“He has interest in continuing to play,” Antonetti said. “We have an academy in the Dominican. He asked if we would be interested in seeing him work out, so we worked him out. That’s really the extent of it.”

At this point, past injuries have essentially rendered the 37-year-old Guerrero a pure designated hitter. He appeared in 137 games as a DH for Baltimore last season, hitting .290 with 13 homers and 63 RBIs. The Indians already have a well-paid full-time DH with a laundry list of recent health woes in Travid Hafner.

In theory, Cleveland could put Hafner and Vladdy into a DH platoon, but that would strike a decisive blow to the versatility manager Manny Acta wants available on his bench. The only way I could see adding Guerrero making sense was if he could handle playing left field.

Asked if Guerrero could play any outfield, Antonetti’s reply was: “He hasn’t played outfield recently.”

Antonetti noted that the Indians had Guerrero track down some fly balls during the workout to see what type of shape he was in for playing the outfield. The GM said Guerrero looked “no different than how he has over the last few years.” That’s hardly a ringing endorsement.

So, as Antonetti suggested, I wouldn’t make too much of this at this point in time. If we’re a month into the season, and injuries haunt Cleveland’s roster once again, and the team is in dire need of offense, well then, hey, sure I could see the Tribe getting more serious about taking a flier on an experienced hitter like Vlad.

Asked if Guerrero stepped into the box to face “Rob” (Indians pitcher Roberto Hernandez/formerly Fausto Carmona), Antonetti allowed himself to crack a smile.

The Indians “reduced their roster” — don’t go calling them roster cuts unless you want to get Manny Acta angry — by three players on Tuesday. The Tribe optioned 3B Lonnie Chisenhall and 1B Matt LaPorta to Triple-A, and also re-assigned OF Chad Huffman to Minor League camp.

Removing Chisenhall from camp cleared the way for Hannahan to win the starting nod at third base for the Indians. Not a big surprise there, but Cleveland insisted it was a competition. Chisenhall (16 Ks against 1 walk this spring) did not show the type of plate discipline the Indians wanted to see from him this preseason.

For all of you upset about Chisenhall’s demotion, keep in mind that the kid is still only 23 years old. He’s actually the third-youngest player on the team’s 40-man roster. The fact that he’s already in the mix for a big league job is impressive, but he is still in need of some offensive development.

The Indians know Hannahan is one of the best defensive third basemen in baseball and they love having him out there, along with Casey Kotchman at 1B, for their groundball-happy pitching staff. That said, Hannahan is eager to prove that he really did turn a corner down the stretch last season in the batter’s box.

Acta said LaPorta had a real opportunity to win a job on the Opening Day roster as either the starting left fielder or a backup outfielder/first baseman/DH off the bench. LaPorta hit .167 with 11 strikeouts and one walk in 14 games for the Tribe this spring. Cleveland needs to see more consistency from him before calling him back to the Majors.

Huffman had a better shot at making the team as a backup outfielder last spring than he did this spring. Still, given the way the outfield competition has gone, Huffman certainly could have played himself into the mix. Instead, he hit .231 and will likely wind up back in Columbus to start the year.

Ubaldo Jimenez started against the White Sox on Tuesday and was solid for the most part. He went five innings, giving up three runs (two earned) with three strikeouts and no walks. The Big U sat around 91-94 mph for the most part and ended with eight groundouts. He logged 90 pitches (54 strikes) and registered 11 first-pitch strikes among the 21 hitters he faced. Ubaldo had six 3-ball counts.

Acta raved about Ubaldo’s secondary pitches and Jimenez said he was pleased with his ability to avoid falling behind in the count as often as he has in other spring outings. He breezed through the first three innings, but ran into a 26-pitch wall during the fourth.

Center fielder Michael Brantley returned to the lineup on Tuesday after having last played a game on March 19 due to a right hamstring injury. He went 0-for-2. Outfielder Fred Lewis, who had been battling a sore right elbow, also returned to game action on Tuesday.

Shelley Duncan went 0-for-4 and saw his spring average drop to .195 on Tuesday, but Antonetti said Duncan had stepped forward as a leading candidate for the left field job. The average isn’t quite there, but Duncan has made consistently solid contact and leads the team with five home runs and 15 RBIs this spring so far.

The Associated Press reported the details of Hernandez’s restructured contract on Monday. Good ol’ Rob will have a base salary of $2.5M in 2012 with another $2.7M available through incentives. He can make $200K each for 20, 23 and 26 starts, $200K each for 150, 170 and 185 innings, and $250K every 15 days on the roster from 95-165 days. Hernandez’s original deal was for $7M this season. His 2013 club option has been reduced to $6M with any bonuses reached tacked on, and another $3M possible through incentives based on innings pitched. That option was originally $9M. The 2014 club option was eliminated. Of course, Hernandez is on MLB’s restricted list and he won’t see a penny until he’s back with the Indians and activated.

Antonetti said he has a couple pitchers in mind for the two available bullpen jobs, but he’s not ready to tip hishand just yet. The GM then went on to note that some of the candidates have performed better of late after poor starts to the spring. That, to me, might be in relation to Dan Wheeler.

Three of the other candidates — Jeremy Accardo, Robinson Tejeda and Henricus van den Hurk — each pitched on Tuesday. Accardo turned in another shutout frame to lower his spring ERA to 1.29 ERA. Tejeda and van den Hurk? Two runs allowed apiece. Right now, I’ve got to think Accardo, Nick Hagadone, Frank Herrmann and Wheeler are the top choices.

Antonetti and Acta have both stated that they want to see Jeanmar Gomez, Kevin Slowey and David Huff each pitch once more before announcing who has won the fifth starter job. Antonetti said they will take the best arm — regardless of their contract situation (see: $1.25M owed Slowey in 2012). With that said, it’s easy to think Gomez will land the job.

A couple Indians-related notes out of Rockies camp: Casey Blake was released on Tuesday and Colorado is moving former Tribe prospect Alex White to the bullpen. Blake is 38, missed time last year and this spring due to neck issues, and hit .150 in Cactus League play. I really don’t see him as a fit for the Indians at this point. As for White — part of the Ubaldo trade — many evaluators believed from the start that he was a future reliever, not starter.

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7 Comments

Why hasn’t the front office demonstrated any interest in bringing in Johnny Damon to play left field? His defense is actually better than he gets credit for, and he still has good speed and some pop left in his bat. It seems like this might be a decent move for the Tribe, particularly in light of recent moves to bring in the likes of Bobby Abreu.

ok – DISCLAIMER – exceedingly small sample size. Watched several games online / MLBTV, and saw a couple in person at Goodyear. LaPorta looked like a whipped puppy. His body language was just plain horrible. I played D1 college ball and you could tell when someone just wanted to be somewhere else. Sorry to say that was what I saw. I hope I’m wrong or that it changes, but I wonder . . . . The Tribe needs him to be what he was expected to be – or at least something a lot closer. C’Mon Matt – it might still be in there somewhere. . . . . Don’t give up yet.

dismissively wiknang I was just at that website, the German one with Mistess Helga .Don’t act like you have not virtually licked Her boot and been dismissively wiknang.P.S. Do you know how she ties her shoes?In little nazis ..WHAT? Too soon?

Newer games won’t run on the school’s ceupmtors so for those types of games you would need your own computer. However it would be probably be possible at an event to use someone else’s computer for a game or two. It can make it harder to play newer pc games because everyone needs ceupmtors.

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1. Introduction {#sec1-viruses-10-00307}
===============

1.1. A Principle {#sec1dot1-viruses-10-00307}
----------------

The following principle (basics-focus principle) is proposed here as a foundation for uses of phages in nanomedicine. The curing of currently intractable, biochemically complex diseases requires understanding of the disease basics, but it does not require understanding of the disease details. Historical justifications for the basics-focus principle include (1) the development of smallpox \[[@B1-viruses-10-00307]\] and rabies \[[@B2-viruses-10-00307]\] vaccines before any details about virus composition and structure were known; (2) the discovery of bacterial cell wall-active \[[@B3-viruses-10-00307],[@B4-viruses-10-00307]\] and ribosome-active \[[@B5-viruses-10-00307]\] antibiotics before the composition and structure of bacterial cell walls and ribosomes were known and (3) the use of phage therapy for infectious disease in the absence of knowledge of the composition and structure of phages \[[@B6-viruses-10-00307],[@B7-viruses-10-00307]\].

Applying the basics-focus principle does not mean neglecting the rest of the science. Louis Pasteur's basics-oriented work on improving wine and beer fermentation was a major part of the foundation for the fields of biochemistry and microbiology \[[@B2-viruses-10-00307],[@B8-viruses-10-00307]\]. Antibiotics became major tools in investigating the composition, structure and dynamics of bacterial cell walls \[[@B4-viruses-10-00307]\] and ribosomes \[[@B5-viruses-10-00307],[@B9-viruses-10-00307]\].

A proposed corollary is the following. Basics-focus on practical aspects of neurodegenerative and other diseases will not compromise the remaining science. Indeed, as we will describe in [Section 6](#sec6-viruses-10-00307){ref-type="sec"}, we think that the remaining science will also be promoted with this approach.

However, to get started, one has to know enough basics. We think likely that, at least in the case of neurodegenerative diseases, some basics will have to be assumed, without rigorous proof. In the discussion below, we will present both key assumptions and the phage-based evidence in the case of neurodegenerative disease. We will also present a basics-oriented strategy for malignant tumor therapy. This strategy includes use of a phage capsid-based drug delivery vehicle (DDV).

1.2. The Scientific Environment {#sec1dot2-viruses-10-00307}
-------------------------------

Articulation of the basics-focus principle is motivated, in part, by a current environment in which progress is politely described as slow for the curing of both neurodegenerative diseases and metastatic cancer. Less politely, but probably more accurately, most (not all) research on neurodegenerative diseases appears to be mired in its focus on complex biochemical details, with only limited symptomatic relief achieved \[[@B10-viruses-10-00307],[@B11-viruses-10-00307],[@B12-viruses-10-00307],[@B13-viruses-10-00307]\]. Focus on these details is the opposite of (1) what has historically been the most successful focus (previous section) and (2) what some fundamentals project to be the optimal focus for developing future therapies for pathogenic virus infections ([Section 2.5](#sec2dot5-viruses-10-00307){ref-type="sec"}), neurodegenerative diseases ([Section 3.2](#sec3dot2-viruses-10-00307){ref-type="sec"}) and cancerous tumors ([Section 4.2](#sec4dot2-viruses-10-00307){ref-type="sec"}). Lack of basics-focus is one possible explanation of why neurodegenerative diseases are incurable at this stage in history.

