text:
Atomic force microscope
Atomic nanoscope
Atom probe
Ballistic conduction
Bingel reaction
Bio-nano generator
Bionanotechnology
Break junction
Brownian motor
Bulk micromachining
Carbon nanotube
CeNTech
Chemical Compound Microarray
Colloid
Comb drive
Computronium
Coulomb blockade
Dielectrophoresis
Dip Pen Nanolithography
DNA machine
Ecophagy
Electrochemical scanning tunneling microscope
Electron beam lithography
Electrospinning
Engines of Creation
Exponential assembly
Femtotechnology
Fermi point
Fluctuation dissipation theorem
Fluorescence interference contrast microscopy
Fullerene
Fungimol
Gas cluster ion beam
Hacking Matter
History of nanotechnology
Hydrogen microsensor
Inorganic nanotube
Ion-beam sculpting
Kelvin probe force microscope
Lab-on-a-chip
Langmuir-Blodgett film
LifeChips
List of nanoengineering topics
List of nanotechnology applications
List of nanotechnology topics
Lotus effect
Magnetic force microscope
Magnetic resonance force microscopy
Mechanochemistry
Mechanosynthesis
MEMS thermal actuator
Mesotechnology
Micro Contact Printing
Microelectromechanical systems
Micromachinery
Molecular assembler
Molecular logic gate
Molecular manufacturing
Molecular motors
Molecular recognition
Nano-abacus
Nanoart
Nanocar
Nanochemistry
Nanocomputer
Nanocrystal
Nanocrystalline silicon
Nanocrystal solar cell
Nanoelectrochemistry
Nanoelectrode
Nanoelectromechanical systems
Nano-emissive display
Nanoengineering
Nanoethics
Nanofactory
Nanoimprint lithography
Nanomanufacturing
Nanomaterial based catalyst
Nanomorph
Nanomotor
Nano-optics
Nanoparticle
Nanoparticle tracking analysis
Nanopore
Nanoprobe
Nanorobot
Nanorod
Nanoscale
Nano-Science Center
Nanosensor
Nanoshell
Nanosight
Nanosocialism
Nanostructure
Nanotechnology education
Nanotechnology in fiction
Nanotoxicity
Nanovid microscopy
Nanowire
National Nanotechnology Initiative
Neowater
Niemeyer-Dolan technique
Ormosil
Picotechnology
Quantum heterostructure
Quantum point contact
Quantum solvent
Quantum well
Quantum wire
Royal Society's nanotech report
Scanning gate microscopy
Scanning probe lithography
Scanning voltage microscopy
Self-assembled monolayer
Self reconfigurable
Self-Reconfiguring Modular Robotics
Self-replication
Smart dust
Smart material
Soft lithography
Spin polarized scanning tunneling microscopy
Stone Wales defect
Supramolecular assembly
Supramolecular chemistry
Supramolecular electronics
Surface micromachining
Surface plasmon resonance
Synthetic molecular motors
Synthetic setae
Tapping AFM
There's Plenty of Room at the Bottom
Transfersome
Utility fog
http://en.wikipedia.org/wiki/Molecular_logic_gate
A molecular logic gate in nanotechnology is a logic gate on a molecular level. Much academic research is dedicated to the development of these systems and several prototypes now exist. Because of their potentional utility in simple arithmetic these systems are also called moleculators.
Molecular logic gates work with input signals based on chemical processes and with output signals based on spectroscopy. One of the earlier water solution-based systems exploit the chemical behavior of compounds A and B in scheme 1 [1].
Compound A is a push-pull olefin with the top receptor containing four carboxylic acid anion groups (and non-disclosed counter cations) capable of binding to calcium. The bottom part is a quinoline molecule which is a receptor for hydrogen ions. The logic gate operates as follows.
Without any chemical input of Ca2+ or H+, the chromophore shows a maximum absorbance in UV/VIS spectroscopy at 390 nm. When calcium is introduced a blue shift takes place and the absorbance at 390 nm decreases. Likewise addition of protons causes a red shift and when both cations are in the water the net result is absorption at the original 390nm. This system represents a XNOR logic gate in absorption and a XOR logic gate in transmittance.
In compound B the bottom section now contains a tertiary amino group also capable of binding to protons. In this system fluorescence only takes place when both cations are present and therefore the system represents an AND logic gate.
With both systems run in parallel and with monitoring of transmittance for system A and fluorescence for system B the result is a half-adder capable of reproducing the equation 1+1=2.
In a modification of system B not two but three chemical inputs are simultaneously processed in an AND logic gate [2].An enhanced fluorescence signal from the compound depicted below is obtained only in the presence of hydrogen, zinc and sodium ions through interaction with respectively the amine, carboxyl and crown ether receptors and this system can be potentially applied in disease screening (lab-on-a-molecule) because these ions are all physiologically relevant.
In another XOR logic gate system the chemistry is based on the pseudorotaxane [3] depicted in scheme 3. In organic solution the electron deficient diazapyrenium salt (rod) and the electron rich 2,3-dioxynaphthalene units of the crown ether (ring) self-assemble by formation of a charge transfer complex.
An added tertiary amine like tributylamine forms a 1:2 adduct with the diazapyrene and the complex gets dethreaded. This process is accompanied by an increase in emission intensity at 343 nm resulting from freed crown ether. Added trifluoromethanesulfonic acid reacts with the amine and the process is reverted. Excess acid locks the crown ether by protonation and again the complex is dethreaded.
A full adder system based on fluorescein [4] is able to compute 1+1+1=3.
↑ Proof-of-Principle of Molecular-Scale Arithmetic A. Prasanna de Silva and Nathan D. McClenaghan J. Am. Chem. Soc.; 2000; 122(16) pp 3965 - 3966; Abstract
↑ Communicating Chemical Congregation: A Molecular AND Logic Gate with Three Chemical Inputs as a "Lab-on-a-Molecule" Prototype David C. Magri, Gareth J. Brown, Gareth D. McClean, and A. Prasanna de Silva J. Am. Chem. Soc.; 2006; 128(15) pp 4950 - 4951; (Communication) Abstract
↑ Logic Operations at the Molecular Level. An XOR Gate Based on a Molecular Machine Alberto Credi, Vincenzo Balzani, Steven J. Langford, and J. Fraser Stoddart J. Am. Chem. Soc.; 1997; 119(11) pp 2679 - 2681; (Article) Abstract
↑ A Molecular Full-Adder and Full-Subtractor, an Additional Step toward a Moleculator David Margulies, Galina Melman, and Abraham Shanzer J. Am. Chem. Soc.; 2006; 128(14) pp 4865 - 4871; (Article) DOI: 10.1021/ja058564w
Retrieved from "http://en.wikipedia.org/wiki/Molecular_logic_gate"
Categories: Logic gates | Nanotechnology


text:
from __future__ import unicode_literals

from django.db import models, migrations

def create_variant_type_module(apps, schema_editor):
    VariantType = apps.get_model('release', 'VariantType')
    VariantType.objects.create(name='module')

class Migration(migrations.Migration):

    dependencies = [
        ('release', '0006_auto_20160512_0515'),
    ]

    operations = [
        migrations.RunPython(create_variant_type_module),
    ]

