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Kaposi sarcoma is an acquired immunodeficiency syndrome-related disease that mainly involves the skin, gastrointestinal gut, and lungs. Whole-body 18F-fluorodeoxyglucose-positron emission tomography and computed tomography (FDG-PET/CT) scanning is useful for simultaneous detection of multiple lesions of Kaposi sarcoma. We present a 67-year-old man with a history of infection with human immunodeficiency virus who presented with numerous cutaneous lesions. FDG-PET/CT images showed lesions in the skin, lung, and lymph nodes. The gastrointestinal lesions were detected using gastric fiberscopy (GF) and colon fiberscopy (CF). After Kaposi sarcoma therapy, the uptake in the lesions of the skin, lung, and lymph nodes decreased, but new lesions were detected in the pancreas and lumbar spine. He had pancreatitis and Candida spondilitis. Whole-body FDG-PET/CT is useful for detecting lesions and determining the extension to which the disease has spread, adding the gastrointestinal lesions by GF and CF. After therapy, FDG-PET/CT can be used to demonstrate which lesions remain active and to determine the overall response to treatment. In this case, we show how useful FDG-PET/CT is and how difficult it is to treat Kaposi sarcoma. [ABSTRACT FROM AUTHOR]

Objective: The purpose of this study was to evaluate the usefulness of 18F-fluorodeoxyglucose (FDG) positron emission tomography (PET) in differentiating pulmonary artery sarcoma from pulmonary embolism. Materials and Methods: We evaluated three patients with pulmonary artery sarcoma and 10 patients with proximal pulmonary embolism (6 men and 7 women, ranging in age from 35 to 94 years). All the patients had evidence of perfusion defects in their proximal pulmonary arteries on contrast-enhanced computed tomography (CT) scans performed prior to PET/CT. The maximum standardized uptake value (SUV(max)) of FDG uptake in all the lesions was measured using PET/CT. The location of lesions, background uptake or thrombi in the legs were evaluated in both groups as basic characteristics. Results: The mean SUV(max) of the pulmonary artery sarcomas (7.63 +/- 2.21, n = 3) and the pulmonary embolisms (2.31 +/- 0.41, n = 10) were significantly different (P < 0.05). The mean times between the initial contrast-enhanced CT scan and PET/CT scan were similar in both groups (P = 0.7804). The differences in the locations in lesions between the three groups (right, left and bilateral) or background uptakes were not significant. Conclusion: FDG PET/CT could distinguish pulmonary artery sarcoma from pulmonary embolism based on the SUV(max) value. [ABSTRACT FROM AUTHOR]

Aims. Soluble urokinase plasminogen activator receptor (suPAR) reflects the immune activation in circumstances of inflammation and infection. It has been considered as a risk biomarker associated with poor outcome in various low-grade inflammation and infectious diseases. The study is aimed at investigating whether suPAR has a predictive value with short-term survival in patients with hepatitis B-related acute-on-chronic liver failure (HB-ACLF). Methods. Serum suPAR expression was compared among patients with different states of chronic hepatitis B virus infection. Sixty HB-ACLF patients were recruited as the training cohort and followed up for 90 days. Serum suPAR level and the clinical relevance with short-term outcome were investigated. The temporal dynamics of suPAR were evaluated in 50 HB-ACLF patients with available serum sequentially at baseline, week 2 and week 4. Another 167 HB-ACLF patients were enrolled to validate the predictive value of suPAR with respect to the prognosis. Results. Serum suPAR level was significantly increased in HB-ACLF patients compared to non-ACLF patients. In the training set of HB-ACLF, we observed higher suPAR level, INR, MELD score, and more complications in nonsurvivors than survivors. Longitudinal analysis revealed an increased trend of suPAR level in nonsurvivors during week 0 to week 4 and the modest decline in survivors. It showed that the synchronous suPAR level was higher in nonsurvivors at all indicated time points. Elevated suPAR level at baseline was identified as a strong predictor of a 90-day mortality of HB-ACLF patients. It was confirmed suPAR>16.26 ng/ml had a positive predictive value of 72.22% and a negative predictive value of 77.88% for poor outcome in the validation cohort. Conclusions. Serum suPAR level increases significantly in HB-ACLF patients and associated with a 90-day mortality. It suggests that suPAR might be a potential biomarker to predict the prognosis of HB-ACLF patients.

Eosinophils are a subset of granulocytes characterized by a high abundance of specific granules in their cytoplasm. To act as effector cells, eosinophils degranulate and form eosinophil extracellular traps (EETs), which contain double-stranded DNA (dsDNA) co-localized with granule proteins. The exact molecular mechanism of EET formation remains unknown. Although the term “EET release” has been used in scientific reports, it is unclear whether EETs are pre-formed in eosinophils and subsequently released. Moreover, although eosinophil degranulation has been extensively studied, a precise time-course of granule protein release has not been reported until now. In this study, we investigated the time-dependent release of eosinophil peroxidase (EPX) and mitochondrial DNA (mtDNA) following activation of both human and mouse eosinophils. Unexpectedly, maximal degranulation was already observed within 1 min with no further change upon complement factor 5 (C5a) stimulation of interleukin-5 (IL-5) or granulocyte/macrophage colony-stimulating factor (GM-CSF)-primed eosinophils. In contrast, bulk mtDNA release in the same eosinophil populations occurred much slower and reached maximal levels between 30 and 60 min. Although no single-cell analyses have been performed, these data suggest that the molecular pathways leading to degranulation and mtDNA release are at least partially different. Moreover, based on these data, it is likely that the association between the mtDNA scaffold and granule proteins in the process of EET formation occurs in the extracellular space.

