Curcumin prevents the non-alcoholic fatty hepatitis via mitochondria protection and apoptosis reduction

Background: Non-alcoholic fatty hepatitis (NASH) is highly prevalent, mitochondria damage is the main pathophysiological characteristic of NASH. However, treatment for mitochondria damage is rarely reported. Methods: NASH model was established in rats, the protective effects of curcumin were evaluated by histological observation; structure and function assessments of mitochondria; and apoptotic genes expression. Results: NASH rats treated with curcumin displayed relatively slight liver damage when compared with NASH livers. The average mitochondrial length and width of NASH (12.0 ± 3.2 and 5.1 ± 1.1 micrometers) were significantly longer than that of normal (6.2 ± 2.1 and 2.1 ± 1.5 micrometers) and NASH treated with curcumin (7.4 ± 1.2 and 3.2 ± 1.5 micrometers) rats. The average malondialdehyde (MDA) and 4-hydroxy nonyl alcohol (HNE) levels in liver homogenates of NASH rats (4.23 ± 0.22 and 19.23 ± 2.3 nmol/Ml) were significantly higher than these in normal (1.32 ± 0.12 and 3.52 ± 0.43 nmol/mL) and NASH treated with curcumin (1.74 ± 0.11 and 4.66 ± 0.99 nmol/mL) rats. The expression levels of CytC, Casp3 and Casp8 of the NASH livers were significantly higher than normal and NASH treated with curcumin rats livers. Conclusion: Our data demonstrated that curcumin prevents the NASH by mitochondria protection and apoptosis reduction and provided a possible novel treatment for NASH.     

生物安全柜中不同包装物影响灭菌口腔器械有效期的研究

目的探讨不同包装对灭菌口腔小器械在生物安全柜中的有效期的影响。方法在生物安全柜中,对高压灭菌后玻璃器皿包装和纸塑包装的口腔小器械在不同时间点进行细菌采样培养实验,在第1天打开玻璃器皿包装的灭菌小器械后的4、8、24 h进行采样,以后每间隔24小时采集1次,连续10 d采样观察其细菌生长情况,同时在每一个时间点均采集一次纸塑包装的灭菌器械作为实验对照。结果在生物安全柜相对无污染的情况下,对照组均无细菌生长,实验组在144 h的培养结果开始有菌落生长,168 h后的培养结果有统计学意义(P<0.05)。结论在生物安全柜中相对无污染的条件下,玻璃器皿包装的口腔诊疗中的小器械的有效期远远超过《医疗机构口腔诊疗器械消毒技术操作规范》所规定的包装灭菌物品一经打开不得超过4 h的标准。     

Different methods for inducing adipose-derived stem cells to differentiate into Schwann-like cells

Introduction

The aim of the study was to explore an effective method to induce adipose-derived stem cells (ADSCs) to differentiate into Schwann-like cells in vitro.

Material and methods

Reagents were applied in two different ways (Dezawa inducing method and modified inducing method) in which inducers including β-mercaptoethanol (β-ME), all-trans-retinoic acid (ATRA), type I collagenase, forskolin, heregulin, basic fibroblast growth factor (BFGF) and brain-derived neurotrophic factor (BDNF) were used in different ways to induce ADSCs of rats to differentiate into Schwann-like cells. After induction, the cell morphologic characteristics and the cellular immunohistochemical staining positive rate of anti-S100 and anti-GFAP (glial fibrillary acidic protein) antibodies and the gray value of immunocytochemical dye with anti-S100 and anti-GFAP antibodies and cell activity measured by the MTT method were compared with each other to evaluate the induction effects.

Results

Both methods can induce differentiation of ADSCs of rats into Schwann-like cells, but the cellular morphology of the modified method was more similar to Schwann cells than that of the Dezawa inducing method, there was a higher cellular immunohistochemical staining positive rate and staining grey value in immunocytochemical dye with anti-S100 and anti-GFAP antibodies, and less damage in the cell activity of the modified inducing method than that of the Dezawa inducing method.

