The effect of posterior cruciate ligament tibial avulsion fracture on functional outcomes in knees with concomitant ipsilateral lower limb fractures: a matched-cohort analysis.

BACKGROUND: At present, the optimal treatment for posterior cruciate ligament tibial avulsion fracture (PCLTAF) combined with concomitant ipsilateral lower limb fractures remains unclear. The present study aimed to assess the preliminary outcomes of treatment for PCLTAF with concomitant ipsilateral lower limb fractures by open reduction and internal fixation (ORIF). MATERIALS AND METHODS: The medical records of patients who sustained PCLTAF with concomitant ipsilateral lower limb fractures between March 2015 and February 2019 and underwent treatment at a single institution were retrospectively reviewed. Imaging examinations performed at the time of injury were applied to identify concomitant ipsilateral lower limb fractures. We used 1:2 matching between patients with PCLTAF combined with concomitant ipsilateral lower limb fractures (combined group; n = 11) and those with isolated PCLTAF (isolated group; n = 22). Outcome data were collected, including the range of motion (ROM) and visual analogue scale (VAS), Tegner, Lysholm, and International Knee Documentation Committee (IKDC) scores. At the final follow-up, the clinical outcomes were compared between the combined and isolated groups and between patients who underwent early-stage surgery and those who underwent delayed treatment for PCLTAF. RESULTS: Thirty-three patients (26 males, 7 females) were included in this study, with eleven patients having PCLTAF and concomitant ipsilateral lower limb fractures and a follow-up of 3.1 to 7.4 years (average, 4.8 years). Compared to patients in the isolated group, patients in the combined group demonstrated significantly worse Lysholm scores (85.7 ± 5.8 vs. 91.5 ± 3.9, p = 0.040), Tegner scores (4.4 ± 0.9 vs. 5.4 ± 0.8, p = 0.006), and IKDC scores (83.6 ± 9.3 vs. 90.5 ± 3.0, p = 0.008). Inferior outcomes were found in patients with delayed treatment. CONCLUSIONS: Inferior results were found in patients with concomitant ipsilateral lower limb fractures, while better outcomes were obtained in patients with PCLTAF through early-stage ORIF using the posteromedial approach. The present findings may help determine the prognoses of patients with PCLTAF combined with concomitant ipsilateral lower limb fractures treated through early-stage ORIF.

MD1 deletion exaggerates cardiomyocyte autophagy induced by heart failure with preserved ejection fraction through ROS/MAPK signalling pathway.

In our previous studies, we reported that myeloid differentiation protein 1 (MD1) serves as a negative regulator in several cardiovascular diseases. However, the role of MD1 in heart failure with preserved ejection fraction (HFpEF) and the underlying mechanisms of its action remain unclear. Eight-week-old MD1-knockout (MD1-KO) and wild-type (WT) mice served as models of HFpEF induced by uninephrectomy, continuous saline or d-aldosterone infusion and a 1.0% sodium chloride treatment in drinking water for 4 weeks to investigate the effect of MD1 on HFpEF in vivo. H9C2 cells were treated with aldosterone to evaluate the role of MD1 KO in vitro. MD1 expression was down-regulated in the HFpEF mice; HFpEF significantly increased the levels of intracellular reactive oxygen species (ROS) and promoted autophagy; and in the MD1-KO mice, the HFpEF-induced intracellular ROS and autophagy effects were significantly exacerbated. Moreover, MD1 loss activated the p38-MAPK pathway both in vivo and in vitro. Aldosterone-mediated cardiomyocyte autophagy was significantly inhibited in cells pre-treated with the ROS scavenger N-acetylcysteine (NAC) or p38 inhibitor SB203580. Furthermore, inhibition with the autophagy inhibitor 3-methyladenine (3-MA) offset the aggravating effect of aldosterone-induced autophagy in the MD1-KO mice and cells both in vivo and in vitro. Our results validate a critical role of MD1 in the pathogenesis of HFpEF. MD1 deletion exaggerates cardiomyocyte autophagy in HFpEF via the activation of the ROS-mediated MAPK signalling pathway.

Knockout of MD1 contributes to sympathetic hyperactivity and exacerbates ventricular arrhythmias following heart failure with preserved ejection fraction via NLRP3 inflammasome activation.

