13 research outputs found
The dynamics of human body weight change
An imbalance between energy intake and energy expenditure will lead to a
change in body weight (mass) and body composition (fat and lean masses). A
quantitative understanding of the processes involved, which currently remains
lacking, will be useful in determining the etiology and treatment of obesity
and other conditions resulting from prolonged energy imbalance. Here, we show
that the long-term dynamics of human weight change can be captured by a
mathematical model of the macronutrient flux balances and all previous models
are special cases of this model. We show that the generic dynamical behavior of
body composition for a clamped diet can be divided into two classes. In the
first class, the body composition and mass are determined uniquely. In the
second class, the body composition can exist at an infinite number of possible
states. Surprisingly, perturbations of dietary energy intake or energy
expenditure can give identical responses in both model classes and existing
data are insufficient to distinguish between these two possibilities. However,
this distinction is important for the efficacy of clinical interventions that
alter body composition and mass
Loss of PTEN is associated with elevated EGFR and HER2 expression and worse prognosis in salivary gland cancer
BACKGROUND: Activity of the tumour-suppressor gene PTEN is reduced in different types of cancer and implicates non-responsiveness to targeted therapy. This study evaluates the gene and protein status of PTEN in salivary gland carcinomas. METHODS: A total of 287 carcinomas of the major and minor salivary glands were investigated for phosphatase and tensin homologue located on chromosome 10 (PTEN) deletion and loss of PTEN expression using fluorescence in situ hybridisation (FISH) and immunohistochemistry (IHC), respectively. Results were correlated to clinicopathological parameters, long-term survival, epidermal growth factor receptor (EGFR) and human epidermal growth factor receptor 2 (HER2) (IHC and FISH) status of the tumours. RESULTS: Hemizygous deletions of PTEN were found in 35 out of 232 (15.1%) carcinomas, while homozygous deletions were observed in 17 out of 232 (7.3%) tumours. Phosphatase and tensin homologue located on chromosome 10 deletion was common in certain histological subtypes and especially homozygous deletion was associated with high-grade malignancy, lymph node metastases and unfavourable long-term prognosis (P<0.001). Loss of PTEN expression was present in 59 out of 273 (21.6%) carcinomas and was significantly correlated to genomic PTEN deletion, high-grade malignancy (P<0.001), increased tumour size (P=0.036), lymph node metastases (P=0.007) and worse disease-specific survival (P=0.002). Genomic PTEN deletion, in particular homogenous deletion (P<0.001) predominantly occurred in tumours with increased gene copy number of EGFR (60.0%) and/or amplification of HER2 (63.6%). Loss of PTEN expression was frequently found in tumours overexpressing EGFR (28.6%) and/or HER2 (52.6%). CONCLUSION: PTEN function is reduced in different types of salivary gland cancer indicating unfavourable prognosis. Its association with EGFR and HER2 signalling might affect targeted therapy
Electroweak parameters of the z0 resonance and the standard model
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124399.pdf (publisher's version ) (Open Access
Comparison of the effects of 52 weeks weight loss with either a high-protein or high-carbohydrate diet on body composition and cardiometabolic risk factors in overweight and obese males
Immunological memory ≠protective immunity
So-called ‘immunological memory' is, in my view, a typical example where a field of enquiry, i.e. to understand long-term protection to survive reexposure to infection, has been overtaken by ‘l'art pour l'art' of ‘basic immunology'. The aim of this critical review is to point out some key differences between academic text book-defined immunological memory and protective immunity as viewed from a co-evolutionary point of view, both from the host and the infectious agents. A key conclusion is that ‘immunological memory' of course exists, but only in particular experimental laboratory models measuring ‘quicker and better' responses after an earlier immunization. These often do correlate with, but are not the key mechanisms of, protection. Protection depends on pre-existing neutralizing antibodies or pre-activated T cells at the time of infection—as documented by the importance of maternal antibodies around birth for survival of the offspring. Importantly, both high levels of antibodies and of activated T cells are antigen driven. This conclusion has serious implications for our thinking about vaccines and maintaining a level of protection in the population to deal with old and new infectious disease