10.7: RNA and Ribosome Export from the Nucleus
A. rRNA and Ribosomes
The synthesis and processing of rRNAs are coincident with the assembly of the ribosomal subunits, as shown below.
The 45S pre-rRNAs initially bind to ribosomal proteins in the nucleolus (that big nuclear body!) to initiate assembly and then and serve as a scaffold for the continued addition of ribosomal proteins to both the small and large ribosomal subunits. After the 5S rRNA added to the nascent large ribosomal subunit, processing (cleavage) of 45S rRNA is completed and the subunits are separated. The separated ribosomal subunits exit the nucleus o the cytoplasm where they will associate with mRNAs to translate new proteins. To better understand what is going on, try summarizing what you see here in the correct order of steps. You can also see this process animated at this link: here .
B. mRNA
The 5’ methyl guanosine cap and the poly(A) tail collaborate to facilitate exit of mRNAs from the nucleus into the cytoplasm. We now understand that proteins in the nucleus participate in the export process. A nuclear transport receptor binds along the mature (or maturing) mRNA, a poly-A-binding protein binds along the poly-A tail of the message, and another protein binds at or near the methyl guanosine CAP itself. These interactions enable transport of the mRNA through nuclear pores. After the mRNA is in the cytoplasm, the nuclear transport receptor re-cycles back into the nucleus while a translation initiation factor replaces the protein bound to the CAP. The nuclear transport process is summarized in the illustration below.
See a more detailed description of mRNA transport from the nucleus at this link: here . The mature mRNA, now in the cytoplasm, is ready for translation. Translation is the process of protein synthesis mediated by ribosomes and a host of translation factors (including the initiation factor in the illustration above. The genetic code directs polypeptide synthesis during translation. Details of translation will be discussed shortly.


6.3: Callbacks
Callbacks are where the real casting happens. Callbacks allow you to see in real time how actors listen to each other, take direction, and make creative choices. Print off scenes for each character and pair up actors to see how they interact and the choices they make. If an actor is good with various people not only are they talented, but they are able to listen and collaborate well with others. Try to see as many different pairings as possible and your goal should be to see which actors make the boldest choices, listen and collaborate, and take direction. Once you have a good sense of the actors talent and skills, cast the most central character first and base your other casting decisions off of that choice. Always cast work ethic over talent, since talented people are often the laziest and most averse to critiques. Remember hard work always beats talent.


3.2: Log Rocker (Kubbestol)
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Log Rocker (
Kubbestol
)
Norwegian-American Maker, workmen at Little Norway; decoration attributed to Olaf Colberson, c.1930 Wood (oak), paint Little Norway Collection, Gift of Scott & Jennifer Winner MHAHS 2015.021.0004 |
Kubbestols , traditional Norwegian log chairs, were created from the trunks of trees, their typically over-sized bases making them appear almost rooted to the ground, immovable. Kubbestols are a source of national pride in Norway and symbols of Norwegian heritage in America. This ethnic tradition is completely transformed when rockers, typically associated with movement, are added. Although this combination is rare, this rocking kubbestol made for Little Norway is a clear example of the reinvention of ethnicity.
For a complete essay on this object, click here.
Often, chairs are considered utilitarian above all other characteristics. We need them for an easy way to sit down, we need them to sit at the table, we need them in crowded theaters, and we prefer different styles based on our comfort needs. However, chairs represent much more than a resting position. They communicate our identity and our lifestyle. Think of a rocking chair, a stool, and an office chair. These are clearly not interchangeable, but they all chairs and it matters which one you are sitting in.
Created in the early 18th century, the rocking chair is a distinctly American invention. One of the most comfortable chairs ever created, the rocking chair is so soothing that people often use it to calm infants. When sitting in a rocking chair, the chair matches your center of gravity and keeps you in an unstressed position.It is a chair that refuses to sit still, but carries out its motion in a soft and serene way, shifting back and forth slowly, lazily, as if lulling you to sleep.
On the other hand, when you sit in a kubbestol, you are rooted to the ground. The other kubbestols in the exhibit vary greatly in size, but this Norwegian chair demands its presence be felt. It represents power and an immovable, proud sense of self. Comparing a rocking chair to a kubbestol is nearly impossible, which is why this object in the exhibit is so rare.
Observing the kubbestol rocker in the exhibit, the details come to life. Scars cover it, traces left by the axe used to carve this rocker out of a giant log. Though this chair is hollowed out in the center, one would not be able to tell upon moving this massive weight, which demands it stay rooted in one spot. Paint on the end of the seat has worn away from use, showing that this was clearly a loved object even though it was made for Little Norway. Olaf Colberson, an artist with a tragic past, did the large and swooping rosemaling along the bottom of the chair. Horseshoes carved on either side of the chair can be easily scanned over in one’s haste to study the rest of the object. A large crack traces the left side of the chair, showing the wood expanding with age, stretching out and making its presence known.
Then there are the rockers. How did they come to be on this kubbestol? This powerful, heavy mass of a chair seems like it would smash the rockers into the ground. This beast of a chair could not possibly move the way the rockers imply. Who thought this was a good idea?  Mount Horeb was a community of immigrants that wanted to pass their culture down to their future generations and they clearly succeeded when you look around the Historical Society. However, this Norwegian culture does not remain untouched. Children of these immigrants not only cared for their Norwegian roots, but they also wanted to grasp the shifting nature of American culture. Both the rocking chair and the kubbestol are symbols of the nostalgia that is a focal point at Little Norway. Combining these two chairs by placing rockers on a kubbestol, this object represents a cultural hybrid of idealized identities, highlighting a theme of reinvention and cultural fusion often practiced by Norwegian-American immigrants.


6.6: Percussion
Introduction
A percussion instrument is a musical instrument that is sounded by being struck or scraped by a beater (including attached or enclosed beaters or rattles); struck, scraped or rubbed by hand; or struck against another similar instrument. The percussion family is believed to include the oldest musical instruments, following the human voice.
The percussion section of an orchestra most commonly contains instruments such as timpani, snare drum, bass drum, cymbals, triangle and tambourine. However, the section can also contain non-percussive instruments, such as whistles and sirens, or a blown conch shell. On the other hand, keyboard instruments, such as the celesta, are not normally part of the percussion section, but keyboard percussion instruments such as the glockenspiel and xylophone (which do not have piano keyboards) are included.
Percussion instruments are most commonly divided into two categories: pitched percussion instruments, which produce notes with an identifiable pitch, and unpitched percussion instruments, which produce notes or sounds without an identifiable pitch.
Percussion is commonly referred to as “the backbone” or “the heartbeat” of a musical ensemble, often working in close collaboration with bass instruments, when present. In jazz and other popular music ensembles, the pianist, bassist, drummer and sometimes the guitarist are referred to as the rhythm section. Most classical pieces written for full orchestra since the time of Haydn and Mozart are orchestrated to place emphasis on the strings, woodwinds, and brass. However, often at least one pair of timpani is included, though they rarely play continuously. Rather, they serve to provide additional accents when needed. In the eighteenth and nineteenth centuries, other percussion instruments (like the triangle or cymbals) have been used, again generally sparingly. The use of percussion instruments became more frequent in the twentieth-century classical music.
Timpani
Timpani, or kettledrums, are musical instruments in the percussion family. A type of drum, they consist of a skin called a head stretched over a large bowl traditionally made of copper. They are played by striking the head with a specialized drum stick called a timpani stick or timpani mallet . Timpani evolved from military drums to become a staple of the classical orchestra by the last third of the eighteenth century. Today, they are used in many types of musical ensembles, including concert bands, marching bands, orchestras, and even in some rock.
The basic timpani drum consists of a drumhead stretched across the opening of a bowl typically made of copper or, in less expensive models, fiberglass and sometimes aluminum. In the Sachs–Hornbostel classification, the timpani are thus considered membranophones. The drumhead is affixed to a hoop (also called a fleshhoop ), which in turn is held onto the bowl by a counterhoop ,which is then held by means of a number of tuning screws called tension rods placed regularly around the circumference. The head’s tension can be adjusted by loosening or tightening the rods. Most timpani have six to eight tension rods.
The shape of the bowl contributes to the quality of the drum. For example, hemispheric bowls produce brighter tones while parabolic bowls produce darker tones. Another factor that affects the timbre of the drum is the quality of the bowl’s surface. Copper bowls may have a smooth, machined surface or a rough surface with many small dents hammered into it.
Timpani come in a variety of sizes from about 84 centimeters (33 inches) in diameter down to piccoli timpani of 30 centimeters (12 inches) or less. A 33-inch drum can produce the C below the bass clef, and specialty piccoli timpani can play up into the treble clef. In Darius Milhaud’s 1923 ballet score La création du monde , the timpanist must play the F sharp at the bottom of the treble clef. Each individual drum typically has a range of a perfect fifth.
Please listen to the timpani’s role in Carmina Burana, Part 1, as played by the Raleigh Symphony Orchestra.
Bass Drum
Bass drums are percussion instruments which vary in size and are used in several musical genres. Three major types of bass drums are as follows:
- The type usually seen or heard in orchestral, ensemble or concert band music is the orchestral, or concert bass drum (in Italian: gran cassa, gran tamburo ). It is the largest drum of the orchestra.
- The kick drum, struck with a beater attached to a pedal, usually seen on drum kits.
- The pitched bass drum, generally used in marching bands and drum corps. This is tuned to a specific pitch and is usually played in a set of three to six drums.
A bass drum is typically cylindrical with the diameter much greater than the height. There is normally a struck head at both ends of the cylinder. The heads may be made of calf skin or plastic. There is normally a means of adjusting the tension either by threaded taps or by strings. Bass drums are built in a variety of sizes, but size has little to do with the volume produced by the drum. The size chosen being based on convenience and aesthetics.
In the following video, Kristen Shiner McGuire gives an introduction to the concert bass drum.
Snare Drum
The snare drum or side drum is a ubiquitous percussion instrument known for its cylindrical shape and powerful, staccato sound. Snare drums are often used in orchestras, concert bands, marching bands, parades, drum lines, drum corps, and more. The snare is also one of the central pieces in a trap set, a collection of percussion instruments designed to be played by a seated drummer, which is used in many popular genres of music. Snare drums are typically played with drum sticks, although there are other options for a completely different sound, such as the brush.
The snare drum originated from the Tabor drum, which was originally used to accompany the flute. It has evolved into more modern versions including the kit snare, marching snare, and the piccolo snare. Each type presents a different dimension and style of percussion. The snare drum that someone might see in a concert is typically used with a backbeat style to create rhythm. In marching bands it can do the same technique but it is mostly used for a front beat.
In comparison with the marching snare, the kit snare is typically smaller in length between the two heads, while the piccolo is the smallest of the three. The snare drum is known for its loud crack when a person strikes it with a drum stick or mallet. The depth of the sound varies from snare to snare because of the different techniques and construction qualities of the drum. Some of these qualities include tightness of the head, dimensions, and brand.