Two recent books appear to be warning signs that public patience is beginning to exhaust. A recent, cancer-oriented book comes very close to laying the slow-progress blame at the feet of science (really, scientists) \[[@B14-viruses-10-00307]\]. A recent, polio vaccine-oriented book suggests the following. Without the intervention of the law partner of an American President, polio vaccine, as we know it, would not have existed as early as it did \[[@B15-viruses-10-00307]\]. A logical rendition of the current state of phage therapy is likely to exhaust public patience to a new level because, in this case, successful application of the basics has already been achieved (\[[@B16-viruses-10-00307]\], reviewed in \[[@B17-viruses-10-00307],[@B18-viruses-10-00307]\]). However, apparently, in the US, one can receive phage therapy only on an ad hoc basis \[[@B16-viruses-10-00307],[@B19-viruses-10-00307]\].

Our entire research history is in the area of phages, with a primary focus on phage assembly. Historically speaking, the Caltech phage group (the home of PS for four years) was, in its early years, supported by the foundation that previously supported the basics focus-oriented work on polio vaccines. This foundation, The March of Dimes (also called the National Foundation), also supported the Pauling-associated work on structure discussed below (see the credits in references \[[@B20-viruses-10-00307],[@B21-viruses-10-00307],[@B22-viruses-10-00307],[@B23-viruses-10-00307]\]). That is to say, the basic philosophy in the current article appears to have an indirect linkage to the distant past.

1.3. Phage Assembly Basics {#sec1dot3-viruses-10-00307}
--------------------------

The composition and structure of phage T3 and its relative, T7, are illustrated in [Figure 1](#viruses-10-00307-f001){ref-type="fig"}d. The phage particle consists of (1) a DNA-encapsulating shell of the protein product of *gene 10*, called gp10; (2) an external structure (tail) adapted for specific binding to host cells and (3) an internal core stack \[[@B24-viruses-10-00307],[@B25-viruses-10-00307],[@B26-viruses-10-00307]\]. The various phage proteins are labeled by gp, followed by the number of the encoding gene. A T3 gene is given the same number as its T7 counterpart \[[@B27-viruses-10-00307]\].

The DNA-containing, protein capsid of all well-studied, double-stranded DNA phages begins its existence as a DNA-free capsid, called a procapsid. The T3/T7 procapsid (also called capsid I) is illustrated in [Figure 1](#viruses-10-00307-f001){ref-type="fig"}a \[[@B24-viruses-10-00307]\]. The procapsid subsequently packages a DNA genome and, while so doing, changes its structure to form a more phage-like capsid, called capsid II for T3/T7 ([Figure 2](#viruses-10-00307-f002){ref-type="fig"}b). At the end of packaging, the T3/T7 tail is attached to a ring (called portal or connector) that is on a DNA-filled capsid ([Figure 2](#viruses-10-00307-f002){ref-type="fig"}c) called a head \[[@B26-viruses-10-00307]\]. The connector (1) is the site of DNA entry; (2) occupies a 5-fold vertex of an icosahedral, DNA-containing gp10 shell and (3) forms the base of the core stack \[[@B24-viruses-10-00307],[@B25-viruses-10-00307]\].

2. Phage Assembly and Dynamic States {#sec2-viruses-10-00307}
====================================

2.1. The Stability of the Icosahedral Shell of the Related Phages, T3 and T7 {#sec2dot1-viruses-10-00307}
----------------------------------------------------------------------------

One's first impression of the mature T3/T7 capsid is that the DNA-enclosing gp10 shell is extremely stable and unlikely to change states. The shell is resistant to both ionic detergent \[[@B28-viruses-10-00307]\] and the proteases, trypsin and subtilisin \[[@B29-viruses-10-00307]\]. In a mature phage T3/T7 capsid, the major shell protein has a conformation \[[@B25-viruses-10-00307]\] in common among the various double-stranded DNA phages. This conformation is called the HK97 fold, named after the first phage found to have this fold \[[@B30-viruses-10-00307]\].

The mature gp10 shell of T7 capsid II also has a surprisingly high stability to elevated temperature, as discussed in [Section 4.3](#sec4dot3-viruses-10-00307){ref-type="sec"}. This characteristic suggests resistance to damage during possible use as a capsid-drug delivery vehicle (DDV).

Nonetheless, dynamism of phage shells is suggested by cryo-electron microscopy (cryo-EM) analysis. After expulsion of DNA from phage HK97, the shell "bows out" more than it does before expulsion \[[@B31-viruses-10-00307]\]. Similarly, T7 capsid II is found 1.4% larger than the mature capsid when purified \[[@B25-viruses-10-00307]\] and in lysates \[[@B32-viruses-10-00307]\]. If one makes the assumption that HK97-type shell proteins have incompressible components, without capacity for storing and releasing energy, the above result with HK97 is impossible. The reason is that DNA expulsion releases pressure from packaged DNA. This would cause contraction, not expansion, if one makes this assumption. Therefore, the shell of HK97 and probably T3/T7 can move internally to store and release energy.

Less direct evidence for shell dynamics arises from analysis of the leakage of DNA from (tail-free) phage T3 heads. The heads are obtained from a T3 mutant; almost no T3 and T7 heads are without a tail in a wild type infection \[[@B26-viruses-10-00307]\]. The DNA leaks from heads in quantized amounts. This phenomenon is seen via the formation of sharp bands during agarose gel electrophoresis of the DNA remaining packaged after 1-hit restriction endonuclease digestion. The DNA remaining packaged is obtained by (1) DNase I-digestion of external DNA; and (2) expulsion from the capsid of DNA remaining packaged \[[@B26-viruses-10-00307]\]. This leakage-quantization phenomenon is best explained by quantized gp10 shell contraction that evolved via selection for control of the rate of infection-initiating DNA injection \[[@B26-viruses-10-00307],[@B33-viruses-10-00307]\].

In addition, some multi-site T3 mutants undergo enhanced in vivo production of the following gp10-shell variants of capsid II: hyper-expanded and contracted. Identification of hyper-expanded capsid II is made by both (1) electron microscopy and (2) calculation of hydration from the density during buoyant density centrifugation in Nycodenz density gradients of a Nycodenz-impermeable (low density, high hydration) capsid II \[[@B34-viruses-10-00307],[@B35-viruses-10-00307]\]. A DNA-free version of these capsids was initially investigated \[[@B34-viruses-10-00307]\].

Next, a DNA-containing version of hyper-expanded capsid II was isolated via its Nycodenz impermeability (sealing) and accompanying low density \[[@B35-viruses-10-00307]\]. This particle underwent contraction in the presence of magnesium ATP, but not magnesium ADP. Binding of ATP to gp10 was proposed to be the source of energy \[[@B35-viruses-10-00307]\]. The following was evidence that the sealing had been evolutionarily selected. For wild type capsid II, cryo-EM revealed the complexity of inter-gp10 subunit interactions to be so high \[[@B25-viruses-10-00307]\] that accidental sealing was improbable. Thus, these capsids were proposed \[[@B35-viruses-10-00307]\] to be in states selected for function during DNA packaging (details \[[@B36-viruses-10-00307]\]). The hyper-expansion required shell thinning to the point that β-sheet was proposed as the likely dominant conformation of gp10 major shell protein \[[@B35-viruses-10-00307]\].

2.2. α-Sheet, Rather than β-Sheet, in Size-Altered Capsid II? {#sec2dot2-viruses-10-00307}
-------------------------------------------------------------

α-sheets resemble parallel β-sheets in having a parallel and extended conformation. However, if the amino acids all have the same chirality (as they do in almost all current proteins), then amino acids alternate side chain positions. That is to say, the conformation is not a helical array of amino acids. If constituent amino acids either alternate in chirality or are all glycine, then an α-sheet can be a helical array of amino acids \[[@B21-viruses-10-00307],[@B22-viruses-10-00307],[@B23-viruses-10-00307],[@B37-viruses-10-00307],[@B38-viruses-10-00307]\]. The above has suggested the possibility that α-sheets began existence abiotically, when proteins were glycine-rich and other amino acids involved were not chiral \[[@B37-viruses-10-00307],[@B38-viruses-10-00307]\].

An α-sheet-like peptide of 3--6 amino acids is called a nest. Nests are typically glycine-rich. α-sheets and nests have α-amino groups segregated on one edge and α-carboxyl groups segregated on the opposing edge \[[@B21-viruses-10-00307],[@B37-viruses-10-00307],[@B38-viruses-10-00307]\]. Nest-associated α-amino groups are known to bind anions, such as phosphate, via the α-amino group edge. P-loop ATP-binding sites typically have a phosphate-binding nest \[[@B37-viruses-10-00307],[@B38-viruses-10-00307]\]. Thus, one projects that a more extensive α-sheet is also likely to bind phosphates, including those part of ATP.

α-sheets were discovered via model building in 1951 \[[@B21-viruses-10-00307]\] and were originally called parallel pleated sheets before parallel β-pleated sheet was known to be the more frequent structure. However, extensive α-sheets were found, by the discoverers, to be unlikely for the real world of left-handed amino acids. The reason was "steric hindrance between adjacent side chains" \[[@B23-viruses-10-00307]\] for left-handed, non-glycine amino acids. Bending of α-sheets can reduce steric hindrance enough to make extensive α-sheet possible \[[@B22-viruses-10-00307]\].

Additional unfavorable energetics are expected from the charge separation of α-sheets in the absence of multiple sheet layers. The α-carboxyl edge is negatively charged; the α-amino edge is positively charged at physiological pH. Indeed, stable proteins have only a small percentage of α-sheet-like nests. Among the proteins stable enough to be characterized, α-sheet-like nests are found primarily in ATP binding sites and in the lining of transmembrane pores \[[@B37-viruses-10-00307],[@B38-viruses-10-00307]\].

The expected increase of α-sheet content for abiotically generated peptides suggests that nests are imprints from times before the existence of living organisms. The idea is that this structure was not completely replaced when increased diversity and chirality arrived for biological amino acids \[[@B37-viruses-10-00307],[@B38-viruses-10-00307]\].

In theory, evolutionary retention of α-sheet structure would be increased if (1) the α-sheet is curved; (2) cooperativity is symmetry-promoted by incorporation of the protein in a symmetrical structure and (3) the protein binds a nest-stabilizing ATP molecule, thereby initiating a cooperative transition to α-sheet structure. Thus, we propose the following hypothesis. During DNA packaging, the observed T3 capsid II shell dynamics (hyper-expansion and contraction) are caused by the adopting by gp10 of ATP-responsive, dynamic α-sheet conformations.

