Silk fibroin is a natural polymer with certain water solubility, structural modification, good biocompatibility and biodegradability, which can be used as a drug delivery carrier material. As a promising drug delivery system, drug-loaded silk fibroin nanoparticles can control drug release, reduce toxicity and improve therapeutic effects. In this paper, the basic characteristics of silk fibroin, the preparation methods of drug-loaded silk fibroin nanoparticles and the application of silk fibroin in nanoparticulate drug delivery systems are reviewed, and on this basis, the further development of drug-loaded silk fibroin nanoparticles is prospected.

AlM: To investigate the association between the degree of anterioruveitis and related factors including inflammatory markers as well as sacroiliac joint imaging in patients with ankylosing spondylitis ( AS) .
METHODS: Anterior changes evaluated by slit lamp, erythrocyte sedimentation rate ( ESR ) , C - reactive protein ( CRP ) and magnetic resonance imaging of 55 cases with AS associateduveitis were retrospectively analyzed. A modified endotoxin-induced uveitis ( ElU ) clinical standard was used for uveitis grading. SPARCC sacroiliac scoring was used to evaluate bone edema of sacroiliac joint. The correlation between the degree of uveitis and sacroiliitis was assessed.
RESULTS: ln the 55 patients with AS, ElU grading scored 2-10, and SPARCC index scored 0-22. Further analysis showed that the severity of uveitis was significantly correlated with ESR (r=0. 869, P<0. 001) and CRP (r=0. 485, P<0. 001). The degree of anterior uveitis in AS patients was not correlated with inflammation of sacroiliac joint (r=0. 237, P=0. 081).
CONCLUSlON: Local autoimmunity of uveitis and sacroiliac joint inflammation with subsequent bone formation in AS might be mutually independent processes.

OBJECTIVETo investigate the influence of total flavonoids of Elsholtzia splendens (TFES) on isolated ischemia/reperfusion rat hearts and its underlying mechanisms.

METHODSHearts isolated from male SD rats were perfused on the Langendorff apparatus and subjected to global ischemia for 30 min followed by 120 min of reperfusion. The cardiac infarct size was measured by TTC staining. Hemodynamic parameters and the level of lactate dehydrogenase (LDH) in the coronary effluent were measured. Absorbance at 520 nm was determined in isolated cardiac mitochondria exposed to 200 micromol/L CaCl2 to detect the opening of the mitochondrial permeability transition pore.

RESULTSPretreatment with TFES (1, 10, 100 microg/ml) for 5 min decreased infarct size and LDH release and improved the recovery of the left ventricular developed pressure. In mitochondria, the decrease of absorbance at 520 nm evoked by CaCl2 was greatly inhibited by TFES.

CONCLUSIONTFES prevents myocardial ischemia/reperfusion injury, and this cardioprotective effect is probably via inhibiting mitochondrial permeability transition pore opening.

Animals ; Cardiotonic Agents ; pharmacology ; Disease Models, Animal ; Flavones ; pharmacology ; In Vitro Techniques ; Lamiaceae ; chemistry ; Male ; Mitochondria, Heart ; drug effects ; Mitochondrial Membrane Transport Proteins ; drug effects ; Myocardial Reperfusion ; Myocardial Reperfusion Injury ; prevention & control ; Rats ; Rats, Sprague-Dawley

OBJECTIVETo observe the impact of adenosine A1 receptor stimulation on extracellular signal-regulated kinase 1/2 (ERK1/2) signal pathways on angiotensin II (AngII) stimulated cardiomyocytes of neonatal rats in vitro.

METHODSCardiomyocytes of neonatal rats were cultured in vitro. Cardiomyocytes hypertrophy was induced by AngII (0.1 µmol/L). The antihypertrophic effect of adenosine A1 receptor stimulation via adenosine A1 receptor agonist R-PIA (1 µmol/L) was observed in the presence or absence of ERK1/2 inhibitor 1, 4-Diamino-2, 3-dicyano-1, 4-bis(o-aminophenylmercapto) butadiene (U0126) 1 µmol/L, PKC inhibitor Ro-31-8220 (50 nmol/L), and pertussis toxin (PTX, 5 mg/L). The total protein content was assayed by the method of Lowry. The expression of mRNA of atrial natriuretic peptide (ANP) was determined by RT-PCR. [Ca(2+)]i was measured by confocal microscope using Fluo-3/AM as fluorescent indicator. The relative expression of ERK1/2 was determined by Western blot.

RESULTSCompared with normal control group, AngII induced significant cardiomyocyte hypertrophy. Compared with AngII group, R-PIA significantly inhibited AngII-induced increase of the protein content, cardiomyocytes volume and expression of ERK1/2, calcium ion fluorescence intensity, similar as U0126 and Ro-31-8220. The inhibitory effects on AngII induced cardiomyocytes hypertrophy of R-PIA were lost when preincubated with PTX.

CONCLUSIONAdenosine A1 receptor can inhibit AngII induced cardiomyocyte hypertrophy through downregulating ERK signal pathways and reducing intracellular Ca(2+).

