Where do various biotechnologies exist on the hype cycle for academic research and industrial research /manufacturing?

To start with, the Hype cycle is an entertaining but inaccurate model so to accept it unquestioningly is itself a problem.

As far as excessive or overenthusiastic promotion of these various biotechnologies is concerned, to add to Ian Welland's summation, Immunotherapy, and specifically Cancer Immunotherapy, currently seem to be coming off of peak hype, given the back-to-back reports of clinical trial deaths from Juno Therapeutics and ZIOPHARM Oncology in early and mid-July 2016, respectively.

Exploring the question's assumptions is a more interesting exercise.

• First, this wording, 'What changes need to be made to reach the plateau of productivity?' suggests a problematic assumption, that not only might a generic tool-kit exist but much like a magic wand, could be easily deployed to any over-hyped technology and so doing, could in short order make the process of its widespread adoption submit to rationality and render it more efficient. Doesn’t such an excessively technocratic approach contradict the way human societies really operate, which on the contrary reveal themselves to be much too haphazard and unpredictable? After all, were the latter not the case, would hype even exist?
• Next, the unquestioning acceptance that the hype cycle 'model' accurately represents how societies adopt technological innovations is also problematic. Where's the proof the hype cycle's even accurate?
• The problem with the hype cycle is it combines two separate phenomena, one, the fallible human tendency to fetishize novelty and all that entails such as contagion, excessive enthusiasm, speculation, in short, hype, and two, the classic S-curve that describes the Diffusion of innovations.
• In a recent meta-analysis of empirical studies on the hype cycle (1), Dedhayir and Steinert emphasize that one of its key weaknesses is it melds these two disparate phenomena that measure different outputs, and artificially forces on them the same y-axis parameter, namely, visibility (or expectations).
• The human hype-centric cycle typically assesses enthusiasm for the new technology. How to measure enthusiasm? This remains unclear since the hype cycle measures it using two different y-axes interchangeably, namely, visibility and expectation, which have different operational definitions. While visibility is defined as 'technology presence rate on media channels, conversations as well as in interpersonal conversations', expectation is defined as 'expected future value of an innovation' (1).
• Meantime, the S-curve for assessing diffusion of innovations measures neither enthusiasm nor visibility nor expectations but rather the innovation's rate of adoption.
• No wonder then that the resulting model doesn't have a track model for successful predictions which is what this recent meta-analysis also suggests (see below from 1).

A Meta-Analysis Suggests The Hype Cycle's A Flawed Model Found In <50% Of Empirical Results

Bibliography

1. Dedehayir, Ozgur, and Martin Steinert. "The hype cycle model: A review and future directions." Technological Forecasting and Social Change 108 (2016): 28-41. https://www.researchgate.net/pro...

https://www.quora.com/Where-do-various-biotechnologies-exist-on-the-hype-cycle-for-academic-research-and-industrial-research-manufacturing/answer/Tirumalai-Kamala

Over the years, the consensus that harms of antibacterial soaps outweigh their benefits has indeed coalesced. But to understand how antibacterial soaps could harm, we first need to understand how they differ from regular soaps. Also referred to as antimicrobial or antiseptic soaps, they contain chemicals that regular soaps don't.

Many liquid soaps labeled antibacterial contain Triclosan, a synthetic compound, specifically a phenylether or chlorinated bisphenol. While the US FDA classifies it as a Class III drug, i.e., a compound with high solubility and low permeability, Triclosan is also a pesticide. Triclocarban is another common chemical found in antibacterial soaps. Many of the concerns about Triclosan also apply to Triclocarban (1).

Since it appeared on the scene in 1972, Triclosan has steadily permeated through the consumer landscape such that it's practically ubiquitous today (see lists below from 1 and 2).

Triclosan's so ubiquitous it's even found embedded in medical devices such as catheters and sutures to prevent infections (3).

As for its beneficial effect, a 2015 study compared bactericidal effect of plain versus Triclosan-containing soaps in conditions that mimic hand washing, and found no difference in their ability to reduce bacterial numbers during a 20 second exposure (4). In other words, dubious benefit when used for routine hand washing under normal circumstances, i.e., only washing hands for a few seconds. After all, most of us don't scrub as though preparing to do surgery every time we wash our hands.

How Triclosan, A Common Antibacterial Soap Ingredient Inhibits/Kills Microbes

In vitro studies show Triclosan can stop bacteria growing at low concentrations (bacteriostatic), and kill them at high concentrations (bactericidal). It also has some activity against some fungi (5) and even parasites such as those that cause malaria, Plasmodium falciparum, and toxoplasmosis, Toxoplasma gondii (6).

Triclosan is able to target many different types of bacteria by blocking the active site for an enzyme essential for bacterial fatty acid biosynthesis (7, 8). Blocking the enzyme enoyl-acyl carrier protein reductase, Triclosan prevents bacteria from synthesizing fatty acid, which they need for their cell membranes and for reproduction.

Problems With Triclosan

I. Triclosan selects for antibiotic resistance

As widespread Triclosan use increased, labs increasingly started finding cross-resistance to antibiotics. Under selection pressure from Triclosan, bacteria mutate to develop resistance mechanisms to it, which end up bestowing antibiotic resistance as well. In other words, studies show Triclosan selects for antibiotic resistance (see table below from 9).