Specifically, single-layered α-sheet is the proposed structure for gp10 in the shell of the most hyper-expanded version of T3 capsid II ([Figure 2](#viruses-10-00307-f002){ref-type="fig"}a; orientation in the shell is discussed in the next paragraph). The thickness is 0.6--0.9 nm \[[@B21-viruses-10-00307],[@B37-viruses-10-00307]\], which is thin enough to make possible covering of the entire surface of the observed hyper-expanded T3 capsid II \[[@B35-viruses-10-00307]\]. In addition, the proposed structure for the contracted versions of T3 capsid II is multi-layer α-sheet ([Figure 2](#viruses-10-00307-f002){ref-type="fig"}c), generated by an event approximating the folding of the single-layered α-sheet ([Figure 2](#viruses-10-00307-f002){ref-type="fig"}b), without loss of gp10 subunits. This latter conversion would be assisted by favorable electrical charge-charge interactions ([Figure 2](#viruses-10-00307-f002){ref-type="fig"}b).

Assembly of multiple [Figure 2](#viruses-10-00307-f002){ref-type="fig"}a-like subunits will be inhibited by charge-charge interactions unless the radial positions of neighboring subunits vary so that the negatively and positively charged edges of neighboring subunits are juxtaposed ([Figure 2](#viruses-10-00307-f002){ref-type="fig"}d). This "staggering" of radial position will cause increase in apparent shell thickness when a shell is visualized in a two-dimensional projection of the three-dimensional structure.

Given the polar nature of the two edges of alpha-sheet, one edge is predicted to be at the outer surface of the capsid's shell; the other is predicted to be at the inner surface of the shell. Most likely, the negatively charged edge will be at the outer surface to minimize interaction with other intracellular proteins, most of which are negatively charged at neutral pH \[[@B39-viruses-10-00307]\].

2.3. Test of a Prediction: Surface Charge {#sec2dot3-viruses-10-00307}
-----------------------------------------

We have tested the prediction of a relatively high negative surface charge for the gp10 shell of hyper-expanded T3 capsid II. This was done for capsid II that had incompletely packaged DNA, abbreviated ipDNA; an ipDNA-containing capsid is called an ipDNA-capsid. The test was performed by native agarose gel electrophoresis in two dimensions (2d-AGE) (recent reference \[[@B26-viruses-10-00307]\]): 0.30% agarose gel in the first dimension; 2.0% agarose gel in the second dimension. A band of hyper-expanded ipDNA-capsid II was seen (labeled HE-CII in [Figure 3](#viruses-10-00307-f003){ref-type="fig"}a) after GelStar staining, nucleic acid-specific. This band was also seen after Coomassie staining, protein-specific. The effective origin of electrophoresis is indicated by the letter o. For comparison, the position of wild type T3 capsid II was also determined by 2d-AGE (dot labeled WT-CII in [Figure 3](#viruses-10-00307-f003){ref-type="fig"}a). The latter 2d-AGE was performed in a separate first and second dimension gel embedded in the same agarose frame as the gel in [Figure 3](#viruses-10-00307-f003){ref-type="fig"}a. The position of capsid I was determined from a separate analysis (dot labeled CI).

The effective radius of a particle (*R*~E~), together with the radius of the gel's effective pore (*P*~E~), uniquely determine the straight line drawn from the effective origin to the position of a particle in the gel. This line (dashed) is indicated for the WT-CII position in [Figure 3](#viruses-10-00307-f003){ref-type="fig"}a (*R*~E~ = 28.6 nm by small angle X-ray scattering \[[@B40-viruses-10-00307]\]). The angle, θ, decreases as *R*~E~ increases \[[@B26-viruses-10-00307]\]. Thus, the particles of the HE-CII band are confirmed in [Figure 3](#viruses-10-00307-f003){ref-type="fig"}a to be relatively large. The shape and orientation of HE-CII band indicate that these particles are also heterogeneous in *R*~E~.

The average particle of the HE-CII band also had an average electrical surface charge density, σ, that was negative and was increased in absolute value. The reasoning is the following. The value of σ has, in general, been found to be proportional to the electrophoretic mobility in the absence of a gel. This mobility has been found to be independent of internal contents, such as ipDNA (\[[@B26-viruses-10-00307]\] and included references). The ratio of σ value for HE-CII to σ value for WT-CII was 1.9. This ratio was determined from the ratio of average distances migrated in the first (low sieving) dimension, corrected for an estimated 5% greater effect of sieving on HE-CII in the first dimension. When CI was substituted for HE-CII, this ratio was also 1.9.

The source of the relatively high negative σ of hyper-expanded ipDNA-capsid II had to be either (1) the σ at the surface of shell-associated gp10 or (2) leakage from the capsid of a segment of (negatively charged) ipDNA, without dissociation of the ipDNA. We concluded that the former possibility was correct because electron micrographs did not reveal any leaked DNA \[[@B35-viruses-10-00307]\]. Thus, qualitatively, the above prediction was confirmed.

Finally, the relatedness of HE-CII and WT-CII particles was confirmed in the 2d-AGE profile of a higher density fraction from the same Nycodenz density gradient. In this case, the HE-CII band was connected to a WT-CII-like band by an arc formed by capsid II particles with intermediate *R*~E~ and σ values ([Figure 3](#viruses-10-00307-f003){ref-type="fig"}b and inset). Contrast enhancement was used in the inset of [Figure 3](#viruses-10-00307-f003){ref-type="fig"}b to make the arc more easily seen. Presumably, the arc-forming particles were also intermediate in structure.

2.4. Electron Microscopy {#sec2dot4-viruses-10-00307}
------------------------

In previous electron micrographs of specimens negatively stained with sodium phosphotungstate, hyper-expanded ipDNA-capsids appeared full \[[@B35-viruses-10-00307]\]. This appearance was caused by impermeability to the negative stain, not by filling with DNA \[[@B35-viruses-10-00307]\]. The low-electron density interior was occupied by dried buffer components. The appearance was similar after negative staining with uranyl acetate ([Figure 4](#viruses-10-00307-f004){ref-type="fig"}). However, the following feature was exaggerated in some particles of hyper-expanded NLD capsid II. A thin, dark layer of negative stain separated the light interior from the light gp10 shell ([Figure 4](#viruses-10-00307-f004){ref-type="fig"}). Apparently, after drying of most of the interior, negative stain leaked through the gp10 shell and then dried in a thin layer. In contrast, a contaminating wild type capsid II-like particle had the traditional negative stain-filled appearance (arrow in [Figure 4](#viruses-10-00307-f004){ref-type="fig"}). The shell of the latter capsids is 2 nm thick.

In the shell-revealing regions of hyper-expanded ipDNA-capsid II particles, the shell usually appears 3--5 nm thick. However, the thickness of the shell is likely to be significantly less than that ([Section 2.2](#sec2dot2-viruses-10-00307){ref-type="sec"}). This difference is enough so that a staining alone is unlikely to be the cause. Thus, the cause of the above difference resides in changes to the gp10 shell that occur in the latter stages of negative staining.

Details were suggested by the observation that, in some regions, the gp10 shell appeared doubled (arrowhead in [Figure 4](#viruses-10-00307-f004){ref-type="fig"}). The radial position staggering proposed in [Figure 2](#viruses-10-00307-f002){ref-type="fig"}d explained the observed doubling via an increase in the staggering distance at the latter stages of negative staining. By this explanation, embedding in the negative stain limited shell disruption to sub-observable levels. The regions of apparent shell thickening, without doubling, could be explained by smaller increase in the staggering distance and superposition of images from multiple planes perpendicular to the direction of observation. In summary, the electron microscopy produced images that were explained by a gp10 structure similar to the one in [Figure 2](#viruses-10-00307-f002){ref-type="fig"}d. Higher resolution, direct determination of structure is needed to test more directly for α-sheet and other structures.

2.5. Possible Pathway to Anti-Viral Therapeutics {#sec2dot5-viruses-10-00307}
------------------------------------------------

The above analysis by 2d-AGE has been performed only for phage T3. This analysis is also a relatively simple, inexpensive, sensitive way to determine whether other viruses produce size-altered capsids like those of phage T3. For now, we make the following extrapolation. Pathogenic viruses do make extensive α-sheet-containing shell intermediates, at least in the case of the capsids of viruses with a double-stranded DNA genome, such as herpes viruses.

If, indeed, this is true, then the following is a possible strategy for anti-viral therapy. Find or design therapeutic compounds that target the backbone of extensive α-sheets. The low frequency of extensive α-sheets suggests low toxicity. This strategy has the projected advantage of being insensitive to bypass via single mutations. In addition, a relatively broad spectrum of viruses is likely to be susceptible. Two major factors in reducing the success of anti-viral drug therapies are evolution of resistant viral mutants and presence of narrow drug specificity (examples \[[@B41-viruses-10-00307]\]).

3. Dynamic States and Neurodegenerative Disease {#sec3-viruses-10-00307}
===============================================

3.1. Some Details {#sec3dot1-viruses-10-00307}
-----------------

Neurodegenerative diseases are all characterized by the presence of protein aggregates collectively called amyloid. This name is derived from starch-like texture. The aggregate-forming protein varies with the neurodegenerative disease (reviews: ALS \[[@B42-viruses-10-00307]\], Alzheimer \[[@B43-viruses-10-00307]\], Huntington \[[@B44-viruses-10-00307]\], Parkinson \[[@B45-viruses-10-00307]\], prion-associated \[[@B46-viruses-10-00307]\]). When various proteins form amyloid, they convert from an original mixed-element structure to a predominantly β-sheet structure.

Although β-sheet is the predominant conformation of accumulating amyloid protein, computer simulations reveal that α-sheet is (1) accessible to amyloid-forming proteins \[[@B47-viruses-10-00307],[@B48-viruses-10-00307]\] and (2) selectively accessible to them at low pH, especially in the protein region thought to initiate the transition to amyloid \[[@B48-viruses-10-00307]\]. The proposal has been made that charge-charge interactions assist assembly to form an α-sheet intermediate that subsequently converts to β-sheet during the formation of amyloid. Molecular dynamics simulation has shown the possibility of conversion of α-sheet to β-sheet \[[@B47-viruses-10-00307],[@B48-viruses-10-00307],[@B49-viruses-10-00307]\].

Given the association of nest-like structures with membrane pores, the theory is that extensive α-sheet-containing amyloid proteins, which are minority species, generate toxicity by making pores in cell membranes \[[@B37-viruses-10-00307],[@B38-viruses-10-00307],[@B47-viruses-10-00307],[@B48-viruses-10-00307]\]. Mature amyloids are complex enough so that the amount of α-sheet associated with the β-sheet structure is, to our knowledge, not known.

