This study reports the high value of VERT breast cancer-targeted education programs in improving RT knowledge and perhaps decreasing patient anxiety. Continued efforts are required to improve patients' accessibility to VERT in Australia, and to better understand the effect of VERT's unique educational features on patients' emotional and physical needs throughout their RT.
Summary
Haemostatic changes in septic patients are complex, with both procoagulant and anticoagulant changes. Thirty‐eight patients with severe sepsis and 32 controls were investigated by coagulation screens, individual factor assays, calibrated automated thrombography (CAT), whole blood low‐dose‐tissue factor activated (LD‐TFA) Rotem and LD‐TFA waveform analysis. Thirty‐six of 38 patients had an abnormal coagulation screen. The mean levels of factors II, V (P < 0·05), VII, X, XI and XII, antithrombin and protein C (P < 0·01) was decreased in sepsis compared with controls. The mean factor VIII and fibrinogen level (P < 0·001) was increased. CAT in platelet rich and poor plasma showed a prolonged lag time (P < 0·02), decreased peak thrombin (P < 0·02) and delayed time to peak thrombin (P < 0·001) in sepsis patients, however, the endogenous thrombin potential was equivalent in sepsis and controls. In LD‐TFA Rotem, septic patients had delayed clot times (P = 0·04) but an increased maximum velocity of clot formation (P < 0·01) and area under the clot elasticity curve (P < 0·01). LD‐TFA waveform analysis showed a delayed onset time but an increased rate of clot formation (P < 0·005). In conclusion, global tests of haemostasis suggest that in this patient group, activation of haemostasis is delayed but once initiated thrombin generation and clot formation are normal or enhanced.
SummaryPatients with haemophilia requires different amounts of FVIII to prevent and treat bleeds. We hypothesise that this is because FVIII has variable effects on individual patients' global haemostasis. Twelve patients with severe haemophilia A were infused with 50 IU/kg FVIII and thrombin generation in platelet rich (PRP) and platelet poor plasma (PPP) and velocity of changing clot elasticity were measured preinfusion and at nine subsequent time points over 72 h. Despite a close correlation between median FVIII and median initial rate of thrombin generation (R 2 0AE94), endogenous thrombin potential (ETP; R 2 0AE94) and peak thrombin (R 2 0AE91) in PPP, there was wide inter-patient variability at each time point. There was, however, a highly predictable intra-patient relationship between FVIII level and thrombin generation. Inter-patient variability was due to both differences in FVIII levels and the variable effect FVIII had on an individuals' thrombin generation. The utility of PRP was limited because, at low-FVIII levels, only rate of thrombin generation was measurable. At low-FVIII concentrations, the rate of thrombin generation in PPP was the most useful test whilst at higher levels ETP and peak thrombin could also be used.
A large body of evidence indicates that the central nervous system plays an essential role in the pathogenesis of hypertension. However, in many cases the specific brain regions involved and the mechanisms by which these regions promote hypertension are not known. In recent years, research in this and other laboratories has attempted to determine the mechanisms by which neural and humoral signals arising in response to pathological conditions (often occurring in the periphery) interact with the central nervous system to produce hypertension. In this article, we illustrate the coupling of peripheral and central factors in the pathogenesis of hypertension by examining the central actions of angiotensin II and mineralocorticoids in the expression of renal hypertension and mineralocorticoid-salt hypertension, respectively. We also review recent data from this laboratory illustrating the involvement of medullary vasomotor centers in the development of neurogenic hypertension after sinoaortic deafferentation and in the maintenance of hypertension in the spontaneously hypertensive rat.
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