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Crisis management skills are often overlooked until a crisis is upon us. Luckily, crisis management skills are leadership skills, applied in unusual, uncomfortable, and often stressful situations.
In a world where there always seems to be a new crisis, leadership is more important than ever.
Crisis Management vs. Crisis Leadership
We tend to look at leadership and management as being two different things when, in fact, management is just one aspect of leadership, under leadership's broad umbrella. Similarly, crisis management is yet another aspect of leadership. There's not "regular" leadership and "crisis" leadership; it's all just leadership.
So, the very same leadership skills that allow you to flourish during "normal" times will help you through a crisis. And that's a good thing, because crises interrupt our "normal" times with little or no warning.
Emotional Intelligence
During a crisis, emotions run high and they aren't usually positive emotions. People involved in or affected by the crisis may be scared, upset, confused or angry. An emotionally intelligent leader is better able to manage their own emotions and those of others. The leader will know how to acknowledge feelings without adding fuel to the emotional fire and calm people without coming across as dismissive of their feelings.
Crises are emotionally challenging and you must often make decisions quickly and with a dearth of information. Emotional Intelligence helps leaders to ensure their actions, reactions and decisions are rational according to the information they have and not the emotions they're feeling.
The ability to motivate others and rally them around a common cause is essential to a leader's effectiveness. That's no different during a crisis. But what is different is how a crisis affects employee motivation and engagement and, therefore, productivity.
During a crisis, workloads may increase or drastically decrease. Work environments and circumstances may change. There will be times when employees feel out of control. Employees may struggle with staying motivated and engaged due to that sense of fear and uncertainty.
Regular check-ins and feedback sessions will help you not only assess your employee's mindset—and their Performance Readiness® Level for changing responsibilities—but provide continuing opportunities to ensure employees understand how their individual performance is connected with your overall crisis response. When employees feel valued and supported, they'll feel increasingly engaged and motivated.
While we know that we'll eventually face a crisis, we often don't know the exact nature of that crisis. Therefore, it's tough to have a predefined response. Your response depends on the situation. But crisis management isn't just one person's response. In fact, while a top-down leadership style may be intuitive it is often ineffective during a crisis. Instead, you'll need to adapt your leadership style to suit the specifics of the crisis situation and the changing responsibilities of your employees.
Anyone can learn leadership skills, and anyone can learn to apply those skills to crisis management, and practice doing so. The one thing you can't learn ahead of time is experience, that comes with time. But while crises are often unforeseen and sudden, you'll be able to quickly adapt if you have a strong foundation of leadership skills.
- What do you think is the most important leadership skill you need to manage a crisis? Why?
- Think of a time when you or your organization was in crisis (it doesn't have to be major). Looking back, what did you (or other leaders) do well or not so well in terms of responding?


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Over at The Government Accountability Project, they use the upcoming film "Official Secrets" to talk about potential national security whistleblower missteps. The film, which opens at the end of August, tells the tale of British intelligence translator Katharine Gun. In 2003, she was charged under the Official Secrets Act for passing a memo to a reporter. She believed the note was from US spies asking for negative information on nations whose votes were needed for UN approval of the Iraq war.
Movies like this one demystify whistleblowing…Nonetheless, the Hollywood version of Gun's whistleblower story contains a few key examples of risky choices that would have likely imperiled the success of a national security whistleblower, at least in the U.S.

subset: commoncrawl


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Quench that stench
If you have ever had your eyes diverted for just a moment or two while driving, then realized how dangerously close you were to heading into the tail-end of another car or swerving into someone else's lane, then you probably also know the 'immediacy' of your reaction to 'correct' your course. You immediately brake, bringing the car back into a safe distance behind the one in front of you, or you get back into the lane you were to be in and then remain vigilant to remain there! With all the texting while driving I see these days, it is easy to see how accidents can be on the rise - for diverted eyes only take a moment to allow the catastrophic to occur. The same is true in our spiritual lives - diversions are dangerous to us - they change our course, put us in harm's way, and can take a little bit more 'over-correction' than we might first imagine.
God, teach me lessons for living so I can stay the course. Give me insight so I can do what you tell me—my whole life one long, obedient response. Guide me down the road of your commandments;
I love traveling this freeway! (Psalm 119:33-35)
God, teach me lessons for living so I can stay the course. Give me insight so I can do what you tell me—my whole life one long, obedient response. Guide me down the road of your commandments;
I love traveling this freeway! (Psalm 119:33-35)
God doesn't go about 'teaching us' stuff from his Word - things about the way he works, what to expect of his careful attentiveness over our lives - just so we can live as we please. He expects us to use these truths to guide us into 'carefully lived' lives ourselves. This means we have to guard against the diversions that come our way. Back in the days when warfare was a little less 'scientific' than it is today, one of the tactics utilized was to 'divert' the supply of water, food, and needed supplies away from the place you were attempting to 'take over'. They did this to cut them off - so they'd get desperate and let their guard down. Desperate people do desperate things - not always all that carefully thought out or purposeful!
If they diverted the flow of water coming into the township, there would arise a panic because water was a necessary part of daily life. If it wasn't available any longer, the chances of survival were significantly reduced. Yes, they could look for alternatives, but eventually they'd need the water. The body isn't made to survive without it. Similarly, the spirit of man isn't meant to be cut-off from God - although one may survive for a while, the vitality of life soon fades and you begin to experience a sense of being 'dry' on the inside. The human spirit needs connection with God's Spirit - continual and uninterrupted. Only then do we sense the 'fullness of grace' that God desires for each of us.
Diversions also lead to chaos in our lives. If you have ever been diverted from doing something that needs to be done, but you chose something else in place of that action, you know what I am referring to with this thought. Leave the laundry just a few days beyond when you should have addressed those piles and you will become desperate for clean underwear at some point! Sure, it could be as simple as 'buying new' to further avoid the needed task, but eventually the piles will require some action on your part. Eventually the stench of dirty laundry will reach your nostrils! Diversions can lead us away from the course we should be on and take us down ones we might find add a little bit of a 'stench' to our lives. When this happens, the stench can only be avoided for so long! Eventually we will desire to 'quench the stench'!
Divert your attention away from God long enough and you will find your living a very barren and dry life filled with all manner of not so 'sweet' a scent to it! The connection we maintain is one of attentive and purposeful choice to stay on course - to not be enticed by diversionary tactics used by the enemy of our soul. I choose not to text and drive. I choose to pay attention to the road. If we can make this purposeful choice in our driving habits, why can't w make similar choices when it comes to our spiritual focus and purposeful connection with a loving God who cares for us so deeply? Just asking!


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Daily Photo Reprise: My Inspirations, 2011
Coffee and a Cookie?
More than that!
Inspiration No. 1: Cookie, ready to start the day! Even though she was never a morning torite she's always been the one to happily accompany me in whatever I do and wherever I go around the house.
Inspiration No. 2: my morning coffee, fresh ground, French-pressed.
Inspiration No. 3: my favorite mug featuring one of the paintings I've always found most inspiring "The Starry Night", by an artist I've always found inspiring, Vincent Van Gogh.
This photo and and others will be included in the 2013 calendar "In The Kitchen With Cookie".
All images used on this site are copyrighted to Bernadette E. Kazmarski unless otherwise noted and may not be used without my written permission. Please ask if you are interested in using one in a print or internet publication. If you are interested in purchasing a print of this image or a product including this image, check my Etsy shop or Fine Art America profile to see if I have it available already. If you don't find it there, visit Ordering Custom Artwork for more information on a custom greeting card, print or other item..


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Tag Archives: Florida Custody Modification
Grounds for Modification of Custody in Florida
It is unrealistic to think that one or both parties of a custody arrangement will be in the same situation in ten, five, or even two years that they were when the agreement was first made. People change, and circumstances change—sometimes for better and sometimes for worse. To compensate for changes, Florida law allows… Read More »


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A film by Marjane Satrapi and Vincent Paronnaud
It's fair to say that Persopolis is unlike any other film you're likely to find this year, and that's not just because the film's fluid narrative gives a rare and illuminating glimpse into the history of Iran over the past 30 years. More distinctively, the film's larger narrative thread is woven into a logistically crazy quilt of a mega-story, involving the twists and turns of a young woman's coming-of-age and cultural exploration in and out of Tehran.
Oh, and did we mention that it's entirely animated, with free diversions and detours into stylistic fancy? If a summary description sounds tedious or stiflingly serious, the end result is anything but: It's a fizzy, deep, irreverent, and highly personal saga told in moving pictures and smart, ripe dialogue. The historical and societal factors are just a backdrop-albeit an ominous and repressive one-to a life unfolding and unveiling.
Based on Iranian artist-writer Marjane Satrapi's autobiographical graphic novel and with the writer's direct involvement in the film, Persopolis is a rare example of how to artfully adapt a graphic novel to film. A world (and a budgetary stratum) away from Ratatouille, Satrapi's visual style is deceptively simple and fluid, moving from realism to the fantastical and back.
In recounting her saga, from life under the Shah through the Islamic Revolution, and up to her self-exile in the early '90s, Satrapi tells a gripping story from the inside out with both the naivete of youth and the hardened wisdom of experience. While her country was going through its machinations, Satrapi's own youthful obsessions follow paths not unlike her Western counterparts, moving from Bruce Lee to the Bee Gees and, in her teen years, Iron Maiden. She goes to school in Vienna, but is far from liberated by Western contact, instead torn between affinities.
In some way, this compact epic tale conveys both the protagonist's passage beyond youth and the legacy of her grandmother, who imparts non-sentimentalized wisdom and a kind of philosophical ballast throughout. As with the best graphic novels, Persopolis-the film-tells its stories not only through words and pictures, but in the very language created through the blending of the two.