II. Discharged Widely Into The Environment, Triclosan Can Affect Biomass Such As Algae & Bacterial Communities

Since it's widely used in such a diverse array of products, Triclosan ends up in soil, ground water and municipal wastewater treatment plants. Such plants require proper functioning of microbes to break down sewage. Triclosan can inhibit methane production in wastewater plant anaerobic digesters as well as select for multidrug resistance in such bacterial communities (10). Triclosan's effects persist even beyond because it's discharged from wastewater treatment plants as effluent. Certain algae species in the vicinity of such plants have been found to be very sensitive to Triclosan (11, 12). Triclosan also affects bacterial communities in rivers (13). Potential environmental risk of Triclosan becomes even more relevant in areas of water scarcity where it doesn't get sufficiently diluted.

III. Triclosan Can Alter Gut Microbiota In Fishes & Rodents, Potentially Alter Human Microbiota, & Even Promote Tumors In Rodents

• Triclosan could profoundly (14) and stably (12) alter fish gut microbiota as well as those of baby rats (15).
• While so far Triclosan doesn't appear to affect human gut microbiome, the data are far from conclusive, being based on just one study with 7 volunteers (16). OTOH, a study on nasal secretions from 90 healthy adults found a positive correlation between presence of Triclosan in nasal secretions and nasal colonization by Staphylococcus aureus (17). This suggests Triclosan indeed has the potential to influence, even alter human microbiota.
• One mouse model even found Triclosan capable of promoting liver tumors (18).

IV. Triclosan Can Disrupt Hormonal Function

Triclosan was found to disrupt thyroid hormone-associated gene expression and altered the rate of frog metamorphosis (19). It could also disrupt thyroid (20, 21), estrogen (22), and testosterone (23) function in rats.

V. Triclosan Bans

Given the increasing litany of concerns about Triclosan's deleterious effects on the physiology of a wide variety of species, which may also increasingly include humans, several governments are either considering banning it or have already done so.

• In March 2010, the European Union banned Triclosan from any products that may come into contact with food (2).
• On 16 May, 2014, the US state of Minnesota banned the sale of Triclosan-containing cleaning products (soaps), giving manufacturers time until early 2017 to phase them out (24).
• As of 2015, Health Canada was considering banning Triclosan. It's estimated ~1730 products including cosmetics, health and personal care products containing Triclosan were available in Canada in 2011 (1).
• The US FDA is mulling its regulation (25), with a report due in September 2016.

Bibliography

1. Dhillon, Gurpreet Singh, et al. "Triclosan: current status, occurrence, environmental risks and bioaccumulation potential." International journal of environmental research and public health 12.5 (2015): 5657-5684. Triclosan: Current Status, Occurrence, Environmental Risks and Bioaccumulation Potential

2. Alliance for the Prudent Use of Antibiotics. "Triclosan." White Paper prepared by the Alliance for the Prudent Use of Antibiotics (APUA) (2011). http://emerald.tufts.edu/med/apu...

3. Stickler, David James, G. Ll Jones, and Allan Denver Russell. "Control of encrustation and blockage of Foley catheters." The Lancet 361.9367 (2003): 1435-1437. http://carambola.usc.edu/Biofilm...

4. Kim, S. A., et al. "Bactericidal effects of triclosan in soap both in vitro and in vivo." Journal of Antimicrobial Chemotherapy (2015): dkv275.

5. Vischer, W. A., and J. Regös. "Antimicrobial spectrum of Triclosan, a broad-spectrum antimicrobial agent for topical application." Zentralblatt für Bakteriologie, Parasitenkunde, Infektionskrankheiten und Hygiene. Erste Abteilung Originale. Reihe A: Medizinische Mikrobiologie und Parasitologie 226.3 (1974): 376.

6. McLeod, Rima, et al. "Triclosan inhibits the growth of Plasmodium falciparum and Toxoplasma gondii by inhibition of Apicomplexan Fab I." International journal for parasitology 31.2 (2001): 109-113. https://www.researchgate.net/pro...

7. McMurry, Laura M., Margret Oethinger, and Stuart B. Levy. "Triclosan targets lipid synthesis." Nature 394.6693 (1998): 531-532.

8. Levy, Colin W., et al. "Molecular basis of triclosan activity." Nature 398.6726 (1999): 383-384.

9. Schweizer, Herbert P. "Triclosan: a widely used biocide and its link to antibiotics." FEMS microbiology letters 202.1 (2001): 1-7. http://femsle.oxfordjournals.org...

10. McNamara, Patrick J., Timothy M. LaPara, and Paige J. Novak. "The impacts of triclosan on anaerobic community structures, function, and antimicrobial resistance." Environmental science & technology 48.13 (2014): 7393-7400. https://www.researchgate.net/pro...

11. Reiss, Richard, et al. "An ecological risk assessment for triclosan in lotic systems following discharge from wastewater treatment plants in the United States." Environmental Toxicology and Chemistry 21.11 (2002): 2483-2492.

12. Lawrence, J. R., et al. "Resilience and recovery: The effect of triclosan exposure timing during development, on the structure and function of river biofilm communities." Aquatic Toxicology 161 (2015): 253-266. https://www.researchgate.net/pro...

13. Ricart, Marta, et al. "Triclosan persistence through wastewater treatment plants and its potential toxic effects on river biofilms." Aquatic Toxicology 100.4 (2010): http://www.clipmedia.net/galera/...

14. Narrowe, Adrienne B., et al. "Perturbation and restoration of the fathead minnow gut microbiome after low-level triclosan exposure." Microbiome 3.1 (2015): 1. Microbiome

15. Hu, Jianzhong, et al. "Effect of postnatal low-dose exposure to environmental chemicals on the gut microbiome in a rodent model." Microbiome 4.1 (2016): 1. Microbiome

16. Poole, Angela C., et al. "Crossover Control Study of the Effect of Personal Care Products Containing Triclosan on the Microbiome." mSphere 1.3 (2016): e00056-15. http://msphere.asm.org/content/m...

