提高肠激惹综合征病人的自我管理

在发达国家中,有17%的妇女患有肠激惹综合征(IBS)。本病最初的症状为:胀气、便秘、肠痉挛。以上这些症状可能与紧张、饮食、炎症、感染有关。美国西雅图的华盛顿大学进行了一项随机试验,以确定一种认知和行为干预是否可以减轻症状,从而改善妇女的生活质量。一组144人的白人妇女,年龄是从18岁到48岁,被确诊患有IBS,将其随机分成3组。两组接受了症状、饮食评估和劝告、放松、认知和行为干预等方面的指导,减轻了病情。其中一些妇女接受了连续8 w的一对一的支持指导(综合纪录组),而其他一些人则参加简单的指导(简单记录组)。第3组的妇女接受…     

Computed tomographic evaluation of mouth breathers among paediatric patients

Objectives

Mouth breathing causes many serious problems in the paediatric population. It has been maintained that enlarged adenoids are principally responsible for mouth breathing. This study was designed to evaluate whether other mechanical obstacles might predispose the child to mouth breathing.

Methods

67 children with ages ranging from 10 to 15 years were studied and grouped into mouth-breathers and nose-breathers. The children first underwent axial CT scans of the brain for which they were originally referred. In addition, they were subjected to a limited coronal CT examination of the paranasal sinuses. Congenital anatomical variations as well as inflammatory changes were assessed.

Results

87% of mouth-breathing children had hypertrophied adenoids, 77% had maxillary sinusitis, 74% had pneumatized middle concha, 55% had a deviated nasal septum, 55% had hypertrophied inferior conchae, 45% had ethmoidal sinusitis and 23% showed frontal sinusitis. Such changes were significantly less prevalent in nose-breathers. 12.9% of mouth-breathing children did not have adenoids. Of these children, only 3.3% had one or more congenital or inflammatory change whereas the other 9.6% showed a completely normal CT scan signifying the incidence of habitual non-obstructive mouth breathing.

Conclusions

It is clear that adenoids have a dominant role in causing mouth breathing. Yet, we recommend that paediatricians should assess other mechanical obstacles if mouth breathing was not corrected after adenoidectomy. Further research should be performed to test the validity of correction of such factors in improving the quality of life of mouth-breathing children.     

Feasibility of catheter ablation renal denervation in “mild” resistant hypertension

Renal denervation (RDN) has been proposed as a novel interventional antihypertensive technique. However, existing evidence was mainly from patients with severe resistant hypertension. The authors aimed to evaluate the efficacy of RDN in patients with resistant hypertension with mildly elevated blood pressure (BP). Studies of RDN in patients with mild resistant hypertension (systolic office BP 140–160 mm Hg despite treatment with three antihypertensive drugs including one diuretic, or mean systolic BP by 24‐hour ambulatory BP measurement [ABPM] 135–150 mm Hg) were included. Two observational and one randomized cohort were identified (109 patients in the RDN group and 36 patients in the control group). Overall, the mean age of patients was 62±10 years, and 69.7% were male. Before‐after comparison showed that RDN significantly reduced ABPM as compared with the baseline systolic ABPM, from 146.3±13 mm Hg at baseline to 134.6±14.7 mm Hg at 6‐month follow‐up and diastolic ABPM from 80.8±9.4 mm Hg at baseline to 75.5±9.8 mm Hg at 6‐month follow up (both P<.001). This significant effect was not observed in the control group. Between‐group comparison showed a greater change in ABPM in the RDN group as compared with that in the control group (change in systolic ABPM: −11.7±9.9 mm Hg in RDN vs −3.5±9.6 mm Hg in controls [P<.001]; change in diastolic ABPM: −5.3±6.3 mm Hg in RDN vs −2.1±5.5 mm Hg in control [P=.007]). RDN was also associated with a significantly decreased office systolic/diastolic BP and reduced number of antihypertensive medications. No severe adverse events were found during follow‐up. RDN seems feasible to treat patients with mild resistant hypertension.     