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TV Tray Tables Before:
We've had these TV tray tables since we received them as a wedding gift over 27 years ago! They've kept pretty well, although somewhere along the way, one was broken beyond repair. So we were left with three sitting on the stand that they came with.
In the pic above, I had already sanded the tops of two of them. You can see the one at bottom left is slightly darker.
I've seen a lot of Farmhouse style tv tray tables over the years on Pinterest and Instagram, and I love the look of stained top and black base.
Essential Stencil
I decided to use these as a stencil demo for one of my weekly Facebook Lives I've been doing for Essential Stencil. As one of their ambassadors, I love to share my best stenciling tips each week on their FB page, and I also add them to my Youtube channel if you ever miss any of the lives. If you are in the USA and want to check out their beautiful stencil range, don't forget to use my code IRESTORESTUFF to save 10% on any purchases there. Link for Essential Stencil
Video Tutorial – Replay
Got your old TV tray tables ready? Here's the replay of the video tutorial I did showing you the steps I took, including staining the tops, stenciling the numbers.
Artisan Natural Chalk finish
On the TV tray tables, I used Artisan's colour, Noir to paint the base AND to create the stain on top. If you missed it in the video above, I created a stain using approx. one part paint to 3 or 4 parts water. You can really water the paint down to any ratio you are happy with. I stock the full Artisan range here on my website, shipping Australia wide. Just head to the Shop tab above.
Once painted and stained and the stencils in place, I used Artisan's Flat Matte Sealer to go over the entire piece. I used a brush for the base, but used a damp cloth to create a smooth matte finish over the TV Tray table tops.
Stencil set used in this project:
Finished TV Tray Tables – Farmhouse Style
Here are the TV tray tables all finished in their black & stained glory!
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I hope you enjoyed that tutorial.
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Bulgaria is located on the east of the Balkans. Tourists visit this country because of its clear sea, good sandy beaches, natural beauty and moderate holiday prices. In addition, Bulgaria has the richest historical and cultural heritage, because the history of the Bulgarian state counts from the Neolithic era! National Bulgarian traditions were formed under the influence of Slavic, Turkish, Greek and Thracian cultures. With a English-language guide you will find fascinating excursions whereby you can see truly unique objects. For example, "1001guide" recommends you to visit the cities of Plovdiv and Veliko Tarnovo, visit ancient museum city Nesebar and the botanical garden in Balchik, see the ancient Aladzha Monastery and, of course, admire the delightful valley of roses.
Popular cities
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Heparan sulfate proteoglycans (HSPGs) are required for various signaling pathways, one of which is the bone morphogenetic protein (BMP) signaling pathway. N-deacetylase/N-sulfotransferase-1 (NDST1) participates in synthesizing heparan sulfate (HS) chains of HSPGs, and is involved in bone and lung development. Here, we report that in spite of the redundant expression of Ndst2, Ndst3 and Ndst4 genes, Ndst1–/– mice display defective differentiation of lung cells and increased cell proliferation. Loss of Ndst1 in the lung enhances downstream BMP signaling in vivo. Noggin, which is an antagonist of BMP, can rescue the Ndst1–/– lung morphogenetic defects in explant cultures. Further studies in vitro indicated that loss of Ndst1 significantly impairs BMP internalization by decreasing BMP binding to endogenous HS. Exogenous heparin can rescue both the BMP signaling and BMP internalization abnormalities in Ndst1–/– lung. Thus, we propose that HS regulates BMP signaling by controlling the balance between BMP binding to HS, and that BMP receptors and NDST1-dependent modification are essential for this process. The results suggest that NDST1-dependent HS is essential for proper functioning of BMP in embryonic lung development.
Lung epithelium and mesenchyme generate essential secreted proteins for each other and thus coordinate lung embryonic morphogenesis. Multiple factors, including bone morphogenetic proteins (BMPs), fibroblast growth factors (FGFs) and hedgehog are reportedly involved in lung formation. Inhibition of BMP signaling with the BMP antagonist, noggin (NOGG) or dominant-negative BMP receptor (dnAlk6) alters expression of FOXJ1, uteroglobin (UTER/CC10) and pulmonary surfactant-associated protein C (PSPC/SFTPC) and causes a severe reduction in distal lung epithelial cell types and an increase in proximal cell types (Weaver et al., 1999). Ectopic expression of gremlin (GREM1), another antagonist of BMP, results in disruption of the proximal-distal pattern in embryonic lung (Lu et al., 2001). In addition, deletion of BMPR1a or BMP4 in mouse lung epithelium leads to reduction in number of type II pneumocyte and a decrease in epithelial proliferation (Eblaghie et al., 2006). Misexpression of BMP4 also causes a decrease of type II cells and inhibition of epithelial proliferation, along with cell death in the mesenchyme during lung development (Bellusci et al., 1996). Abnormal septa in alveolar were observed in mice with deletions of FGFR3 and FGFR4 (Weinstein et al., 1998). Overexpression of Sonic hedgehog leads to an abundance of mesenchyme and loss of typical alveoli (Bellusci et al., 1997). Additional signals such as EGF, Wnt and TGFβ are also important in lung development.
A number of signaling pathways including BMP, FGF, hedgehog and Wnt depend on heparan sulfate proteoglycans (HSPGs) (Hacker et al., 2005; Lin, 2004). HSPGs are macromolecules composed of heparan sulfate glycosaminoglycan (GAG) side chains covalently bound to core proteins. Biosynthesis of heparan sulfate (HS) is initiated from a chain composed of repeated D-glucuronic acid (GlcUA) N-acetyl-D-glucosamine (GlcNAc) residues. The glucosaminoglycan chains first undergo N-deacetylation and N-sulfation of selected GlcNAc residues by GlcNAc N-deacetylase/N-sulfotransferase (NDST) (Lindahl et al., 1998; Salmivirta et al., 1996). The subsequent modifications, such as C-5 epimerization of GlcA to iduronic acid (IdoA) and O-sulfation at various positions, are dependent on the prior N-sulfation of GlcN units created by NDST (Esko and Selleck, 2002; Lindahl et al., 1998). NDST has a key role in the modification of the HS polysaccharide chain.
Genes encoding four known NDST isozymes, Ndst1-Ndst4, have been identified in mammals (Aikawa and Esko, 1999; Aikawa et al., 2001; Eriksson et al., 1994; Hashimoto et al., 1992; Kusche-Gullberg et al., 1998). Ndst1 and Ndst2 are expressed ubiquitously in both embryonic and adult mice, whereas Ndst3 and Ndst4 are mostly expressed during embryonic development (Ford-Perriss et al., 2002; Grobe et al., 2002; Miettinen et al., 1997; Yabe et al., 2005). Mice lacking Ndst2 have abnormal mast cells without properly sulphated heparin and mast-cell proteases (Forsberg et al., 1999; Humphries et al., 1999), and those lacking Ndst3 have no obvious phenotype (Grobe et al., 2002). However, disruption of Ndst1 results in severe malformations in lung, brain, cranial facial, lens, vascular, skeletal, and lacrimal gland development (Abramsson et al., 2007; Fan et al., 2000; Grobe et al., 2005; Hu et al., 2007; Pan et al., 2008; Pan et al., 2006; Ringvall et al., 2000). Thus, NDST1 is an essential NDST isozyme in mouse embryonic development.
Previously we reported that Ndst1 mutant mice developed atelectasis and respiratory distress and died shortly after birth (Fan et al., 2000). However, the detailed developmental defects and the underlying mechanisms of NDST1-depedent HS modulation of signaling pathways remain unclear. Here, we report that BMP signaling is affected in Ndst1 mutant lung, which could be one of the causes of defective lung development.
Abnormal lung morphogenesis in Ndst1 mutants
Mouse lung arises from the laryngotracheal groove at 9.5 days post coitum (d.p.c.). Terminal sacs and vascularization develop in the period of 16.5-17.5 d.p.c. After 17.5 d.p.c., the number of terminal sacs and vascularization increase and type I and type II cells differentiate (Warburton et al., 2000). Previous studies have demonstrated that Ndst1-null mice develop pulmonary hypoplasia and neonatal respiratory distress (Fan et al., 2000; Ringvall et al., 2000). To further characterize the phenotype of the mutants, histological examination of embryonic lung development in mutant mice was performed by hemotoxylin and eosin staining lung sections of mice at 16.5 and 18.5 d.p.c. At 16.5 d.p.c., the terminal sacs were less dilated in lungs of Ndst1 mutants than those in the wild type (Fig. 1A,B,E,F). The mesenchyma in 16.5 d.p.c. mutant lungs was also thicker than that in their wild-type littermates (Fig. 1A,B). At 18.5 d.p.c., mutant lungs exhibited less dilated sacs and thicker septa compared with wild-type lungs (Fig. 1C,D,G,H). Furthermore, BrdU labeling of 16.5 and 18.5 d.p.c. embryos indicated that mutant lungs had many more proliferative cells than normal littermates (Fig. 1I-K), consistent with the observation that mesenchyma and septa were thicker in mutant lungs than in wild-type lungs.
Expression of NDST genes during lung development
Although NDST1 is essential for lung morphogenesis, it is not the only NDST protein expressed during lung development. Lung samples from Ndst1 mutants and normal littermates were examined for expression levels of NDST genes by RT-PCR. At 17.5 d.p.c., all four NDST isozymes were expressed in normal lungs. In the Ndst1–/– lung, expressions of Ndst2, Ndst3 and Ndst4 mRNA transcripts were upregulated (Fig. 1L), suggesting a potential redundant effect among the NDST enzymes. Because it is considered to be the less prevalent phenotype in Ndst2 or Ndst3 mutant mice (Forsberg et al., 1999; Grobe et al., 2002; Humphries et al., 1999), NDST1 might be the most important isoform in the NDST family. The phenotype observed in Ndst1–/– mice might form as a result of lack of NDST1 function that cannot be compensated by other members of this enzyme family.
Defective differentiation of lung cells in Ndst1 mutants
Neonatal respiratory distress observed in Ndst1 mutants might be caused by reduced production of surfactant proteins (Fan et al., 2000). Immunostaining analyses revealed a striking reduction in expression of two surfactant proteins, SFTPC and SFTPA in lungs of Ndst1-knockout mice. At 16.5 d.p.c., staining of SFTPC was specifically detected in the distal epithelium (Fig. 2C), whereas staining of SFTPA was detected throughout the epithelium, including proximal and distal parts, in lungs of wild-type mice (Fig. 2A). Significantly, both proteins were barely detectable in mutant lungs (Fig. 2B,D). Furthermore, analysis of the mutant lungs at 18.5 d.p.c. revealed a notable decrease of SFTPC-positive cells (Fig. 2E-G). In parallel, real-time RT-PCR assay indicated that mRNA levels of Sftpc, Sftpa and Sftpb were significantly reduced in mutant lung at 17.5 d.p.c. (Fig. 2Y). These observations imply that inactivation of Ndst1 leads to defective development of distal epithelium and immaturity of type II alveolar cells, which fail to produce surfactant proteins.
Type I alveolar cells were also found to be immature in Ndst1-null mice. From 17.5 d.p.c., type I alveolar cells arise from their precursor cells. Both cell types characteristically express aquaporin-5 (AQP5), a water channel protein (Krane et al., 1999; Kreda et al., 2001). Immunofluorescent examination of 16.5 and 18.5 d.p.c. mutant mouse lungs indicated that the number of AQP5-positive cells was significantly reduced in Ndst1-null mice (Fig. 2H-L). Consistently, the mRNA level of Aqp5 was also reduced in lungs of 17.5 d.p.c. mutant animals (Fig. 2Y).
The expression pattern of the proximal bronchiole epithelium marker CC10 (UTER/Clara Cell 10 protein), did not alter between Ndst1 mutant and control lungs (Fig. 2M,N). Immunofluorescent examination revealed that the number of CC10-immunoreactive cells did not change in mutant lungs (Fig. 2O-Q). However, the bronchioles lining with these cells were less dilated in mutant lungs than in normal littermates (Fig. 2O,P), suggesting that development of proximal bronchiole epithelium was affected by Ndst1 inactivation.
There is a close relationship between blood vessel and lung structural development. Immunofluorescent examination showed that the mutant lungs had no significant alteration in distributions of caveolin-1 (CAV1) and α-smooth muscle actin (SMA), which are molecular markers of blood vessels (Fig. 2R-V for caveolin-1; Fig. 2W,X for SMA). It appears that inactivation of Ndst1 does not affect the lung blood vessel development.
BMP signaling pathway is upregulated in Ndst1–/– lungs
The embryonic lung in Grem1–/– mice exhibits an abnormal `proximalized' phenotype, which is caused by BMP-signaling dysregulation (Michos et al., 2004). Thus, BMP signaling was examined in Ndst1–/– lungs. Binding of BMPs to preformed heteromeric receptor complexes results in the phosphorylation of Smad proteins, and subsequent stimulation of expression of Id1 (Hollnagel et al., 1999; Nohe et al., 2002), Dlx5 (Holleville et al., 2003; Miyama et al., 1999) and Tbx1 (Bachiller et al., 2003). Phosphorylated Smad1 (Smad1-P) was highly upregulated in lungs of 16.5 d.p.c. mutant mice (Fig. 3A,B), and upregulation of ID1 protein was evident at 18.5 d.p.c. (Fig. 3E,F). Interestingly, overexpressed ID1 in mutant lungs seemed to localize not only in the nucleus, but also in the cytoplasm. A similar phenomenon was observed in small cell lung cancer with upregulated ID1, although the reason for this was not clear (Kamalian et al., 2008). mRNA levels of both Dlx5 and Tbx1 were also increased in lungs of Ndst1-deficient animals (Fig. 3I). All these data demonstrate that the BMP-signaling pathway is upregulated in Ndst1–/– lungs. However, mRNA levels of Bmp2, Bmp4, Bmp5 and Bmp7 were not changed in Ndst1 mutant lungs (Fig. 3J), indicating that the upregulation of BMP signaling in the mutants was not caused by an increased BMPs.
Blockade of BMP signaling rescues the defective differentiation of type I and type II cells in Ndst1-null mice
To determine whether dysregulated BMP signaling caused the defective differentiation of type I and type II cells in Ndst1-null lungs, Noggin, a BMP antagonist, was applied to block BMP signaling. Similarly to wild-type lung explants (Fig. 4A-H), treatment of 15.5 d.p.c. Ndst1–/– lungs with noggin resulted in significantly downregulated expression of Smad1-P protein (Fig. 4K,L), and upregulation of SFTPC (Fig. 4M,N) and AQP5 (Fig. 4O,P). Furthermore, BrdU labeling indicated that cell proliferation was decreased in the presence of noggin (Fig. 4I,J). These results demonstrate that block of BMP signaling could rescue the developmental failure in type I and type II cells, or their precursor cells, in mutant lungs. And it reinforced the idea that upregulation of BMP signaling contributes to the defective lung development in Ndst1 mutants. However, exogenous noggin inhibited the proliferation of both wild-type and mutant lungs (Fig. 4R), indicating that a physiological concentration of BMP is essential for cellular processes, including DNA synthesis and mitosis.
Decreased binding of BMP2 and BMP4 to endogenous HS in Ndst1 mutant lungs
Since NDST1 catalyzes the first modification step in biosynthesis of HS and the HS structure in most basement membrane is affected in Ndst1–/– mice, the HS chain in mutant lungs is therefore probably affected. Thus, endogenous HS in wild-type and mutant lungs was detected using an antibody that reacts with O-sulfated N-acetylated glucosamine residues of HSPGs (Fig. 5A-D). Wild-type lungs showed a strong signal, whereas no signal was detected in mutant lungs. This demonstrates that loss of NDST1 causes failure in the synthesis of normal HS chains, which is consistent with a previous report in the Ndst-1–/– lens (Pan et al., 2006). BMPs are reportedly involved in lung morphogenesis, and bind to heparin. To investigate how the BMP-signaling pathway is regulated in Ndst1 mutant lungs, histochemical assays were performed to test the interaction between secreted proteins and endogenous HS in mutant lungs. At 18.5 d.p.c., the binding of BMP2 and BMP4 was less in mutant lungs than that in normal littermates (Fig. 5E-H), suggesting that the capacity of the secreted BMP proteins to bind to HS was decreased in Ndst1–/– lungs. Pre-treatment of lung sections with heparitinase greatly reduced the binding in Ndst1-null mice and wild-type littermates (Fig. 5I,J), indicating that the binding of these secreted proteins is indeed HS dependent.
HS-dependent binding of BMP to cell surface is essential for BMP internalization in lung cells
Based on our data and previous reports (Ruppert et al., 1996; Fisher et al., 2006; Jiao et al., 2007), HS seems to have an inhibitory role in the BMP-signaling pathway. Thus HS-dependent BMP binding appears to be distinct from receptor-dependent BMP binding. To study the function of HS-dependent BMP binding to the cell surface, BMP internalization was monitored in lung epithelial cells. In cultured wild-type lung epithelial cells, heparitinase treatment significantly reduced BMP binding to the cell surface and its consequent internalization (Fig. 6A,C,M,O,U). This demonstrates that HS-dependent binding of BMP is essential for BMP internalization.
To test whether BMP receptors are involved in BMP internalization, noggin, which inhibits BMP signaling by binding to BMPs and preventing their interaction with receptors (Smith and Harland, 1992; Zimmerman et al., 1996), was applied to internalization assays. BMP2 binding to the cell surface and internalization in normal and Ndst1 mutant lung epithelium were not changed in the presence of noggin (Fig. 6E,G). It is conceivable that BMP internalization occurs mainly via binding to HS chains rather than binding to BMP receptors. In Ndst1–/– lung cells, the binding of BMPs and consequent internalization was also markedly attenuated (Fig. 6B,D,F,H,U), indicating the necessity of NDST1-dependent HS modification during this process. Similar results were obtained with mesenchymal cells (Fig. 6Q-T).
It was unexpected that exogenous heparin could largely rescue BMP2 binding to the cell surface and consequent internalization in Ndst1–/– mice (Fig. 6J,L,U), whereas its effect on wild-type cells was much less significant (Fig. 6I,K,U). It seems that not only cell surface HS, but also extracellular HS, participates in the internalization of BMP.
Exogenous heparin could also rescue the phenotype of Ndst1–/– lung
Since exogenous heparin could rescue the BMP binding and internalization, it might be also able to rescue the dysregulated BMP signalling and consequent morphogenetic defects in Ndst1–/– lungs. Treatment of 15.5 d.p.c. wild-type and Ndst1–/– lung explants with 10 μg/ml exogenous heparin, which has a higher content of N-sulfation than HS, reduced the expression of Smad1-P (Fig. 7A,B,G,H) and enhanced the expression of SFTPC and AQP5 (Fig. 7C-F,I-L). The findings confirm that impaired BMP signaling with N-sulfation or heparin can facilitate the differentiation of type I and type II alveolar cells.
Consistently, in wild-type lungs, BMP4 and heparin together led to the decreased expression of Smad1-P (Fig. 7M,N) and increased expression of SFTPC, compared with that in lungs treated with BMP4 alone (red in Fig. 7O,P), but did not affect the expression of caveolin-1 (Fig. 7O,P, green).
Western blot assays were also performed. Similarly to results of the histochemical assays, Ndst1–/– lung explants displayed a much higher level of phosphorylation of Smad1 than wild-type lung explants, whereas treatment with noggin or heparin dramatically reduced this abnormal high level (Fig. 7Q). This confirmed the inhibitory function of heparin in BMP signaling.
NDSTs might compensate for each other in knockout mice
Here, we found that loss of Ndst1 in lung results in defective BMP signaling even with the redundantly enhanced expression of Ndst2, Ndst3 and Ndst4, whereas FGF signalling, but not hedgehog signalling, was also affected in mutant lungs (supplementary material Figs S1 and S2). Ndst1-null mice display severe brain and facial defects, which might be consistent with impaired sonic hedgehog (Shh) and FGF interaction with mutant HS (Grobe et al., 2005) in some mutants. It is also possible that only part of NDST1's function could be compensated by other NDST isozymes in lung development. For instance, it is possible that the hedgehog signaling in lung was compensated. Although multiple abnormalities previously described in Ndst1–/– mice were not observed in Ndst2 or Ndst3 mutant mice, it is likely that other isoforms of the NDST enzyme family might have compensated for the loss of Ndst2 or Ndst3. Considering that NDST1 modulates FGF signaling, but not BMP and Wnt during lens development (Abramsson et al., 2007; Pan et al., 2006), compensation between NDSTs seemed to be tissue dependent. Moreover, in lungs, we found that blood vessel formation was not affected by loss of NDST1 whereas differentiation of lung epithelium cells was. This implies that the compensation might even be cell-type dependent.
NDST1-dependent modification is essential for HS modulation of the BMP-signaling pathway and BMP internalization
Here, we propose that dysregulation of BMP signaling pathway contributes to the defective morphogenesis in Ndst1-null lung. Consistently, similar abnormal septation of the lung airway epithelium was observed in embryonic lung when GREM1, an antagonist of BMP, was deficient (Michos et al., 2004). By contrast, overexpression of BMP4 in embryonic distal lung epithelium results in thicker mesenchyma than observed in control and in the `emphysematous' phenotype (Bellusci et al., 1996). Nog–/– mice exhibit abnormal morphology with a malformed and truncated lobe (Weaver et al., 2003). There are several possible explanations for these discrepancies. First, endogenous GREM1 is expressed in proximal airway epithelium (Weaver et al., 1999), whereas noggin is normally expressed in the distal mesenchyme (Lu et al., 2001). By inhibition of BMP signaling, GREM1 and noggin might have different roles in spatial and temporal regulation of lung development. Thus, the phenotypes observed in these mice models result from deficiencies in partial epithelium or mesenchyme differentiation alone. Similarly, ectopic expression of BMP4 in distal epithelium had no obvious affect on the epithelium in the proximal airway (Bellusci et al., 1996). HS plays an upstream regulatory role in the BMP-signaling pathway, and thereby modulates the differentiation of all the epithelium and mesenchyme. To determine how HS does this, further conditional gene knockout studies are needed. In addition, depending on concentration, BMP promotes mesenchyme proliferation or death (Bellusci et al., 1996). In Bmp4 transgenic mice, a high level of BMP4 resulted in cell death and inhibition of cell proliferation. However, in our model and in GREM1-deficient mice, cell proliferation increased, probably because of the occurrence of endogenous BMP at proper concentrations. Finally, HS modulates not only BMP signaling, but also other important pathways during lung development, including the FGF-signaling pathway (supplementary material Fig. S1). Thus, the phenotype we report here might result from dysregulation of several signaling pathways.
Accordingly, we asked how NDST1-dependent HS was involved in the BMP-signaling pathway. It is reported that HS binds to the N-terminal of BMP-2 and modulates the function of BMP2 in chick limb bud assays (Ruppert et al., 1996). In C2C12 myoblast cells, blockade of cell surface HSPG sulfation or removal of the GAG chain enhanced BMP2 signaling and bioactivity, which could be attenuated by exogenous heparin (Jiao et al., 2007). In this study, we further proved that the binding of HS to BMP inhibits BMP signalling, rather than facilitates it, in lung development. In particular, NDST1-dependent modification is essential for the activity of HS in the regulation of BMP-signaling pathways. In addition to regulating BMP binding, HS also has a role in binding noggin to the cell surface. Therefore, reduced noggin binding in Ndst1 mutant lungs might also contribute to the hyperactivity of the BMP-signaling pathway (Viviano et al., 2004).
Recent studies have implied that cell surface HSPGs are also involved in cellular internalization of proteins (Belting, 2003; Jiao et al., 2007; Payne et al., 2007). Live-cell imaging indicates that HSPGs mediate cationic ligand internalization via a clathrin- and caveolin-independent, but flotillin- and dynamin-dependent pathway (Payne et al., 2007). Our data further demonstrate that the NDST1-dependent HS modifications, including N-deacetylation and N-sulfation, are required for BMP internalization. We also observed that HS-mediated BMP internalization might be independent of BMP receptors (Fig. 6C,G). More interestingly, we found that exogenous heparin could partly rescue the BMP internalization defects caused by loss of NDST1 (Fig. 6J,L). This implies that, not only cell-surface HS, but also extracellular heparin or HS, also contribute to BMP internalization, which has not been reported before.
Taken together, it is postulated that BMPs that bind to HS prefer to internalise, whereas BMPs that bind to receptors prefer to activate downstream signaling. The balance between BMP binding to HS and to receptors might control BMP signaling.
Compared with our previous work on Ndst1 mutant bone (Hu et al., 2007), the activity of HS in modulating signaling pathways seems variable in different tissues. First, unlike in embryonic lung, exogenous heparin might not be able to rescue the morphogenetic defects in Ndst1–/– embryonic limb bone. Second, FGF1 binding to the cell surface is attenuated in mutant lung but not in mutant bone. It is conceivable that other factors participate in the process of HS binding to cytokines.
In summary, previous studies on the Ndst1-knockout mouse indicate that HS could regulate various secreted ligands in different tissue contexts. Therefore, the tissue-specific regulation of HS and secreted ligands might contribute to the observation that HS plays a vital role in different developmental tissues via various signaling pathways. In this study, we provide a mouse model for exploring the function of HS in BMP signaling. We point out the different roles of HS in regulating BMP signaling and BMP internalization, and thus present an explanation for the mechanistic involvement of NDST1-dependent HS in modulation of the BMP-signaling pathway during lung development,
In addition to insights into developmental regulation, our study also has important clinical implications. We found an inhibitory effect of heparin on the modulation of BMP signalling, which might provide an explanation for the clinical observations that heparin can improve outcome in small-cell lung cancer (SCLC) (Altinbas et al., 2004; Lebeau et al., 1994), in which BMP8 is overexpressed (Henderson et al., 2005).
Materials and Methods
The generation of the Ndst1-deficient mice and molecular examination by PCR to distinguish wild-type and mutant Ndst1 alleles have been reported previously (Fan et al., 2000). All mice used in this study were bred and maintained at Shanghai Institute of Biological Sciences under specific pathogen-free conditions in accordance with institutional guidelines.
Histological and immunohistochemical analysis
Embryonic lungs were fixed overnight in 4% buffered formaldehyde at 4°C and embedded in paraffin for sectioning. For histological analysis, 5 μm sections were stained with hematoxylin and eosin, mounted in xylene-based medium and photographed. For immunohistochemistry, 5 μm tissue sections were pretreated with 10 mM sodium citrate buffer (pH 6.0) at 95°C, and then incubated overnight at 4°C with anti-CC10 (T-18), anti-SFTPA (N-19), anti-SFTPC (M-20), anti-AQP5 (G-19), anti-caveolin-1 (N-20), anti-Smad1-P (Ser463-Ser465), anti-Id1 (C-20), anti-Patched (G-19), anti-Gli1 (N-16) (all from Santa Cruz Biotechnology, Santa Cruz, CA), anti-SMA (Sigma, St Louis, MO) or anti-HepSS-1 (Seikagaku Corp., Tokyo, Japan). For enzymatic staining, biotinylated secondary antibodies and the ABC staining system (Santa Cruz) were applied. The images were captured on a cooled CCD camera (SPOT II, Diagnostic Instruments, Sterling Heights, MI) on an Olympus BX51 microscope. For immunofluorescence, secondary antibodies conjugated with appropriate fluorochrome, FITC, Cy3, Cy5 (Jackson ImmunoResearch, West Grove, PA), were used. Digital images were analyses by confocal laser-scanning microscope (Leica SP2 system) and processed using Adobe Photoshop. At least three embryos for each genotype were analyzed for each antibody.
Total RNA was isolated from lungs of 17.5 d.p.c. Ndst1–/– and wild-type embryos using Trizol Reagent (Invitrogen, Paisley, UK), and then reverse transcribed with Super-scriptase (Invitrogen). The primers used in PCR assays were Ndst1 (forward, 5′-CTG CCC TGG CGT GCC TCC-3′; reverse, 5′-TGG GCC GTG TCA CAT AGA GCA GT-3′); Ndst3 (forward, 5′-TCA CAT GCA GCC CCA CCT CTT-3′; reverse, 5′-GCT CCC CTC CAT GAA TAC TCT TGT-3′); Ndst2, Ndst4 (Pan et al., 2006); Bmp2 (forward, 5′-TCT TCC GGG AAC AGA TAC AGG-3′; reverse, 5′-TCT CCT CTA AAT GGG CCA CTT-3′); Bmp4 (Zhang et al., 2007), β-actin (Actb) (forward, 5′-CTG GCT GGC CGG GAC CTG ACA-3′; reverse, 5′-ACC GCT CGT TGC CAA TAG TGA TGA-3′). Actb was used as an internal control for quantification.
Real-time PCR assays were performed on a DNA Engine Opticon 2 (MJ Research, Watertown, MA) using the DyNAmo SYBR Green qPCR kit (FinnzymesOy, Espoo, Finland). The data were expressed as relative mRNA (gene) copies, which were normalized to the expression level of Actb. The following primers were used: Aqp5 (forward, 5′-AGC CTT ATC CAT TGG CTT GTC-3′; reverse, 5′-TGA GAG GGG CTG AAC CGA T-3′); SftpA (Okubo and Hogan, 2004); SftpB (forward, 5′-ACG TCC TCT GGA AGC CTT CA-3′; reverse, 5′-TGT CTT CTT GGA GCC ACA ACA G-3′); SftpC (forward, 5′-ACC CTG TGT GGA GAG CTA CCA-3′; reverse, 5′-TTT GCG GAG GGT CTT TCC T-3′); Dlx5 (forward, 5′-GTC CCA AGC ATC CGA TCC G-3′; reverse, 5′-GCT TTG CCA TAA GAA GCA GAG G-3′); Tbx1 (forward, 5′-AGG CAG ACG AAT GTT CCC C-3′; reverse, 5′-GCT TGT CAT CTA CGG GCA CA-3′).
BrdU labeling and detection
Mouse embryos were labeled with BrdU (BrdU labeling and detection kit II, Roche, Germany) by intraperitoneal injection of 10 mM BrdU (1-2 ml per 100 g body weight) into pregnant females 1 hour before sacrifice. Cultured lung explants were treated with 100 μM BrdU for 1.5 hours before harvesting, and then were fixed in 95% ethanol at 4°C and embedded in paraffin. Antibody staining of embryo sections was carried out according to the manufacturer's instructions. The number of BrdU-positive nuclei and total cells in each field of vision was estimated from eight sections from three animals for each genotype.
In situ HS-binding assays
The assays were performed on paraffin-embedded sections essentially as previously described for cryosections (Chang et al., 2000; Friedl et al., 1997). Briefly, after blocking, sections were incubated with 15 nM BMP2, 15 nM BMP4 and 30 nM FGF1 (all from R&D Systems, Wiesbaden, Germany), respectively. Then, sections were incubated with anti-BMP2, anti-BMP4, anti-FGF1 antibodies (all from R&D Systems) and stained using the ABC staining system (Santa Cruz).
Organ culture of embryonic lung explants
Mouse embryonic lungs were cultured essentially as previously described (Dean et al., 2005; del Moral et al., 2006). Briefly, lungs were isolated from 15.5 d.p.c. crosses of Ndst1+/– mice. They were placed in a six-well plate on an 8 μm Nucleopore membrane floating in 1 ml BGJ-B medium (GibcoBRL, Grand Island, NY) with antibiotic/antimycotic (Life Technologies, Paisley, UK) and 0.1% BSA, and were maintained at 37°C in a humidified 5% CO2 incubator. Lung explants were cultured in medium supplemented with 10 μg/ml heparin (Sigma) or with 500 ng/ml noggin (R&D Systems) for 3 days and were compared with explants cultured in BGJ-B medium. The medium was changed every day.
Primary lung epithelial and mesenchymal cell cultures
Epithelial and mesenchymal cell cultures were obtained by differential adhesion as previously described (Lebeche et al., 1999). Briefly, whole lungs were dissected at 15.5 d.p.c. and digested with 0.4% dispase 0.8% Collagenase (37°C, 60 minutes; GibcoBRL) to give rise to single cells. The resulting filtered suspension was plated in 30 mm dishes and incubated at 37°C in a humidified 5% CO2 incubator for 1 hour for differential adhesion. The supernatant containing epithelium cells was removed and centrifuged at 1000 r.p.m. for 10 minutes at room temperature. The cell pellet was resuspended in Dulbecco's modified Eagle's medium (DMEM) with 10% heat-inactivated fetal bovine serum, and plated in dishes. The mesenchymal cells attached to the dish were washed with PBS and cultured with fresh medium.
BMP internalization assays
BMP2 internalization was performed mostly as previously described (Jiao et al., 2007). Briefly, BMP2 (12 μl of 400 ng/ml; R&D systems) was incubated with goat anti-BMP2 antibody (40 μl of 500 ng/ml; Santa Cruz) for 30 minutes at 37°C to form the BMP2-anti-BMP2 complex. Lung epithelial or mesenchymal cells, seeded on glass coverslips in 24-well plates, were incubated with BMP2-anti-BMP2 complex at 4°C for 30 minutes. After a wash with ice-cold serum-free DMEM, the cells were incubated at 37°C for 30 minutes. Cells were then incubated with FITC-conjugated secondary antibody (Jackson ImmunoResearch) and 4,6-diamidino-2-phenylindole (DAPI) and examined by confocal laser-scanning microscope (Leica SP2 system) after being fixed.
Western blot
Lung explants were homogenized and lysed after treated with noggin and heparin. Then lysates were collected after brief concentration. Immunoblotting was performed as described previously (Huang et al., 2002) with primary antibodies against Smad1-P (Cell Signaling Technology), Smad1 (a kind gift from Yeguang Chen, Tsinghua University, Beijing, China) and β-actin (Sigma).
Statistical analysis
The Student's t-test was used to determine levels of difference between groups, and P values for significance were set to 0.05. Values for all measurements were expressed as the means ± s.d.
We are grateful to Xinhua Lin and Xiaoyan Ding for helpful discussions and Yeguang Chen for supplying antibody against Smad1. This work was supported by Minster for Science and Technology Grant G1998051007 and Chinese High-Tech R&D Program (863)-2001AA231011 and 0022Z2002.