17. Syed, Adnan K., et al. "Triclosan promotes Staphylococcus aureus nasal colonization." MBio 5.2 (2014): e01015-13. Triclosan Promotes Staphylococcus aureus Nasal Colonization

18. Yueh, Mei-Fei, et al. "The commonly used antimicrobial additive triclosan is a liver tumor promoter." Proceedings of the National Academy of Sciences 111.48 (2014): 17200-17205. http://www.pnas.org/content/111/...

19. Veldhoen, Nik, et al. "The bactericidal agent triclosan modulates thyroid hormone-associated gene expression and disrupts postembryonic anuran development." Aquatic Toxicology 80.3 (2006): 217-227. https://www.researchgate.net/pro...

20. Crofton, Kevin M., et al. "Short-term in vivo exposure to the water contaminant triclosan: evidence for disruption of thyroxine." Environmental Toxicology and Pharmacology 24.2 (2007): 194-197. https://www.researchgate.net/pro...

21. Zorrilla, Leah M., et al. "The effects of triclosan on puberty and thyroid hormones in male Wistar rats." Toxicological Sciences 107.1 (2009): 56-64. The Effects of Triclosan on Puberty and Thyroid Hormones in Male Wistar Rats

22. Stoker, Tammy E., Emily K. Gibson, and Leah M. Zorrilla. "Triclosan exposure modulates estrogen-dependent responses in the female wistar rat." Toxicological Sciences (2010): kfq180. Triclosan exposure modulates estrogen-dependent responses in the female Wistar rat

23. Kumar, Vikas, et al. "Alteration of testicular steroidogenesis and histopathology of reproductive system in male rats treated with triclosan." Reproductive Toxicology 27.2 (2009): 177-185.

24. SF 2192 Status in the Senate for the 88th Legislature (2013

25. Kuehn, Bridget M. "FDA pushes makers of antimicrobial soap to prove safety and effectiveness." JAMA 311.3 (2014): 234-234.

https://www.quora.com/Does-anti-bacterial-soap-do-more-harm-than-good/answer/Tirumalai-Kamala

When we hear the word epidemic, we typically think of diseases, often communicable diseases but maybe we shouldn't, at least not always. An epidemic that isn't so much potential but real has been with us for at least a century and is only increasing in importance, namely, road injuries. Also important to remember that one doesn't need to be a driver to fall victim to road injuries. Victims include cyclists, motorcyclists, passengers and pedestrians as well.

Rubbernecking was one of the first phrases I added to my vocabulary when I came to the US. Needless to say I learned it in the context in which it is perhaps most often used, drivers slowing down to see what happened in a road accident. A 2014 report reckoned 1.2 billon vehicles that were expected to increase to 2 billion by 2035 (1).

The thing about hidden epidemics is we somehow learn to internalize certain costs, get habituated to them and keep on moving. Dangers inherent to an automobile in motion are precisely the type of costs our brains seem wired to discount. I hear or read an all too familiar regurgitation every time there's a plane crash, a statistical accounting of how much safer, despite that particular crash, plane travel is compared to automobiles. Numbers aren't apparently enough to leave an impression though. As prosperity increases around the world, increasing numbers of the newly affluent are taking to the roads in their new cars the world over, and inevitably, increasing numbers are dying or injured. After all, the driving habit is taking off in those places just as electronic distractions proliferate as well.

In my time behind the wheel, I've seen it all. From a seemingly endless stream of drivers with their eyes glued to their phones to someone looking in their vanity mirror, carefully applying mascara, another wielding an eyelash curler, someone else mouthing a spoonful, the other hand holding a bowl, drivers all. Wait a minute. That last one, did I really see that? I had to make sure I really did see it. Yes, no doubt about it, a driver behind the wheel eating their breakfast using a bowl and spoon, hands-free driving as far as I could tell. Rubbernecking. Did any of them or even me for that matter seriously consider we would rubberneck or be the object of someone else's rubbernecking that day as we got in our cars and started driving? Of course not. If we'd done that, how could we overcome our fear-induced paralysis to start driving? Sheer habituation and following inevitably in its wake, a hidden in plain sight epidemic of road injuries and deaths. The fact remains that in the US, the lifetime chances of dying in a car accident are apparently 1 in 606 compared to 1 in 174, 426 by lightning (2).

So let's look at some more numbers to better understand the contours of this particular epidemic. In 2015, the Lancet helpfully published a massive report by the Bill and Melinda Gates Foundation-funded Institute for Health Metrics and Evaluation on global causes of mortality (3).

First off the bat, they include road injuries as one of the top ten causes of global death in a list that includes the likes of heart disease, respiratory infections and stroke (see below from 3).

Their analysis further concludes road injuries jumped up the list from #10 in 1990 to #5 in 2013 (see below from 3).

While adding more granularity to road injury data, the WHO 's 2015 Global status report on road safety is the typical Curate's egg, some good bits but mostly bad (4). According to them, though road traffic fatalities plateaued between 2007 and 2013, they're increasing in middle- and low-income countries (see figure below from 4).

Unfortunately, middle-income countries are where most of the world lives (see figure below from 4).

While Africa leads the world road injury fatalities per 100000 (see figure below from 4).

So what can be done? Can anything be done? The WHO data suggests it's going to be something we've seen before, a long, hard slog to enact and enforce safe driving practices. This includes traffic partitioning to protect those most vulnerable, tough drink-driving and helmet laws, strictly enforced speed limits and vehicles that meet not just basic safety standards, which shockingly most of them don't right now, but those that meet preferably the most stringent safety standards (see figure below from 4).