NEW FINDINGS: What is the central question of this study? In this study, we investigated whether MD1 interacted with the sympathetic nerves in ventricular arrhythmia (VA) during heart failure with preserved ejection fraction (HFpEF). What is the main finding and its importance? Mice with HFpEF showed increased susceptibility to VA, adverse electrical remodelling, impaired heart rate variability, enhanced sympathetic hyperactivity, activation of the NLRP3 inflammasome and increased interleukin-1ß release. These changes induced by HFpEF were exacerbated by MD1 deficiency. ABSTRACT: Sympathetic hyperactivity can promote malignant ventricular arrhythmia (VA), and myeloid differentiation 1 (MD1) has been reported to play an important role in obesity-induced VA. However, it is not known whether an interaction of MD1 with sympathetic hyperactivity contributes to the VA induced by heart failure with preserved ejection fraction (HFpEF). The aim of this study was to investigate the potential interaction between MD1 and sympathetic hyperactivity in HFpEF-induced VA and the underlying mechanism. Eight-week-old MD1-knockout (MD1-KO) and wild-type (WT) mice were subjected to a model of HFpEF induced by uninephrectomy, a continuous saline or d-aldosterone infusion and provision of drinking water containing 1.0% sodium chloride for 4 weeks. Echocardiography and haemodynamics were used to verify the model of HFpEF. An isolated electrophysiological study was performed to assess the susceptibility to VA. Four weeks later, the mice with HFpEF showed an increased heart weight to tibia length ratio, decreased left ventricular minimum rates of pressure rise (dP/dtmin ), increased τ, lung weight to tibia length ratio and preserved left ventricular ejection fraction compared with WT mice. The mice with HFpEF exhibited increased susceptibility to VA, as shown by the shortened effective refractory period, prolonged action potential duration (APD), increased APD alternans threshold and higher incidence of VA. Moreover, we also found that mice with HFpEF showed impaired heart rate variability, sympathetic hyperactivity, activation of the NLRP3 inflammasome and increased interleukin-1ß release. These changes induced by HFpEF were exacerbated by MD1 deficiency. We conclude that MD1-KO contributes to sympathetic hyperactivity and facilitates VA in HFpEF via activation of the NLRP3 inflammasome. Treatment targeting MD1 and NLRP3 might decrease the risk of HFpEF-induced VA.

The Value of the CHADS2 and CHA2DS2-VASc Score for Predicting the Prognosis in Lacunar Stroke with or without Atrial Fibrillation Patients.

BACKGROUND: The CHADS2 and CHA2DS2-VASc scoring systems have been proved efficacy to stratify stroke and thromboembolism risk in patients with atrial fibrillation (AF). Whether CHADS2 and CHA2DS2-VASc score has predictive value for the prognosis in lacunar stroke (LS) patients remains unclear. METHODS: A total of 763 consecutive patients with LS (mean age: 66 ± 12 years; 464 male) were enrolled in this study between January 2013 and December 2014. Patients were divided into LS without AF (LS; n = 679) and LS with AF (LS-AF; n = 84) groups. Measures of performance for the risk scores were evaluated at predicting mortality and restroke in LS-AF and LS without AF patients. All patients were evaluated with respect to clinical features and in-hospital clinical results. RESULTS: During the mean follow-up period of 20 ± 5.8 months, 29 patients (3.8%) experienced all-cause death, 105 patients (13.8%) experienced recurrence of ischemic stroke. Multivariate analysis revealed that CHADS2 and CHA2DS2-VASc score were independently associated with all-cause death (all P < .05). On receiver operating characteristic curve analysis, area under the curve (AUC) for CHADS2 score was .942 with a similar accuracy of the CHA2DS2-VASc score (AUC: .908) in predicting mortality in LS-AF patients. Kaplan-Meier curves were conducted according to the cut-off value of CHA2DS2-VASc score. When CHADS2 score greater than or equal to 4 point or CHA2DS2-VASc score greater than or equal to 5 point, the mortality in LS-AF patients was significantly higher compared with those CHADS2 score less than 4 point or CHA2DS2-VASc score less than 5 point. However, after adjusting for clinical covariates, CHADS2 and CHA2DS2-VASc score could not predict both mortality and restroke in LS without AF patients. CONCLUSIONS: The CHADS2 and CHA2DS2-VASc score have excellent predictive value for mortality in LS-AF patients but could not predict both mortality and restroke in LS without AF patients.

Usefulness of Red Blood Cell Distribution Width to Predict Heart Failure Hospitalization in Patients with Hypertrophic Cardiomyopathy.

Red cell distribution width (RDW) has been associated with heart failure (HF) hospitalization in the general population, but the correlation to HF hospitalization in patients with hypertrophic cardiomyopathy (HCM) is unclear.Ninety-eight HCM patients without a history of HF were enrolled and RDW was assessed as a predictor.During a 16.8 ± 9.0 month follow-up period, 17 subjects were hospitalized due to HF. HF hospitalization patients had higher RDW than non-HF patients (14.7 ± 1.4% versus 13.0 ± 0.9%, P < 0.001). The cut-off value of RDW for predicting HF hospitalization was 14% with a sensitivity of 83.2% and a specificity of 82.7%. Multivariate analysis demonstrated that brain natriuretic protein (BNP) (HR 1.028, 95% CI 1.011-1.045, P = 0.001) and RDW (HR 1.711, 95% CI 1.042-2.809, P = 0.034) were predictors of HF hospitalization.High RDW is an independent predictor of HF hospitalization and might be useful for predicting the prognosis in HCM patients.