The snare drum is constructed of two heads—both typically made of plastic—along with a rattle of metal wires on the bottom head called the snares. The wires can also be placed on the top, just like on the Tarol Snare. The top head is typically called the batter head because that is where the drummer strikes it, while the bottom head is called the snare head because that is where the snares are located. Tension of the drum heads is held constant through the tension rods. The ability to tighten them provides an opportunity to differ the sound of the hit. The strainer is a lever that releases and tightens the snare. If the strainer is relaxed, the sound of the snare is more like that of a tom because the snares are not present. The rim is the metal ring around the batter head, which can be used for a variety of things, although it is notably used to sound a piercing rimshot with the drumstick.
The following video gives an overview of playing the snare drum.
Cymbals
Cymbals consist of thin, normally round plates of various alloys. The majority of cymbals are of indefinite pitch, although small disc-shaped cymbals based on ancient designs sound a definite note. Cymbals are used in many ensembles ranging from the orchestra, percussion ensembles, jazz bands, heavy metal bands, and marching groups. Drum kits usually incorporate at least a crash, ride or crash/ride, and a pair of hi-hat cymbals.
The anatomy of the cymbal plays a large part in the sound it creates. A hole is drilled in the center of the cymbal and it is used to either mount the cymbal on a stand or straps (for hand playing). The bell, dome, or cup is the raised section immediately surrounding the hole. The bell produces a higher “pinging” pitch than the rest of the cymbal. The bow is the rest of the surface surrounding the bell. The bow is sometimes described in two areas: the ride and crash area. The ride area is the thicker section closer to the bell while the crash area is the thinner tapering section near the edge. The edge or rim is the immediate circumference of the cymbal.
Cymbals are measured by their diameter often in inches or centimeters. The size of the cymbal affects its sound, larger cymbals usually being louder and having longer sustain. The weight describes how thick the cymbal is. Cymbal weights are important to the sound they produce and how they play. Heavier cymbals have a louder volume, more cut, and better stick articulation (when using drum sticks). Thin cymbals have a fuller sound, lower pitch, and faster response.
The profile of the cymbal is the vertical distance of the bow from the bottom of the bell to the cymbal edge (higher profile cymbals are more bowl shaped). The profile affects the pitch of the cymbal: higher profile cymbals have higher pitch.
The following video gives a first lesson in cymbals.
Contributors and Attributions
- Percussion instrument. Provided by : Wikipedia. Located at : https://en.Wikipedia.org/wiki/Percussion_instrument . License : CC BY-SA: Attribution-ShareAlike
- Timpani. Provided by : Wikipedia. Located at : https://en.Wikipedia.org/wiki/Timpani . License : CC BY-SA: Attribution-ShareAlike
- HardtkePauken von Timpani21 aus der deutschsprachigen. . Located at : https://de.Wikipedia.org/wiki/Pauke#/media/File:HardtkePauken.jpg . License : CC BY-SA: Attribution-ShareAlike
- Snare drum. Provided by : Wikipedia. Located at : https://en.Wikipedia.org/wiki/Snare_drum . License : CC BY-SA: Attribution-ShareAlike
- 2006-07-06 snare 14 . Authored by : Stephan Czuratis (Jazz-face). Located at : https://commons.wikimedia.org/wiki/File:2006-07-06_snare_14.jpg#/media/File:2006-07-06_snare_14.jpg . License : CC BY-SA: Attribution-ShareAlike
- 2006-07-06 Crash Zildjian 14 . Authored by : Stephan Czuratis (Jazz-face). Located at : https://commons.wikimedia.org/wiki/File:2006-07-06_Crash_Zildjian_14.jpg#/media/File:2006-07-06_Crash_Zildjian_14.jpg . License : CC BY-SA: Attribution-ShareAlike
- My Drums. Authored by : Joshua Davis. Located at : https://www.flickr.com/photos/18092593@N03/2620170206/ . License : CC BY: Attribution
- Carmina Burana part 1 Raleigh Symphony Orchestra - Timpani. Authored by : Craig Zerbe. Located at : https://youtu.be/F1DEyrAZofU . License : All Rights Reserved . License Terms : Standard YouTube License
- Concert Bass Drum with Kristen Shiner McGuire. Authored by : GroverProPerc. Located at : https://youtu.be/xi9UPLhNYr4 . License : All Rights Reserved . License Terms : Standard YouTube License
- Snare Drum Lesson #1. Authored by : 215th Army Band - Massachussetts Army National Guard. Located at : https://youtu.be/ES3QpDN2AyY . License : All Rights Reserved . License Terms : Standard YouTube LIcense
- Cymbals Lesson. Authored by : 215th Army Band - Massachussetts Army National Guard. Located at : https://youtu.be/K0xFJR4iuMA . License : All Rights Reserved . License Terms : Standard YouTube License
- Mozart - Overture The Abduction from the Seraglio (K.384) - Wiener Symphoniker - Fabio Luisi (HD). Authored by : kocaonur. Located at : https://youtu.be/GrFbiw77_90 . License : All Rights Reserved . License Terms : Standard YouTube LIcense
- 1919 Ludwig New Inspiration Model bass drum. Authored by : By Ludwig & Ludwig . Provided by : Wikimedia Commons. Located at : https://upload.wikimedia.org/Wikipedia/commons/7/78/1919_Ludwig_New_Inspiration_Model_bass_drum.jpg . License : Public Domain: No Known Copyright


2.3: The ijth Entry of a Product
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In previous sections, we used the entries of a matrix to describe the action of matrix addition and scalar multiplication. We can also study matrix multiplication using the entries of matrices.
What is the \(ij^{th}\) entry of \(AB?\) It is the entry in the \(i^{th}\) row and the \(j^{th}\) column of the product \(AB\).
Now if \(A\) is \(m \times n\) and \(B\) is \(n \times p\), then we know that the product \(AB\) has the form \[\left[ \begin{array}{cccc} a_{11} & a_{12} & \cdots & a_{1n} \\ a_{21} & a_{22} & \cdots & a_{2n} \\ \vdots & \vdots & \ddots & \vdots \\ a_{m1} & a_{m2} & \cdots & a_{mn} \end{array} \right] \left[ \begin{array}{cccccc} b_{11} & b_{12} & \cdots & b_{1j} & \cdots & b_{1p} \\ b_{21} & b_{22} & \cdots & b_{2j} & \cdots & b_{2p} \\ \vdots & \vdots & & \vdots & & \vdots\\ b_{n1} & b_{n2} & \cdots & b_{nj} & \cdots & b_{np} \end{array} \right]\nonumber \]
The \(j^{th}\) column of \(AB\) is of the form \[\left[ \begin{array}{cccc} a_{11} & a_{12} & \cdots & a_{1n} \\ a_{21} & a_{22} & \cdots & a_{2n} \\ \vdots & \vdots & \ddots & \vdots \\ a_{m1} & a_{m2} & \cdots & a_{mn} \end{array} \right] \left[ \begin{array}{c} b_{1j} \\ b_{2j} \\ \vdots \\ b_{nj} \end{array} \right]\nonumber \] which is an \(m\times 1\) column vector. It is calculated by \[b_{1j} \left[ \begin{array}{c} a_{11} \\ a_{21} \\ \vdots \\ a_{m1} \end{array} \right] + b_{2j}\left[ \begin{array}{c} a_{12} \\ a_{22} \\ \vdots \\ a_{m2} \end{array} \right] +\cdots + b_{nj}\left[ \begin{array}{c} a_{1n} \\ a_{2n} \\ \vdots \\ a_{mn} \end{array} \right]\nonumber \]
Therefore, the \(ij^{th}\) entry is the entry in row \(i\) of this vector. This is computed by \[a_{i1}b_{1j}+a_{i2}b_{2j}+\cdots + a_{in}b_{nj}=\sum_{k=1}^{n}a_{ik}b_{kj}\nonumber \]
The following is the formal definition for the \(ij^{th}\) entry of a product of matrices.
Definition \(\PageIndex{1}\): The \(ij^{th}\) Entry of a Product
Let \(A=\left[ a_{ij}\right]\) be an \(m\times n\) matrix and let \(B=\left[ b_{ij}\right]\) be an \(n\times p\) matrix. Then \(AB\) is an \(m\times p\) matrix and the \(\left( i, j \right)\)-entry of \(AB\) is defined as \[(AB)_{ij}=\sum_{k=1}^{n}a_{ik}b_{kj} \nonumber \] Another way to write this is \[(AB)_{ij}=\left[ \begin{array}{cccc} a_{i1} & a_{i2} & \cdots & a_{in} \end{array} \right] \left[ \begin{array}{c} b_{1j} \\ b_{2j} \\ \vdots \\ b_{nj} \end{array} \right] = a_{i1}b_{1j} + a_{i2}b_{2j} + \cdots + a_{in}b_{nj}\nonumber \]
In other words, to find the \(\left( i, j \right)\)-entry of the product \(AB\), or \((AB)_{ij}\), you multiply the \(i^{th}\) row of \(A,\) on the left by the \(j^{th}\) column of \(B\). To express \(AB\) in terms of its entries, we write \(AB = \left[ (AB)_{ij} \right]\).
Consider the following example.
Example \(\PageIndex{1}\): The Entries of a Product
Compute \(AB\) if possible. If it is, find the \(\left( 3,2 \right)\)-entry of \(AB\) using Definition \(\PageIndex{1}\) . \[A = \left[ \begin{array}{cc} 1 & 2 \\ 3 & 1 \\ 2 & 6 \end{array} \right], B = \left[ \begin{array}{ccc} 2 & 3 & 1 \\ 7 & 6 & 2 \end{array} \right]\nonumber \]
Solution
First check if the product is possible. It is of the form \(\left( 3\times 2\right) \left( 2\times 3\right)\) and since the inside numbers match, it is possible to do the multiplication. The result should be a \(3\times 3\) matrix. We can first compute \(AB\): \[\left[ \left[ \begin{array}{rr} 1 & 2 \\ 3 & 1 \\ 2 & 6 \end{array} \right] \left[ \begin{array}{r} 2 \\ 7 \end{array} \right] ,\left[ \begin{array}{rr} 1 & 2 \\ 3 & 1 \\ 2 & 6 \end{array} \right] \left[ \begin{array}{r} 3 \\ 6 \end{array} \right] ,\left[ \begin{array}{rr} 1 & 2 \\ 3 & 1 \\ 2 & 6 \end{array} \right] \left[ \begin{array}{r} 1 \\ 2 \end{array} \right] \right]\nonumber \] where the commas separate the columns in the resulting product. Thus the above product equals \[\left[ \begin{array}{rrr} 16 & 15 & 5 \\ 13 & 15 & 5 \\ 46 & 42 & 14 \end{array} \right]\nonumber \] which is a \(3\times 3\) matrix as desired. Thus, the \(\left( 3,2 \right)\)-entry equals 42.
Now using Definition \(\PageIndex{1}\) , we can find that the \(\left( 3,2 \right)\)-entry equals \[\begin{aligned} \sum_{k=1}^{2}a_{3k}b_{k2} &=a_{31}b_{12}+a_{32}b_{22} \\ &=2\times 3+6\times 6=42\\\end{aligned}\] Consulting our result for \(AB\) above, this is correct!