Adenosine A1 Receptor Agonists ; pharmacology ; Angiotensin II ; pharmacology ; Animals ; Calcium ; metabolism ; Cardiomegaly ; chemically induced ; prevention & control ; Cells, Cultured ; Female ; MAP Kinase Signaling System ; Male ; Myocytes, Cardiac ; drug effects ; metabolism ; pathology ; Rats ; Rats, Sprague-Dawley ; Receptor, Adenosine A1 ; drug effects ; metabolism

AIM: To screen TIGR/myocilin gene (MYOC) mutation in high myopic Chinese children with family history.METHODS: Gene sequencing was performed in exon 3 of the TIGR gene in high myopic Chinese Children. The coding sequence of TIGR exon 3 was screened by capillary electrophoresis sequencing. The sequence alterations were analyzed by bioinformatics.RESULTS: TIGR gene mutation was not found in high myopic patients and normal controls group.CONCLUSION: No identified gene mutation is found in TIGR gene in high myopic Chinese children.

Abstract: Objective　To investigate the molecular characteristic and evolutionary trends of full-genome sequences of coxsackievirus A2 (CV-A2) and A5 (CV-A5) in Changsha City. Methods　The CV-A2 and CV-A5 strains were isolated and detected from patients with hand, foot and mouth disease (HFMD) cases. The full-genome sequences of CV-A2 and CV-A5 strains were obtained using NGS sequencing. Homology and phylogenetic tree analysis were performed, and the recombination regions of the strains were examined by SimPlot software. Results　The full-genome sequences of CV-A2 and CV-A5 strains were obtained from routine surveillance cases of HFMD in Changsha in 2019. The CV-A2 strain was named S281/Changsha/CHN/2019 with the full-genome sequence of 7 422 bp long; the CV-A5 strain was named S272/Changsha/CHN/2019 with the full-genome sequence of 7 425 bp long. Homology analysis of the isolates by comparison with the nucleic acid sequences of CV-A2 and other CV-A2 strains in China showed that the non-structural protein region shared lower similarity than that of structural protein region. The CV-A2 showed 79.20% similarity with Fleetwood strain (NC038306), showed the highest similarity 95.60% with MN419014 strain from Hubei Province. The non-structural protein 3C and 3D region shared the lowest similarity with MN419014, 90.51 and 92.06%, respectively. Phylogenetic tree analysis showed that 3C and 3D regions were located in the CV-A4 branch. Amino acid mutation sites were found in non-structural protein region, and the amino acid sequence in structural protein region was conserved. SimPlot analysis showed that genetic recombination was found in the 3C and 3D region of CV-A2 strains. The full-genome sequence of CV-A5 showed 80.7% similarity with the Swartz (AY421763) and 97.43% similarity with the strain (MH111030) from Australian. Homology analysis showed that the non-structural protein region shared lower similarity than that of structural protein region, based on full-genome of CV-A5. Phylogenetic tree analysis showed that CV-A5 and MH111030 were in the same branch, indicating that CV-A5 strain not from local. The amino acid sequence of CV-A5 strain was conserved. Conclusions　The CV-A2 strain in Changsha City shared genome sequence information with CV-A4, and the CV-A5 strain was imported from abroad. Our findings are expected to understand the molecular and recombination characteristics of CV-A2 and CV-A5, provided the data of evolution and genetic features of the coxsackievirus, and interrupt disease transmission in a timely and effective manner.

