In February Microsoft published an article to parents on how to interpret "leetspeak" so that parents could understand what their kids were saying. The article is off the wall funny. Microsoft seems so serious in its presentation of the facts. Below are some excerpts from the article. The full article can be found here.

1. While it has many nicknames, information-age slang is commonly referred to as leetspeek, or leet for short. Leet (a vernacular form of "elite") is a specific type of computer slang where a user replaces regular letters with other keyboard characters to form words phonetically—creating the digital equivalent of Pig Latin with a twist of hieroglyphics.

2. Rules of grammar are rarely obeyed. Some leetspeekers will capitalize every letter except for vowels (LiKe THiS) and otherwise reject conventional English style and grammar, or drop vowels from words (such as converting very to "vry").

3. Non-alphanumeric characters may be combined to form letters. For example, using slashes to create "//" can substitute for the letter M, and two pipes combined with a hyphen to form "|-|" is often used in place of the letter H. Thus, the word ham could be written as "|-|4//."

4. The suffix "0rz" is often appended to words for emphasis or to make them plural. For example, "h4xx0rz," "sk1llz0rz," and "pwnz0rz," are plural or emphasized versions (or both) of hacks, skills, and owns.

Hello Gents, I wanted to connect my Logitech Ultrathin Keyboard Folio m1 which worked OK in the past but now is not typing anything. The battery is freshly charged and connected. Removing/Adding...

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It’s hard not to enjoy the constant stream of Chinese electric cars coming down the pipe. Another day, another ridiculously cheap model. This LUQI M1 EV300 electric car is reminiscent of the Renault Twizy (£6950), but with a touch more room and polish. Of course it’s only a city runabout (or should we say crawlabout?), but it’s definitely got bags of cute. Unfortunately there are pathetically few specifications to hand, apart from the fact that it’s Chinese, costs $900,  comes...

The post LUQI M1 EV300 – $900 for your next super slow EV? appeared first on The Red Ferret Journal.

SIBU: An elderly man lost RM136,000 after being duped in an online business transaction scam, said Sibu District police chief ACP Zulkipli Suhaili.

He said the victim, in his 60s and unemployed, fell victim when he clicked on a link on Facebook on Oct 9 and was taken to an e-commerce platform which used the WhatsApp application.

“The victim was offered a business opportunity selling branded cosmetics items online exclusively, on the condition that he provides the capital first to enjoy the profits.

“The victim agreed and was then told to download the ‘ask-oshop’ application for confirmation of sales and to increase the capital for the stock of sales items,“ he said in a statement today.

He said that from Oct 13 till Nov 7, the victim made 32 cash transactions into 11 bank accounts on the instruction of the suspect, purportedly to increase the stock of sales items in the app.

On Sunday (Nov 10), the suspect was told that the ‘ask-oshop’ app had been frozen and was instructed to make an additional payment of RM70,000.

“Realising that he has been cheated, the victim lodged a police report at the Commercial Crime Investigation Division of the Sibu District Police Headquarters here yesterday,” he said, adding that the case is being investigated under Section 420 of the Penal Code for cheating.

There are a few nights at the Holiday Inn: Milton Keynes East M1, Jct.14 where the 5k IHG Bonus Points rate is either a few pounds less than the discount rate or the same (based on a lower room category being available). November 14, 17, 21, 28,...

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Gerson Chaverra Castro presidente de la Corte Suprema de Justicia señaló que la elección demostró su unidad y robustez institucional con la elección de la nueva fiscal General.

CARM1 is a protein arginine methyltransferase (PRMT) that acts as a coactivator in a number of transcriptional programs. CARM1 orchestrates this coactivator activity in part by depositing the H3R17me2a histone mark in the vicinity of gene promoters that it regulates. However, the gross levels of H3R17me2a in CARM1 KO mice did not significantly decrease, indicating that other PRMT(s) may compensate for this loss. We thus performed a screen of type I PRMTs, which revealed that PRMT6 can also deposit the H3R17me2a mark in vitro. CARM1 knockout mice are perinatally lethal and display a reduced fetal size, whereas PRMT6 null mice are viable, which permits the generation of double knockouts. Embryos that are null for both CARM1 and PRMT6 are noticeably smaller than CARM1 null embryos, providing in vivo evidence of redundancy. Mouse embryonic fibroblasts (MEFs) from the double knockout embryos display an absence of the H3R17me2a mark during mitosis and increased signs of DNA damage. Moreover, using the combination of CARM1 and PRMT6 inhibitors suppresses the cell proliferation of WT MEFs, suggesting a synergistic effect between CARM1 and PRMT6 inhibitions. These studies provide direct evidence that PRMT6 also deposits the H3R17me2a mark and acts redundantly with CARM1.

