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Background Non-traumatic hemoperitoneum is a potentially life threatening condition that requires prompt diagnosis and intervention in the emergency department (ED). There are many causes of non-traumatic hemoperitoneum, but spontaneous rupture of a peritoneal seeding tumor is rare. Case report We describe two cases of spontaneous rupture of a peritoneal seeding hepatocellular carcinoma (HCC), following spontaneous rupture of HCC in the ED. Two patients, with a history of ruptured HCC presented with acute left upper quadrant and right lower quadrant abdominal pain. Vital signs were stable, and the diagnosis was made by contrast-enhanced computed tomography scan of abdomen. The patients survived because of early diagnosis and surgical intervention. Conclusion This report highlights that spontaneous rupture of peritoneal seeding HCC can occur after spontaneous rupture of HCC. Emergency physicians should be aware of this rare complication, particularly in Asian countries. Surgical intervention is the appropriate choice for definitive treatment.

The ubiquitously expressed molecular chaperone GRP78 (78 kDa glucose-regulated protein) generally localizes to the ER (endoplasmic reticulum). GRP78 is specifically induced in cells under the UPR (unfolded protein response), which can be elicited by treatments with calcium ionophore A23187 and sarcoplasmic/endoplasmic reticulum Ca2+-ATPase inhibitor TG (thapsigargin). By using confocal microscopy, we have demonstrated that GRP78 was concentrated in the perinuclear region and co-localized with the ER marker proteins, calnexin and PDI (protein disulphide-isomerase), in cells under normal growth conditions. However, treatments with A23187 and TG led to diminish its ER targeting, resulting in redirection into a cytoplasmic vesicular pattern, and overlapping with the mitochondrial marker MitoTracker. Cellular fractionation and protease digestion of isolated mitochondria from ER-stressed cells suggested that a significant portion of GRP78 is localized to the mitochondria and is protease-resistant. Localizations of GRP78 in ER and mitochondria were confirmed by using immunoelectron microscopy. In ER-stressed cells, GRP78 mainly localized within the mitochondria and decorated the mitochondrial membrane compartment. Submitochondrial fractionation studies indicated further that the mitochondria-resided GRP78 is mainly located in the intermembrane space, inner membrane and matrix, but is not associated with the outer membrane. Furthermore, radioactive labelling followed by subcellular fractionation showed that a significant portion of the newly synthesized GRP78 is localized to the mitochondria in cells under UPR. Taken together, our results indicate that, at least under certain circumstances, the ER-resided chaperone GRP78 can be retargeted to mitochondria and thereby may be involved in correlating UPR signalling between these two organelles.

Several binding activities recognizing ultraviolet (UV)-induced DNA damage were detected in cell-free extracts of the unicellular alga, Chlorella pyrenoidosa by gel shift assay. A UV-damaged-DNA binding activity was isolated from algal extracts by a series of chromatography on diethylaminoethyl-cellulose (DEAE-cellulose) and heparin-sepharose columns. The binding activity was detected in the flowthrough (FT) of heparin affinity chromatography. Quantitative analysis of the shifted bands after gel shift assay indicated that the ratio of UV-specific (18 kJ m −2 ) to non-specific binding increased about 15-fold from the first DEAE fractionation to heparin affinity chromatography. When the heparin-FT was fractionated again on a DEAE-cellulose column, UV-dependent binding was detected only in the fraction eluted by NaCl between 0.20 and 0.21 M. Three polypeptides in this NaCl eluate, estimated to be 72, 80 and 90 kDa in molecular mass by sodium dodecyl sulfate polyacrylamide gel electrophoresis (SDS-PAGE), were shown to bind directly to UV-damaged DNA. This binding activity, however, showed only 25% of the binding affinity provided by the heparin-FT, implying that some modulating factors for UV-dependent binding might exist in the heparin-FT. Thus, the three polypeptides may represent a core UV-damaged-DNA binding activity in algal extracts. This core binding activity also recognized DNA lesions induced by DNA alkylating agent cisplatin, and the binding to cisplatin-damaged DNA could be competed by UV-irradiated DNA. Our data suggest that this binding activity may be involved in the damage-recognition step of nucleotide excision repair (NER) in C . pyrenoidosa .

