General factors such as male sex, elderly patients, mandibular anterior location, bone augmentation and short implants were associated with implant loss.

No abstract

Astrocytes play an important role in the coupling between neuronal activity and brain blood flow via their capacity to "sense" neuronal activity and transmit that information to parenchymal arterioles. Here we show another role for astrocytes in neurovascular coupling: the ability to act as a signaling conduit for the vitally important process of upstream vasodilation (represented by pial arterioles) during both excessive (seizure) and physiological (sciatic nerve stimulation) increases in cerebral cortical neuronal activity. The predominance of an astrocytic rather than a vascular route was indicated by data showing that pial arteriolar-dilating responses to neuronal activation were completely blocked following selective disruption of the superficial glia limitans, whereas interference with interendothelial signaling was without effect. Results also revealed contributions from connexin 43, implying a role for gap junctions and/or hemichannels in the signaling process and that signaling from the glia limitans to pial arterioles may involve a diffusible mediator.

Background and Purpose-Recent findings indicate that estrogen (ie, 17␤-estradiol [E 2 ]) provides neuroprotection in models of transient global and focal ischemia. Enhanced postischemic leukocyte adhesion and infiltration have been linked to neuropathology in the brain as well as other tissues. We recently showed that estrogen reduces leukocyte adhesion in the cerebral circulation of female rats during resting conditions. Methods-We compared leukocyte adhesion in pial venules in vivo in intact, ovariectomized (OVX), and E 2 -treated OVX female rats subjected to transient forebrain ischemia (30-minute right common carotid artery occlusion and hemorrhagic hypotension) and reperfusion. Adherent rhodamine-6G-labeled leukocytes were viewed through a closed cranial window with the use of intravital microscopy. Leukocyte adhesion was measured before ischemia and at different times after reperfusion. Results-Before ischemia, leukocyte adhesion (measured as a percentage of venular area occupied by adherent leukocytes) was 2 to 3 times greater in OVX versus intact or E 2 -treated OVX rats (7.0%, 3.4%, and 2.2%, respectively). This difference disappeared at 120 minutes of reperfusion, when comparable levels of enhanced leukocyte adhesion were observed in all groups. In OVX rats, leukocyte adhesion remained elevated after 4 and 6 hours of reperfusion (11.6% and 12.9%, respectively), while the other 2 groups showed significantly lower levels (5.0% and 5.8% for intact rats and 7.0% and 7.2% for E 2 -treated OVX rats). Conclusions-Present

We examined whether damage to the glia limitans (GL), via exposure to the gliotoxin L-␣-aminoadipic acid (L-␣AAA), alters hypercapniainduced pial arteriolar dilation in vivo. Anesthetized female rats were prepared with closed cranial windows. Pial arteriolar diameters were measured using intravital microscopy. L-␣AAA (2 mM) was injected into the space under the cranial windows 24 h before the study, and injury to the GL was confirmed by light microscopy. L-␣AAA was associated with a reduction in pial arteriolar CO 2 reactivity to 40 -50% of the level seen in vehicle-treated controls, with no further reduction in the CO 2 response after nitric oxide (NO) synthase (NOS) inhibition via N -nitro-L-arginine (L-NNA). Subsequent blockade of prostanoid synthesis, via indomethacin (Indo), reduced CO2 reactivity to 10 -15% of normal. In vehicle-treated controls, L-NNA, followed by Indo, reduced the response to ϳ50% and then to 15-20% of the normocapnic value, respectively. On the other hand, L-␣AAA had no effect on vascular responses to the endothelium-dependent vasodilator acetylcholine or the NO donor SNAP and did not alter cortical somatosensory evoked responses. This indicates an absence of any direct L-␣AAA actions on pial arterioles or influence on neuronal transmission. Furthermore, L-␣AAA did not alter the vasodilation elicited by topical application of an acidic artificial cerebrospinal fluid solution, suggesting that the GL influences the pial arteriolar relaxation elicited by hypercapnic, but not local extracellular (EC), acidosis. That differences exist in the mechanisms mediating hypercapniaversus EC acidosis-induced pial arteriolar dilations was further exemplified by the finding that topical application of a neuronal NOS (nNOS)-selective blocker (ARR-17477) reduced the response to hypercapnia (by ϳ65%) but not the response to EC acidosis. Disruption of GL gap junctional communication, using an antisense oligodeoxynucleotide (ODN) connexin43 knockdown approach, was accompanied by a 33% lower CO 2 reactivity versus missense ODN-treated controls. These results suggest that the GL contribution to the hypercapnic vascular response appears to involve the NO-dependent component rather than the prostanoid-dependent component and may involve gap junctional communication. We speculate that the GL may act to facilitate the spread, to pial vessels, of hypercapnia-induced vasodilating signals arising in the comparatively few scattered nNOS neurons that lie well beneath the GL. connexin; gap junction; hypercapnia; L-␣-aminoadipic acid; nitric oxide; prostanoids BECAUSE OF THE INTIMATE ANATOMIC RELATIONSHIP between cerebral resistance vessels and astrocytes (19), it has been postulated that astrocytes play a vital role in the regulation of local perfusion in the brain (7). In fact, experimental evidence to that effect has been published (43). Small pial arterioles (Ͻ50 m), although exhibiting a relative paucity of direct neural connections (8, 33), nevertheless appear to be regulated by extravascular influences (23,38). F...