Inhibitory Mechanism of Epigallocatechin Gallate on Fibrillation and Aggregation of Amidated Human Islet Amyloid Polypeptide.

The abnormal fibrillation of human islet amyloid polypeptide (hIAPP) is associated with development of type II diabetes mellitus (T2DM). (-)-Epigallocatechin gallate (EGCG) can bind amyloid proteins to inhibit the fibrillation of these proteins. However, the mechanic detail of EGCG inhibiting amyloid formation is still unclear at the molecular level. In the present work, we sought to investigate the effect of EGCG on amidated hIAPP (hIAPP-NH2 ) fibrillation and aggregation by using spectroscopic and microscopic techniques, and also sought to gain insights into the interaction of EGCG and hIAPP22-27 by using spectroscopic experiments and quantum chemical calculations. ThT fluorescence, real-time NMR, and TEM studies demonstrated that EGCG inhibits the formation of hIAPP-NH2 fibrils, while promoting the formation of hIAPP-NH2 amorphous aggregates. Phenylalanine intrinsic fluorescence and NMR studies of the EGCG/hIAPP22-27 complex revealed three important binding sites including the A ring of EGCG, residue Phe23, and residue Ile26. DFT calculations identified the dominant binding structures of EGCG/Phe23 and EGCG/Ile26 complexes, named structure I and structure II, respectively. Our study demonstrates the inhibitory mechanism of EGCG on fibrillation and aggregation of hIAPP-NH2 in which EGCG interacts with hIAPP-NH2 through hydrogen bonding and π-π interactions between the A ring and residue Phe23 as well as hydrophobic interactions between the A ring and residue Ile26, which can thus inhibit the interpeptide interaction between hIAPP-NH2 monomers and finally inhibit fibrillation of hIAPP-NH2 . This study agrees with and reinforces previous studies and offers an intuitive explanation at both the atomic and molecular levels. Our findings may provide an invaluable reference for the future development of new drugs in the management of diabetes.

Self-seeded growth of five-fold twinned copper nanowires: mechanistic study, characterization, and SERS applications.

A comprehensive mechanistic study conducted on the formation mechanism of five-fold twinned copper nanowires by heating copper(I) chloride with oleylamine at 170 °C is presented. Electron microscopy and UV-visible absorption spectra are used to analyze the growth mechanism of copper nanowires. High-resolution transmission electron microscopy and selected-area electron diffraction are used to investigate the detailed structure of copper nanowires and nanoparticles, and a five-twinned structure is shown to exist in the copper nanowires and nanoparticles. Additionally, experiments have been performed to indirectly confirm that oleylamine preferentially adsorbs on the {100} facets of growing crystals. On the basis of the above results, the self-seeded growth of copper nanowires is confirmed. In the initial stage of reactions, copper nanoparticles with two distinctive sizes are formed. As the reaction proceeds, larger five-twinned copper nanoparticles serve as seeds for anisotropic crystal growth. Further, copper atoms generated from an Ostwald ripening process or reduction reactions of a copper(I) chloride-oleylamine complex continue to deposit and crystallize on the twin boundaries. Once the {110} planes are generated, oleylamine preferentially adsorbs on the newly formed {100} facets and then guides the formation of nanowires. The electrical resistivity of a single copper nanowire is measured to be 41.25 nΩ-m, which is of the same order of magnitude as the value of bulk copper (16.78 nΩ-m). Finally, an effective surface-enhanced Raman spectroscopy active substrate made of copper nanowire is used to detect the 4-mercaptobenzoic acid molecules.

Electrical spin injection and detection in Mn5Ge3/Ge/Mn5Ge3 nanowire transistors.