Bibliography

1. 1.2 Billion Vehicles On World's Roads Now, 2 Billion By 2035: Report

2. Mortality Risk

3. Naghavi, Mohsen, et al. "Global, regional, and national age-sex specific all-cause and cause-specific mortality for 240 causes of death, 1990-2013: a systematic analysis for the Global Burden of Disease Study 2013." Lancet 385.9963 (2015): 117-171. http://www.thelancet.com/pdfs/jo...

4. The WHO 's Global status report on road safety 2015 http://www.who.int/violence_inju...

https://www.quora.com/What-are-some-potential-epidemics-that-nobody-is-talking-about-as-of-2016/answer/Tirumalai-Kamala

What (if any) were the long-term effects or repercussions of the "dotbusters" incidents against Indian-Americans in NJ during the 1980s?

New Jersey's Dotbusters

According to Elizabeth Gutierrez (1), in the 9-month period from June 1987 to Feb 1988, >15 Indians were brutally attacked in and around Jersey City, New Jersey. A group calling itself 'Dotbusters' sent a letter to the The Jersey Journal in August 1987 stating their intention to force Indians out of this community, by violence if necessary (see below from 1).

'If I'm walking down the street and I see a Hindu and the setting is right, I will just hit him or her'

The shocking 1987 attacks on Navroze Mody (on Sep 27, 1987 in Hoboken, New Jersey), which left him dead, and on Kaushal Saran (on Sep 24, 1987 in Jersey City, New Jersey, which left him with permanent neurological damage, didn't lead to appropriate punishments for the culprits. Mody's killers were convicted for merely aggravated assault and simple assault (2) while Saran's attackers were acquitted (3, 4). In fact, even Mody's father's complaint that the police didn't do enough to ensure his son's protection (2) was dismissed by the 3rd Circuit of the US Court of Appeals.

One of the most shocking and certainly flagrant aspects of these beatings and killing is that a mere 2 weeks earlier, on Sep 12, 1987, two of the brothers convicted on the aggravated assault charge for Mody's killing had apparently beaten two other Indians, Stevens Institute of Technology students Syed Hasan and Vikas Aggarwal. As the 3rd Circuit of the US Court of Appeals itself notes (from 2, emphasis mine),

'On September 12, 1987, two Asian Indian students from Stevens Institute of Technology (Stevens) in Hoboken, Syed Hasan (Hasan) and Vikas Aggarwal (Aggarwal), were walking to a restaurant named East L.A., two blocks from Stevens, for dinner. At 9:00 p.m., as they were about to enter the restaurant, someone stepped in front of them and stole Hasan's umbrella. Hasan turned and saw a man holding a baseball bat and another running away with the umbrella. When Aggarwal stepped forward and asked for the umbrella back, he was punched in the face by one of the men. About this time, an unknown person hit Hasan on his left side with a metal bar.

Hasan and Aggarwal entered the restaurant to escape their assailants. Aggarwal was bleeding profusely from his mouth. From inside the restaurant, he and Hasan could not see whether their assailants had left the area. They decided to walk back to Stevens and call security. Hasan only got as far as the curb when he was hit from behind with a baseball bat and fell into the road. Two men then picked Hasan up bodily, slammed him against the door of an adjoining store and punched and kicked him for about five minutes. Hasan ran back to Stevens alone. None of the men tried to rob Hasan. In the meantime, Aggarwal had also been attacked and struck senseless. He too was not robbed during the attack and, after the Hoboken police found him, he was taken to St. Mary's Hospital.

Mr. Ivan Sales (Sales), a man of Hispanic origin employed at a nearby restaurant called "Chicken Galore," saw the attack and called to the men beating Hasan and Aggarwal to stop. In response, three of the attackers ran over to Sales and assaulted and robbed him. The attackers fled as police responded to the scene.

After receiving medical treatment for their injuries, Hasan and Aggarwal gave signed statements to the Hoboken police about the attacks. While Hasan said he would recognize "the tall chap" if Hasan saw him again, neither Hasan nor Aggarwal could identify the attackers. Sales was able to identify two of them as "Chinito" and "Chinito's" brother. App. at 372-73. Hasan and Aggarwal were not asked whether they wanted to file complaints against their attackers. After they gave the police their respective dorm hall phone numbers and addresses so the police could reach them if needed, they left thinking that there was nothing further for them to do in order to press charges. Later Hasan did contact the Hoboken police to give them the phone number of his uncle's house in Queens, New York where he was staying while he recuperated from the attack.

Three days after the assaults, Detective Cahill learned that William Acevedo, also known as "Chinito," "was telling his friends in Hoboken High School how he had beat up two Indians and the Chicken man." Id. at 371. On September 17, 1987, William and Luis Acevedo went to the Hoboken police station. Detective Cahill reported that he then called Hasan and his roommate, Aggarwal, but Hasan said he did not want to file a complaint. The phone number Detective Cahill said he called was not the phone number of either Hasan or Aggarwal, and Hasan and Aggarwal were not roommates. Hasan and Aggarwal said they never told the Hoboken police that they did not want to press charges. Indeed, Aggarwal said he was never contacted by the police after he reported the incident. Hasan testified that he once received a message at his dormitory that the police had called and would call back, but they never did. Detective Cahill did contact Sales. Contrary to earlier statements, Sales now said that he did not want to file a complaint.

