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Abstract@#With the successive liberalization of the two child and three child policies in China, the issue of sibling relationships has been paid more and more attention by society. Severe sibling jealousy has a negative impact on the physical and mental health development of both young children and their siblings. The study reviewed the influencing factors of sibling jealousy, and analyzed the effect of applying six related intervention methods to the sibling jealousy intervention.The review aims to provide theoretical and empirical basis for children s sibling jealousy intervention, to reduce the level of sibling jealousy through the intervention, and to promote the physical and mental health of young children and their brothers and sisters.
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<p><b>OBJECTIVE</b>To investigate the expression of N-cadherin in bone marrow leukemic cells derived from acute leukemia patients and its clinical significances.</p><p><b>METHODS</b>A total of 113 patients with acute leukemia were enrolled in this study. Flow cytometry was employed to detect the expression of N-Cadherin in bone marrow leukemic cells from acute leukemia patients and the relationships between the N-cadherin expression and the clinical characteristics of patients with acute leukemia were analyzed.</p><p><b>RESULTS</b>The expression of N-Cadherin in bone marrow leukemic cells deriveted from patients with acute leukemia was variable with 0%-99.7%. For adult AML patients, the positive rate of CD34 in N-cadheringroup was significantly higher than that in N-cadheringroup(67.39% vs 33.33%)(P=0.013), while the differences of total CR rate and rate of CR after 1 cycle of induction treatment were not significant between these 2 groups(P>0.05). As to ALL patients, N-cadheringroup had significant lower WBC count (21.31±7.07 vs 51.10±23.69)(P=0.008) and lower percentage of peripheral blood blast (43.22±5.75% vs 66.45±5.65%)(P=0.015). The CR rate after 1 cycle of induction treatment and rate of overall CR were lower and the relapse rate was higher in N-cadherinALL group than those in N-cadherinALL group, but the differences were not significant (P>0.05). For childhood ALL, the positive rate of CD33 in N-cadheringroup was significantly higher than that in N-cadheringroup(47.62% vs 0%)(P=0.012). The relapse rate was higher in N-cadheringroup than that in N-cadheringroup (30.00% vs 0%)(P=0.115). The median survival time, 3-year overall OS rate and 3-year relapse-free survival rate in N-cadheringroups of adult AML, non-M3 AML, ALL and chidhood ALL paients were superior to N-cadheringroups, but the differences were not significant.</p><p><b>CONCLUSION</b>The expression of N-cadherin in bone marrow leukemic cells relates to some clinical features of patients with acute leukemia and to some extent has inferior effect on survival of patients with acute leukemia.</p>
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<p><b>OBJECTIVE</b>To explore the expression of PD-L1 in acute leukemia patients, and to analyze the relationship of PD-L1 expression with the patients' clinical characteristics and prognosis.</p><p><b>METHODS</b>The expression of PD-L1 in leukemia cells of 75 patients including 59 de novo patients and 16 relapse/refractory patients with acute leukemia was detected by the flow cytometry, the clinical information was collected, and the therapeutic efficacy of de novo patients was analyzed.</p><p><b>RESULTS</b>The PD-L1 was expressed in human acute leukemia cells with total expression rate 32% (24/75), and its expression level in AML-M5 was higher than that in other leukemias [56.3% (9/16) vs 25.4% (15/59)], there was statistical significance (P = 0.019). The PD-L1 possitive rate in relapse/refractory group was higher than that in de novo patient group [(56.3% (9/16) vs 25.4% (15/59)], and there was statistical significance (P = 0.019). In 59 de novo patients, the CR rate of PD-L1 positive group after 1 course of chemotherapy was lower than that in PD-L1 negative group (66.7% vs 71.4%), the CR rate of PD-L1 positive group after 2 courses of chemotherapy was also lower than that in PD-L1 negative group (70% vs 88.6%). The relapse rate and the proportion of refractory patients in PD-L1 possitive group were higher than those in PD-L1 negative group. The expression of PD-L1 did not correlated with the clinical parameters, such as sex, age, extramedullary infiltration, percentage of blast cells in bone marrow, counts of WBC, RBC and platelet, as well as molecular biological features and cytogenetical characteristics.</p><p><b>CONCLUSION</b>PD-L1 is expressed in human acute leukemia cells, and may be involved in the immune escape and primary resistant mechanisms, PD-L1 may be used as an indicator for evaluation of the the patients' prognosis and reocurrence.</p>
