Verfahren und Vorrichtung zur Bestimmung der Position eines Fahrzeugs

DE 3725896 A UPAB: 19930923 The detecting is operative for a distance of several metres. Each target mark with a preset strip pattern is scanned by a light beam over a preset scanning angle. The backscattered pattern is received by a photo-detector, while the time appearance of the receiver signals, according to the strip pattern, is measured. Pref. the angular position is determined by discerning the time ratio needed for the light beam over the distance between two pattern strips in left- and right-hand region of the target marking. The time determination for the light beam sweep may use the distance to the target marking. The measuring may take place over preset angular range. USE/ADVANTAGE - Satellites of transport vehicles, e.g. in warehouses and storage shelving, with precision steering towards storage position. 0/

MEASUREMENT OF THE LOCAL LONGITUDINAL STRAIN IN THE UNIAXIAL TENSILE TEST UP TO HIGH STRAIN RATES

Répartition des déformations dans l'essai de traction uniaxial jusqu'aux vitesses d'allongement élevées. Lors d'un essai de traction uniaxial, il importe de mesurer simultanément l'allongement, la striction et la force. On a présenté récemment un procédé optique permettant de mesurer ces deux types de déformation. Le procédé a été modifié de manière à s'appliquer également aux vitesses de déformation élevées et à fournir la répartition des déformations le long de 1'éprouvette.In the uniaxial tensile test force, longitudinal and transversal elongation must be measured simultaneously. Recently we presented a non instrusive method to measure both elongations in one experiment. To get more information about the material behaviour beyond the yield stress we modified this test equipment. Now we obtain the strain distribution along the whole sample

Eliminating the breast cancer surgery paradigm after neoadjuvant systemic therapy: current evidence and future challenges

In patients with operable early breast cancer, neoadjuvant systemic treatment (NST) is a standard approach. Indications have expanded from downstaging of locally advanced breast cancer to facilitate breast conservation, to in vivo drug-sensitivity testing. The pattern of response to NST is used to tailor systemic and locoregional treatment, that is, to escalate treatment in nonresponders and de-escalate treatment in responders. Here we discuss four questions that guide our current thinking about 'response-adjusted' surgery of the breast after NST. (i) What critical diagnostic outcome measures should be used when analyzing diagnostic tools to identify patients with pathologic complete response (pCR) after NST? (ii) How can we assess response with the least morbidity and best accuracy possible? (iii) What oncological consequences may ensue if we rely on a nonsurgical-generated diagnosis of, for example, minimally invasive biopsy proven pCR, knowing that we may miss minimal residual disease in some cases? (iv) How should we design clinical trials on de-escalation of surgical treatment after NST?Surgical oncolog

Pre-diagnostic smoking behaviour and poorer prognosis in a German breast cancer patient cohort - Differential effects by tumour subtype, NAT2 status, BMI and alcohol intake

Contains fulltext : 136562.pdf (publisher's version ) (Closed access)BACKGROUND: Inconsistent associations of smoking and breast cancer-specific mortality might be explained by subgroups of patients with different susceptibility to harmful effects of smoking. METHODS: We used a prospective cohort of 3340 postmenopausal breast cancer patients aged 50-74 and diagnosed with invasive tumours 2001-2005 in Germany, with a median follow-up time of 6 years. The effect of pre-diagnostic smoking behaviour on mortality outcomes and risk of recurrence was investigated using delayed entry Cox regression analysis. Differential effects according to N-acetyltransferase (NAT2) status, BMI, alcohol consumption, and tumour subtypes were assessed. RESULTS: Overall, smoking at time of breast cancer diagnosis versus never/former smoking was non-significantly associated with increased breast cancer-specific mortality and risk of recurrence (HR 1.23, 95% CI 0.93-1.64, and HR 1.29, 95% CI 0.95-1.75, respectively). Associations were consistently stronger in NAT2 slow than in fast acetylators for all mortality outcomes. Breast cancer-specific mortality was significantly increased in smokers with NAT2 slow acetylating status (HR 1.77, 95% CI 1.13-2.79) but not in those with fast acetylating status (HR 1.09, 95% CI 0.60-1.98; Pheterogeneity=0.19). Smoking was associated with significantly poorer outcomes for triple negative and luminal A-like tumours (e.g. all-cause mortality: HR 1.93, 95% CI 1.02-3.65, and HR 2.08, 95% CI 1.40-3.10, respectively). Risk of recurrence was significantly increased for women with HER2 positive tumours (HR 3.64, 95% CI 1.22-10.8). There was significant heterogeneity by BMI for non-breast cancer-specific mortality (/=25 kg/m(2): HR 0.94, 95% CI 0.38-2.36; Pheterogeneity=0.04). CONCLUSION: The harmful effects of smoking may be particularly relevant for certain subgroups of breast cancer patients. This may include patients with NAT2 slow acetylation status or with tumour subtypes other than luminal B, such as luminal A tumours who usually have a rather good prognosis. Emphasis on smoking cessation programmes for all cancer patients should be strengthened

CaM kinase II-δ is required for diabetic hyperglycemia and retinopathy but not nephropathy.

Type 2 diabetes has become a pandemic and leads to late diabetic complications of organs including kidney and eye. Lowering hyperglycemia is the typical therapeutic goal in clinical medicine. However, hyperglycemia may only be a symptom of diabetes but not the sole cause of late diabetic complications, Instead, other diabetes-related alterations could be causative. Here, we studied the role of CaM Kinase II δ (CaMKIIδ) that is known to be activated through diabetic metabolism. CaMKIIδ is expressed ubiquitously and might therefore affect several different organ systems. We crossed diabetic leptin receptor mutant mice to mice lacking CaMKIIδ globally. Remarkably, CaMKIIδ-deficient diabetic mice did not develop hyperglycemia. As potential underlying mechanisms, we provide evidence for improved insulin sensing with increased glucose transport into skeletal muscle but also reduced hepatic glucose production. Despite normoglycemia, CaMKIIδ-deficient diabetic mice developed the full picture of diabetic nephropathy but diabetic retinopathy was prevented. We also unmasked a retina-specific gene expression signature that might contribute to CaMKII-dependent retinal diabetic complications. These data challenge the clinical concept of normalizing hyperglycemia in diabetes as a causative treatment strategy for late diabetic complications and call for a more detailed analysis of intracellular metabolic signals in different diabetic organs