[Early onset Epstein-Barr virus-negative diffuse large B cell lymphoma after bilateral lung transplantation: a case report].

Lymphoma after solid organ transplantation is one of the manifestations of post-transplant lymphoproliferative disorders(PTLD). Here we reported a 39-year-old male patient presented with intermittent fever, markedly elevated level of peripheral blood lymphocytes and lactate dehydrogenase(LDH), rapid decrease in hemoglobin and platelet count ten months after bilateral lung transplantation. After systematic evaluation, the patient excluded infectious diseases. Positron emission tomography-computed tomography (PET/CT) revealed diffuse increasing of standard uptake value in bones throughout the body. The bone marrow aspiration, flow cytometric analysis and histopathology confirmed the diagnosis of diffuse large B-cell lymphoma (DLBCL) with negative Epstein-Barr virus-encoded small RNA (EBER) hybridization in situ. Meanwhile, complicated hemophagocytic lymphohistiocytosis was also diagnosed in the patient based on hypertriglyceridemia, abnormally elevated level of serum ferritin and solvable CD25 (sCD25). Treatment regimen included reduction of immunosuppression, anti-CD20 antibody (CD20+ B cell inhibitor, rituximab) and etoposide. Repeated PET/CT and bone marrow biopsy showed complete remission of lymphoma after 4 months of therapy.

ISOC1 promotes the proliferation of gastric cancer cells by positively regulating CDK19.

OBJECTIVE: To explore the role and potential mechanism of isochorismatase domain-containing 1 (ISOC1) in gastric cancer. PATIENTS AND METHODS: The expression levels of ISOC1 in gastric cancer (GC) tissues, as well as corresponding cell lines, was evaluated by quantitative Real Time-Polymerase Chain Reaction (qRT-PCR). A cell line stably expressing ISOC1 was constructed by vector construction and cell transfection, and the proliferation ability of the stably transfected cells was examined. Subsequently, the ISOC1 target database was screened, which suggested that CDK19 may be the potential target. The correlation between ISOC1 and CDK19 mRNA and protein expressions in clinical tissue specimens and cell lines was evaluated by qRT-PCR and Western blot, and the Luciferase reporter gene experiment was applied to verify the regulatory effect of ISOC1 on CDK19. RESULTS: ISOC1 was shown to be markedly increased in GC tissues compared to adjacent cancer tissues by qRT-PCR. In addition, compared with patients with low ISOC1 expression, the pathological stage and tumor size of gastric cancer patients with high ISOC1 expression were remarkably larger. Then, the ISOC1 knockdown cell line was established, and it was found through cell proliferation function experiments that the proliferation rate of gastric cancer cells was remarkably slower than the control group after knocking down ISOC1. Subsequently, bioinformatics and Luciferase reporter gene experiments suggested that ISOC1 had a direct regulatory effect on CDK19. In addition, recovery experiments also demonstrated that CDK19 overexpression could reverse the effect of ISOC1 silencing on cell proliferation. CONCLUSIONS: ISOC1 was markedly upregulated in GC tissues. It could positively regulate its downstream target CDK19, which in turn promoted the proliferation of GC cells. Therefore, our study may provide new ideas for understanding the progression of GC.

Effect of recombinant human endostatin on the expression of c-Myc and bFGF in mouse gastric cancer cells.

The aim of this study was to observe the effects of re-combinant human endostatin on the proliferation and apoptosis of mouse gastric cancer cells, and explore some possible mechanisms of recom-binant human endostatin inhibition of cancer. A murine gastric cancer xenograft model was established. A total of 20 mice were divided into two groups (control and experimental groups). The expression of c-Myc and basic fibroblast growth factor (bFGF) was determined by reverse transcription-polymerase chain reaction, Western blotting, and immu-nohistochemical staining methods. Tumor volume was measured and a growth curve was calculated. The tumor diameter in the experimental group was significantly smaller than that in the control group after treat-ment with endostatin for 21 days. The expression levels of c-Myc and bFGF in the experimental group were significantly lower than those of the control group (P < 0.05). There was a positive correlation between the expression of c-Myc and bFGF in the experimental group. Microvessel density was significantly inhibited in the experimental group (P < 0.05). These results demonstrated that recombinant human endostatin could in-hibit tumor metastasis by inhibition of the expression of c-Myc and bFGF in gastric cancer tissue as well as by inhibition of angiogenesis.