In-beam γ ray spectroscopy with γ singles spectra, γγ coincidences and γ ray angular distributions has been performed with several target-projectile combinations:Ca +S,Ca +Ca,Fe +N,Ni +C,Ni +N,Zn +O,Zn +O. Level schemes ofGe,Ge,As,Se,Kr,Sr andSr have been deduced. The following level energies and spin-parity assignments have been found:Ge: 957.4 keV, 2; 1693.7; 2174.7, (4); 3685.7; 4207.5;Ge: 1015.8, 2; 1777.9, 2; 2267.9, 4; 2428.8, 3(); 2649.1, 3; 3582.3, (5); 3649.3, (5); 3696.2, (6); 3883.3, (6); 4054.4, (7); 4454.6; 4837.3;As: 98.2; 164.6;789.6;863.2; 1306;2160;2210.4;2831.5;3258.3;3263.5;3991.1;5195.7;Se: 945.4, 2; 1600.9; 2039.4, (4);Kr: 455.7, 2; 1013.5, (4); 1781.5;Sr: 385.4, 2; 980.2, (4); 1763.2, (6);Sr: 573.4, 2; 1328.5,(4); 2229.6,(6). γ ray activity spectra have been measured after the bombardment of natural Ca withS. The half-life of the new isotopeSe has been found to be 27±3 sec. Recoil distance Doppler-shift measurements have been performed with the reactionsNi,zn(O, 2 n) Kr,Sr. The following half-lives have been determined:Kr: 423.8 keV, 2, 37±5 psec; 1034.2,4, 5.7±1.6;Kr: 455.3, 2, 25±3; 1120.0, 4, 3.8±1;Sr: 385.4, 2, 44±6. The energy and half-life systematics of the first excited state of even-even nuclei suggest a maximum of nuclear deformation in the region 28≦N, Z≦50 nearSr orZr. [ABSTRACT FROM AUTHOR]

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Pneumococcal meningitis causes apoptosis of developing neurons in the dentate gyrus of the hippocampus. The death of these cells is accompanied with long-term learning and memory deficits in meningitis survivors. Here, we studied the role of the PI3K/Akt (protein kinase B) survival pathway in hippocampal apoptosis in a well-characterized infant rat model of pneumococcal meningitis. Meningitis was accompanied by a significant decrease of the PI3K product phosphatidylinositol 3,4,5-trisphosphate (PIP3) and of phosphorylated (i.e., activated) Akt in the hippocampus. At the cellular level, phosphorylated Akt was decreased in both the granular layer and the subgranular zone of the dentate gyrus, the region where the developing neurons undergo apoptosis. Protein levels and activity of PTEN, the major antagonist of PI3K, were unaltered by infection, suggesting that the observed decrease in PIP3 and Akt phosphorylation is a result of decreased PI3K signaling. Treatment with the PTEN inhibitor bpV(pic) restored Akt activity and significantly attenuated hippocampal apoptosis. Co-treatment with the specific PI3K inhibitor LY294002 reversed the restoration of Akt activity and attenuation of hippocampal apoptosis, while it had no significant effect on these parameters on its own. These results indicate that the inhibitory effect of bpV(pic) on apoptosis was mediated by PI3K-dependent activation of Akt, strongly suggesting that bpV(pic) acted on PTEN. Treatment with bpV(pic) also partially inhibited the concentration of bacteria and cytokines in the CSF, but this effect was not reversed by LY294002, indicating that the effect of bpV(pic) on apoptosis was independent of its effect on CSF bacterial burden and cytokine levels. These results indicate that the PI3K/Akt pathway plays an important role in the death and survival of developing hippocampal neurons during the acute phase of pneumococcal meningitis.

The protozoan Leishmania mexicana parasite causes chronic non-healing cutaneous lesions in humans and mice with poor parasite control. The mechanisms preventing the development of a protective immune response against this parasite are unclear. Here we provide data demonstrating that parasite sequestration by neutrophils is responsible for disease progression in mice. Within hours of infection L. mexicana induced the local recruitment of neutrophils, which ingested parasites and formed extracellular traps without markedly impairing parasite survival. We further showed that the L. mexicana-induced recruitment of neutrophils impaired the early recruitment of dendritic cells at the site of infection as observed by intravital 2-photon microscopy and flow cytometry analysis. Indeed, infection of neutropenic Genista mice and of mice depleted of neutrophils at the onset of infection demonstrated a prominent role for neutrophils in this process. Furthermore, an increase in monocyte-derived dendritic cells was also observed in draining lymph nodes of neutropenic mice, correlating with subsequent increased frequency of IFNγ-secreting T helper cells, and better parasite control leading ultimately to complete healing of the lesion. Altogether, these findings show that L. mexicana exploits neutrophils to block the induction of a protective immune response and impairs the control of lesion development. Our data thus demonstrate an unanticipated negative role for these innate immune cells in host defense, suggesting that in certain forms of cutaneous leishmaniasis, regulating neutrophil recruitment could be a strategy to promote lesion healing.