Returning to the biology, the hypothesis has previously been proposed \[[@B50-viruses-10-00307]\] (and expanded \[[@B51-viruses-10-00307]\]) that one of the normal (non-toxic) functions of amyloid-forming proteins is innate immunity. This innate immunity occurs via neutralizing of products of both pathogen-generated and physical insults. By this hypothesis, neurodegenerative disease occurs when control of this insult-neutralizing activity is lost and, in some cases, the innate immune proteins start neutralizing themselves. A result is accumulation of toxic aggregates. Indeed, more recent studies have shown anti-bacterial and anti-viral effects of the amyloid for Alzheimer disease \[[@B52-viruses-10-00307],[@B53-viruses-10-00307]\].

The expanded proposal \[[@B51-viruses-10-00307]\] originally was that the neutralizing interaction occurred via the extension by innate immune proteins of β-sheet structure generated by the insult. However, the above considerations suggest substitution of α-sheet structure for β-sheet structure.

3.2. A Proposal for Reduction to Practice {#sec3dot2-viruses-10-00307}
-----------------------------------------

We propose the following working assumptions to implement the basics-focus principle for neurodegenerative diseases. (1) Pathogenic viral infection and other insults trigger activation of amyloid-forming host innate immune proteins. These proteins convert to extensive α-sheet structure and, then, co-assemble with and inactivate extensive α-sheet-rich structures generated by the insults. These activities are currently obscure; (2) Extensive α-sheets are rare to non-existent in endogenous proteins of the virus host, other than activated innate immune system proteins; (3) Neurodegenerative diseases are caused by α-sheet-dependent damage caused by hyper-produced, activated innate immune proteins. These proteins eventually form β-sheet-rich amyloid.

Other virus-induced innate immunity activities (cytokine-induced neuroinflammation, for example) are known to be associated with the onset of neurodegenerative disease \[[@B54-viruses-10-00307]\]. By the above hypothesis, these activities are secondary.

The proposal of (1)--(3) includes the fundamental idea that higher organisms have retained an immune system that has anciently derived targets and mode of action. This system is based on an abiotically derived protein structure. This system is difficult to analyze because proteins with more recently evolved composition and structure force both the innate immune system and its targets into intermittent status.

A way to reduce these ideas to practice is the following, as similarly suggested \[[@B51-viruses-10-00307]\] before the introduction of the above α-sheet proposal. (1) Select for low-pathogenicity viruses that yield unstable, α-sheet-rich complexes when innate immune system proteins co-assemble with intracellular intermediates of this virus; (2) Infect patients with these viruses. To manage adaptive immunity, several such viruses would be used in succession. To isolate the needed viruses, one could begin by trying to find cases of spontaneous (presumably limited) disease-remission that have a correlation with a previous virus infection. The correlation would presumably not be dramatic and finding it would require determination. The reason is that most infections are expected to have the opposite effect, i.e., to trigger disease \[[@B54-viruses-10-00307],[@B55-viruses-10-00307]\]. Therefore, the desired post-infection remissions are likely to be rare.

Of course, selecting for any immune system-avoiding virus has an obvious potential danger of ending with a problem of virus virulence. Presumably, virus virulence would be carefully monitored during selection. In any case, the selection would include screening for low virulence. Low virulence might, indeed, be necessarily co-selected during selection for an immune complex-disrupting phenotype.

4. Phage Assembly and Development of Gated, Targeted Drug Delivery Vehicles {#sec4-viruses-10-00307}
===========================================================================

4.1. Avoiding Immune Systems {#sec4dot1-viruses-10-00307}
----------------------------

Here, we change direction to discuss use of phage capsids as DDVs for the therapy of cancerous tumors. Administration of phage capsids is accompanied by the problem of phage capsid removal/neutralization by host immune systems. Both adaptive and innate immune systems will act to remove or neutralize foreign nanoparticles, including phages \[[@B56-viruses-10-00307]\]. Optimization of a DDV-based strategy must include a response to this problem. One response to adaptive immunity is to serially change the phage-source of the DDV, in analogy to what is proposed above for low-virulence, therapeutic, eukaryotic viruses. In addition, phages propagate rapidly enough so that directed evolution can be used to reduce removal of a phage-derived DDV by any immune system.

However, probably the most significant potential advantage of a phage capsid-DDV is gating via the connector (formed by gp8 for T3/T7; [Figure 1](#viruses-10-00307-f001){ref-type="fig"}). The connector of phages T3 and T7 also exists for all other studied double-stranded DNA phages (reviews \[[@B57-viruses-10-00307],[@B58-viruses-10-00307]\]). Thus, if connectors can, in general, be used as gates to capsid-DDVs, nature will provide many immunologically unrelated DDVs.

Before adaptive immunity becomes limiting (which takes 1--2 weeks in the case of phage K \[[@B56-viruses-10-00307]\]), innate immune systems reduce effectiveness of any unprotected nanoparticle. Apparently the most active system is the mononuclear phagocyte system (MPS), formerly called the reticuloendothelial system. The MPS moves nanoparticles primarily to the liver and spleen \[[@B59-viruses-10-00307],[@B60-viruses-10-00307]\]. Published tests of the efficiency of the MPS have been made with phages lambda, P22 and K. Phages lambda and P22 are lysogenic. When in a lysogenic state, lambda and P22 presumably could not have experienced and adapted to their environments. In contrast, phage K is lytic and had continuously experienced and adapted to its environment. Therefore, one expects that past genetic adaptation would cause phage K to have a longer lifetime in mouse circulation. This is the case. Complete removal occurs in over 24 hr for phage K \[[@B56-viruses-10-00307]\] and 3--4 h for phages lambda and P22 \[[@B61-viruses-10-00307],[@B62-viruses-10-00307]\].

That the above difference in lifetimes can be adaptive for phage lambda was shown by 10-cycles of the following: mutagenic growth, followed by mouse passage \[[@B61-viruses-10-00307]\]. The adapted lambda was removed from mouse circulation more slowly than wild type lambda. Removal was by approximately a factor of 10 per day, several orders of magnitude more slowly than before adaptation \[[@B61-viruses-10-00307]\]. A comparable removal rate was found for lytic phage T3 without any laboratory adaptation \[[@B63-viruses-10-00307]\]. Apparently, the needed adaptation had occurred for T3 in the wild. Systematic attempts to make lytic phages more long-lived in circulation have not been made to our knowledge.

4.2. Targeting Tumors {#sec4dot2-viruses-10-00307}
---------------------

Perhaps the most dramatic potential application of the basics-focus principle is to the therapy of cancerous tumors, including metastatic tumors. Focus on details (rather than basics) leads to targeting of either tumor-concentrated biochemistry or a patient's immune systems. However, the biochemistry of tumors overlaps the biochemistry of normal cells. Thus, essentially all drug and radiation therapies are toxic, which limits the extent of the therapy and makes patients sick \[[@B64-viruses-10-00307],[@B65-viruses-10-00307],[@B66-viruses-10-00307]\]. Multi-faceted toxicity of immunotherapy is emerging as a problem \[[@B67-viruses-10-00307]\]. In addition, when a cancer becomes metastatic, none of the above therapies can systematically block bypass of the therapy via evolution of cancer cells.

However, tumors do have one targetable, basic characteristic that they apparently cannot evolve to eliminate. This characteristic is the presence of 10--200 nm-sized pores in the blood vessels that feed tumors. Healthy blood vessels do not have these pores \[[@B68-viruses-10-00307],[@B69-viruses-10-00307]\].

Thus, one should be able to achieve specific drug delivery to tumors with the following strategy: use of a DDV small enough to fit in these pores, but too large to pass through healthy blood vessels. In addition, tumors have relatively poor lymphatic drainage. Thus, when a DDV enters a tumor, it is slow to leave. The combined effect of the pores and the poor drainage is called the enhanced permeability and retention (EPR) effect \[[@B68-viruses-10-00307],[@B69-viruses-10-00307]\].

Knowledge of the EPR effect is not new. The EPR effect has been the foundation for improved drug delivery via liposomal DDVs. Several products are FDA approved \[[@B70-viruses-10-00307]\], the earliest being Doxil \[[@B71-viruses-10-00307]\]. However, results have been disappointing. A recent review indicates the following limitations \[[@B72-viruses-10-00307]\]: (1) "rapid loss of the drug cargo ... often immediately after ... systemic administration"; (2) "in many cases, less than 1% of the administered nanoparticle dose reaches the malignant tissue"; (3) "lack of release of drug in tumors"; (4) safety of the DDV; (5) safety of impurities (bacterial endotoxin which can generate a cytokine storm); (6) immunotoxicity (complement-generated, for example) and (7) standardization during manufacturing scale-up. A major uncertainty is the extent of the EPR effect in early metastases.

In evaluating the use of a phage capsid-DDV, we initially note that phages have never been found to be toxic to humans. Phages T3 and T7 were presumably isolated from sewage \[[@B73-viruses-10-00307]\] and have passed through humans many times with the associated likelihood that they and their capsids already have evolved to avoid human immune systems. Furthermore, phage capsids with DDV potential are assembled in vivo and easily purified with structure uniform enough to obtain a 3--4 Å cryo-EM structure of the shell in the case of T7 \[[@B25-viruses-10-00307]\]. If gated, a phage capsid is well on its way to removing the above limitations.

Indeed, one form of T3 capsid II is sufficiently gated so that it does not allow Nycodenz (molecular weight = 821) in its internal cavity until the temperature is raised. That is to say, the elevated temperature opens a gate. The gate is closed by lowering temperature, with the loaded Nycodenz not leaking detectably. The connector is the likely location of the gate \[[@B74-viruses-10-00307]\].

4.3. Adequate Loading of a Phage Capsid-DDV {#sec4dot3-viruses-10-00307}
-------------------------------------------

Nonetheless, a major barrier still exists to implementation of a gated T3 phage capsid-DDV. When we used elevated temperature to increase permeability (open the gate) in the presence of 10 mg/mL doxorubicin, the T3 gp10 shell was damaged. Native gel electrophoresis suggested disassembly to small aggregates, possibly monomers of gp10 (unpublished data). This limitation was possibly caused by detergent characteristics of doxorubicin, which has a positively charged and a hydrophobic region. These two regions are also present in most anti-cancer drugs.

Although this limitation has not yet been bypassed, we have found that the T7 counterpart of the loadable T3 capsid II is much more stable (80--83 °C). Future work will focus on the T7 version of this capsid II.

5. Prospects for the Future {#sec5-viruses-10-00307}
===========================

Hypothesis-derived theory and practice can differ, possibly because of variables not in the theory. Also, hypotheses can be incorrect. The above proposals for treating neurodegenerative disease and cancerous tumors are not exempt from this pattern. Nonetheless, when basic considerations point in a simple direction, attempts to go in that direction should, it seems to us, be made. However, in the absence of a change in priorities, the probability is very close to zero that the above strategies will be tested experimentally within the next few years.

