Adult neurogenesis in the hippocampus is a notable process due not only to its uniqueness and potential impact on cognition but also to its localized vertical integration of different scales of neuroscience, ranging from molecular and cellular biology to behavior. This review summarizes the recent research regarding the process of adult neurogenesis from these different perspectives, with particular emphasis on the differentiation and development of new neurons, the regulation of the process by extrinsic and intrinsic factors, and their ultimate function in the hippocampus circuit. Arising from a local neural stem cell population, new neurons progress through several stages of maturation, ultimately integrating into the adult dentate gyrus network. The increased appreciation of the full neurogenesis process, from genes and cells to behavior and cognition, makes neurogenesis both a unique case study for how scales in neuroscience can link together and suggests neurogenesis as a potential target for therapeutic intervention for a number of disorders.

WCE size is related to aging, not to CVD risk. CVD risk in most persons with WCH is comparable to age- and risk-adjusted normotensive control subjects.

Stroke is the world's leading cause of disability with limited brain repair treatments which effectively improve long-term neurological deficits. The neuroinflammatory responses persist into the late repair phase of stroke and participate in all brain repair elements, including neurogenesis, angiogenesis, synaptogenesis, remyelination and axonal sprouting, shedding new light on post-stroke brain recovery. Resident brain glial cells, such as astrocytes not only contribute to neuroinflammation after stroke, but also secrete a wide range of trophic factors that can promote post-stroke brain repair. Alternatively, activated microglia, monocytes, and neutrophils in the innate immune system, traditionally considered as major damaging factors after stroke, have been suggested to be extensively involved in brain repair after stroke. The adaptive immune system may also have its bright side during the late regenerative phase, affecting the immune suppressive regulatory T cells and B cells. This review summarizes the recent findings in the evolving role of neuroinflammation in multiple post-stroke brain repair mechanisms and poses unanswered questions that may generate new directions for future research and give rise to novel therapeutic targets to improve stroke recovery.

We report anodic formation of Ti-Nb-O nanotubes on top of a Ti35Nb alloy, and in vitro bioactivity and stem cell response of the anodic nanotubes. It was found that the amorphous Ti-Nb-O nanotubes presented a significantly enhanced in vitro bioactivity (in simulated body fluids) compared to those of undoped TiO2 nanotubes and porous Ti-Nb-O without nanotubular structure. Similar to undoped TiO2 nanotubes, the Ti-Nb-O nanotubes also promote mesenchymal stem cell adhesion and fast formation of extracellular matrix (ECM) materials. The above findings make it possible to further explore the biological properties, such as cell proliferation and drug delivery, of a variety of Ti-alloy-based oxide nanotubes.

Abstract-The ambulatory arterial stiffness index (AASI) is derived from 24-hour ambulatory blood pressure recordings.We investigated whether the goodness-of-fit of the AASI regression line in individual subjects (r 2 ) impacts on the association of AASI with established determinants of the relation between diastolic and systolic blood pressures. We constructed the International Database on the Ambulatory Blood Pressure in Relation to Cardiovascular Outcomes (7604 participants from 6 countries). AASI was unity minus the regression slope of diastolic on systolic blood pressure in individual 24-hour ambulatory recordings. AASI correlated positively with age and 24-hour mean arterial pressure and negatively with body height and 24-hour heart rate. The single correlation coefficients and the mutually adjusted partial regression coefficients of AASI with age, height, 24-hour mean pressure, and 24-hour heart rate increased from the lowest to the highest quartile of r 2 . These findings were consistent in dippers and nondippers (night:day ratio of systolic pressure Ն0.90), women and men, and in Europeans, Asians, and South Americans. The cumulative z score for the association of AASI with these determinants of the relation between diastolic and systolic blood pressures increased curvilinearly with r 2 , with most of the improvement in the association occurring above the 20th percentile of r 2 (0.36). In conclusion, a better fit of the AASI regression line enhances the statistical power of analyses involving AASI as marker of arterial stiffness. An r 2 value of 0.36 might be a threshold in sensitivity analyses to improve the stratification of cardiovascular risk. (Hypertension. 2008;52:1038-1044.) Key Words: ambulatory arterial stiffness index Ⅲ arterial stiffness Ⅲ blood pressure measurement/monitoring Ⅲ epidemiology Ⅲ population science Ⅲ statistical analysis I n 1914, MacWilliam and Melvin 1 already noticed that loss of elasticity in the arterial system impacted on the relation of diastolic with systolic pressure. We recently defined the ambulatory arterial stiffness index (AASI) as unity minus the regression slope of diastolic on systolic blood pressure in individual 24-hour ambulatory blood pressure recordings. 2,3 The stiffer the arterial tree, the closer the regression slope and AASI are to 0 and 1, respectively. We validated AASI against other markers of arterial stiffness, such as the systolic augmentation index and aortic pulse wave velocity. 2 In spite of the prognostic accuracy of AASI over and beyond classical risk factors, including pulse pressure 3-5 and pulse wave velocity, 6 some researchers criticized AASI. It would be a surrogate marker of arterial stiffness not different from pulse pressure. 7 Schillaci et al 8 reported that AASI decreased with less nocturnal dipping in blood pressure. Gavish et al 9 suggested that symmetrical regression might provide a better estimate of AASI less affected by the nocturnal blood pressure fall and the goodness-of-fit of the regression slope, as expressed by the c...