About a week after the attack, Peter Van Schaick (Van Schaick), a friend of Hasan's family and an attorney practicing in Hoboken, went to the Hoboken Police Department to talk with Lieutenant Kiely upon learning from Hasan that the police had taken no action in the matter. Lieutenant Kiely explained that no action had been taken because none of the victims had filed a complaint, but he admitted that he could legally pick up the attackers without awaiting a filed complaint from the victims. This explanation surprised Van Schaick since Hasan and Aggarwal had told him they did want the police to press charges. Van Schaick also told Lieutenant Kiely that he suspected the Hoboken police were not pressing the matter because the victims were Asian Indians. Later, another member of the Hoboken police force told Van Schaick that gangs and the "dot busting" problem were not high on the police department's priority list'

In other words, future violence and certainly Mody's killing was likely preventable if police had acted expeditiously in apprehending Hasan and Aggarwal's attackers. Why didn't this happen? Institutional indifference, bias? All these years later, we each have to fill the blanks ourselves as per our disposition. Violence to Mody and Saran was preventable because not being held accountable for the Sep 12 student beatings sent a strong, univocal message to those perpetrators that their open season mayhem on the Indian-American community in their neck of the woods was, if not officially sanctioned, somehow allowed.

Community Activism, Legal Repercussions And Consequences Of New Jersey Dotbuster Attacks In The 1980s

Such concerted attacks within a short time period caused the Indian American community in this area to coalesce around this issue. Following numerous public protests (5, 6), the US Justice Department became involved (7) and only then did local city officials begin to pursue a more aggressive approach against these crimes.

These 'dotbuster' incidents may have played a role in the passing of the bias crimes law (ethnic intimidation law) in August 1990 by the New Jersey State Assembly or so asserts the senior US Senator from New Jersey, Bob Menendez (8).

However, though frequency of such attacks definitely abated from their 1980s highs, hate crimes against Indian Americans in this region of New Jersey haven't stopped.

• In June 2010, 49-year old Divyendu Sinha, a 49-year old Stevens Institute of Technology professor was savagely beaten and killed in Old Bridge Township, New Jersey, ~30 miles south of Jersey City, while he was out for a walk with his two sons near his home (9). At that time, the Indian population in this predominantly white town of 70,000 had increased to ~6%. Two of the 5 accused high school students, though tried as adults, were finally acquitted of all the most serious charges and instead only found guilty of simple assault, 'a 4th degree crime that carries the presumption of non-incarceration' (10). One was sentenced to >12 years in prison (11), another to 7 years for aggravated manslaughter (12) and the fifth to 15 years (13).
• As recently as July 2015, 57 year old Rohit Patel was apparently the victim of a hate crime attack (beating) in North Brunswick, New Jersey (14), ~32 miles south of Jersey City.

Indian Population Demographic Changes In Jersey City, New Jersey post-1980s

Inexplicably, dotbuster attacks appear to not have prevented Indian immigration into this area. Indian population in Jersey City has expanded steadily, regardless of these attacks. While some have speculated that Indians' tendency to cluster spatially both residentially and in business in this area made them more visible as targets for the 1980s attacks (1), it may be that counter-intuitively, the same tendency helped sustain their continuing immigration into this region. Strength is in numbers after all.

• In 1992, the New York Times (15) quotes the Census Bureau as stating that 'During the 1980's, Jersey City's Asian Indian population increased from 2,303 to 7,361’.
• By 1989, it had apparently increased to 15000 (16), a >2X increase in just 2 years, ~6.5% of the total.
• While Jersey City Indians numbered 27111 in 2010 (17), representing 10.9% of the overall Jersey City population, their number further increased to 27603 by 2013 (18), a 1.8% increase over 3 years.

Bibliography

1. Gutierrez, Elizabeth. "THE-DOTBUSTER-ATTACKS: HATE CRIME AGAINST ASIAN INDIANS IN JERSEY CITY, NEW JERSEY." Middle States Geographer 5 (1996): 30-38. http://msaag.org/wp-content/uplo...

2. 959 F.2d 461

3. New York Times, Feb 11, 1993. 3 Are Acquitted on a Count In Indian Physician's Beating

4. Hudson Reporter, Ricardo Kaulessar, Mar 5, 2009. ‘DotBusters’ victim looks back<br><font size=2><i>Now in Oklahoma; racial attack nearly killed JC resident in 1987</font></i><br>

5. New York Times, Oct 8, 1987. Jersey City Indian Community Protests Rash of Racial Attacks

6. New York Times, Dec 16, 1987. Protesters Want Four Tried As Adults in Killing of Indian

7. New York Times, Oct 12, 1987. In Jersey City, Indians Protest Violence

8. Menendez Letter To TIME On Joel Stein's Essay About Indian-Americans In NJ | U.S. Senator Bob Menendez of New Jersey

9. Jersey Journal, Stephen Sterling, July 1, 2010. http://blog.nj.com/ledgerlocal/p...

10. Jersey Journal, Sue Epstein, Oct 1, 2013. Acquittals in Old Bridge beating death spark tears of relief, tears of frustration

11. Jersey Journal, Sue Epstein, Apr 3, 2014. Last of 5 charged in fatal Old Bridge beating case sentenced to 12 years in prison

12. News12, Oct 18, 2013. 3 sentenced in fatal beating of Old Bridge man

13. Jersey Journal, Sue Epstein, June 12, 2014. Appeals court upholds Old Bridge teen's 15-year prison term in Old Bridge fatal beating

14. Times of India, July 7, 2015. Indian man attacked in apparent hate crime in New Jersey - Times of India

15. New York Times, Sep 12, 1992. 3 Indicted in Beating of Indian Doctor

16. New York Times, Apr 10, 1989. Indian-Americans Protest Verdicts in Jersey City

17. American FactFinder - Results

18. American FactFinder - Results

19. American FactFinder - Results

https://www.quora.com/What-if-any-were-the-long-term-effects-or-repercussions-of-the-dotbusters-incidents-against-Indian-Americans-in-NJ-during-the-1980s/answer/Tirumalai-Kamala

If garlic is such a great antibacterial, does it also kill our good bacteria? If not why?