You may wish to use this method to verify that the rest of the entries in \(AB\) are correct.
Here is another example.
Example \(\PageIndex{2}\): Finding the Entries of a Product
Determine if the product \(AB\) is defined. If it is, find the \(\left( 2, 1 \right)\)-entry of the product. \[A= \left[ \begin{array}{rrr} 2 & 3 & 1 \\ 7 & 6 & 2 \\ 0 & 0 & 0 \end{array} \right], B =\left[ \begin{array}{rr} 1 & 2 \\ 3 & 1 \\ 2 & 6 \end{array} \right]\nonumber \]
Solution
This product is of the form \(\left( 3\times 3\right) \left( 3\times 2\right)\). The middle numbers match so the matrices are conformable and it is possible to compute the product.
We want to find the \(\left( 2, 1 \right)\)-entry of \(AB\), that is, the entry in the second row and first column of the product. We will use Definition \(\PageIndex{1}\) , which states \[(AB)_{ij}=\sum_{k=1}^{n}a_{ik}b_{kj}\nonumber \] In this case, \(n=3\), \(i=2\) and \(j=1\). Hence the \(\left( 2, 1 \right)\)-entry is found by computing \[(AB)_{21} = \sum_{k=1}^{3}a_{2k}b_{k1} = \left[ \begin{array}{ccc} a_{21} & a_{22} & a_{23} \end{array} \right] \left[ \begin{array}{c} b_{11} \\ b_{21} \\ b_{31} \end{array} \right]\nonumber \] Substituting in the appropriate values, this product becomes \[\left[ \begin{array}{ccc} a_{21} & a_{22} & a_{23} \end{array} \right] \left[ \begin{array}{c} b_{11} \\ b_{21} \\ b_{31} \end{array} \right] = \left[ \begin{array}{ccc} 7 & 6 & 2 \end{array} \right] \left[ \begin{array}{c} 1 \\ 3 \\ 2 \end{array} \right] = 1 \times 7 + 3 \times 6 + 2 \times 2 = 29\nonumber \]
Hence, \((AB)_{21} = 29\).
You should take a moment to find a few other entries of \(AB\). You can multiply the matrices to check that your answers are correct. The product \(AB\) is given by \[AB = \left[ \begin{array}{cc} 13 & 13 \\ 29 & 32 \\ 0 & 0 \end{array} \right]\nonumber \]


7.6: Female Prisoners
Incarcerated women pose is significant difference from incarcerated men. The primary concern is that often times, women are the prime caretaker for children. When they are incarcerated, who cares for the children left behind? This may mean the children must be cared for by the father or extended family members, but this is not always possible, and the children may end up in foster care. To compound this problem, there are fewer female prisons, so they are farther away from their children making visits difficult if not impossible. These issues can have significant impact on the growth and development for the children and women. It can also make the reunification problem difficult.
Another issue for female prisoners is they may be pregnant or have other significant medical issues during incarceration. What happens to the child upon delivery is a significant concern for incarcerated females. They may be unsure of long-term care for the newborn or how to cope with the separation immediately after birth. This can contribute to significant psychological issues for the female prisoner and could affect behavior and treatment.
More and more institutions are recognizing these concerns for female prisoners and started unique programs to address these issues. For example, the State of California has developed the Community Prisoner Mother Program:
The Community Prisoner Mother Program (CPMP) is a community substance abuse treatment program where non-serious, nonviolent female offenders may serve a sentence up to six years. The CPMP has been in existence since 1985 and is mandated by Penal Code (PC) Section 3410. Women are placed in the program from any of the female institutions. Pursuant to PC 3410, program eligibility requires that the female offender have up to two children less than six years of age, have no active felony holds, nor any prior escapes. The female offender must sign a voluntary placement agreement to enter the program, followed by three years of parole. The CPMP facilities are not the property of CDCR, and a private contractor provides program services at our Pomona facility. The treatment program addresses substance issues, emotional functioning, self-esteem, parenting skills, and employment skills.
Figure 7.3 Female Inmate Education Class . Photo by CoreCivic . Image is under a CC.By 2.0 license.
Basic Program Components of the CPMP
- Pregnant and/or parenting mothers and their children under six years of age are provided programs and support services to assist in developing the skills necessary to become a functioning, self-sufficient family that positively contributes to society.
- Individual Treatment Plans are developed for both the mother and child to foster development and personal growth. Program services focus on trauma-informed substance abuse prevention, parenting and educational skills.
- The program provides a safe, stable, and stimulating environment for both the mother and the child, utilizing the least restrictive alternative to incarceration consistent with the needs for public safety.
- Program goals facilitate the mother/child bond, reunite the family, enhance community reintegration, foster successful independent living, and enhance self-reliance and self-esteem. The resultant mission is to break the inter-generational chain of crime and social services dependency.
The primary focus of the CPMP is to reunite mothers with their child(ren) and re-integrate them back into society as productive citizens by (a) providing a safe, stable, wholesome and stimulating environment, (b) establishing stability in the parent-child relationship and providing the opportunity for in-mate mothers to bond with their children and strengthen the family unit. Specific goals are:
- To PROMOTE community reintegration, independent living and self-reliance;
- To REDUCE the use of alcohol and drugs, involvement in criminal behavior, the rate of recidivism, Factors which result in trauma to children of incarcerated parents and ultimately long-term costs to the state;
- To INCREASE parenting skills, emotional stability, and educational and vocational opportunities;
- To ADDRESS substance abuse issues, behavioral and psychological factors which impact emotional stability, self-esteem, self-reliance, parent-child relationship and appropriate child development;
- To PROVIDE pre-release planning, employment skills, educational, vocational and parenting skills. (CDCR Website)


12.4: Material Hoists and Elevators
Material Hoists, Personnel Hoists and Elevators
General requirements
The employer shall comply with the manufacturer's specifications and limitations applicable to the operation of all hoists and elevators. Where manufacturer's specifications are not available, the limitations assigned to the equipment shall be based on the determinations of a professional engineer competent in the field.
Rated load capacities, recommended operating speeds, and special hazard warnings or instructions shall be posted on cars and platforms. The use of endless belt-type manlifts on construction shall be prohibited.
Material Hoists
Operating rules
Operating rules shall be established and posted at the operator's station of the hoist. Such rules shall include signal system and allowable line speed for various loads. Rules and notices shall be posted on the car frame or crosshead in a conspicuous location, including the statement "No Riders Allowed."
No person shall be allowed to ride on material hoists except for the purposes of inspection and maintenance.
Hoistway entrances
All entrances of the hoistways shall be protected by substantial gates or bars, which shall guard the full width of the landing entrance. All hoistway entrance bars and gates shall be painted with diagonal contrasting colors such as black and yellow stripes.
Overhead protection
Overhead protective covering of two inch planking, 3/4-inch plywood, or other solid material of equivalent strength, shall be provided on the top of every material hoist cage or platform.
Hoist towers
Hoist towers may be used with or without an enclosure on all sides. However, whichever alternative is chosen, the following applicable conditions shall be met:
- When a hoist tower is enclosed, it shall be enclosed on all sides for its entire height with a screen enclosure of 1/2-inch mesh, No. 18 U.S. gauge wire or equivalent, except for landing access.
- When a hoist tower is not enclosed, the hoist platform or car shall be totally enclosed (caged) on all sides for the full height between the floor and the overhead protective covering with 1/2-inch mesh of No. 14 U. S. gauge wire or equivalent. The hoist platform enclosure shall include the required gates for loading and unloading. A six foot high enclosure shall be provided on the unused sides of the hoist tower at ground level.
- Car arresting devices shall be installed to function in case of rope failure. All material hoist towers shall be designed by a licensed professional engineer.
Personnel Hoists
Outside hoist towers
Hoist towers outside the structure shall be enclosed for the full height on the side or sides used for entrance and exit to the structure. At the lowest landing, the enclosure on the sides not used for exit or entrance to the structure shall be enclosed to a height of at least 10 feet. Other sides of the tower adjacent to floors or scaffold platforms shall be enclosed to a height of 10 feet above the level of such floors or scaffolds.
Inside Hoist towers
Towers inside of structures shall be enclosed on all four sides throughout the full height. Towers shall be anchored to the structure at intervals not exceeding 25 feet. In addition to tie-ins, a series of guys shall be installed. Where tie-ins are not practical, the tower shall be anchored by means of guys made of wire rope at least one-half inch in diameter, securely fastened to anchorage to ensure stability.
Personnel hoist requirements
Hoistway doors or gates shall be not less than six feet six inches high and shall be provided with mechanical locks which cannot be operated from the landing side, and shall be accessible only to persons on the car. Cars shall be permanently enclosed on all sides and the top, except sides used for entrance and exit, which have car gates or doors. A door or gate shall be provided at each entrance to the car, which shall protect the full width and height of the car entrance opening. Overhead protective covering of two inch planking, 3/4- inch plywood or other solid material or equivalent strength shall be provided on the top of every personnel hoist. Doors or gates shall be provided with electric contacts, which do not allow movement of the hoist when door or gate is open. An emergency stop switch shall be provided in the car and marked "Stop."
Data plate
Cars shall be provided with a capacity and data plate secured in a conspicuous place on the car or crosshead.
Inspection
Following assembly and erection of hoists and before being put in service an inspection and test of all functions and safety devices shall be made under the supervision of a competent person. A similar inspection and test is required following major alteration of an existing installation. All hoists shall be inspected and tested at not more than three month intervals. The employer shall prepare a certification record which includes the date the inspection and test of all functions and safety devices was performed; the signature of the person who performed the inspection and test; and a serial number, or other identifier, for the hoist that was inspected and tested. The most recent certification record shall be maintained on file.
Specifications
All personnel hoists used by employees shall be constructed of materials and components, which meet the specifications for materials, construction safety devices, assembly, and structural integrity as stated in the American National Standard A 10.4-1963, Safety Requirements for Workmen Hoists.
Hoist tower that is not enclosed
When a hoist tower is not enclosed, the hoist platform or car shall be totally enclosed (caged) on all sides for the full height between the floor and the overhead protective covering with
3/4-inch mesh of No. 14 U. S. gauge wire or equivalent. The hoist platform enclosure shall include the required gates for loading and unloading.
These hoists shall be inspected and maintained on a weekly basis. Whenever the hoisting equipment is exposed to winds exceeding 35 miles per hour it shall be inspected and put in operable condition before reuse.


11.11: End of Chapter Problems
Fatty Acids
1. In terms of structure what distinguishes:
a. fatty acids from carboxylic acids
b. saturated fatty acid from unsaturated fatty acid.
2. Which has lower melting point? Explain.
a. lauric acid or myristic acid.
b. linoleic acid or oleic acid
Waxes
1. List the biological functions of waxes.
2. What property of waxes allows them to fulfill their primary biological functions?
Triglycerides
1. Construct a triglyceride from myristic acid, palmitic acid, oleic acid, and glycerol. Would you expect the triglyceride to be a liquid or a solid at room temperature? Explain.
