[Multiple pulmonary masses with diffuse cystic lesions].

A 50-year-old female patient, presenting with a past history of Reynaud's syndrome, xerostomia and xerophthalmia, was admitted to Fujian Provincial Hospital because of coughing for 10 days and left anterior chest pain for 1 day. Chest imaging showed multiple nodules and masses, and diffuse cystic lesions in both lungs. Based on the differential diagnosis of multiple pulmonary masses and diffuse cystic lesions respectively, autoantibodies, radionuclide dynamic imaging of the parotid, positron emission tomography-CT, CT-guided percutaneous transthoracic needle biopsy, and other examinations were performed. The diagnosis of diffuse large B-cell lymphoma stage ⅣA (lung, parotid gland) and Sjögren's syndrome was confirmed. By analyzing the imaging features and pathogenesis in detail, the diffuse cystic lesions of both lungs were considered to be related to lymphocytic interstitial pneumonia caused by Sjögren's syndrome. The pulmonary space-occupying lesions in the lungs were significantly absorbed after RCHOP regimen for lymphoma.

Benchmark Experiment to Prove the Role of Projectile Excited States Upon the Ion Stopping in Plasmas.

We report on a precision energy loss measurement and theoretical investigation of 100 keV/u helium ions in a hydrogen-discharge plasma. Collision processes of helium ions with protons, free electrons, and hydrogen atoms are ideally suited for benchmarking plasma stopping-power models. Energy loss results of our experiments are significantly higher than the predictions of traditional effective charge models. We obtained good agreement with our data by solving rate equations, where in addition to the ground state, also excited electronic configurations were considered for the projectile ions. Hence, we demonstrate that excited projectile states, resulting from collisions, leading to capture-, ionization-, and radiative-decay processes, play an important role in the stopping process in plasma.

Determination of Hydrogen Density by Swift Heavy Ions.

A novel method to determine the total hydrogen density and, accordingly, a precise plasma temperature in a lowly ionized hydrogen plasma is described. The key to the method is to analyze the energy loss of swift heavy ions interacting with the respective bound and free electrons of the plasma. A slowly developing and lowly ionized hydrogen theta-pinch plasma is prepared. A Boltzmann plot of the hydrogen Balmer series and the Stark broadening of the H_{ß} line preliminarily defines the plasma with a free electron density of (1.9±0.1)×10^{16} cm^{-3} and a free electron temperature of 0.8-1.3 eV. The temperature uncertainty results in a wide hydrogen density, ranging from 2.3×10^{16} to 7.8×10^{18} cm^{-3}. A 108 MHz pulsed beam of ^{48}Ca^{10+} with a velocity of 3.652 MeV/u is used as a probe to measure the total energy loss of the beam ions. Subtracting the calculated energy loss due to free electrons, the energy loss due to bound electrons is obtained, which linearly depends on the bound electron density. The total hydrogen density is thus determined as (1.9±0.7)×10^{17} cm^{-3}, and the free electron temperature can be precisely derived as 1.01±0.04 eV. This method should prove useful in many studies, e.g., inertial confinement fusion or warm dense matter.

Energy deposition by heavy ions: additivity of kinetic and potential energy contributions in hillock formation on CaF2.

Modification of surface and bulk properties of solids by irradiation with ion beams is a widely used technique with many applications in material science. In this study, we show that nano-hillocks on CaF2 crystal surfaces can be formed by individual impact of medium energy (3 and 5 MeV) highly charged ions (Xe(22+) to Xe(30+)) as well as swift (kinetic energies between 12 and 58 MeV) heavy xenon ions. For very slow highly charged ions the appearance of hillocks is known to be linked to a threshold in potential energy (Ep) while for swift heavy ions a minimum electronic energy loss per unit length (Se) is necessary. With our results we bridge the gap between these two extreme cases and demonstrate, that with increasing energy deposition via Se the Ep-threshold for hillock production can be lowered substantially. Surprisingly, both mechanisms of energy deposition in the target surface seem to contribute in an additive way, which can be visualized in a phase diagram. We show that the inelastic thermal spike model, originally developed to describe such material modifications for swift heavy ions, can be extended to the case where both kinetic and potential energies are deposited into the surface.