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Cancer Care Accelerator: An Innovative Transdisciplinary Approach to Redress Cancer Disparities in Harlem
Main Article Content
Accelerators, an innovation in trans-disciplinary team science, are a new model to spark ideas and approaches to redress disparities. We describe the Cancer Care Accelerator, a cross-sector collaboration comprising cancer advocates, patients, clinicians, researchers, public health leaders and funders charged to reduce disparities and the cancer burden in Harlem. We describe the process and early initiatives of this Accelerator which began its focus on key risk factors for cancers with undue burden in Harlem, namely, access and insurance. First, the group helped design a project connecting patients with social distress to a community organization that can address social needs. Plans to expand research and educational in-reach and outreach for cancers that are highly prevalent with disparate outcomes are underway. Early projects focus on discrete achievable outcomes of treatment, screening and education. Subsequent works will utilize community-based cancer needs assessment findings to stimulate new projects. The Accelerator may serve as a model to aid with priority setting, idea generation and implementation for endeavors addressing population-level cancer disparities.
Article Details
The Medical Research Archives grants authors the right to publish and reproduce the unrevised contribution in whole or in part at any time and in any form for any scholarly non-commercial purpose with the condition that all publications of the contribution include a full citation to the journal as published by the Medical Research Archives.
2. https://grants.nih.gov/grants/guide/pa-files/PAR-20-043.html
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6. Kaplan GA, Everson SA, Lynch JW. Promoting Health: Intervention Strategies from Social and Behavioral Research. Washington DC: National Academies Press (US); 2000.
7. Bay Area Regional Health Inequities Initiative BARHII conceptual framework. http://barhii.org/framework
8. Donaldson MS, Sox HC Jr. Committee on Priorities for Assessment and Reassessment of Health Care Technologies. Washington DC: National Academies Press (US); 1992.
9. Marin DB, Costello Z, Sharma V, Knott CL, Lam D, Jandorf L. Adapting Health through Early Awareness and Learning Program into a New Faith-Based Organization Context. Progress in Community Health Partnerships: Research, Education, and Action 2019;13(3):321-329. https://mshsstaff.auntbertha.com
10. Bickell NA, Lin JJ, Abramson SR, et al. Racial Disparities in Clinically Significant Prostate Cancer Treatment: The Potential Health Information Technology Offers. J Oncol Pract. 2018;14(1):e23-e33.
11. www.scan360.com
12. Walker DM, McAlearney AS, Sova LN, Lin JJ, Abramson S, Bickell NA. Comparing Prostate Cancer Treatment Decision Making in a Resource-rich and a Resource-poor Environment: A Tale of two Hospitals. J Natl Med Assoc. 2016;108(4):211-219.
13. Fei K, Lin JJ, Supoyo S, Rebeca Franco R, Abramson S, Hoke G, Oh W, Stock R, Bickell NA.Impact of Age and Life-expectancy on Treatment Receipt in High-risk Prostate Cancer. Journal of Advances in Medicine and Medical Research 2019; 30(11): 1-9. ISSN: 2456-8899 (NLM ID: 101570965).
14. Kinney PL, Aggarwal M, Northridge ME, Janssen NA, Shepard P. Airborne concentrations of PM(2.5) and diesel exhaust particles on Harlem sidewalks: a community-based pilot study. Environ Health Perspect. 2000;108(3):213-218.
15. Northridge ME, Yankura J, Kinney PL, et al. Diesel exhaust exposure among adolescents in Harlem: a community-driven study. Am J Public Health. 1999;89(7):998-1002.
16. https://www.uspreventiveservicestaskforce.org/Page/Document/RecommendationStatementFinal/prostate-cancer-screening1
17. Morrison RS, Wallenstein S, Natale DK, Senzel RS, Huang LL. "We don't carry that"--failure of pharmacies in predominantly nonwhite neighborhoods to stock opioid analgesics. N Engl J Med. 2000;342(14):1023-1026.


