Objective To investigate the early diagnosis and treatment of pneumocystosis after renal transplantation. Methods The clinical data of 6 cases of renal transplant recipients from 2000-2001 who developed pneumocystosis were discussed. Results Six patients were diagnosed as having pneumocystosis and subjected to the treatment of SMZ_ CO (SMZ 60-70 mg/kg daily, TMP 12-14 mg/kg daily) for 3 weeks. Immunosuppressive regimene was regulated. Except one case died due to abandonment of treatment, the remaining 5 cases were cured and had normal renal function. Conclusion The diagnosis of pneumocystosis was established by visualization of pathogen in bronchialveolar lavage (BAL) samples. SMZ_ CO is still the most commonly used drug for pneumocystosis at present and administration for individual is important because of its renal toxicity. The dosage of immunosuppressive agent for each patient with pneumocystosis must be adjusted.

Objective To study the influence of tumor necrosis factor-alpha (TNF-?) gene polymorphism on infections in old kidney allograft recipients. Methods The TNF-? genotype in -308 promoter position was determined in 87 old kidney transplant recipients from January 1998 to January 2001 by PCR using sequence -specific primer(PCR-SSP), and then the effects of genotypes on the frequency of rejection and infection, and the survival rate of the patient and graft were observed. Results 58 recipients were low TNF-? production genotype and 29 were high TNF-? production genotype. There were no significant differences in the frequency of rejection, median day of first infection and kinds of infections between the two genotypes. The frequency and times of infections were higher in low TNF-? genotype recipients than those in high TNF-? genotype recipients(67 2% vs 41 4%, P=0 021; 1 68 vs 0 86, P=0 017). The survival rates of the patients and grafts were equal in both the two groups. Conclusion The old recipients with low TNF-? production genotype may be susceptible to infections under routine immunosuppression. It is helpful for old recipients to perform more individual immunosuppression regimens according to TNF-? genotype.

Aim To investigate the effect of bufalin on proliferation and expression of WT1 in K562 cells. Methods The colony number of K562 cell was detec-ted with semi-solid culture assay. The cell cycle was measured by flowcytometry, and the expression of WT1 was observed with immunocytochemistry. Subcutaneous tumor models established by K562 cells in BALB/C nu/nu mice were divided into three groups, including model group, bufalin group and positive control group. After 21 days, the subcutaneous tumors were removed for calculating the inhibitory rate of tumor growth. HE staining and immunohistochemistry were used to ob-serve the morphological changes and the expression of WT1 . Results ① Bufalin could significantly decrease the colony number of K562 cell, arrest it at G0/G1 phase and down-regulate its expression of WT1 in a dose-dependent manner. ② Compared with the model group, the tumor inhibitory rate was much higher, while the volume and the weight were obviously lower in the other two groups. ③Bufalin could induce apop-tosis, necrosis, hemorrhage and fibrosis with HE stai-ning, and down-regulate the expression of WT1. Con-clusion Bufalin could inhibit the proliferation, arrest the cell cycle at G0/G1 phase and down-regulate the expression of WT1 in vitro. Bufalin could inhibit the tumor inhibitory rate, the volume and the weight of the subcutaneous tumors, induce apoptosis, necrosis, hemorrhage and fibrosis with HE staining and down-regulate the expression of WT1 .

Objective To investigate the interventional treatment timing of patients with non-ST segment elevation myocar-dial infarction with ST segment elevation in lead aVR.Methods Totally 57 cases with non-ST segment elevation myocardial infarc-tion with ST segment elevation in lead aVR in our hospital from July 2010 to July 2013 were selected.They were divided into two groups,30 cases in group A and they were given emergency PCI treatment with in 12 hours of onset,27 cases in group B and they were given emergency PCI treatment within 12-24 hours of onset.Compare the therapeutic efficacy and adverse cardiovascular e-vents after discharge.Results Therapeutic efficacy of group A was better than group B after 1,6,12 month follow up and rate of adverse cardiovascular events of group A was shorter than group B.Conclusion Emergency PCI treatment within 12 hours can im-prove the prognosis of patients with non-ST segment elevation myocardial infarction with ST segment elevation in lead aVR.

