Category Archives: Reveryplay

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In this case, there are at least two disks that I probably need to configure, since /dev/sde seems to be parking as often as about every 4 minutes (0.004 Hz) and /dev/sdc is only parking slightly less often. The smartmon_load_cycle_count_value metric seems like it would be the right one to query, but that actually expresses a percentage value (0-100) representing how many load cycles remain in the specified lifetime- on reaching 0 the disk has done a very large number of load cycles. It does support reading arbitrary metrics from text files written by other programs with its textfile collector however, which is fairly easy to integrate with arbitrary other tools. These communities are filled with knowledgeable individuals who can offer more personalized advice and help you navigate the complexities of long-term data storage.

Microsoft Remote Desktop

However, I noticed that my HDD’s heads park (particulary Seagate Exos) every 3 minutes. ZFS is widely trusted for large-scale storage, but production environments expose design mistakes,… When dealing with critical data, you only get one chance to do it right. The status field is a bitmask supporting a number of different options, but the main ones we care about are 1 (OK), and 2 (FAULTED). When combined with a JSON parser like jq, this can be used to automate tasks for each disk.

Is AnyDesk free?

• It’s hard to imagine why your drives are that loud!
• For quietness, a noise reducing case, move it somewhere else, quieter drives, maybe SSD instead of hard drives, etc.
• It refreshes the disks SMART information every 5 min.
• In this article we will discuss some strategies and tools to make managing disk arrays on FreeBSD (and related platforms like TrueNAS Core) much easier.
• NVMe on the other hand, supports multiple queues (often 64 queues, but the official specification allows for up to 65,536 queues) allowing for many commands to be run concurrently.
• At somewhat larger scales, a number of drives can be connected directly to a SAS (or SATA) controller PCIe card.

The parking rate basically drops to zero at the time I updated the settings for the Seagate drives, and the Western Digital one hasn’t changed because it needs to be powered off to change that setting and I haven’t done so yet. The other slight annoyance when setting the idle3 timer on WD drives is that changes only take effect when the drive is powered on, usually meaning the host computer must be fully shut down and started back up for any changes to be seen- this makes experimentation to determine how raw timer values are interpreted a slower and more tedious process. Of particular note, WD Green drives ship configured to park the heads after only 8 seconds of inactivity which could notionally wear out the disk in a matter of months if the heads are cycling more-or-less continuously! For drives made by Western Digital, the inactivity timer for parking the heads is called the idle3 timer.
While I have been aware of this in my home server as well, it is easy to forget to ensure that disks are not silently killing themselves by cycling the heads. With modern, especially Enterprise grade hard drives being able to have hundreds of thousands of head park operations in their service life, is this really an isssue? With the tools presented here, the reader is well armed to react to failed disks and ensure that the wrong disk isn’t accidentally pulled. However, if a disk has died entirely, or a slot is empty, it might not have a device name. Sesutil can also be used to locate the disk in the physical array.While the SES data tells us that there is an 8 TB disk in Slot 06, it does not tell us which slot in the chassis corresponds to 06. Looking at a few items from the output, we can see the device names (/dev/da0 and /dev/da7 respectively) of the disks in Slot00 and Slot07.

Collecting SMART metrics

Obligatory word of warning – mucking with low-level drive settings like this can cause issues. Has anyone found a tool that can use EPC to change the Idle_b and Idle_c values for Exos drives? View an ad to download for free It’s self-hosted and self-managed, so data remains within your company network.Bank-Level EncryptionBanking-standard TLS 1.2 technology protects your computer from unauthorized access. Unparalleled PerformanceOur proprietary video-codec, DeskRT, compresses image data to reduce bandwidth and latency to a level imperceptible to the human eye. With decades of experience in IT management and later as a writer and tutor, she combines technical knowledge with a passion for clear communication.

Smart Check Intervals & HDD Head Parking

If your system has multipath SAS, each disk will be present more than once, and you should use the gmultipathcommand to deduplicate your disks and for labeling as well. FreeBSD supports a number of different ways to label the disk, depending on your use case. The map command displays all of the SES devices and each element (this is the nomenclature in SES) connected to them. Of course, all of this chassis management technology isn’t very effective without tools to make it usable. It also provides information about each slot in the enclosure (even if empty), including a flag to indicate if the device has recently been swapped.