Stromal interaction molecule 1 (STIM1) plays a pivotal role in store-operated Ca2+ entry (SOCE), an essential mechanism in cellular calcium signaling and in maintaining cellular calcium balance. Because O-GlcNAcylation plays pivotal roles in various cellular function, we examined the effect of fluctuation in STIM1 O-GlcNAcylation on SOCE activity. We found that both increase and decrease in STIM1 O-GlcNAcylation impaired SOCE activity. To determine the molecular basis, we established STIM1-knockout HEK293 (STIM1-KO-HEK) cells using the CRISPR/Cas9 system and transfected STIM1 WT (STIM1-KO-WT-HEK), S621A (STIM1-KO-S621A-HEK), or T626A (STIM1-KO-T626A-HEK) cells. Using these cells, we examined the possible O-GlcNAcylation sites of STIM1 to determine whether the sites were O-GlcNAcylated. Co-immunoprecipitation analysis revealed that Ser621 and Thr626 were O-GlcNAcylated and that Thr626 was O-GlcNAcylated in the steady state but Ser621 was not. The SOCE activity in STIM1-KO-S621A-HEK and STIM1-KO-T626A-HEK cells was lower than that in STIM1-KO-WT-HEK cells because of reduced phosphorylation at Ser621. Treatment with the O-GlcNAcase inhibitor Thiamet G or O-GlcNAc transferase (OGT) transfection, which increases O-GlcNAcylation, reduced SOCE activity, whereas treatment with the OGT inhibitor ST045849 or siOGT transfection, which decreases O-GlcNAcylation, also reduced SOCE activity. Decrease in SOCE activity due to increase and decrease in O-GlcNAcylation was attributable to reduced phosphorylation at Ser621. These data suggest that both decrease in O-GlcNAcylation at Thr626 and increase in O-GlcNAcylation at Ser621 in STIM1 lead to impairment of SOCE activity through decrease in Ser621 phosphorylation. Targeting STIM1 O-GlcNAcylation could provide a promising treatment option for the related diseases, such as neurodegenerative diseases.

Acute lung injury (ALI), is a rapidly progressing heterogenous pulmonary disorder that possesses a high risk of mortality. Accumulating evidence has implicated the activation of the p65 subunit of NF-κB [NF-κB(p65)] activation in the pathological process of ALI. microRNAs (miRNAs), a group of small RNA molecules, have emerged as major governors due to their post-transcriptional regulation of gene expression in a wide array of pathological processes, including ALI. The dysregulation of miRNAs and NF-κB activation has been implicated in human diseases. In the current study, we set out to decipher the convergence of miR-99b and p65 NF-κB activation in ALI pathology. We measured the release of pro-inflammatory cytokines (IL-1β, IL-6, and TNFα) in bronchoalveolar lavage fluid using ELISA. MH-S cells were cultured and their viability were detected with cell counting kit 8 (CCK8) assays. The results showed that miR-99b was up-regulated, while PRDM1 was down-regulated in a lipopolysaccharide (LPS)-induced murine model of ALI. Mechanistic investigations showed that NF-κB(p65) was enriched at the miR-99b promoter region, and further promoted its transcriptional activity. Furthermore, miR-99b targeted PRDM1 by binding to its 3'UTR, causing its down-regulation. This in-creased lung injury, as evidenced by increased wet/dry ratio of mouse lung, myeloperoxidase activity and pro-inflammatory cytokine secretion, and enhanced infiltration of inflammatory cells in lung tissues. Together, our findings indicate that NF-κB(p65) promotion of miR-99b can aggravate ALI in mice by down-regulating the expression of PRDM1.