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Humans , Acute Disease , B7-H1 Antigen , Flow Cytometry , Leukemia , Prognosis , RecurrenceABSTRACT
To investigate the protective effects of eplerenone on adriamycin-induced renal injury and the possible mechanisms involved, 36 male Sprague-Dawley rats were randomly divided into control group, adriamycin nephropathy (AN) group and eplerenone-treated group (100 mg·kg(-1)·d(-1) eplerenone). Blood pressure, 24-h urinary protein, serum potassium, sodium and creatinine were measured 28 days after adriamycin injection (a single tail intravenous injection of 6.5 mg/kg adriamycin). The morphological changes of renal tissues were observed by light and electron microscopy. Immunohistochemistry and Western blotting were performed to examine the expression of TGF-β(1) and desmin in renal cortex. The results showed that 28 days after adriamycin injection, there were no significant changes in the level of serum potassium, sodium, creatinine concentrations and blood pressure values in the rats of the three groups. Meanwhile, the 24-h proteinuria excretion in the AN group was significantly higher than that in the control group (P<0.01), but that in the eplerenone-treated group was substantially reduced when compared with that in the AN group (P<0.05). Mild mesangial cell proliferation and matrix expansion, diffuse deformation and confluence of foot processes in podocytes were found in the AN group. By contrast, rats in the eplerenone-treated group exhibited obvious attenuation of these morphological lesions. The protein expression of TGF-β(1) and desmin in the AN group was markedly up-regulated in contrast to that in the control group (P<0.01), whereas that in the eplerenone-treated group was much lower than in the AN group (P<0.05). It was concluded that eplerenone may ameliorate the proteinuria and the development of pathological alteration in adriamycin-induced nephropathy presumably via the inhibition of cytokine release, and restore the morphology of podocytes independent of its blood pressure-lowing effects.
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Objective To access the effects of aldosterone (ALD) and its receptor antagonist- spironolactone (SPI) on the production of reactive oxygen species (ROS) and apoptosis in podocytes and to explore the possible mechanism involved. Methods Conditionally immortalized mouse podocytes were divided into control group, ALD group, SPI group and SPI +ALD group. The level of ROS production and the expression of nephrin protein were assayed by fluorescent spectrophotometry and indirect immunofluorescence technology. The apoptosis rate of podocytes was monitored by flow cytometry. The expression of bax and bcl-2 mRNA and protein was detected by RT-PCR and Western blotting methods. The anti-oxidant N-acetylcysteine (NAC)was applied to determine whether the effects of ALD on podocytes were mediated by ROS pathway.Results Compared with the control group, ALD significantly increased ROS production in podocytes (P＜0.05). SPI completely abolished the above-mentioned effect of ALD (P＜0.05). ALD induced the down-regulation of the expression of nephrin and the up-regulation of podocytes apoptosis (P＜0.05), which was accompanied with the elevated expression of bax mRNA and protein and the reduced expression of bcl-2 mRNA and protein (P＜0.05). SPI or NAC prevented the above-mentioned changes induced by ALD (P＜0.05). Conclusion ALD increases theexpression of pro-apoptotic factor (bax) but decreases the expression of anti-apoptotic factor (bcl-2)to induce podocytes apoptosis through the mineralocorticoid receptor (MR) possibly via the mechanisms involving ROS pathway.