redpajama_set_name: RedPajamaGithub


PCB Assembly & Components - Hemeixin Electronics Co.,Ltd.
Quote is based on RFQ Data provided at the time of this quote and is subject to change if data has changed at the time of order. We do not perform a full DFM analysis nor do we identify all the issues at the time of quoting. For turnkey quotes, the availability of components varies every day; and we do not guarantee that all the components will be readily available at the time of order without any lead-time issues.
Consigned parts shortage: If regardless of shortage, customer has asked us to proceed to the assembly phase and if customer does not send the parts within 2 days of starting the order, then we will complete all assemblies with whatever components were consigned to us, and all assemblies (including shortage assemblies) will be shipped and invoiced as per order, and the order would be deemed to be completed. Subsequently, if the customer ships the shortage assemblies with the shortage parts to us for rework, such rework assembly would be performed by HemeixinPCB at a suitable rework charge to be determined by HemeixinPCB.
Turnkey parts shortage: where it is known that some parts cannot be quickly procured due to unavailability or long lead times or other reasons, and customer specifically asks us to start the job nevertheless, such assemblies (including shortage assemblies) will be shipped and invoiced as per order, and the order would be deemed to be completed. When HemeixinPCB receives the ordered long lead-time components, customer may EITHER elect to ship those parts shipped to them (in which case no additional rework is involved); OR customer may send the shortage assemblies BACK to HemeixinPCB for completion rework (Rework & Re-Shipping charges will apply).
Assembly data : Completeness of Assembly data: It is customer's responsibility to provide complete and correct assembly data, BOM in excel spreadsheet, Assembly Gerbers, assembly drawings, Special instructions if any, and XY Pick and Place Data for SMT parts. If customer is unable to provide correct XY Data, additional charges will apply.
Discrepancy in data: Customer is responsible for providing data that is consistent and has no discrepancy in information. HemeixinPCB tries to identify any discrepancies in customer data but will not be responsible if some discrepancy is not caught. Any issues caused due to such discrepancy in customer data is solely customer's responsibility.
Turn Time: Assembly Turn Time will start when the kit is complete AND all assembly data related issues are resolved.
On-Time: HemeixinPCB may make partial shipments for your order. You order will be considered shipped on-time if at least 90% of assemblies are shipped by the due date.
Order Completeness: Orders may be considered complete, if the quantity shipped is within +/- 5% of the original quantity.
If you have asked for a consigned assembly (or partial turnkey) quote, then at the time of placing the order you will be sending us the components for assembly. Please note our requirements for kitting the components.
4. Insufficient attrition will be construed as parts shortage.
5. All consigned parts must be shipped to us in a properly kitted form (each line item of BOM in a separate bag, properly marked for identifying the component unambiguously).


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World War 3 Something Went Wrong – How To Fix
World War 3 Something Went Wrong: The Farm 51 created the tactical first-person shooter game called World War 3. The game takes place in an imagined universe where different circumstances led to a third global war, as its name suggests.
The World War 3 creators aimed to capture the conflict as accurately as they could. They did that by putting into use tools, techniques, and equipment that were directly derived from the real world.
Many World War 3 gamers, however, are having trouble customising their characters while playing games.
"Something went wrong" during World War 3. mistake after selecting "Customize"
The problem arises when players try to use the customisation menu to change their character's loadout in the middle of a game.
Users will see the error message "Something went wrong" after choosing the "Custom" option.
The error message causes the game to crash and start again from scratch. You are so expelled from the game, which may be considered an abandonment.
With the modification, World War 3 already caused issues in January. However, that particular time, while attempting to completely create a match or when selecting a custom match, error messages were displayed.
The business at that time indicated that they were conscious of the problem and were addressing it.
Already Working on a Solution:
The World War 3 devs have acknowledged that they're all conscious of the problem with character customisation not being possible during a match.
However, there are currently no specifics on the anticipated release timing for a patch. We will keep this article up-to-date with any fresh information as soon as it becomes available.
How to Fix "Something Went Wrong" in World War 3:
The entire planet is your battlefield in the tactical multiplayer online FPS game World War 3.
With a vast selection of weapons, machines, tools, and drone at your fingertips, you can outgun the opposition in thrilling team-based battles.
However, a number of users report having gameplay and technical problems.
Are you receiving a World War 3 "something went wrong" error?
Many players experience the same error.
"[151] Something Went Wrong" is the Full Error Message:
In this post, we'll talk about the causes of the World War 3 "Something went wrong" issue and how to remedy it.
Why Did Anything Go Wrong And Cause World War 3 Error?
You experience error 151. Due to the World War 3 game's overloaded server or excessive player count, something went wrong and caused an error.
Additionally, it's conceivable if World War 3 is undergoing maintenance.
Many players attempt to join the WW3 game concurrently.
The WW3 network is overload due to traffic strain.
The WW3 infrastructure is under pressure from heavy traffic.
How to Uninstall World War 3 Games Yourself Easily
Underwater Map Overwatch 2 – New Map
Bai Yi Path to Nowhere Wiki Guide and Review

redpajama_set_name: RedPajamaCommonCrawl


All Paul McCartney items listed below are authentic and very limited. We do not carry multiple items. All prices and availability are subject to change. All prices include shipping and handling for all USA customers. All other destinations will require actual shipping cost to complete transaction. Have a question? Ask us before purchasing the item. Thank You.
Description: 1989 Paul McCartney World Tour Band Laminate. Official Tour laminate owned and used by sound engineer David "Cowboy" Conyers. Front and back pass displayed.
NOTE: Item is VG+ condition and has a photo of Cowboy under laminate.
Laminate comes with nylon landyard.
Description: Paul McCartney World Tour promo Tour Book. This book was handed out at the end of each show. Photos and insight of the tour and Paul McCartney.
Description: 7x9 full color Paul McCartney 2001 Japanese concert handbill.
Description: Paul McCartney 1988 Club Sandwich University of Sussex. 11x17 color cover BW pages. Full Paul McCartney issue.
Note: Is folded, creased in the middle. Overall VG+ condition.
Description: Paul McCartney Rock magazine foldout poster.
Note: This item VG+ condition. Comes folded, has creases.
Description: Paul McCartney Band On The Run 25th Anniversary Promo Poster.
Note: This item VG condition. Some wear, creases, bottom gray is folded.


text:
La glossodynie, appelée aussi syndrome de la bouche brûlante ou syndrome de la langue de feu , est une douleur au niveau de la langue qui se situe le plus souvent sur la pointe ou les bords de la langue. La glossodynie est une forme topographique particulière de stomatodynie qui a des origines diverses : glossite, trouble psychosomatique ou inconnue. La glossodynie est classée dans les paresthésies buccales psychogènes, symptômes d'une dépression.

Leur physiopathologie demeure mal comprise, mais les glossodynies pourraient correspondre à une neuropathie.

La fréquence des glossodynies est estimée entre 0,7 et 4,6 % de la population générale. La douleur est décrite comme une brûlure chronique, souvent accompagnée d'un cortège de manifestations fonctionnelles (picotements, sensation de bouche sèche, troubles du goût…). Les douleurs augmentent progressivement au fur et à mesure de la journée, sont majorées par le stress mais disparaissent pendant le sommeil et sont améliorées pendant les repas.

Le retard diagnostique est fréquent et source d'anxiété pour le patient, entraî-nant une multiplication des consultations médicales et une majoration de l'intensité des douleurs.

La prise en charge des glossodynies est complexe. La reconnaissance de la réalité des douleurs est fondamentale pour le patient. Le traitement médicamenteux peut faire appel à des traitements médicamenteux, ou des traitements locaux
. Certaines personnes ont la langue de feu après avoir consommé du Roquefort ou des fruits moisis.

Notes et références

Voir aussi

Article connexe
 Paresthésie

Liens externes
 Association langue de feu consacré à la glossodynie
 Forum consacré à la glossodynie et stomatodynie

