Primary chondrosarcoma of the liver: A case report.

BACKGROUND: Primary chondrosarcoma of the liver are extremely rare. Moreover, there are few reports focusing on typical clinical symptoms and imaging characteristics. Therefore, the diagnosis of chondrosarcoma of the liver remains a challenge. CASE SUMMARY: A 59-year-old male was admitted due to a lesion occupying the right liver lobe that was found by physical examination. Magnetic resonance imaging showed a lobular mass with high T2 weighted image and low T1 weighted image with enhanced internal separation and edge in the right liver. He was diagnosed with liver cystadenoma by using magnetic resonance imaging. At 3 mo later, the magnetic resonance scan showed that the mass was enlarged. Laparoscopic liver tumor resection was performed with a pathological diagnosis of liver chondrosarcoma. Then he received a surgical resection for the recurrent lesion. However, intrahepatic and abdominal metastases were found again at 8 mo after the second operation. The patient then received conservative management and is now under follow-up. CONCLUSION: Primary liver chondrosarcoma generally is presented as lobulated and heterogeneous density/signal, cystic, solid masses without calcification with enhanced edge, internal septa and solid part. The imaging features are closely related to pathology, which may be helpful for clinical diagnosis.

Asiaticoside Mitigates the Allergic Inflammation by Abrogating the Degranulation of Mast Cells.

The effects of asiaticoside (AS) on allergic responses mediated by mast cells were investigated. AS showed no obvious cytotoxicity on RPMCs (rat peritoneal mast cells). AS reduced the intracellular calcium in RPMCs and deprived the histamine release and degranulation. AS also decreased the generation of antigen-induced tumor necrosis factor α, interleukin (IL)-4, IL-8, and IL-1ß in RBL-2H3 cells sensitized by IgE. The suppression of AS on pro-inflammatory cytokines was related with the activation of the intracellular FcεRI and the inhibition of the nuclear factor-κB signaling pathway. In addition, AS disabled the phosphorylation of antigen-induced Syk, Lyn, Gab2, and PLCγ1, thus suppressing the downstream Akt phosphorylation and MAPKs pathways. It also increased HO-1 and Nrf2 expression time dependently. In summary, we demonstrate that AS suppresses the allergic inflammation mediated by mast cells and this effect might be mediated by FcεRI-dependent signaling pathways.

Inhibition of protein kinase C delta attenuates allergic airway inflammation through suppression of PI3K/Akt/mTOR/HIF-1 alpha/VEGF pathway.

Vascular endothelial growth factor (VEGF) is supposed to contribute to the pathogenesis of allergic airway disease. VEGF expression is regulated by a variety of stimuli such as nitric oxide, growth factors, and hypoxia-inducible factor-1 alpha (HIF-1α). Recently, inhibition of the mammalian target of rapamycin (mTOR) has been shown to alleviate cardinal asthmatic features, including airway hyperresponsiveness, eosinophilic inflammation, and increased vascular permeability in asthma models. Based on these observations, we have investigated whether mTOR is associated with HIF-1α-mediated VEGF expression in allergic asthma. In studies with the mTOR inhibitor rapamycin, we have elucidated the stimulatory role of a mTOR-HIF-1α-VEGF axis in allergic response. Next, the mechanisms by which mTOR is activated to modulate this response have been evaluated. mTOR is known to be regulated by phosphoinositide 3-kinase (PI3K)/Akt or protein kinase C-delta (PKC δ) in various cell types. Consistent with these, our results have revealed that suppression of PKC δ by rottlerin leads to the inhibition of PI3K/Akt activity and the subsequent blockade of a mTOR-HIF-1α-VEGF module, thereby attenuating typical asthmatic attack in a murine model. Thus, the present data indicate that PKC δ is necessary for the modulation of the PI3K/Akt/mTOR signaling cascade, resulting in a tight regulation of HIF-1α activity and VEGF expression. In conclusion, PKC δ may represent a valuable target for innovative therapeutic treatment of allergic airway disease.

Treatment and mortality rate of bullous pemphigoid in China: a hospital-based study.

Bullous pemphigoid (BP) has been reported to be associated with significant morbidities and a considerable mortality rate. We retrospectively studied 94 patients with BP in a Chinese tertiary medical center between 2005 and 2010 to evaluate the treatment of BP and prognostic factors for the mortality of BP. Cerebrovascular diseases (42.55%) and hypertension (39.36%) were the most common pre-existing conditions. Cardiopathy, diabetes and psoriasis pre-existed in 24.47%, 22.34% and 5.32%, respectively. Eighty of all 94 patients were treated by systemic corticosteroid at prednisone 0.3 mg/kg to 1.5 mg/kg daily. Patients were followed up for a minimum of 1 year or until the time of death. The mean duration of follow-up was 32 months. Kaplan-Meier analysis showed a 1-year survival probability of 76.6% (standard error 4.4%), with a 95% confidence interval (68.04%, 85.16%). Multivariate analysis revealed that increased age, bedridden condition, presence of cerebrovascular diseases at diagnosis, pre-existing cardiopathy and low serum albumin level were associated with the elevated 1-year mortality rate of BP.