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When It Comes to Guns,
"Oh, never mind. Congress hasn't passed a single piece of gun control legislation, beyond voting in 2013 to renew an expiring ban on plastic firearms, which could potentially bypass security checkpoints at airports and other locations. Most recently, Senate lawmakers worked to block a package of gun violence legislation, including a measure to bar individuals on terror watch lists from purchasing firearms." (Ref. 1) Following the school shooting in Sandy Hook, Connecticut, "New York City Mayor Michael Bloomberg issued a strong statement responding to Friday's elementary school shooting in Connecticut, calling on Congress to take action on gun control. " 'For every day we wait, 34 more people are murdered with guns,' Bloomberg said. 'Today, many of them were five-year-olds.' "Bloomberg, a co-chair of Mayors Against Guns, also slammed President Barack Obama's earlier statement on the shooting, saying that it did not go far enough to address the issue of gun violence. " 'President Obama rightly sent his heartfelt condolences to the families,' he continued. 'But the country needs him to send a bill to Congress' " 'Calling for 'meaningful action' is not enough. We need immediate action.' "Shortly after the statement went out, the NYC Mayors Office tweeted out a new Mayors Against Guns 'Demand A Plan' petition calling for Obama and Congress to address gun violence." (Ref. 2) That was more than five years ago. Nothing came of the outcry for congressional action and Mayor Bloomberg's call for more than words. Instead, America's gun violence has gotten worse and school shootings continue. When it comes to guns, it's business as usual! Young lives don't seem to matter. In fact, no American life seems to matter when it comes to the Second Amendment and the "God-given right" to own and use guns - legal or illegal! Politicians spout bromides and pontificate, but do nothing meaningful while the carnage continues. They go through the motions of seeming to act, but, in reality do nothing constructive. They dance around the issue, mouth ineffective bromides, and issue sad-faced expressions of sympathy for the victims and their families, but they refuse to take the one brave, bold and necessary step to end the death-spiral of gun violence in America - the repeal of the Second Amendment to the U.S. Constitution. The time has come to find and elect politicians who will not shy away from finally instituting the one step that has yet to be tried and which can begin the process of reducing gun deaths and injuries in America! Continued inaction is no longer an option! "For evil to succeed, all it needs is for good men to do nothing." — Martin Luther King Jr. Continuing the charade of appearing to take action while actually doing nothing, President Trump, in early March of 2018, "unveiled a bare-bones plan to combat school shootings that marked his retreat from gun control policies he had repeatedly championed just weeks ago, in a move likely to soothe the powerful National Rifle Association. [Emphasis mine] "Trump's new plan focuses on 'hardening' schools with increased security and expresses support for boosting some background checks. But it punts the issue of gun control to a commission, headed by his pro-gun Education Secretary . . . , to review. It also leaves NRA-backed proposals, such as arming teachers, on the table — but defers such policies to the states to decide. "The proposals are a stark departure from Trump's comments at a White House meeting last month during which he endorsed the idea of raising the age to purchase AR-15s and other high-powered long guns from 18 to 21 in the wake of the Feb. 14 shootings at Marjory Stoneman Douglas High School in Parkland, Fla., that left 17 dead at the hands of a 19-year-old wielding an AR-15-style rifle. "At his meeting, held days after the massacre, Trump {hypocritically} chided GOP lawmakers for not including an age-hike provision in legislation they proposed, telling them it was 'because you're afraid of the NRA, right?' The very next night, Trump held an unscheduled White House meeting with NRA leaders, tweeting afterward: 'Good (Great) meeting in the Oval Office tonight with the NRA!' [Emphasis mine] "Since then, the president has gradually backed off the idea of gun purchase age limits. "A White House official said that the president reacted not to opposition by the NRA, but from lawmakers — a distinction without a difference, given the legislative scorecard the NRA uses to determine whether to attack lawmakers come re-election time. "Gun-control advocates said the president missed a crucial opportunity to lead. " 'President Trump has offered only drips of water in response to a five-alarm fire,' [Emphasis mine] said {the} co-president of the Brady Campaign to Prevent Gun Violence." (Ref. 3) In fairness to President Trump, his action (and actually his inaction) is no different than that of President Obama and other presidential predecessors, as well of that of most of congressional elected officials. Simply put, When it comes to guns, it's business as usual! From Massachusetts to the White House, meaningless gun control measures were the theme of the week following the Florida school massacre as politicians scrambled to appear to be opposed to gun violence. U.S. Senator Ed Markey from Massachusetts, in keeping with his liberal/Democratic solution of throwing money at any-and-all problems, came out "with his proposed solution to the nation's gun violence problem, and it amounts to, of all things, a wonky federal grant program. "Markey wants to offer states financial incentives to change their laws to look more like the laws in Massachusetts. For example, police chiefs here are empowered to approve or revoke gun licenses for local residents; Markey's plan would make states that adopt similar measures over the next five years eligible for federal money. "Massachusetts does indeed boast many sensible gun policies. But a federal handout won't be the thing that convinces, say, the state of Wyoming to emulate the laws of this very blue commonwealth. The same might even be said of Maine, New Hampshire and Vermont. "Meanwhile President Trump is out with his plan to address the school shooting problem, but it's missing a central element that he embraced after the shooting in Parkland, Fla.: a federal increase in the minimum age to purchase a long gun, from 18 to 21. "Now, the president insists he is not afraid to stand up to the National Rifle Association — not like those weak-kneed members of Congress of his own party that he called out publicly a few weeks ago. No, it appears the president is afraid only of the NRA's lawyers. "The NRA has sued the state of Florida, which . . . officially increased its age limit to purchase assault-style weapons to 21. Some national retailers have also been sued for acting on their own to raise the age. In a tweet . . . Trump said he is 'watching court cases and rulings before acting' on age limits. "But the idea that the president of the United States would hold off on pursuing a policy he supports because of the critical case of 'Some Guy' vs. Dick's Sporting Goods is quite simply ludicrous. "The White House plan addresses bump stocks, calls for improvements in mental health care and encourages states to authorize gun violence restraining orders. All fine as far as they go. "But it also rushes to arm teachers while slow-walking a sensible restriction on gun sales. That is the NRA's dream scenario, and no denial-by-tweet will change that." (Ref. 4) By the way. With all the fuss over the issue of outlawing bump stocks, exactly how many school shootings have involved guns with bump stocks? Answer: ZERO! How many mass shootings have involved guns with bump stocks? Answer: ONE! The bump stock controversy is simply another red herring being thrown out to confuse and distract from the real issue – that of reducing the number of guns in the hands of would be mass killers! The real questions needing answers are: how many school shootings have involved guns? Answer: ALL OF THEM! And, how many mass shootings have involved guns? Answer: ALL OF THEM! "The Pew Research Center in 2017 suggested 7 out of 10 Americans favor an assault weapons ban (including 5 out of 10 gun owners). In our closely divided county, this level of agreement is rare. "Why, then, are we once again sending our 'thoughts and prayers' after a mass killing involving an assault weapon? . . . "For evil to succeed, all it needs is our continued 'thoughts and prayers' instead of meaningful action to let our local representatives know how we feel." (Ref. 5) Gun rights advocates vigorously lay down a smoke screen of irrelevant issues to head off any meaningful actions on gun control. For example, in early March of this year. Senator Marco Rubio (R-FL) sent a letter to the Federal Education Secretary, "asking her to rescind the Obama administration's 2014 guidance aimed at reducing disproportionate discipline of students of color and promoting alternatives to punitive discipline. The premise of Rubio's letter isn't unusual—conservative critics have claimed for years that this guidance was federal overreach and prevented schools from disciplining students. But what is unusual is that Rubio's letter went even further and claimed that the guidance contributed to the terrible massacre at Marjory Stoneman Douglas High School in Parkland, Florida [Emphasis mine] . . . Of course, none of Rubio's argument is actually true . . . The attempt to blame the shooting on the discipline reforms advocated in the Obama-era guidance is another in a long line of attempted distractions from the real issue: the need to strengthen our nation's gun laws to help reduce the epidemic of gun violence in this country. "The distraction of the discipline guidance follows on the heels of other distractions that claimed that gun violence is a mental health issue, not a guns issue, and that schools should arm teachers. . . All of these are just more false claims that prevent a serious discussion about gun safety. . . - - - "It's clear that none of the arguments connecting the discipline guidance to the Parkland tragedy hold up under serious scrutiny. What's also clear is that instead of talking about arming teachers or ignoring the disparate rates of discipline of students of color, policymakers should be talking about real solutions to the problem of gun violence. [Emphasis mine] They can start by banning assault weapons and high capacity magazines, allowing the Centers for Disease Control and Prevention to research gun violence as a public health issue, requiring background checks for all gun sales, supporting local violence reduction programs, and ensuring that all domestic abusers don't have access to guns. These solutions are straightforward and have broad support across the country." (Ref. 6) What is abundantly clear is that meaningful action to end gun violence has been continually and effectively sidetracked by gun enthusiast with smokescreens, red herrings and the inevitable reliance on the claim that any-and-all steps to control access to guns is prohibited by the Second Amendment to the Constitution. Instead, potentially effective action is sidetracked with halting and ineffectual "baby steps" and groveling appeasement of the pro-gun lobby with more of the "same old, same old". According to the NRA, instead of dramtically reducing the number of guns in the United States, we need to put more guns on the streets of America by arming teachers. Unbelievably, we have elected officials who go along with the NRA proposal. "Unfortunately, the likelihood of Congress passing meaningful gun reform is close to zero. Even as the urgency of American gun violence increases, Congress does nothing. "Many Republicans depend on support from the powerful gun lobby. They have every reason not to bend. Ditto the Democrats. Having taken so many political hits on gun politics over the last two decades, and sensing a sea-change that gives them the political upper-hand, why ease up now? The Democratic Party has every incentive to exploit the issue for political gain rather than concede even an inch and settle for a bill that can garner support from an increasingly elusive group of moderates. "The Republican intransigence on guns stems from fear of a powerful gun lobby led by the National Rifle Association. The NRA once took a bi-partisan approach, supporting members of either party it trusted on guns. But no more: Now the NRA is all in on the GOP. It spends tremendous amounts of money and mobilizes its membership base on behalf of the Republican lawmakers who toe its line. "GOP officials rightly fear that any willingness to compromise on gun issues will provoke the NRA's wrath — which could result in the gun lobby backing a future primary opponent. In the middle of a presidential campaign where many fear that usually engaged political supporters may sit on the sidelines, to anger the NRA could be political suicide. "Democrats used to cower in fear of the NRA as well. For a generation, the party viewed gun issues as an untouchable third rail of politics. - - - "If there's hope, it's that the public is increasingly fed up with the never-ending drumbeat of gun violence that claims more 90 American lives each day. Only when the public demands that Congress elevates public safety over partisan politics — and makes that demand in the voting booth — will there be any real chance for federal legislation that will meaningfully combat American gun violence." (Ref. 7) "To pass any significant gun control legislation through the United States Congress, President Trump would have had to exert the full power of his office. Trump would have had to twist the arms of his Republican colleagues and burn through significant political capital with his conservative base. So it's not exactly surprising that over the weekend he backed away from pushing the more ambitious gun reforms that have circulated in Congress since the school shooting in Parkland, Florida. Without Trump on board, universal background checks and a host of other policies appear to have missed their moment for the millionth time. " 'I think we could all see it coming,' . . . a leading Senate Democratic voice on guns, told reporters . . . 'I've been skeptical since the beginning that the president and his party were really willing to break with the NRA.' . . . 'it will likely take an election where they pay a price for their fealty to the gun lobby' for meaningful action to take place. Don't hold your breath. "The only real glimmer of hope came . . . when the president seemed keen on a few pro–gun control policies during a televised meeting with members of Congress from both parties. He supported lifting the age of purchase for all firearms from 18 to 21, and he backed expanding background checks to cover gun show and online sales. He didn't outright reject a resurrected assault weapons ban, either. Senate Democrats took some of the ideas Trump said he supported and quickly translated them into a legislative proposal, in the hopes of capitalizing on the president's comments before he could change his mind. "But the president had lunch with top officials at the National Rifle Association just a few days after that meeting, and his willingness to buck the organization has steadily diminished since then. The White House position has been whittled down to support for the Fix NICS Act, a bipartisan bill to ensure better reporting of information into the National Instant Criminal Background Check System, as well as offering Justice Department assistance for training educators to use firearms and establishing a commission to make recommendations for other reforms. In Washingtonese, this is known as 'punting.' The White House also urged states to pursue a policy of restraining orders allowing law enforcement to temporarily disarm those showing signs of danger. (Trump appears to have been convinced, now, that it's worth securing warrants for such search and seizure instead of 'taking the guns first.') "(Ref. 8) As past history has shown, meaningful reform on guns or "school safety" may be nearing a quiet death, just weeks after demands for action peaked following the Parkland shooting. Unless-and-until the American public rises up and says ENOUGH, nothing meaningful will happen! Public outrage must clearly emphasize that the position that When it comes to guns, it's business as usual! will no longer be tolerated. Unfortunately, as of now, "Sources on Capitol Hill now universally say they do not expect legislation—even the narrowed down variety—to pass, while senior officials at the White House appear committed to spotlighting the influence they suggest violent video games are having on our nation's youth. "Frustration with the inertia bubbled over this week, sparking a round of finger-pointing over who exactly and which party is at fault. But the outcome should not have caught anyone by surprise. Doing nothing in the aftermath of a prior mass-shooting is a right of passage for Congress. [Emphasis mine] - - - "As the state of Florida moved new measures into law, hints of gridlock on the federal level grew more visible in recent days. The simplest of legislative responses—a bill that would strengthen federal reporting requirements on background checks for gun purchases known as Fix NICs—has garnered 62 Senate co-sponsors, including the second-ranking Senate Republican. "That is enough for passage. And yet, the bill has stalled. [Emphasis mine] - - - " 'Senate Republicans haven't devoted one second to the gun safety debate on the Senate floor' . . . 'That fact says everything about their willingness to buck the NRA and get something real done.' - - - "The Trump administration, for its part, could not be clearer in its determination to let the news cycle move on from the shooting. A president who had, just last week, spoken about his ostensible desire to push comprehensive background checks and restrictions on buying AR-15s, spent the close of the week watching video games instead." (Ref. 9) After a mass shooting, politicians offer condolences and prayers, observe moments of silence and order flags flown at half-staff. But afterward, legislative efforts are deferred and ultimately derailed. Invariably, the refrain is: not now, later; There will be a time and place for a political debate, but not now. Now is the time for us to mourn and unite as a country. And the time for political debate and meaningful action never comes. It's always the same old story – now is not the time, later. When it comes to guns, it's business as usual! Will the American public continue to avoid taking the first hard step toward reversing this trend? Or, will the American public finally stand up and demand that their elected representatives institute meaningful, effective and innovative legislation to reverse the trend of gun violence in the United States? Will the American public demand the repeal of the Second Amendment to the Constitution, followed by the enactment of radical and restrictive gun control laws that will put an end to these senseless killings? When it comes to gun violence, will the American public finally demand an end to the business as usual attitude of its elected officials? Isn't now finally the right time? ----------------------------------------------------------------------------------------------------------------- References:
19 March 2018 {Article 319; Suggestions?_10} |