Kallistatin, a novel anti-angiogenesis agent, inhibits angiogenesis via inhibition of the NF-κB signaling pathway.

Development of a novel angiogenesis inhibitor will be essential for the improvement of therapeutics against cancer. Kallistatin had been recognized as an endogenous angiogenesis inhibitor. Here, we demonstrated kallistatin's strong anti-angiogenesis and anti-metastasis activity stimulated by breast cancer cells (MCF-7) and its mechanism of action in vitro. The anti-angiogenesis effect in vivo was evaluated by chicken chorioallantoic membrane (CAM) neovascularisation. Because of the underlying molecular mechanism of its anti-angiogenesis activity remains poorly understood. In this study, we examined whether the NF-κB signaling pathway was involved in the anti-angiogenesis and anti-metastasis activity of kallistatin. Kallistatin significantly inhibited TNF-α-induced nuclear factor-κB activation in a dose-dependent manner. Addition of kallistatin inhibited TNF-α induced IκBα degradation; phosphorylation of IκBα kinase (IKK), nuclear factor-κB-p65 protein; and nuclear translocation of p65/50. Meanwhile, we investigated the effects of kallistatin on the expression of vascular endothelial growth factor (VEGF) and other angiogenesis-related gene in human umbilical vein endothelial cells (HUVECs). We found that kallistatin decreased the expression of VEGF and some angiogenesis-related genes, which promoted angiogenesis in cancer. Taken together, we suggested that kallistatin would inhibit tumor angiogenesis via inhibition of the NF-κB signaling pathway and finally abrogate NF-κB-dependent gene expression. All the results revealed that kallistatin would have potential as a novel.

Mass measurements of the neutron-deficient 41Ti, 45Cr, 49Fe, and 53Ni nuclides: first test of the isobaric multiplet mass equation in f p-shell nuclei.

Isochronous mass spectrometry has been applied to neutron-deficient 58Ni projectile fragments at the HIRFL-CSR facility in Lanzhou, China. Masses of a series of short-lived T(z)=-3/2 nuclides including 41Ti, 45Cr, 49Fe, and 53Ni have been measured with a precision of 20-40 keV. The new data enable us to test for the first time the isobaric multiplet mass equation (IMME) in fp-shell nuclei. We observe that the IMME is inconsistent with the generally accepted quadratic form for the A=53, T=3/2 quartet. We perform full space shell model calculations and compare them with the new experimental results.

Results of carbon ion radiotherapy for skin carcinomas in 45 patients.

UNLABELLED: BACKGROUND; Heavy ions represent the best tool for external radiotherapy (RT) of inoperable tumours. Heavy ion RT has been used in the treatment of various tumours, especially for radioresistant tumours mediated by hypoxia, localized near organs at risk. Most of these treatments are concentrated in deep-seated tumours such as those of the brain, head, lung, liver, rectum and urogenital organs, and treatment of skin carcinomas is limited. OBJECTIVES: To evaluate the outcome and toxicity after carbon ion RT for skin carcinomas at the Heavy Ion Research Facility in Lanzhou, China. METHODS: Between November 2006 and March 2009, 45 patients with skin carcinoma [squamous cell carcinoma (SCC) (n = 16), basal cell carcinoma (BCC) (n = 12), malignant melanoma (MM) (n = 7), Bowen disease (n = 8) and Paget disease (n = 2)] were treated with carbon ion RT within a clinical Phase I trial. Patients received total doses of 60-70 GyE for SCC and BCC, 61-75 GyE for MM, 60 GyE for Bowen disease and 42·5 GyE for Paget disease, administered in 6-11 fractions over 6-11 days, with a fraction dose of 7-10 GyE. RESULTS: The mean follow-up was 24 months, range 12-36 months. The actuarial local control rates at 1 and 3 years were 90·9% and 65·5% for SCC, 91·7% and 80·2% for BCC, 85·7% and 42·9% for MM, 90% and 90% for Bowen and Paget diseases, respectively. The actuarial 1- and 3-year overall survival rates for 45 patients were 88·9% and 86%, respectively. No severe side-effects greater than Common Toxicity Criteria grade 3 have been observed. CONCLUSIONS: The results demonstrated that heavy ion RT offers high local tumour control and progression-free survival rates without significant radiation-induced toxicity for patients with skin carcinomas.