In this Letter, we report the electrical spin injection and detection in Ge nanowire transistors with single-crystalline ferromagnetic Mn5Ge3 as source/drain contacts formed by thermal reactions. Degenerate indium dopants were successfully incorporated into as-grown Ge nanowires as p-type doping to alleviate the conductivity mismatch between Ge and Mn5Ge3. The magnetoresistance (MR) of the Mn5Ge3/Ge/Mn5Ge3 nanowire transistor was found to be largely affected by the applied bias. Specifically, negative and hysteretic MR curves were observed under a large current bias in the temperature range from T = 2 K up to T = 50 K, which clearly indicated the electrical spin injection from ferromagnetic Mn5Ge3 contacts into Ge nanowires. In addition to the bias effect, the MR amplitude was found to exponentially decay with the Ge nanowire channel length; this fact was explained by the dominated Elliot-Yafet spin-relaxation mechanism. The fitting of MR further revealed a spin diffusion length of lsf = 480 ± 13 nm and a spin lifetime exceeding 244 ps at T = 10 K in p-type Ge nanowires, and they showed a weak temperature dependence between 2 and 50 K. Ge nanowires showed a significant enhancement in the measured spin diffusion length and spin lifetime compared with those reported for bulk p-type Ge. Our study of the spin transport in the Mn5Ge3/Ge/Mn5Ge3 nanowire transistor points to a possible realization of spin-based transistors; it may also open up new opportunities to create novel Ge nanowire-based spintronic devices. Furthermore, the simple fabrication process promises a compatible integration into standard Si technology in the future.

Sorafenib plus transarterial chemoembolization vs sorafenib alone for patients with advanced hepatocellular carcinoma: A systematic review and meta-analysis.

BACKGROUND: Although the past decade has seen remarkable advances in treatment options for hepatocellular carcinoma (HCC), the dismal overall prognosis still envelops HCC patients. Several comparative trials have been conducted to study whether transarterial chemoembolization (TACE) could improve clinical outcomes in patients receiving sorafenib for advanced HCC; however, the findings have been inconsistent. AIM: To study the potential synergies and safety of sorafenib plus TACE vs sorafenib alone for treating advanced HCC, by performing a systematic review and meta-analysis. METHODS: This study was conducted following the PRISMA statement. A systematic literature search was conducted using the Cochrane Library, Embase, PubMed, and Web of Science databases. Data included in the present work were collected from patients diagnosed with advanced HCC receiving sorafenib plus TACE or sorafenib alone. Data synthesis and meta-analysis were conducted using Review Manager software. RESULTS: The present study included 2780 patients from five comparative clinical trials (1 was randomized control trial and 4 were retrospective studies). It was found that patients receiving sorafenib plus TACE had better prognoses in terms of overall survival (OS), with a combined hazard ratio (HR) of 0.65 [95% confidence interval (95%CI): 0.46-0.93, P = 0.02, n = 2780]. Consistently, progression free survival (PFS) and time to progression (TTP) differed significantly between the sorafenib plus TACE arm and sorafenib arm (PFS: HR = 0.62, 95%CI: 0.40-0.96, P = 0.03, n = 443; TTP: HR = 0.73, 95%CI: 0.64-0.83, P < 0.00001, n = 2451). Disease control rate (DCR) was also significantly increased by combination therapy (risk ratio = 1.36, 95%CI: 1.02-1.81, P = 0.04, n = 641). Regarding safety, the incidence of any adverse event (AE) was increased due to the addition of TACE; however, no significant difference was found in grade ≥ 3 AEs. CONCLUSION: The combination of sorafenib with TACE has superior efficacy to sorafenib monotherapy, as evidenced by prolonged OS, PFS, and TTP, as well as increased DCR. Additional high-quality trials are essential to further validate the clinical benefit of this combination in the treatment of advanced HCC.

Comprehensive profiling of Epstein-Barr virus-encoded miRNA species associated with specific latency types in tumor cells.

BACKGROUND: Epstein-Barr virus (EBV) is an etiological cause of many human lymphocytic and epithelial malignancies. EBV expresses different genes that are associated with three latency types. To date, as many as 44 EBV-encoded miRNA species have been found, but their comprehensive profiles in the three types of latent infection that are associated with various types of tumors are not well documented. METHODS: In the present study, we utilized poly (A)-tailed quantitative real-time RT-PCR in combination with microarray analysis to measure the relative abundances of viral miRNA species in a subset of representative lymphoid and epithelial tumor cells with various EBV latency types. RESULTS: Our findings showed that the miR-BHRF1 and miR-BART families were expressed differentially in a tissue- and latency type-dependent manner. Specifically, in nasopharyngeal carcinoma (NPC) tissues and the EBV-positive cell line C666-1, the miR-BART family accounted for more than 10% of all detected miRNAs, suggesting that these miRNAs have important roles in maintaining latent EBV infections and in driving NPC tumorigenesis. In addition, EBV miRNA-based clustering analysis clearly distinguished between the three distinct EBV latency types, and our results suggested that a switch from type I to type III latency might occur in the Daudi BL cell line. CONCLUSIONS: Our data provide a comprehensive profiling of the EBV miRNA transcriptome that is associated with specific tumor cells in the three types of latent EBV infection states. EBV miRNA species represent a cluster of non-encoding latency biomarkers that are differentially expressed in tumor cells and may help to distinguish between the different latency types.