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While the music industry has spent the last week or so enveloped by Kanye West's ongoing The Life of Pablo album release saga, it's due time we switch gears a little and settle in for the three-way battle of Taylor Swift, Kendrick Lamar, and The Weeknd at the 58th Annual Grammy Awards. LL Cool J is back to host the event tonight at the Staples Center in Los Angeles. There will be quite a few powerhouse performances from artists like Adele, Rihanna, and Justin Bieber, as well as Lady Gaga doing some renditions of David Bowie classics and the cast of Hamilton performing the play's opening number.
The show goes from 8PM ET to 11:30PM ET on CBS, which is also providing the only (legal) way to watch the event online. The pre-show, from 3:30PM ET to 6:30PM ET can be watched for free at CBS.com or grammylive.com.
As far as awards go, Lamar, Swift, and The Weeknd are dominating the main categories. Lamar is up for the most Grammys with 11 nominations, while Swift and The Weeknd are tied with seven each. Adele's record-smashing 25 didn't make the eligibility cutoff for this year's show, so expect it to sweep 2017's.
Kendrick Lamar, Taylor Swift, and The Weeknd are battling for the biggest categories
Unlike the byzantine collection of streaming methods available for this year's Super Bowl, the process of watching the Grammys online is remarkably simpler thanks to CBS's streaming service, CBS All Access. The network has owned the exclusive broadcasting rights to the show since 1973, meaning the only way to legally watch it online is by subscribing over at CBS.com/all-access. The monthly cost is $5.99, but you can always sign up for a free one-week trial and cancel the service following the show. Here's how to get CBS All Access up and running on every device:
Watching on a smartphone or tablet
If you're itching to watch the Grammys and don't have a larger screen, download the free CBS app from the iOS App Store, the Google Play Store, or Microsoft's Windows 10 marketplace. From there, you can log in with your All Access credentials and enjoy the live Grammys stream. Make sure to login into the mobile app with the same account you used to sign up for All Access. If you used your Facebook credentials to log in, use the same on mobile. If you used a standard email address and password, use those credentials to log in or else All Access won't recognize your account.
Watching on a PC or Mac
CBS All Access members can stream CBS live through a web browser but only in select markets. A full list of live TV locales can be found here, but it's safe to say the company has most of the US's larger markets covered at this point. If you have a cable subscription, you can watch the Grammys live from anywhere through CBS's main website.
Watching on a game console or set-top box
CBS, being a slow-moving old-school behemoth of a corporation, is painfully behind on making All Access available on more than a select few set-top box and game console platforms. The company has the most popular devices covered — Apple TV, Roku, Chromecast, Amazon's Fire TV, and Android TV devices all support the new service via either CBS's main app or a dedicated All Access app. Make sure to get the All Access app if it's available on your desired platform. For instance, Apple TV, Fire TV, and Android TV all have dedicated All Access "channels," separate from the main CBS app. Chromecast, however, only works with the CBS mobile app or by mirroring your computer screen with the Google Cast Chrome extension.
As for game consoles, however, All Access is only available on the Xbox 360. It's absurd, and there's we can do about it until the company decides to bring its service that launched in October 2015 to game consoles that came out in November 2013. If you happen to have an old Xbox lying around, search for the All Access app and enter the code you see on your screen after sign-in over at CBS.com/xbox360 using a mobile or web browser.
Watching outside the United States
CBS doesn't offer a legal streaming option for viewers who want to tune into the Grammys outside the United States, even if they pay for All Access. That said, you can use a VPN service or a similar DNS proxy service to trick CBS into thinking your internet connection resides in America. A product like TunnelBear is a sophisticated VPN service for all your geoblocking avoidance needs. But simpler services like Unblockus, Getflix, and Media Hint effectively do the same thing with less hassle. The Verge's Thomas Ricker wrote about proxy services last year and has a great guide to getting started with the somewhat messy world of streaming service workarounds.


