Objective The objective of this study is to investigate the psychological stress status of Chinese college students ,and to provide evidence for mental health education in colleges and universities .Methods A random sampling method was conducted to perform the questionnaire (psychological stress scale for college students by Zhang Lin ,Che Wenbo ,etc .) on psychological stress a‐mong 205 college students .Results The main sources of psychological stress on college students were job‐seeking pressure ,school pressure ,academic pressure ,emotion pressure and interpersonal pressure .The scores on college environment and learning task stress of engineering and technology students were significantly higher than other divisions (P< 0 .05) .Male students showed markedly higher stress level than female students in love pressure ,inferiority pressure and academic pressure (P< 0 .05) .The scores on frustration pressure and family pressure of students with siblings were significantly higher than students from one‐child family (P<0 .05) .The scores on family pressure of rural students were significantly higher than those from towns and cities (P<0 .01) .Conclusion The psychological stress of college students in Hainan province are overall in good condition .There are some differences among different groups .We should pay more attention to college students′mental health problems ,and make separate counseling according to the profession and family background difference .

Purpose To observe the pathologic types of glomerular diseases which have high renal interstitial foam cells infiltration and to evaluate the relationship between infiltration of foam cells (FC) in renal interstitial tissue and pathologic parameters.Methods A total of 2 862 patients who had received renal biopsy were enrolled in this study. Patients with Alport syndrome (AS,n=5), membranous proliferative glomerular nephritis (MPGN,n=28), focal segmental glomerulosclerosis (FSGS,n=144), idiopathic membranous nephropathy (IMN,n=132), IgA nephropathy (IgAN,n=893) were divided into two groups:FC+ group with foam cells and FC- group without foam cells.Results Infiltration of foam cells in renal interstitial tissue was commonly seen in AS.The frequency of interstitial foam cells was 46.43% in MPGN, 20.14% in FSGS, 13.64% in IMN, and 6.27% in IgAN. It was found that the segmental glomerular sclerosis and interstitial fibrosis were more severe in FC+ group than that in FC- group.Conclusions The renal interstitial foam cells are most common in patients with AS, but also seen in patients with MPGN, FSGS, IMN and IgAN. There might be a relationship between glomerular sclerosis, interstitial fibrosis and infiltration of foam cells. The present of foam cells in the renal interstitial tissue may contribute to the progression of renal diseases.

In order to investigate the effects of connective tissue growth factor (CTGF) antisense oligodeoxynucleotide (ODN) on plasminogen activator inhibitor-1 (PAI-1) expression in renal tubular cells induced by transforming growth factor beta1 (TGF-beta1) and to explore the role of CTGF in the degradation of renal extracellular matrix (ECM), a human proximal tubular epithelial cell line (HKC) was cultured in vitro. Cationic lipid-mediated CTGF antisense ODN was transfected into HKC. After HKC were stimulated with TGF-beta1 (5 microg/L), the mRNA level of PAI-1 was detected by RT-PCR. Intracellular PAI-1 protein synthesis was assessed by flow cytometry. The secreted PAI-1 in the media was determined by Western blot. The results showed that TGF-beta1 could induce tubular CTGF and PAI-1 mRNA expression. The PAI-1 mRNA expression induced by TGF-beta1 was significantly inhibited by CTGF antisense ODN. CTGF antisense ODN also inhibited intracellular PAI-1 protein synthesis and lowered the levels of PAI-1 protein secreted into the media. It was concluded that CTGF might play a crucial role in the degradation of excessive ECM during tubulointerstitial fibrosis, and blocking the biological effect of CTGF may be a novel way in preventing renal fibrosis.

In order to explore the role of connective tissue growth factor (CTGF) in the pathogenesis of renal tubulointerstitial fibrosis, 48 Wistar rats were randomly divided into sham-operated and unilateral ureteral obstruction (UUO) group. On the postoperative day 1, 3, 7 and 14, the rats were killed and the kidneys were removed. The renal tubulointerstitial injury index was evaluated according to the MASSON staining. The mRNA levels of CTGF, transforming growth factor-β1(TGF-β1), collagen Ⅰ (col Ⅰ ), and plasminogen activator inhibitor-1 (PAI-1) were detected using reverse transcriptional-polymerase chain reaction (RT-PCR). Immunohistochemistry was performed to evaluate the protein expression of the above factors, and the relations among them were analyzed. Quantitative expression of CTGF protein in the kidneys was also assessed using Western blot. The results showed that TGF-β1 mRNA level was increased at first day after UUO, followed by a marked elevation of CTGF mRNA level, which began to increase 3 days after UUO (P＜0.01). With the progression of the disease, the mRNA expression of CTGF, col Ⅰ and PAI-1 was increased progressively. Immunohistochemistry revealed that the CTGF protein expression was significantly increased in fibrotic areas and tubular epithelial cells 3 days after UUO. On the post-UUO day 7, the protein level of CTGF was positively related to the renal tubulointerstitial injury index (r =0.62, P＜0.01), the expression of TGF-β1 (r=0.85, P＜0.01), col Ⅰ (r=0.78, P＜0.01),and PAI-1(r=0.76, P＜0.01). Upon Western blot analysis, CTGF protein expression began to increase 3 days after UUO, and appeared progressively throughout the time course (P＜0. 01, as compared with sham-operated group). It is concluded that CTGF can be induced by TGF-β and mediate various profibrotic actions of this cytokine, such as increasing extracellular matrix (ECM)synthesis and decreasing ECM degradation. The increased expression of CTGF may play a crucial role in the development and progression of tubulointerstitial fibrosis.

In order to investigate the effects of connective tissue growth factor (CTGF) antisense oligodeoxynucleotide (ODN) on plasminogen activator inhibitor-1 (PAI-1) expression in renal tubular cells induced by transforming growth factor β1 (TGF-β1) and to explore the role of CTGF in the degradation of renal extracellular matrix (ECM), a human proximal tubular epithelial cell line (HKC) was cultured in vitro. Cationic lipid-mediated CTGF antisense ODN was transfected into HKC. After HKC were stimulated with TGF-β1 (5 μg/L), the mRNA level of PAI-1 was detected by RT-PCR. Intracellular PAI-1 protein synthesis was assessed by flow cytometry. The secreted PAI-1 in the media was determined by Western blot. The results showed that TGF-β1 could induce tubular CTGF and PAI-1 mRNA expression. The PAI-1 mRNA expression induced by TGF-β1 was significantly inhibited by CTGF antisense ODN. CTGF antisense ODN also inhibited intracellular PAI-1 protein synthesis and lowered the levels of PAI-1 protein secreted into the media. It was concluded that CTGF might play a crucial role in the degradation of excessive ECM during tubulointerstitial fibrosis, and blocking the biological effect of CTGF may be a novel way in preventing renal fibrosis.