Read the in depth Review of Samsung Galaxy M14 5G Mobile Phones. Know detailed info about Samsung Galaxy M14 5G configuration, design and performance quality along with pros & cons, Digit rating, verdict based on user opinions/feedback.

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Chemotherapy-induced peripheral neuropathy (CIPN) is a common side effect of chemotherapy treatment, routinely manifesting as increased pain sensitivity (allodynia) in distal extremities. Despite its prevalence, effective treatment options are limited. Cannabinoids are increasingly being evaluated for their ability to treat chronic pain conditions, including CIPN. While previous studies have revealed sex differences in cannabinoid-mediated antinociception in acute and chronic pain models, there is a paucity of studies addressing potential sex differences in the response of CIPN to cannabinoid treatment. Therefore, we evaluated the long-term antiallodynic efficacy of cannabinoid receptor type 1 (CB₁)-selective, cannabinoid receptor type 2 (CB₂)-selective, and CB₁/CB₂ mixed agonists in the cisplatin CIPN model, using both male and female mice. CB₁ selective agonism was observed to have sex differences in the development of tolerance to antiallodynic effects, with females developing tolerance more rapidly than males, while the antiallodynic effects of selective CB₂ agonism lacked tolerance development. Compound-specific changes to the female estrous cycle and female plasma estradiol levels were noted, with CB₁ selective agonism decreasing plasma estradiol while CB₂ selective agonism increased plasma estradiol. Chronic administration of a mixed CB₁/CB₂ agonist resulted in increased mRNA expression of proinflammatory cytokines and endocannabinoid regulatory enzymes in female spinal cord tissue. Ovarian tissue was noted to have proinflammatory cytokine mRNA expression following administration of a CB₂ acting compound while selective CB₁ agonism resulted in decreased proinflammatory cytokines and endocannabinoid regulatory enzymes in testes. These results support the need for further investigation into the role of sex and sex hormones signaling in pain and cannabinoid-mediated antinociceptive effects.

Highly efficient SoCs offer up to 10 CPU cores, 32 GPU cores, 64GB of 400GB/s RAM.

Prices start at $699 for Apple Silicon 'M1' based Mac Mini, $999 for Macbook Air, and $1299 for the 13-Inch MacBook Pro.

A slim entrant to the Apple Silicon lineup 

The show has driven subscriber growth for JioCinema at a faster pace than many shows launched in the past, said Alok Jain, President - General Entertainment, Viacom18

The new budget tablet from the Chinese brand throws in a functional stylus at a great price point.

The Tab M10 Plus (3rd Gen) is powered by an octa-core Qualcomm Snapdragon 680 chipset with 6GB RAM and 128GB storage​ to deliver good multimedia experience and mobile gaming performance

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Contact between inflammatory cells and endothelial cells (ECs) is a crucial step in vascular inflammation. Recently, we demonstrated that the cell-surface level of endomucin (EMCN), a heavily O-glycosylated single-transmembrane sialomucin, interferes with the interactions between inflammatory cells and ECs. We have also shown that, in response to an inflammatory stimulus, EMCN is cleared from the cell surface by an unknown mechanism. In this study, using adenovirus-mediated overexpression of a tagged EMCN in human umbilical vein ECs, we found that treatment with tumor necrosis factor α (TNF-α) or the strong oxidant pervanadate leads to loss of cell-surface EMCN and increases the levels of the C-terminal fragment of EMCN 3- to 4-fold. Furthermore, treatment with the broad-spectrum matrix metalloproteinase inhibitor batimastat (BB94) or inhibition of ADAM metallopeptidase domain 10 (ADAM10) and ADAM17 with two small-molecule inhibitors, GW280264X and GI254023X, or with siRNA significantly reduced basal and TNFα-induced cell-surface EMCN cleavage. Release of the C-terminal fragment of EMCN by TNF-α treatment was blocked by chemical inhibition of ADAM10 alone or in combination with ADAM17. These results indicate that cell-surface EMCN undergoes constitutive cleavage and that TNF-α treatment dramatically increases this cleavage, which is mediated predominantly by ADAM10 and ADAM17. As endothelial cell-surface EMCN attenuates leukocyte–EC interactions during inflammation, we propose that EMCN is a potential therapeutic target to manage vascular inflammation.

