Objective To explore the clinical and radiological findings of skeletal desmoplastic fibromas.Methods Radiographs of six patients with desmoplastic fibromas proved by pathology were retrospectively reviewed.Results Two tumors arose in femur,two in tibia,one in radius and one in humur.In plain radiography,these lesions were always metaphyseal and expansile lytic with a reactive bony rim(n=6).They often had a trabeculated or honeycomb appearance into lesion and four tumors invaded adjacent soft tissue.Conclusion Desmoplastic fibromas of long bones are nearly always metaphyseal.Radiographs disclose a expansile lytic lesion with a sclerotic rim and a trabeculated apperance into it.And the "root hair"sign is fairly characteristic for this tumor.No calcification and periosteal reaction can be seen.

Objective To investigate the stroke occurrence of chronic kidney disease (CKD) and its related factors, especially the carotid atherosclerosis. Methods The data of stroke occurrence in 700 CKD patients hospitalized in Renji Hospital during 2007 were analyzed retrospectively. The incidences of stroke were compared among CKD [Ⅰ-Ⅱ, CKD Ⅲ-Ⅴ non-dialysis patients and dialysis patients. Carotid atherosclerosis of 409 CKD patients was examined by color Doppler ultrasound. The related factors were selected by Spearmnan correlation analysis and Logistic regression analysis. Results Of 700 CKD patients, 67 cases (9.57%) experienced at least one episode of stroke, which was much higher than that of general population. The related factors of stroke in CKD included GFR, age, SBP, CRP, Lpa, serum glucose, pre-albumin, HDL and carotid atherosclerosis. Logistic regression revealed that SBP (β=1.021, P=0.042), CRP (β=1.008, P=0.024) and carotid atherosclerosis (β =3.456, P=0.025) were risk factors of stroke in CKD. Incidence of carotid atherosclerosis was high (50.37%) in CKD patients, besides it was significantly higher in CKD patients with stroke history as compared to those without stroke history (80.0% vs 47.4%, P<0.01). Conclusions The incidence of stroke is quite high in CKD patients, which is closely associated with hypertension, inflammation and glyeolipid metabolism disorder. Carotid atherosclerosis is common in CKD patients with stroke, which may be helpful in screening cerebrovascular diseases in CKD patients.

Objective To investigate the effect and the mechanism of epithelial-mesenchymal transition (EMT) in renal tubular cells induced by uric acid.Methods Normal rat kidney tubular cell line (NRK-52E) were exposed to different concentrations of uric acid (100,200,400,600,800 μmol/L UA) for 48 hours to induce EMT.Morphological changes of the NRK-52E cells were examined under an inverted phase contrast microscope.The protein expression of E-cadherin,α-SMA,p-Akt and Akt were detected by Western blotting.The distribution of E-cadherin and α-SMA were detected by immunofluorescence.NRK-52E cells were pretreated by different concentrations of LY294002(0,2.5,5,10,15 μmol/L),the inhibitor of PI3K/p-Akt signaling pathway,and then processed by uric acid (400 μmol/L) for 48 hours.Western blotting was used to detect the protein expression of p-Akt and Akt.NRK-52E cells were then divided into four groups:normal group (N),uric acid group (UA),LY294002 group (LY),uric acid with LY294002 group (UA + LY).The protein expression of E-cadherin and α-SMA were detected by Western blotting,the distribution of E-cadherin,α-SMA and p-Akt were detected by immunofluorescence.Results There was abundant cellular expression of E-cadherin in unstimulated renal tubular cells whereas its expression was significantly decreased in uric acidstimulated cells (P ＜ 0.05).In addition,uric acid induced de novo expression of α-SMA in contrast to almost negative staining in untreated cells (P ＜ 0.05).p-Akt were obviously increased in high uric acid group (P ＜ 0.05) and Akt changed not significantly (P ＞ 0.05).NRK-52E cells transformed into elongated fibroblast-like cells from cuboidal clustered epithelial cells.These indicated that uric acid has induced EMT and activated PI3K/p-Akt signaling pathway in NRK-52E cells.However,the above effects of uric acid were abolished when p-Akt was blocked by the PI3K inhibitor (10,15 μmol/L LY294002),indicated that LY294002 has reversed the trend of EMT.Conclusions High uric acid induces phenotypic transition of renal tubular cells probably via activating PI3K/Akt signaling pathway.