2. List biological functions of triglycerides.
3. Why are triglycerides not found in cell membranes?
4.
5. Explain with IMF's why canola oil is a liquid at room temperature?
6. True or False
a. Triglycerides are carboxylic acids
b. Saturated fats contain only saturated fatty acids.
c. Unsaturated fats contain only unsaturated fatty acids.
Reactions of Lipids
1. Vegetable oils tend to become rancid more quickly than animal fats. Why?
2. Vegetable oils are easier to digest than animal fats. Why?
3. List four different ways to slow the spoilage (rancidity) of vegetable oil.
4. What does it mean to partially hydrogenate vegetable oil?
5. What are trans fats? How are they produced? Why do restaurants ban the use of trans fats in Ca?
6. Why do food companies partially hydrogenate vegetable oils? Why do they not fully hydrogenate vegetable oils?
7. Which is likely to have most trans-fats: vegetable oil, margarine, or butter? Explain.
8. Draw the products formed when the triglyceride below is saponified. Label each compound in the reaction based on the solubility classification.
9. Draw a picture of a soap micelle and clearly label the parts that interact with water and grease. Explain how soap works to clean grease in your hands.
10. What is hard water? Explain what happens when a soap interacts with a hard water ion.
Steroids
1. How is cholesterol used in the human body?
2. What are the biological functions of HDL and LDL?
3. What are the signs of heart disease in terms of HDL and LDL?
4. A person whose diet contains no cholesterol can still have high cholesterol levels. Explain.
5. What is the role of bile salts in digestion?
Membranes & Transport
1. Draw a sketch of the lipid bilayer. Name the kinds of lipids that make up membrane structure? Why are these lipids used to make up membrane structure?
2. What is the role of cholesterol in membranes?
3. Plant membranes contain a higher proportion of unsaturated fatty acids than do animal membranes. Which type of membrane would you expect to be more fluid (flexible), plant or animal?
4. The phospholipid known as Lecithin is an emulsifying agent but triglycerides are not. Account for the difference.
5. The lipids present in the cell membranes of fish, especially fish that live in cold water, contain more unsaturated fatty acid residues than do lipids found in the membranes of land animals. Explain why.
6. To function properly, membranes must flexible or fluid. In light of this fact, propose an explanation of why cell membranes in the feet and legs of reindeer contain a higher percentage of unsaturated fatty acids than do the cell membranes in the interior of its body.
7. Compare diffusion and facilitated diffusion. How are they similar and different?
8. Compare facilitated diffusion and active transport. How are they similar and different?
Digestion of Triglycerides
1. What part of the digestive system is involved in the digestion of triglycerides?
2. Name the functional group hydrolyzed when a triglyceride undergoes digestion.
3. Name an enzyme that catalyzes the digestion of triglycerides.
4. What products are formed when a triglyceride undergoes digestion?
5. Explain the role of bile salts in lipid digestion?
Fatty Acid Catabolism
1. Answer the following question based on a spiral of fatty acid catabolism:
a. What is the function of FAD in step 1 of the spiral?
b. Identify the type of reaction in step 2 of the spiral?
c. What is the function of NAD + in step 3 of the spiral?
d. What is the harvest of each spiral? (note: last spiral is different)
e. What is different about the harvest in the last spiral?
2. Calculate the net number of ATP’s produced when a myristic acid is activated, undergoes oxidation via adequate number of spirals, acetyl-CoA's pass through the correct number of citric acid cycles, and all the reduced coenzymes (NADH & FADH 2 ) pass through the electron transport chain.
3. Calculate the net number of ATP’s produced when one 10-carbon fatty acid is activated, undergoes oxidation via adequate number of spiral, acetyl-CoA's pass through the correct number of citric acid cycles, and all the reduced coenzymes (NADH & FADH 2 ) pass through the electron transport chain.
4. Where in a cell does fatty acid oxidation take place?
5. a. What are ketone bodies?
b. Why is acidosis (low blood pH) associated with the overproduction of ketone bodies?
c. In 2004 a low carb diet craze swept the US. People on the diet had very bad breath. What molecule is the reason for the bad breath?


4.9: Culture (2) الثقافة
In this section, you will be able to:
- Learn about modern hobbies in Arab countries.
Modern Hobbies in the Arab World:
Beyond traditional pastimes and leisure activities, Arabs engage in a wide array of hobbies that reflect their diverse interests, passions, and values. From recreational pursuits that celebrate cultural heritage to activities that foster personal growth and community engagement, the hobbies embraced by Arabs encompass a spectrum of interests and pursuits. In this context, exploring additional examples sheds light on the multifaceted nature of leisure and personal enrichment in Arab societies:
1.
2. Reading: The world of Arab literature is rich and varied, offering novels, poetry, and religious texts to those who enjoy reading as a pastime.
3. Gardening: Many Arabs, especially those residing in the countryside or with access to outdoor spaces, derive pleasure from nurturing gardens and cultivating plants, flowers, and herbs as a hobby.
4. Birdwatching: Nature enthusiasts throughout the Arab world pursue a hobby of observing and appreciating birds in their natural habitats.
5. Astronomy: Amateur astronomers in Arab countries enjoy studying stars, planets and observing celestial events as a hobby.
6. Traveling: For people who relish discovering new cultures and landscapes, exploring various regions, cities, and countries both domestically and internationally within the Arab world is a favorite pastime.
7. Sports: Many Arabs have a common hobby of participating in or watching sports such as soccer, basketball, volleyball, and tennis. Soccer is particularly popular among the sports. Many children play soccer in the streets at a very young age, and children and adults alike love watching and supporting Western teams, especially Real Madrid and Barcelona.
8. DIY projects: People who enjoy getting creative with their hands often pursue hobbies such as woodworking, home improvement projects, and crafting. These activities, collectively known as do-it-yourself (DIY), involve engaging in hands-on projects for personal enjoyment and satisfaction.
In essence, the hobbies cherished by Arabs serve as avenues for self-expression, connection with others, and the exploration of the world around them. Whether through traditional arts, outdoor adventures, or intellectual pursuits, these hobbies underscore the vibrancy and dynamism of Arab culture and society. By embracing a diverse range of leisure activities, Arabs enrich their lives and contribute to the tapestry of human experience in meaningful and diverse ways.
Activities:
Choose the correct option:
Choose the correct option:
Choose the correct option:


26.1: Physics of the Eye
Learning Objectives
By the end of this section, you will be able to:
- Explain the image formation by the eye.
- Explain why peripheral images lack detail and color.
- Define refractive indices.
- Analyze the accommodation of the eye for distant and near vision.
The eye is perhaps the most interesting of all optical instruments. The eye is remarkable in how it forms images and in the richness of detail and color it can detect. However, our eyes commonly need some correction, to reach what is called “normal” vision, but should be called ideal rather than normal. Image formation by our eyes and common vision correction are easy to analyze with the optics discussed in "Geometric Optics."
Figure 1 shows the basic anatomy of the eye. The cornea and lens form a system that, to a good approximation, acts as a single thin lens. For clear vision, a real image must be projected onto the light-sensitive retina, which lies at a fixed distance from the lens. The lens of the eye adjusts its power to produce an image on the retina for objects at different distances. The center of the image falls on the fovea, which has the greatest density of light receptors and the greatest acuity (sharpness) in the visual field. The variable opening (or pupil) of the eye along with chemical adaptation allows the eye to detect light intensities from the lowest observable to \(10^{10}\) times greater (without damage). This is an incredible range of detection. Our eyes perform a vast number of functions, such as sense direction, movement, sophisticated colors, and distance. Processing of visual nerve impulses begins with interconnections in the retina and continues in the brain. The optic nerve conveys signals received by the eye to the brain.
Refractive indices are crucial to image formation using lenses. The table shows refractive indices relevant to the eye. The biggest change in the refractive index, and bending of rays, occurs at the cornea rather than the lens. The ray diagram in Figure 2 shows image formation by the cornea and lens of the eye. The rays bend according to the refractive indices provided in the table. The cornea provides about two-thirds of the power of the eye, owing to the fact that speed of light changes considerably while traveling from air into cornea. The lens provides the remaining power needed to produce an image on the retina. The cornea and lens can be treated as a single thin lens, even though the light rays pass through several layers of material (such as cornea, aqueous humor, several layers in the lens, and vitreous humor), changing direction at each interface. The image formed is much like the one produced by a single convex lens. This is a case 1 image. Images formed in the eye are inverted but the brain inverts them once more to make them seem upright.
| Material | Index of Refraction |
| Water | 1.33 |
| Air | 1.0 |
| Comea | 1.38 |
| Aqueous humor | 1.34 |
| Lens | 1.41 average (varies throughout the lens, greatest in center) |
| Vitreous humor | 1.34 |
Refractive Indices Relevant to the Eye
As noted, the image must fall precisely on the retina to produce clear vision -- that is, the image distance \(d_{i}\) must equal the lens-to-retina distance. Because the lens-to-retina distance does not change, the image distance \(d_{i}\) must be the same for objects at all distances. The eye manages this by varying the power (and focal length) of the lens to accommodate for objects at various distances. The process of adjusting the eye’s focal length is called accommodation . A person with normal (ideal) vision can see objects clearly at distances ranging from 25 cm to essentially infinity. However, although the near point (the shortest distance at which a sharp focus can be obtained) increases with age (becoming meters for some older people), we will consider it to be 25 cm in our treatment here.
Figure 3 shows the accommodation of the eye for distant and near vision. Since light rays from a nearby object can diverge and still enter the eye, the lens must be more converging (more powerful) for close vision than for distant vision. To be more converging, the lens is made thicker by the action of the ciliary muscle surrounding it. The eye is most relaxed when viewing distant objects, one reason that microscopes and telescopes are designed to produce distant images. Vision of very distant objects is called totally relaxed, while close vision is termed accommodated , with the closest vision being fully accommodated.
We will use the thin lens equations to examine image formation by the eye quantitatively. First, note the power of a lens is given as \(p = 1/f\), so we rewrite the thin lens equations as \[P = \frac{1}{d_{o}} + \frac{1}{d_{i}} \label{26.2.1}\] and \[\frac{h_{i}}{h_{o}} = -\frac{d_{i}}{d_{o}} = m \label{26.2.2}.\] We understand that \(d_{i}\) must equal the lens-to-retina distance to obtain clear vision, and that normal vision is possible for objects at distances \(d_{o} = 25 cm\) to infinity.
TAKE-HOME EXPERIMENT: THE PUPIL
Look at the central transparent area of someone’s eye, the pupil, in normal room light. Estimate the diameter of the pupil. Now turn off the lights and darken the room. After a few minutes turn on the lights and promptly estimate the diameter of the pupil. What happens to the pupil as the eye adjusts to the room light? Explain your observations.
The eye can detect an impressive amount of detail, considering how small the image is on the retina. To get some idea of how small the image can be, consider the following example.