Drivers were caught driving at 'extreme speeds' on quiet roads over the Easter weekend, including a man who was clocked at 151mph on the M1 near London as he led police on a high-speed chase.

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Product Information

Round Oil-resistive Smartclick Connectors for E2E NEXT Series proximity sensors, that are Resistant to Oil, and that Reduce Installation Work(XS5 NEXT Series)

The invention is directed to a pulverulent compound of the formula NiaM1bM2cOx(OH)y where M1 is at least one element selected from the group consisting of Fe, Co, Zn, Cu and mixtures thereof, M2 is at least one element selected from the group consisting of Mn, Al, Cr, B, Mg, Ca, Sr, Ba, Si and mixtures thereof, 0.3≦a≦0.83, 0.1≦b≦0.5, 0.01≦c≦0.5, 0.01≦x≦0.99 and 1.01≦y≦1.99, wherein the ratio of tapped density measured in accordance with ASTM B 527 to the D50 of the particle size distribution measured in accordance with ASTM B 822 is at least 0.2 g/cm3·μm. The invention is also directed to a method for the production of the pulverulent compound and the use as a precursor material for producing lithium compounds for use in lithium secondary batteries.

The present disclosure describes antibodies that target HM1.24. In various aspects, the antibodies have specific CDR, variable, or full length sequences, have modifications with the parent antibody, or include at least one modification relative to a parent antibody that alters affinity to an FcγR or alters effector function as compared to the parent antibody. Nucleic acids encoding the antibodies and methods of using the antibodies are also disclosed.

LFO Store has announced the release of 50 Analog & Ambient Sounds, a collection of patches for the iconic Korg M1 synthesizer and music workstation from the 90s. It sounds fantastic but many of the sounds was overused in years & we didn’t find any modern recreations around the globe. So we made a challenge […]

The post LFO Store releases 50 Analog & Ambient Sounds for Korg M1 appeared first on rekkerd.org.

The pair continued south on the M1 before again confronting a driver of a vehicle near the Palm Beach exit.

For more than 20 years, 178 children have stared at motorists driving along the busy M1 on the Gold Coast. We dispel the urban myths of who they are and why they are there.

Commuters can expect long delays heading north from Sydney on the M1, with two lanes closed and traffic stretching back 21 kilometres after a man died in a crash between a ute and semi-trailer at Mt White, north of Sydney.

Although CEACAM1 (CC1) glycoprotein resides at the interface of immune liver injury and metabolic homeostasis, its role in orthotopic liver transplantation (OLT) remains elusive. We aimed to determine whether/how CEACAM1 signaling may affect hepatic ischemia-reperfusion injury (IRI) and OLT outcomes. In the mouse, donor liver CC1 null mutation augmented IRI-OLT (CC1-KO→WT) by enhancing ROS expression and HMGB1 translocation during cold storage, data supported by in vitro studies where hepatic flush from CC1-deficient livers enhanced macrophage activation in bone marrow–derived macrophage cultures. Although hepatic CC1 deficiency augmented cold stress–triggered ASK1/p-p38 upregulation, adjunctive ASK1 inhibition alleviated IRI and improved OLT survival by suppressing p-p38 upregulation, ROS induction, and HMGB1 translocation (CC1-KO→WT), whereas ASK1 silencing (siRNA) promoted cytoprotection in cold-stressed and damage-prone CC1-deficient hepatocyte cultures. Consistent with mouse data, CEACAM1 expression in 60 human donor liver biopsies correlated negatively with activation of the ASK1/p-p38 axis, whereas low CC1 levels associated with increased ROS and HMGB1 translocation, enhanced innate and adaptive immune responses, and inferior early OLT function. Notably, reduced donor liver CEACAM1 expression was identified as one of the independent predictors for early allograft dysfunction (EAD) in human OLT patients. Thus, as a checkpoint regulator of IR stress and sterile inflammation, CEACAM1 may be considered as a denominator of donor hepatic tissue quality, and a target for therapeutic modulation in OLT recipients.

