Modern approaches to the treatment of breast cancer

Breast cancer is the most common cause of cancer death in women in this country. Until recently, the traditional treatment has been radical surgery with or without radiation therapy for patients with primary breast cancer, and palliative endocrine therapy followed by chemotherapy for patients with advanced disease. These treatments have met with limited effectiveness in terms of eradicating the disease. Studies in the past decade have given cause for optimism for breast cancer patients. Adjuvant systemic therapy after local treatment appears promising for certain subsets of patients with primary breast cancer. The development of estrogen receptor assays has markedly changed our approach to the disease and improved patient care. Estrogen receptor is an important prognostic factor and is useful in planning appropriate therapy for patients with primary breast cancer as well as those with advanced disease. Further research is urgently needed to improve the dismal survival of certain women with this common malignancy.     

The influence of (public) health expenditure on longevity

Objectives

We report new evidence on the contribution of health expenditure to increasing life expectancy in OECD countries, differentiating the effects of public and private health expenditures.

Methods

A theoretical model is presented and estimated though a cross-country fixed effects multiple regression analysis for a sample of OECD countries over the period 1980–2000.

Results

Although the effect of aggregate health expenditure is not conclusive, public health expenditure plays a significant role in enhancing longevity. However, its influence diminishes as the size of the public health sector on GDP expands, reaching a maximum around the 8 %.

Conclusions

With the influence of public health expenditure being positive, the ambiguous effect of the aggregate expenditure suggests that the weight of public and private health sectors matters, the second having a lower impact on longevity. This might explain the poor evolution of the life expectancy in countries with a high amount of private resources devoted to health. In such cases, an extension of public services could give rise to a better outcome from the overall health investment.     

Recreational football is medicine against non-communicable diseases: A systematic review

The purpose of this research was to conduct a systematic review of published articles related to the effect of recreational football on non-communicable diseases. A systematic review of Web of Science, SPORTDiscus, MEDLINE, and PubMed databases was performed according to PRISMA guidelines. Only empirical studies were included. There were no restrictions on the types of study design eligible for inclusion. The primary outcome measures result from the potential effects of recreational football on non-communicable diseases (eg, blood pressure, bone density, LDL cholesterol, and fat mass). A total of 44 articles met the inclusion criteria and were included. Recreational football is shown to: (a) decrease blood pressure and resting heart rate, improve cardiac structure and functioning, as well as increase maximal oxygen uptake in both sexes; (b) reduce cholesterol and triglycerides levels, increase insulin sensitivity, and have a positive impact on glycemic control; (c) improve bone mineralization, increase both bone mineral density and content, as well as acting as a stimulus for osteogenesis; and (d) be clearly beneficial for bone health, while slightly beneficial for body composition, muscle strength, and maximal oxygen uptake in adults with prostate cancer. The present systematic review demonstrated the benefits of recreational football practice on non-communicable diseases related to cardiovascular and bone health, body composition, type 2 diabetes, and prostate cancer. The effectiveness of recreational football on the aforementioned diseases may be related to age and gender; however, further research is required.     

Beneficial effects of Ginkgo biloba extract on insulin signaling cascade,dyslipidemia, and body adiposity of diet-induced obese rats

Ginkgo biloba extract (GbE) has been indicated as an efficient medicine for the treatment of diabetes mellitus type 2. It remains unclear if its effects are due to an improvement of the insulin signaling cascade, especially in obese subjects. The aim of the present study was to evaluate the effect of GbE on insulin tolerance, food intake, body adiposity, lipid profile, fasting insulin, and muscle levels of insulin receptor substrate 1 (IRS-1), protein tyrosine phosphatase 1B (PTP-1B), and protein kinase B (Akt), as well as Akt phosphorylation, in diet-induced obese rats. Rats were fed with a high-fat diet (HFD) or a normal fat diet (NFD) for 8 weeks. After that, the HFD group was divided into two groups: rats gavaged with a saline vehicle (HFD+V), and rats gavaged with 500 mg/kg of GbE diluted in the saline vehicle (HFD+Gb). NFD rats were gavaged with the saline vehicle only. At the end of the treatment, the rats were anesthetized, insulin was injected into the portal vein, and after 90s, the gastrocnemius muscle was removed. The quantification of IRS-1, Akt, and Akt phosphorylation was performed using Western blotting. Serum levels of fasting insulin and glucose, triacylglycerols and total cholesterol, and LDL and HDL fractions were measured. An insulin tolerance test was also performed. Ingestion of a hyperlipidic diet promoted loss of insulin sensitivity and also resulted in a significant increase in body adiposity, plasma triacylglycerol, and glucose levels. In addition, GbE treatment significantly reduced food intake and body adiposity while it protected against hyperglycemia and dyslipidemia in diet-induced obesity rats. It also enhanced insulin sensitivity in comparison to HFD+V rats, while it restored insulin-induced Akt phosphorylation, increased IRS-1, and reduced PTP-1B levels in gastrocnemius muscle. The present findings suggest that G. biloba might be efficient in preventing and treating obesity-induced insulin signaling impairment.     