Example \(\PageIndex{1}\):Size of Image on Retina
What is the size of the image on the retina of a \(1.20 \times 10^{-2}\) cm diameter human hair, held at arm’s length (60.0 cm) away? Take the lens-to-retina distance to be 2.00 cm.
Strategy:
We want to find the height of the image \(h_{i}\), given the height of the object is \(h_{o} = 1.20 \times 10^{-2}\) cm. We also know that the object is 60.0 cm away, so that \(d_{o} = 60.0 cm\). For clear vision, the image distance must equal the lens-to-retina distance, and so \(d_{i} = 2.00 cm\). The equation \(\frac{h_{i}}{h_{o}} = - \frac{d_{i}}{d_{o}} = m\) can be used to find \(h_{i}\) with the known information.
Solution
The only unknown variable in the equation \(\frac{h_{i}}{h_{o}} = -\frac{d_{i}}{d_{o}} = m\) is \(h_{i}\): \[\frac{h_{i}}{h_{o}} = -\frac{d_{i}}{d_{o}}.\] Rearranging to isolate \(h_{i}\) yields \[h_{i} = -h_{o} \cdot \frac{d_{i}}{d_{o}}. \label{26.2.3}\] Substituting the known values gives \[h_{i} = - \left( 1.20 \times 10^{-2} cm \right) \frac{2.00 cm}{60.0 cm}\] \[= -4.00 \times 10^{-4} cm.\]
Discussion:
This truly small image is not the smallest discernible -- that is, the limit to visual acuity is even smaller than this. Limitations on visual acuity have to do with the wave properties of light and will be discussed in the next chapter. Some limitation is also due to the inherent anatomy of the eye and processing that occurs in our brain.
Example \(\PageIndex{2}\):Power Range of the Eye
Calculate the power of the eye when viewing objects at the greatest and smallest distances possible with normal vision, assuming a lens-to-retina distance of 2.00 cm (a typical value).
Strategy:
For clear vision, the image must be on the retina, and so \(d_{i} = 2.00 cm\) here. For distant vision, \(d_{o} \approx \infty\), and for close vision, \(d_{o} = 25.0 cm\), as discussed earlier. The equation \(P = \frac{1}{d_{o}} + \frac{1}{d_{i}}\) as written just above, can be used directly to solve for \(P\) in both cases, since we know \(d_{i}\) and \(d_{o}\). Power has units of diopters, where \(1 D = 1/m\), and so we should express all distances in meters.
Solution
For distant vision, \[P = \frac{1}{d_{o}} + \frac{1}{d_{i}} = \frac{1}{\infty} + \frac{1}{0.0200m}.\] Since \(1/ \infty = 0\), this gives \[P = 0 + 50.0/m = 50.0 D \left(distant~vision\right).\] Now, for close vision, \[P = \frac{1}{d_{o}} + \frac{1}{d_{i}} = \frac{1}{0.250 m} + \frac{1}{0.0200 m}\] \[= \frac{4.00}{m} + \frac{50.0}{m} = 4.00D + 50.0 D\] \[= 54.0 D \left( close~vision \right)l\]
Discussion:
For an eye with this typical 2.00 cm lens-to-retina distance, the power of the eye ranges from 50.0 D (for distant totally relaxed vision) to 54.0 D (for close fully accommodated vision), which is an 8% increase. This increase in power for close vision is consistent with the preceding discussion and the ray tracing in Figure 3. An 8% ability to accommodate is considered normal but is typical for people who are about 40 years old. Younger people have greater accommodation ability, whereas older people gradually lose the ability to accommodate. When an optometrist identifies accommodation as a problem in elder people, it is most likely due to stiffening of the lens. The lens of the eye changes with age in ways that tend to preserve the ability to see distant objects clearly but do not allow the eye to accommodate for close vision, a condition called presbyopia (literally, elder eye). To correct this vision defect, we place a converging, positive power lens in front of the eye, such as found in reading glasses. Commonly available reading glasses are rated by their power in diopters, typically ranging from 1.0 to 3.5 D.
Summary
- Image formation by the eye is adequately described by the thin lens equations: \[P = \frac{1}{d_{o}} + \frac{1}{d_{i}} and \frac{h_{i}}{h_{o}} = -\frac{d_{i}}{d_{o}} = m.\]
- The eye produces a real image on the retina by adjusting its focal length and power in a process called accommodation.
- For close vision, the eye is fully accommodated and has its greatest power, whereas for distant vision, it is totally relaxed and has its smallest power.
- The loss of the ability to accommodate with age is called presbyopia, which is corrected by the use of a converging lens to add power for close vision.
Glossary
- accommodation
- the ability of the eye to adjust its focal length is known as accommodation
- presbyopia
- a condition in which the lens of the eye becomes progressively unable to focus on objects close to the viewer


6.6: Huff Gravity Model
- Use the Huff gravity model to estimate potential sales for a site
You have narrowed your possible new sites down to three locations. Each has met various aspects of what exactly you are looking for in a location. How might you want to proceed to compare these three to determine the best one? One option might be the Huff Model.
The trading area is the area where a business will be pulling customers from. Remember back to our model:
We have a primary trading area, secondary trading area and fringe trading area to review. Huff’s model may be useful for helping us determine how many shoppers we may get in each of these areas.
Huff’s model is a mathematical model that recognizes the correlation between patronage and distance from the location of the store. So in other words, the further a consumer is from your location, the less likely it will be for that person to shop there. This model does not account for other factors that may affect a customer patronizing your store, such as having a product or service that is specialized, that they cannot get elsewhere. It simply looks at the distance from the retail location.
This model can help you to determine areas with high and low sales potential based on several factors including how many people live within a certain radius of your proposed location and what the disposable income is in this market. Incorporating the Huff model along with GIS and census information can give potential new businesses a great deal of information about several possible sites.
Learn More
If you would love to look further at how this model works, check out “ How the Huff Gravity Model Predicts How Many Customers Will Visit Your Store ” or “Huff Model” on ArcGIS.com for all the mathematical details!
Contributors and Attributions
- Huff Gravity Model. Authored by : Freedom Learning Group. Provided by : Lumen Learning. License : CC BY: Attribution
- Fringe, Secondary, and Primary Trading Areas Image. Authored by : Lumen Learning . Provided by : Lumen Learning. License : CC BY: Attribution


15.3: Virulence Factors
- Explain how virulence factors contribute to signs and symptoms of infectious disease
- Differentiate between endotoxins and exotoxins
- Describe and differentiate between various types of exotoxins
- Describe the mechanisms viruses use for adhesion and antigenic variation
In the previous section, we explained that some pathogens are more virulent than others. This is due to the unique virulence factors produced by individual pathogens, which determine the extent and severity of disease they may cause. A pathogen’s virulence factors are encoded by genes that can be identified using molecular Koch’s postulates. When genes encoding virulence factors are inactivated, virulence in the pathogen is diminished. In this section, we examine various types and specific examples of virulence factors and how they contribute to each step of pathogenesis.
Virulence Factors for Adhesion
As discussed in the previous section, the first two steps in pathogenesis are exposure and adhesion. Recall that an adhesin is a protein or glycoprotein found on the surface of a pathogen that attaches to receptors on the host cell. Adhesins are found on bacterial, viral, fungal, and protozoan pathogens. One example of a bacterial adhesin is type 1 fimbrial adhesin, a molecule found on the tips of fimbriae of enterotoxigenic E. coli (ETEC). Recall that fimbriae are hairlike protein bristles on the cell surface. Type 1 fimbrial adhesin allows the fimbriae of ETEC cells to attach to the mannose glycans expressed on intestinal epithelial cells. Table \(\PageIndex{1}\) lists common adhesins found in some of the pathogens we have discussed or will be seeing later in this chapter.
| Pathogen | Disease | Adhesin | Attachment Site |
|---|---|---|---|
| Streptococcus pyogenes | Strep throat | Protein F | Respiratory epithelial cells |
| Streptococcus mutans | Dental caries | Adhesin P1 | Teeth |
| Neisseria gonorrhoeae | Gonorrhea | Type IV pili | Urethral epithelial cells |
| Enterotoxigenic E. coli (ETEC) | Traveler’s diarrhea | Type 1 fimbriae | Intestinal epithelial cells |
| Vibrio cholerae | Cholera | N-methylphenylalanine pili | Intestinal epithelial cells |
The presence of bacteria in Michael’s blood is a sign of infection, since blood is normally sterile. There is no indication that the bacteria entered the blood through an injury. Instead, it appears the portal of entry was the gastrointestinal route. Based on Michael’s symptoms, the results of his blood test, and the fact that Michael was the only one in the family to partake of the hot dogs, the physician suspects that Michael is suffering from a case of listeriosis.
Listeria monocytogenes , the facultative intracellular pathogen that causes listeriosis, is a common contaminant in ready-to-eat foods such as lunch meats and dairy products. Once ingested, these bacteria invade intestinal epithelial cells and translocate to the liver, where they grow inside hepatic cells. Listeriosis is fatal in about one in five normal healthy people, and mortality rates are slightly higher in patients with pre-existing conditions that weaken the immune response. A cluster of virulence genes encoded on a pathogenicity island is responsible for the pathogenicity of L. monocytogenes . These genes are regulated by a transcriptional factor known as peptide chain release factor 1 (PrfA). One of the genes regulated by PrfA is hyl , which encodes a toxin known as listeriolysin O (LLO), which allows the bacterium to escape vacuoles upon entry into a host cell. A second gene regulated by PrfA is actA, which encodes for a surface protein known as actin assembly-inducing protein (ActA). ActA is expressed on the surface of Listeria and polymerizes host actin. This enables the bacterium to produce actin tails, move around the cell’s cytoplasm, and spread from cell to cell without exiting into the extracellular compartment.
Michael’s condition has begun to worsen. He is now experiencing a stiff neck and hemiparesis (weakness of one side of the body). Concerned that the infection is spreading, the physician decides to conduct additional tests to determine what is causing these new symptoms.
- What kind of pathogen causes listeriosis, and what virulence factors contribute to the signs and symptoms Michael is experiencing?
- Is it likely that the infection will spread from Michael’s blood? If so, how might this explain his new symptoms?
Bacterial Exoenzymes and Toxins as Virulence Factors
After exposure and adhesion, the next step in pathogenesis is invasion, which can involve enzymes and toxins. Many pathogens achieve invasion by entering the bloodstream, an effective means of dissemination because blood vessels pass close to every cell in the body. The downside of this mechanism of dispersal is that the blood also includes numerous elements of the immune system. Various terms ending in –emia are used to describe the presence of pathogens in the bloodstream. The presence of bacteria in blood is called bacteremia. Bacteremia involving pyogens(pus-forming bacteria) is called pyemia. When viruses are found in the blood, it is called viremia. The term toxemiadescribes the condition when toxins are found in the blood. If bacteria are both present and multiplying in the blood, this condition is called septicemia.