Electrical probing of magnetic phase transition and domain wall motion in single-crystalline Mn5Ge3 nanowire.

In this Letter, the magnetic phase transition and domain wall motion in a single-crystalline Mn(5)Ge(3) nanowire were investigated by temperature-dependent magneto-transport measurements. The ferromagnetic Mn(5)Ge(3) nanowire was fabricated by fully germaniding a single-crystalline Ge nanowire through the solid-state reaction with Mn contacts upon thermal annealing at 450 °C. Temperature-dependent four-probe resistance measurements on the Mn(5)Ge(3) nanowire showed a clear slope change near 300 K accompanied by a magnetic phase transition from ferromagnetism to paramagnetism. The transition temperature was able to be controlled by both axial and radial magnetic fields as the external magnetic field helped maintain the magnetization aligned in the Mn(5)Ge(3) nanowire. Near the magnetic phase transition, the critical behavior in the 1D system was characterized by a power-law relation with a critical exponent of α = 0.07 ± 0.01. Besides, another interesting feature was revealed as a cusp at about 67 K in the first-order derivative of the nanowire resistance, which was attributed to a possible magnetic transition between two noncollinear and collinear ferromagnetic states in the Mn(5)Ge(3) lattice. Furthermore, temperature-dependent magneto-transport measurements demonstrated a hysteretic, symmetric, and stepwise axial magnetoresistance of the Mn(5)Ge(3) nanowire. The interesting features of abrupt jumps indicated the presence of multiple domain walls in the Mn(5)Ge(3) nanowire and the annihilation of domain walls driven by the magnetic field. The Kurkijärvi model was used to describe the domain wall depinning as thermally assisted escape from a single energy barrier, and the fitting on the temperature-dependent depinning magnetic fields yielded an energy barrier of 0.166 eV.

Effect of a novel proteoglycan PTP1B inhibitor from Ganoderma lucidum on the amelioration of hyperglycaemia and dyslipidaemia in db/db mice.

Protein tyrosine phosphatase 1B (PTP1B) is implicated in the negative regulation of the insulin signalling pathway by dephosphorylating the insulin receptor (IR) and IR substrates. Ganoderma lucidum has traditionally been used for the treatment of diabetes in Chinese medicine; however, its anti-diabetic potency and mechanism in vivo is still unclear. Our previously published study reported a novel proteoglycan PTP1B inhibitor, named Fudan-Yueyang-Ganoderma lucidum (FYGL) from G. lucidum, with a half-maximal inhibitory concentration (IC50) value of 5·12 (sem 0·05) µg/ml, a protein:polyglycan ratio of 17:77 and 78 % glucose in polysaccharide, and dominant amino acid residues of aspartic acid, glycine, glutamic acid, alanine, serine and threonine in protein. FYGL is capable of decreasing plasma glucose in streptozotocin-induced diabetic mice with a high safety of median lethal dose (LD50) of 6 g/kg. In the present study, C57BL/6 db/db diabetic mice were trialed further using FYGL as well as metformin for comparison. Oral treatment with FYGL in db/db diabetic mice for 4 weeks significantly (P < 0·01 or 0·05) decreased the fasting plasma glucose level, serum insulin concentration and the homeostasis model assessment of insulin resistance. FYGL also controlled the biochemistry indices relative to type 2 diabetes-accompanied lipidaemic disorders. Pharmacology research suggests that FYGL decreases the plasma glucose level by the mechanism of inhibiting PTP1B expression and activity, consequently, regulating the tyrosine phosphorylation level of the IR ß-subunit and the level of hepatic glycogen, thus resulting in the improvement of insulin sensitivity. Therefore, FYGL is promising as an insulin sensitiser for the therapy of type 2 diabetes and accompanied dyslipidaemia.

Shensong Yangxin attenuates metabolic syndrome-induced atrial fibrillation via inhibition of ferroportin-mediated intracellular iron overload.

