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Background Ambulatory blood pressure monitoring (ABPM) on the oscillometric method is applicable in patients with atrial fibrillation, but the mean pulse rate is or not similar to the ventricular rate from the Holter in atrial fibrillation patients remains unknown. Methods This study included 228 persistent atrial fibrillation patients who received simultaneous 24-h ABPM and 24-h Holter. The mean 24-h pulse rate and the mean 24-h ventricular rate were calculated, and mVR-mPR was used to reflect the difference between them. The SD of 24-h pulse rate values was calculated as SD-pulse rate. Furthermore, according to the SD-pulse rate, the patients were divided into ≤5, 6-10, 11-15 and >15 bpm subgroups. Results For the total population, the mean 24-h pulse rate is positively correlated with the mean 24-h ventricular rate, and the Bland-Altman plot showed quite wide 95% limits. As the SD-pulse rate increased, the 24-h mVR-mPR also increased. The mean 24-h mVR-mPR was 0.5 bpm when SD-pulse rate ≤5, 3.5 bpm when SD-pulse rate of 6-10, 7.6 bpm when SD-pulse rate of 11-15, and 12.5 bpm when SD-pulse rate >15 bpm, respectively. Meanwhile, in the SD-pulse rate 0-10 subgroup, the 95% limits were only from -13.8 to 19.7 bpm, while in the >10 subgroup, these values were from -19.5 to 36.5 bpm. Conclusion The mean 24-h pulse rate should not be used to represent the true ventricular rate for all atrial fibrillation patients. However, when lower the SD-pulse rate, the mVR-mPR becomes smaller.

Herein, we have proposed a colorimetric biosensor for detection of acid phosphatase based on human serum albumin (HSA) templated MnO2 nanosheets (HSA-MnO2 NSs). HSA-MnO2 NSs as an efficient biomimetic oxidase could catalyze the oxidization of 3,3',5,5'-tetramethylbenzidine (TMB) to the coloured oxidation product (oxTMB). Acid phosphatase (ACP) could hydrolyze l-ascorbic acid-2-phosphate (AAP) to produce ascorbic acid, and ascorbic acid could lead to the decomposition of MnO2 NSs to Mn2+ ions, inhibiting the production of oxTMB. On the basis of this, we have demonstrated a novel colorimetric approach for the detection of acid phosphatase with the linear range from 50 μU mL-1 to 1500 μU mL-1 and a detection limit of 40 μU mL-1. The MnO2 NS-based colorimetric method has been successfully used to determine the content of acid phosphatase in real samples with satisfactory results.

The narrow-QRS tachycardias are the most common form of cardiac arrhythmias observed in clinical practice. Most of narrow-QRS tachycardias are with supraventricular origins, i.e., supraventricular tachycardia (SVT). In this chapter, we have focused on differential diagnosis of narrowly defined SVTs, including atrial tachycardia, atrioventricular nodal reentrant tachycardia (AVNRT), and atrioventricular reentrant tachycardia (AVRT), using non-invasive methods at the bedside. Atrial fibrillation and atrial flutter, which belong to broadly defined SVTs, are not specifically discussed. In this chapter, we have also shown usefulness of intracardiac recordings from implantable devices like pacemaker and implantable cardioverter defibrillator in diagnosis of SVT. Finally, we have briefly induced the transesophageal recording and atrial pacing, a versatile non-invasive method that is popularly used for diagnosis and treatment for SVT at the bedside in hospital and clinical settings in some countries.

Nasopharyngeal carcinoma (NPC) has a unique and complex etiology, which is not completely understood. The aim of this study is to investigate the expression patterns of phosphatidylinositol 3-kinase (PI3K), protein kinase B (PKB), and mammalian target of rapamycin (mTOR) proteins in patients with NPC and their relationship with NPC progression and prognosis. Between January 2008 and March 2010, PI3K, PKB, and mTOR protein expressions were detected using immunohistochemistry among 119 patients with NPC and 30 healthy people. A 5-year follow-up was conducted for all patients. Correlations of PI3K, PKB, and mTOR proteins with the clinicopathological features and prognosis of NPC were evaluated using Spearman's rank correlation coefficient and Kaplan-Meier curve. Cox's regression analysis was performed to analyze the risk factors for the prognosis of NPC. First, PI3K, PKB, and mTOR were highly expressed in patients with NPC. The expressions of PI3K, PKB, and mTOR proteins were associated with T stage, N stage, clinical stage, relapse, and distant metastasis. Meanwhile, PI3K is positively correlated with PKB and PKB is positively correlated with mTOR in NPC. Higher PI3K, PKB, and mTOR protein expressions were related to a shorter survival time and a lower survival rate in NPC. Cox regression analysis revealed that age, T stage, N stage, PI3K, PKB, and mTOR were independent risk factors for NPC patient survival. Altogether, our data suggest that overexpression of PI3K, PKB, and mTOR proteins is an important indicator of poor survival in NPC. In addition, inhibition of PI3K-PKB-mTOR signaling may also contribute to the development of new therapeutic strategies for NPC.

