ObjectiveTo investigate the effects and mechanisms of Fangji Fulingtang （FFD） on mitochondrial function in the mouse model of myocardial fibrosis （MF）. MethodsSixty SPF-grade male C57BL/6J mice were randomly allocated into six groups （n=10 per group）： control， model， low-dose， medium-dose， and high-dose （3.315， 6.63， and 13.26 g·kg^-1， respectively） FFD， and captopril （20 mg·kg^-1）. MF was induced by subcutaneous injection of isoproterenol （10 mg·kg^-1·d^-1） in other groups except the control group for 14 consecutive days， with simultaneous gavage of corresponding drugs. Left ventricular ejection fraction （LVEF） and left ventricular fractional shortening （LVFS） were measured by echocardiography. Serum levels of creatine kinase-MB （CK-MB）， cardiac troponin I （cTnI）， N-terminal pro-brain natriuretic peptide （NT-pro BNP）， tumor necrosis factor-α （TNF-α）， interleukin-1β （IL-1β）， and interleukin-6 （IL-6） were determined by enzyme-linked immunosorbent assay （ELISA）. Malondialdehyde （MDA）， superoxide dismutase （SOD）， and glutathione （GSH） levels were measured by biochemical assays. Reactive oxygen species （ROS） were detected by dihydroethidium （DHE） fluorescence staining. Hematoxylin-eosin （HE）， Masson's trichrome， and wheat germ agglutinin （WGA） staining were performed to evaluate myocardial structure and fibrosis. Mitochondrial ultrastructure and function were assessed by transmission electron microscopy， adenosine triphosphate （ATP） colorimetric assay， and JC-1 fluorescence staining. The protein levels of phosphorylated adenosine monophosphate-activated protein kinase α subunit （p-AMPKα）， AMPKα， peroxisome proliferator-activated receptor gamma coactivator-1α （PGC-1α）， mitofusin 2 （MFN2）， pyruvate kinase M2 isoform （PKM2）， lactate dehydrogenase A （LDHA）， and hypoxia-inducible factor 1 alpha （HIF-1α） were analyzed by Western blot. ResultsCompared with the control group， the model group exhibited decreased LVEF and LVFS， increased heart weight index and heart weight-to-tibia length ratio （P<0.01）， elevated levels of myocardial injury markers （CK-MB， cTnI， and NT-pro BNP）， inflammatory cytokines （TNF-α， IL-1β， and IL-6）， and MDA， along with reduced SOD and GSH levels （P<0.01）. Enhanced interstitial collagen deposition and cardiomyocyte hypertrophy were observed in the model group （P<0.01）. Transmission electron microscopy and JC-1 staining revealed mitochondrial swelling， crista disruption， decreased ATP content， and reduced red/green fluorescence ratio in the model group （P<0.01）. Western blot analysis demonstrated downregulation of p-AMPKα， PGC-1α， and MFN2 and upregulation of PKM2， LDHA， and HIF-1α in the model group （P<0.01）. Compared with the model group， treatment with FFD or captopril improved LVEF and LVFS， reduced heart weight index and heart weight-to-tibia length ratio （P<0.05， P<0.01）， lowered the serum levels of CK-MB， cTnI， NT-pro BNP， TNF-α， IL-1β， IL-6， and MDA， increased the SOD and GSH levels （P<0.05， P<0.01）， attenuated the myocardial fibrosis and cardiomyocyte hypertrophy （P<0.01）， and restored the mitochondrial ultrastructure. The medium and high-dose FFD groups as well as the captopril group showed increased ATP production and red/green fluorescence ratio （P<0.05， P<0.01）. Furthermore， FFD upregulated the expression of p-AMPKα and PGC-1α while downregulating the expression of LDHA and HIF-1α （P<0.05， P<0.01）. ConclusionFFD activates the AMPK/PGC-1α/MFN2 signaling pathway and inhibits the PKM2/LDHA/HIF-1α axis to restore mitochondrial function and energy metabolic homeostasis， thereby attenuating isoproterenol-induced myocardial fibrosis.