BACKGROUND: Shensong Yangxin (SSYX) is a traditional Chinese medicine been widely used clinically to treat various arrhythmias including atrial fibrillation (AF). However, the role and precise mechanism of SSYX in MS-induced AF have not yet been elucidated. PURPOSE: To elucidate the protective effects of SSYX on MS-induced AF and its possible mechanisms of action. METHODS: Male Wistar rats (180-220 g) were fed a 16-week high-carbohydrate, high-fat (HCHF) diet together with 25% fructose in drinking water to produce a MS model. Low-concentration (SSYX-L, 0.4 g/kg) and high-concentration (SSYX-H, 0.8 g/kg) of SSYX were given by daily gavage 8-weeks following HCHF diet for 8-weeks. In vivo electrophysiological study, histological analysis, RNA-sequence (RNA-Seq) and gene ontology (GO) analysis, qRT-PCR and western blot were performed. RESULTS: Both low-concentration and high-concentration of SSYX could inhibit MS-induced AF susceptibility, electrical remodeling and structural remodeling. Results from RNA-sequence analysis revealed intracellular iron homeostasis mediated the protective effect of SSYX against MS. In vivo and in vitro experiments both demonstrated that SSYX up-regulated ferroportin (Fpn) expression and ameliorated intracellular iron overload induced by MS. To verified whether Fpn is the target of SSYX and intracellular iron overload mediated the protective effect of SSYX against MS, adeno-associated virus type 9 (AAV9) delivery system was used. Knocking down Fpn (AAV9-shFpn) markedly aggravated the reactive oxygen species (ROS) production, electrical remodeling and atrial fibrosis induced by MS, leading to a further increase of AF susceptibility induced by MS. CONCLUSION: Our study demonstrated for the first time that SSYX reduced AF susceptibility, inhibited electrical remodeling and structural remodeling via up-regulating Fpn, decreasing intracellular iron overload and reducing ROS production. These results suggest that SSYX might be a potential therapeutic agent for the treatment of MS-induced AF.

Clinical efficacy of electromagnetic field therapy combined with traditional Chinese pain-reducing paste in myofascial pain syndrome.

BACKGROUND: Pulsed electromagnetic field (PEMF) therapy is widely used to treat myofascial pain syndrome (MPS). Damp-clearing and pain-reducing paste (DPP) comprises medical herbs and has been a traditional method of reducing myofascial pain in China for a long time, and it is usually administered with heating. However, the synergistic effect of PEMF therapy on heating-DPP in patients with MPS is unclear. AIM: To investigate the synergistic effect of PEMF therapy plus heating-DPP in lumbar MPS. METHODS: This double-blind, randomized, placebo-controlled trial was conducted on 120 patients with lumbar MPS who were randomly divided into an experimental group (EG, n = 60) and a control group (CG, n = 60). Patients in both groups were treated with heating-DPP combined with PEMF therapy; however, the electromagnetic function of the therapeutic apparatus used in the CG was disabled. Each treatment lasted for 20 min and was applied five times a week for two weeks. The short-form McGill Pain Questionnaire was applied at five time points: pretest, end of the first and second weeks of treatment, and end of the first and fourth week after completing treatment. Visual analog scale (VAS), present pain intensity index (PPI), and pain rating index (PRI; total, affective pain, and sensory pain scores) scores were then analyzed. RESULTS: Compared with the CG, the VAS, PPI and PRI scores (total, affective pain and sensory pain scores) in the EG were significantly lower after treatment and during follow-up. CONCLUSION: PEMF therapy combined with heating-DPP showed better efficacy than heating-DPP alone in reducing the overall intensity of pain and sensory and affective pain.

Rare case report and literature review of intracranial mesenchymal chondrosarcoma.

Intracranial mesenchymal chondrosarcoma (IMC) is a rare primary malignant tumor in the skull, but mostly originates from the abnormal residual chondrocytes in the embryonic period, which grow slowly, and primarily occurs at the junction of the cartilage of the skull base. IMC is difficult to diagnose by preoperative imaging and is easily misdiagnosed. It needs to be differentiated from meningiomas, gliomas, hemangioma, fibroids, etc.; this article introduces a case of primary IMC in a 38-year-old female teacher, and reviews the literature on the diagnosis and treatment of symptoms. The patient suffered from persistent severe headaches without nausea and vomiting. There was no obvious abnormality in the physical examination. Magnetic resonance imaging (MRI) of the head showed a circular space-occupying lesion on the right frontal bone and forehead; the mass was approximately 5.9 cm × 5.2 cm × 5.5 cm, and there was a large edema band surrounding it. The space-occupying effect was obvious; bilateral ventricles were compressed, and on the right side, the midline structure was shifted to the left. The patient was initially diagnosed with simple meningioma. After admission, the right frontal lobe meningioma was resected under general anesthesia, and the tumor tissue was completely removed in blocks. The postoperative pathology report stated: malignant tumor of the right frontal lobe; consider mesenchymal chondrosarcoma. Following a difficult pathological consultation at the Provincial Medical Association, the tumor was found to be consistent with mesenchymal chondrosarcoma. Intracranial chondrosarcoma is a very rare malignant tumor. Other intracranial masses, such as meningioma and glioma, should be distinguished through differential diagnosis. At present, more attention is paid to surgical intervention and combined radiotherapy and chemotherapy for the treatment of IMC, which should also be the future treatment option.