Terme médical
Maladie des muqueuses
Symptôme en dermatologie

redpajama_set_name: RedPajamaWikipedia


text:
Los Gatos Priest Confronted By 2nd Alleged Victim; Beating Trial Delayed
Filed Under:Assault, Beating, Catholic, Crime, Jerold Lindner, Los Gatos, Mike Colgan, Priest Abuse, Religion, Sex abuse, Will Lynch, William Lynch
Will Lynch seen outside the courtroom (CBS) Will Lynch seen outside the courtroom following a previous day's hearing. (CBS)
SAN JOSE (KCBS) – The judge overseeing the trial of a man accused of beating a Los Gatos priest Jerold Lindner sent the jury delayed testimony in the case because of legal questions over whether the cleric may have perjured himself on the witness stand.
Lindner testified on Wednesday that he did not molest William Lynch, the man facing felony assault and elder abuse charges for allegedly attacking him at a retirement home.
Thursday morning, yelling could be heard outside the courtroom as a witness in the case, who claimed Lindner had also abused her as a child, confronted Lindner in the hallway as he was about to enter the courtroom.
KCBS' Mike Colgan Reports:
Inside the courtroom, Judge David Cena sent jurors home, saying the trial needed to be halted temporarily because there were significant issues in the case that have to be discussed in chambers. He did not say what those issues were, but there was speculation that Lindner may have perjured himself.
On Wednesday, defense attorney Pat Harris said he would "make sure" that Lindner was charged with perjury after Deputy District Attorney Vicki Gemetti told the jury in her opening statement that Lindner would probably lie by denying he molested Lynch.
When Lindner later took the witness stand Wednesday, he indeed denied having molested Lynch or his brother.
Lynch claims Lindner raped him and his brother during a church camping trip in 1975 when the boys were 7 and 4 years old.
Lynch and his brother settled a civil lawsuit with the Jesuits in 1998 related to the alleged abuse, and Harris said the settlement included an agreement that Lindner would admit to the abuse and apologize for it.
However, the settlement is not legally an admission of guilt and it is unclear whether a perjury charge would stand up in court.
There was also speculation that Lindner is refusing to testify further.
A number of Lynch's supporters gathered outside the courthouse this morning, talking, holding hands and carrying signs, some of which read "Vatican Stop the Cover-Up."
Some in the group said Lindner also abused them, and some claimed to have been on the camping trip in the 1970s on which Lynch says Lindner raped and sodomized him and forced him to have sex with his 4-year-old brother.
Deb Lukas, the woman who confronted Linder and yelled at him outside of court Thursday morning, was also part of the group.
Standing in a circle with other Lynch supporters, she embraced Lynch's sister Amanda, who told Lukas she was proud of her.
"I talked to who I needed to talk to," Lukas said. "He hasn't seen me for 30 years. He had to look me in the eye today."
Lynch's attorney has denied that her client intended to assault Lindner when he confronted the priest in May, 2010, and said jurors should question the credibility of his testimony.
The judge said testimony would not resume until 1:30 p.m. Friday while the questions surrounding that unusual legal maneuver were investigated.