Conclusions

The effect of the modified method to induce ADSCs to differentiate into Schwann-like cells in vitro is superior to that of the Dezawa inducing method.     

Multifactor‐dimensionality reduction reveals interaction of important gene variants involved in allergy

Elevated IgE levels in the atopic triad of asthma, allergic rhinitis and atopic dermatitis is a multifactorial condition whose genetic component involves interaction of several gene loci. One hundred and two matched pairs of allergic and nonallergic individuals were phenotyped for total serum IgE level using enzyme‐linked immunosorbent assay (ELISA). Atopic status was defined by serum IgE concentration ≥100 IU mL^?1. SNPs genotyped include the IL4 ‐590C>T (rs2243250), FCER1B E237G (rs569108), CD14 ‐159C>T (rs2569190), IL4RA Q551R (rs1801275) and ADRB2 R16G (rs1042713). Gene–gene interaction was analysed using multifactor‐dimensionality reduction (MDR). Significant association between atopic allergy and the IL4 ‐590C>T polymorphism was confirmed in three genetic models. Interaction among the 5 gene variants was validated by MDR. The five‐locus model was chosen as the best to describe the interaction of the SNPs within the context of atopy. The strongest interaction was between IL4 ‐590C>T and IL4RA Q551R and between FCER1B E237G and ADRB2 R16G. The IL4 variant also interacts synergistically with the FCER1B and ADRB2 coding variants. CD14 ‐159C>T, in general, interacts antagonistically with the rest of the SNPs. In conclusion, a five‐locus interaction exists among IL4 ‐590C>T, FCER1B E237G, CD14 ‐159C>T, IL4RA Q551R and ADRB2 R16G in Filipino cases of atopic allergy.     

Differentiation between tuberculosis and leukemia in abdominal and pelvic lymph nodes: evaluation with contrast-enhanced multidetector computed tomography

PURPOSE:

To compare the characteristics of tubercular vs. leukemic involvement of abdominopelvic lymph nodes using multidetector computed tomography (CT).

MATERIALS AND METHODS:

We retrospectively reviewed multidetector computed tomography features including lymph node size, shape, enhancement patterns, and anatomical distribution, in 106 consecutive patients with newly diagnosed, untreated tuberculosis (55 patients; 52%) or leukemia (51 patients; 48%). In patients with leukemia, 32 (62.7%) had chronic lymphocytic leukemia, and 19 (37.3%) had acute leukemias; of these, 10 (19.6%) had acute myeloid leukemia, and 9 (17.6%) had acute lymphocytic leukemia.

RESULTS:

The lower para-aortic (30.9% for tuberculosis, 63.2% for acute leukemias and 87.5% for chronic lymphocytic leukemia) and inguinal (9.1% for tuberculosis, 57.9% for acute leukemias and 53.1% for chronic lymphocytic leukemia) lymph nodes were involved more frequently in the three types of leukemia than in tuberculosis (both with p <0.017). Tuberculosis showed peripheral enhancement, frequently with a multilocular appearance, in 43 (78.2%) patients, whereas patients with leukemia (78.9% for acute myeloid leukemia and acute lymphocytic leukemia, 87.5% for chronic lymphocytic leukemia) demonstrated predominantly homogeneous enhancement (both with p <0.017). For the diagnosis of tuberculosis, the analysis showed that a peripheral enhancement pattern had a sensitivity of 78.2%, a specificity of 100%, and an accuracy of 88.7%. For the diagnosis of leukemia, the analysis showed that a homogeneous enhancement pattern was associated with a sensitivity of 84.3%, a specificity of 94.5%, and an accuracy of 89.6%.

CONCLUSION:

Our findings indicate that the anatomical distribution and enhancement patterns of lymphadenopathy seen on multidetector computed tomography are useful for differentiating between untreated tuberculosis and leukemia of the abdominopelvic lymph nodes.     