Single-crystalline Ni2Ge/Ge/Ni2Ge nanowire heterostructure transistors.

In this study, we report on the formation of a single-crystalline Ni(2)Ge/Ge/Ni(2)Ge nanowire heterostructure and its field effect characteristics by controlled reaction between a supercritical fluid-liquid-solid (SFLS) synthesized Ge nanowire and Ni metal contacts. Scanning electron microscopy (SEM) and transmission electron microscopy (TEM) studies reveal a wide temperature range to convert the Ge nanowire to single-crystalline Ni(2)Ge by a thermal diffusion process. The maximum current density of the fully germanide Ni(2)Ge nanowires exceeds 3.5 × 10(7) A cm(-2), and the resistivity is about 88 µΩ cm. The in situ reaction examined by TEM shows atomically sharp interfaces for the Ni(2)Ge/Ge/Ni(2)Ge heterostructure. The interface epitaxial relationships are determined to be [Formula: see text] and [Formula: see text]. Back-gate field effect transistors (FETs) were also fabricated using this low resistivity Ni(2)Ge as source/drain contacts. Electrical measurements show a good p-type FET behavior with an on/off ratio over 10(3) and a one order of magnitude improvement in hole mobility from that of SFLS-synthesized Ge nanowire.

[Reversion of resistance to cisplatin induced by MG132 in cervical cancer line HCE1 multicellular spheroid].

OBJECTIVE: To investigate the effect of the ubiquitin-proteasome pathway inhibitor MG132 on the natural resistance to cisplatin in the human cervical cancer line (HCE1) multicellular spheroid (HCE1/MCS) model and to probe it if MG132 could reverse the HCE1/MCS resistance to cisplatin, as well as the possible mechanism of drug resistance. METHODS: (1) HCE1/MCS was obtained using liquid overlay and rotating technique. (2) Four groups were established (MG132 group, cisplatin group, MG132+cisplatin group, the control group). Cell viability were measured by trypan blue exclusion assay. Cell cycle and apoptosis were detected by flow cytometry. (3) The expression of nuclear factor (NF) kappaB of both HCE1 monolayer cells (HCE1/MC) and HCE1/MCS was detected by western blot, and the expression of B cell lymphoma/leukemia-2 (bcl-2) was detected by immunohistochemistry. RESULTS: (1) HCE1/MCS was established successfully. (2) Cell inhibited rate of HCE1/MC and HCE1/MCS was: in MG132 group, (11.67+/-2.34)% vs (10.78+/-1.17)% (P>0.05); in MG132+cisplatin group, (92.67+/-2.52)% vs (91.33+/-2.18)% (P>0.05); in cisplatin group, (45.01+/-7.44)% vs (9.45+/-5.98)% (P<0.05). (3) The rate of apoptosis of HCE1/MC and HCE1/MCS were: in MG132 group, 8.14% and 5.97%; in MG132+cisplatin group, 99.01% and 95.22%; in cisplatin group, 33.61% and 0.88%. (4) The expression level of NF-kappaB and the high expression rate of bcl-2 were: in HCE1/MCS of control group, 0.67 and 60%; in HCE1/MCS of cisplatin group, 0.85 and 83%; in HCE1/MCS of MG132 group, 0.39 and 20%; in HCE1/MCS of MG132+cisplatin group, 0.47 and 33%. CONCLUSIONS: (1) HCE1/MCS present natural resistance to cisplatin and may become a good model for the study of cervical cancer drug resistance in vitro. (2) MG132 could induce the inhibition and apoptosis of HCE1/MCS cells and partially reverse the natural resistance of HCE1/MCS to cisplatin, of which partially reverse the natural resistance may be in relation to the down-regulation of NF-kappaB and bcl-2 expression.

Shensong Yangxin Protects Against Metabolic Syndrome-Induced Ventricular Arrhythmias by Inhibiting Electrical Remodeling.