text:
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NCBI Bookshelf. A service of the National Library of Medicine, National Institutes of Health.
National Research Council (US) Committee on Diet and Health. Diet and Health: Implications for Reducing Chronic Disease Risk. Washington (DC): National Academies Press (US); 1989.
Diet and Health: Implications for Reducing Chronic Disease Risk.
National Research Council (US) Committee on Diet and Health.
Washington (DC): National Academies Press (US); 1989.
Hardcopy Version at National Academies Press
26Dental Caries
Dental caries is the localized demineralization of the tooth surface caused by organic acid metabolites of oral microorganisms such as Streptococcus mutans. The disease leads to a chronic, progressive destruction of the teeth.
The prevalence of dental caries is most often expressed as dmft (decayed, missing, and filled teeth) for primary dentition and DMFT for permanent teeth (Barmes and Sardo-Infirri, 1977). Internationally, prevalence rates of dmft in 6-year-olds and DMFT in 12-year-olds range from a high of 9.3 per child in Japan and 10.6 per child in Switzerland, respectively, to a low of 0.9 per child in Cameroon and 0.1 in Zambia, respectively. U.S. prevalence rates are intermediate; dmft in 6-year-olds is 3.4 per child and DMFT in 12-year-olds is 4.0 per child (Sreebny, 1982a).
Caries prevalence in the United States has declined in the past 30 years. During 1971-1974, children from 5 to 17 years of age had decay or fillings in an average of 7.06 teeth. By 1981 this number had dropped to 4.77, a 32% decrease (NIDR, 1981). Caries of the tooth crown is still predominantly a disease of children and adolescents, although caries of the root surface of the teeth, secondary to exposure of the root by recession of the gingivae, is becoming more prevalent among older adults (Miller et al., 1987). Less is known about the causes of root caries than about caries of the tooth crown, but possible risk factors include increased longevity of the population and longer retention of teeth in adults (Carlos, 1984).
Although declining in prevalence, dental caries in the United States remains a significant health problem. Rates are highest in the Northeast, lowest in the Southwest, and at intermediate levels elsewhere (NIDR, 1981). Prevalence rates are highest in females of every age group (NIDR, 1981) and in people of both sexes in the lower socioeconomic groups (Ismail et al., 1987). The estimated costs of dental care in the United States amounted to $25.1 billion in 1984, or 6.5% of total health care costs (Levit et al., 1985). In 1990, the costs are projected to be as high as $42 billion (Arnett et al., 1986).
Evidence Associating Dietary Factors with Dental Caries
The relationship of diet to dental caries risk was suspected as early as the fourth century B.C., when Aristotle hypothesized that dental caries was caused by consumption of sweet figs, which stuck to the tooth (Forster, 1927). Current evidence from studies in humans and animals indeed indicates that dental caries does not develop in the absence of fermentable carbohydrates in the diet (Brown, 1975). Evidence also suggests that the cariogenic effect of fermentable carbohydrates can be amplified or attenuated by other dietary factors as well as by oral microflora and host factors (e.g., genetic susceptibility and the composition and flow of saliva). However, as McDonald (1985a) points out, even after 23 centuries we know only a little more than Aristotle about the relative cariogenicity of foods.
Epidemiologic and Clinical Studies
Among the major carbohydrates in the diet—complex carbohydrates (e.g., starches) and simple sugars (e.g., sucrose and lactose)—sucrose appears to have the greatest cariogenic potential. Using data collected by the World Health Organization, Sreebny (1982a) reported a correlation coefficient of .72 between sugar availability in grams per person per day and DMFT in 12-year-old children in 47 countries. However, the correlation coefficient for dmft in 6-year-old children in 23 countries was only .31. Takeuchi (1961) provided time-trend data supportive of Sreebny's cross-sectional findings and reported that the prevalence of dental caries in Japanese children decreased precipitously during the late 1940s in association with the severe reduction in sugar supplies during World War II. Similar observations were made in Europe (Sognnaes, 1948; Toverud, 1957). In the United States, correlation analyses of time-trend data on per-capita sugar consumption and caries incidence suggest (1) that caries incidence increases when per-capita sugar consumption exceeds 40 g/day in the absence of fluoride use and 50 g/day when fluoride is used and (2) that the increase in caries incidence reaches a plateau when the per-capita consumption reaches approximately 130 g/day (Lehner, 1980; Newbrun, 1982; Sheiham, 1983, 1984; Sreebny, 1982b). As Glinsmann et al. (1986) noted, these data suggest that the current mean intake of added and total sugars in the United States (53 and 95 g/day, respectively) contributes substantially to overall caries risk and that reduction in sugar intake could be expected to reduce that risk. However, findings of other studies indicate that the correlation between sugar intake and caries occurrence is not entirely consistent. For example, caries incidence in Great Britain did not change appreciably from 1940 to 1977, despite an apparent doubling of sugar intake (Jackson, 1979). Likewise, the 32% decline in caries prevalence in the United States in the 1970s appears to have occurred despite a continued high intake of sugars. A similar observation was made in a study by DePaola et al. (1982), who noted that caries incidence in Massachusetts schoolchildren dropped markedly during a period in which total sugar consumption increased and then leveled out. Although total sugar consumption increased during the study period, however, the amount of sucrose consumed actually decreased.
Sucrose in solution stimulates the formation of plaque (Geddes et al., 1978)—a substance comprising microbial colonies embedded in a matrix of salivary proteins and extracellular polymers, which may serve as a medium for growth of caries-promoting bacteria. It also increases the mineral content of plaque and saliva, suggesting increased mineral resorption from the teeth (Tenovuo et al., 1984). Frequent rinsing with a sucrose solution over 2 months produced changes characteristic of early demineralization of tooth surfaces (Geddes et al., 1978). Small slabs of bovine enamel attached to human teeth for short periods also underwent demineralization when frequently exposed to sucrose (Pearce and Gallagher, 1979; Tehrani et al., 1983).
Sucrose in foods is also cariogenic. In a clinical trial at the University of Turku in Finland (Scheinin et al., 1975a,b), three groups consuming diets containing sucrose, fructose, and xylitol, respectively, were followed for 2 years. By the study's end, the average number of decayed, missing, or filled tooth surfaces (DMFS) was twice as high in the group consuming sucrose than in the fructose group. The xylitol group had virtually no DMFS. The lower cariogenicity of fructose relative to sucrose may explain in part the inability of some studies to demonstrate a cariogenic potential of presweetened foods such as cereals (Finn and Jamison, 1980; Glass and Fleisch, 1974), which differ considerably in their content of specific sugars (Glinsmann et al., 1986). The decline in caries prevalence in the United States since the 1970s, despite a continued high consumption of total sugars, may be partially due to the nation's increasing consumption of corn-derived sweeteners such as fructose and the declining use of sucrose (Glinsmann et al., 1986).
The composition of dietary carbohydrate also appears to influence cariogenicity. Early enamel erosion, a risk factor for caries, was noted in 12 children ages 9 to 15 years who had consumed large quantities of soft drinks (Asher and Read, 1987). The authors concluded that a major contributing factor was the high citric acid content and resulting low pH of the drinks. Consumption of canned pears and apples has also been noted to lower plaque pH—a factor believed to promote tooth demineralization (Shaw, 1987)—to a greater degree than sugar alone (Abelson and Pergola, 1984; Imfeld et al., 1978; Jensen and Schachtele, 1983). Likewise, comparisons of snack foods commonly consumed in the United States and in the United Kingdom demonstrate a wide variability in their ability to increase plaque and salivary acidity (Bibby et al., 1986; Edgar et al., 1975). In these studies, the sugar-to-starch ratio of the snack foods appears to be important, since some items low in sugar but high in starch caused a more severe and prolonged increase in plaque and saliva acidity than snacks high in sugar alone (Bibby et al., 1986; Mörmann and Mühlemann, 1981). The degree of plaque and salivary acidification does not necessarily correlate with the amount of enamel destruction that follows or with the extent of subsequent caries (McDonald, 1985a).
The sequence in which carbohydrate-containing foods are eaten also appears to influence cariogenesis. For example, a sharp decrease in the pH of saliva and plaque has been noted after use of a sugar rinse. The pH returns to baseline after approximately 30 minutes. However, when cheese is consumed 5 minutes after a sugar rinse, the sharp increase in acidity is blunted and the pH returns quickly to baseline (Edgar, 1981; Edgar et al., 1982; Schachtele and Jensen, 1983).
The frequency of carbohydrate consumption also appears to influence caries formation. In a classic cohort study conducted in a mental institution in Vipeholm, Sweden, the frequency of dental caries activity in adult patients was monitored over several years while their diet and eating schedule were controlled. Two important findings were noted. First, dental caries appeared to be influenced more by frequency of sucrose intake than by total amount consumed. Second, solid forms of sugar, which are more easily retained in teeth, appear to be more cariogenic than liquid forms of sucrose (Gustafsson et al., 1952).
In general, epidemiologic and clinical findings support the notion that all dietary carbohydrates are cariogenic to some degree and that cariogenesis is influenced not only by the composition of carbohydrate-containing foods but also by the sequence and frequency with which they are consumed. Beyond this, there are two basic reasons why little is known about the cariogenic potential of specific carbohydrate-containing foods: (1) because of cost and ethical considerations, few studies of specific foods and caries in humans have been or will be conducted and (2) findings from such studies are difficult to generalize to noninstitutionalized humans. Furthermore, it is probably not possible to develop a valid cariogenic index for individual foods, since studies of caries incidence comparing groups consuming and not consuming various food items show little effect due to the strong cariogenic challenge from the rest of the diet (McDonald, 1985a).
Certain foods appear to be protective. As noted previously, consumption of cheese blunts the drop in pH characteristically seen after a sugar rinse (Edgar, 1981). Regular milk consumption by 14-year-old Danish schoolchildren was associated with a lower incidence of caries, but regular milk consumption was a marker of a better diet and could also have been an indicator of better preventive dental care (Hölund, 1987). Consumption of salted peanuts and cheddar cheese increases oral alkalinity (Geddes et al., 1977; Imfeld et al., 1978; Jensen and Schachtele, 1983)—a factor believed to protect against caries formation. Cocoa also contains substances that inhibit oral acidification (Paolino, 1982). Starchy fibrous foods require increased mastication and may inhibit cariogenesis by stimulating saliva and maintaining neutral plaque pH (Krasse, 1982). Studies suggest that polyols (sugar alcohols, including the 6-carbon sorbitol and 5-carbon xylitol) are noncariogenic and possibly even anticariogenic. Sorbitol-containing chewing gum, unlike sugar-containing gum, does not appear to promote tooth decay in children (Glass, 1983). Also, as noted earlier, the group on the xylitol diet in the University of Turku study had no DMFS. That finding was attributed to the fact that xylitol is not metabolized by oral microbes (Scheinin, 1976; Scheinin et al., 1975a,b). Substitution of xylitol for sucrose in many Finnish food products has been associated with a dramatic decrease in caries incidence over a 2-year period (Scheinin et al., 1975b). Similarly, the use of xylitol-containing chewing gum was associated in one study with low caries incidence, even in subjects who did not otherwise modify their diets. This led the authors to hypothesize that xylitol is actively anticariogenic rather than noncariogenic (Scheinin et al., 1975c).
With the exception of data on fluoride, there are few data relating dietary components to caries risk in humans. Several investigators have found a beneficial effect of supplemental vitamin D in children up to the age of 10 (McDonald, 1985b) and have suggested that the optimal daily intake is approximately 400 IU (Shaw, 1952). However, other studies have produced conflicting findings (Navia, 1970). As a result, the relationship of vitamin D to caries risk remains unresolved (McDonald, 1985b).
Of all dietary components exhibiting a protective effect against caries, the most effective is fluoride. In the 1930s, large-scale epidemiologic trials conducted in several suburban Chicago communities and later in 21 cities in four states demonstrated a strong inverse association between natural fluoride concentrations in community water supplies and DMFT prevalence in children ages 12 to 14 years (Dean et al., 1941, 1942). In these studies, DMFT prevalence was found to be approximately 60% lower in populations drinking water with natural flouride concentrations of 1 part per million (ppm) during tooth development than in populations consuming little or no fluoride. Once it was determined that the 1 ppm concentration of fluoride in drinking water is both optimal and safe and that the benefit of fluoride ingestion persists into middle age, a decision was made to undertake a large community trial in which water was fluoridated in three communities in North America (Grand Rapids, Michigan; Newburgh, New York; and Brantford, Ontario). A 50 to 60% reduction in caries prevalence was observed in all three communities, and no major adverse effects were noted in residents of any age (McClure, 1970). The findings from these and subsequent large-scale community trials led the American Dental Association and the U.S. Public Health Service in 1950 to endorse widespread fluoridation of the water supply as a preventive measure against dental caries (Schrotenboer, 1981). At present, approximately 130.8 million people in the United States are drinking water from public supplies with either natural fluoride at optimal levels (i.e., 0.7 to 1.2 ppm, depending on ambient temperature) or with fluoride added to meet optimal levels (T. Reeves, Centers for Disease Control, personal communication, 1987).
Ingestion of fluoride at such levels reduces caries risk in people of all ages. For example, consumption of optimally fluoridated water has been associated with an almost 50% reduction in caries incidence in children (Burt et al., 1986; Driscoll et al., 1981) as well as a reduced risk of root caries in adults (Anonymous, 1987; Stamm and Banting, 1980). Consumption of fluoridated water before the emergence of permanent molars appears most effective—producing an average risk reduction of 50 to 60%, which continues for the lifetime of the teeth as long as fluoride intake is maintained (Deatherage, 1943). If fluoride intake is discontinued, caries become more prevalent, but not to the degree that would be expected if there had been no previous exposure to fluoride (Lemke et al., 1970; Weatherell et al., 1977).
Although fluoridated water has been shown to be an effective, safe, and low-cost means of reducing caries risk in the general population, more than 45% of the U.S. population continues to drink water with less than optimal levels of fluoride (T. Reeves, Centers for Disease Control, personal communication, 1987). To address this need, the American Dental Association, the American Academy of Pediatrics, and the American Academy of Pediatric Dentistry have issued guidelines on fluoride supplementation for children receiving less than adequate levels of fluoride in their drinking water (see Table 26-1).
TABLE 26-1
Recommended Daily Fluoride Supplements for Children in Three Age Categories, Based on Fluoride Concentration in the Water Supply.
The extent of dietary fluoride supplementation in the United States is not known. In a 1982 survey of 4,000 dentists and 2,000 pediatricians, only 60% of the dentists and 70% of the pediatricians who responded reported prescribing dietary fluoride supplements (Gift and Hoerman, 1985). These figures are comparable with those of an earlier survey in which 81% of pediatricians and 63% of family physicians reported prescribing supplements (Margolis et al., 1980). The lower proportion of prescribers among dentists in both surveys may reflect a smaller number of children under age 2 in dentists' practices or a bias resulting from the survey's relatively low response rates, e.g., 75% and 49% among dentists and physicians, respectively, in the 1982 survey (Gift and Hoerman, 1985).7
The mechanism by which fluoride protects against root and surface caries is not well understood (Brown and König, 1977; Seichter, 1987). Since fluoride is found in enamel as well as in dentin, it is believed to inhibit caries formation primarily by promoting remineralization of early demineralized areas of the tooth (Driscoll, 1985; Silverstone, 1984) and by exerting an antimicrobial effect, thus suppressing cariogenic oral microflora (Shaw, 1987).
Fluoride is absorbed both systemically and topically (Brown et al., 1977; Ericsson, 1977; Weatherell et al., 1977). During tooth development, systemic fluoride appears to be incorporated into the tooth structure (Sognnaes, 1965; Weatherell et al., 1977). After tooth formation, fluoride is incorporated into the surface crystalline structure of the tooth, primarily through topical agents such as fluoridated water and dentifrices (Weatherell et al., 1977).
Overconsumption of fluoride during tooth development can lead to dental fluorosis characterized by mottling of the tooth surfaces. Consumption of water fluoridated at 1 ppm rarely results in clinical fluorosis of either the teeth or skeleton (Carr et al., 1985); however, other fluoride sources can add to overall fluoride load. For example, fluoride in the food chain is believed to contribute on average 0.2 to 0.6 mg of fluoride per person per day. Foods especially rich in fluoride include chicken, seafoods, and brewed tea (tea can contain as much as 1 to 4 mg of fluoride per cup) (Levy, 1986; McClure, 1970; Newbrun, 1975; Richmond, 1985). Fluoride can also be unintentionally ingested from fluoridated dentifrices, which can provide an average daily fluoride intake of as much as 0.3 mg for children under age 5 (Barnhart et al., 1974). Concern has also been expressed about the elevated fluoride levels in some baby formulas and foods (Adair and Wei, 1978; Singer and Ophaug, 1979). Because fluoride levels can vary considerably with the type of formula or food and where it is processed, manufacturers of infant formulas have reduced levels in their products (American Dental Association Council on Dental Therapeutics, 1984).
Overall, however, as noted in a review by Richmond (1985), the amount of fluoride ingested from foods and from the supervised use of fluoridated dentifrices is small, and when combined with levels in optimally fluoridated drinking water, is well within the margin of safety defined by the American Dental Association Council on Dental Therapeutics (1984). The large data base on fluoride indicates that consumption of optimal levels of fluoride substantially reduces caries incidence with little risk of side effects (e.g., dental fluorosis) and that the growing availability of fluoridated water is probably responsible for much of the decline in caries incidence in the United States over the past 15 to 20 years (Dunning, 1979).
Results of animal studies on dietary carbohydrate and cariogenesis are consistent with those of studies in humans. In rats, for example, the incidence of caries increases with increases in the amounts of sucrose added to the diet; a cariogenic effect is seen at levels as low as 0.1% by weight of diet (Michalek et al., 1977). An increase in caries incidence with increasing sucrose dose has been observed at levels ranging from 8% (Kreitzman and Klein, 1976) to 40% of dietary sucrose (Hefti and Schmid, 1979). The cariogenic potential of sucrose is greater than that of equivalent amounts of glucose, fructose, or invert sugars (a mixture of dextrose and fructose obtained by hydrolyzing sucrose) (Birkhed et al., 1981; Horton et al., 1985).
As in humans, the cariogenicity of dietary carbohydrates in animal models appears to be influenced by the frequency, form, and composition of the diet. For example, frequent consumption of carbohydrates markedly accelerates caries formation in rats (Firestone et al., 1982; Skinner et al., 1982). Studies of the cariogenic potential of various forms of dietary carbohydrates in rats indicate that certain carbohydrate-containing foods, such as bananas, are much more cariogenic than sucrose alone or even sucrose-topped chocolate fed frequently in meals (Shrestha and Kreutler, 1983). Consumption of a cereal base with added sugar caused fewer caries in rats than did consumption of presweetened cereals with equal sucrose levels (McDonald and Stookey, 1977). Likewise, carbohydrates in the form of maize or wheat starch had virtually no cariogenic activity when consumed by gnotobiotic rats and macaques, respectively (Beighton and Hayday, 1984; Horton et al., 1985).
Studies of dietary composition in rats indicate that addition of certain cheeses (e.g., cheddar cheese) to a cariogenic diet protects against buccal (cheek side) decay both alone (Edgar et al., 1982; Harper et al., 1986) and with sulcal caries (toward the linear depression in the occlusal surface of the tooth) (Rosen et al., 1984). Other dietary substances inhibiting sucrose cariogenicity in animal models include mineral concentrates containing protein, calcium, and phosphate (Harper et al., 1987); cocoa (Paolino, 1982); and xylitol (Leach and Green, 1981; Shyu and Hsu, 1980) in rats; and saccharin in inbred hamsters (Linke, 1980). The mechanisms by which these items inhibit sucrose cariogenicity in animal models are not clearly understood, but may include enzyme inhibition in oral bacteria (Paolino, 1982); stimulation of saliva, which helps to maintain plaque pH in a neutral range (Krasse, 1982); and the influence of the texture and casein or calcium-phosphate content of cheeses (Harper et al., 1986).
The cariogenicity of other dietary components, including protein, vitamin D, niacin, pyridoxine, calcium, phosphorus, and certain trace elements, has also been investigated in animal studies. Offspring of rats fed marginal protein diets during pregnancy and lactation developed molars that were much more prone to caries than offspring of rats fed adequate protein diets (Shaw and Griffiths, 1963). Shaw (1987) hypothesized that the decreased amount and altered protein content of saliva in the protein-depleted rats may account for part of their increased caries susceptibility. Other studies have shown that children with protein-calorie malnutrition have not only a high rate of caries but also reduced salivary levels of immunoglobulin A (IgA), the predominant immunoglobulin in body secretions (McMurray et al., 1977; Reddy et al., 1976). McDonald (1985b) hypothesized that protein malnutrition disturbs IgA salivary concentration, thereby increasing caries risk.
In one early study in puppies, vitamin D deficiency was shown to disturb the rate of tooth eruption, tooth position, and calcification of enamel on permanent teeth (Mellanby, 1918). The B-complex vitamins niacin and pyridoxine were also shown in early studies to modify cariogenesis in animals; however, unlike vitamin D, their effect did not appear to be systemic. Niacin was believed to promote caries formation in the Syrian hamster by stimulating oral microflora (Orland et al., 1950). Unlike niacin, pyridoxine seemed to suppress caries formation in animals (Strean et al., 1956) and in humans (Strean, 1958). The paucity of more recent evidence on these vitamins suggests that neither plays a major role in cariogenesis.
The roles of calcium and phosphorus, both major constituents of teeth, were also the subject of early research (McDonald, 1985b). Reduction of dietary calcium in rats was shown to increase caries risk (Constant et al., 1954; Gustafson et al., 1963), whereas the addition of calcium chloride, calcium gluconate, or phosphorus decreased risk (Gustafson et al., 1964; Stanmeyer, 1963). There has been no confirmation of these findings, however. A number of trace elements, including aluminum, barium, boron, cadmium, copper, lead, and selenium, have also been examined for cariostatic potential, but again, no definitive data have been obtained (Losee and Ludwig, 1970).
Animal studies support findings in humans that dietary carbohydrates, especially sucrose, are a major risk factor for caries and that the frequency and sequence of carbohydrate consumption as well as the composition of the carbohydrates can also influence cariogenicity. Interpretation of the results from such studies must be tempered, however, by the knowledge that most of them are derived from a single animal species—the rat. The rat has been favored because of the rapidity with which it develops dental caries in the laboratory and the similarity of its sulcal and smooth-surface carious lesions to those of humans (Glinsmann et al., 1986); however, its feeding patterns and oral physiology (e.g., microbial composition, oral pH, salivary composition, flow rate, and buffering capacity) differ greatly from those of humans (McDonald, 1985a). For example, rats nibble throughout the day, and it is known that meal frequency correlates positively and strongly with caries formation in animals (Firestone et al., 1982; Skinner et al., 1982) and in humans (Gustafsson et al., 1952). Furthermore, foods must be given to rats in powdered form—not in the physical form usually consumed by humans. This can complicate attempts to assess cariogenicity of specific foods (Krasse, 1985). Differences in oral physiology may also .influence findings. For example, although most types of phosphates effectively reduce caries in rats when added to sucrose-containing diets, phosphate supplementation in the human diet has been markedly unsuccessful in reducing caries incidence (Nizel and Harris, 1964).
Evidence Associating Nondietary Factors with Dental Caries
Studies suggest that fermentable carbohydrates in the diet contribute to caries formation but are not sufficient by themselves to cause dental caries. Oral microflora and appropriate host factors must also be present and must interact with diet if caries are to form and progress (Navia, 1977).
Oral Microflora
The oral cavity is host to a variety of microbial flora that thrive in the moist nutrient-rich environment. At birth, the mouth is usually sterile; soon afterward, colonization occurs (Gibbons and van Houte, 1978). The cariogenic role of oral microflora was first noted in studies of rats delivered by Caesarean section and maintained under sterile conditions. The germ-free rats were caries-free from birth and remained so, even when fed a cariogenic diet (Orland et al., 1954).
Streptococcus mutans is most commonly associated with cariogenesis. S. mutans has been found in all human populations and is concentrated in plaque over the most active carious lesions (Kristofferson et al., 1985). Bacteriocin typing of S. mutans demonstrates that the mother is the major source of oral infection in the infant (Berkowitz and Jordan, 1975; Rogers, 1981). The mother also determines the extent of infection, since highly infected mothers tend to have children with higher counts of S. mutans than mothers with low infection rates (Köhler and Bratthall, 1978).
Both the presence and the extent of S. mutans infection in children are associated with caries risk. Köhler et al. (1986) reported that in children infected with S. mutans before age 2, caries prevalence is 8 times greater than in children not infected until age 4. Similarly, children who are more heavily infected tend to develop more caries than children with lower counts (Köhler et al., 1984).
Monoinoculation of germ-free rats with various isolates of human oral microflora has demonstrated that most strains of S. mutans can cause caries in the fissures and smooth surfaces of the teeth, although strains vary in virulence. Other microorganisms associated to various degrees with caries formation include Streptococcus salivarius, S. sanguis, Lactobacillus casei, and several strains of Actinomyces (Miller, 1981). However, generalizing these findings to humans should be approached with caution, since monoinfection in gnotobiotic rats does not mimic the process that occurs in the oral environment of humans where various microflora compete for available niches (Shaw, 1987).
The mechanisms by which S. mutans, S. sanguis, and other microorganisms promote caries are not well understood. S. sanguis is believed to help establish colonization of the tooth surface by S. mutans and other oral microflora (van Houte, 1976). If unimpeded, progressive colonization of the tooth surface results in plaque (Hardie and Bowden, 1976). Plaque holds acidic microbial metabolic by-products close to the tooth surface, protecting them from the buffering effect of saliva. These by-products are believed to demineralize the tooth surface and promote decay. The microbial content of plaque can vary considerably, however, both across a single tooth surface and over time. This limits our ability to identify specific causative agents. Furthermore, S. mutans is often not detectable in plaque over apparently active carious lesions (Shaw, 1987). Whether this results from an inability to measure small microbial concentrations, from mistaken sampling of inactive lesions, or from a true lack of effect is not known. However, the association of S. mutans infection with caries incidence in children and the fact that plaque concentrations over active lesions are reduced when sugar consumption is curtailed suggests that S. mutans is a major etiologic agent for caries of the tooth crown.
Host Factors
The role of genetic susceptibility in caries causation appears to be minor. Although monozygotic twins in one longitudinal twin study were found to have a more concordant incidence rate of caries than dizygotic twins (Kent and Moorrees, 1979), corroborative evidence is lacking.
The composition and the rate of flow of saliva appear to influence cariogenesis in several ways, although there is no evidence for genetic determination of these factors (Shaw, 1987). Saliva can act as a buffer, neutralizing acid by-products of oral microflora found on tooth surfaces and in carious lesions. The high concentrations of calcium and phosphorus and the low levels of fluoride found in saliva may facilitate remineralization of early carious lesions and form caries-resistant surface enamel (Silverstone, 1984). Saliva may also inhibit the metabolism and growth of cariogenic microflora, since it contains several potentially bacteriostatic agents, including lysozyme, lactoferrin, and secretory immunoglobulins (Cole et al., 1976; Evans et al., 1976; Pollock et al., 1976).
Decreasing saliva flow in rodents through removal or ligation of some or all the major salivary glands substantially increases caries incidence (Muhler and Shafer, 1957; Schwartz and Shaw, 1955; Schwartz and Weisberger, 1955). Destruction or absence of salivary glands in humans results in a marked increase in caries incidence (Bertram, 1967).
Dental caries is a multifactorial disease. Diet and oral microflora are implicated in caries causation along with such host factors as salivary composition and flow. Genetic susceptibility does not appear to be a major risk factor for caries.
Fermentable carbohydrates appear to be the only component of the diet capable of inducing caries. All fermentable dietary carbohydrates, especially sucrose, are potentially cariogenic, but sucrose is generally accepted as the most cariogenic dietary factor. Sucrose consumption has been associated most strongly by and consistently with the frequency of dental caries in humans. Other sugars such as glucose and fructose have also been shown to be potentially cariogenic in human and laboratory studies, although they appear to be less cariogenic than sucrose. The cariogenic potential of carbohydrate-containing foods depends on their characteristics (e.g., stickiness), and the frequency and sequence of their consumption. The addition of certain foods and nonnutritive sweeteners, such as cheddar cheese, cocoa, and xylitol, to the diet appears to reduce the cariogenic potential of a sucrose-containing meal.
Caries will neither form nor progress in the absence of a suitable substrate (e.g., oral microflora). Of the oral microflora that have been implicated in caries causation, S. mutans has been the most consistently and strongly associated.
Consumption of fluoride in optimal amounts reduces caries incidence in people of all ages. Fluoride is strongly anticariogenic if consumed in optimal amounts before eruption of permanent teeth. Widespread fluoridation of water supplies and the use of topical fluorides (e.g., fluoridated dentifrices), combined with changing trends in sugar consumption (e.g., decreasing sucrose consumption), are probably the two factors most responsible for the recent decline in caries prevalence rates in the United States.
Directions for Research
Research should be continued on plaque and its specific role in cariogenesis and on dietary factors and food intake patterns that can modify plaque ecology or prevent plaque accumulation.
More research should be undertaken on the environmental and genetic factors that influence risk of tooth and root cavities.
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Horton, W.A., A.E. Jacobs, R.M. Green, V.F. Hillier, and D.B. Drucker. 1985. The cariogenicity of sucrose, glucose and maize starch in gnotobiotic rats mono-infected with strains of the bacteria Streptococcus mutans , Streptococcus salivarius, and Streptococcus milleri. Arch. Oral Biol. 30:777-780. [PubMed: 3868967]
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Jackson, D. 1979. Caries experience in deciduous teeth of five-year-old English children: 1974-1977. Probe 20:404-406. [PubMed: 293645]
Jensen, M.E., and C.F. Schachtele. 1983. The acidogenic potential of reference foods and snacks at interproximal sites in the human dentition. J. Dent. Res. 62:889-892. [PubMed: 6575037]
Kent, R.L., Jr., and C.F.A. Moorrees. 1979. Associations in interproximal caries prevalence from a longitudinal twin study. J. Dent. Res. (sp. iss.) 58:225.
Köhler, B., and D. Bratthall. 1978. Intrafamilial levels of Streptococcus mutans and some aspects of the bacterial transmission. Scand. J. Dent. Res. 86:35-42. [PubMed: 273301]
Köhler, B., I. Andréen, and B. Jonsson. 1984. The effect of caries-preventive measures in mothers on dental caries and the oral presence of the bacteria Streptococcus mutans and lactobacilli in their children. Arch. Oral Biol. 29:879-883. [PubMed: 6596034]
Köhler, B., I. Andreen, and B. Jonsson. 1986. Streptococcus mutans infection and dental caries in young children—a longitudinal study. Caries Res. 20:171.
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Copyright © 1989 by the National Academy of Sciences.
Bookshelf ID: NBK218734
National Research Council (US) Committee on Diet and Health. Diet and Health: Implications for Reducing Chronic Disease Risk. Washington (DC): National Academies Press (US); 1989. 26, Dental Caries.
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May 7th is National Child and Youth Mental Health day, a day dedicated to raising awareness about the importance of children's mental health and showing that positive mental health is essential to a child's healthy development. I see the truth in this message in the work I do every day with children and youth in Regent Park, many of whom are coping with difficult and complex situations in their lives.
As adults, we often don't remember that young people are impacted by things happening in different areas of their lives – they're impacted by what's happening in school, at home, in their communities. We also sometimes forget that young people are physically and hormonally going through lots of changes, while lacking the decision-making abilities, impulse control, and emotional regulation that we have as adults.
The combination of these stressors and significant physical changes and developments can result in a perfect storm of emotional turbulence, meaning many youth feel alone, overwhelmed, or hopeless. They may feel like they have no one to turn to, or that their early experiences in life will forever define them or limit their opportunities for future success and happiness. This is why Dixon Hall's Summer Camp program is about so much more than just daily activities and fun. It's a place that provides structure, safe and consistent support, relationship building skills, and opportunities and experiences for learning so that youth develop self-confidence and are prepared to pursue their own visions of greatness and take risks.
I can speak to the positive effects of Summer Camp because I attended Dixon Hall from 3 years old, up until I became a Counsellor in Training (CIT) in my teen years, ultimately working as a Camp Counsellor for 4 consecutive summers. Summer Camp at Dixon Hall directly contributed to the woman I am today and to my career path. Working with campers from Monday toFriday is an incredible opportunity for us as a trusted and safe adult presence in the lives of our campers.
By being together with the campers all day and in so many different situations, without the stress of school, we're able tofoster strong relationships and model healthy relationships that youth can apply to other areas oftheir lives. We teach youth that they teach people how they want to be treated, and watch as they apply this concept in their own circles. We encourage our campers to talk about their emotions and show them they're not alone, normalizing their feelings and experiences. Being aware of the issues they're facing, naming them, and recognizing they're not the only ones struggling with them is a huge step in fighting stigma and taking steps to make real, lasting changes in their lives.
Having camp counsellors and trusted adults who grew up in the same neighbourhood and attended the same camp is extremely beneficial for the campers. Understanding, empathy, positive role models, and the chance to just be carefree kids has incredible results. There are many campers who take a very similar path to my own – starting out as small children attending camp, and continuing on as CITs and Counsellors. It's a very proud moment when we see young children grow into capable youth, flourishing in planning camp activities, working with young children, and communicating with parents effectively. Summer camp gives young people something to aspire to.
It's an innate human need to feel like you're part of something and connected to one another. Some of our campers have really strong connections with one another. Some of our campers are connected to the sports aspect of camp and being part of a team. Some of them are connected to our staff and call them first when something happens in their lives, whether it's good or bad news. No matter what the connection, we emphasize the same message to our campers: you are worthy and you matter, we care and we see your light. Summer camp teaches our campers that their experiences in life don't have to be limited – they deserve to see and do things, and to broaden their experiences. Summer camp reminds them that they can do anything.
Help us send a Regent Park youth to camp this summer.
Sandra Costain is Dixon Hall's Director of Children & Youth Services. Born and raised in Regent Park, Sandra is knowledgeable about the community, dedicated and passionate about her work, and trusted by the youth she serves. She completed her education in Social Work at Ryerson University, and has a wealth of experience with agencies across Toronto, including Toronto Public Health and Mothercraft.