ObjectiveTo investigate the effects and mechanisms of Fangji Fulingtang （FFD） on mitochondrial function in the mouse model of myocardial fibrosis （MF）. MethodsSixty SPF-grade male C57BL/6J mice were randomly allocated into six groups （n=10 per group）： control， model， low-dose， medium-dose， and high-dose （3.315， 6.63， and 13.26 g·kg^-1， respectively） FFD， and captopril （20 mg·kg^-1）. MF was induced by subcutaneous injection of isoproterenol （10 mg·kg^-1·d^-1） in other groups except the control group for 14 consecutive days， with simultaneous gavage of corresponding drugs. Left ventricular ejection fraction （LVEF） and left ventricular fractional shortening （LVFS） were measured by echocardiography. Serum levels of creatine kinase-MB （CK-MB）， cardiac troponin I （cTnI）， N-terminal pro-brain natriuretic peptide （NT-pro BNP）， tumor necrosis factor-α （TNF-α）， interleukin-1β （IL-1β）， and interleukin-6 （IL-6） were determined by enzyme-linked immunosorbent assay （ELISA）. Malondialdehyde （MDA）， superoxide dismutase （SOD）， and glutathione （GSH） levels were measured by biochemical assays. Reactive oxygen species （ROS） were detected by dihydroethidium （DHE） fluorescence staining. Hematoxylin-eosin （HE）， Masson's trichrome， and wheat germ agglutinin （WGA） staining were performed to evaluate myocardial structure and fibrosis. Mitochondrial ultrastructure and function were assessed by transmission electron microscopy， adenosine triphosphate （ATP） colorimetric assay， and JC-1 fluorescence staining. The protein levels of phosphorylated adenosine monophosphate-activated protein kinase α subunit （p-AMPKα）， AMPKα， peroxisome proliferator-activated receptor gamma coactivator-1α （PGC-1α）， mitofusin 2 （MFN2）， pyruvate kinase M2 isoform （PKM2）， lactate dehydrogenase A （LDHA）， and hypoxia-inducible factor 1 alpha （HIF-1α） were analyzed by Western blot. ResultsCompared with the control group， the model group exhibited decreased LVEF and LVFS， increased heart weight index and heart weight-to-tibia length ratio （P<0.01）， elevated levels of myocardial injury markers （CK-MB， cTnI， and NT-pro BNP）， inflammatory cytokines （TNF-α， IL-1β， and IL-6）， and MDA， along with reduced SOD and GSH levels （P<0.01）. Enhanced interstitial collagen deposition and cardiomyocyte hypertrophy were observed in the model group （P<0.01）. Transmission electron microscopy and JC-1 staining revealed mitochondrial swelling， crista disruption， decreased ATP content， and reduced red/green fluorescence ratio in the model group （P<0.01）. Western blot analysis demonstrated downregulation of p-AMPKα， PGC-1α， and MFN2 and upregulation of PKM2， LDHA， and HIF-1α in the model group （P<0.01）. Compared with the model group， treatment with FFD or captopril improved LVEF and LVFS， reduced heart weight index and heart weight-to-tibia length ratio （P<0.05， P<0.01）， lowered the serum levels of CK-MB， cTnI， NT-pro BNP， TNF-α， IL-1β， IL-6， and MDA， increased the SOD and GSH levels （P<0.05， P<0.01）， attenuated the myocardial fibrosis and cardiomyocyte hypertrophy （P<0.01）， and restored the mitochondrial ultrastructure. The medium and high-dose FFD groups as well as the captopril group showed increased ATP production and red/green fluorescence ratio （P<0.05， P<0.01）. Furthermore， FFD upregulated the expression of p-AMPKα and PGC-1α while downregulating the expression of LDHA and HIF-1α （P<0.05， P<0.01）. ConclusionFFD activates the AMPK/PGC-1α/MFN2 signaling pathway and inhibits the PKM2/LDHA/HIF-1α axis to restore mitochondrial function and energy metabolic homeostasis， thereby attenuating isoproterenol-induced myocardial fibrosis.

To summarize the nursing care of a patient with acute myocardial infarction complicated with cardiogenic shock before operation.The main nursing points are as follows:in the acute stage,the integrated rescue was implemented with rapid on-machine coordination of external cardiopulmonary resuscitation,multidisciplinary collaboration to ensure safe patient transport;during the bridging period,the combined operation care of extracorporeal membrane oxygenation,intra-aortic balloon counter pulsation and continuous kidney replacement therapy was carried out with goal-oriented anticoagulation care,prevention of catheter-related infection with the assistance of mechanical circulation,and neurological function monitoring.The patient successfully passed the waiting period for heart transplantation and underwent heart transplantation 21 days after admission.With the follow-up for 1 year,the patient recovered well.