Docetaxel is a novel type of chemotherapy drug that actively treats a number of malignant tumors. The aim of the present study was to explore the severity and natural course of tissue damage induced by docetaxel extravasation and to confirm the vesicant potential of docetaxel. Rats were selected for the establishment of the ulcer model. Different volumes and concentrations were explored to induce the skin ulcer and to confirm the optimum rational injection model. The natural course of tissue injury and pathological changes produced by docetaxel extravasation were observed by comparing to vinorelbine extravasation. A 0.4 ml volume and a 6 mg/ml concentration were the optimum rational injection model for the induction of the skin ulcer. The docetaxel extravasation induced local tissue necrosis, followed by granuloma formation and hyperpigmentation or scar formation. The severity of the injury depended on the concentration of the extravasation used in the rat model. The injury occurred on the first day following extravasation and lasted 4-6 weeks. The damage from docetaxel was weaker than vinorelbine in association with the depth and extension of necrosis. In conclusion, docetaxel extravasation can induce tissue necrosis. However, the severity of necrosis was weaker than that of vinorelbine. Docetaxel has superficial vesicant properties.

A new phthalocyanine material, 2,9,16,23-tetrakis [4-(hexafluoroisopropanol)-anilinomethyl]phthalocyaninato zinc (ZnPcF 24 N 4 O 4 ) was designed and synthesized. The chemoselective material was coated on a 300 MHz surface acoustic wave (SAW) device using cyclic voltammetry for the detection of sarin (GB) vapor. It was found that the observed frequency shifts were linear to the concentrations of sarin in the range of 0.6–43.4 mg/m 3 with a high sensitivity of 205.8 Hz/mg/m 3 . The influences of other interfering vapors on the sensor response were also examined. The results showed that the phthalocyanine-based SAW sensor exhibited a fairly fast response, excellent reversibility, linearly sensitivity, and a high selectivity to vapor of the organophosphorus nerve agent GB.

Immunophenotype is critical for diagnosing common B-cell acute lymphoblastic leukemia (common ALL) and detecting minimal residual disease. We developed a protocol to explore the immunophenotypic profiles of common ALL based on the expression levels of the antigens associated with B lymphoid development, including IL-7Rα (CD127), cytoplasmic CD79a (cCD79a), CD19, VpreB (CD179a), and sIgm, which are successive and essential for progression of B cells along their developmental pathway. Analysis of the immunophenotypes of 48 common ALL cases showed that the immunophenotypic patterns were highly heterogeneous, with the leukemic cell population differing from case to case. Through the comprehensive analysis of immunophenotypic patterns, the profiles of patient-specific composite leukemia cell populations could provide detailed information helpful for the diagnosis, therapeutic monitoring, and individualized therapies for common ALL.

Hypertrophy of non-clamped liver lobes and the atrophy of clamped lobes have been shown to be interactive. Here, a rat model of selective lobe occlusion was established to study the effect of contralateral ischemia/reperfusion (I/R) on regeneration of non-clamped lobes.Left lateral and middle liver lobes were pretreated with I/R. In the experimental (IR + PVL) group, portal veins of the left and middle lobes were ligated. A group given similar portal vein ligation but no I/R (PVL) was the positive control.Compared with the PVL group, the IR + PVL had higher, but not remarkable, levels of serum transaminases; weights of non-clamped lobes in the IR + PVL group comparatively increased much more notably. At 24-h post-surgery, the IR + PVL group's PCNA mRNA was up-regulated compared with the PVL group. At 72-h post-surgery, PCNA protein was up-regulated significantly, while TGF-β1 was down-regulated in the IR + PVL group notably, compared with the PVL group.The I/R pretreatment given to the clamped lobes facilitates liver regeneration of non-clamped lobes after selective portal vein ligation, which may result from down-regulated TGF-β1 expression in non-clamped lobes.