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JP Harris & The Tough Choices
Jake Owen Gives Big Boost to Arizona's Tony Martinez
Well apparently Jake Owen isn't just a man of talk, he's a man of action, and one country artist from Arizona is set to be the beneficiary of Owen's good nature, and desire to see more substance in the format. Tony Martinez is a well-seasoned traditional country artist and touring sideman for multiple projects, and by a strange twist of fate, will be playing on Jake Owen's Days of Gold arena tour.
Arizona, Dana Armstrong, Days Of Gold Tour, Eli Young Band, Hank Williams III, Hank3, Jake Owen, Jerry Reed, JP Harris & The Tough Choices, Junction 10, Ray Lawrence Jr., Robert Perez, The Bluegrass Inn, The Cadillac Three, Tony Martinez, Valley Fever, Waylon Jennings
Independent Music Awards Announces 12th Annual Nominees (& Winners)
The Independent Music Awards has announced their 12th Annual nominations, and it includes many great names from the independent country/roots world like Rachel Brooke, The Boomswagglers, Lucky Tubb, The Steel Wheels, Tom VandenAvond, Langhorn Slim, and The Carper Family to name a few. The Awards honor exceptional independent artists traditionally ignored by mainstream media and big box retailers.
12th Annual, 2013, Brandi Carlisle, INdependent Music Awards, Jim Lauderdale, JP Harris & The Tough Choices, Langhorn Slim, Lucky Tubb, Nominees, Rachel Brooke, The Bommswagglers, The Carper Family, The Steel Wheels, Tom VandenAvond, Tom Waits, Weird Al Yankovic Kevin Lyman
Saving Country Music's 25 Essential Albums for 2012
Here is the list of 25 albums Saving Country Music deems essential for 2012 listening, and then I added an extra one I couldn't leave off. Please note this list only includes albums that have been reviewed so far. There are a few more good and important albums in 2012 that have yet to be reviewed. The first 7 albums on the list (from Little Victories to Lee Bains) were all serious considerations for SCM's Album of the Year.
Billy Don BUrns, Carolina Chocolate Drops, Chris Knight, Davy Jay Sparrow, Don Williams, essential albums, Foghorn Stringband, Jackson Taylor, James Leg, Joe Buck, Joseph Huber, JP Harris & The Tough Choices, Justin Townes Earle, Lee Bains III & The Glory Fires, Left Lane Cruiser, Lone Wolf, Marty Stuart, McDougall, Paige Anderson, Rachel Brooke, Ray Wylie Hubbard, Restavrant, Reverend Peyton's Big Damn Band, Sara Watkins, The Alabama Shakes, The Calamity Cubes, Tom VandenAvond, Willie Nelson