Silibinin attenuates allergic airway inflammation in mice.

Allergic asthma is a chronic inflammatory disease regulated by coordination of T-helper2 (Th2) type cytokines and inflammatory signal molecules. Silibinin is one of the main flavonoids produced by milk thistle, which is reported to inhibit the inflammatory response by suppressing the nuclear factor-kappa B (NF-κB) pathway. Because NF-κB activation plays a pivotal role in the pathogenesis of allergic inflammation, we have investigated the effect of silibinin on a mouse ovalbumin (OVA)-induced asthma model. Airway hyperresponsiveness, cytokines levels, and eosinophilic infiltration were analyzed in bronchoalveolar lavage fluid and lung tissue. Pretreatment of silibinin significantly inhibited airway inflammatory cell recruitment and peribronchiolar inflammation and reduced the production of various cytokines in bronchoalveolar fluid. In addition, silibinin prevented the development of airway hyperresponsiveness and attenuated the OVA challenge-induced NF-κB activation. These findings indicate that silibinin protects against OVA-induced airway inflammation, at least in part via downregulation of NF-κB activity. Our data support the utility of silibinin as a potential medicine for the treatment of asthma.

[Anthocyanidin inhibits immunoglobulin E-mediated allergic response in mast cells].

This study is to investigate the anti-allergic effect of anthocyanidin and to explore its possible mechanism. The experiments of passive cutaneous anaphylaxis reaction (PCA) and colorimetry were used to determine the effect of anthocyanidin on degranulation of mast cells in vivo. For in vitro study, various concentrations of anthocyanidin (100, 50 and 25 micromol x L(-1)) were added to the culture medium of mast cells cultured with 100 microg x L(-1) of dinitrophenyl (DNP) specific IgE overnight. The azelastine (100 micromol x L(-1)) was selected as the positive control. The antigen (DNP-human serum albumin, DNP-HAS)-induced release of degranulation was measured by enzymatic assay, histamine was determined by EIA, and interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-alpha) were measured by Western blotting, separately. In addition, the effects of anthocyanidin on phosphorylation of NF-kappaB, p38MAPK and Akt were observed by Western blotting. The results showed that treatments with anthocyanidin (100 and 50 mg x kg(-1)) were followed by a decrease in PCA of rats. Anthocyanidin (100 and 50 micromol x L(-1)) obviously suppressed the degranulation from mast cells, whereas results from anthocyanidin (100 and 50 micromol x L(-1)) group indicated significant inhibitory effect on histamine, the calcium uptake, TNF-alpha, IL-6, phosphorylation of NF-kappaB, p38MAPK and Akt of mast cells induced by antigen. Anthocyanidin may suppress the anaphylactic reaction by inhibiting the action of mast cells. NF-kappaB, p38MAPK and Akt at least in part contribute to this event.

Cornuside suppresses lipopolysaccharide-induced inflammatory mediators by inhibiting nuclear factor-kappa B activation in RAW 264.7 macrophages.

Cornuside, a secoiridoid glucoside compound, was isolated from the fruit of Cornus officinalis SIEB. et ZUCC. Cornuside has been reported to possess immunomodulatory and anti-inflammatory activities. However, the effects and mechanism of action of cornuside in inflammation have not been fully characterized. The present study was therefore designed to examine whether cornuside suppresses inflammatory response in lipopolysaccharide (LPS)-stimulated RAW 264.7 macrophage cells. Cornuside significantly inhibited the LPS-induced production of nitric oxide, prostaglandin E(2), tumor necrosis factor-alpha, interleukin-6 (IL-6), and IL-1beta. The mRNA and protein expressions of inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) were also decreased by cornuside. Furthermore, cornuside significantly attenuated the LPS-stimulated phosphorylation and degradation of inhibitory kappa B-alpha and the subsequent translocation of the p65 subunit of nuclear factor-kappa B (NF-κB) to the nucleus. Cornuside also reduced the phosphorylations of extracellular-signal-related kinase (ERK1/2), p38, and c-Jun N-terminal kinase (JNK1/2). These results suggest that the anti-inflammatory property of cornuside is related to the downregulations of iNOS and COX-2 due to NF-κB inhibition as well as the negative regulation of ERK1/2, p38, and JNK1/2 phosphorylations in RAW 264.7 cells.

Protective effect of cornuside against carbon tetrachloride-induced acute hepatic injury.

This study elucidated the effects of cornuside on carbon tetrachloride (CCl4)-induced hepatotoxicity. Rats were treated intraperitoneally with 0.5 mL/kg of CCl4. Sixteen h after CCl4 treatment, the levels of serum aminotransferases, tumor necrosis factor-α (TNF-α), and lipid peroxidation were significantly elevated, whereas the hepatic antioxidative enzyme activities were decreased. These changes were attenuated by cornuside. Histological studies also indicated that cornuside inhibited CCl4-induced liver damage. Furthermore, the contents of hepatic nitrite, inducible nitric oxide synthase (iNOS), and cyclooxygenase-2 (COX-2) were elevated after CCl4 treatment, while cytochrome P450 2E1 (CYP2E1) expression was suppressed. Cornuside treatment inhibited the formation of liver nitrite, and reduced the overexpression of iNOS and COX-2 proteins, but restored the liver CYP2E1 content as compared with the CCl4-treated rats. Our data indicate that cornuside protects the liver from CCl4-induced acute hepatotoxicity, perhaps due to its ability to restore the CYP2E1 function and suppress inflammatory responses, in combination with its capacity to reduce oxidative stress.