Cyclin-dependent kinase 10 (Cdk10) is a Cdc2-related kinase and plays an essential role in the progression from the G2 to M phase of the cell cycle. However, relative little is known about its expression pattern, clinical relevance, and biological function in hepatocellular carcinoma (HCC). In the present study, we investigated the mRNA and protein expression levels of Cdk10 in 127 pairs of HCC samples and adjacent nontumorous liver tissues and evaluated its clinical significance. Additionally, we assessed the effects of restoration of Cdk10 on cell proliferation and drug sensitivity in HCC cells. We showed that the Cdk10 mRNA and protein expression was markedly decreased in HCC samples compared to adjacent nontumorous liver tissues. Quantitative real-time polymerase chain reaction and immunohistochemical studies revealed that reduced Cdk10 expression was significantly associated with alpha-fetoprotein levels, tumor size, and tumor stage. Ectopic expression of Cdk10 reduced HCC cell proliferation, blocked the cell cycle at the G0-G1 phase, as well as inhibited cell migration and anchorage-independent growth. Additionally, Cdk10 overexpression enhanced the chemosensitivity of HCC cells to cisplatin and epidoxorubicin, two chemotherapeutic agents commonly used in HCC. These data collectively demonstrate that reduced Cdk10 expression is closely linked to HCC development and progression. Restoration of its expression may have therapeutic benefits in treating this malignancy.

Cyclin-dependent kinase 10 (CDK10) is a member of the Cdc2 family of kinases, and has been demonstrated to be an important determinant of resistance to endocrine therapy for breast cancer. To investigate the expression and possible function of CDK10 in biliary tract cancer (BTC), we systematically examined CDK10 in tissues and cell lines. We found that expression of CDK10 was downregulated in both biliary tract tumors and cell lines. Remarkably, the expression of CDK10 correlated with clinical characteristics. Overexpression or knockdown of CDK10, respectively, inhibited or promoted cell proliferation, colony formation and migration. This suggests that CDK10 functions as a tumor suppressor gene in BTC. Overexpression of CDK10 caused malignant cells to become sensitive to chemotherapy and other hostile environments, suggesting that CDK10 functions to regulate survivability of BTC cells. We investigated the expression of six genes to resolve the mechanism. c-RAF was negatively regulated by CDK10 in both cells and specimens. Our results indicate that CDK10 plays a crucial role in the growth and survivability of biliary tract cancer, and offers a potential therapeutic target for this fatal disease.

Adenosquamous carcinoma rarely occurs in the pancreas, and is characterized by the presence of cellular components from both duct adenocarcinoma and squamous carcinoma. Here, we describe a rare case of pancreatic adenosquamous carcinoma with sarcomatous change. Immunohistochemistry showed that the sarcomatous lesion lost the epithelial marker and aberrantly expressed of acquired mesenchymal markers, which indicated that this special histological phenotype may be attributed to epithelial-mesenchymal transition. This case also indicated that a routine radical surgery without aggressive treatment strategies was still appropriate for adenosquamous carcinoma of the pancreas with sarcomatoid change.

Background Oxidative stress and inflammation are implicated in the process of liver regeneration. Lactulose orally administered can be bacterially fermented and induces dramatic amounts of endogenous hydrogen. Hydrogen has been confirmed to have antioxidant and anti-inflammatory properties. This study investigated the potential influence of lactulose administration on liver regeneration. Materials and methods Antibiotics were used to suppress bacterial fermentation of lactulose, and hydrogen-rich saline was used as a supplementary measure of exogenous hydrogen. The liver regeneration model was produced in Sprague–Dawley rats through 70% partial hepatectomy. Results Compared with non–lactulose-treated group, lactulose administration remarkably increased the weights of remnant liver and inhibited increases in serum levels of transaminases more notably. In the lactulose-treated group, increases of markers for regeneration, such as proliferating cell nuclear antigen and cyclin D1, were highly elevated. Biochemically, lactulose administration increased liver superoxide dismutase activity and decreased malondialdehyde content. In the lactulose-treated group, excessive increases in inflammatory cytokines, such as interleukin-6 and tumor necrosis factor-α, were inhibited significantly. Increased heme oxygenase-1 and superoxide dismutase 2 expression were also observed after lactulose treatment. The antibiotics suppressed the regeneration-promoting effect of lactulose by reducing hydrogen production, whereas supplementing hydrogen by hydrogen-rich saline would get a similar regeneration-promoting effect as lactulose administration. Conclusions Lactulose administration accelerates posthepatectomized liver regeneration in rats by inducing hydrogen, which may result from attenuation of the oxidative stress response and excessive inflammatory response.