As support for this pessimism, exhibit A is the current status of phage therapy of infectious disease. For phage therapy, the basics point in a clear direction (details \[[@B17-viruses-10-00307]\]). In addition, going in this direction is supported by (1) historical \[[@B6-viruses-10-00307],[@B7-viruses-10-00307],[@B73-viruses-10-00307]\] and present-day \[[@B16-viruses-10-00307]\] examples of dramatic success of doing that and (2) recent development of technologies that should dramatically improve results, if deployed. These include technologies of computerized database use/phage storage/phage retrieval, in addition to updated procedures of phage isolation and characterization. Yet, few, if any, systematic attempts at implementation are being made. Phage therapy is performed on an ad hoc basis \[[@B16-viruses-10-00307],[@B75-viruses-10-00307]\], which slows implementation, sometimes to the point that it is too late.

6. Relationship to Scientific Details {#sec6-viruses-10-00307}
=====================================

In [Section 1.1](#sec1dot1-viruses-10-00307){ref-type="sec"}, we gave examples of scientific output triggered by de facto past clinically oriented use of the basics-focus principle. The finding of a curative, low-virulence virus, as proposed above, should do the same in the case of neurodegenerative diseases. Existence of such a virus would likely trigger experiments that use the virus to determine the interaction of virus metabolism and assembly with cellular events. Cellular events would be better understood. One finding might be that the above assumptions need to be modified or abandoned. However, the overall direction embodied in the assumptions could still be accurate enough to obtain a cure.

A gated, uniform-size, uniform-structure DDV can also be used to track the progression of tumors via the loading of the DDV with a trackable compound. Nycodenz, for example, is x-ray opaque and can be tracked by use of micro-CT. Such tracking would be used both clinically and also to analyze pathways of receptor mediated endocytosis and lysosome targeting of endocytic vesicles.

In other words, the division between basic science and clinical practice is not sharp.

We thank Martin Adamo and Richard Ludueña for comments on drafts of this manuscript. This work was supported by the Welch Foundation (AQ-764) and the San Antonio Area Foundation.

P.S. wrote the manuscript, designed the experiment for [Figure 3](#viruses-10-00307-f003){ref-type="fig"} and performed the electron microscopy; E.T.W. contributed procedural suggestions, performed the 2d-AGE and prepared specimens for electron microscopy.

The authors declare no conflict of interest. The founding sponsors had no role in the design of the study; in the collection, analyses, or interpretation of data; in the writing of the manuscript, and in the decision to publish the results.

![The progression of capsids during the in vivo assembly of phages T3 and T7. (**a**) capsid I; (**b**) capsid II packaging DNA; (**c**) head; (**d**) mature phage.](viruses-10-00307-g001){#viruses-10-00307-f001}

![A line drawing of the proposed α-sheet-generating polypeptide backbone of the gp10 subunits of (**a**) hyper-expanded T3/T7 capsid II; (**b**) an intermediate converting from its state in hyper-expanded to its state in contracted capsid II and (**c**) contracted capsid II. N and C indicate the N- and C-terminals of gp10; (**d**) Assembly of two gp10 subunits is shown with the proposed radial staggering. The staggering improves electrical charge-charge-derived energetics. The + symbols indicate the + electrical charge of the α-amino edge; the − symbols indicate the − electrical charge of the α-carboxyl edge.](viruses-10-00307-g002){#viruses-10-00307-f002}

![Analysis by 2d-AGE of hyper-expanded T3 ipDNA-capsid II. The ipDNA-capsid II is from the Nycodenz gradient-isolation in [Figure 4](#viruses-10-00307-f004){ref-type="fig"}b of reference \[[@B35-viruses-10-00307]\]. Two fractions of the Nycodenz density gradient were analyzed by 2d-AGE, the (**a**) 1.073 g/mL and (**b**) 1.099 g/mL fractions. The procedure of 2d-AGE is described in reference \[[@B26-viruses-10-00307]\]. The first dimension was run in a 0.30% agarose gel at 2.0 V/cm for 5.0 h. The second dimension was run in a surrounding 2.0% agarose gel at 1.8 V/cm V/cm for 16.0 h. The electrophoresis buffer was 0.09 M Tris-acetate, pH 8.3, 0.001 M MgCl~2~. The temperature was 25 ± 0.3 °C. Seakem LE agarose was used (Lonza, Basel, Switzerland). The arrowheads indicate the leading edges of sample wells. The arrows indicate the directions of the first (I) and second (II) dimension electrophoresis. The curved dashed lines indicate the profile of variable length DNAs (no protein attached) from the DNA fraction of the same Nycodenz gradient. The DNA profile was obtained in a separate quadrant embedded in the same agarose frame as the gels of (**a**,**b**).](viruses-10-00307-g003){#viruses-10-00307-f003}

![Electron microscopy of hyper-expanded NLD capsid II. The sample was the same as the sample used for [Figure 2](#viruses-10-00307-f002){ref-type="fig"}a. Particles in the sample were negatively stained with 1% uranyl acetate. The procedures of specimen preparation and EM were the same as used in reference \[[@B35-viruses-10-00307]\].](viruses-10-00307-g004){#viruses-10-00307-f004}


It’s all so painfully familiar: with a crunch date of February 3, the Democratic Party in Iowa decided to charge ahead with an IT rollout that comprised an entirely new software system spread out across thousands of sites to record the result of the Democratic caucus for its presidential nominee.

It was, inevitably, a complete failure. The results from the Iowa caucus were supposed to come in nearly 24 hours ago. Instead, it has become a rolling news cycle of tech catastrophe.

We’re not even going to bother to dig into lessons learned because they are the same ones that every sysadmin since the dawn of time has dealt with – and spends their entire career warning the suits about, to greater and lesser degrees of success.

Let’s start with the app. It was produced by a bunch of IT hotshots who have advised previous Democratic campaigns, including those used by Obama and Hillary Clinton, and set up a for-profit company called, for some reason, “Shadow.” The biz won the contract to create an app that would do a simple task: allow people on the ground to type in the result of headcounts in town halls and gymnasiums across Iowa and send them to a central processing point.

All people had to do was download the app, punch in a security code – only one per precinct, of which there are 1,765 – tap in the results and hit send. What could go wrong?

Lots, as it turns out. For one, the app was only launched several weeks ago so nobody that had to use it was familiar with it. That was fine for the occasional 20-something that acted as a caucus chair and who is perfectly comfortable with downloading and trying out new smartphone apps; navigating a new user-interface is just part of life.

But the majority of caucus managers are retired, some in their 70s and 80s, many of whom have done the same job every four years. They needed a smartphone app like they needed a hole in the head.

Sticking PINs in your eyes

But it was fine: Democratic headquarters sent instructions via email about how to use the new software.

So all they had to do was find a smartphone, find the download instructions, download it, figure out how to log in, navigate a new interface, and figure out how to input the right numbers in the right boxes. And read the email instructions. Which include the fact that the test PIN they had been sent to try it out wouldn’t work on the day of voting. For security reasons, they’d get a new one. No one was given any training. And no one was on hand to set it up or answer questions.

One chair from Poweshiek County, John Grennan, told the New York Times that seven of the 10 people running precincts in his area never downloaded the app. But those that did had trouble with the changing security PIN and couldn’t get into it. “A lot of people were like, ‘I’m getting a virus on my phone’ and just quit it,” he told the paper.

Amazingly this last-minute rollout may have been intentional rather than the result of poor project management. Democratic Party heads appeared to believe that providing no information about the app and providing it a week or so before the actual vote was a good security measure. That sound you hear? That’s every IT manager across the world banging their heads on their desk.

The app had only been tested in controlled environments; there was no state-wide testing. No one visited the more rural parts of Iowa where data speeds made the entire download, authentication, data input and sending process an exercise in frustration. There was, seemingly, no independent security review either.

It was also claimed the app's development team was relatively new and inexperienced.

Entirely inevitably, a lot of local managers decided to reject the whole thing. One precinct chair, Deb Copeland, told the Des Moines Register that she “didn’t even bother” to download it. They had phoned in their results for decades and would do the same again in 2020. Others tried. And immediately hit problems: they “couldn’t get the app to download” and “couldn’t get it to work.”

FAQ-you

The brilliant minds at Shadow – who were paid $60,000 to produce the app and have picked up another $60,000 for a different version for Nevada – probably figured people would access its FAQ and Help pages. Had they actually existed, which they didn’t.

But they wouldn’t have anyway. As Deb Copeland noted: “We had an informal Facebook group and people were saying they couldn’t get it to do anything and had so many questions.” So no training, inadequate support, a rushed rollout and a complete inability to think through the obvious resistance to new technology from those required to use the app. Anything else? Oh yes, plenty.

The Iowan Democratic Party – which contracted with Shadow and, somewhat amazingly, defended the app rollout two weeks ago to skeptical journalists – was keen to point out that the app had not been hacked or compromised. Great! Except reports coming in suggest that it simply didn’t work properly.

The data input appears to have worked correctly (although some managers complained that they couldn’t get it to do the maths) but it appears as though it was only partially outputting the results, causing massive tabulation errors. Oh, and the app crashed for lots of people, requiring them to shut it down and log back in again.

It actually gets worse than that: for the first time, the caucuses were reporting three sets of numbers rather than one. That’s thanks to the extremely tight results in 2016 when Hillary Clinton very narrowly beat out Bernie Sanders, Sanders’ team successfully argued that there needed to be results recorded throughout the somewhat convoluted multi-stage voting process that Iowa uses, rather than just the end result.

So all the volunteers were not only required to do their job differently to before – providing three sets of figures instead of one – but they were also expected to do so through an entirely new system that hadn’t been properly bug-tested.

Very hot hotline

And so with the whole system falling over, everyone responsible for reporting their results did the obvious thing and called the election hotline. And guess what? It was overwhelmed by everyone having problems, leaving them on hold for hours.

You can easily secure America's e-voting systems tomorrow. Use paper – Bruce Schneier READ MORE

Another caucus manager said it took her four hours just to get someone on the phone to take the results after she abandoned the app thanks to repeat crashes. Another manager said he managed to successfully send the results but didn’t get a confirmation and so was unsure whether it had really been sent; a fear that only grew as more and more people reported problems.

We could write pages and pages of reports about how differently people experienced this almighty IT cock-up but what’s the point? If you’re reading The Reg you already know what the problem is and the details quickly become irrelevant.

