Cavernous hemangiomas of the temporalis muscle with prominent formation of phleboliths: Case report and review of the literature.

Rationale: Hemangiomas are benign tumors characterized by an abnormal proliferation of blood vessels, most often occur in the skin and subcutaneous tissue, intramuscular hemangioma, a distinctive type of hemangioma within the skeletal muscle, account for <1% of all hemangiomas, temporalis muscle is a very uncommon site, cavernous hemangioma of the temporalis muscle with prominent formation of phleboliths is rare reported.

Patient Concerns: A 62-year-old man presented with a slowly increased mass in his right temporal fossa.

Diagnoses: Computed tomography (CT) scan showed the lesion across the zygomatic arch, with many calcified nodules differ in sizes and no erosion to the bone, magnetic resonance imaging (MRI) showed an oval lesion with hypointense and isointense on T2-weighted imaging within the temporal muscle, and preoperation diagnosis was hemangioma.

Effect of artesunate supplementation on bacterial translocation and dysbiosis of gut microbiota in rats with liver cirrhosis.

Aim: To evaluate the effect of artesunate (AS) supplementation on bacterial translocation (BT) and gut microbiota in a rat model of liver cirrhosis.

Methods: Fifty-four male Sprague-Dawley rats were randomly divided into a normal control group (N), a liver cirrhosis group (M) and a liver cirrhosis group intervened with AS (MA). Each group was sampled at 4, 6 and 8 wk.

[Protective effect of tanshinol on the hepatopulmonary syndrome in rat].

Objective: To explore the mechanism of tanshinol on alleviate the inflammatory injury of lung tissue in rat hepatopulmonary syndrome (HPS).

Methods: SD rats were randomly divided into normal control group (n = 8), hepatopulmonary syndrome (HPS) group (n = 11) and tanshinol intervention group (n = 9). HE staining was used to observe the histopathology changes of pulmonary and hepatic tissues, and to count the number of macrophages in lung tissues.

Heme oxygenase-1 prevents liver fibrosis in rats by regulating the expression of PPARγ and NF-κB.

Aim: To investigate the effects of heme oxygenase (HO)-1 on liver fibrosis and the expression of peroxisome proliferator-activated receptor gamma (PPARγ) and nuclear factor-kappa B (NF-κB) in rats.

Methods: Sixty Wistar rats were used to construct liver fibrosis models and were randomly divided into 5 groups: group A (normal, untreated), group B (model for 4 wk, untreated), group C (model for 6 wk, untreated), group D [model for 6 wk, treated with zinc protoporphyrin IX (ZnPP-IX) from week 4 to week 6], group E (model for 6 wk, treated with hemin from week 4 to week 6). Next, liver injury was assessed by measuring serum alanine aminotransferase (ALT), aspartate aminotransferase (AST) and albumin levels.

Preparation and characterization of coverage-controlled CaCO3 nanoparticles.

CaCO(3) nanoparticles were coated with stearate through a salt-exchange procedure. Their coverage had been successfully controlled by extraction in a Soxhlet apparatus, based on which a series of CaCO(3) nanoparticles were obtained with different surface coverages. They were characterized with thermogravimetric analysis, X-ray photoelectron spectroscopy and Fourier transform infrared spectroscopy.

Intestinal endotoxemia plays a central role in development of hepatopulmonary syndrome in a cirrhotic rat model induced by multiple pathogenic factors.

Aim: To characterize the correlation between severity of hepatopulmonary syndrome (HPS) and degree of hepatic dysfunction, and to explore how intestinal endotoxemia (IETM) affects the development of HPS in cirrhotic rats.

Methods: Male Wister rats were fed with a diet containing maize flour, lard, cholesterol, and alcohol and injected subcutaneously with CCl(4) oil solution every two days for 8 wk to induce typical cirrhosis and development of HPS. The animals were also given a nitric oxide (NO) production inhibitor, N(omega)-nitro-L-arginine methyl ester (L-NAME) intraperitoneally, and an iNOS inhibitor, aminoguanidine hydrochloride (AG) via gavage daily from the end of the 4th wk to the end of the 6th or 8th wk, or a HO-1 inhibitor, zinc protoporphyrin (ZnPP) intraperitoneally 12 h prior to killing.

[Expression of HMGB-1 and its extracellular release of cultured primary hepatic parenchymal cells and Kupffer cells induced by LPS].

Objective: To investigate HMGB-1 expression and its extracellular release of cultured primary hepatic parenchymal cells (HC) and Kupffer cells (KC) that were induced by lipopolysaccharides (LPS).

Methods: Primary hepatic parenchymal cells and Kupffer cells were cultured in flasks, and some cells were treated with 500 microg/L LPS for 24 hours (induced group) and some were not treated with LPS and served as controls. All of the cells were repeatedly frozen-thawed, and the expression levels of HMGB1-mRNA and HMGB1 proteins were detected by semi-quantitative RT-PCR and Western blot respectively.

Multiple pathogenic factor-induced complications of cirrhosis in rats: a new model of hepatopulmonary syndrome with intestinal endotoxemia.

Aim: To develop and characterize a practical model of Hepatopulmonary syndrome (HPS) in rats.

Methods: The experimental animals were randomized into five feeding groups: (1) control (fed standard diet), (2) control plus intraperitoneal injection with lipopolysaccharide (LPS), (3) cirrhosis (fed a diet of maize flour, lard, cholesterol, and alcohol plus subcutaneously injection with carbon tetrachloride (CCl(4)) oil solution), (4) cirrhosis plus LPS, and (5) cirrhosis plus glycine and LPS. The blood, liver and lung tissues of rats were sampled for analysis and characterization.

Inhibition of hepatitis B virus expression and replication by RNA interference in HepG2.2.15.

Aim: To observe the inhibition of hepatitis B virus replication and expression by transfecting vector-based small interference RNA (siRNA) pGenesil-HBV X targeting HBV X gene region into HepG2.2.15 cells.

[A new method for amplification and sequence analysis of the full-length of HBV genome].

Objectives: To develop a new method for amplifying and sequencing the full-length of HBV genome.

Methods: A pair of primers located at the nick region of HBV molecule and a thermostable polymerase with high fidelity and sensitivity were used. After cloning the PCR products into a plasmid, the sequences of HBV genome were analyzed.