Organ shortage continues to limit the lives of patients who require liver transplantation. While extending criteria for liver organs provides a needed resource, tissue damage from prolonged ischemic injury can result in early allograft dysfunction and consequent rejection. In this issue of the JCI, Nakamura et al. used a mouse transplantation model with prolonged ex vivo cold storage to explore liver graft protection. The authors found that liver grafts with absent carcinoembryonic antigen-related cell adhesion molecule 1 (CEACAM1) exhibited increased ischemia-reperfusion injury inflammation and decreased function in wild-type recipients. The authors went on to correlate CEACAM1 levels with postreperfusion damage in human liver transplant recipients. Notably, this study identified a potential biomarker for liver transplant donor graft quality.

The respiratory epithelium comprises polarized cells at the interface between the environment and airway tissues. Polarized apical and basolateral protein secretions are a feature of airway epithelium homeostasis. Human respiratory syncytial virus (hRSV) is a major human pathogen that primarily targets the respiratory epithelium. However, the consequences of hRSV infection on epithelium secretome polarity and content remain poorly understood. To investigate the hRSV-associated apical and basolateral secretomes, a proteomics approach was combined with an ex vivo pediatric human airway epithelial (HAE) model of hRSV infection (data are available via ProteomeXchange and can be accessed at https://www.ebi.ac.uk/pride/ with identifier PXD013661). Following infection, a skewing of apical/basolateral abundance ratios was identified for several individual proteins. Novel modulators of neutrophil and lymphocyte activation (CXCL6, CSF3, SECTM1 or CXCL16), and antiviral proteins (BST2 or CEACAM1) were detected in infected, but not in uninfected cultures. Importantly, CXCL6, CXCL16, CSF3 were also detected in nasopharyngeal aspirates (NPA) from hRSV-infected infants but not healthy controls. Furthermore, the antiviral activity of CEACAM1 against RSV was confirmed in vitro using BEAS-2B cells. hRSV infection disrupted the polarity of the pediatric respiratory epithelial secretome and was associated with immune modulating proteins (CXCL6, CXCL16, CSF3) never linked with this virus before. In addition, the antiviral activity of CEACAM1 against hRSV had also never been previously characterized. This study, therefore, provides novel insights into RSV pathogenesis and endogenous antiviral responses in pediatric airway epithelium.

The respiratory epithelium comprises polarized cells at the interface between the environment and airway tissues. Polarized apical and basolateral protein secretions are a feature of airway epithelium homeostasis. Human respiratory syncytial virus (hRSV) is a major human pathogen that primarily targets the respiratory epithelium. However, the consequences of hRSV infection on epithelium secretome polarity and content remain poorly understood. To investigate the hRSV-associated apical and basolateral secretomes, a proteomics approach was combined with an ex vivo pediatric human airway epithelial (HAE) model of hRSV infection (data are available via ProteomeXchange and can be accessed at https://www.ebi.ac.uk/pride/ with identifier PXD013661). Following infection, a skewing of apical/basolateral abundance ratios was identified for several individual proteins. Novel modulators of neutrophil and lymphocyte activation (CXCL6, CSF3, SECTM1 or CXCL16), and antiviral proteins (BST2 or CEACAM1) were detected in infected, but not in uninfected cultures. Importantly, CXCL6, CXCL16, CSF3 were also detected in nasopharyngeal aspirates (NPA) from hRSV-infected infants but not healthy controls. Furthermore, the antiviral activity of CEACAM1 against RSV was confirmed in vitro using BEAS-2B cells. hRSV infection disrupted the polarity of the pediatric respiratory epithelial secretome and was associated with immune modulating proteins (CXCL6, CXCL16, CSF3) never linked with this virus before. In addition, the antiviral activity of CEACAM1 against hRSV had also never been previously characterized. This study, therefore, provides novel insights into RSV pathogenesis and endogenous antiviral responses in pediatric airway epithelium.

Minjuan Ma
Mar 30, 2020; 0:jlr.RA120000664v1-jlr.RA120000664
Research Articles