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The Royal Treatment Trailer: It's Nice To Know There Are Still Hot Princes From Fictional Countries
By Jenna Busch/Dec. 21, 2021 3:58 pm EST
If you can't get your fill of Hallmark Christmas movies and you're wondering how you'll cope with the loss when January hits, I have good news for you. There is a single royal in town, engaged to a total jerk who is just looking for a girl with financial issues to come and love him for who he is. What? You've seen this story in one form or another before? Well, you must like it, because they keep making them. From "The Princess Diaries" to "Coming to America," the royal love story is so hot right now — and has been forever. You can become a princess, win the heart of a prince, etc., just by being your own goofy self. Someone in the story (whether love interest, royal Grandma or something like that) will encourage your goofiness, your clumsiness, or your hairdressing dream, there will be some sort of mishap, misunderstanding, or fiance who is a vile person under that icy-yet-charming exterior, and then you'll fall in love and live happily ever after.
Today we have a new trailer for "The Royal Treatment" from Netflix. Here is the info for you:
Isabella (Laura Marano) runs her own salon and isn't afraid to speak her mind, while Prince Thomas (Mena Massoud) runs his own country and is about to marry for duty rather than love. When Izzy and her fellow stylists get the opportunity of a lifetime to do the hair for the royal wedding, she and Prince Thomas learn that taking control of their own destiny requires following their hearts.
'I'm Izzy, of 183rd Street'
"The Royal Treatment" stars Laura Marano ("Austin & Ally") as Izzy of 183rd Street in NYC and Mena Massoud ("Aladdin") as Prince Thomas of ... some fictional kingdom. Izzy is hired (along with her entire salon, it appears) to fix Prince Thomas' hair for the royal wedding for $50,000. There must be some movie magic here, because I did makeup for years, sometimes for celebrities, and let's just say it doesn't pay that much. Thomas is engaged to a person who doesn't speak in the trailer, and Izzy's got some sort of Brooklyn accent that comes and goes.
"Oh no," you say. "They don't match up!" Fear not, romantic story fans. Of course, they're going to fall in love!
Though you don't see it in the trailer, I would venture to guess that Izzy has a best friend who will also fall in love with the Prince's best friend at some point, and someone is absolutely getting a makeover. It's probably Prince Thomas, going by the hair comment at the beginning of the trailer. Ooh, can we get a royal prince outfit montage?
'Best Freakin' Hair Salon in New York'
Forgive me. I'm only half making fun of this, I swear. I enjoy a good love story, and frankly, something like this is kind of just what the doctor ordered in these days of "Pandemic III: the Omicron Variant." I tease because I care. I'm someone who watches "Practical Magic" every year around Halloween the way other people watch horror movies. My dad is obsessed with Hallmark Christmas movies because they are predictable and have happy endings.
January is looking to be a rough month since we're likely to see a post-holiday Covid spike. We're all going to need to be soothed. A gentle bit of hot royal from a foreign country falling in love with a rough-around-the-edges-with-a-heart-of-gold commoner might just do the trick.
"The Royal Treatment" will premiere on Netflix on January 20, 2022. Please tell me your favorite commoner/royal love story films. I must know them all!