That this, that or the other Medicinal plants/extract is antibacterial is usually a marketing claim based on a bunch of dubious reports, largely anecdotes, and not on sound, rigorously tested and reproducible science (1). See for example 2, the US National Institutes of Health’s summation of garlic’s health benefits. Certainly no verifiable reports of its ‘proven’ antibacterial properties listed there.

What if instead we probe the underlying premise, as to why antibacterial even became perceived to be a desirable quality? A more illuminating journey attends such a quest, revealing how certain concepts take root, how their underlying flaws lie hidden in plain sight, sometimes for far too long, all until a newer body of work permeates our collective consciousness, forcing us to confront the untenable aspects of the original concept and eventually to incorporate this newer knowledge within its fold. In doing so, our understanding of something fundamental about nature changes. In this case, it’s about recalibrating our overwhelmingly adversarial stance towards bacteria, a stance that rooted and took off sometime in the mid-20th century.

When did antibacterial become a sought after aim and is it really always beneficial? Such a notion is of fairly recent vintage. How could it be otherwise when Bacteria itself pervaded collective human consciousness only after the late 19th century concept of Germ theory of disease took hold?

Word usage frequency reveals how use of antibacterial tracks with that of Antibiotics, itself an early 20th century discovery (See figures below from Google Ngrams for the words antibacterial, antibiotics and bacteria in the English corpus of books, 3).

With their large-scale manufacture streamlined post-WWII, antibiotics became mainstream medicine starting in the early 1950s. With them spread the linked notion that getting rid of bacteria somehow bestowed health. Antibacterial thus became established as a desirable end goal in and of itself, even among the healthy, or at least it became a commercially exploitable goal for health product manufacturers and their marketers. So it continued for the good part of half a century or more.

Much more recently, this premise of antibacterial benefit started crashing into a dead end with the mainstreaming of the Microbiota concept, the idea that the human body isn't so much a single individual as each a unique eukaryote-microbe ecosystem. After all, we do acquire our final 'tissue', our microbiota, post-birth as our body gets rapidly and permanently colonized by microbes from our environment.

Back when antibiotics and antibacterial were all the rage, who'd stop to think and consider 'good' bacteria? Bacteria were then largely seen as 'germs', to be summarily rid of without a second thought. But now? Now we have to seriously consider the consequences. Data's increasing by the day on the harms that attend the thoughtless meddling with and ridding of our microbiota (4), largely through widespread indiscriminate use of antibiotics and other antibacterials (4, 5, 6). Such harms are many, ranging from increasing rates of allergies and autoimmunities to obesity.

Each individual has unique microbiota, the result of unique life history (c-section or natural birth for example), genetics and epigenetics (which largely determine the processes that attend stable microbial colonization), age, diet, gender, infection and treatment history, lifestyle choices and location. Consider the infamous Typhoid Mary. Even as she worked as a cook in household after household, spreading Typhoid fever in her wake (7), Mary Mallon herself remained unharmed from the disease she was spreading. In the context of the human-microbiota ecosystem, 'good' bacteria is thus inherently contextual and individual. Of course, we already understand this implicitly. After all, our knowledge of human biology is incomplete enough that the process of regulator approval of drugs and therapies is guided by their average, and not individual, efficacy (8).

How then is it possible for one plant/extract to eliminate the 'bad' bacteria, leaving the 'good' untouched in those who consume/apply it? In this light, the claim that garlic or some other plant extract is antibacterial is revealed for the parlous and now increasingly untenable marketing ploy it really is, especially when it lacks clear data showing it can kill or inhibit specific bacteria when used at specific doses, similar to how antibiotic potency is assessed. And even antibiotics do rid our bodies of helpful microbes even as they eliminate the harmful ones (9).

This is not to say garlic or other medicinal plant extracts aren't beneficial to human health. They certainly appear to be and the largely anecdotal data supporting such assertions are obviously long-standing. However, we currently lack a clear understanding of exactly how they are beneficial, when, where and in whom. We won't know without rigorously controlled scientific studies. This is where the science funded by grant agencies like the National Center for Complementary and Integrative Health (NCCAM) becomes critical, for plugging these major gaps in our knowledge and understanding of ancient 'home' remedies.

Bibliography

1. Tirumalai Kamala's answer to Where do I find a table showing anything edible and which kind of bacteria it is effective against?

2. https://nccih.nih.gov/sites/ncca...

3. Original Google Ngram paper: Michel, Jean-Baptiste, et al. "Quantitative analysis of culture using millions of digitized books." science 331.6014 (2011): 176-182. http://www.librarian.net/wp-cont...

4. An Epidemic of Absence: A New Way of Understanding Allergies and Autoimmune Diseases. Moises Velasquez-Manoff, An Epidemic of Absence: A New Way of Understanding Allergies and Autoimmune Diseases Reprint, Moises Velasquez-Manoff - Amazon.com

5. Missing Microbes: How the Overuse of Antibiotics is Fueling Our Modern Plagues. Martin J. Blaser. Missing Microbes: How the Overuse of Antibiotics Is Fueling Our Modern Plagues: 9780805098105: Medicine & Health Science Books @ Amazon.com

6. Tirumalai Kamala's answer to If we know that overusing antibiotics will cause resistant bacteria, why do we still give out so much of it? Especially in some parts of the world?