Here’s what’s happened: the suits hired a company because they were swayed by their CVs and sales talk and didn’t run it past anyone that knew what they were doing. Then the suits didn’t listen to all the people telling them it was a bad idea and they should delay rollout. And they didn’t allow sufficient time for testing and training.

In light of the debacle Shadow has apologized for the code cock-up, albeit rather grudgingly. It maintains that the app was "sound and accurate," but says problems occurred in data transmission.

Meanwhile, Nevada has cancelled its contract with Shadow and is presumably asking for its money back. ®


Esteve perto de ser o tricampeonato para Portugal, mas o Brasil ganhou a final do Mundial de futebol de sub-20, vencendo por 3-2, após prolongamento.

É o quinto título dos brasileiros na categoria, conquistado numa final intensa, de resultado incerto até ao fim e em que a selecção portuguesa só caiu na segunda parte do prolongamento.

A equipa de Ilídio Vale deixa a Colômbia como vice-campeã mundial, a segunda melhor posição da sua história, só batida pelos títulos de 1989 e 1991.

A final era o confronto entre a melhor defesa e o melhor ataque. E começou por cair para o lado brasileiro. Portugal, que ainda não tinha sofrido qualquer golo neste Mundial, não resistiu sequer cinco minutos ao Brasil: Óscar apontou um livre do lado direito e a bola entrou na baliza portuguesa, com Sérgio Oliveira a ser o último a tocar na bola – a FIFA atribuiu o golo a Óscar.

A selecção portuguesa, no entanto, reagiu muito bem à primeira situação de desvantagem neste Mundial. Quatro minutos depois, Nélson Oliveira assistiu Alex, que repôs a igualdade (9’).

O empate permitiu a Portugal não se desviar da estratégia inicial, assente num bloco compacto a defender.

O Brasil voltou a assustar logo a seguir, com a bola a bater na trave, num lance em que Mika evitou o golo “in extremis”, ficando até a dúvida sobre a se a bola entrou ou não na baliza.

Com a defesa portuguesa a dar cada vez menos espaço ao ataque adversário, o Brasil começou a tentar remates de longe, como fez William (20’, para boa defesa de Mika) e Juan Jesus (43’).

Pelo meio, Portugal conseguiu finalmente estender-se no campo e forçou o Brasil a recuar, criando um par de boas oportunidades, sempre com Nélson Oliveira como protagonista.

O avançado do Benfica rematou duas vezes por cima (35’ e 39’) e noutra ocasião foi desarmado quando se preparava para marcar (36’).

Ao intervalo, o Brasil fez duas substituições, apostando mais no ataque, com Danilo (contratado pelo FC Porto ao Santos) a passar de lateral-direito para o meio-campo.

Portugal cedeu a iniciativa de jogo e no contra-ataque chegou à vantagem. Nélson Oliveira foi novamente o protagonista: o avançado correu um quarto de campo sozinho contra os defesas brasileiros e, já com pouco ângulo, rematou, com o guarda-redes brasileiro a não segurar a bola.

Em vantagem, e mesmo com um lateral-direito adaptado (Cédric saiu lesionado e Pelé teve de fazer o lugar), Portugal conseguiu durante longos minutos “secar” o ataque brasileiro e até poderia ter ampliado a vantagem no contra-ataque, com o guarda-redes brasileiro a evitar o golo de Nélson Oliveira (73’).

E quando Portugal já contava os minutos para o final, o Brasil repôs o empate, com Óscar a marcar na recarga, após cruzamento de Dudu defendido por Mika para a frente (78’).

Foi, assim, necessário recorrer ao prolongamento, em que a selecção portuguesa até dispôs da primeira grande oportunidade. Só que Caetano, isolado perante Gabriel, tentou o chapéu e permitiu a defesa ao guarda-redes (97’).

Já o Brasil teve mais capacidade física e também mais sorte. Aos 111’, Óscar queria fazer um cruzamento e a bola entrou directamente na baliza, passando por cima de Mika.

Portugal acabou mesmo o jogo reduzido a dez elementos, porque Danilo saiu lesionado a cinco minutos do fim, quando já estavam esgotadas as substituições. E o Brasil até podia ter feito o 4-2, não fosse Mika defender o remate de Henrique (118’). Mas já não foi preciso mais nada para os brasileiros vencerem, ao contrário do que aconteceu em Lisboa há 20 anos.

Decisivo nos golos de Portugal. Assistiu no primeiro e marcou o segundo. É o mais talentoso desta selecção e terminou Mundial como melhor marcador da equipa, com quatro golos.

Joga como médio-defensivo e é o pêndulo da selecção. Muito forte fisicamente, sabe também passar a bola. Mário Rui e Alex também se destacaram.

Foi a referência da defesa de Portugal no Mundial e na final não fugiu à regra, com sobriedade e excelente sentido de colocação.

Esteve nos três golos do Brasil e isso diz tudo. Dudu também foi importante para a “canarinha” obrigar ao prolongamento.

Não entrou bem em jogo e falhou a melhor oportunidade portuguesa no prolongamento.

Brasil 3Portugal 2

Jogo no Estádio Nemésio Camacho “El Campín”, em Bogotá (Colômbia).

Gabriel; Danilo, Bruno Uvini, Juan Jesus, Gabriel Silva (Allan, 46’); Fernando, Casemiro, Willian (Negueba, 46’), Óscar; Coutinho (Dudu, 62’), Henrique. Treinador: Ney Franco.

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Mika; Cédric (Júlio Alves, 57’), Nuno Reis, Roderick, Mário Rui; Danilo, Pelé, Saná (Dias, 100’); Sérgio Oliveira, Alex (Caetano, 82’), Nélson Oliveira. Treinador: Ilídio Vale

Árbitro: Mark Geiger (EUA).Amarelos: Roderick (28’), Pelé (36’), Sérgio Oliveira (38’), Henrique (45+1’), Juan Jesus (75’), Júlio Alves (85’), Saná (88’), Nélson Oliveira (98’),

1-0, por Sérgio Oliveira (p.b.), aos 5’

1-1, por Alex, aos 9’

1-2, por Nelson Oliveira, aos 59’

2-2, por Óscar, aos 78’

3-2, por Óscar, aos 111’


Q:

Unable to click button on Mobile App in android

I am new of mobile app automation tested using Appium with TestNG.Am practicing to automate amazon app, App was launching successfully but when I try to click login option, it's getting:

"FAILED: login org.openqa.selenium.NoSuchElementException: An
  element could not be located on the page using the given search
  parameters. (WARNING: The server did not provide any stacktrace
  information) Command duration or timeout: 0 milliseconds"

    public void login() throws InterruptedException{

        System.out.println("Login check");
        Thread.sleep(3000);
//      String sample = driver.findElementByXPath("//*[@class='android.widget.Button' and @index='5']").getText();
        System.out.println("Next sleep");

//      driver.findElement(By.xpath("//[@class='android.widget.Button' and @index='5']')]")).click();
//      driver.findElement(By.id("in.amazon.mShop.android.shopping:id/sign_in_button")).click();
        driver.findElement(By.xpath("//android.widget.Button[@index='5']")).click();
        Thread.sleep(3000);
        System.out.println("Pass");

    }

Image:

A:

"//android.widget.Button[@index='5']" is invalid xpath locator. If you will ever what to use index (but I strongly suggest not to do it), do it this way:
"(//android.widget.Button)[5]"
But in your case the best is to search by resource-id:
driver.findElement(By.id("sign_in_button")).click();

And if it still doesn't work you can print app screen xml structure just before you search for element:
System.out.println(driver.getPageSource())
Analyse the xml you get if it contains your button and what are the attributes of it.


GM Joins With Sandia To Advance Hydrogen Storage

Date:

January 11, 2005

Source:

Sandia National Laboratories

Summary:

General Motors Corp. and Sandia National Laboratories have launched a partnership to design and test an advanced method for storing hydrogen based on metal hydrides. Metal hydrides — formed when metal alloys are combined with hydrogen — can absorb and store hydrogen within their structures.

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FULL STORY

A critical aspect of hydride storage tank development is the act of recharging and discharging hydrogen. Here, Sandia National Laboratories engineer Mark Zimmerman integrates a hydride bed with temperature monitoring sensors.

Credit: Photo by Bud Pelletier

A critical aspect of hydride storage tank development is the act of recharging and discharging hydrogen. Here, Sandia National Laboratories engineer Mark Zimmerman integrates a hydride bed with temperature monitoring sensors.

Credit: Photo by Bud Pelletier

DETROIT, Mich., and LIVERMORE, Calif. — General Motors Corp. and Sandia National Laboratories have launched a partnership to design and test an advanced method for storing hydrogen based on metal hydrides.

Metal hydrides — formed when metal alloys are combined with hydrogen — can absorb and store hydrogen within their structures. When subjected to heat, the hydrides release their hydrogen. In a fuel cell system, the hydrogen can then be combined with oxygen to produce electricity.

GM and Sandia, a National Nuclear Security Administration lab, have embarked on a 4-year, $10 million program to develop and test tanks that store hydrogen in a complex hydride, sodium aluminum hydride — or sodium alanate for short. The goal is to develop a pre-prototype solid-state hydrogen storage tank that would store more hydrogen onboard a fuel cell vehicle than current conventional hydrogen storage methods. Researchers also hope to create a tank design that could be adaptable to any type of solid-state hydrogen storage.

“Hydrides have shown significant early promise to one day increase the range of fuel cell vehicles,” says Jim Spearot, director, GM Advanced Hydrogen Storage Program. “We know a lot of research still needs to be done, both on the types of hydrides we use, as well as the tanks we store them in. We think our work on projects like this with Sandia will get us another step closer to our goal.”

GM and Sandia say the program is part of a concerted effort to find a way to store enough hydrogen onboard a fuel cell vehicle to equal the driving range obtained from a tank of gas, which will be key to customer acceptance of fuel cell vehicles.

The current leading methods of storage are liquid and compressed gas. However, to date, neither of these technologies has been able to provide the needed range and running time for fuel cell vehicles.

“We are designing a hydrogen storage system with challenging thermal management requirements and limits on volume and weight,” says Chris Moen, manager of science and engineering technologies at Sandia. “Our staff researchers are excited to apply their unique, science-based design and analysis capabilities to engineer a viable solution.”

“This is the kind of public private research partnership that will help us realize the President’s vision, communicated in his 2003 State of the Union Address, that ‘the first car driven by a child born today can be powered by hydrogen, and pollution-free,’” said DOE Secretary Spencer Abraham. “Over the long term, because of the President’s visionary leadership, clean, efficient hydrogen fuel technologies like this will help make our nation far less reliant on foreign sources of energy.”