Patients with septicemia are described as septic, which can lead to shock, a life-threatening decrease in blood pressure (systolic pressure <90 mm Hg) that prevents cells and organs from receiving enough oxygen and nutrients. Some bacteria can cause shock through the release of toxins (virulence factors that can cause tissue damage) and lead to low blood pressure. Gram-negative bacteria are engulfed by immune system phagocytes, which then release tumor necrosis factor, a molecule involved in inflammation and fever. Tumor necrosis factor binds to blood capillaries to increase their permeability, allowing fluids to pass out of blood vessels and into tissues, causing swelling, or edema(Figure \(\PageIndex{1}\)). With high concentrations of tumor necrosis factor, the inflammatory reaction is severe and enough fluid is lost from the circulatory system that blood pressure decreases to dangerously low levels. This can have dire consequences because the heart, lungs, and kidneys rely on normal blood pressure for proper function; thus, multi-organ failure, shock, and death can occur.
Exoenzymes
Some pathogens produce extracellular enzymes, or exoenzymes, that enable them to invade host cells and deeper tissues. Exoenzymes have a wide variety of targets. Some general classes of exoenzymes and associated pathogens are listed in Table \(\PageIndex{2}\). Each of these exoenzymes functions in the context of a particular tissue structure to facilitate invasion or support its own growth and defend against the immune system. For example, hyaluronidase S, an enzyme produced by pathogens like Staphylococcus aureus , Streptococcus pyogenes , and Clostridium perfringens , degrades the glycoside hylauronan (hyaluronic acid), which acts as an intercellular cement between adjacent cells in connective tissue (Figure \(\PageIndex{2}\)). This allows the pathogen to pass through the tissue layers at the portal of entry and disseminate elsewhere in the body (Figure \(\PageIndex{2}\)).
| Class | Example | Function |
|---|---|---|
| Glycohydrolases | Hyaluronidase S in Staphylococcus aureus | Degrades hyaluronic acid that cements cells together to promote spreading through tissues |
| Nucleases | DNAse produced by S. aureus | Degrades DNA released by dying cells (bacteria and host cells) that can trap the bacteria, thus promoting spread |
| Phospholipases | Phospholipase C of Bacillus anthracis | Degrades phospholipid bilayer of host cells, causing cellular lysis, and degrade membrane of phagosomes to enable escape into the cytoplasm |
| Proteases | Collagenase in Clostridium perfringens | Degrades collagen in connective tissue to promote spread |
Pathogen-produced nucleases, such as DNAse produced by S. aureus, degrade extracellular DNA as a means of escape and spreading through tissue. As bacterial and host cells die at the site of infection, they lyse and release their intracellular contents. The DNA chromosome is the largest of the intracellular molecules, and masses of extracellular DNA can trap bacteria and prevent their spread. S. aureus produces a DNAse to degrade the mesh of extracellular DNA so it can escape and spread to adjacent tissues. This strategy is also used by S. aureus and other pathogens to degrade and escape webs of extracellular DNA produced by immune system phagocytes to trap the bacteria.
Enzymes that degrade the phospholipids of cell membranes are called phospholipases. Their actions are specific in regard to the type of phospholipids they act upon and where they enzymatically cleave the molecules. The pathogen responsible for anthrax, B. anthracis, produces phospholipase C. When B. anthracis is ingested by phagocytic cells of the immune system, phospholipase C degrades the membrane of the phagosome before it can fuse with the lysosome, allowing the pathogen to escape into the cytoplasm and multiply. Phospholipases can also target the membrane that encloses the phagosome within phagocytic cells. As described earlier in this chapter, this is the mechanism used by intracellular pathogens such as L. monocytogenes and Rickettsia to escape the phagosome and multiply within the cytoplasm of phagocytic cells. The role of phospholipases in bacterial virulence is not restricted to phagosomal escape. Many pathogens produce phospholipases that act to degrade cell membranes and cause lysis of target cells. These phospholipases are involved in lysis of red blood cells, white blood cells, and tissue cells.
Bacterial pathogens also produce various protein-digesting enzymes, or proteases. Proteases can be classified according to their substrate target (e.g., serine proteases target proteins with the amino acid serine) or if they contain metals in their active site (e.g., zinc metalloproteases contain a zinc ion, which is necessary for enzymatic activity).
One example of a protease that contains a metal ion is the exoenzyme collagenase. Collagenase digests collagen, the dominant protein in connective tissue. Collagen can be found in the extracellular matrix, especially near mucosal membranes, blood vessels, nerves, and in the layers of the skin. Similar to hyaluronidase, collagenase allows the pathogen to penetrate and spread through the host tissue by digesting this connective tissue protein. The collagenase produced by the gram-positive bacterium Clostridium perfringens , for example, allows the bacterium to make its way through the tissue layers and subsequently enter and multiply in the blood (septicemia). C. perfringens then uses toxins and a phospholipase to cause cellular lysis and necrosis. Once the host cells have died, the bacterium produces gas by fermenting the muscle carbohydrates. The widespread necrosis of tissue and accompanying gas are characteristic of the condition known as gas gangrene (Figure \(\PageIndex{3}\)).
Toxins
In addition to exoenzymes, certain pathogens are able to produce toxins, biological poisons that assist in their ability to invade and cause damage to tissues. The ability of a pathogen to produce toxins to cause damage to host cells is called toxigenicity.
Toxins can be categorized as endotoxins or exotoxins. The lipopolysaccharide (LPS) found on the outer membrane of gram-negative bacteria is called endotoxin (Figure \(\PageIndex{4}\)). During infection and disease, gram-negative bacterial pathogens release endotoxin either when the cell dies, resulting in the disintegration of the membrane, or when the bacterium undergoes binary fission. The lipid component of endotoxin, lipid A, is responsible for the toxic properties of the LPS molecule. Lipid A is relatively conserved across different genera of gram-negative bacteria; therefore, the toxic properties of lipid A are similar regardless of the gram-negative pathogen. In a manner similar to that of tumor necrosis factor, lipid A triggers the immune system’s inflammatory response (see Inflammation and Fever ). If the concentration of endotoxin in the body is low, the inflammatory response may provide the host an effective defense against infection; on the other hand, high concentrations of endotoxin in the blood can cause an excessive inflammatory response, leading to a severe drop in blood pressure, multi-organ failure, and death.
A classic method of detecting endotoxin is by using the Limulus amebocyte lysate (LAL) test. In this procedure, the blood cells (amebocytes) of the horseshoe crab ( Limulus polyphemus ) is mixed with a patient’s serum. The amebocytes will react to the presence of any endotoxin. This reaction can be observed either chromogenically (color) or by looking for coagulation (clotting reaction) to occur within the serum. An alternative method that has been used is an enzyme-linked immunosorbent assay (ELISA) that uses antibodies to detect the presence of endotoxin.
Unlike the toxic lipid A of endotoxin, exotoxins are protein molecules that are produced by a wide variety of living pathogenic bacteria. Although some gram-negative pathogens produce exotoxins, the majority are produced by gram-positive pathogens. Exotoxins differ from endotoxin in several other key characteristics, summarized in Table \(\PageIndex{3}\). In contrast to endotoxin, which stimulates a general systemic inflammatory response when released, exotoxins are much more specific in their action and the cells they interact with. Each exotoxin targets specific receptors on specific cells and damages those cells through unique molecular mechanisms. Endotoxin remains stable at high temperatures, and requires heating at 121 °C (250 °F) for 45 minutes to inactivate. By contrast, most exotoxins are heat labile because of their protein structure, and many are denatured (inactivated) at temperatures above 41 °C (106 °F). As discussed earlier, endotoxin can stimulate a lethal inflammatory response at very high concentrations and has a measured LD 50 of 0.24 mg/kg. By contrast, very small concentrations of exotoxins can be lethal. For example, botulinum toxin, which causes botulism, has an LD 50 of 0.000001 mg/kg (240,000 times more lethal than endotoxin).
| Characteristic | Endotoxin | Exotoxin |
|---|---|---|
| Source | Gram-negative bacteria | Gram-positive (primarily) and gram-negative bacteria |
| Composition | Lipid A component of lipopolysaccharide | Protein |
| Effect on host | General systemic symptoms of inflammation and fever | Specific damage to cells dependent upon receptor-mediated targeting of cells and specific mechanisms of action |
| Heat stability | Heat stable | Most are heat labile, but some are heat stable |
| LD 50 | High | Low |
The exotoxins can be grouped into three categories based on their target: intracellular targeting, membrane disrupting, and superantigens. Table \(\PageIndex{4}\) provides examples of well-characterized toxins within each of these three categories.
| Category | Example | Pathogen | Mechanism and Disease |
|---|---|---|---|
| Intracellular-targeting toxins | Cholera toxin | Vibrio cholerae | Activation of adenylate cyclase in intestinal cells, causing increased levels of cyclic adenosine monophosphate (cAMP) and secretion of fluids and electrolytes out of cell, causing diarrhea |
| Tetanus toxin | Clostridium teta | niInhibits the release of inhibitory neurotransmitters in the central nervous system, causing spastic paralysis | |
| Botulinum toxin | Clostridium botulinum | Inhibits release of the neurotransmitter acetylcholine from neurons, resulting in flaccid paralysis | |
| Diphtheria toxin | Corynebacterium diphtheriae | Inhibition of protein synthesis, causing cellular death | |
| Membrane-disrupting toxins | Streptolysin | Streptococcus pyogenes | Proteins that assemble into pores in cell membranes, disrupting their function and killing the cell |
| Pneumolysin | Streptococcus pneumoniae | ||
| Alpha-toxin | Staphylococcus aureus | ||
| Alpha-toxin | Clostridium perfringens | Phospholipases that degrade cell membrane phospholipids, disrupting membrane function and killing the cell | |
| Phospholipase C | Pseudomonas aeruginosa | ||
| Beta-toxin | Staphylococcus aureus | ||
| Superantigens | Toxic shock syndrome toxin | Staphylococcus aureus | Stimulates excessive activation of immune system cells and release of cytokines (chemical mediators) from immune system cells. Life-threatening fever, inflammation, and shock are the result. |
| Streptococcal mitogenic exotoxin | Streptococcus pyogenes | ||
| Streptococcal pyrogenic toxins | Streptococcus pyogenes |
The intracellular targeting toxins comprise two components: A for activity and B for binding. Thus, these types of toxins are known as A-B exotoxins (Figure \(\PageIndex{5}\)). The B component is responsible for the cellular specificity of the toxin and mediates the initial attachment of the toxin to specific cell surface receptors. Once the A-B toxin binds to the host cell, it is brought into the cell by endocytosis and entrapped in a vacuole. The A and B subunits separate as the vacuole acidifies. The A subunit then enters the cell cytoplasm and interferes with the specific internal cellular function that it targets.
Four unique examples of A-B toxins are the diphtheria, cholera, botulinum, and tetanus toxins. The diphtheria toxin is produced by the gram-positive bacterium Corynebacterium diphtheriae , the causative agent of nasopharyngeal and cutaneous diphtheria. After the A subunit of the diphtheria toxin separates and gains access to the cytoplasm, it facilitates the transfer of adenosine diphosphate (ADP)-ribose onto an elongation-factor protein (EF-2) that is needed for protein synthesis. Hence, diphtheria toxin inhibits protein synthesis in the host cell, ultimately killing the cell (Figure \(\PageIndex{6}\)).