• Then, click on “Connect” to access the other device.
• The status field is a bitmask supporting a number of different options, but the main ones we care about are 1 (OK), and 2 (FAULTED).
• NVMe connects storage devices directly to the PCIe bus, offering extremely low latency and high throughput.
• When dealing with critical data, you only get one chance to do it right.
• Looking at a few items from the output, we can see the device names (/dev/da0 and /dev/da7 respectively) of the disks in Slot00 and Slot07.

I will optimize settings later for the security/quietness tradeoff however, I’m very pleased with it for now. How can I set this value on the Truenas interface? Keeping it spinning but not accessing data is safer. I would still recommend against idling your drive as that reduces longevity. I also set the tunable vfs.zfs.txg.timeout to a somewhat large value so the regular syncs don’t happen every 5 seconds.
This will activate the fault LED for element 9 (Slot 08) on the first SES device. You can avoid any uncertainty by enabling the “locate” or “fault” LED for the drive you mean to replace. This example creates a new GPT partition scheme on da36, creates a 4 GiB swap partition aligned to 1 MiB boundaries, and then adds a ZFS partition with the label e3s01-ZGY0XH87 using the remainder of the space on the disk.
SAS disk reservations provide the ability to connect to the disk redundantly—or even across multiple machines—while ensuring it is only used by one of them at a time. SAS provides many more features than SATA does—including full duplex operations, advanced error recovery, multipath, and disk reservations. It too was an extension on an existing interface bus which offered greatly improved performance. SATA+AHCI improved data transfer speeds, simplicity of communication, and included abilities that we today take for granted, such as “hot swap” and command queueing. These concepts also apply to other operating systems, but the tools might differ slightly.

I moved the system dataset to the boot pool. I don’t move any data, no apps are running, this is a vanilla Scale install so far, yet the HDD is in constant work. 1 SSD to boot and 1 HDD to store data. Agree, I have used SeaChest with good results for this same issue on scale plus drive cache. If you do it on a live pool, I’d back up your data first.
Direct Attached deployments require a bit more hardware and cabling. The NVMe interface is also extensible to allow operating over the network (where it is known as NVMe Over Fabric or NVMe-oF). NVMe on the other hand, supports multiple queues (often reveryplay 64 queues, but the official specification allows for up to 65,536 queues) allowing for many commands to be run concurrently. While both SATA and SAS allow multiple commands to be issued at once to the device, these commands cannot actually be executed concurrently—instead, they are queued for sequential operation.
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CD56highCD16+/− NK cells aredescribed by NKG2A, low level of perforin, and are primarily characterized bycytokine production.16,30,31 Therefore, it is likely that the changes in the frequencies oftwo subsets of NK cells during the disease recovery are protective mechanisms toeliminate the SARS-COV2 and thereby reducing inflammation occurred in the earlystages of disease. Our data revealed that the percentages of Th1, Th2, andTh17 cells were significantly lower in patients than healthy control (Figure 3(a)–(c) and (j)–(l), P Figure 3(d)–(h) and (m)–(q), P Figure 3(f), (h), (o), and (q), P Figure3(d), (e),(g), (m), (n), and (p)). The number of CD56low CD16+ NK cells in patients wassignificantly increased compared to healthy subjects. To determine the percentages of activated T cells, exhausted T cells, Th1 cells,Th2 cells, Th17 cells, Tregs, B cells, NK cells, and monocytes in peripheralblood of COVID-19 patients (the first day and 10 days of initiation oftherapeutic approaches) and healthy subjects, PBMCs were stained with differentmonoclonal antibodies or matched to isotype control IgG for 30 min at4○C. These changes may play afundamental role in reducing disease severity through regulating cytokineproductions involved in the inflammation and functions of various immune cells.Nevertheless, larger and more multicenter studies are needed to validate theseconclusions. A limitation of the study was the lack of determinationof immune system differences between alive and dead patients with COVID-19 during arecovery period.
The stained cells were washedtwice with PBS and centrifuged at 300 × g for 10 min at roomtemperature. Fixation and permebilization of the cells were performed for stainingsome intracellular molecules with different antibodies according to themanufacturer’s guideline (eBiosciences, USA). The isolated cells were washed twice with phosphate buffered saline(PBS) at 300 × g for 10 min. Peripheral bloodmononuclear cells (PBMCs) were isolated from whole blood by Ficoll-Paquecentrifugation according to the manufacturer’s instructions (Lymphodex,Germany).
The RRF funding amounts shown for measures are based on the initial cost estimates provided by the Member States included in the recovery and resilience plans and may as such differ from finalized Commission financial reports, which follow eventual project implementation. The map exclusively serves information purposes and is not an exhaustive database of projects supported by the Recovery and Resilience Facility. Improving access to and the quality of general, vocational, and higher education; focusing on digital education, early childhood education and care; supporting youth employment. The funding amounts shown reflect the initial cost estimates included in the national recovery and resilience plans. It is not an exhaustive database of projects supported by the Facility and will be regularly updated as the implementation progresses.
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Moreover, Qinet al. indicated that suppressor and helper T cell percentages were lower inpatients than normal group. In the next step, the adaptive immune system of COVID-19 subjects was studied after 1and 10 days of initiation of therapeutic methods. In an attempt to discover the frequency of other cells of innateimmunity, the number of monocytes was also assessed. As shown inFigure 4(a)–(d),statistically significant reduction in the levels of pro-inflammatory cytokines(IL-1α, IL-1β, IL-6, and TNF-α) in patients were observed during a recovery,with the exception of IL-1β level (P Figure 4(e),P Figure 4(f)). Having considered that severe COVID-19 is largely related to a cytokine storm,cytokine profiles of COVID patients were assessed during a recovery.