Identification of the anterior sectoral trunk with particular reference to the hepatic hilar plate and its clinical importance.

BACKGROUND: At the hilum of the liver, there is a structure called the hilar plate, which is of great surgical importance because all variations in the bile ducts and blood vessels occur within this region. The Rex-Cantlie line does not always pass the point of portal bifurcation. Classifying portal vein (PV) variations based on the shape and origin of anterior sectoral trunk (AST) within the hepatic plate system will be of higher anatomical and surgical value than the conventional method based on PV ramification. METHODS: We investigated PV variations in the hilar plate in terms of combinations of 4 hepatic sectoral trunks rather than successive ramification of the PV. The combination patterns of each sectoral trunk were analyzed using data from adult cadaver liver dissection (n = 64) and multi-detector computed tomography (n = 216) of human livers. RESULTS: The AST root position on the hilar plate varies, in contrast to the other sectoral trunks, which are relatively consistent in their root position. Three types of PV variations were identified based on the AST root position. In addition, 4 similar but different shapes (I, Y, V, and U) of AST were identified. CONCLUSION: Not only the root position in the hepatic hilar plate but also the shape of AST can be considered as the major determinants of PV variations.

Ramification of Glisson's sheath peripheral branches and clinical implications in the era of local ablation therapy.

PURPOSE: Classical anatomical resection does not always guarantee tumor-free margins when the tumor overrides traditional anatomical planes. Surgeons and interventionists frequently need to focus on the peripheral branches of Glisson's sheath in patients with poor hepatic reserves, particularly when the tumor is deep seated. The present study used anatomical liver dissection to investigate the spatial distribution of the branches of Glisson's sheath in each of four liver sectors. METHODS: Sixty-four adult human liver specimens were dissected. The size and ramification patterns of Glisson's sheath in each sector were analyzed in terms of bilateral homology within two paramedian sectors and within two lateral sectors. RESULTS: Each liver sector had a characteristic Glisson's sheath in terms of trunk shape and ramification pattern. The two paramedian sectors showed point symmetry. Most of the branches of the two paramedian sectors emerged from the top of a short stout trunk. Although the two paramedian sectors were similar in terms of basic configuration, the ramification axes were almost perpendicular to each other. Unlike the paramedian sectors, the two lateral sectors showed not much homology. CONCLUSIONS: The peripheral branches of Glisson's sheath were generally longer (approximately 5 cm) and thicker than anticipated. Extirpation strategies should take into account that each liver sector has a characteristic Glisson's sheath ramification pattern.

Anatomical variations of the origin of the segment 4 hepatic artery and their clinical implications.

The threat of ischemic complications following massive resection, especially in living donor hepatectomy or split liver transplantation, has been haunting surgeons for many years. Postmortem dissections of 62 livers were performed to investigate anatomical variations of the principal artery for segment 4 (A4). The origin of A4 was examined separately in the liver with (n = 46) or without (n = 16) an aberrant left hepatic artery (abLHA). A4s were found to be extrahepatic or intrahepatic branches of the right hepatic artery (RHA), left hepatic artery, or proper hepatic artery and were categorized into 4 different types according to their origins. The RHA type, originating from the RHA or right anterior hepatic artery (RAHA), was the most common pattern in our series. The A4 roots had a strong tendency of stemming from the RHA (n = 12) even in the livers with abLHA (n = 16). Among the RHA-type A4s, the A4 arising from RAHA (n = 2) is supposed to be the most dangerous variant because it can cause an ischemic change in the remaining part of the liver after right hepatectomy. In conclusion, in the era of living donor liver transplantation, paying particular attention to the point of origin of A4 is a prerequisite, especially when the lateral section is relatively small. Arterial injuries to A4 during split liver transplantation may also increase the risk of hepatic artery thrombosis and ischemic cholangiopathy.

Endovascular management of early portal vein thrombosis caused by coronary vein steal after liver transplantation and its outcome.

Early portal vein thrombosis (PVT), after orthotopic liver transplantation (OLT), is relatively uncommon and is a serious complication that can compromise graft and patient survival. The factors predisposing to PVT after OLT include rejection, technical problems during the surgery, use of vein grafts and conduits, preoperative PVT, previous portasystemic shunts and splenectomy, hypercoagulable state, and significant development of gastroesophageal collaterals. Among them, few cases of PVT caused by coronary vein (CV) steal after OLT have been reported. Herein, we present a case with early PVT caused by CV steal after OLT, which is treated by a percutaneous transportal approach, with a review of the relevant literature.