Observation of the decay psi(2S)-->K0SK0L.

The decay psi(2S)-->K(0)(S)K(0)(L) is observed using psi(2S) data collected with the Beijing Spectrometer at the Beijing Electron-Positron Collider; the branching fraction is determined to be B(psi(2S)-->K(0)(S)K(0)(L))=(5.24+/-0.47+/-0.48)x10(-5). Compared with J/psi-->K(0)(S)K(0)(L), the psi(2S) branching fraction is enhanced relative to the prediction of the perturbative QCD "12%" rule. The result, together with the branching fractions of psi(2S) decays to other pseudoscalar meson pairs (pi(+)pi(-) and K+K-), is used to investigate the relative phase between the three-gluon and the one-photon annihilation amplitudes of psi(2S) decays.

Observation of a near-threshold enhancement in the pp mass spectrum from radiative J/psi-->gammapp decays.

We observe a narrow enhancement near 2m(p) in the invariant mass spectrum of pp pairs from radiative J/psi-->gammapp decays. No similar structure is seen in J/psi-->pi(0)pp decays. The results are based on an analysis of a 58 x 10(6) event sample of J/psi decays accumulated with the BESII detector at the Beijing electron-positron collider. The enhancement can be fit with either an S- or P-wave Breit-Wigner resonance function. In the case of the S-wave fit, the peak mass is below 2m(p) at M=1859(+3)(-10) (stat)+5-25(syst) MeV/c(2) and the total width is Gamma<30 MeV/c(2) at the 90% confidence level. These mass and width values are not consistent with the properties of any known particle.

Measurements of the cross section for e(+)e(-) --> hadrons at center-of-mass energies from 2 to 5 GeV.

We report values of R = sigma(e(+)e(-)-->hadrons)/sigma(e(+)e(-)-->mu(+)mu(-)) for 85 center-of-mass energies between 2 and 5 GeV measured with the upgraded Beijing Spectrometer at the Beijing Electron-Positron Collider.

Antihypertensive and renal-protective effects of losartan in streptozotocin diabetic rats.

OBJECTIVE: To assess the renal benefits of a specific angiotensin II receptor antagonist, losartan, in diabetic rats with renal impairment. DESIGN AND METHODS: Uninephrectomized streptozotocin diabetic spontaneously hypertensive rats (SHR) were randomly assigned to receive vehicle, or to receive losartan or captopril, or both, intraperitoneally via osmotic minipumps for 8 weeks. RESULTS: Blood pressure and urinary protein excretion in the diabetic SHR increased progressively during the experimental period. Both captopril treatment and losartan treatment completely blocked the development of hypertension in diabetic SHR. Simultaneous administration of captopril and losartan did not enhance the antihypertensive effects of losartan treatment or captopril treatment. Furthermore, losartan treatment, captopril treatment and losartan + captopril treatment all significantly decreased urinary protein excretion, urinary albumin excretion and serum creatinine to the same extent. These effects were sustained for the entire experimental period and were not associated with any significant changes in body weight, urine volume, urine sugar and urinary electrolytes excretion. These results were confirmed by morphological analysis of kidneys in each group of rats. Losartan treatment, captopril treatment and losartan+captopril treatment all significantly and effectively protected against an increase in the percentage of focal glomerular sclerosis. Losartan treatment and captopril treatment both significantly attenuated the increase in heart weight: body weight ratio. The heart weight: body weight ratio in the losartan-treated group was significantly lower than in the captopril-treated group. CONCLUSIONS: These results indicate that hypertension could accelerate diabetic renal impairment and that losartan has antihypertensive and renoprotective effects in this rat model. They also suggest that the antihypertensive and renoprotective effects of captopril treatment in this rat model are caused mainly by inhibition of angiotensin II production rather than stimulation of the kallikrein-kinin system or of vasodilator prostaglandins. The difference in potency between losartan treatment and captopril treatment to attenuate the increase in heart weight: body weight ratio might partly explain the existence in the heart of angiotensin-forming pathways, which are not dependent on angiotensin converting enzyme.