The present study is concerned with the buoyancy-driven airflow in an cumulus between two asymmetrically heated horizontal eccentric elliptical cylinders. Flow patterns and heat transfer characteristics for various geometric configurations and heating conditions are predicted. The governing equations are discretized with the finite volume method on a curvilinear grid system generated numerically by the body-fitted coordinate transformation. Dependence of the equivalent conductivity on the physical and geometric parameters, such as the Rayleigh number, the dimensionless eccentricity, and the ratio of the areas of the cylinders, has been evaluated. Results show that, for Ra > 104, the strength of the buoyancy-driven fluid motion as well as the enhancement in the heat transfer becomes appreciable. Among the nine possible geometric configurations considered in this study, case Vv exhibits the highest heat transfer performance. For some special cases, the numerical solutions are compared with existing...

Spontaneous renal artery dissection (SRAD) is a rare entity. We reported a 30-year-old healthy man presenting with sudden onset of left flank pain. Abdominal plain film and sonography were unremarkable. The contrast-enhanced abdominal computed tomographic (CT) scan demonstrated a dissecting intimal flap of the left distal renal artery (RA) complicating infarction. Selective angiography of the renal artery disclosed a long dissection of left distal RA with a patent true lumen and occlusion of left accessory RA. Conservative treatment with control of blood pressure and antiplatelet agent was prescribed. The patient was discharged with an uneventful condition on day 5.

Although the differential expression of heat shcok proteins, Hsp90alpha and Hsp90beta was extensively studied in many kinds of cells, the post-transcriptional regulation of Hsp90 isoforms remains unclear. In control and GA-treated rat gliosarcoma cells, it has been reported that the translational efficiency of hsp90alpha is higher than hsp90beta. In this study, we present evidences identifying the roles for leaky scanning and 5'-UTR sequence in translational regulation of Hsp90beta. The result of in vitro transcription and translation (IVTT) experiment showed that hsp90alpha exhibited higher translation efficiency than hsp90beta. Sequence analysis revealed that there is an out-of-frame downstream AUG codon in hsp90beta gene. However, elimination of the downstream AUG by site-directly mutagenesis or introducing Kozak context sequence around the initiator AUG of hsp90beta open reading frame increased its translational efficiency, which indicated that leaky scanning might be a possible mechanism regulating hsp90beta. Furthermore, we also constructed a firefly luciferase reporter system to verify the effect of subsequent translation at the downstream out-of-frame AUG codon in 9L and A549 cells. Furthermore, it is believed that 5'-untranslated region (5'-UTR) also plays a significant role in translational control. We showed hsp90beta 5'-UTR gives rise to the reduction of the translation efficiency in IVTT experiment. Additionally, the reductive effect of hsp90beta 5'-UTR was further confirmed by luciferase reporter assay using truncated deletion analyses of 5'-UTR of hsp90beta. Our results support the hypothesis that ribosome leaky scanning mechanism and 5'-UTR sequence acts as negative regulators in hsp90beta mRNA.