Autoinflammatory diseases in childhood,part 1: monogenic syndromes

Autoinflammatory diseases constitute a family of disorders defined by aberrant stimulation of inflammatory pathways without involving antigen-directed autoimmunity. They may be divided into monogenic and polygenic types. Monogenic autoinflammatory syndromes are those with identified genetic mutations, such as familial Mediterranean fever, tumor necrosis factor receptor-associated periodic fever syndrome (TRAPS), mevalonate kinase deficiency or hyperimmunoglobulin D syndrome, cryopyrin-associated periodic fever syndromes (CAPS), pyogenic arthritis pyoderma gangrenosum and acne (PAPA) syndrome, interleukin-10 and interleukin-10 receptor deficiencies, adenosine deaminase 2 deficiency and pediatric sarcoidosis. Those without an identified genetic mutation are known as polygenic and include systemic-onset juvenile idiopathic arthritis, idiopathic recurrent acute pericarditis, Behçet syndrome, chronic recurrent multifocal osteomyelitis and inflammatory bowel disease among others. Autoinflammatory disorders are defined by repeating episodes or persistent fever, rash, serositis, lymphadenopathy, arthritis and increased acute phase reactants, and thus may mimic infections clinically. Most monogenic autoinflammatory syndromes present in childhood. However, because of their infrequency, diverse and nonspecific presentation, and the relatively new genetic recognition, diagnosis is usually delayed. In this article, which is Part 1 of a two-part series, the authors update monogenic autoinflammatory diseases in children with special emphasis on imaging features that may help establish the correct diagnosis.

     

Autoinflammatory diseases in childhood,part 2: polygenic syndromes

Autoinflammatory diseases are a family of disorders characterized by aberrant stimulation of inflammatory pathways without involvement of antigen-directed autoimmunity. They can be further divided in monogenic and polygenic types. Those without an identified genetic mutation are known as polygenic and include systemic-onset juvenile idiopathic arthritis, idiopathic recurrent acute pericarditis, Behçet syndrome, chronic recurrent multifocal osteomyelitis and inflammatory bowel disease among others. Autoinflammatory diseases are characterized by recurrent flares or persistent systemic inflammation and fever, as well as lymphadenopathy and cutaneous, abdominal, thoracic and articular symptoms. Although these syndromes can mimic infections clinically, the inflammatory lesions in autoinflammatory disorders are aseptic. However, because of their infrequency, varied and nonspecific presentation, and the new genetic identification, diagnosis is usually delayed. In this article, which is Part 2 of a two-part series, the authors review the main polygenic autoinflammatory diseases that can be seen in childhood, with special emphasis wherever applicable on imaging features that may help establish the correct diagnosis. However, the major role of imaging is to delineate organ involvement and disease extent.

     

In vivo characterization of emerging white matter microstructure in the fetal brain in the third trimester

The third trimester of pregnancy is a period of rapid development of fiber bundles in the fetal white matter. Using a recently developed motion‐tracked slice‐to‐volume registration (MT‐SVR) method, we aimed to quantify tract‐specific developmental changes in apparent diffusion coefficient (ADC), fractional anisotropy (FA), and volume in third trimester healthy fetuses. To this end, we reconstructed diffusion tensor images from motion corrected fetal diffusion magnetic resonance imaging data. With an approved protocol, fetal MRI exams were performed on healthy pregnant women at 3 Tesla and included multiple (2–8) diffusion scans of the fetal head (1–2 b = 0 s/mm² images and 12 diffusion‐sensitized images at b = 500 s/mm²). Diffusion data from 32 fetuses (13 females) with median gestational age (GA) of 33 weeks 4 days were processed with MT‐SVR and deterministic tractography seeded by regions of interest corresponding to 12 major fiber tracts. Multivariable regression analysis was used to evaluate the association of GA with volume, FA, and ADC for each tract. For all tracts, the volume and FA increased, and the ADC decreased with GA. Associations reached statistical significance for: FA and ADC of the forceps major; volume and ADC for the forceps minor; FA, ADC, and volume for the cingulum; ADC, FA, and volume for the uncinate fasciculi; ADC of the inferior fronto‐occipital fasciculi, ADC of the inferior longitudinal fasciculi; and FA and ADC for the corticospinal tracts. These quantitative results demonstrate the complex pattern and rates of tract‐specific, GA‐related microstructural changes of the developing white matter in human fetal brain.