Objective:To explore the relationships between sarcopenia and the clinical efficacy and prognosis of elderly patients with esophageal cancer who were treated by radical radiotherapy.Methods:The clinicopathological data of 134 elderly patients with esophageal cancer who received radical radiotherapy in Department of Radiotherapy, Affiliated Hospital of Yangzhou University from January 2013 to December 2018 were retrospectively analyzed. The muscle cross-sectional area at the level of the third lumbar vertebra was measured by using computed tomography (CT) images. These patients were divided into sarcopenia group ( n=56) and non-sarcopenia group ( n=78) according to the skeletal muscle index before radiotherapy. The efficacy and incidence of adverse reactions of the two groups were compared. Kaplan-Meier method was used to plot the survival curve, and Cox regression model was used to analyze prognostic factors. Results:There was a significant difference in the objective response rate between the sarcopenia and non-sarcopenia group at 1 month after radiotherapy [53.57% (30/56) vs. 71.79% (56/78) , χ2=4.71, P=0.030]. There was no significant difference in the disease control rate between the two groups [94.64% (53/56) vs. 91.03% (71/78) , χ2=0.21, P=0.651]. There was a significant difference in the total incidence of adverse reactions between the sarcopenia and non-sarcopenia group [67.86% (38/56) vs. 47.44% (37/78) , χ2=5.52, P=0.019]. By the end of the follow-up, the 1-, 3- and 5-year overall survival (OS) rates of 134 elderly patients with esophageal cancer who received radical radiotherapy were 91.0%, 73.1% and 55.2% respectively. The median OS of patients in the sarcopenia and non-sarcopenia group were 14 months and 26 months respectively, with a statistically significant difference ( χ2=9.84, P=0.002) . The median progression-free survival (PFS) of the two groups were 7 months and 18 months respectively, with a statistically significant difference ( χ2=9.91, P=0.002) . Univariate analysis showed that cT stage ( HR=2.45, 95% CI: 1.26-4.74, P=0.008) , cN stage ( HR=1.63, 95% CI: 1.06-2.50, P=0.027) , cTNM stage ( HR=2.04, 95% CI: 1.28-3.27, P=0.003) , body mass index (BMI) ( HR=2.23, 95% CI: 1.01-4.90, P=0.046) , pre-radiotherapy sarcopenia ( HR=2.45, 95% CI: 1.27-4.72, P=0.007) and chemotherapy ( HR=0.30, 95% CI: 0.11-0.83, P=0.020) were prognostic factors for OS; cT stage ( HR=2.27, 95% CI: 1.18-4.39, P=0.015) , cN stage ( HR=1.61, 95% CI: 1.04-2.47, P=0.030) , cTNM stage ( HR=1.90, 95% CI: 1.19-3.02, P=0.007) , BMI ( HR=1.98, 95% CI: 1.06-3.79, P=0.032) , pre-radiotherapy sarcopenia ( HR=1.79, 95% CI: 1.06-3.04, P=0.031) and adverse reactions ( HR=0.60, 95% CI: 0.38-0.97, P=0.037) were prognostic factors for PFS. Multivariate analysis showed that pre-radiotherapy sarcopenia ( HR=1.91, 95% CI: 1.22-3.00, P=0.005) was an independent prognostic factor for OS; BMI ( HR=1.80, 95% CI: 1.03-3.15, P=0.039) and pre-radiotherapy sarcopenia ( HR=2.00, 95% CI: 1.27-3.14, P=0.003) were independent prognostic factors for PFS. Conclusion:Sarcopenia before radiotherapy can be a useful predictor for prognosis in elderly patients with esophageal cancer who received radical radiotherapy, and patients with sarcopenia benefit less from treatment.

Objective To study the mechanism of marcosomia by investigating insulin-like growth factor 2(IGF_2)imprinting status,expression level and the promoter usage in the placenta of macrosomia. Methods We selected heterozygous cases for Apa Ⅰ polymorphism in exon 9 of IGF_2 gene and then analyzed its imprinting status in 168 placentas of macrosomia and normal pregnancies.IGF_2 transcription levels and promoter usages in macrosomic and normal placenta were evaluated by using semi-quantitative RT- PCR assay.Results Thirty specimens of macrosomic placenta and 30 of normal placenta were identified as heterozygous for IGF_2.All of the heterozygous specimens showed maintenance of imprinting.The expression of placental IGF_2 mRNA(2.2?1.2)was significantly higher in macrosomia than that of normal weight group (1.6?0.6,P 0.05).Conclusion It is possible that over expression of IGF_2 in placenta contributes to macrosomia while the promoter usage and imprinting status are not associated with macrosomia.

OBJECTIVETo determine whether auricularia auricular polysaccharide (AAP) protects heart against ischemia/reperfusion (1/ R) injury and its underlying mechanisms.

METHODSMale Sprague-Dawley rats, pretreated with AAP (50, 100, 200 mg/(kg x d), gastric perfusion) for 4 weeks, were used for Langendorff isolated heart perfusion. The hearts were subjected to global ischemia for 30 min followed by 120 min of reperfusion and the left ventricular hemodynamic parameters were measured. Formazan, a product of 2, 3, 5-triphenyl-tetrazolium chloride (TTC), which is proportional to myocardial viability, was measured at 490 nm, and the level of lactate dehydrogenase (LDH) in the coronary effluent was measured to evaluate the cardiac injury. The cardiac malondialdehyde (MDA), a product of lipid peroxidation, and superoxide dismutase (SOD) activity were determined after myocardial I/R.

RESULTSThe pretreatment with AAP at 50, 100, 200/(kg d) for 4 weeks before I/R increased myocardial formazan content, reduced LDH release, improved the recovery of the left ventficular developed pressure, maximal rise rate of left ventricular pressure, and rate pressure product (left ventricular developed pressure multiplied by heart rate) attenuated the decrease of coronary flow during reperfusion. The cardiac protective effect of high dose AAP was more potent than that of compound radix salviae miltiorrhizae (CRSM, 4 ml/(kg x d), gastric perfusion for 4 weeks). Pretreatment with AAP (100 mg/(kg x d)) markedly inhibited the increase of MDA level and the decrease of SOD activity induced by I/R in myocardium.

CONCLUSIONThe findings indicate that in the isolated rat heart, AAP protects myocardium against ischemia/reperfusion injury via enhancing the activity of SOD and reducing lipid peroxidation in heart.

Animals ; Basidiomycota ; chemistry ; Male ; Myocardial Ischemia ; pathology ; physiopathology ; Myocardial Reperfusion Injury ; physiopathology ; prevention & control ; Oxidative Stress ; drug effects ; Polysaccharides ; isolation & purification ; pharmacology ; Protective Agents ; pharmacology ; Rats ; Rats, Sprague-Dawley ; Superoxide Dismutase ; metabolism