This thesis started by using geldanamycin (GA) to treat rat brain tumor (RBT) 9L cells. By observing cell stress response, we initiated the study of the differentially inductive mechanisms on heat shock protein 90 isoforms. Geldanamycin (GA) is an ansamycin-derivative benzoquinone compound, which was originally isolated as a natural product with anti-fungal activity. GA could inhibit the essential ATPase activity of HSP90 and results in inactivation, destabilization, and degradation of HSP90 client proteins, including a wide variety of signal-transducing proteins that regulate cell growth and differentiation, such as protein kinases and steroid hormone receptors. But reports had shown that GA treatment could also induce heat-shock response; especially including HSP70, GRP78 and GRP94 in RBT 9L cells. In this study, we found only a 1/10 dose of GA (i.e., 0.5 贡M) could induce HSP90, compared to 5 贡M GA to induce those heat shock proteins like HSP70, GRP78 and GRP94. Furthermore, HSP90 exists two highly consistent isoforms, HSP90α and HSP90β, in mammalian cells. We further separated HSP90 isoforms by decrease pH (to 8.0) and percentage (9%) of PAGE gel; the results showed apparently differential induction of HSP90 isoforms through GA treatment (HSP90α > HSP90β). On the other hand, the consistencies were confirmed from RNA to protein level by real time qPCR analysis, Western Blotting and de novo synthetic analysis. Our results demonstrated that gene level regulation controlled the differential induction of HSP90 isoforms. According to the promoter sequences of hsp90α and hsp90β, we evaluated the different importance of some transcriptional elements by Electrophoresis Mobility Shift Assay (EMSA). Interestingly, differential induction of HSP90α and β is related to the differential binding activities to HSEs in hsp90α and hsp90β promoters. In addition, we also observed the binding strengths on HSEs might imply how HSP90α is more inducible isoforms than HSP90β. On the other hand, the results of binding activities on basic transcription elements showed that GC-box (sp-1 site) involved in inductive level of HSP90α汹and HSP90β the binding on TATA-box and CRE were respectively related to the induction of HSP90α and HSP90β. In conclusion, treatment with GA facilitate HSF1 binding to the distinct HSE sites on the promoters of hsp90α and hsp90β and further induce HSP90s. It agreed with the observations of differential induction on mRNA and protein level in 9L cells under treatment with GA.

Both geldanamycin (GA) and radicicol (RA) are HSP90 binding agents that possess antitumour activities. Although the in vitro data indicated that the inhibitory constant of RA is much bigger than that of GA, the in vivo data on drug efficacy might reveal different results. We have recently shown that treatment with GA induces a heat-shock response and that calcium mobilization may be involved in the process. By using induction of HSP70 as the endpoint assay, we found changes in upstream signaling mediators, including HSF1 and calcium mobilization, as well as possible involvement of protein kinase in human non-small cell lung cancer H460 cells treated with GA and RA. Our results demonstrated that calcium mobilization, a calcium dependent and H7-sensitive protein kinase, along with HSF1 activation by phosphorylation, are all involved in the HSP70 induction process triggered by the drugs. However, only GA, but not RA, can provoke a rapid calcium mobilization and thereby result in an instant induction of HSP70. Furthermore, the rapid calcium influx, followed by instant HSP induction, could be achieved in GA- or RA-treated cells placed in a medium containing excessive calcium while the response was completely abolished in cells depleted of calcium. Taken together, our findings suggest that differential calcium signaling may account for the differential induction of HSP and the action of GA and RA.

Mitral regurgitation (MR) was recognized by Corvisart. In the last decade, the availability of Doppler echocardiography and angiography, widely using pure MR as the end-effect of rheumatic heart disease (RHD), has shown (MR) to be a fairly common condition. Now, the interest has shifted to a variety of nonrheumatic forms of MR. This paper attempts to review rheumatic and nonrheumatic cases in our area in patients under the age of 14 years.

BackgroundEosinophilic granulocytes are important for the human immune system. Many cationic proteins with cytotoxic activities, such as eosinophil cationic protein (ECP) and eosinophil-derived neurotoxin (EDN), are released from activated eosinophils. ECP, with low RNase activity, is widely used as a biomarker for asthma. ECP inhibits cell viability and induces apoptosis to cells. However, the specific pathway underlying the mechanisms of ECP-induced cytotoxicity remains unclear. This study investigated ECP-induced apoptosis in bronchial epithelial BEAS-2B cells and elucidated the specific pathway during apoptosis.ResultsTo address the mechanisms involved in ECP-induced apoptosis in human BEAS-2B cells, investigation was carried out using chromatin condensation, cleavage of poly (ADP-ribose) polymerase (PARP), sub-G1 distribution in cell cycle, annexin V labeling, and general or specific caspase inhibitors. Caspase-8-dependent apoptosis was demonstrated by cleavage of caspase-8 after recombinant ECP treatment, accompanied with elevated level of tumor necrosis factor alpha (TNF-α). Moreover, ECP-induced apoptosis was effectively inhibited in the presence of neutralizing anti-TNF-α antibody.ConclusionIn conclusion, our results have demonstrated that ECP increased TNF-α production in BEAS-2B cells and triggered apoptosis by caspase-8 activation through mitochondria-independent pathway.