No abstract

. Diagnosis of radial scar based on core needle biopsy is likely to be reliable when there is no associated atypical hyperplasia at percutaneous biopsy, when the biopsy includes at least 12 specimens, and when mammographic findings are reconciled with histologic findings. When the lesion diagnosed by core needle biopsy as radial scar does not meet these criteria, excisional biopsy is indicated.

Prolonged sitting has been shown to promote endothelial dysfunction in the lower legs. Furthermore, it has been reported that simple sitting-interruption strategies, including calf raises, prevent leg endothelial dysfunction. However, it is unclear whether prolonged sitting affects central cardiovascular health, or whether simple sitting-interruption strategies prevent impaired central cardiovascular health. This study sought to answer two questions: in young, healthy adults 1) does prolonged sitting (3 h) lead to increased aortic stiffness, and 2) do intermittent calf raise exercises to prevent pooling prevent aortic stiffening. Twenty young, healthy participants (21.7 ± 2.5 yr, 70% female, 25.5 ± 6.1 kg/m2) were randomized to 3 h of sitting with (CALF) or without (CON) 10 calf raises every 10 min. Aortic stiffening [carotid-femoral pulse wave velocity (PWV)] was measured in the supine position pre- and post-sitting. Venous pooling during sitting was estimated with total hemoglobin (tHB) concentration using near-infrared spectroscopy. There were no condition × time interactions. Following 3 h of sitting, PWV significantly increased (0.30 ± 0.46 m/s, P < 0.001). There was no condition effect for PWV ( P = 0.694), indicating the intermittent calf rises did not preserve central cardiovascular health. tHb was not significantly affected by sitting ( P = 0.446) but was 1.9 μM higher for CON versus CALF ( P = 0.106). Sitting increases aortic stiffness in young, healthy individuals, a process that may be influenced by lower extremity blood pooling. Calf raises, which have been reported to preserve vascular function in the legs, do not appear to provide sufficient stimulus for maintaining central cardiovascular health. NEW & NOTEWORTHY Although simple strategies, such as fidgeting or calf raises, are sufficient for preserving vascular function in the legs, data from the current study indicate that such strategies are not sufficient for maintaining central cardiovascular health, which is linked to cardiovascular disease.

No abstract

Percutaneous stereotactic CNB is an accurate method to establish a histopathologic diagnosis of nonpalpable breast lesions. Accuracy increases when additional surgery is performed for lesions with anticipated sampling error or when CNB findings are discordant with mammographic findings. An understanding of the interrelationship among these parameters is necessary to properly assess results.

Endothelial function typically exhibits a hormetic response to exercise. It is unknown whether endothelial damage occurs in response to acute exercise and could be a contributing mechanism. We sought to determine the effects of acute exercise on endothelial-derived circulating factors proposed to reflect endothelial integrity and activation. Young, healthy men ( n = 10) underwent 30-min moderate continuous (MOD) and high-intensity interval (HII) cycling exercise bouts. Venous blood samples were taken immediately before and after exercise for quantification of circulating endothelial cells (CECs), circulating angiogenic cells (CACs), apoptotic and activated endothelial microvesicles (EMVs), thrombomodulin (TM), von Willebrand factor (vWF), syndecan-1, and circulating microRNAs (ci-miRs) 126–3p and 126–5p. Endothelial function was assessed by flow-mediated dilation (FMD) of the brachial artery before, 10 min after, and 60 min after exercise. Numbers of CECs and EMVs were unchanged by either exercise bout ( P > 0.05). Numbers of all measured CAC subtypes decreased in response to MOD (21%–34%, P < 0.05), whereas only CD31+/34+/45dim/− CACs decreased following HII (21%, P < 0.05). TM and syndecan-1 increased with both exercise intensities (both ~20%, P < 0.05). HII, but not MOD, increased vWF (88%, P < 0.001), ci-miR-126–3p (92%, P = 0.009) and ci-miR-126–5p (110%, P = 0.01). The changes in several circulating factors correlated with changes in FMD following either one or both intensities. Changes in circulating factors do not support the concept of exercise-induced endothelial cell denudation, apoptosis, or activation, though slight disruption of endothelial glycocalyx and membrane integrity may occur. A related loss of mechanotransduction along with mechanisms underlying endothelial activation and ci-miR-126 secretion may relate to changes in endothelial function. NEW & NOTEWORTHY Using circulating endothelial-derived factors, we show that endothelial denudation, apoptosis, and activation do not appear to increase, whereas disrupted endothelial glycocalyx and membrane integrity may occur during both high-intensity interval and moderate intensity cycling. Increases in factors nonspecific to endothelial damage, including von Willebrand factor and microRNA-126, occurred only after high-intensity interval exercise. These results shed light on the hypothesis that disrupted endothelial integrity contributes to the endothelial function response to exercise.