In mammalian species, ovulation occurs following a massive release of hypothalamic gonadotropin-releasing hormone (GnRH). Several chemicals, including norepinephrine (NE) and neuropeptide Y (NPY), are responsible for the initiation and/or magnitude and duration of this pre-ovulatory GnRH surge. In the central nervous system, NE neural cell bodies are located in the brainstem; some are co-localized with NPY neurons and/or co-express the NE transporter (NET) gene which dictates NET protein production. The activity of NET at NE terminals is critical for synaptic NE function. In the rabbit, coitus induces a hypothalamic NE release which precedes the GnRH surge. We hypothesize that the coital stimulus is transmitted to the brainstem and transformed and integrated into GnRH-stimulating signals via NE, NET and/or NPY. However, very little is known about the distribution of cells expressing NET, NPY and tyrosine hydroxylase (TH, the rate-limiting enzyme of NE synthesis) in this species. Therefore, we utilized the sensitive in situ hybridization technique to identify the presence of these messages in conjunction with the location of NE cells, the latter being marked by dopamine β-hydroxylase (DBH), the specific enzyme for NE synthesis. Three non-mated New Zealand White does were perfused with 4% paraformaldeyde and their brainstems were sectioned at 20-μm thick between 2 mm caudal to the obex and the rostral pons. Serial sections were immunohistochemically stained for DBH and hybridized with rabbit-specific TH and NET cRNAs and a human NPY probe. The data suggest that several DBH-positive areas in the medulla expressed one or more messages, i.e. the lateral tegmentum (A1) and the nucleus of the solitary tract (A2) expressed all three mRNAs, the area postrema (AP) contained NET and TH mRNAs but not NPY cells. In the pons, the locus coeruleus (LC), subnucleus of coeruleus (LCs) and lateral tegmental nuclei (A5) expressed NET and TH mRNAs but contained little or no NPY message. The distribution patterns of TH and NET appeared to be similar in the LC, LCs, A2 and AP.

MicroRNAs (miRNAs) are involved in the development of most cancers. However, few studies have been conducted to determine their relationship to biliary tract cancer (BTC). Farnesoid X receptor (FXR) has been reported to be a tumor suppressor for hepatocellular carcinoma and breast cancer; but few studies have focused on its correlation with BTC. In this study, we identified miR-421 as a potential regulator of FXR expression. We found that their expression amount was inversely correlated as FXR was aberrantly down-regulated in both primary tumor specimens and cell lines; while miR-421 was significantly up-regulated. Ectopic expression of miR-421 significantly decreased FXR protein concentration in BTC cells and promoted cell proliferation, colony formation and migration in vitro. Furthermore, a decrease in miR-421 expression induced G(0)/G(1) cell cycle arrest. In conclusion, our study identified microRNA-421 functions as an oncomiR in BTC by targeting FXR. This finding may provide a novel therapeutic strategy for treatment of biliary tract cancer.

Gastric cancer is the fourth most common cancer worldwide, with a high rate of death and low 5-year survival rate. To date, there is a lack of efficient therapeutic protocols for gastric cancer. Recent studies suggest that cancer stem cells (CSCs) are responsible for tumor initiation, invasion, metastasis, and resistance to anticancer therapies. Thus, therapies that target gastric CSCs are attractive. However, CSCs in human gastric adenocarcinoma (GAC) have not been described. Here, we identify CSCs in tumor tissues and peripheral blood from GAC patients. CSCs of human GAC (GCSCs) that are isolated from tumor tissues and peripheral blood of patients carried CD44 and CD54 surface markers, generated tumors that highly resemble the original human tumors when injected into immunodeficient mice, differentiated into gastric epithelial cells in vitro, and self-renewed in vivo and in vitro. Our findings suggest that effective therapeutic protocols must target GCSCs. The capture of GCSCs from the circulation of GAC patients also shows great potential for identification of a critical cell population potentially responsible for tumor metastasis, and provides an effective protocol for early diagnosis and longitudinal monitoring of gastric cancer.

Bile duct injuries (BDIs) are difficult to avoid absolutely when the biliary tract has a malformation, such as accessory hepatic duct. Here, we investigated the management strategies for BDI combined with accessory hepatic duct during laparoscopic cholecystectomy.

Between 1995 and 1999, 12 difficult primary total hip arthroplasties were performed on 7 patients (7 hips) with failed initial treatment of traumatic dislocation of the hip and 5 patients (5 hips) with untreated congenital dislocation of the hip. The arthroplasties were performed in the position of the true acetabulum in all patients who had either congenital or posttraumatic dislocation of the hip. After a mean follow-up of 24 months, 11 hips showed considerable improvement concerning pain, gait, and mobility based on Harris’ score, except that 1 had sciatic nerve injury due to over- lengthening of the limb. Although it is technically demanding and presents a difficult surgical problem, total hip arthroplasty is a reasonable treatment option and satisfactory solution for patients who present with either failed treatment of traumatic fracture and dislocation of the hip or painful neglected congenital dislocation of the hip.