Objective To assess the impact of physical training on physiological function of adult renal transplant recipients by meta-analysis and to provide theoretical guidance for clinical practice.Methods Randomized controlled trials of physical training for the treatment of renal transplant recipients until October 2017 were searched in the database of Cochrane library,PubMed,Embase,Web of Science,Wanfang Data and CNKI.Data extracted from the literatures were analyzed with RevMan software (version 5.3).Results A total of 10 studies in 10 manuscripts met the inclusion criteria,and 557 cases were included.Meta-analysis results were as follows.Compared with the control group (routine drug therapy),the level of peak exercise oxygen uptake (peak VO2) was significantly increased in physical training group (routine drug therapy and physical training) (MD=2.40,95％ CI 0.15-4.64,P=0.04).However,there was no statistically significant difference in the change of blood lipid,blood pressure,hemoglobin and serum creatinine between the two groups (all P ＞0.05).Conclusions Physical training can improve cardio respiratory fitness of renal transplant recipients in the early stage,but it has no obvious effect on blood pressure,blood lipid,hemoglobin and blood creatinine.

OBJECTIVETo detect the expression of pan-neuronal marker protein gene product (PGP)9.5 and its clinicopathologic significance in breast cancer.

METHODSThe expression of PGP9.5 was examined by immunohistochemistry EnVision method in 196 cases during 2007 to 2011, including 20 normal tissues, 14 cases of fibroadenoma, 18 cases of ductal carcinoma in situ (DCIS) and 144 cases of invasive ductal carcinoma (IDC) of the breast. The relationship between PGP9.5 expression and clinicopathologic characteristics of IDC was assessed.

RESULTSPGP9.5 expression was localized in the stroma of all normal breast tissues, but there was no expression observed in all fibroadenomas and DCIS. Overall, the expression rate of PGP9.5 in IDC was 61.8% (89/144). PGP9.5 expression increased from grade 1 tumors (29.4%, 10/34) to grade 2-3 tumors (71.8%, 79/110; P = 0.000). In addition, patients with less than 3 years disease-free survival tended to show higher PGP9.5 expression (64.8%, 35/54), compared to patients with equal to and/or more than 3 years disease-free survival (46.7%, 42/90; P = 0.035). However, there was no correlation between PGP9.5 expression and tumor size, tumor stage, lymph metastasis, hormone receptor expression.

CONCLUSIONPGP9.5 expression is correlated with tumor grade and prognosis in IDC of the breast.

Adult ; Aged ; Biomarkers, Tumor ; metabolism ; Breast Neoplasms ; metabolism ; pathology ; Carcinoma, Ductal, Breast ; metabolism ; pathology ; Carcinoma, Intraductal, Noninfiltrating ; metabolism ; pathology ; Disease-Free Survival ; Female ; Fibroadenoma ; metabolism ; pathology ; Humans ; Middle Aged ; Neoplasm Grading ; Ubiquitin Thiolesterase ; metabolism

[This corrects the article DOI: 10.1016/j.apsb.2022.06.016.].

Near-infrared (NIR)-light-triggered nanomedicine, including photodynamic therapy (PDT) and photothermal therapy (PTT), is growing an attractive approach for cancer therapy due to its high spatiotemporal controllability and minimal invasion, but the tumor eradication is limited by the intrinsic anti-stress response of tumor cells. Herein, we fabricate a tumor-microenvironment responsive CRISPR nanoplatform based on oxygen-deficient titania (TiO_2-x ) for mild NIR-phototherapy. In tumor microenvironment, the overexpressed hyaluronidase (HAase) and glutathione (GSH) can readily destroy hyaluronic acid (HA) and disulfide bond and releases the Cas9/sgRNA from TiO_2-x to target the stress alleviating regulators, i.e., nuclear factor E2-related factor 2 (NRF2) and heat shock protein 90α (HSP90α), thereby reducing the stress tolerance of tumor cells. Under subsequent NIR light illumination, the TiO_2-x demonstrates a higher anticancer effect both in vitro and in vivo. This strategy not only provides a promising modality to kills cancer cells in a minimal side-effects manner by interrupting anti-stress pathways but also proposes a general approach to achieve controllable gene editing in tumor region without unwanted genetic mutation in normal environments.