Participant-level meta-analyses assessed the age-specific relevance of office blood pressure to cardiovascular complications, but this information is lacking for out-of-office blood pressure. At baseline, daytime ambulatory (n=12 624) or home (n=5297) blood pressure were measured in 17 921 participants (51.3% women; mean age, 54.2 years) from 17 population cohorts. Subsequently, mortality and cardiovascular events were recorded. Using multivariable Cox regression, floating absolute risk was computed across 4 age bands (≤60, 61–70, 71–80, and >80 years). Over 236 491 person-years, 3855 people died and 2942 cardiovascular events occurred. From levels as low as 110/65 mm Hg, risk log-linearly increased with higher out-of-office systolic/diastolic blood pressure. From the youngest to the oldest age group, rates expressed per 1000 person-years increased ( P <0.001) from 4.4 (95% CI, 4.0–4.7) to 86.3 (76.1–96.5) for all-cause mortality and from 4.1 (3.9–4.6) to 59.8 (51.0–68.7) for cardiovascular events, whereas hazard ratios per 20-mm Hg increment in systolic out-of-office blood pressure decreased ( P ≤0.0033) from 1.42 (1.19–1.69) to 1.09 (1.05–1.12) and from 1.70 (1.51–1.92) to 1.12 (1.07–1.17), respectively. These age-related trends were similar for out-of-office diastolic pressure and were generally consistent in both sexes and across ethnicities. In conclusion, adverse outcomes were directly associated with out-of-office blood pressure in adults. At young age, the absolute risk associated with out-of-office blood pressure was low, but relative risk high, whereas with advancing age relative risk decreased and absolute risk increased. These observations highlight the need of a lifecourse approach for the management of hypertension.

Objectiveβ-blockers (BBs) with different pharmacological properties may have heterogeneous effects on sympathetic nervous activity (SNA) and central aortic pressure (CAP), which are independent cardiovascular factors for hypertension. Hence, we analyzed the effects of bisoprolol and atenolol on SNA and CAP in hypertensive patients.MethodsThis was a prospective, randomized, controlled study in 109 never-treated hypertensive subjects randomized to bisoprolol (5 mg) or atenolol (50 mg) for 4–8 weeks. SNA, baroreflex sensitivity (BRS) and heart rate (HR) variability (HRV) were measured using power spectral analysis using a Finometer. CAP and related parameters were determined using the SphygmoCor device (pulse wave analysis).ResultsBoth drugs were similarly effective in reducing brachial BP. However, central systolic BP (−14±10 mm Hg vs −6±9 mm Hg; P<0.001) and aortic pulse pressure (−3±10 mm Hg vs +3±8 mm Hg; P<0.001) decreased more significantly with bisoprolol than with atenolol. The augmentation index at a HR of 75 bpm (AIxatHR75) was significantly decreased (29%±11% to 25%±12%; P = 0.026) in the bisoprolol group only. Furthermore, the change in BRS in the bisoprolol group (3.99±4.19 ms/mmHg) was higher than in the atenolol group (2.66±3.78 ms/mmHg), although not statistically significant (P>0.05). BRS was stable when RHR was controlled (RHR≤65 bpm), and the two treatments had similar effects on the low frequency/high frequency (HF) ratio and on HF.ConclusionBBs seem to have different effects on arterial distensibility and compliance in hypertensive subjects. Compared with atenolol, bisoprolol may have a better effect on CAP.Trial RegistrationClinicalTrials.gov NCT01762436

Progressive neurological deterioration poses enormous burden on the aging population with ischemic stroke and neurodegenerative disease patients, such as Alzheimers' disease and Parkinson's disease. The past two decades have witnessed remarkable advances in the research of neurovascular unit dysfunction, which is emerging as an important pathological feature that underlies these neurological disorders. Dysfunction of the unit allows penetration of blood-derived toxic proteins or leukocytes into the brain and contributes to white matter injury, disturbed neurovascular coupling and neuroinflammation, which all eventually lead to cognitive dysfunction. Recent evidences suggest that aging-related oxidative stress, accumulated DNA damage and impaired DNA repair capacities compromises the genome integrity not only in neurons, but also in other cell types of the neurovascular unit, such as endothelial cells, astrocytes and pericytes. Combating DNA damage or enhancing DNA repair capacities in the neurovascular unit represents a promising therapeutic strategy for vascular and neurodegenerative disorders. In this review, we focus on aging related mechanisms that underlie DNA damage and repair in the neurovascular unit and introduce several novel strategies that target the genome integrity in the neurovascular unit to combat the vascular and neurodegenerative disorders in the aging brain.