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Eukaryotic expression vectors carrying the small hairpin RNA (shRNA) for TRPC6 mRNA were constructed, and the effects of knocking-down TRPC6 on puromycin aminonucleoside (PAN)-induced apoptosis of mouse podocytes were observed. Two eukaryotic expression vectors containing small hairpin structure targeting TRPC6 named pGCsi-TRPC6A and pGCsi-TRPC6B were designed and synthesized. The plasmids were transfected into conditionally immortalized murine podocyte cell line by liposome. The changes in the TRPC6 mRNA and protein expression were observed by RT-PCR and Western blot after 48 h. Cultured podocytes were divided into four groups: control group, PAN treatment group, PAN treatment+shRNA transfection group, and PAN treatment+ negative control group. The expression of Bax and Bcl-2 mRNA and proteins was detected by RT-PCR and Western-blot respectively. The apoptotic rate of podocytes was measured by flow cytometry. The results showed that the expression of TRPC6 mRNA and protein was decreased in the podocytes when transfected with pGCsi-TRPC6A, and pGCsi-TRPC6B. The expression of Bax was increased, and that of Bcl-2 was decreased at protein and mRNA levels in the podocytes after treated with PAN for 48 h. These changes was attenuated by knocking-down TRPC6. Knocking-down TRPC6 could effectively decrease the PAN-induced apoptosis of podocytes. It was concluded that TRPC6 may play an important role in the PAN-induced apoptosis of podocytes. Knocking-down TRPC6 gene could effectively prevent the podocytes from apoptosis induced by PAN.
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This study examined the effect of sulodexide on podocyte injury in rats with adriamycin nephropathy (AN). A total of 36 healthy male SD rats were randomly assigned to three groups: control group, AN group and sulodexide treatment group. Rat models of AN were established by a single tail intravenous injection of adriamycin (6.5 mg/kg) in both AN group and sulodexide treatment group. Sulodexide (10 mg/kg) was administered the rats in the treatment group once daily by garage from the first day of model establishment until the 14th day or the 28th day. Samples of 24-h urine and renal cortex tissues were harvested at day 14, 28 after the model establishment. Excretion of 24-h urinary protein was measured by Coomassie brilliant blue method. The pathological changes in renal tissues were observed by light microscopy and electron microscopy respectively. Heparanase mRNA was detected by RT-PCR. Expressions of desmin, CD2AP and heparanase were determined by immunohistological staining. The results showed that the expressions of heparanase mRNA and protein were increased in the glomeruli of AN rats at day 14 and 28 after the model establishment, which was accompanied by the increased expression of desmin and CD2AP. The mRNA and protein expression of heparanase was decreased in the sulodexide-treated rats as compared with AN rats at day 14 and 28. And, the protein expression of desmin and CD2AP was reduced as with heparanase in the sulodexide- treated rats. Proteinuria and podocyte foot process effacement were alleviated in the AN rats after sulodexide treatment. There was a positive correlation between the expression of heparanase and the expression of desmin and CD2AP (as well as 24-h urinary protein excretion). It was concluded that increased heparanase is involved in podocyte injury. Sulodexide can maintain and restore podocyte morphology by inhibiting the expression of heparanase in AN.
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To investigate the effects of albumin on the production of matrix metalloproteinases-2 (MMP-2) and matrix metalloproteinases-9 (MMP-9) in podocytes. Podocytes were treated with bovine serum albumin (BSA) at the concentration of 0.1, 0.5, 1, 2 g/L, respectively. Conditioned media were harvested 12, 24, 48 and 72 h after the treatment. The expression of MMP-2 and MMP-9 was assayed by gelatin zymography, RT-PCR and Western blotting analysis. Our results showed that in comparison with the control group, BSA increased the expression of MMP-2 and MMP-9 mRNA and protein in a dose- and time-dependent manner (P<0.05). Meanwhile, the enzymatic activities of MMP-2 and MMP-9 in the culture supernatants of podocytes were also increased (P<0.05). It is concluded that albumin up-regulated the expression of MMP-2 and MMP-9 at gene and protein levels in a time- and dose-dependent manner.