In 2003, President Bush announced the Hydrogen Fuel Initiative with $1.2 billion over five years (FY 2004-FY 2008) to accelerate hydrogen research. Sandia’s research activities in hydrogen storage support the President’s long term vision for commercially viable hydrogen-powered vehicles to reverse America’s growing dependence on foreign oil.

The GM-Sandia project, privately funded and separate from the President’s initiative, will be conducted in two phases. In Phase One, the program will study engineering designs for a sodium alanate storage tank. Researchers will analyze these designs using thermal and mechanical modeling, develop controls systems for hydrogen transfer and storage, and develop designs for external heat management. GM and Sandia scientists will also be testing various shapes — from cylindrical to semi-conformable — to see which are the most promising.

A possible scenario for filling up with a solid-state storage solution such as sodium alanate could look like this: The alanate would come preloaded in the tank, where it would remain, giving up its hydrogen, and becoming a mixture of sodium hydride and aluminum. The customer would fill up using gaseous hydrogen. During filling, the mixture of aluminum and sodium hydride would absorb the hydrogen and turn it back into alanate, which would be ready to yield hydrogen when needed by the fuel cell. Once the tank is filled, the hydrogen would be stored at low pressure.

While it has shown good potential, hydride-based hydrogen storage also has some hurdles to clear. One current drawback is that most complex metal hydrides, such as sodium alanate, still operate at too high a temperature, which causes an inefficiency that forces some of the hydrogen to be used up in order to release the remaining hydrogen. Another challenge is reducing the time it takes to reabsorb hydrogen. It currently takes at least 30 minutes to recharge.

In separate, independent projects outside of this collaboration, both GM and Sandia are working to identify alloys that will store greater amounts of hydrogen that can be released at lower temperatures. Reducing filling and recharging times is another key area of research.

The research conducted through the GM-Sandia partnership is independent from that of Sandia’s participation in the Metal Hydride Center of Excellence. The Center of Excellence, to be funded in Fiscal Year 2005 through a U.S. Department of Energy “Grand Challenge,” aims to develop a new class of materials capable of storing hydrogen safely and economically.

###

General Motors Corp. (NYSE: GM), the world’s largest vehicle manufacturer, employs about 325,000 people globally. Founded in 1908, GM has been the global automotive sales leader since 1931. GM today has manufacturing operations in 32 countries and its vehicles are sold in 192 countries. In 2003, GM sold nearly 8.6 million cars and trucks, about 15 percent of the global vehicle market. GM’s global headquarters are at the GM Renaissance Center in Detroit. More information on GM and its products can be found on the company’s corporate website at http://www.gm.com.

Sandia is a multiprogram laboratory operated by Sandia Corporation, a Lockheed Martin company, for the U.S. Department of Energy’s National Nuclear Security Administration. Sandia has major R&D responsibilities in national security, energy and environmental technologies, and economic competitiveness.

Aug. 1, 2015  After debuting the world's first solar air battery last fall, researchers have now reached a new milestone. They report that their patent-pending design -- which combines a ... read more

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If William Shakespeare had ever dared to explore the animal kingdom, he might have come up with “BoJack Horseman.” Even in a long line of TV narcissists — Archie Bunker, Frasier Crane, Barbara Walters — BoJack stood out, insisting he was still riding high in the saddle when he was really just an ex-sitcom star with serious addiction problems, threatening anyone in his orbit.

So, to be or not to be? That is the question creator Raphael Bob-Waksberg should be answering in the animated show’s final eight episodes, which dropped this past Friday on Netflix.

Viewers have plenty of reasons to root for the title character, despite his self-centered nature, sexist impulses and habit of always wearing the same sweater. As we’ve learned over the course of six seasons, he suffered a traumatic childhood. He has financially supported man-child Todd Chavez, the most annoying roommate since Felix Unger, and Diane Nguyen, a freelancer suffering from a lifetime of writer’s block. At times, he’s tried to better himself. In this last batch of stories, a newly sober BoJack has taken a job as a drama professor, if only to mend fences with his estranged sister. Just hearing the voice of the golden-throated Will Arnett makes you want to smile — and go out and buy a new car.

But for every hoof up, there’s two hooves back.

In Season 2, BoJack’s journey of self-discovery took a horrid detour when he crossed the line with an ex-girlfriend’s underage daughter. Much of Season 5 dealt with BoJack learning firsthand what it’s like to be sexually objectified. But the lesson didn’t stick. During a psychotic break, he nearly chokes his girlfriend to death.

And our “hero” only checked himself into rehab to escape the enormous guilt he felt from talking his former co-star Sarah Lynn into a drug binge with fatal results.

As BoJack gallops toward the finish line, it’s Bob-Waksberg’s job to decide if his protagonist is headed for redemption or ruin.

He doesn’t fulfill his duty.

Those who haven’t binged to the end of the series may want to stop reading now. (Are they gone? Good, let’s move forward.)

At one point, the show appears to have determined the character’s fate. During a relapse, BoJack breaks into his former house and proceeds to do an impersonation of William Holden’s corpse in “Sunset Boulevard.” In the penultimate episode, BoJack finds himself at a dinner party surrounded by deceased friends and family (and Zach Braff as a butler) followed by a surreal variety show that’s more painful to watch than the “Star Wars Holiday Special.” It’s a disturbing, shocking journey — and instantly ranks among the most brilliant episodes in the show’s history.

But Bob-Waksberg can’t quite commit to the darkness. In the very next installment, BoJack is still with us, at least enough to direct a production of “Hedda Gabler” behind prison bars.

In the final scene, the temporarily released horse finds himself lying on a rooftop with Diane, who is also still stuck at the crossroads.

“Life’s a bitch,” Diane says. “And then you keep living.”

OK — but just what kind of life are these two crazy kids going to lead?

Bob-Waksberg could be trying to emulate the ambiguous ending of “The Sopranos.” Maybe Netflix balked at the idea of banishing one of its most popular characters to hell. Either way, fans of the most brilliant animated series of the decade deserved a better ending — even if it meant putting BoJack out of his misery.

Neal Justin covers the entertainment world, primarily TV and radio. He also reviews stand-up comedy. Justin is the founder of JCamp, a non-profit program for high-school journalists, and works on many fronts to further diversity in newsrooms.


The Hamas-linked Council on American-Islamic Relations (CAIR) wants and needs hate crimes against Muslims, because they’re the currency they use to buy power and influence in our victimhood-oriented society, and to deflect attention away from jihad terror and onto Muslims as putative victims. Hamas-linked CAIR, designated a terror organization by the United Arab Emirates, and other Muslims have on many occasions not hesitated to stoop even to fabricating “hate crimes,” including attacks on mosques. Most notably, in February, a New Jersey Muslim was found guilty of murder that he tried to portray as an “Islamophobic” attack, and in 2014 in California, a Muslim was found guilty of killing his wife, after first blaming her murder on “Islamophobia.”

“Woman arraigned in false report of attack on Fordson,” by George Hunter, The Detroit News, February 19, 2016 (thanks to Steve):

A woman has been charged with making a false police report after she allegedly fabricated a plot to blow up Dearborn Fordson High School to retaliate against the November terrorist attacks in Paris.

Saida Chatti was arraigned Thursday in Dearborn’s 18th District Court on charges of false report or threat of a bomb/harmful device, a felony punishable by more than five years in prison. Bond was set at $2,500.

Police say Chatti called Dearborn investigators Nov. 19, six days after Islamic extremists killed 130 people in Paris. Suicide bombers and gunmen struck a sports stadium during a soccer match, a theater during a rock concert, cafes and restaurants.

The Islamic State claimed responsibility.

Chatti “contacted the Dearborn Police Department to report that an ‘anonymous’ friend had overheard a group of individuals at Twelve Oaks Mall in Novi threatening to bomb Fordson High School in retaliation for the attacks in Paris,” according to a Dearborn police press release.

Fordson has a predominantly Arab-American student body.

“We get a number of threats against Dearborn, mostly from people on Twitter and Facebook, especially after high-profile events like Paris, because of our Muslim population,” Lt. Ron Beggs of the Dearborn police investigative division told The Detroit News on Friday. “So we take these very seriously.

“We expended a lot of resources to investigate this woman’s claim. It became apparent there were holes in her story. When we presented her with the evidence, she admitted it was a false report.”…


Q:

Node.js body-parser won't parse input names with square brackets in json

I have a problem with Express body-parser in Node.js
I have inputs like this:
<input id="personEmail1" type="email" name="person[0][email]" placeholder="Email1" class="form-control">
<input id="personEmail2" type="email" name="person[1][email]" placeholder="Email2" class="form-control">

After when I submit my form I got this in my console.log:
{ 'person[0][email]': 'info@sss.sss', 'person[1][email]': 'info@ggg.ggg' }

But I want it to be parsed in json format:
{ person: [{email: 'info@sss.sss'}, {email: 'info@ggg.ggg'}] }

What I'm doing wrong?

A:

for express version 4.x when you need to manually install body-parser and multer, and you want to get nested properties from the post, e.g. data[test] in the form of req.body.data.test, you need to set:
app.use(bodyParser.urlencoded({ extended: true }));


Cow Face: October Yoga Pose of the Month

Stretches the hips, ankles and shoulders while opening chest and lengthening spine.

Cow Face Pose (Sanskrit: Gomukhasana)

1. Bend your knees with feet on floor. Slide right foot under the left knee to the outside of the left hip. Then cross your left leg over the right, stacking the left knee on top of the right and bring the left foot to the outside of the right hip. Try to bring the heels by hips evenly. Sit evenly on the sitting bones. You may sit on a block to elevate hips. If this isn’t available to you, simply sit in an easy seated pose.
2. Inhale and stretch your left arm straight out to the left, parallel to the floor. Flip thumb down towards floor. This movement will roll your left shoulder slightly up and forward. With a full exhalation, sweep the arm behind your torso and tuck the forearm in the hollow of your lower back, parallel to your waist, with the left elbow against the left side of your torso. Roll the shoulder back and down, then work the forearm up your back until it is parallel to your spine. The back of your hand will be between your shoulder blades. Ensure that your left elbow doesn't slip away from torso.
3. Inhale and lengthen right arm in front of you parallel to the floor. Turn the palm up on the exhale. With another inhalation, stretch the arm straight up toward the ceiling, palm turned back. Lift actively through your right arm. With an exhalation, bend the elbow and reach down for the left hand. If possible, hook the right and left fingers. This is where the strap comes in handy.
4. Lift the right elbow toward the ceiling with left elbow toward the floor. Firm your shoulder blades against your back ribs and lift your chest. Try to keep the right arm beside the right side of your head.
5. Stay in pose ~5-10 breaths. Release arms, uncross legs and repeat with the arms and legs reversed for the same length of time. Remember that whichever leg is on top, the same-side arm is lower.

