Our study indicates the constant effect of SG in the acceleration of gastric emptying of solids, which occurs faster, not only in short but also in long-term postoperatively. Such effects on gastric motility, in combination with the reported alterations in gut hormones, may explain how this 'food limiting' operation results in weight loss.
We conclude that combination of radiotherapy with Stealth liposomal doxorubicin is feasible. The potential role of such a regimen in the treatment of highly angiogenic tumors requires further investigation.
68Ga-DOTATOC is a promising tool for evaluation of the expression of SSTR2 in NETs. The combination of [18F]FDG and 68Ga-DOTATOC dynamic PET studies provides different information regarding the biological properties of lesions in patients with metastatic NETs in whom 90Y-DOTATOC therapy is planned. While the global 68Ga-DOTATOC uptake is influenced mostly by K1, the global [18F]FDG uptake is mostly influenced by VB. Only patients with enhanced 68Ga-DOTATOC uptake (SUV >5.0) were referred to 90Y-DOTATOC therapy.
SG accelerates gastric emptying and small bowel transit of semisolids. In addition, it delays the initiation of cecal filling and T ICVt. This early and prolonged contact of food with the distal small bowel mucosa may explain the metabolic effects of SG occurring before substantial weight loss.
DOTATOC uptake in NETs is mainly dependent on k (1) (receptor binding) and V(b) (fractional blood volume). Pharmacokinetic data analysis can help to separate blood background activity (V(b)) from the receptor binding (k (1)), which may help to optimise planning of (90)Y-DOTATOC therapy.
Permanent ventricular pacing is associated with alterations in regional myocardial perfusion. Furthermore, abnormalities of microvascular flow, as indicated by reduced coronary flow reserve in the defect-related artery, are at least partially responsible for the uncertain specificity of dipyridamole myocardial perfusion scintigraphy.
The results demonstrated moderate (68)Ga-DOTATOC uptake in primary NSCLC but did not provide any evidence for SSTR2 expression in metastases. This may be caused by loss of the gene expression in metastases as compared with the primary tumours.
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