of ASMI may be related to the reserve function of islet β cells.

Objective:To investigate the role and mechanism of long non-coding RNA (lncRNA) gastric cancer associated transcript 3 (GACAT3) in glioma radioresistance.Methods:Real-time reverse transcription PCR (RT-qPCR) was used to detect the expression of lncRNA GACAT3 and miR-497 in human astrocyte NHA cells and glioma cells U251. NC-siRNA and GACAT3-siRNA were transfected into U251 cells, and the cells were treated with X-ray irradiation. Colony formation assay was used to detect the survival fraction of U251 cells. The apoptosis of U251 cells was detected by flow cytometry. Western blot was used to detect the expression of cysteine containing aspartate specific protease 3 (Caspase-3) in U251 cells. Bioinformatics software and dual luciferase reporter gene assay were used to predict and verify the targeting relationship between lncRNA GACAT3 and miR-497, and between miR-497 and Yes-associated protein 1 (YAP1), respectively. NC mimic, miR-497 mimic, GACAT3-siRNA and NC inhibitor, GACAT3-siRNA and miR-497 inhibitor were co-transfected into U251 cells. Colony formation assay, flow cytometry and Western blot were adopted to evaluate the effect of miR-497 overexpression and lncRNA GACAT3 on the radiosensitivity of U251 cells by regulating miR-497.Results:Compared with NHA cells, the expression of lncRNA GACAT3 in U251 cells was significantly up-regulated, and the expression of miR-497 in U251 cells was significantly down-regulated (both P<0.05). After knockdown of GACAT3, the survival fraction of irradiated U251 cells was significantly decreased, while the apoptosis rate and Caspase-3 protein expression were significantly increased (all P<0.05). lncRNA GACAT3 targeted and negatively regulated the expression of miR-497. Overexpression of miR-497 significantly reduced the survival fraction of U251 cells after irradiation, and increased the apoptosis rate and Caspase-3 protein expression. Inhibition of miR-497 significantly reversed the promoting effect of lncRNA GACAT3 knockdown on the radiosensitivity of U251 cells. miR-497 targeted and negatively regulated the expression of YAP1. Conclusion:Knockdown of lncRNA GACAT3 can enhance the radiosensitivity of glioma cells by regulating the miR-497/YAP1 axis.

Objective:To observe the changes of macular morphology and blood flow after minimally invasive vitrectomy (PPV) in patients with severe non-proliferative diabetic retinopathy (sNPDR).Methods:A prospective clinical study. From January 2020 to April 2021, 17 consecutive sNPDR patients with 17 eyes who were diagnosed and received PPV treatment at the Zhongshan Ophthalmic Center of Sun Yat-sen University were included in the study. There were 12 males with 12 eyes and 5 females with 5 eyes; the average age was 55 years old; the average duration of diabetes was 11 years; the average glycosylated hemoglobin was 7.9%. Before the operation and 1, 3, and 6 months after the operation, all the affected eyes underwent best corrected visual acuity (BCVA), standard 7-field fundus color photography, and optical coherence tomography angiography (OCTA). An OCTA instrument was used to scan the macular area of the affected eye with in the range of 3 mm×3 mm to measure the central subfoveal thickness (CST), the thickness of the ganglion cell complex (GCC) in the macular area, the thickness of the retinal nerve fiber layer (RNFL), and the superficial capillary plexus (SCP) vessel density and perfusion density in the macular area, macular avascular zone (FAZ) area, a-circularity index (AI). Before the operation and 6 months after the operation, the least significant difference test was used for the pairwise comparison.Results:Before the operation, 1, 3, and 6 months after the operation, the FAZ area of the macular area were 0.34±0.14, 0.35±0.10, 0.37±0.10, 0.36±0.13 mm 2, respectively; AI were 0.52±0.13, 0.54±0.11, 0.57±0.10, 0.60±0.11; CST was 282.6±66.7, 290.4±70.9, 287.2±67.5, 273.2± 49.6 μm; GCC thickness were 77.1±15.5, 74.3±13.9, 72.6±16.2, 78.5±18.3 μm; the thickness of RNFL was 97.9±13.8, 101.3±14.6, 97.7±12.0, 96.1±11.4 μm, respectively. The overall blood flow density of SCP in the macula were (16.79±1.43)%, (16.71±1.82)%, (17.30±2.25)%, (17.35±1.22)%; the overall perfusion density were 0.32±0.02, 0.32±0.03, 0.33±0.03, 0.33±0.02, respectively. After the operation, the CST increased first and then decreased; the thickness of RNFL increased 1 month after the operation, and then gradually decreased. Comparison of the parameters before and 6 months after the operation showed that the AI improved, and the difference was statistically significant ( P=0.049); the difference in FAZ area and the thickness of CST, GCC, and RNFL was not statistically significant ( P=0.600, 0.694, 0.802, 0.712); There was no statistically significant difference in the retina SCP blood flow density and perfusion density in the macular area ( P=0.347, 0.361). Conclusion:Compared with before surgery, there is no significant change in macular structure and blood flow density in sNPDR patients within 6 months after minimally invasive PPV.