Cholera toxin is an enterotoxin produced by the gram-negative bacterium Vibrio cholerae and is composed of one A subunit and five B subunits. The mechanism of action of the cholera toxin is complex. The B subunits bind to receptors on the intestinal epithelial cell of the small intestine. After gaining entry into the cytoplasm of the epithelial cell, the A subunit activates an intracellular G protein. The activated G protein, in turn, leads to the activation of the enzyme adenyl cyclase, which begins to produce an increase in the concentration of cyclic AMP (a secondary messenger molecule). The increased cAMP disrupts the normal physiology of the intestinal epithelial cells and causes them to secrete excessive amounts of fluid and electrolytes into the lumen of the intestinal tract, resulting in severe “rice-water stool” diarrhea characteristic of cholera.
Botulinum toxin (also known as botox) is a neurotoxin produced by the gram-positive bacterium Clostridium botulinum . It is the most acutely toxic substance known to date. The toxin is composed of a light A subunit and heavy protein chain B subunit. The B subunit binds to neurons to allow botulinum toxin to enter the neurons at the neuromuscular junction. The A subunit acts as a protease, cleaving proteins involved in the neuron’s release of acetylcholine, a neurotransmitter molecule. Normally, neurons release acetylcholine to induce muscle fiber contractions. The toxin’s ability to block acetylcholine release results in the inhibition of muscle contractions, leading to muscle relaxation. This has the potential to stop breathing and cause death. Because of its action, low concentrations of botox are used for cosmetic and medical procedures, including the removal of wrinkles and treatment of overactive bladder.
Another neurotoxin is tetanus toxin, which is produced by the gram-positive bacterium Clostridium tetani . This toxin also has a light A subunit and heavy protein chain B subunit. Unlike botulinum toxin, tetanus toxin binds to inhibitory interneurons, which are responsible for release of the inhibitory neurotransmitters glycine and gamma-aminobutyric acid (GABA). Normally, these neurotransmitters bind to neurons at the neuromuscular junction, resulting in the inhibition of acetylcholine release. Tetanus toxin inhibits the release of glycine and GABA from the interneuron, resulting in permanent muscle contraction. The first symptom is typically stiffness of the jaw (lockjaw). Violent muscle spasms in other parts of the body follow, typically culminating with respiratory failure and death. Figure \(\PageIndex{7}\) shows the actions of both botulinum and tetanus toxins.
Membrane-disrupting toxins affect cell membrane function either by forming pores or by disrupting the phospholipid bilayer in host cell membranes. Two types of membrane-disrupting exotoxins are hemolysins and leukocidins, which form pores in cell membranes, causing leakage of the cytoplasmic contents and cell lysis. These toxins were originally thought to target red blood cells (erythrocytes) and white blood cells (leukocytes), respectively, but we now know they can affect other cells as well. The gram-positive bacterium Streptococcus pyogenes produces streptolysins, water-soluble hemolysins that bind to the cholesterol moieties in the host cell membrane to form a pore. The two types of streptolysins, O and S, are categorized by their ability to cause hemolysis in erythrocytes in the absence or presence of oxygen. Streptolysin O is not active in the presence of oxygen, whereas streptolysin S is active in the presence of oxygen. Other important pore-forming membrane-disrupting toxins include alpha toxin of Staphylococcus aureus and pneumolysin of Streptococcus pneumoniae .
Bacterial phospholipases are membrane-disrupting toxins that degrade the phospholipid bilayer of cell membranes rather than forming pores. We have already discussed the phospholipases associated with B. anthracis, L. pneumophila, and Rickettsia species that enable these bacteria to effect the lysis of phagosomes. These same phospholipases are also hemolysins. Other phospholipases that function as hemolysins include the alpha toxin of Clostridium perfringens , phospholipase C of P. aeruginosa , and beta toxin of Staphylococcus aureus .
Some strains of S. aureus also produce a leukocidin called Panton-Valentine leukocidin (PVL). PVL consists of two subunits, S and F. The S component acts like the B subunit of an A-B exotoxin in that it binds to glycolipids on the outer plasma membrane of animal cells. The F-component acts like the A subunit of an A-B exotoxin and carries the enzymatic activity. The toxin inserts and assembles into a pore in the membrane. Genes that encode PVL are more frequently present in S. aureus strains that cause skin infections and pneumonia. 1 PVL promotes skin infections by causing edema, erythema (reddening of the skin due to blood vessel dilation), and skin necrosis. PVL has also been shown to cause necrotizing pneumonia. PVL promotes pro-inflammatory and cytotoxic effects on alveolar leukocytes. This results in the release of enzymes from the leukocytes, which, in turn, cause damage to lung tissue.
The third class of exotoxins is the superantigens. These are exotoxins that trigger an excessive, nonspecific stimulation of immune cells to secrete cytokines (chemical messengers). The excessive production of cytokines, often called a cytokine storm, elicits a strong immune and inflammatory response that can cause life-threatening high fevers, low blood pressure, multi-organ failure, shock, and death. The prototype superantigen is the toxic shock syndrome toxin of S. aureus . Most toxic shock syndrome cases are associated with vaginal colonization by toxin-producing S. aureus in menstruating women; however, colonization of other body sites can also occur. Some strains of Streptococcus pyogenes also produce superantigens; they are referred to as the streptococcal mitogenic exotoxins and the streptococcal pyrogenic toxins.
- Describe how exoenzymes contribute to bacterial invasion.
- Explain the difference between exotoxins and endotoxin.
- Name the three classes of exotoxins.
Virulence Factors for Survival in the Host and Immune Evasion
Evading the immune system is also important to invasiveness. Bacteria use a variety of virulence factors to evade phagocytosis by cells of the immune system. For example, many bacteria produce capsules, which are used in adhesion but also aid in immune evasion by preventing ingestion by phagocytes. The composition of the capsule prevents immune cells from being able to adhere and then phagocytose the cell. In addition, the capsule makes the bacterial cell much larger, making it harder for immune cells to engulf the pathogen (Figure \(\PageIndex{8}\)). A notable capsule-producing bacterium is the gram-positive pathogen Streptococcus pneumoniae , which causes pneumococcal pneumonia, meningitis, septicemia, and other respiratory tract infections. Encapsulated strains of S. pneumoniae are more virulent than nonencapsulated strains and are more likely to invade the bloodstream and cause septicemia and meningitis.
Some pathogens can also produce proteases to protect themselves against phagocytosis. As described in Adaptive Specific Host Defenses , the human immune system produces antibodies that bind to surface molecules found on specific bacteria (e.g., capsules, fimbriae, flagella, LPS). This binding initiates phagocytosis and other mechanisms of antibacterial killing and clearance. Proteases combat antibody-mediated killing and clearance by attacking and digesting the antibody molecules (Figure \(\PageIndex{8}\)).
In addition to capsules and proteases, some bacterial pathogens produce other virulence factors that allow them to evade the immune system. The fimbriae of certain species of Streptococcus contain M protein, which alters the surface of Streptococcus and inhibits phagocytosis by blocking the binding of the complement molecules that assist phagocytes in ingesting bacterial pathogens. The acid-fast bacterium Mycobacterium tuberculosis (the causative agent of tuberculosis) produces a waxy substance known as mycolic acid in its cell envelope. When it is engulfed by phagocytes in the lung, the protective mycolic acid coat enables the bacterium to resist some of the killing mechanisms within the phagolysosome.
Some bacteria produce virulence factors that promote infection by exploiting molecules naturally produced by the host. For example, most strains of Staphylococcus aureus produce the exoenzyme coagulase, which exploits the natural mechanism of blood clotting to evade the immune system. Normally, blood clotting is triggered in response to blood vessel damage; platelets begin to plug the clot, and a cascade of reactions occurs in which fibrinogen, a soluble protein made by the liver, is cleaved into fibrin. Fibrin is an insoluble, thread-like protein that binds to blood platelets, cross-links, and contracts to form a mesh of clumped platelets and red blood cells. The resulting clot prevents further loss of blood from the damaged blood vessels. However, if bacteria release coagulase into the bloodstream, the fibrinogen-to-fibrin cascade is triggered in the absence of blood vessel damage. The resulting clot coats the bacteria in fibrin, protecting the bacteria from exposure to phagocytic immune cells circulating in the bloodstream.
Whereas coagulase causes blood to clot, kinases have the opposite effect by triggering the conversion of plasminogen to plasmin, which is involved in the digestion of fibrin clots. By digesting a clot, kinases allow pathogens trapped in the clot to escape and spread, similar to the way that collagenase, hyaluronidase, and DNAse facilitate the spread of infection. Examples of kinases include staphylokinases and streptokinases, produced by Staphylococcus aureus and Streptococcus pyogenes , respectively. It is intriguing that S. aureus can produce both coagulase to promote clotting and staphylokinase to stimulate the digestion of clots. The action of the coagulase provides an important protective barrier from the immune system, but when nutrient supplies are diminished or other conditions signal a need for the pathogen to escape and spread, the production of staphylokinase can initiate this process.
A final mechanism that pathogens can use to protect themselves against the immune system is called antigenic variation, which is the alteration of surface proteins so that a pathogen is no longer recognized by the host’s immune system. For example, the bacterium Borrelia burgdorferi , the causative agent of Lyme disease, contains a surface lipoprotein known as VlsE. Because of genetic recombination during DNA replication and repair, this bacterial protein undergoes antigenic variation. Each time fever occurs, the VlsE protein in B. burgdorferi can differ so much that antibodies against previous VlsE sequences are not effective. It is believed that this variation in the VlsE contributes to the ability B. burgdorferi to cause chronic disease. Another important human bacterial pathogen that uses antigenic variation to avoid the immune system is Neisseria gonorrhoeae , which causes the sexually transmitted disease gonorrhea. This bacterium is well known for its ability to undergo antigenic variation of its type IV pili to avoid immune defenses.
- Name at least two ways that a capsule provides protection from the immune system.
- Besides capsules, name two other virulence factors used by bacteria to evade the immune system.
Based on Michael’s reported symptoms of stiff neck and hemiparesis, the physician suspects that the infection may have spread to his nervous system. The physician decides to order a spinal tap to look for any bacteria that may have invaded the meninges and cerebrospinal fluid (CSF), which would normally be sterile. To perform the spinal tap, Michael’s lower back is swabbed with an iodine antiseptic and then covered with a sterile sheet. The needle is aseptically removed from the manufacturer’s sealed plastic packaging by the clinician’s gloved hands. The needle is inserted and a small volume of fluid is drawn into an attached sample tube. The tube is removed, capped and a prepared label with Michael’s data is affixed to it. This STAT (urgent or immediate analysis required) specimen is divided into three separate sterile tubes, each with 1 mL of CSF. These tubes are immediately taken to the hospital’s lab, where they are analyzed in the clinical chemistry, hematology, and microbiology departments. The preliminary results from all three departments indicate there is a cerebrospinal infection occurring, with the microbiology department reporting the presence of a gram-positive rod in Michael’s CSF.
