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The persist() method of the StorageManager interface requests permission to use persistent storage, and returns a Promise that resolves to true if permission is granted and bucket mode is persistent, and false otherwise.


What contributes to these persistent wage gaps? Research shows that a majority of each of these gaps can be explained by differences in education, labor force experience, occupation or industry and other measurable factors.

If a value is wrapped in $persist, on initialization Alpine will register its own watcher for that value. Now everytime that value changes for any reason, Alpine will store the new value in localStorage.

$persist works with primitive values as well as with arrays and objects.However, it is worth noting that localStorage must be cleared when the type of the variable changes.Given the previous example, if we change count to a value of $persist( value: 0 ), then localStorage must be cleared or the variable 'count' renamed.

If you want to use $persist with, you need to use a standard function instead of an arrow function so Alpine can bind a custom this context when it initially evaluates the component scope.

Adversaries also have a way to reestablish persistence using a lingering federated session. As noted earlier, AWS documentation on the GetFederationToken API stated prior to the release of this blog post:

The results for each search are saved in a CSV file that is available for 7 days. Results are deleted after this time period. When a search has a Pending status for 24 hours, its status changes to Failed. When a search has a Failed status, you can try to persist the search again. The available statuses are:

If you want to enable selected users to persist searches, you can add the Persist Search permission to their global permissions. To learn how to assign a global permission, see Using the Global Permissions Feature.

The analysis underscores how vaccine disparities have improved as availability has opened up and Biden administration officials have attempted to prioritize equitable distribution. Still, gaps persist even as minority groups have suffered much higher mortality rates from the pandemic than whites and are at risk of infection as states move to reopen and lift mask mandates.

The decreased numbers of total mDCs, CD1c+ mDCs and pDCs found in acute SARS-CoV-2 infected patients were in accordance with previous publications [5, 6]. This fact might be explained by different mechanisms, including apoptosis due to increased inflammatory mediators produced by abortive SARS-CoV-2 infection of myeloid cells [25]. Another nonexclusive explanation could be that DCs migrate from peripheral blood to tissues or inflammatory sites, such as CD1c+ mDCs preferential migration to the lungs in patients with severe COVID-19 [6]. These defects were accompanied by alterations mainly found in activation, migration and tolerogenic markers that importantly persisted 7 months after infection in previously hospitalized and also in nonhospitalized patients. Especially persistent in the total and DC subsets was the decreased expression of integrin β7. The expression of αEβ7 defines migration to antigen presentation sites within lymph nodes [26] and α4β7 on mDCs and pDCs is indicative of migration of these cells to gut [27]. Remarkably, SARS-CoV-2 has been shown to infect and productively replicate in human small intestinal organoids, increasing cytokine production and human angiotensin-converting enzyme 2 expression [28]. It has been also reported, that the disruption in gut barrier integrity contributes to COVID-19 severity [29]. Thus, the lower percentage of DCs expressing integrin β7 in peripheral blood might be a consequence of ongoing DC migration to the gut or other tissues or inflammatory sites up to 7 months after infection. In fact, necropsy studies in SARS-CoV-2 infected patients have shown mononuclear inflammatory infiltrates in different organs [30]. Also prominent was the deficit in IDO expressing DCs 7 months after infection. In contrast, IDO+ CD1c+ and CD16+ mDC levels in acute infection were dramatically increased compared to HD. This is in agreement with other acute respiratory infections such influenza [31] and respiratory syncytial virus [32] in which IDO expression is increased in order to counteract excessive inflammation as happen after acute SARS-CoV-2 infection. However, in this infection, the tissue damage in low respiratory tract is prominent [33] and may persist at the long-term what may cause the exhaustion of IDO producing DCs and/or migration of these cells to inflammatory focus even after 7 months after infection. Although these defects were present independently of whether or not the participants were previously at the hospital, hospitalized patients showed additional defects. These were, lower expression of the co-stimulatory molecule CD86, found in acute infection also by other authors [5, 7, 24] that persisted 7 months after infection together with lower levels of CD4+ DCs. Low levels of activation molecules, such as CD86 have been related with a possible impairment in T cell and DCs response to the virus. Specifically, we and others have found pDC hyporesponsiveness to HIV after CD4 downregulation in this cell type [15, 34]. On the contrary, CCR7+ pDCs remained at high levels even after 7 months after infection indicating again ongoing migration to lymph node or other inflammatory foci. In this line, the higher expression of other chemokine receptors such as CCR1, CCR3, and CCR5 has previously described in SARS-CoV-1 infected monocyte derived DCs [35].

It is unknown whether these defects in the DCs compartment will be reversible after longer follow up or specific therapies may be needed for the normalization of these defects. What is clear is that persisting symptoms and unexpected substantial organ dysfunction are observed in an increasing number of patients who have recovered from COVID-19 [12]. Actually, Huang et al. recently described that 7 months after illness onset, 76% of the SARS-CoV-2 infected patients reported at least one symptom that persisted, being fatigue or muscle weakness the most frequently reported symptoms [36]. In addition, many of those previously hospitalized patients presented residual chest imaging abnormalities, impaired pulmonary diffusion capacity and other extrapulmonary manifestations as a low estimated glomerular filtration rate [36]. The immune mechanisms that might be involved in the development of these persisting symptoms are still unknown. However, it would be expected that 7 months after SARS-CoV-2 infection there is still an inflammatory response due to persistent tissue damage or persistence presence of viral antigens in the absence of viral replication which may cause these deficits in DC. In fact, it has been reported that SARS-CoV-2 can persist in the intestines up to 7 months following symptoms resolution [37]. Thus, we postulate that the decrease in peripheral DCs numbers, along with the alterations in DC homing and activation markers 7 months after the infection might be indicative of DC migration to inflammatory sites which may be contributing to long-term symptoms, a phenomenon also known as long COVID.

One of the limitations of this study might be that, for a more precise identification of pDCs, CD2+, CD5+, and AXL+ cells should have been excluded [38]. Nevertheless, since these cell populations are barely represented within PBMCs, the showed results correspond mainly to pDCs, although some contamination with AS-DC cannot be excluded. The same happened with CD123+ mDCs, which were not included in our gating strategy, however, the levels of this subset was so low that did not change total mDC levels (data not shown). Moreover, a limitation of this work might be that all patients included in this study belong to the first wave of COVID-19 in Spain. It would have been interesting to have access to tissue samples, however due to safety issues at that moment of the pandemic it was not possible. At that time, different experimental treatments with very limited but transitory immunosuppressive effects were administered what may have affected the levels of immune parameters. However, the agreement of our observations with other data in the literature during acute infection and the persistence of these defects 7 months after infection minimized the potential bias of these treatments in our results.

The MySQL server maintains system variables that configure its operation. A system variable can have a global value that affects server operation as a whole, a session value that affects the current session, or both. Many system variables are dynamic and can be changed at runtime using the SET statement to affect operation of the current server instance. SET can also be used to persist certain global system variables to the mysqld-auto.cnf file in the data directory, to affect server operation for subsequent startups. RESET PERSIST removes persisted settings from mysqld-auto.cnf.

The capability of persisting global system variables at runtime enables server configuration that persists across server startups. Although many system variables can be set at startup from a my.cnf option file, or at runtime using the SET statement, those methods of configuring the server either require login access to the server host, or do not provide the capability of persistently configuring the server at runtime or remotely: 041b061a72


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