Shensong Yangxin (SSYX) is a traditional Chinese medicine, which has been proven to improve the clinical symptoms of arrhythmia. However, the role of SSYX in metabolic syndrome (MetS)-induced electrical remodeling remains to be fully elucidated. Here, we sought to clarify whether SSYX can alter the electrophysiological remodeling of cardiac myocytes from MetS rats by regulating transient outward potassium current (I to) and calcium current (I Ca-L). Male Wistar rats were subjected to 16 weeks of high-carbohydrate, high-fat to produce a MetS model group. SSYX (0.4 g/kg) was administrated by daily gavage 8 weeks following high-carbohydrate, high-fat for 8 weeks. In vivo electrophysiological study was performed to evaluated ventricular arrhythmias (VA) vulnerability and electrophysiological properties. The potential electrical mechanisms were estimated by whole-cell patch-clamp and molecular analysis. The H9C2 cells were used to verify the protective role of SSYX in vitro. After 16-week high-carbohydrate, high-fat feeding, MetS model rats showed increased body weight (BW), blood pressure (BP), blood sugar (BS), heart rate (HR) and heart weights to tibia length (HW/TL) ratio. Furthermore, MetS rats depicted increased VA inducibility, shortened effective refractory period (ERP) and prolonged action potential duration (APD). Lower I Ca-L and I to current densities were observed in MetS rats than CTL rats. Additionally, MetS rats exhibited significantly increased cardiac fibrosis, decreased Cx43 expression and protein levels of Cav1.2, Kv4.2, Kv4.3 than CTL group. As expected, these MetS-induced effects above were reversed when SSYX was administrated. Mechanistically, SSYX administrated significantly down-regulated the TLR4/MyD88/CaMKII signaling pathway both in vivo and in vitro. Collectively, our data indicated that the electrical remodeling induced by MetS contributed to the increased VA susceptibility. SSYX protects against MetS-induced VA by inhibiting electrical remodeling through TLR4/MyD88/CaMKII signaling pathway.

Efficacy and Mechanism of a Chinese Classic Prescription of Yueju in Treating Nonalcoholic Steatohepatitis and Protecting Hepatocytes from Apoptosis.

Yueju, a famous classic Chinese prescription, has been extensively used in treating depression syndromes for hundreds of years. Recent studies have reported that Yueju showed good effects in treating metabolic diseases, such as obesity and hyperlipidemia. Nonalcoholic steatohepatitis (NASH), which leads to cirrhosis and severe cardiovascular diseases, is closely linked to obesity and abnormal lipid metabolism. In this study, Yueju could decrease the levels of alanine aminotransferase, aspartate transaminase, triglyceride, cholesterol, and low-density lipoprotein-C but increase the high-density lipoprotein-C in the serum of the NASH rat model induced by high-fat and high-cholesterol diet. Yueju could alleviate hepatosteatosis by increasing the phosphorylation of acetyl-CoA carboxylase and inhibiting the expression of fatty acid synthase and stearoyl-CoA desaturase 1. Yueju downregulated the expression of α-smooth muscle actin and collagen type 1A1, ameliorating the liver fibrilization. Yueju could also protect the hepatocytes from apoptosis by upregulating antiapoptosis protein Bcl-2 and X-linked inhibitor of apoptosis protein and downregulating apoptotic proteins Bax and cleaved poly ADP-ribose polymerase. Thus, Yueju could improve liver function, regulate lipid metabolism, alleviate hepatosteatosis and fibrosis, and protect hepatocytes from apoptosis against NASH. Yueju may be used as an alternative effective medicine for NASH treatment.

[Relationship between epithelial-mesenchymal transition and basal cell-like phenotype in breast cancer].

OBJECTIVES: To evaluate the relationship between epithelial-mesenchymal transition and basal cell-like phenotype breast cancer (BLBC). METHODS: Three hundred and eighty two cases of breast cancers including basal cell-like, luminal A, luminal B and Her-2 subtypes were collected from 458 cases of invasive breast cancers based on their immunophenotypes. They were then stained immunohistochemically with FOXC-2, vimentin, Syndecan-1 and E-cadherin. The relationship of these markers with the basal cell-like phenotype of breast cancer was studied. RESULTS: Of the 41 BLBC cases, FOXC-2, vimentin and Syndecan-1 were positive in 14 cases (34.1%), 18 cases (43.9%) and 36 cases (87.7%) respectively; E-cadherin expression was reduced in 26 cases (63.4%). The positive rates of FOXC-2 and vimentin were higher in BLBC than in other subtypes of breast cancer (P < 0.01). The expression of E-cadherin was the lowest among the 4 subtypes of breast cancers (P < 0.01). Syndecan-1 was positive in the stromal cells adjacent to cancer cells in 17 cases (41.5%) BLBC and the expression was higher than that in other subtypes (P = 0.007). There existed a correlation between FOXC-2 and vimentin expression in BLBC (r = 0.607, P < 0.01). The rates of positive lymph nodes in FOXC-2 and vimentin positive BLBC cases were 71.4% and 66.7% respectively, and both were higher than those of FOXC-2 and vimentin negative BLBC cases (P = 0.002 and P = 0.001). CONCLUSION: Epithelial-mesenchymal transition is probably related to the basal cell-like phenotype of breast cancers, and this may be one of the reasons accounting for the different biological behavior of BLBC from other subtypes of breast cancer.