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Travel disruption warning as scenic St Ives railway line gets long-overdue upgrade
The new track will be more reliable, says Network Rail
Edward ChurchTrainee Reporter
The new track should be finished by February 8, 2021 (Image: Western Network Rail)
Our Saturday morning email features the very best news and exclusive content from our team of reporters
One of Cornwall's most popular stretches of railway is getting a £3m refit in the largest track investment in the county since the 1950s.
Passengers looking to travel on the scenic St Ives to Carbis Bay line should check before they travel from January 3 until February 8, since there will be disruptions while the upgrade is fitted.
Great Western Railway has confirmed a rail replacement service between St Ives and St Erth while the track is being upgraded.
To maintain social distancing, GWR has asked passengers to plan ahead and avoid busy times on the popular coastal line.
Network Rail announced the refit, which will see the decades-old track ripped out and a new one fitted.
One-and-a-half miles of replacement track is being laid over the five-week period with 3,600 new sleepers and around 400 tonnes of stone for the rail to sit on.
While no additional services on the line are being planned, Network Rail hopes it will be more reliable in time for the busy tourist season later in 2021.
Mark Chorley, GWR regional station manager, said: "We have been working hard to make sure that people can be confident to travel safely, and that includes running as many replacement buses as we can to make extra room, as well as enhanced cleaning and social distancing measures.
"This work is important to ensure we can continue to maintain and improve reliability on this very popular and scenic branch line and we thank customers for their patience in advance."
According to GWR, the mainline between Plymouth and Penzance will operate as normal while the St Ives bay line is upgraded.
Councillor Andrea Davis, chairman of Peninsula Rail Task Force, said: "At this time of uncertainty with the ongoing pandemic it is heartening that Network Rail are investing in the Cornish network, this substantial upgrade is very welcome and will give a much needed boost to the far South West economy as we move to the recovery phase."