7. Tirumalai Kamala's answer to Does an asymptomatic disease induce immunity?

8. http://www.fda.gov/downloads/Dru...

9. Tirumalai Kamala's answer to Does taking CIPRO eliminate bacterial immunities that might have been acquired over years of traveling?

https://www.quora.com/If-garlic-is-such-a-great-antibacterial-does-it-also-kill-our-good-bacteria-If-not-why/answer/Tirumalai-Kamala

Why are biologists starting to publish preprints now so long after it became the norm in physics?

Refers to: http://www.nytimes.com/2016/03/16/science/asap-bio-biologists-published-to-the-internet.html?_r=1

In other words, where's scientific publishing headed? Clearly, we're deep in the trenches of a confusing and at times ugly transition phase. Intrepid open-access advocates like Alexandra Elbakyan have wrong-footed incumbents like Elsevier into taking potentially futile and counter-productive rearguard actions like lawsuits (1). This is scientific publishing's Napster moment after all. Such David versus Goliath battles draw mainstream media interest and with that, the story's hopelessly flawed core stands revealed.

Much of basic science research is taxpayer-funded. Scientists perform peer-review of each other's work pro bono. Editing processes are outsourced to back offices in developing countries to cut administrative costs to the bone. Electronic publishing costs a fraction of print. And peer-review's unacceptably slow in the era of instant updates. Why then do for-profit scientific publishing heavyweights own the copyright to scientists' published work? And why do they charge an arm and a leg for accessing just one paper, even for scientists who publish in those same journals and who perform pro bono peer-review on their behalf? For e.g., electronic access per-paper can range from US $6 to $36, even for papers published decades earlier. Annual subscriptions to thousands of journals are an onerous financial burden even for Harvard (2), one of the best-endowed universities in the world. Clearly, shining a spotlight on scientific publishing is akin to turning over the proverbial rock, and such scrutiny doesn't augur well for the prevailing order. How could such an untenable status quo even continue to exist? Obviously something's got to give and soon. Preprints, especially by biologists, are a clear sign of this happening. After all, when it comes to the digital era, biologists have tended to follow, not lead.

At heart, the issue's about unprecedented changes in knowledge communication and perusal. Perhaps one of the most persuasive arguments for where they might lead us comes from the physicist Michael Nielsen, one of the first scientists to embrace the digital landscape by blogging on his own web-site since 2003.

In a blog article titled, 'Where will the key ideas shaping the future of scientific publishing come from?', Nielsen explores the counter-intuitive idea that scientific publishing's future will be shaped by none of the key stakeholders of the scientific ecosystem, i.e., neither by leading scientists nor journal publishers nor librarians nor policy makers, etc. Instead, he argues key features of future scientific publishing will be invented over the next few decades 'by two groups of outsiders: exceptionally creative user interface designers, and people who design group experiences' (3).

Nielsen interprets Henry Oldenburg, Johannes Gutenberg and Aldus Manutius to essentially be interface designers, and defines scientific journals as 'user interface to humanity’s scientific knowledge'. Nielsen argues their present-day counterparts are 'attempting to invent powerful new representations for knowledge, representations that will let us manipulate and comprehend knowledge in new ways'. He reminds how two staples of user experience, the hyperlink and search box, have transformed how we relate to knowledge. Nielsen declares 'journals are also a medium for collective intelligence' but that the 'design of media for collective intelligence isn’t yet a widely recognized field'. He argues that collective scientific experience will be shaped by the work being done by the likes of Ned Gulley, Robin Hanson, Bobby McFerrin, Jane McGonigal, Elan Lee.

Nielsen concludes that scientific publishing's future won't be monolithic as in the past but instead include a variety of forms, ranging from the informal to the collaborative to the prevailing model, i.e., the 'paper of record'. I'm inclined to agree. It'll be confusing for a while. Some approaches will likely crash and burn. Others will become mainstays. Unlikely it'll be monolithic. A fast moving science story like Zika had researchers uploading raw data online in real time (4). Unthinkable in the monolithic era. Seen in this light, physicists were ahead of the curve by publishing preprints. Biologists? Far behind. Both, however, are responding to the way the digital world has wrought unprecedented changes in how scientific knowledge is shared. If Nielsen's right, preprints will be but one form of how that's done.

Bibliography

1. https://scholar.google.com/schol...

2. The Guardian, Ian Sample, April 24, 2012. Harvard University says it can't afford journal publishers' prices

3. Michael Nielsen, May 10, 2015. Where will the key ideas shaping the future of scientific publishing come from?

4. Nature, Declan Butler, Feb 23, 2016. Zika researchers release real-time data on viral infection study in monkeys

https://www.quora.com/Why-are-biologists-starting-to-publish-preprints-now-so-long-after-it-became-the-norm-in-physics/answer/Tirumalai-Kamala

How often are seniors in nursing homes under-monitored?

Assuming under-monitoring implies neglect, it's important to note that in contrast to other types of more explicit abuse such as physical, psychological, verbal or emotional, neglect is the most common type of senior abuse.

What is Neglect?

The WHO recognizes abuse and neglect of seniors as global health problems (1). However, unlike explicit physical and mental abuse which are easier to identify and therefore define, neglect is trickier. Was it unintentional (for e.g., incontinent resident left unchanged for long periods of time because of inadequate, over-worked staff) or intentional (for e.g., staff refusing to change incontinent residents when they are wet). As well, physical signs of neglect such as pressure ulcers, skin tears, malnutrition and dehydration can be just as easily attributed to chronic disease.

Neglect is defined to various degrees of detail, each definition helpful in its own way in helping to identify it.