We report a family of glucocorticoid-remediable aldosteronism (GRA). A 20-year-old man presented with early-onset hypertension accompanied by hypokalemia was admitted to our hospital. Clinical data and family history were collected. Following genetic analyses with PCR and Sanger sequencing to document the chimeric gene and crossover site, respectively, we identified CYP11B1/CYP11B2 and determined the breakpoint of unequal crossover to be located in 264-380 nucletide, which was considered as GRA. There were 4 cases of GRA in the family, the average age of onset was 28 years, and all had different degrees of hypertension. Among them, the proband′s uncle suffered from moyamoya disease and died 6 months later due to sudden cerebral hemorrhage. In order to improve the understanding of this rare disease, the pathogenesis, biochemical profiles, diagnosis and treatment of GRA were summarized and analyzed.

Objective:To analyze the urine of normal healthy left-behind children under 1 year old and left-behind children with zinc deficiency under 1 year old in Zunyi area using hydrogen nuclear magnetic resonance ( 1HNMR), thus providing a new biomarker for the early diagnosis of zinc deficiency. Methods:From January to August 2018, a total of 40 normal healthy left-behind children under 1 year old in Zunyi area(healthy control group)[22 males and 18 females, average age of (7.78±3.62) months, average height of (65.01±2.67) cm and average body mass of (7.15±1.59) kg] and 40 age-matched left-behind children with zinc deficiency in the same region(zinc deficiency group)[19 males and 21 females, average age of (7.89±3.57) months, average height of (64.25±2.95) cm and average body mass of (7.02±1.68) kg] were included for a cross-sectional study by stratified sampling.The urine 1HNMR spectra of children in the 2 groups were measured, and the age, height, body mass and serum zinc content of children in the 2 groups were compared.The metabolites of the 2 groups were compared by metabono-mics technology combined with multivariate statistical analysis, and the differential metabolites of children with zinc deficiency were screened out. Results:There were no significant differences in age, height and body mass between the 2 groups (all P>0.05). The serum zinc level of healthy control group was significantly higher than that of zinc deficiency group [(54.3±3.06) mmol/L vs.(39.2±3.77) mmol/L, t=22.65, P<0.05]. Urine 1HNMR spectrogram results showed that compared with healthy controls, 4-hydroxyphenylpyruvic acid, phenyl acetyl glycine, and hippuric acid salt water were significantly lower in zinc deficiency group ( r=-0.620, -0.689, and -0.721, respectively, all | r|>0.602, all P<0.05). Conclusions:Zinc deficiency in left-behind children under 1 year old in Zunyi area is mainly manifested by decreased metabolites of 4-hydroxyphenylpyruvic acid, phenylacetyl glycine and horse-urate, suggesting metabolic disorder of intestinal flora.Differentially expressed metabolites have a potential application value in the early diagnosis of zinc deficiency.

Objective:To explore the clinical charecteristics, imaging features, therapy and prognosis of stroke in children, and provide help for clinical treatment.Methods:The clinical data of 49 children with stroke were collectedand retrospectively analyzed in the Children′s Hospital of Soochow University from January 1, 2019 to December 31, 2019.Results:A mong the 49 children with stroke, 35 were male and 14 were female, aged 1-178 (65.69 ± 55.22) months; the specific etiologies were cerebrovascular malformation, craniocerebral trauma, tumor, vitamin K deficiencies, infectious diseases, rheumatic immune diseases, hemophilia and congenital heart disease. The first symptoms of stroke were disturbance of consciousness, hemiplegia, convulsions, vomiting and headache. The arterial ischemic stroke (18 cases) were mainly caused by craniocerebral trauma and cerebrovascular malformation. The hemorrhagic stroke (31 cases) were mainly caused by arteriovenous malformation, vitamin K deficiency and tumor. The surgical rate in the arterial stroke group was significantly lower than that in the hemorrhagic stroke group.Conclusions:Traumatic cerebral infarction and intracranial arteriovenous malformation are the main causes of arterial ischemic stroke and hemorrhagic stroke in children. Early diagnosis and treatment can significantly improve prognosis.

Objective To investigate the management of Graves' disease in Jiangsu province. Methods According to the 2011 management of GD survey from American Thyroid Association and the 2013 survey from European Thyroid Association, a questionnaire was designed for this survey to acquire the diagnosis, treatment, and follow-up of Graves' disease among endocrinologists from 35 tertiary hospitals in Jiangsu province. Results A total of 476 valid questionnaires were collected. For patients with symptoms of hyperthyroidism, a large majority of respondents monitored serum FT3 , FT4 , TSH, thyroid peroxidase antibody, thyroglobulin antibody, TSH receptor antibody, and finding of thyroid ultrasound, accounted for 95. 6％, 95. 0％, 95. 4％, 95. 8％, 90. 3％, 90. 5％, and 93. 9％physicians, respectively. 91.2％ of physicians preferred anti-thyroid drugs as the first-line treatment, and 92. 6％ of them gave priority to the use of methimazole. For the duration of anti-thyroid drugs therapy, 41.2％of endocrinologists chose 24 months, while 20％ chose 18 months. When patients have moderate and active ophthalmopathy, most respondents with medium or senior professional titles preferred anti-thyroid drugs, while most resident physicians chose radioactive iodine plus corticosteroids. When pregnancy was confirmed in the patients of Graves' disease, 88％ of respondents preferred propylthiouracil during the first trimester of pregnancy, and 58. 4％ of them would continue propylthiouracil into the second trimester. Conclusions The mastering of basic perception of Graves' disease knowledge is satisfactory among the endocrinologists. But by comparing to the American and European survey results and related guidelines, there are still some differences in diagnosis and treatment. Therefore, physicians should notice those differences and make improvement on standardized treatment for patients to raise the response ratio while reducing the recurrent events.