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Other results of the currentstudy revealed that the percentage of another subset of NK cells(CD56highCD16+/− NK cells) was significantly increased atthe first day of recovery. TheCD56lowCD16+ NK cells have high expression levels ofkiller inhibitory receptors, the maturation marker (CD57), and natural andantibody-dependent cellular cytotoxicity which is mediated by releasing high levelsof perforin and enhanced killing.16,30,31 These findings suggest thatthe reduced number of CD56lowCD16+ NK cells may contribute todisease susceptibility in the early stages of disease. COVID-19, as a pandemic disease, is responsible for considerable mortality and morbidity.25 Immune system functions have fundamental role in the pathogenesis and outcomeof disease.26 Therefore, the current study focused on determining how immune system changesduring a recovery were correlated to disease severity. Thepercentages of Th1, Th2, Th17, Tregs, exhausted CD4+ T cells, exhaustedCD8+ T cells, activated CD4+ T cells, activated CD8+ T cells, and Bcells were assessed using flow cytometry (a–i) and then analyzed (j–r).The depicted results are representative of 57 independent experimentsfor COVID-19 patients at the first day of treatment, 51 independentexperiments for COVID-19 patients in 10 days of treatment, and 40independent experiments for healthy groups. The frequencies of innate immune cells in COVID-19 and control subjects.The percentages of CD56low CD16+ NK cells,CD56high CD16+/− NK cells, and monocytes werestudied by flow cytometry (a and b) and then analyzed (c–e).
In disagreement with other reports showing increasedfrequency of B cells in the late stage of recovery,17 we observed that the percentage of this cell was decreased followingrecovery. Moreinterestingly, the percentages of exhausted CD4+ T cells and exhausted CD8+ T cellswere higher in the early stage of recovery than the late stage of recovery. Thisobservation was in contrast with previous study showing severe cases of COVID-19tend to have lower percentages of monocytes.24 This discrepancy may be attributed to disease stage which patients wereevaluated.