'Neglect. Defined as neglect by staff or other caregivers such as failure to rotate or flip the person to prevent bed sores; failure to provide a person with food, water, shelter, hygiene, medicine, comfort, or personal safety; or ignoring requests for help'

(2).

'Neglect is perhaps the most common, but also the most difficult type to prove. It may be as omissions (for example, not providing care for an elder who is incapable of caring for him/herself, not providing medication that is required for chronic or acute problems) or as commissions (over medicating an elder to keep him/her docile, or putting the elder through unnecessary procedures or medical treatments). Examples of neglect include failing to provide proper nutrition or clothing, failing to attend to the hygiene of those who may be bedridden, failing to provide private bathroom arrangements, or leaving incapacitated adults unsupervised for long periods of time (Department of Justice, 2007). Neglect may also be self-inflicted (McDonald, Collins & Dergal, 2006).'

(3).

The National Center on Elder Abuse (NCEA) defines elder neglect more succinctly as (4)

'refusal or failure to fulfill any part of a person's obligations or duties to an elder. Neglect may also include failure of a person who has fiduciary responsibilities to provide care for an elder (e.g., pay for necessary home care services) or the failure on the part of an in-home service provider to provide necessary carer'

According to Sorenson, communication neglect is lack of meaningful and personable conversations with the seniors or caregiver avoiding physical or social contact with the care receiver (5). This can also be intentional, 'silent treatment' or talking over them to a 3rd party, all ways to punish and/or 'discipline' the senior care receiver.

Communication neglect may also ensue when the caregiver is either simply stretched for time or subject to stereotypes that conversations with seniors are long, tedious and repetitive (6).

Some Data On Neglect Of Seniors In Nursing Homes

Data on senior abuse and neglect are hard to come by. For e.g., the US lacks a systematic nation-wide database on rates of abuse and neglect among seniors, be they in residences, assisted care facilities or nursing homes. As well, studies more often focus on explicit abuse, not neglect. Data thus has to be sought from the few individual studies that did examine neglect.

• 37% of certified nursing assistants in a 2010 US survey reported witnessing neglect of residents in a nursing home (7).
• Shockingly the 2003 Atlanta Long-Term Care Ombudsman Study found 95% of residents interviewed reporting having experienced neglect or witnessing neglect of other residents (8).
• Data in a 2004 NCEA report (9) represented the FY 2003 data from Adult Protective Services (APS) in all 50 US states, the District of Columbia and Guam. Among adults >60 years, APS received 253,426 reports across 26 states, investigated 192, 243 across 29 states and substantiated 88, 455 across 24 states. It found 58% involved neglect. However, this includes all types of seniors, both those in and outside nursing homes.
• An Israeli questionnaire-based study of staff working at 24 of 300 long-term nursing homes for older people in Israel (n=510) also found physical and mental neglect were the most common form of elder abuse, 30 and 34%, respectively (see table below from 10).

Signs and Symptoms of Senior Neglect

Since it's difficult to distinguish whether symptoms ensue from neglect or chronic disease, Anglin and Homeier suggest making use of a detailed checklist (see list and photos below from 11). Tell-tale signs include overgrown toe nails, pressure sores, dirty clothing, and poor body and oral hygiene among others.

Most Common Reasons for Senior Neglect

• According to the WHO, owners of private facilities often enforce cuts in areas essential for quality care such as human resources (1). Inadequate staff numbers inevitably culminate in neglect.
• An Israeli questionnaire-based study (n=510) found highest correlation of physical and mental neglect with inadequate staff numbers and high staff turnover (10).

Bibliography

1. Krug, E. G. "World report on violence and health/edited by Etienne G." Krug...[et al.]: Geneva: World Health Organization (2002). http://apps.who.int/iris/bitstre...

2. Page, Connie, et al. "The effect of care setting on elder abuse: results from a Michigan survey." Journal of Elder Abuse & Neglect 21.3 (2009): 239-252.

3. Sev'er, Aysan. "More than wife abuse that has gone old: a conceptual model for violence against the aged in Canada and the US." Journal of Comparative Family Studies (2009): 279-292. https://tspace.library.utoronto....

4. Types of Abuse

5. Sorenson, Helen. "Verbal abuse and communication neglect in the elderly." Elder Abuse: A Public Health Perspective (2006): 117-129.

6. Lin, Mei-Chen, and Howard Giles. "The dark side of family communication: a communication model of elder abuse and neglect." International Psychogeriatrics 25.8 (2013): 1275-1290. https://www.researchgate.net/pro...

7. Zhang, Zhenmei, et al. "Neglect of older adults in Michigan nursing homes." Journal of Elder Abuse & Neglect 23.1 (2010): 58-74. https://www.researchgate.net/pro...

8. Hawes, C., and J. Kayser-Jones. "Abuse and neglect in nursing homes and institutions." Annals of Long Term Care 11 (2003): 17-21.

9. Teaster P: A 2004 Survey of State Adult Protective Services: Abuse of Adults 60 Years of Age and Older. Washington, DC: National Center on Elder Abuse (NCEA); 2006. http://www.ncea.aoa.gov/Resource...

10. Natan, Merav Ben, Pat Matthews, and Ariela Lowenstein. "Study of factors that affect abuse of older people in nursing homes: Merav Ben Natan and Ariela Lowenstein explore the maltreatment of care home residents." Nursing management 17.8 (2010): 20-24.

11. Anglin, Deirdre, and Diana C. Homeier. "Elder Abuse and Neglect." http://cdn3.slremeducation.org/w...

https://www.quora.com/How-often-are-seniors-in-nursing-homes-under-monitored/answer/Tirumalai-Kamala