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For SCN patients, the primary treatment is G-CSF induction therapy. However, many SCN patients develop leukemia over the period of G-CSF therapy. Since CSF3R mutations are present in most SCN-AML, and CSF3R -mutant clones appear to precede leukemic transformation, it will be clinically relevant to monitor the CSF3R gene to evaluate disease progression in SCN patients.

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Although granulocyte-colony stimulating factor has been widely used in clinics to successfully treat a wide range of life-threatening conditions associated with low neutrophil numbers, its prolonged use is related to CSF3R mutations and leukemia in SCN patients. Therefore, the research community and ultimately the SCN patient could greatly benefit from a clear understanding of the molecular mechanism underlying G-CSF therapy and disease progression influenced by its prolong use. One major issue of prolong use of G-CSF is the development of hyporesponse or nonresponse to the treatment in SCN patients. Understanding the signaling mechanism downstream of activated G-CSFR may help us to overcome G-CSF hyporesponse/nonresponse issue in current SCN patients. Similarly, more than 80% of CNL patients carry a CSF3R mutations (specifically T618I) but show a completely different disease characterized by an uncontrolled numbers of neutrophils. Given the high frequency of proximal mutation, it is likely that T618I works as a driver mutation in CNL; however, the mechanism responsible for the T618I mutation leading to CNL remains largely unresolved.

Overall, it is clear that G-CSFR signaling is essential for neutrophil development. However, how the receptor signaling gets differentially perturbed in proximal and truncation mutations leading to different disease conditions, remains to be explored. In the preceding sections of this review, the current knowledge base for our understanding of G-CSFR signaling has been presented along with what is known about the relationship and mechanisms of mutations to the receptor from the various disease manifestations. While considerable progress has been made, there are still major gaps in our understanding of the underlying mechanisms of disease development and progression. These gaps are in part due to both the complexity of the signaling systems and perhaps some of the models systems and technologies that have been applied to study them. For example, while JAK/STAT, PI3K/pAKT, and MAPK/ERK signaling have been established as central players in G-CSFR activation ( figures 2 ), there are clearly other signaling changes that are emerging that are not directly related to these signaling pathway (e.g. redox controlled signaling mechanism involving Prdx1 and Prdx2 etc.) ( Footlocker Finishline Online Best Sale Cheap Online KNITWEAR Jumpers Miss Goodlife Original Clearance Sale Latest Collections Online Ic7jc
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). In addition, the role that phosphatases play in controlling these events is just beginning to be explored (SHIPs, SHP1 and SHP2). Additional understanding of the broad phosphorylation network associated with both normal G-CSFR activation and activation in disease-specific mutation will likely provide further insight into the regulation or dysregulation of this complex signaling network. Fortunately, both targeted phosphorylation array technologies and global phosphoproteomics methods have now become more commonplace and thus could represent new areas to develop a deeper understanding of G-CSFR signaling. Another underexplored area is the interplay between STAT3 and STAT5 signaling pathways from normal and disease-specific G-CSFR (truncation versus proximal mutations). How this interplay works between these branches of JAK2 signaling resulting in healthy versus abnormal neutrophil productions requires further investigation possibly utilizing conditional knockdown/knockout of STAT 3/5 in mouse models. These models have been effectively utilized to study JAK/STAT signaling in normal granulopoiesis previously ( 78 80 ) but have not yet been integrated into CSF3R mutation models and thus could have an impact on distinguishing their roles in the disease phenotypes.

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Filed to: surveillance

Microsoft’s president and chief legal officer, Brad Smith, called for federal regulation of face recognition in a new blog post on Friday. Half of all adults already have their face in a federal database, andvendors are supplying face recognition technology to schools, airports, and baseball stadiums. Federal regulation could help meetnumerous privacy concerns while also giving the public a voice in the tech’s advancement, he argues.

Smith calls for federal regulation because, in our currently unregulated state, leaving individual companies to make ethical decisions on face recognition “is an inadequate substitute for decision making by the public and its representatives in a democratic republic.”

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“We live in a nation of laws, and the government needs to play an important role in regulating facial recognition technology,” Smith writes. “As a general principle, it seems more sensible to ask an elected government to regulate companies than to ask unelected companies to regulate such a government.”

Smith urges congress to convene a bipartisan commission of experts to essentially create a homegrown version of the , a regulatory framework that balances both the potential of face recognition with the need to prevent misuses. “This should build on recent work by academics and in the public and private sectors to assess these issues and to develop clearer ethical principles for this technology,” he writes.

The statement continues by prompting readers to consider whether we should press the government to install varying regulatory measures advanced by privacy experts. It’s widely know that face recognition software can be buggy and inaccurate on darker skinned people. Smithraised the question of a federal law defining a minimum performance level on accurate identifications, banning face recognition software with unacceptably high mis-identification rates. Another possibility: requiring police agencies to post public notices anywhere face recognition is used on the public. This would apply to retailers as well, who have quietly sought patents to identify shoppers and match them with details on their preferences.

“It may seem unusual for a company to ask for government regulation of its products, but there are many markets where thoughtful regulation contributes to a healthier dynamic for consumers and producers alike,” Smith writes. Theoretically, setting a minimum benchmark for face recognition accuracy would push all suppliers to refine the tech, prompting fewer false positives. If shoppers are informed which stores use face recognition, they could avoid those locations, sending a clear message to companies on whether they consent to the practice.

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