Objective: To explore the characteristic changes in urinary metabolites in left-behind children with vitamin D deficiency under 1 year old in Zunyi area by metabolomic nuclear magnetic resonance (NMR) in order to provide new biomarkers for early diagnosis of vitamin D deficiency. Methods: From January to August 2018, blood tests and urine collection were carried out on the left-behind children under 1 year old in Fenggang county, Bozhou district and Zheng′an county under Zunyi city by stratified sampling.Forty children diagnosed as a vitamin D deficiency were selected as a vitamin D deficiency group, and 40 children with normal urine test were selected as a healthy control group.For urine sampling, SIMCA-P+ software was applied to analyze the integral value of hydrogen spectrogram by principal component analysis (PCA) and partial least squares discriminant analysis (PLS-DA) was used to distinguish the difference in urine metabolites between two groups of the left-behind children.Orthogonal partial least squares discriminant analysis (OPLS-DA) was used to screen different metabolites. Results: The serum level of 25-hydroxy vitamin D[25-(OH)D][(32.0±3.6) nmol/L ] in the healthy control group was higher than that in the vitamin D deficiency group[(15.8±2.3) nmol/L], and the difference was statistically significant (P<0.05). PCA and PLS-DA analysis showed significant differences in urine metabolites between the healthy control group and the vitamin D deficiency group (P<0.05). OPLS-DA indicated R²X=0.365, Q²=0.978, which further verified the difference of metabolites.Compared with the healthy control group, the urine of methyl malonic acid, 3-hydroxy butyrate, N-acetyl glycoprotein signal, glutamic acid, dimethyl glycine, 2-ketone glutaric acid, taurine, fumaric acid salt level increased significantly in the vitamin D deficiency group, and the differences were statistically significant (|r|>0.602, all P<0.05, df=39). However, the levels of ethyl malonic acid, creatine, choline, glycerophosphalocholine and equine were significantly decreased, and the differences were statistically significant (|r|>0.602, all P<0.05, df=39). Conclusions The left-behind children under 1 year old with vitamin D deficiency in Zunyi region are mainly characterized by disorder in energy metabolism, lipid metabolism, amino acid metabolism and intestinal microbial meta-bolism disorders, and their differential metabolites have potential application value in early diagnosis and pathogenesis of vitamin D deficiency.

Objective: To investigate the etiology, clinical features, treatment and outcome of nephrotic syndrome associated with chronic mercury poisoning. Methods: From June 2013 to April 2018, Beijing Chaoyang Hospital, Capital Medical University received 33 patients with chronic mercury-neutral nephrotic syndrome. The clinical manifestations, laboratory tests, treatment methods, and outcomes were analyzed. Results: Among the 33 patients, 27 patients had mercury exposure due to daily-life contact and the other 6 patients were caused by iatrogenic mercury. The symptom was characterized by typical nephrotic syndrome such as lower extremity edema and proteinuria at first onset. The treatment was based on mercury-removing treatment, 19 cases were treated with mercury removal alone, 16 cases were completely relieved; 10 cases were treated with mercury removal and glucocorticoids, all of which were completely relieved; 4 cases were treated with mercury removal, glucocorticoids and immunosuppressive agents, all complete remission; clinical complete remission rate is about 90.9% (30 cases in total) . Urinary mercury levels decreased the fastest between the first and second courses of mercury treatment, but the total amount of urine protein increased. As the amount of urinary mercury excreted increased, the total amount of urine protein decreased gradually (Z=2.86, P<0.01) . Conclusion The clinical features of chronic mercury-induced nephrotic syndrome are non-specific, easy to be misdiagnosed and missed. The treatment is mainly treated with mercury removal treatment. The prognosis is good. In severe cases, glucocorticoid therapy can be supplemented.