• Data were analyzed by GraphPad Prism 6 (GraphPad Software, USA) and are expressedas the mean standard error of the mean (SEM) and mean ± standard deviation (SD).The normal distribution of data was determined by Kolmogrov–Smirnov test.
• TheCD56lowCD16+ NK cells have high expression levels ofkiller inhibitory receptors, the maturation marker (CD57), and natural andantibody-dependent cellular cytotoxicity which is mediated by releasing high levelsof perforin and enhanced killing.16,30,31 These findings suggest thatthe reduced number of CD56lowCD16+ NK cells may contribute todisease susceptibility in the early stages of disease.
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• Thepercentages of Th1, Th2, Th17, Tregs, exhausted CD4+ T cells, exhaustedCD8+ T cells, activated CD4+ T cells, activated CD8+ T cells, and Bcells were assessed using flow cytometry (a–i) and then analyzed (j–r).The depicted results are representative of 57 independent experimentsfor COVID-19 patients at the first day of treatment, 51 independentexperiments for COVID-19 patients in 10 days of treatment, and 40independent experiments for healthy groups.
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• The CD3+ cell population was also determined using the gating oflymphocyte population and was then used to measure the percentages of B cells(CD3− CD19+ CD22+ cells), exhausted CD4+ T cells (CD3+ CD4+ PD-1+ cells),exhausted CD8+ T cells (CD3+ CD8+ PD-1+ cells), CD56lowCD16+ NK cells (CD3− CD56lowCD16+ cells), and CD56high CD16+/− NK cells(CD3−CD56high CD16+/− cells).

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Having considered that innate immunity provides the early line of defense againstviral infections, some innate immune cells were studied in the course of 10 daysafter initiation of treatment, which is almost a period that the disease isdeteriorated and may result in death or recovery from COVID-19.27,28 Our datashowed that CD56lowCD16+ NK cell number was significantlylower in the early stage of recovery than the late stage of recovery; however itsfrequency was noticeably increased compared to healthy subjects. Moreover, the authors have shown that CD4+and CD8+ T cell numbers were notably decreased.17 In agreement with previous study, our data revealed that the frequencies ofTh cells (Th1, Th2, and Th17 cells) in patients were significantly lower in theearly recovery stage than the late recovery stage and healthy individuals. B cells showed an increasedpercentage in patients compared to healthy subjects, while this increase wassignificantly reduced in the late stage of recovery (Figure 3(i) and (r),P Open in a new tabThe percentages of adaptive immune cells in COVID-19 and healthyindividuals. Its frequency wassignificantly higher in the late recovery stage than early recovery stage (Figure 2(a) and (c),P highCD16+/− NK cells in the early stage of recovery was significantlyincreased in comparison with the late stage of recovery and healthy individuals(Figure 2(a) and(d),P Figure2(b) and (e),P Open in a new tabThe frequencies of innate immune cells in COVID-19 and control subjects.The percentages of CD56low CD16+ NK cells,CD56high CD16+/− NK cells, and monocytes werestudied by flow cytometry (a and b) and then analyzed (c–e).
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• Thesefindings were consistent with other reports indicating the number of CD8+ T cellswas markedly decreased and its function was exhausted in COVID-19 patients.29 In contrast with the percentage of activated CD4+ T cell which was increasedin the early stage of recovery, the activated CD8+ T cell had the reduced frequency;however its number was significantly increased in the late stage of recovery, unlikeactivated CD4+ T cell number.
• PBMCs were isolated from healthy subjects and COVID-19patients and then stained with different monoclonal antibodies.
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• The stained cells were washedtwice with PBS and centrifuged at 300 × g for 10 min at roomtemperature.

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The resultsare representative of 57 independent experiments for COVID-19 patientsat the first day of treatment, 51 independent experiments for COVID-19patients in 10 days of treatment, and 40 independent experiments forhealthy individuals. The demographic, laboratory, and clinical characteristics of COVID-19 andhealthy subjects. Table2 depicts the demographic and other characteristics of COVID-19 andhealthy subjects. Of the 57 patients, 51 (89.48%) weredischarged from hospital and 6 (10.52%) died during the study. Antibodies used for determing the changes of the immune system ofCOVID-19 patients by flow cytometry.