These results confirm what his physician had suspected: Michael’s new symptoms are the result of meningitis, acute inflammation of the membranes that protect the brain and spinal cord. Because meningitis can be life threatening and because the first antibiotic therapy was not effective in preventing the spread of infection, Michael is prescribed an aggressive course of two antibiotics, ampicillin and gentamicin, to be delivered intravenously. Michael remains in the hospital for several days for supportive care and for observation. After a week, he is allowed to return home for bed rest and oral antibiotics. After 3 weeks of this treatment, he makes a full recovery.
Viral Virulence
Although viral pathogens are not similar to bacterial pathogens in terms of structure, some of the properties that contribute to their virulence are similar. Viruses use adhesins to facilitate adhesion to host cells, and certain enveloped viruses rely on antigenic variation to avoid the host immune defenses. These virulence factors are discussed in more detail in the following sections.
Viral Adhesins
One of the first steps in any viral infection is adhesion of the virus to specific receptors on the surface of cells. This process is mediated by adhesins that are part of the viral capsid or membrane envelope. The interaction of viral adhesins with specific cell receptors defines the tropism (preferential targeting) of viruses for specific cells, tissues, and organs in the body. The spike protein hemagglutinin found on Influenzavirus is an example of a viral adhesin; it allows the virus to bind to the sialic acid on the membrane of host respiratory and intestinal cells. Another viral adhesin is the glycoprotein gp20, found on HIV. For HIV to infect cells of the immune system, it must interact with two receptors on the surface of cells. The first interaction involves binding between gp120 and the CD4 cellular marker that is found on some essential immune system cells. However, before viral entry into the cell can occur, a second interaction between gp120 and one of two chemokine receptors (CCR5 and CXCR4) must occur. Table \(\PageIndex{5}\) lists the adhesins for some common viral pathogens and the specific sites to which these adhesins allow viruses to attach.
| Pathogen | Disease | Adhesin | Attachment Site |
|---|---|---|---|
| Influenzavirus | Influenza | Hemagglutinin | Sialic acid of respiratory and intestinal cells |
| Herpes simplex virus I or II | Oral herpes, genital herpes | Glycoproteins gB, gC, gD | Heparan sulfate on mucosal surfaces of the mouth and genitals |
| Human immunodeficiency virus | HIV/AIDS | Glycoprotein gp120 | CD4 and CCR5 or CXCR4 of immune system cells |
Antigenic Variation in Viruses
Antigenic variation also occurs in certain types of enveloped viruses, including influenza viruses, which exhibit two forms of antigenic variation: antigenic drift and antigenic shift (Figure \(\PageIndex{9}\)). Antigenic drift is the result of point mutations causing slight changes in the spike proteins hemagglutinin (H) and neuraminidase (N). On the other hand, antigenic shift is a major change in spike proteins due to gene reassortment. This reassortment for antigenic shift occurs typically when two different influenza viruses infect the same host.
The rate of antigenic variation in influenza viruses is very high, making it difficult for the immune system to recognize the many different strains of Influenzavirus. Although the body may develop immunity to one strain through natural exposure or vaccination, antigenic variation results in the continual emergence of new strains that the immune system will not recognize. This is the main reason that vaccines against Influenzavirus must be given annually. Each year’s influenza vaccine provides protection against the most prevalent strains for that year, but new or different strains may be more prevalent the following year.
- Describe the role of adhesins in viral tropism.
- Explain the difference between antigenic drift and antigenic shift.
Key Concepts and Summary
Virulence factors contribute to a pathogen’s ability to cause disease. Exoenzymes and toxins allow pathogens to invade host tissue and cause tissue damage. Exoenzymes are classified according to the macromolecule they target and exotoxins are classified based on their mechanism of action. Bacterial toxins include endotoxin and exotoxins . Endotoxin is the lipid A component of the LPS of the gram-negative cell envelope. Exotoxins are proteins secreted mainly by gram-positive bacteria, but also are secreted by gram-negative bacteria. Bacterial pathogens may evade the host immune response by producing capsules to avoid phagocytosis, surviving the intracellular environment of phagocytes, degrading antibodies, or through antigenic variation . Viral pathogens use adhesins for initiating infections and antigenic variation to avoid immune defenses. Influenza viruses use both antigenic drift and antigenic shift to avoid being recognized by the immune system.
Footnotes
- 1 V. Meka. “Panton-Valentine Leukocidin.” http://www.antimicrobe.org/h04c.file...L-S-aureus.asp


10.1: Advocacy Introduction
Learning Objectives
- Advocate for client rights and needs
- Utilize advocacy resources appropriately
- Evaluate implications of contemporary health care policy for health care consumers and nursing practice
- Explore the role of professional organizations in nursing practice
- Discuss legislative policy-making activities that influence nursing practice and health care
- Examine various positions on unions and collective bargaining
- Compare and contrast various workplace advocacy models
What do you think of when you hear the word “advocacy”?  Nurses have a long history of acting as client advocates. Early nurses advocated for professional nurses’ value and knowledge and fought for implementation of best practices, safety measures, and other quality improvements. Florence Nightingale advocated for practice changes that improved environmental conditions in health care and reduced life-threatening infections by using data to support her recommendations. Lillian Wald worked to establish public health nursing and improve the lives of immigrant communities.
More recently, nurses led the establishment of Nurse Practice Acts in each state and pushed for multistate licensing via the Nurse Licensure Compact (NLC). The American Nurses Association (ANA) declared 2018 as the “Year of Advocacy” to highlight the importance of advocacy in the nurse’s role. Nurses continue to advocate for building healthier communities as demonstrated in the Future of Nursing 2020-2030: Charting a Path to Achieve Health Equity report. [1]
In this chapter, we will review how every nurse is responsible for client advocacy and examine the powerful influence nurses can have on local, state, and federal health care policies that affect the nation’s health and the profession of nursing.
Read the Future of Nursing 2020-2030: Charting a Path to Achieve Health Equity at Future of Nursing: Campaign for Action .
- National Academies of Sciences, Engineering, and Medicine. (2021). The Future of nursing 2020-2030: Charting a path to achieve health equity. The National Academies Press. https://doi.org/10.17226/25982 ↵


5.2: General class names and Common names of monosaccharides
- Assign and interpret class names of monosaccharides.
- Assign D/L stereodescriptors to the common names and define epimers.
- Draw structure from the name and vice versa for important monosaccharides, including D-ribose, D-glucose, D-mannose, and D-galactose.
General class names of monosaccharides
Monosaccharides are either polyhydroxy aldehydes that take aldo as prefixes or polyhydroxy ketones that take keto as prefixes in their general name. The general formula of monosaccharides is \(\ce{C_{n}H_{2n}O_{n}}\) where n can be 3, 4, 5, 6, 7, or 8 representing triose, tetrose, pentose, hexose, heptose, or octose, respectively, in the general name. For example, D-glucose belongs to aldohexose, where the aldo- prefix tells it is an aldehyde, -hex- in the middle of the name tells it has six \(\ce{C's}\), and -ose suffix denotes it is a carbohydrate. D-fructose belongs to ketohexose, i.e., it is a monosaccharide with a ketone group and six \(\ce{C's}\). D-glyceraldehyde is an aldotriose, i.e., a monosaccharide with an aldehyde group and three \(\ce{C's}\).
Common names of monosaccharides
Common names are specific for each monosaccharide. All \(\ce{C's}\) in a monosaccharide are chiral centers except the two terminal \(\ce{C's}\) and the \(\ce{C}\) of ketone group if it is a ketose. The absolute configuration of the penultimate \(\ce{C}\), i.e., the second-last \(\ce{C}\), is explicitly expressed by D- or L-stereochemical descriptors and the absolute configuration of all other chiral centers is implicit in the common name of the monosaccharide. There is one set of common names for all D-isomers, and their mirror images (enantiomers) have the same common name with D- replaced with L-. For example, D-glyceraldehyde and L-glyceraldehyde, D-glucose, and L-glucose are enantiomer pairs shown in Figure \(\PageIndex{1}\).
If the \(\ce{-OH}\) group on the second-last carbon (penultimate \(\ce{C}\) or the second \(\ce{C}\) from the bottom end) in Fisher projection of a monosaccharide is on the right side, it is assigned D- and if it is on the left side, it is assigned L-configuration. Monosaccharides that are enantiomer pairs have the same common name, but D- is replaced with L- or vice versa. For example, D-glyceraldehyde and L-glyceraldehyde, D-glucose and L-glucose enantiomer pairs are shown in Figure \(\PageIndex{1}\). with the penultimate \(\ce{C}\) defining D- or L-configuration shown in red color.
D-configuration of monosaccharides is commonly found in nature. The D/L stereodescriptors do not indicate the rotation of the plane polarized light, i.e., the enantiomer's dextro/levo rotatory nature. However, if one enantiomer is dextro (d-), the other is levo (l-) to the same degree, and vice versa.
The structures as Fisher projections and common names of D-aldoses are shown in Figure \(\PageIndex{2}\). and those of D-ketoses are shown in Figure \(\PageIndex{3}\). These are the most common monosaccharides found in nature.
Some important monosaccharides
D-Glucose is the most abundant monosaccharide in nature. Plants produce it in a photosynthesis process. D-Galactose and D-mannose are two important diastereomers of D-glucose that differ from D-glucose in the configuration of only one chiral center.
Epimers are diastereomers that differ in absolute configuration of only one chiral center. For example, D-galactose configuration is different from D-glucose only at \(\ce{C}\)#4, i.e., D-galactose is a \(\ce{C}\)4-epimer of D-glucose. Similarly, D-mannose is \(\ce{C}\)2-epimer of D-glucose.
D-Fructose is another important monosaccharide that differs at \(\ce{C}\)#1 and \(\ce{C}\)#2 from glucose. That is, the \(\ce{C=O}\) is an aldehyde group at \(\ce{C}\)#1 in D-glucose, but it is a ketone at \(\ce{C}\)#2 in D-fructose. Fisher projections of D-glucose, D-galactose, D-mannose, and D-fructose are shown in Figure \(\PageIndex{4}\). with the differences from D-glucose highlighted by red-color fonts. D-ribose is another important monosaccharide present in RNA.
Drawing structures of important monosaccharides
D-ribose is aldopentose, i.e., an aldehyde with five \(\ce{C's}\). All chiral \(\ce{C's}\) have \(\ce{-OH}\) groups oriented towards the right in the Fisher projection. D-allose is aldohexose with the same structural features as D-ribose, i.e., all chiral \(\ce{C's}\) have \(\ce{-OH}\) groups oriented towards the right in the Fisher projection. D-glucose is \(\ce{C}\)3 epimer of D-allose. The other three important monosaccharides can be drawn by relating them to D-glucose, i.e., D-galactose is a \(\ce{C}\)4 epimer, D-mannose is a \(\ce{C}\)2 epimer of D-glucose, and D-fructose has a ketone group at \(\ce{C}\)2 in the place of aldehyde group of D-glucose at \(\ce{C}\)1.