Note: In addition to utilizing a strap, you may sit on a yoga block or elevate your hips to assist you with the lower body portion of this pose.

Contraindications: If you have any shoulder issues or knee concerns, please do not perform that half of the pose. As with all yoga and exercise, seek guidance from a medical provider to ensure you are ready to partake.

About Author

Celeste has been in the science, health and wellness field over twenty years. As a chemist, she conducted research which brought her into the mindset of proactive wellness and prevention. After receiving her Masters in Health Education from East Carolina University, she ventured into the mind/body world receiving training in Mindfulness-Based Stress Reduction and Yoga. Shortly after, she received the 2003 Wellness in the Workplace Award for a large health system in the state of Virginia. In 2004, Celeste joined SAS Institute, Inc. and continues to be passionate in her position as Wellness Supervisor. She loves working with her team members, teaching yoga and meditation, presenting seminars and nurturing healthy lifestyle changes to the SAS community. Celeste is a published author, the wife of a fun-loving husband, mother of a high school daughter, yogini and professional front porch meditator. She is a nationally Master Certified Health Education Specialist (MCHES), an Experienced Registered Yoga Teacher (E-RYT) with the National Yoga Alliance, Mindfulness-Based Stress Reduction (MBSR) Instructor, Certified Wellness and Health Coach (CWHC), Certified Yin-Yang Yoga and Mindfulness Meditation Instructor and Certified Yoga Therapist (CYT). Follow @ccooperpeel on Twitter and Instagram.


Chicken Tzedakah

Kä-pä-r the Hebrew word root of Kippur, as in Yom Kippur, translates to cover or to ignore. Through the narrowly practiced Kaparot with live chickens, bought for around $20 to $30 apiece, waved over one’s head to transfer one’s sins to the animal. The chickens, or their value must be donated to the poor. In addition to prayer and repentance, hundreds of people and their families gave Tzedakah in this manner to avert the most awful judgments that Yom Kippur could bring. Despite verbal and written assurances these people received, their Tzedakah, or philanthropic justice, never reached the promised poor. Hundreds of chickens went directly into the garbage and landfill rather than to the needy.

Judaism’s Sages recognized that it is harder to disburse charitable funds than it is to raise those funds. Therefore the Talmud prescribes that at least two people must be present when collecting food or money for the communal fund. Three people are needed to distribute it to the poor. In the case of this year’s chicken Tzedakah there were many people collecting the price of the chickens and kosher killing them, but literally no one to distribute them to the poor or needy. The killed chickens went directly to the Department of Sanitation garbage truck at all the sites I observed in the Pico-Robertson area.

No chicken feathers were plucked, no butchering, no refrigeration or any preparation of the chicken Tzedakah for human or animal consumption was observed. The typical chicken Tzedakah ruse had people paying for their chicken Tzedakah, usually receiving a receipt for their donation at a table set up outside a temporary structure in a parking lot, later repurposed as a Sukkah. The temporary structure was partitioned so that the person completed a Kaparah prayer with a 5 to 7 lb. live chicken Tzedakah, handed it over to one or more kosher slaughterers who immediately slit the chicken Tzedakah’s neck and tossed the still reflexively moving chicken Tzedakah into a large 55 gallon barrel covered with a lid with a chute to prevent many of the still moving chickens from inadvertently getting out. After filling the 55 gal. garbage bag lined drum with about 10 chicken Tzedakahs one of the slaughterers removed the usually opaque black plastic bag, tied the top, then took and tossed it onto a growing, several foot high, pile of similar bags on the parking lot next to the temporary structure.

This was the only handling of just killed, or up to 72 hours killed, chickens until they were picked up by the Department of Sanitation. In the words of the non-Jewish Department of Sanitation municipal employee tossing the bags onto his garbage truck: “What a waste of food.”

I estimate that I personally saw at two locations over 50 large garbage bags of dead chickens, some of whom I could feel or see through the plastic. That would be about 500 chickens that people had paid minimally an aggregated $10,000 for that they thought was going to Tzedakah. I witnessed several people being directly assured their chicken Tzedakah would be given to the needy. Other Los Angeles chicken Tzedakah sites also had their killed chickens hauled to the landfill and a conservative estimated total of $50,000 to $100,000 of intended Tzedakah may have been direct to the landfill during this year’s Days of Awe. All indications locally point to that this is not a new phenomenon, and the total of thrown away Tzedakah could have easily reached over a million dollars over the past decade or so.

It's been sixteen years since a Los Angeles Jewish Population Survey gave information about the community’s needy. This chicken Tzedakah situation is a direct outcome of not expending the resources communally to know who and where the community’s poor or needy are. Ignore the demography of the poor or needy and it's impossible to effectively contact and get services or Tzedakah to them. Without communal research there can be no documented communal benefit. Egregious communal harm and misdirection may be dressed up by the fundraisers to appear beneficial and it's not the exclusive characteristic of any one particular segment of the community. Jewish individual, organizational and communal oversight mechanisms and culture in Los Angeles demonstrate an aversion to their responsibilties.

When the needy and poor are invisible to the community, Tzedakah is destroyed or misdirected into pockets it was never intended for.

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Q:

ember.js v1.0.0-rc.1 -- Using a modal outlet, how do I route out of the modal on close?

I'm attempting to render all my modals through application routing, but I'm having trouble figuring out the proper way to return to a previous state after I dismiss the modal.
Here's the basic setup:
I have an outlet in my application template which I'm using to display modal dialogs.
It looks something like:
{{ outlet modal }}

In my route mappings, I've defined hooks for the individual modal. For instance, my help dialog pops up with:
App.HelpRoute = Ember.Route.extend({
    renderTemplate: function(controller, model) {
        this.render({ outlet: 'modal' });
    }
});

Right now, I can display my modal through the uri:
   foo.com/#/help

I have a hook to dismiss the modal using jQuery:
$('#modalHelpWindow').modal('hide');

But this doesn't really help, because I'm just hiding the element. I need to update URI on dismissal. If I hit the same route again, the modal is already hidden, and doesn't display.
What methods should I be using to dismiss the modal, and route the application back to its previous state? Should I just be using history.back()?
Note, I am aware of this SO question, but the solution is not the preferred 'ember' way of doing things, as programmatically created views will not have their controllers associated properly  What's the right way to enter and exit modal states with Ember router v2?

A:

Looks like I can hook up the hidden handler to do a history.back() call in my view's didInsertElement method, a la:
   didInsertElement: function() {
        var $me = this.$();
        $me.modal({backdrop:"static"});
        $me.on('hidden', function() {
            history.back();
        });
    },


Q:

What's the easiest way to test a gateway?

I want to test a toy gateway I wrote. The testing will occur on Linux machines. I would like to do this in the easiest way possible, ideally writing no code and using existing utilities. This boils down to two questions:

Is there an existing utility that can send packets with simple stuff in them(like a string that I supply) to a host through a user-specified gateway, without reconfiguring Linux's network settings? If so, what syntax would I use for the utility?
Is there a simple utility I can run on the receiving end to verify that the correct packet was received? If so, what syntax would I use for the utility?

A:

I don't know about the first, but I don't think it's that hard to modify your routing table:
route add -host 1.2.3.4 gw 5.6.7.8
(replace 1.2.3.4 by your target IP and 5.6.7.8 by the IP of your gateway).
For 2.:
On the target server type netcat -l 1234 and on the client then type netcat 1.2.3.4 1234. (1234 is a "random" port number)(depending on your distribution netcat might be called simple "nc".) If a connection gets established you can just type data on the client or the server machine, press enter and see the data arriving on the other machine.


Louise:

We are presently working with Jody Pierce to get the accounting system for the turbine book in place, and a turbine report form prepared. We will have this to you in the next 10 business days. The only recent news is the sale of the steam turbine for $400k, and that we intend to utilize an outside consulting firm (Navigant) to enhance our ability to get some interest going on the SW501D5A. Lastly, we are reviewing the possibility of having the Ft. Pierce project use MHI unit #3 instead of unit #1 in light of the apparent market interest in units 1 and 2, and the current Ft. Pierce construction schedule which is better suited for unit #3 than unit #1.

Mike Coleman is putting together a budget and program to monitor (from a technical perspective) and maintain the 501D5A and the 501Fs.

Please let me know if you have any other questions.

Regards,

Ben

 -----Original Message-----
From: 	Kitchen, Louise
Sent:	Friday, July 20, 2001 8:16 AM
To:	Wiggs, Brett; Jacoby, Ben; Calger, Christopher F.
Subject:	FW: MHI 501 F Disposition Planning

All valid points - I wouldn't mind an update on where we are on the turbine book (including yesterday's good news).

Thanks

Louise

 -----Original Message-----
From: 	Coleman, Mike
Sent:	Thursday, July 19, 2001 5:50 PM
To:	Wiggs, Brett; Jacoby, Ben; Calger, Christopher F.
Cc:	Virgo, Robert; Mays, Wayne; Tapscott, Ron; Fairley, David; Golden, Bruce; Kitchen, Louise
Subject:	MHI 501 F Disposition Planning

With the shipment of two of the four units from MHI scheduled for August and no viable place to ship them, our exposure to increasing costs associated with these units will start to climb quickly.  We need to move agressively to minimize our risk in this position.

Based on discussion with a number of people, I would strongly recommend that we make full efforts to sell units 1 and 2 as quickly as possible.  John Garrison has identified a number of potential buyers, and I believe that Brett Wiggs in in communication with one or more of them as we speak.

We should inform MHI that we will now target unit 3 for Fort Pierce, given the slowdown in the Fort Pierce schedule and the inability to get further reductions in pricing from MHI on unit 1.  If we also drop the dual fuel requirement for Fort Pierce, we should provide some project savings to that project.  Prior to informing MHI, we shoud have Jackson Chaeng status the auxiliaries for unit 3 so we have a basis for understanding any appropriate cancellation costs.

I also recommend that we tentatively target unit 4 for Tallahassee, unless sale of units 1 and 2 were contingent on delivering a 3rd unit to a buyer.  In the next three weeks we will review Tallahassee versus best turbine fit and availability of alternative equipment to determine if we want to continue to target unit 4 to that project.

Finally, MHI has requested that we allow an extention of ship date for unit 1 from August 2 to the end of August.  I think it is in our best interests to agree to that directly, given that we can't tell them where to ship it and would immediately face claims for storage costs if we insist on an August 2 ship date.  We should ask that they forgo storage costs on auxiliaries until the later ship date.

Probably everyone knows some of this, and some know all of this, but hopefully the overall picture is of value.

Thanks!

Mike Coleman