Necrotizing fasciitis caused by perforated appendicitis: a case report

Acute appendicitis is one of the most common causes of acute abdominal pain. Accurate diagnosis is often hindered due to various presentations that differ from the typical signs of appendicitis, especially the position of the appendix. A delay in diagnosis or treatment may result in increased risks of complications, such as perforation, which is associated with increased morbidity and mortality rates. Necrotizing fasciitis caused by perforated appendicitis is extremely rare. We herein report a case of 50-year-old man presenting with an appendiceal abscess in local hospital. After ten days of conservative treatment with intravenous antibiotics, the patient complained about pain and swelling of the right lower limb and computed tomography (CT) demonstrated a perforated appendix and gas and fluid collection extending from his retroperitoneal cavity to the subcutaneous layer of his right loin and right lower limb. He was transferred to our hospital and was diagnosed with necrotizing fasciitis caused by perforated appendicitis. Emergency surgery including surgical debridement and appendectomy was performed. However, the patient died of severe sepsis and multiple organ failure two days after the operation. This case represents an unusual complication of a common disease and we should bear in mind that retroperitoneal inflammation and/or abscesses may cause necrotizing fasciitis through lumbar triangles.     

Role of CD11b+Gr-1+ myeloid cells in AGEs-induced myocardial injury in a mice model of acute myocardial infarction

Aims: Polymorph neutrophils are the predominant inflammatory cells and play a crucial role on the pathogenesis of myocardial injury at the early stage of acute myocardial infarction (AMI). However, the precursors and the differentiation of neutrophils are not fully understood. Here we explored the role of CD11b⁺Gr-1⁺ myeloid-derived suppressor cells (MDSCs) on myocardial injury in the absence and presence of advanced glycation end-products (AGEs) in a mice model of AMI. Methods and Results: Male C57BL/6J mice were selected. Fluorescent actived cell sortor (FACS) data demonstrated significantly increased CD11b⁺Gr-1⁺ MDSCs both in peripheral blood circulation and in the ischemic myocardium at 24 hours post AMI. Quantitative-real-time PCR results also revealed significantly upregulated CD11b and Ly6G mRNA expression in the ischemic myocardium. AGEs treatment further aggravated these changes in AMI mice but not in sham mice. Moreover, AGEs treatment also significantly increased infarction size and enhanced cardiomyocyte apoptosis. The mRNA expression of pro-inflammatory cytokine IL-6 and iNOS2 was also significantly increased in AMI + AGEs group compared to AMI group. Conclusion: These data suggest enhanced infiltration of MDSCs by AGEs contributes to aggravated myocardial injury in AMI mice, which might be one of the mechanisms responsible for severer myocardial injury in AMI patients complicating diabetes.     

Molecular pathology and potential therapeutic targets in esophageal basaloid squamous cell carcinoma

Basaloid squamous cell carcinoma (BSCC) is a rare and poorly differentiated variant of typical squamous cell carcinoma. Emerging studies show that genetic alterations are more frequent in BSCC than in conventional SCC, and some of which led to the identification of potential therapeutic targets in esophageal BSCC. Approximately half of the esophageal BSCC cases harbor either an EGFR mutation or amplification, and these occur in a mutually exclusive fashion. Therefore, the application of tyrosine kinase inhibitors may be beneficial to esophageal BSCC patients. This tumor is partly characterized by the activation of the Wnt and Hedgehog (HH) signaling pathways. Wnt signaling is activated by SFRP2 promoter hypermethylation and HH signaling is activated by the frequent mutations in PTCH1. Increasing evidence shows that the Wnt signaling pathway is involved in cross-talk with other developmental pathways, including the HH pathway. Therefore, pharmaceutical therapy targeting both the HH and Wnt pathways would be quite effective in patients with esophageal BSCC with highly malignant potential. In this review, we discuss the pathology, prognostic factors, genetic alterations and potential therapeutic targets in BSCC of esophagus.