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VOICE OF PROFESSIONALS
How to increase egg production with Gut health
The egg industry is currently going through its fair share of challenges. Producers are looking for more ways to improve the efficiency of their businesses.
To try to achieve this, many are looking into how they can:
• Improve eggshell quality.
• Increase the number of eggs laid, with regular discussions around a target of 500 eggs per bird.
• Lengthen the laying cycle.
With these objectives in mind, the role of layer gut health in production has never been more pertinent.
Egg production, for the laying hen, is a taxing process, considering the energy they use and the stress they endure. It is a biologically complex procedure, and to achieve the highest-quality eggs, the bird's performance needs to be optimal. By trying to push the boundaries of a bird's laying capability, we run the risk of compromising the quality of the end result.
If gut health in layers is not at its best, you will see the effects in the eggs they produce. In fact, gastrointestinal challenges are known to be connected to:
• Fragile shells.
• Dirty eggs.
• Short and less abundant laying cycles.
These are issues that will not only hurt your birds but, in the long term, hurt your profits, too.
By making gut health a priority, we can ensure that layers have the resources they need to produce successfully. On top of this, when we talk about pushing the boundaries in terms of what our birds can do, optimal gut health is the key to safely achieving these goals.
EGGSHELL ESSENTIALS
When aiming to "improve eggshell quality," it is essential to distinguish precisely what that means. Generally, a good-quality shell is one that does not crack easily and, as a result, will reduce the number of seconds. However, increasing shell thickness does not necessarily improve quality; it is the structure of the shell that is crucial.
Many enzymes and minerals are involved in the creation of the shell structure. Layers receive the required minerals through their diet, but these minerals must be readily bioavailable for them to be useful in the egg-creation process. The small intestine cannot absorb non-bioavailable minerals.
We also need to be wary of how much of a mineral is included in the diet formulation, as well as the interactions of that mineral once it is consumed. Calcium carbonate, for example, is crucial for eggshell formation, and it is often presumed that increasing the amount of calcium in the diet will automatically lead to more durable shells. However, there is a negligible balance to be considered. Calcium, when dissolved in the gastrointestinal system, can interact with other minerals, reducing their absorption. This, in turn, can have a direct impact on other structural components of the egg, diminishing quality.
With these factors in mind, the best method for ensuring optimum bioavailability is to use chelated minerals in the diet. They will have fewer reactions with other minerals, allowing the bird to absorb more of the mineral. By ensuring that layers are getting the most out of their feed, we give them the best chance to maintain a healthy gut and, as a result, produce high-quality eggs.
LAYING HEALTHIER AND LONGER
The laying hen can naturally continue to produce eggs for many years, but her peak production will naturally decline with age. Genetic advances in recent years have allowed birds to produce nearly one egg per day, from week 18 to week 75. In some cases, however, the push for large eggs — which come at end-of-lay — has extended this period to 80+ weeks.
Lengthening the egg-laying period puts more stress on the bird, as she must create a metabolically rich egg while also maintaining her body weight and dealing with any additional challenges from the environment that may impact the immune system.
It is worth noting that if the energy requirements of the bird are not being met, at a certain point, her body will shut down the reproductive system that was producing the eggs in favor of supporting her body weight and providing energy for vital bodily systems.
HEALTHY GUT, HEALTHY LAY
Between 50–80% of the immune system functions in some way through the gut. Many factors can trigger the immune system, such as:
• Mycotoxins.
• New diets.
• High levels of potentially pathogenic bacteria, known as dysbacteriosis.
The immune response in the gut generally takes the form of inflammation, which produces additional mucous layers. Added mucous creates an extra barrier for the minerals to pass through before being absorbed. This means that if an inflammatory response is underway, it is unlikely that the bird will receive its full mineral requirement, impacting eggshell structure and, therefore, strength and quality.
Maintaining and promoting gut health in flocks:
• Increases villi height.
• Reduces villi-crypt ratio.
• Improves tight junctions between cells.
Villi with improved height will have an enhanced surface area and, therefore, can absorb more nutrients to sustain the hen for longer lay cycles. Improving tight junctions will prevent bacteria from becoming translocated into the bloodstream, which can lead to a multitude of problems — including, in the worst cases, diseases like colisepticemia.
The addition of Actigen®, a unique bioactive product derived from the Saccharomyces cervisiae yeast strain, in layer feed can help to optimize gut health. Actigen works to normalize and promote diverse gut bacteria. This helps with the maintenance of the bird's gastrointestinal integrity and stability, which, in turn, supports its immune defense and gut health.
GETTING THE BALANCE RIGHT
In a natural setting, the microbiome — the microbial population in the gut — is developed from the mother as the chick is raised in the nest. Our modern systems mean that this does not happen, so the creation and maintenance of the microbiome should be considered when determining management practices. Keeping the microbiome balanced will go a long way to improving layer gut health and egg production.
Many producers have been successful in improving gut health and the microbiome via the implementation of Alltech's Seed, Feed, Weed program to manage the composition of the intestinal microbial community. This involves accelerating the evolution of the microbial community to a steady state and then maintaining the status quo. The Seed, Feed, Weed program achieves this by:
• Seeding the gut with favorable organisms.
• Feeding these favorable organisms.
• Weeding out the unfavorable organisms.
By helping to maintain the microbiome balance, this program works to improve shell quality and enable a healthier, longer lay.
Producers in the egg industry are desperately seeking out ways to help their birds continue to lay more in the safest way possible. Quality food will help layers produce quality eggs — but this is only effective if the bird is able to absorb the beneficial nutrients that come from it in the first place. Improving the gut health of birds in lay will enable them to absorb a higher proportion of their feed. This will not only aid the overall wellbeing of the layer but will also give them the foundations to successfully and safely produce better eggs for a longer period of time.
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