Aim To investigate the effect of resveratrol on proliferation and differentiation in K562 cells. Methods K562 cells were treated with different con-centrations of resveratrol for 6d. The colony number of K562 cells was detected with semi-solid culture assay. Expression of GATA-1 and PU. 1 in K562 cells was re-spectively measured with immunocytochemistry and Western blot. Expression of differentiation related anti-gen, CD11b, CD14 and CD42b, was measured with flowcytometry on K562 cells. Results Resveratrol
could significantly decrease the colony number of K562 cells in a dose-dependent manner, and enhance the ex-pression of GATA-1,PU. 1,CD11b, CD14 and CD42b in K562 cells. Conclusion Resveratrol could inhibit the proliferation and induce differentiation of K562 cells via up-regulating the expression of GATA-1 and PU. 1 protein.

Objective To investigate the effect and underlying mechanisms of ghrelin in a rat model of renal fibrosis. Methods Male Sprague-Dawley rats were divided into 4 groups , including sham operation +saline or brain gut peptide treatment group , model + saline or brain gut peptide treatment group. Unilateral ureteral obstruction (UUO) was established by left ureteral ligation. 7 days and 14 days after operation, the rats were sacrificed , while the kidney tissue of obstruction side was harvested for pathlogical changes through Masson coloration. Expression of α-smooth muscle actin (α-SMA), transforming growth factor beta1 (TGF-β1) and phosphorylated Smad3 (p-Smad3) in renal tissues were analyzed through immunohistochemistry. Expression of α-SMA and TGF-β1 mRNA was detected by real-time-PCR. Apoptosis kidneys cells were marked with TUNEL. Results Ghrelin inhibited renal fibrosis by reducing the production of collagen , restraining extracellular matrix (ECM) deposition and decreasing the expression of α-SMA. Meanwhile, ghrelin inhibited the accumulation of myofibroblasts by blocking the transforming growth factor-β1/Smad3 (TGF-β1/Smad3) signaling pathway. Moreover, ghrelin could attenuate renal tubular cell apoptosis induced by UUO injury. Conclusion Ghrelin can reduce renal fibrosis and renal cell apoptosis induced by UUO , demonstrating that ghrelin is a potent antifibrotic agent that may have therapeutic potential for patients with obstructive nephropathy.

The serum TSH levels of 107 infants with subclinical hypothyroidism (SH) were > 20 mIU/L after 1-8 check-up, along with FT4, TT4, within low normal range. After given small dosage L-T4, for 4 weeks, blood TSH level obviously descended while FT4, TT4, ascended (all P <0.01). Seven cases of thyroid hypogenesis and 7 strumas were found by ultrasonography. It seems appropriate to use dosage of 3-4 μg·kg·-1·d-1 L-T4 in treating SH.

Objective To evaluate the efficacy of percutaneous transluminal angioplasty (PTA) in the treatment of transplanted renal artery stenosis (TRAS)-induced renal dysfunction and hypertension. Methods Between July 1998 and January 2007, PTA was performed on 16 patients with RTAS. Color Doppler uhrasonography preceded the intra-arterial angiographic investigation,with false-negative results in 18. 75 % of patients. Sixteen cases of TRAS were examined at 1 st week,6th month and 13 years after PTA. Hypertension improvement was defined as mean arterial pressure decrease of at least 15 % from the pre-PTA value. Graft function was evaluated by SCr levels, and the improvement was defined as a 20% change. Results Angioplasty was technically feasible in 100 %.Sixteen patients with RTAS were cured clinically. During the follow-up period, graft function was improved in 81.25 %, 68. 75 %, 62. 5 %, 56. 25 %, 50 % of patients respectively at 1st week, 6th month and 1-3 years after PTA. The blood pressure was decreased in 62. 5%, 75 %, 75 %,56. 25 %, 50 % of patients respectively, but no patient remained hypotensor medication free.Conclusion PTA improved renal dysfunction and hypertension induced by TRAS, and it is a safe and effective treatment for TRAS.