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In this regard, the FlowJosoftware (v10.1, FlowJo, Ashland, OR, USA) was used to gate lymphocytepopulation using forward and side scatter to exclude debris or dead cells fromthe analysis of different cells. The cell markers used to determine thefrequencies of the stained cells are indicated in Table 1. The percentages of the stained cells were measured by a FACSCalibursystem (Becton Dickinson, San Jose, CA).
The CD3+ cell population was also determined using the gating oflymphocyte population and was then used to measure the percentages of B cells(CD3− CD19+ CD22+ cells), exhausted CD4+ T cells (CD3+ CD4+ PD-1+ cells),exhausted CD8+ T cells (CD3+ CD8+ PD-1+ cells), CD56lowCD16+ NK cells (CD3− CD56lowCD16+ cells), and CD56high CD16+/− NK cells(CD3−CD56high CD16+/− cells). Afterwards, the lymphocyte population was gatedto assess the frequencies of the CD4+ cells which were used to determine thepercentages of Th1 cells (CD4+ T-bet+ IFN-γ+ cells), Th2 cells (CD4+ IL-4+GATA3+ cells), Th17 cells (CD4+ IL-17α+ RORγt+ cells), Tregs (CD4+CD127low FoxP3+ cells), and activated CD4+ T cells (CD4+ CD25+CD69+ cells). At the first day (the early recovery stage) and 10 days of initiation oftherapeutic methods (the late recovery stage), heparinized blood samples (5 ml)were obtained from patients. All patients had pulmonary involvement and were not on treatment withdrugs influencing the immune system and antibodies production (i.e. steroids,sulfasalazine, phenytoin, and antimalarial drugs) prior to study initiation.

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In 1996, Craig starred in the BBC drama serial Our Friends in the North as the troubled George ‘Geordie’ Peacock. Craig was featured in the poorly received Disney film A Kid in King Arthur’s Court (1995). In 1994, Craig appeared in The Rover, a filmed stage production and Les Grandes Horizontales, a stage production at the National Theatre Studio, where he first met Rachel Weisz, who would become his second wife.
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• Craig next starred as a man who is stalked by a stranger (played by Rhys Ifans) after they witness a deadly accident together in Enduring Love (2004).
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In 2019, Craig starred in Rian Johnson’s black comedy murder-mystery Knives Out as Benoit Blanc, a detective investigating the sudden death of a family patriarch. The film premiered in September 2017 and was distributed by the Orchard the following year. Craig starred alongside Halle Berry in the drama Kings set during the 1992 Los Angeles riots. In 2017, Craig co-starred in Steven Soderbergh’s comedy Logan Lucky, about two brothers who pull off a heist during a NASCAR race. Diane Snyder of The Daily Telegraph praised his “chilling” portrayal of Iago in the play. The production starred David Oyelowo as the titular character and Craig as the main antagonist, Iago.

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He and his wife Weisz starred in a Broadway play titled Betrayal, which ran from October 2013 to January 2014. Craig then co-starred with Harrison Ford and Olivia Wilde in Cowboys & Aliens, an American science fiction Western film, based on Scott Mitchell Rosenberg’s 2006 graphic novel of the same name. In his final release of 2008, the war film Defiance, Craig starred as Tuvia Bielski, the leader of the Bielski partisans, fighting in the forests of Belarus during World War II, saving 1,200 people. Craig starred opposite Nicole Kidman in the science fiction horror film The Invasion in 2007, the fourth film adaptation of the novel The Body Snatchers by Jack Finney, which was met with a negative reception.