Direct mass measurements of short-lived A=2Z-1 nuclides (63)Ge, (65)As, (67)Se, and (71)Kr and their impact on nucleosynthesis in the rp process.

Mass excesses of short-lived A=2Z-1 nuclei (63)Ge, (65)As, (67)Se, and (71)Kr have been directly measured to be -46,921(37), -46,937(85), -46,580(67), and -46,320(141) keV, respectively. The deduced proton separation energy of -90(85) keV for (65)As shows that this nucleus is only slightly proton unbound. X-ray burst model calculations with the new mass excess of (65)As suggest that the majority of the reaction flow passes through (64)Ge via proton capture, indicating that (64)Ge is not a significant rp-process waiting point.

Evidence for functional role of epsilonPKC isozyme in the regulation of cardiac Na(+) channels.

Investigation of the role of individual protein kinase C (PKC) isozymes in the regulation of Na(+) channels has been largely limited by the lack of isozyme-selective modulators. Here we used a novel peptide-specific activator (epsilonV1-7) of epsilonPKC and other peptide isozyme-specific inhibitors in addition to the general PKC activator phorbol 12-myristate 13-acetate (PMA) to dissect the role of individual PKCs in the regulation of the human cardiac Na(+) channel hH1, heterologously expressed in Xenopus oocytes. Peptides were injected individually or in combination into the oocyte. Whole cell Na(+) current (I(Na)) was recorded using two-electrode voltage clamp. epsilonV1-7 (100 nM) and PMA (100 nM) inhibited I(Na) by 31 +/- 5% and 44 +/- 8% (at -20 mV), respectively. These effects were not seen with the scrambled peptide for epsilonV1-7 (100 nM) or the PMA analog 4alpha-phorbol 12,13-didecanoate (100 nM). However, epsilonV1-7- and PMA-induced I(Na) inhibition was abolished by epsilonV1-2, a peptide-specific antagonist of epsilonPKC. Furthermore, PMA-induced I(Na) inhibition was not altered by 100 nM peptide-specific inhibitors for alpha-, beta-, delta-, or etaPKC. PMA and epsilonV1-7 induced translocation of epsilonPKC from soluble to particulate fraction in Xenopus oocytes. This translocation was antagonized by epsilonV1-2. In native rat ventricular myocytes, PMA and epsilonV1-7 also inhibited I(Na); this inhibition was antagonized by epsilonV1-2. In conclusion, the results provide evidence for selective regulation of cardiac Na(+) channels by epsilonPKC isozyme.

Autoantibodies from mothers of children with congenital heart block downregulate cardiac L-type Ca channels.

Congenital heart block (CHB) affects offspring of mothers with autoantibodies (positive IgG) to intracellular SSA/Ro and SSB/La ribonucleoproteins and is associated with high morbidity and mortality. Here, we show that maternal anti-Ro/La antibodies immunoreact with human fetal cardiomyocyte sarcolemma, recognize human L-type Ca channel alpha(1C)-protein and functionally inhibit expressed current in oocytes injected with alpha(1C) cRNA and Purkinje L-type Ca current. Furthermore, cardiac myocytes from pups born to SSA/Ro-immunized mice exhibited reduced L-type Ca current density. All together, the data establish that L-type calcium channel is a target for maternal antibodies and may provide a functional basis for the electrocardiographic abnormalities seen in infants with CHB.

Down-regulation of L-type calcium channel in pups born to 52 kDa SSA/Ro immunized rabbits.

