102,011 research outputs found
A temperature gradient may support mother-infant thermal identification and communication in the breast crawl from birth to breastfeeding
Aim: The human female's nipple-areolar complex (NAC) is the point of arrival of a natural progression from birth to breastfeeding, linked to functional, chemical and biophysical cues that promote the breast crawl soon after birth. We investigated the thermal gradient generated by the lips of the neonate and warmth of the NAC, which may drive the infant directly to the nipple. Methods: We prospectively studied 41 full-term singleton infants and their mothers at the Policlinico Abano Terme, Italy, between January 1, 2015, and February 28, 2015. NAC and breast quadrant temperatures were assessed 6 ± 2 hours prepartum and one and two days postpartum, together with the neonates’ lip temperature. Results: The temperature of the neonates’ lips was significantly lower than the forehead temperature on days one and two postpartum (delta = −1.24°C, p < 0.001 and delta = −1.02°C, p < 0.001, respectively). Thus, the thermal gradient between the NAC and the neonates’ lips was −1.66 ± 1.07°C on day one (p < 0.001) and −1.68 ± 0.63°C (p < 0.001) on day two postpartum. Conclusion: These findings demonstrate, for the first time, that a temperature gradient may support mother-infant thermal identification and communication in the breast crawl and in the natural progression of the continuum from birth to breastfeeding
A Survey of Central Association Members About the Definition, Management, and Complications of Shoulder Dystocia
Vitamin E and enzymatic/oxidative stress-driven oxysterols in amnestic Mild Cognitive Impairment subtypes and Alzheimer’s disease
Oxidative stress, which contributes to neuronal damage, is thought to be a pathophysiological mechanism of Alzheimer's disease (AD). Markers of oxidative stress may appear early in the preclinical, mild cognitive impairment (MCI) phase of AD. We investigated the interaction among enzymatic-derived oxysterols (24S-hydroxycholesterol and 27-hydroxycholesterol), markers of oxidative stress, including free radical-related oxysterols (7β-hydroxycholesterol and 7-ketocholesterol), and vitamin E in AD patients and two amnestic MCI subtypes, amnestic single-domain MCI (a-MCI) subjects, and multi-domain MCI (md-MCI) subjects, compared to healthy control subjects (HC). The study included 37 patients with AD, 24 with a-MCI, 29 with md-MCI, and 24 HC. Plasma assessments were made using isotope dilution-mass spectrometry.
Although we found no significant change in free radical- or enzymatic-derived oxysterol concentrations in AD or MCI patients, vitamin E levels corrected for cholesterol were reduced in AD patients compared to HC. Results suggest that AD patients have upregulated cerebral oxidative stress or a nutritional deficit of vitamin E. The oxysterols investigated here are not useful markers for diagnosing AD or MCI
Cilostazol promotes angiogenesis after peripheral ischemia through a VEGF-dependent mechanism
Background/objectives: Cilostazol has been found to be effective for the treatment of intermittent claudication (IC). This compound has several beneficial effects on platelet aggregation, serum lipids and endothelial cells, but how these might relate to improvements in walking is not entirely understood. The aim of this work was to investigate the effects of cilostazol on angiogenic response in a murine model of peripheral ischemia and to clarify the underlying molecular mechanisms of that response. Methods: We studied ischemia-induced neovascularization in the ischemic hindlimb of cilostazol-treated and untreated control mice. Results: We found that the perfusion recovery was significantly improved in treated compared with control mice. Interestingly, there was a higher level of circulating endothelial progenitor cells (EPCs) in mice treated with cilostazol than in untreated mice. Furthermore, cilostazol administration resulted in upregulation of granulocyte colony-stimulating factor (G-CSF) and vascular endothelial growth factor (VEGF) in the ischemic muscle of treated mice. Finally, inhibiting VEGF activity significantly reduced cilostazol-induced angiogenesis. Conclusions: The results of this study show that cilostazol administration enhances collateral blood flow in the ischemic hindlimbs of mice through a VEGF-dependent mechanism. These data may help to explain the beneficial effects that this drug has on patients with peripheral arterial disease (PAD) and IC. © 2012 Elsevier Ireland Ltd
Fas expression in germ cells in meiotic and in post meiotic arrest of spermatogenesis and in human testes with normal spermatogenesis
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