KiSS1 mediates platinum sensitivity and metastasis suppression in head and neck squamous cell carcinoma

Although surgery and radiotherapy have been the standard treatment modalities for head and neck squamous cell carcinoma (HNSCC), the integration of cisplatin (CDDP)-based therapy has led to improvements in local and regional control of disease for patients. However, many trials show that only 10-20% of patients benefit from this treatment intensification, which can result in profound treatment-associated morbidity and mortality. Moreover, the marginal survival improvement suggests that CDDP resistance is an innate characteristic of HNSCC. To elucidate the biological mechanisms underpinning CDDP resistance in HNSCC, we utilized an experimental model of CDDP resistance in this disease. We first observed significant enhancements in local tumor growth and metastasis, as well as adverse survival, in CDDP-resistant (CR) tumors compared with sensitive tumors. To elucidate the molecular mechanisms of this phenotype, we undertook a systems biology-based approach utilizing high-throughput PCR arrays, and we identified a significant suppression of KiSS1 mRNA and protein expression in the CR cells, but no significant regions of genomic loss with array comparative genomic hybridization. Genetic suppression of KiSS1 in CDDP-sensitive cell lines rendered them CR, an observation that was mechanistically linked to alterations in glutathione S-transferase-π expression and function. We next confirmed that, in human HNSCC tumors, loss of KiSS1 expression was associated with metastatic human HNSCC tumors compared with non-metastatic tumors. Genetic reconstitution of KiSS1 in CR cells abrogated cellular migration and induced CDDP sensitivity. To confirm these findings in a murine model, either CR or KiSS1-transfected CR cells were studied in an orthotopic model of HNSCC, or survival studies revealed significant improvement in survival of the mice bearing CR-KiSS1 tumors. Mechanistically, alterations in apoptotic pathways and CDDP metabolism contributed to KiSS1-associated chemotherapy sensitization. These studies provided further direct evidence for the role of KiSS1 loss in biologically aggressive HNSCC and suggest potential targets for therapy in CR cancers.     

Potent cytotoxic effects of Calomeria amaranthoides on ovarian cancers

Background

Ovarian cancer remains the leading cause of death from gynaecological malignancy. More than 60% of the patients are presenting the disease in stage III or IV. In spite of combination of chemotherapy and surgery the prognosis stays poor for therapy regimen.

Methods

The leaves of a plant endemic to Australia, Calomeria amaranthoides, were extracted and then fractionated by column chromatography. In vitro cytotoxicity tests were performed with fractions of the plant extract and later with an isolated compound on ovarian cancer cell lines, as well as normal fibroblasts at concentrations of 1-100 μg/mL (crude extract) and 1-10 μg/mL (compound). Cytotoxicity was measured after 24, 48 and 72 hours by using a non-fluorescent substrate, Alamar blue.In vivo cytotoxicity was tested on ascites, developed in the abdomen of nude mice after inoculation with human OVCAR₃ cells intraperitoneally. The rate of change in abdomen size for the mice was determined by linear regression and statistically evaluated for significance by the unpaired t test.

Results

Two compounds were isolated by chromatographic fractionation and identified by ¹H-NMR, ¹³C-NMR and mass spectrometry analyses, EPD, an α-methylene sesquiterpene lactone of the eremophilanolide subtype, and EPA, an α-methylene carboxylic acid.Cytotoxicity of EPD for normal fibroblasts at all time points IC₅₀ was greater than 10 μg/mL, whereas, for OVCAR₃ cells at 48 hours IC₅₀ was 5.3 μg/mL (95% confidence interval 4.3 to 6.5 μg/mL).Both, the crude plant extract as well as EPD killed the cancer cells at a final concentration of 10 μg/mL and 5 μg/mL respectively, while in normal cells only 20% cell killing effect was observed. EPA had no cytotoxic effects.Changes in abdomen size for control versus Cisplatin treated mice were significantly different, P = 0.023, as were control versus EPD treated mice, P = 0.025, whereas, EPD versus Cisplatin treated mice were not significantly different, P = 0.13.

Conclusions

For the first time both crude plant extract from Calomeria amaranthoides and EPD have been shown to have potent anti-cancer effects against ovarian cancer.