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Despite this, Craig supported Barack Obama in the 2008 and 2012 US presidential elections. The role involves raising awareness for the UN Mine Action Service (UNMAS), and political and financial support for the cause. In 2024, he starred as William Lee in Luca Guadagnino’s adaptation of William S. Burroughs novel Queer. In 2022, Craig starred in a contemporary revival of Macbeth opposite Ruth Negga on Broadway. Two days before the film’s release in the US, Craig was awarded a star on the Hollywood Walk of Fame which is located at 7007 Hollywood Boulevard (referring to Bond’s code number “007”), and next to the star of fellow Bond actor Roger Moore. After delays due to the COVID-19 pandemic, Craig’s fifth and final Bond film, No Time to Die, was released in September 2021 and received favourable reviews.
When you sign up with us, you’ll enjoy easy access to a huge selection of state-of-the-art games that can be enjoyed on desktop or mobile. The next year, Craig worked with Orbis International in Mongolia to raise support and awareness of the Orbis medical team and their Flying Eye Hospital. Craig starred in 2011 in a short film narrated by Judi Dench, which was produced for International Women’s Day. Craig next starred in a third Benoit Blanc film titled Wake Up Dead Man, with Johnson directing again.
He portrayed Lord Asriel in The Golden Compass, the 2007 film adaptation of Philip Pullman’s novel. Craig’s debut as James Bond came with Casino Royale, premiering on 14 November 2006 and grossing US$594,239,066 worldwide, making it the highest-grossing Bond film until the release of Skyfall in 2012. Although the choice of Craig was controversial, numerous actors publicly voiced their support. Throughout the entire production period, Internet campaigns expressed their dissatisfaction and threatened to boycott the film in protest. He asked Pierce Brosnan at an event for advice and Brosnan told him, “Go for it. Just go for it.” He stated he “was aware of the challenges” of the Bond franchise, which he considered “a big machine that makes a lot of money”.
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He is currently livingupdate in Orange County and has an online art gallery, featuring original works of impressionist-style paintings, drawings and sculptures, many with sports-related themes. After a successful spring coaching the Coyotes’ quarterbacks and volunteering with local youth throughout the Coachella Valley, Marinovich made his case to play for the team in a quest to become the oldest starting quarterback in pro football. Marinovich was named to the all-rookie team, and as the Avengers’ franchise player, but the day he received his signing bonus he was arrested for buying heroin.
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(C) The reduced L1 starvation survival rate of ain-1(lf) mutants was significantly suppressed by a null allele of unc-31. Compromising overall miRNA function dramatically reduces the survival rate of L1 worms in starvation-induced diapause, and the effect can be significantly suppressed by an age-1/PI3K mutation. Our genetic analysis indicated that for both L1 diapause survival and developmental recovery functions, miR-71 regulates expressions of genes in both the insulin receptor-dependent and -independent pathways. (F) Fluorescence and DIC images showing that an hbl-1 3′UTR reporter was repressed in mir-71(+) worms and slightly derepressed in mir-71(lf) mutants. (E) DIC images showing that hbl-1(RNAi) caused precocious VPC divisions in late L2/early L3 in both wild-type and mir-71(lf) worms recovered from 4 d of L1 starvation. (C) Bar graph showing that the delayed VPC timing defects of mir-71(lf) worms was suppressed by an unc-31(lf) mutation and partially suppressed by an age-1(rf) mutation.

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The transcript level of unc-31 was increased in mir-71(lf) worms, compared with that of wild-type controls that were normalized to the value of 1. MiR-71 represses the expression of age-1 and unc-31 through the actions on their 3′UTR, but miR-71 is not required for arresting M cell division during L1 diapause. We found that the poor survival rate of daf-16(mu86)(lf) was further decreased by mir-71(lf) (Fig. 2C), consistent with the notion that a portion of miR-71 activities regulate genes that act in parallel to UNC-31–mediated InsR/PI3K signaling for long-term survival during L1 diapause. (B) The severely reduced survival rate of the mir-71(lf) mutant was suppressed by a null allele of unc-31(e928).
This result suggests that the high expression of miR-71 during L1 diapause is induced or maintained by other signaling pathways. We asked whether the expression of miR-71 was regulated by DAF-16, which is required during L1 diapause for long-term survival (2). It is possible that other miRNAs, including those in the let-7 family, control developmental timing in other tissues during the recovery phase after L1 starvation. We speculate that the expression of heterochronic genes controlling the L2/L3 programs, including that of hbl-1 and lin-42, are increased during L1 diapause to arrest the developmental progression, and miR-71 is probably required to suppress these “excess” signals during the recovery phase (Fig. S5). As pointed out above, multiple miRNAs in addition to miR-71 and the let-7 family miRNAs have roles in L1 diapause, and they may regulate the expression of many diverse targets that may include, but are not limited to, factors involved in UNC-31–InsR-signaling activities. Although the complete removal of miRNA functions causes embryonic lethality or infertility in worms, a partial disruption of overall miRNA functions by mutating either ain-1 or ain-2 provides an effective way to investigate miRNA functions (16, 17).

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