BACKGROUND:Chitosan biological materials can induce bone marrow mesenchymal stem cells to differentiate toward neurons. As a derivative of chitosan, carboxymethyl chitosan has a series of excelent properties. However, whether carboxymethyl chitosan can induce the neuronal differentiation of bone marrow mesenchymal stem cells remains unclear.OBJECTIVE:To investigate the effect of carboxymethyl chitosan thermosensitive hydrogel on the differentiation of bone marrow mesenchymal stem cells into neurons and the possible mechanism.METHODS:Passage 3 bone marrow mesenchymal stem cells from rats were selected and cultured in carboxymethyl chitosan thermosensitive hydrogel extracts in different concentrations (0, 50, 100, 150, 200, 500 g/L). Control cells were cultured in culture medium with no addition of carboxymethyl chitosan thermosensitive hydrogel extracts. MTT assay was performed to investigate the effects of different concentrations of carboxymethyl chitosan thermosensitive hydrogel extracts on bone marrow mesenchymal stem cell proliferation. Western blot assay was used to explore the effect of 150 g/L carboxymethyl chitosan thermosensitive hydrogel extracts on the expression of neuron-specific enolase, Nestin, Vimentin, NF-M, microtubule associated protein 2, glial fibrillary acidic protein, β3-tubulin, Notch1 and Jag1 protein.RESULTS AND CONCLUSION:MTT assay showed that carboxymethyl chitosan thermosensitive hydrogel promoted the cell proliferation, and the proliferation rate reached the peak at the concentration of 150 g/L. Western blot assay showed that the cells induced by 150 g/L carboxymethyl chitosan thermosensitive hydrogel extract had significant increases in neuron-specific enolase, Nestin, Vimentin, NF-M, microtubule associated protein 2, glial fibrillary acidic protein, and β3-tubulin protein expression, and obvious decreases in Notch1 and Jag1 protein expression in comparison with the control group. These results indicate that the carboxymethyl chitosan thermosensitive hydrogel induces rat bone marrow mesenchymal stem cells to differentiate toward neurons, and suppresses the activity of Notch signal pathway in the process of differentiation.

BACKGROUND:Bone marrow stromal cel s can differentiate into nerve cel s to promote nerve tissue repair, but the exact mechanism has not been ful y elucidated.
OBJECTIVE:To explore the influence of adenovirus-mediatedβnerve growth factor transfection on bone marrow stromal stem cel transplantation fighting against brain injury in rats.
METHODS:(1) Rat bone marrow stromal stem cel s were cultured in vitro, transfected with the adenovirus-mediatedβnerve growth factor and directional y induced usingβ-mercaptoethanol. (2) A total of 210 Sprague-Dawley rats were randomized into induction+tranfection group, induction+non-transfection group, induction+medium group, model group, and sham group (n=42 per group). Rat skul injury models were made, and given corresponding treatments at different time points (12, 24, 36, 48, 72 hours). Neurological function of rats was evaluated based on neurological severity scores on the day that the rats were given transplantation, and 1, 2, 3, 4 weeks after transplantation. (3) Another 75 Sprague-Dawley rats were also divided into five groups (n=15 per group) as above, fol owed by model establishment and corresponding treatments at 24 hours after modeling. Neurological severity scores were recorded at the same day, 1, 2, 3, 4 weeks after transplantation. Five rats from each group were sacrificed to detect levels of malondialdehyde and superoxide dismutase in the rat brain at the same day, 2 and 4 weeks after transplantation, respectively.
RESULTS AND CONCLUSION:If the cel s were transplanted within 48 hours after modeling, the neurological severity scores in the induction+transfection group decreased significantly compared with the induction+non-transfection group and model group at 1 and 2 weeks after transplantation (P<0.05). If the cel s were transplanted at different time, the neurological severity scores in the induction+transfection group were decreased significantly compared with the induction+non-transfection group and model group at 3 and 4 weeks after transplantation (P<0.05). If the cel s were transplanted within 24 hours after modeling, the neurological severity scores in the induction+transfection group decreased significantly compared with the model group at 1 week after transplantation (P<0.05), and the neurological severity scores in the induction+transfection group and induction+non-transfection group both were significantly lower than those in the model group (P<0.05). Two weeks after cel transplantation, the level of superoxide dismutase was significantly higher in the induction+transfection group than the induction+medium group and model group (P<0.05), but the level of malondialdehyde was significantly lower (P<0.05). Al these findings indicate that adenovirus-mediatedβnerve growth factor transfer plays a certain neuroprotective role in bone marrow stromal stem cel transplantation for brain injury in rats.

BACKGROUND:Choosing an effective means to label and trace the distribution, differentiation and migration of celsin vivo help to further explore the specific mechanism of cels that exert a therapeutic effect. OBJECTIVE:To understand the migration and localization of BrdU-labeled human umbilical cord mesenchymal stem cels in brain injury model rats. METHODS:Human umbilical cord blood samples were obtained, and the isolation of human umbilical cord mesenchymal stem cels was carried out. The primary and passage culture were performed. The phenotype of cels was detected by flow cytometry. Passage 3 human umbilical cord mesenchymal stem cels were labeled using BrdU, and the cel proliferation was detected using MTT method. BrdU-labeled cels were injected into brain injury ratsvia the tail vein. At 14 days after transplantation, brain tissues in the injury region were cut into sections and the migration and location of the umbilical cord mesenchymal stem cels were observed under inverted
fluorescence microscope. RESULTS AND CONCLUSION: Cel surface specific markers CD45 and CD34 were detected by flow cytometry, but the cels could not express CD44, CD105 and CD29. Based on the cel growth curve, the cels came into a conditioning period at 1-3 days of seeding and came into a logarithmic phase at 3-5 days. BrdU-positive cels were visible at the injury region after 14 days, indicating that in the rats, transplanted human umbilical cord mesenchymal stem cels migrated from the peripheral blood to the site of brain injury to achieve the effective repair of injured parts. Cite this article:Liu HL, Liu ZJ, Chen XB, Hu WZ, Ding BQ. Migration and localization of umbilical cord mesenchymal stem cels implanted into brain injury model rats. Zhongguo Zuzhi Gongcheng Yanjiu. 2016;20(1):31-35.