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objective To assess the effect of aldosterone on the production of matrix metalloproteinase-2 (MMP-2), matrix metalloproteinase-9 (MMP-9)and collagen Ⅳ in culture supematants of podocytes and the possible molecular mechanisms involved in the influence of aldosterone on the synthesis and degradation of extracellular matrix produced by podocytes. Methods Podecytes were treated with aldosterone at the concentration of 10-11, 10-9, 10-7 mol/L respectively. Cultured podocytes were examined at 24, 48 and 72 hours respectively. Spironolactone, a receptor antagonist of aldosterone, was added to observe the blocking effect on aldosterone. An inhibitor of TGF-β1 receptor was used to determine whether the effect of aldosterone on podocytes were mediated through TGF-β1 system. The enzymatic activities of MMP-2 and MMP-9 were assayed by gehtin zymography. Collagen Ⅳ 0.5 chain and TGF-β1 proteins released into culture supematants were assessed by Western blot and ELISA analysis. The adhesion rate of podocytes was monitored by flow cytometry. Results Aldosterone increased the activities of MMP-2 and MMP-9 in a dose- and time-dependent manner (P<0.05). Aldosterone decreased the level of collagen Ⅳ or5 chain protein in culture supernatants (P<0.05). Meanwhile, the expression of TGF-β1 was also increased (P<0.05). Spironolactone completely abolished the above-mentioned changes(P< 0.05). Blockage of TGF-β1 signaling with SB431542 prevented the aldosterone-induced upregulation of MMP-2 and MMP-9 as well as the downregulation of the collagen Ⅳ α5 chain protein and the adhesion rate of podocytes (P<0.05). Conclusions Aldosterone increases the activities of MMP-2 and MMP-9 but decreases the expression of collagen Ⅳ α5 chain and the adhension rate of podocytes possibly via TGF-β1 signaling pathway. Such alterations may contribute to glomerular podocyte injury associated with the GBM abnormality caused by the imbalance between matrix synthesis and degradation.
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Objective To study the effect of overexpression of TRPC6 on Ang Ⅱ-induced apoptosis of mouse podocytes in vitro and to explore the possible mechanisms. Methods Mouse TRPC6 cDNA eukaryotie expression vector pEGFP-NI-mTRPC6 was transfected to conditionally immortalized routine podocyte cell line by liposome. The fluorescent microscopy was used to examine the expression of EGFP after 24 hours. The change of TRPC6 protein expression was observed by Western-blot. Podocytes were treated by different concentrations of Ang Ⅱ. The podocyte intracellular calcium concentration was measured with laser-scanning con_focal microscope. The expression of Bax and Bcl-2 mRNA was assessed by RT-PCR and the expression of Bax and Bcl-2 protein was measured by Western-blot. The apoptotic ratio of podocytes was monitored by flow cytometry and Hoechst staining. Results About 35% of the cells expressed EGFP. An up-regulation of protein expression of TRPC6 was detected in podocytes when transfected with pEGFP-N1-mTRPC6 (P<0.01). The overexpression of TRPC6 promoted the Ang Ⅱ-induced influx of extracellular calcium and elevated the expression of Bax but decreased the expression of Bcl-2 (P<0.01, P<0.05). The apoptotic ratio of podocyte was (2.50±0.72)% when treated by low-dose Ang Ⅱ (10-10 mol/L), and it was increased to (4.33±0.45)% when transfected with pEGFP-N1-mTRPC6 (P <0.05 ). Transfection with pEGFP-NI-mTRPC6 increased apoptosis rate from (15.46± 1.40)% to (18.33±0.87)%(P<0.01) by high-dose Ang Ⅱ (10-6 mol/L). Conclusion TRPC6 plays an important role in the Ang Ⅱ-induced apoptosis of podocytes by promoting the influx of extraeellular calcium, which leads to the apoptosis cascade initiation.
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<p><b>OBJECTIVE</b>To evaluate the effect of mixed composite skin graft on the deep partial thickness burn wounds after tangential excision in burn patients.</p><p><b>METHODS</b>Tangential excision was performed in 30 extremities of 23 burn patients within 3 postburn days (PBDs). Then large pieces of homologous acellular dermal matrix were grafted onto the superficial fascia with razor thin autoskin on top of them. The survival rate of skin grafts, the appearance and the functional recovery of the extremities were observed on 10 to 12 post operative day (POD). Skin samples from a healed wound of a patient were harvested three months after the injury for pathologic examination.</p><p><b>RESULTS</b>The survival rate of the composite skin grafts was 93%. Necrosis was encountered in 7% of the grafts in the lower extremities due to the poor fixation of the grafts leading to separation of autologous skin and the dermal template, and also due to infection resulting in lysis of the grafts. The grafted skin was excellent in the appearance and elasticity, and function of the injured extremities recovered well after grafting after 3 - 6 months of follow-up. Epidermal and dermal texture was also good as shown by pathologic examination.</p><p><b>CONCLUSION</b>Mixed composite skin grafting after early tangential excision might be an ideal and effective method in the management of deep partial thickness burn wounds.</p>