We examined whether the glia limitans (GL) influences pial arteriolar relaxation elicited in vivo by the purinergic (P(2)Y(1) receptor) agonist ADP in female rats, and whether that influence is altered in ovariectomized (Ovx) females. A validated model for GL injury was used, topical application of the gliotoxin L-alpha-aminoadipic acid (L-alphaAAA), 24 h before the study. In both intact and Ovx females, L-alphaAAA had no effect on responses to the NO donor, S-nitroso-N-acetyl penicillamine, but ADP-induced pial arteriolar dilations were significantly reduced (by 33-90%), compared with vehicle-treated controls. When N(G)-nitro-L-arginine (L-NNA) was administered to L-alphaAAA-treated rats, the ADP response was virtually lost in intact females, but no further reductions were observed in the Ovx rats. On the other hand, in L-alphaAAA-treated Ovx females, when the gap junction blocker, Gap 27, was subsequently added to the suffusate, ADP reactivity fell to very low levels. In vehicle-treated control rats, L-NNA and Gap 27 reduced ADP reactivity by approximately 50% in intact and Ovx females, respectively. An earlier study indicated that the endothelium was a key site of influence for L-NNA (intact) and Gap 27 (Ovx). Thus present and previous results imply that the ADP response in pial arterioles represents the additive actions of an endothelial and a GL component. That supposition was confirmed in the present study by the finding that combining endothelial and GL injury produced an essentially complete loss of ADP reactivity in both intact and Ovx females. Finally, topical application of the selective P(2)Y(1) antagonist, MRS-2179, was associated with a nearly complete suppression of the ADP response in both intact and Ovx females. These results suggest that 1) ADP-induced pial arteriolar dilation involves additive contributions from P(2)Y(1) receptors present in both vascular endothelium and the GL; 2) the influence of the GL component is not altered by ovariectomy; and 3) the gap junction-dependent component of the ADP response in Ovx females is unlikely to include the GL and probably resides in the vessels themselves.

We report Shanghai Tian Ma Radio Telescope detections of several long carbonchain molecules at C and Ku band, including HC 3 N, HC 5 N, HC 7 N, HC 9 N, C 3 S, C 6 H and C 8 H toward the starless cloud Serpens South 1a. We detected some transitions (HC 9 N J=13-12 F=12-11 and F=14-13, H 13 CCCN J=2-1 F=1-0 and F=1-1, HC 13 CCN J=2-1 F=2-2, F=1-0 and F=1-1, HCC 13 CN J=2-1 F=1-0 and F=1-1) and resolved some hyperfine components (HC 5 N J=6-5 F=5-4, H 13 CCCN J=2-1 F=2-1) for the first time in the interstellar medium. The column densities of these carbon-chain molecules in a range of 10 12 -10 13 cm −2 are comparable to two carbon-chain molecule rich sources, TMC-1 and Lupus-1A. The abundance ratios are 1.00:(1.11±0.15):(1.47±0.18) for [H 13 CCCN]:[HC 13 CCN]:[HCC 13 CN]. This result implies that the 13 C isotope is also concentrated in the carbon atom adjacent to the nitrogen atom in HC 3 N in Serpens south 1a, which is similar to TMC-1. The [HC 3 N]/[H 13 CCCN] ratio of 78±9, the [HC 3 N]/[HC 13 CCN] ratio of 70±8, and the [HC 3 N]/[HCC 13 CN] ratio of 53±4 are also comparable to those in TMC-1. In any case, Serpens South 1a proves a testing ground for understanding carbon-chain chemistry.

No abstract