Aim To explore the protective roles of lic-ochalcone A ( LA) on mice with cigarette smoke-medi-ated acute lung injury and the related mechanisms. Methods In vivo: Mice were exposed to cigarette smoke ( CS) to establish acute lung injury model. The bronchoalveolar lavage fluid ( BALF ) was conducted for cell counting. The mRNA and protein expression of keratinocyte-derived chemokine ( KC ) , tumor necrosis factor alpha ( TNF-α) , interleukin 1β ( IL-1β) and matrix metalloproteinases ( MMP)-9 in lungs were de-termined. The myeloperoxidase ( MPO ) , superoxide dismutase ( SOD ) activities and glutathione ( GSH ) levels in lungs were quantified. The paraffin sections of lungs were prepared and stained with HE. In vitro:Human lung epithelial cells (BEAS-2B) were exposed to cigarette smoke extract ( CSE ) , which induced cell injury. The releases of interleukin 8 (IL-8) and MMP-9 were assessed. The phosphorylation of mitogen-acti-vated protein kinases ( MAPKs, including ERK1/2, p38 and JNK ) and nuclear factor-κB ( NF-κB ) p65 protein were analyzed by Western blot. Results In vi-vo: The accumulation of inflammatory cells was lower in LA groups than that in model group. In comparison with normal control group, the mRNA and protein lev-els of KC, TNF-α, IL-1βand MMP-9 were significant-ly increased in model group. Following treatment with LA, the above indicators were significantly decreased as compared to model group. In the CS-exposed mice, the MPO activity in lungs was significantly increased, meanwhile the SOD activity and GSH level were signif-icantly decreased compared with the air-exposed ani-mals. CS-induced activity of MPO was significantly in-hibited, which were accompanied by increases in SOD and GSH levels by LA. In vitro: CSE-induced mRNA levels of IL-8 and MMP-9 were significantly inhibited by LA at 2 . 5 and 5 μmol · L-1 . The CSE-induced phosphorylation of ERK1/2 and nucleus NF-κB p65 protein expression were prevented by pretreatment with LA. Conclusions LA has protective effects on CS-ex-posed acute lung injury in mice by preventing CS-in-duced pulmonary inflammation, oxidative stress and protease rise. The exploration of the mechanisms sug-gests that LA exerts protective effects via suppressing ERK1/2/NF-κB pathways.

Objective To explore the clinical features and feasibility of renal transplantation for end-stage renal disease (ESRD) following hematopoietic stem cell transplantation (HSCT).Method A retrospective study was done in one case of renal transplantation for ERSD following HSCT.Clinical manifestations were summarized and prognosis was described.The 22-year-old male recipient had received HLA allele matched related bone marrow transplantation from his sister in 2001 and accepted renal transplantation 14 years after HSCT because of delayed renal dysfunction.Donor was a cardiac death patient,the preoperative Panel Reactive Antibody Testing was negative and there were 1.5 HLA antigen mismatches of 6 HLA-A,B,DR antigens of donor and recipient.The recipient received immunosuppressive therapy of tacrolimus + mycophenolate mofetil + steroid after renal transplantation.Result The patient's renal function remained stable and serum creatinine level was 65 μmol/L.The outcome of the patient was fairly good during the follow-up period of short-term.Conclusion Renal transplant is a feasible alternative for patients with ESRD following HSCT.If the transplanted kidney and abbr.hematopoietic stem cells are from different donors,irnmunosuppressive treatment is essential after renal transplantation.Long-term follow-up and adjustment of immunosuppression treatment are needed to prevent and treat postoperative complications.