The mechanism by which gonadal steroids modulate GH secretion is not known. We have used the reverse hemolytic plaque assay to examine whether gonadal steroid-induced modulation of GH secretion is effected by changes in the population of somatotrophs and/or alterations in their secretory properties. Two groups of Sprague-Dawley rats were studied: group 1 (n = 6) comprised male (M), castrate (Cx), and testosterone-replaced castrate male (Cx + T) rats and group 2 (n = 5) consisted of male (M), female (F), and 17 beta-estradiol-replaced castrate male (Cx + E) rats. The number of plaque-forming cells (expressed as both absolute number and a percentage of all cells) was determined, and secretory status was assessed by measuring plaque areas in response to 0, 0.01, 0.1, 1, 10, and 100 nM GHRH. While mean basal GH plaque areas were similar among the treatment groups of group 1, the maximal GH plaque area was significantly decreased in Cx [16.8 +/- 2.4 vs. 26.4 +/- 3.9 X 10(6) microns2 (mean +/- SEM); P less than 0.05], but not in Cx + T (27.5 +/- 4.1 microns2) rats. The GHRH EC50 was unaffected by castration or T replacement. The percentage and absolute population of somatotrophs were reduced in Cx, but not in Cx + T, rats, while the numbers of lactotrophs remained unchanged in these treatment groups. For group 2, the mean peak GH plaque area was reduced in Cx + E (16.5 +/- 2.9 microns2; P less than 0.001) compared to that in M rats (36.2 +/- 2.3 microns2), but was not significantly different from that in F (13.0 +/- 1.5 microns2) rats. The EC50 was significantly (P less than 0.025) greater in Cx + E (10.9 +/- 2.3 nM) and F (7.9 +/- 1.6 nM) compared to M rats (2.8 +/- 0.7 nM). The absolute somatotroph and lactotroph populations were increased in Cx + E compared to M and F rats, as were the populations of other pituitary cell types. Testosterone enhances GH secretion by increasing the secretory capacity, but not the sensitivity, of somatotrophs to GHRH and by recruiting the function of a subpopulation of somatotrophs. Estradiol reduces the secretory capacity and sensitivity of somatotrophs to GHRH, but increases the population of somatotrophs, lactotrophs, and non-GH- and non-PRL-secreting cells.(ABSTRACT TRUNCATED AT 400 WORDS)

Exposure to acute prolonged sitting reportedly leads to decreased cerebral blood flow. However, it is unclear whether this exposure translates to decreased cerebral perfusion and executive function or whether simple strategies to break up sitting can maintain cerebral perfusion and executive function. This study sought to answer two questions: in young, healthy adults, (a) does prolonged (3 hr) sitting lead to decreased cerebral perfusion and executive function? and (b) does breaking up prolonged sitting, using intermittent calf raise exercises, prevent changes in cerebral perfusion and executive function? Twenty young, healthy participants (21.7 [2.5] years, 70% female, 25.5 [6.1] kg/m2) were randomized to 3 hr sitting with 10 calf raises every 10 min (CALF) and 3 hr sitting without intermittent calf raises (CON). Prefrontal cortex perfusion was assessed using near‐infrared spectroscopy to monitor total hemoglobin (tHB) concentration and tissue saturation index (TSI, oxygenated hemoglobin). Executive function was assessed using the Stroop word and color tasks. Following 3 hr sitting, tHb was significantly lower in CALF versus CON (−2.1 μM, 95% CI [−3.1, −1.1]). TSI was not significantly different between conditions (p = .667). Word (1.6 ms, 95% CI [0.7, 2.5]) and color (1.3 ms, 95% CI [−0.2, 2.8]) completion times were longer (worse) for CALF compared to CON. In conclusion, calf raises decreased both cerebral perfusion and executive function. Simple strategies, such as fidgeting or calf raises, which have been reported to preserve vascular function in the legs, appear not to be sufficient to benefit cerebral perfusion or executive function.