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User agents may provide users the option of disabling the window.performance.timing and window.performance.navigation interfaces. When these interfaces are disabled, both window.performance.timing and window.performance.navigation must return a null value.

Example

A user agent may maintain instances of the PerformanceTiming and PerformanceNavigation interfaces until the Window object associated with the current document is created, when window.performance.timing and window.performance.navigation are replaced with these instances.

Illustration

This illustration is non-normative.

The following graph illustrates the timing attributes defined by the PerformanceTiming interface and the PerformanceNavigation interface with or without redirect, respectively. Attributes underlined may not be available in navigation involving documents from different Merrell Freewheel Lace Charcoal Mens Shoes From China Free Shipping Clearance Clearance Store Pay With Paypal Online Clearance Release Dates kXPr7lq
. User agents may perform internal processing in between timings, which allow for non-normative intervals between timings.

Return to step 11 if the user agent fails to send the request or receive the entire response, and needs to reopen the connection.

Example

When persistent connection [ RFC 2616 ] is enabled, a user agent may first try to re-use an open connect to send the request while the connection can be asynchronously closed . In such case, connectStart, connectEnd and requestStart should represent timing information collected over the re-open connection.

There are implied strong references from the window object to its window.performance.timing and window.performance.navigation objects.

The value of the timing attributes must monotonically increase to ensure timing attributes are not skewed by adjustments to the system clock during the navigation. The difference between any two chronologically recorded timing attributes must never be negative. For all navigations, including subdocument navigations, the user agent must record the system clock at the beginning of the root document navigation and define subsequent timing attributes in terms of a monotonic clock measuring time elapsed from the beginning of the navigation.

Vendor-specific proprietary user agent extensions are discouraged. If such extensions are needed, e.g., for experimental purposes, vendors must use the following extension mechanisms:

There is the potential for disclosing an end-user's browsing and activity history by using carefully crafted timing attacks. For instance, the unloading time reveals how long the previous page takes to execute its unload handler, which could be used to infer the user's login status. These attacks have been mitigated by enforcing the same Lab Pal Zileri FOOTWEAR Laceup shoes su YOOXCOM Discount Limited Edition Best Sale Cheap hLTPTS
policy when timing information involving the previous navigation is accessed.

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Annual analysis of airline sector economics, trends, and performance.

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Fig. 3.

Minocycline prevents MPTP-induced MAC-1 transcription. , , Ventral midbrain MAC-1 mRNA levels but not GFAP mRNA levels are increased by 24 hr after MPTP injection compared with those of saline- or minocycline-injected mice. Minocycline prevents MPTP-induced MAC-1 mRNA increases. MAC-1 and GFAP mRNA values are normalized with GAPDH. Values are mean ± SEM ratios ( = 5–7 mice per group)., Saline-treated; minocycline-treated;, MPTP-treated; , MPTP plus minocycline-treated. * < 0.05, higher than both saline- and minocycline-injected control groups. ** < 0.05, lower than MPTP-injected group and not different from both control groups.

Fig. 4.

Minocycline prevents MPTP-induced microglia reaction. Microglia cells () and TH-positive neurons () are seen in both SNpc and striatum of all mice. One day after the last MPTP injection, numerous activated microglia (larger cell body, poorly ramified short and thick processes) are seen in SNpc (, ) and striatum (, ). Mice injected with both MPTP and minocycline show minimal microglial activation in SNpc () and striatum (); here, microglial cell bodies are small and processes are thin and ramified (, ). Scale bar:, , , , 1 mm; , , ,, 100 μm.

Fig. 5.

Minocycline does not affect MPTP-induced astrocytic reaction. One day after the last injection of MPTP, there is a mild astrocytic response (, ), but 7 d after the last injection of MPTP, it becomes conspicuous (, ). Minocycline does not affect the astrocytic response (, ) 7 d after MPTP administration. Scale bar: ,, , 1 mm; ,, , 100 μm.

Given the effect of minocycline on MPTP-induced microglial activation, we assessed whether the production of known microglial noxious mediators such as IL-1β, ROS, and NO will also be inhibited by minocycline (Fig. Calvin Klein Magnus Bit Driver Top Quality For Sale e2fzQT6j
). The levels of ventral midbrain IL-1β differed significantly among the four group of mice ( F (3,21) = 7.946; p < 0.001) (Fig. Churchs Consul Nevada calf leather shoes Recommend Online B62AT4Un
A ). Ventral midbrain levels of the proinflammatory cytokine IL-1β in MPTP-injected mice (18 mg/kg for four injections) were significantly increased (Fig. Discount Visit New GELHUNTER 3 Volleyball shoes poseidon/white/safety yellow Sale Low Cost Discount Pictures 14d08
A ). However, MPTP produced significantly smaller increases in IL-1β levels in ventral midbrain of MPTP mice treated with minocycline (45 mg/kg twice daily) (Fig. 6 A ). iNOS activity ( F (3,24) = 9.055; p < 0.001) and the ratio of membrane/total p67 phox ( F (3,23) = 4.336; p < 0.05) also varied significantly among the various groups. iNOS and NADPH–oxidase, two prominent enzymes of activated microglia that produce NO and ROS, respectively, exhibited induction patterns similar to those described for IL-1β in that ventral midbrain iNOS activity was increased by 200% (Fig. 6 B ) and NADPH–oxidase activation, evidenced by the translocation of its subunit p67 phox from the cytosol to the plasma membrane, was increased by 80% 24 hr after the last injection of MPTP (Fig. 6 C , D ). MPTP-induced iNOS activity and NADPH–oxidase were both abolished by minocycline administration (Fig. 6 B–D ).

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