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Often times solar energy contractors talk about a solar power system, but what solar equipment makes up a solar power system? There are three way you can utilize your solar power system, which we'll discuss in our next section.
On-Grid Solar System
This is what most residential homes have as most solar energy contractors offer this. An on-grid solar system works with and connects to your utility grid. This system comes with an option of net metering. With this system you can create your own electricity during the day, then when the sun goes down you can get electricity from the grid. This system reduces your electricity bill but won't eliminate it. An on-grid system is easy to install and cost less than an off-grid solar system. If you have a reliable grid and your electricity bills are high, then an on-grid solar system is a reasonable option. Though here in Texas our grid isn't reliable so this may not be your best option. This option eliminates your electricity bill completely.
Off-Grid Solar System
With Texas being such a big state there many rural areas that struggle getting sufficient electricity. Texas is infamous for its many power outages. For these areas, solar energy contractors say an off-grid solar system is greatly beneficial. Being connected to the grid is not necessary to have power. This system does require solar batteries to store the energy generated by the solar panels. The batteries will make sure you have power when the sun goes down. Often times a generator is added to this solar system to ensure you have access to extra electricity during emergencies. Solar energy contractors recommend off-grid solar systems to those that don't have reliable electricity connection.
Hybrid Solar System
A hybrid system can work with or without the grid. With this solar system you get the best of both worlds which is why it's used more commercially. This is the best option since it used both the grid and batteries for excess power. When your solar batteries are fully charged, you'll be automatically sending electricity back to the grid. This will drastically reduce your electric bill and on occasions eliminate it altogether.
Dependent on What Your Solar Energy Contractor Can Offer
Which solar system you go with can often depend on what solar energy contractor you choose. Not all solar energy contractor offers batteries or generators. That's why it's important to choose a reputable solar energy contractor, that can offer you everything you want out of solar energy.
Helpful Links:


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"Fighting ten times harder"
"I have never given up. I have never stopped fighting. I will never stop fighting until the Lord takes me home. Until that day, I'm going to fight for me."
When Brandi Jones was 17, she temporarily lost function of the entire right side of her body. An inflamed optic nerve, weakness in her hands and feet, bladder dysfunction, pain and tingling were just a few of the symptoms that rendered her immobile.
This would be a jarring experience for anyone, but it was particularly difficult for Brandi, who had welcomed her first child only a few months beforehand. Suddenly, she couldn't even hold her daughter.
After being seen by her primary care physician, Brandi was referred to a neurologist. An MRI and spinal tap revealed that Brandi had Multiple Sclerosis (MS), an unpredictable disease of the central nervous system that disrupts the flow of information within the brain, and between the brain and body.
It's been 20 years since Brandi was diagnosed with MS, and she's been fighting ever since. But managing the disease hasn't always been easy.
Throughout her teens, she tried various medications, but nothing seemed to help. In her 20s and 30s, Brandi struggled to find the quality of care she needed, at times feeling dismissed by providers who failed to properly address the severity of her symptoms.
"When you're a minority and you have an autoimmune disease, you're fighting ten times harder," said Brandi, acknowledging the racial disparities in healthcare that still exist today.
Research indicates that Black people with MS may have more aggressive disease progression, greater disability, different symptoms, more frequent relapses with poorer recovery, and earlier disability onset. Scientists still don't know why these differences exist, and not enough clinical trials have been completed to find answers.
"Most doctors don't know enough research on how MS affects minority patients," said Brandi. "I haven't had one provider who said, 'Hey, I know a doctor who specializes in minorities and might be able to help you.'"
And then Brandi heard about Jay Avasarala, a neurologist at UK HealthCare's Kentucky Neuroscience Institute. In addition to his extensive experience in the diagnosis and treatment of MS, Dr. Avasarala has been advocating for minority patients and specifically studying MS in Black patients since 2014.
"By the time I saw Dr. Avasarala, I was screaming for somebody to truly understand what I was going through and to know that it's different," said Brandi. "It was a weight lifted off my shoulders because this is somebody who has seen it for himself. He's done the research. He knew the statistics. I didn't have him questioning the likelihood or severity of my pain. He told me to advocate for my own health care."
Under Dr. Avasarala's care, Brandi was prescribed a drug called OCREVUS®—an infusion therapy that's given through an IV (administered by a healthcare professional) twice a year.
"Dr. Avasarala explained why this treatment was going to be good for me—not just because I had MS, but why it would be good for me as an African American woman," she said.
Since beginning infusion treatments nearly two years ago, Brandi's MRI scans have shown no MS lesions. Dr Avasarala says that from a clinical perspective, she's doing well. But Brandi's story is only one of many—and according to Dr. Avasarala, more research and studies must be done to ensure more favorable health outcomes for Black people with MS.
"The disease is aggressive in minority populations," said Dr. Avasarala. "That's not to say Caucasians don't have severe cases of MS. They absolutely do. But the proportion of individuals with severe disease is significantly different between the groups. It would make sense in a drug trial, that if you treat the most aggressive population effectively, that would be your ticket to success. We need to really reach for the stars and try to combat the disease at its worst."
While smaller trials, repositories and data banks on MS in African Americans do exist, Dr. Avasarala said they are not large enough to represent the broader population. Forming a consortium on minority health issues pertaining to MS, at both university and federal levels, would be a step in the right direction. But this would require continuous funding for research, and the advocacy of both providers like Dr. Avasarala and patients like Brandi, to come to fruition.
"African Americans need to advocate for research and become leaders," said Dr. Avasarala. "There is no better voice than speaking up and showing up."
With 20 years of MS now under her belt, Brandi has become one of those leaders. She's turned her challenges into triumphs, helping raise awareness as a district activist leader for the National Multiple Sclerosis Society and through her podcast, 1SicB. Brandi defines the term as "A strong individual that fights/faces through unimaginable, undeniable, courageous battles that life throws at you without warning but you refuse to carry the spirit of brokenness." The podcast is a platform that "embodies, empowers, educates and invokes the Conversation between Kings and Queens thriving with MS and other autoimmune diseases."
"I strive for efficacy within our community," said Brandi. "When you go through an autoimmune disease, you already lose so much. But I ask, 'What can you bring of value to help others, and what brings value to your situation?' There are so many people going through the same thing I am, but they either don't have the support system or are scared to speak up. You have to speak up for yourself. If you back yourself into a corner, how are you going to get the proper treatment?"
See how we care for patients like Brandi