Congenital heart block is considered a model of passively acquired autoimmune disease in which the mother generates anti-SSA/Ro and/or anti-SSB/La antibodies that cross the placenta and presumably injure the heart of developing fetus. CHB is accompanied by ECG abnormalities including AV block, sinus bradycardia, and ventricular dysfunction. Our previous data indicate that these abnormalities are caused by maternal autoantibody-mediated disturbance of L-type Ca channels. To investigate the consequence of chronic exposure of L-type Ca channels in newborn pups to maternal autoantibodies during pregnancy, we immunized female rabbits with human 52 kDa-SSA/Ro (Ro52) recombinant protein. ECG revealed that pups from the immunized group had varying degrees of conduction defects. In addition, I(CaL) density and protein were reduced in hearts of pups from the immunized group. Sera and purified IgG from immunized rabbits inhibited I(Ba) recorded from oocytes with expressed alpha(1C) and beta(2a) subunits of L-type Ca channel. Pups born to Ro52 immunized mothers exhibited down-regulation of L-type calcium channels in heart. The data provide new insight into the pathogenesis of congenital heart block.

Direct inhibition of expressed cardiac l- and t-type calcium channels by igg from mothers whose children have congenital heart block.

BACKGROUND: Congenital heart block (CHB) is a disease that affects the offspring of mothers with autoimmune diseases. We recently reported that maternal sera containing antibodies against SSA/Ro and SSB/La ribonucleoproteins (positive IgG) inhibited L-type Ca current in isolated cardiac myocytes and induced sinus bradycardia in a murine model of CHB. The direct interaction of positive IgG with L-type Ca channel proteins and the possible inhibition of T-type Ca current that could account for the sinus bradycardia remain unknown. METHODS AND RESULTS: The 2-electrode voltage-clamp technique was used to record currents via L-type (I(Ba)-alpha(1C) or I(Ba)-alpha(1C)+beta(2a)+alpha(2)/delta) and T-type (I(Ba)-alpha(1H)) Ca channels, Na channels (I(Na)-hH1), and K channels (I(Ks)-minK+KvLQT1) expressed in Xenopus oocytes. Positive IgG (350 microgram/mL) inhibited I(Ba)-alpha(1C) by 50.6+/-4.7% (P<0.01) and I(Ba)-alpha(1C)+beta(2a)+alpha(2)/delta by 50.9+/-4.2% (P<0.01); I(Ba)-alpha(1H) was reduced by 18.9+/-1.0% (P<0.01). Immunoblot data show cross-reactivity of positive IgG with alpha(1C) subunit. Pretreatment of oocytes with atropine (1 micromol/L) or acetylcholine (10 micromol/L) did not affect the inhibitory effect of IgG on I(Ba)-alpha(1C) and I(Ba)-alpha(1C)+beta(2a)+alpha(2)/delta (P<0.05). Positive IgG had no effect, however, on either I(Na)-hH1 or I(Ks)-minK+KvLQT1. CONCLUSIONS: Positive IgG inhibited expressed L-type I:(Ba) and cross-reacted with the alpha(1C) subunit in Xenopus oocytes, providing strong evidence that maternal antibodies interact directly with the pore-forming alpha(1)-subunit of Ca channels. In addition, we show for the first time that positive IgG also inhibited T-type I(Ba) but not I(Na)-hH1 or I(Ks)-minK+KvLQT1. This could provide, in part, the ionic basis of sinus bradycardia reported in animal models of CHB and clinically in humans.

[Observation on eosinophilic intranuclear inclusions in hepatocytes of patients with advanced schistosomiasis japonica].

Wedge biopsies of liver from 155 patients with advanced schistosomiasis japonica were observed pathologically, and HBsAg and HBcAg in liver were tested with double bridge peroxidase-anti-peroxidase (PAP) method. 88 of 155 cases (56.8%) were found to be HBsAg and/or HBcAg (HBAg) positive in liver. Eosinophilic intranuclear inclusions were observed in the hepatocytes of 30 cases (19.4%), in which 18 (60%) were also HBAg positive in liver. These inclusions were considered to be the markers of several virus infections, such as cytomegalovirus, herpes simplex virus, etc. The patients with positive HBAg and/or inclusion in liver had significantly more severe pathological changes in liver parenchyma. The results indicate that in addition to hepatitis B, complication with other viral infections in liver, which produce eosinophilic intranuclear inclusion, may also aggravate the pathological changes in liver and may be one of the causes of portal cirrhosis in patients with advanced schistosomiasis japonica (Fig. 1). schistosomiasis japonica