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The mission, focused on the Didymos-Dimorphos binary asteroid system, proved that an asteroid's orbit can be altered by kinetic impactor technology.
Rocks from space have walloped Earth for eons, and it's only a matter of time until our planet lands yet again in the crosshairs of a very large asteroid. But unlike other forms of life—here's looking at you, dinosaurs—humans have a fighting chance of altering our cosmic destiny. At AGU's Fall Meeting 2022 held in December, researchers presented a slate of new results from NASA's Double Asteroid Redirection Test (DART) mission, the first demonstration of asteroid deflection.
Peering at an Orbit
DART's target, the Didymos-Dimorphos asteroid system, was first discovered in the mid-1990s. But astronomers back then spotted only its larger member, Didymos, which is roughly 800 meters (half a mile) in diameter. It wasn't until 2003 that scientists realized that a much smaller body, dubbed Dimorphos, was also present. Dimorphos is about one fifth the size of Didymos, and its orbit takes it in front of and behind Didymos as seen from Earth. That's serendipitous, because by monitoring how the brightness of the Didymos-Dimorphos asteroid system varies over time, scientists were able to precisely determine how long it took Dimorphos to complete an orbit: 11 hours and 55 minutes.
"We needed to understand the Didymos-Dimorphos system before we changed it," said Cristina Thomas, a planetary scientist at Northern Arizona University in Flagstaff, at AGU's Fall Meeting 2022.
The primary goals of the DART mission were simple, at least in concept: Hit Dimorphos with the roughly 570-kilogram (half-ton) DART spacecraft to alter the orbital period of Dimorphos around Didymos significantly and measure that change and characterize the physics of the impact. If successful, it would be the first demonstration of deflecting an asteroid using so-called kinetic impactor technology. (In 2005, another NASA mission, Deep Impact, tested kinetic impactor technology with a comet.)
On 23 November 2021, a Falcon 9 rocket lifted off from California's Vandenberg Space Force Base. By then, the SpaceX-designed rocket had notched more than 100 successful launches, but for members of the DART mission, the event was anything but ordinary: Nestled within the rocket's nose cone was the spacecraft they'd spent well over a decade designing, building, and testing.
The launch went smoothly, and DART soon entered into orbit around the Sun. For roughly 10 months, the spacecraft largely tracked the orbit of Earth, essentially waiting to catch up to the Didymos-Dimorphos asteroid system, which orbits the Sun between Earth and Mars. "We stayed close to Earth the entire time and just caught up with the Didymos system at its closest approach to Earth," said Elena Adams, DART mission systems engineer at the Johns Hopkins University Applied Physics Laboratory in Laurel, Md.
Approaching the Unknown
It was only around July of 2022 that DART's onboard camera—the Didymos Reconnaissance and Asteroid Camera for Optical navigation (DRACO)—caught its first glimpse of Didymos. But Dimorphos wouldn't come into view until much, much later: Just an hour before impact, at a distance of roughly 25,000 kilometers, the tiny moonlet was still a mere two pixels across in DRACO images.
"We didn't see Dimorphos until late in the game," said Adams. To prepare for the uncertainties of impacting a body they knew virtually nothing about, DART team members ran thousands of Monte Carlo simulations beforehand in which they varied the moonlet's size, shape, albedo, and a slew of other parameters.
The DART spacecraft successfully impacted Dimorphos on 26 September 2022. The event was recorded by a cadre of Earth-based telescopes and also the Light Italian Cubesat for Imaging of Asteroids (LICIACube), a briefcase-sized spacecraft carrying two cameras that launched with DART and was released from the spacecraft 15 days prior to impact.
A Serendipitous Boost
Researchers had calculated that the impact, which occurred roughly head-on, would shorten Dimorphos's orbital period by just under 10 minutes. That was assuming the simplest case of no ejecta being produced, said Andy Cheng, DART investigation team lead at the Johns Hopkins University Applied Physics Laboratory, at a press conference.
"The amount of momentum that you put in the target is exactly equal to the momentum that the spacecraft came in with." But if ejecta flies off the asteroid after impact, physics dictates that the asteroid can get an extra boost, said Cheng. "You end up with a bigger deflection."
That's good news when it comes to pushing a potentially harmful space rock out of the way, said Cheng. "If you're trying to save the Earth, that makes a big difference."
And ejecta there was, in spades—on the basis of detailed follow-up observations of the Didymos-Dimorphos system, scientists discovered that Dimorphos is now traveling around Didymos once every 11 hours and 22 minutes. That's a full 33 minutes shorter than its original orbital period, a finding that implied that a substantial amount of ejecta was produced. Imagery obtained from ground- and space-based telescopes has borne that out—a plume of debris tens of thousands of kilometers long currently stretches out from Dimorphos. Researchers have estimated that at least a million kilograms (1,100 U.S. tons) of material were blasted off the asteroid by the impact. That's enough debris to fill several rail cars, said Andy Rivkin, DART investigation team lead at the Johns Hopkins University Applied Physics Laboratory, at a press conference at the Fall Meeting.
Follow the Debris
Interestingly, the ejecta shed by Dimorphos has remained in distinctly more plumelike configurations than the debris shed by comet 9P/Tempel 1 when NASA's Deep Impact spacecraft intentionally crashed into it in 2005. "The Dimorphos ejecta has a lot of morphological features," said Jian-Yang Li, a planetary scientist at the Planetary Science Institute in Fairfax County, Virginia, and a member of the DART team, at the Fall Meeting.
The reason is probably the different compositions and surface features of the two bodies, he said. Tempel 1 is rich in volatiles and fine-grained dust; Dimorphos's surface, on the other hand, is littered with boulders. Scientists plan to continue to monitor Dimorphos's debris plume through at least March.
The DART mission has also enabled scientists to investigate a fundamental question about the Didymos-Dimorphos asteroid system: Do the two asteroids have the same composition? It's a common assumption when it comes to binary asteroids, but it's never been confirmed. Thomas, leader of the DART Observations Working Group, presented new results on the subject at a press conference at the Fall Meeting. She shared near-infrared spectra of the binary asteroid system that astronomers had collected both before and after impact using a NASA telescope in Hawaii.
Observations obtained prior to impact (when the overwhelming majority of the sunlight reflected off the asteroid system came from Didymos) and after impact (when the debris shed by Dimorphos was responsible for more than two thirds of the reflected light) revealed very similar spectra, with characteristic dips at wavelengths of 1 and 2 micrometers in both cases. That's strong evidence that the two asteroids have similar compositions, said Thomas.
Scientists aren't yet finished with Didymos and Dimorphos: In 2024, researchers involved in the European Space Agency's Hera mission plan to launch a spacecraft to the system to further characterize the asteroids—including accurately measuring the mass of Dimorphos—and to study the crater created by the DART impact.


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12 Nov Boost Your Concentration Using Incense
When it comes to concentrating on a particular purpose, it seems challenging for many. If you cannot focus and employ all your mental energy at a particular task, here is something important for you to learn. It is not only you who is dealing with concentration challenges; there are many who are not able to focus in a moment and think of attending different tasks at a time.
Furthermore, there are many ways to keep your concentration at a peak. And one of them is going with aromatherapy. Yes, it is a popular yet proven way to boost your concentration. Also, many monks and ascetics from different cultures believe that aroma really works when they try to concentrate their minds for meditation. If you also want to increase concentration with aroma, you can use incense such as comeback incense powder. You can burn incense with your desired fragrance while meditating or trying to focus on a subject. There is a range of incense fragrances you can use to improve your concentration. In addition to it, you can also buy a room odorizer online to spread a pleasant scent around your room. After all, here are some popular incense fragrances you can try to boost your focus.
Peppermint is one of the best fragrances you can use to improve your focus. It works by soothing your nervous system and increasing your alertness at the same time. It allows the senses to focus and increase your productivity when you are involved in a particular task. If you are pursuing your academic career, it can be a great solution for you. You can shop for incense with peppermint aroma such as comeback incense powder.
Lavender produces a sweet smell that can have a calming effect on your mind. Once you feel this smell, you can't forget it easily. Lavender has been used for aromatherapy for some time and works best for dealing with work and school-related anxiety. You can buy room odorizers online with lavender fragrances and use them when you need to focus on a particular task. You can feel a boost in your productivity after using lavender incense.
It has the ability to stimulate your mind and boy when you receive aromatherapy. Also, this fragrance has a history in using for the treatment of dementia and Alzheimer's. You can use this fragrance for your overall mental and physical well-being. That's all you need to know about improving your concentration through incense.


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