2.2: Official Statistics
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- Alison S. Burke, David Carter, Brian Fedorek, Tiffany Morey, Lore Rutz-Burri, & Shanell Sanchez
- Southern Oregon University via OpenOregon
Despite being aware that crime does go unreported, it is still important to estimate and attempt to measure crime in the country. However, it is essential always to be aware of the data sources strengths and weaknesses when reading crime statistics. Also, be cautious of how changing data collection techniques may alter statistics. For example, if a survey never collected data on prescription drug abuse but then all of a sudden does it could seem like prescription drugs are being abused at high rates. However, it is most likely just because it is the first time the questions got asked and there are no comparison groups.
Official statistics are gathered from various criminal justice agencies, such as the police and courts, and represent the total number of crimes reported to the police or the number of arrests made by that agency. Remember, if an officer uses discretion and does not arrest a person, even if a crime was committed, this does not get reported.
The Federal Bureau of Investigation’s (FBI’s) Uniform Crime Reports (UCR) is the largest, most common data on crime currently available. The UCR lists the number of crimes that were reported to the police and the number of arrests made. The link below can take you to the UCR homepage www.fbi.gov/services/cjis/ucr.
The UCR Program’s primary objective is to generate reliable information for use in law enforcement administration, operation, and management. Various groups and agencies rely upon the UCR crime data, such as law enforcement executives, students, researchers, the media, and the public at large seeking information on crime in the nation. [1] The UCR began in 1929 by the International Association of Chiefs of Police to meet the need for reliable uniform crime statistics for the nation. In 1930, the FBI was tasked with collecting, publishing, and archiving those statistics. Every year there are four annual publications produced from data received from more than 18,000 city, university and college, county, state, tribal, and federal law enforcement agencies voluntarily participating in the program. [2]
The UCR Program consists of four data collections: The National Incident-Based Reporting System (NIBRS), the Summary Reporting System (SRS), the Law Enforcement Officers Killed and Assaulted (LEOKA) Program, and the Hate Crime Statistics Program. The UCR also publishes special reports on Cargo Theft, Human Trafficking, and NIBRS topical studies. The UCR Program will manage the new National Use-of-Force Data Collection.
National Incident-Based Reporting System, or NIBRS
The National Incident-Based Reporting System, or NIBRS, was created to improve the overall quality of crime data collected by law enforcement. NIBRS is unique because it collects data on crimes reported to the police, but also incidents where multiple crimes are committed, for example when a robbery escalates into a rape. [3] NIBRS also collects information on victims, known offenders, relationships between victims and offenders, arrestees, and property involved in the crimes. See the link to go directly to NIBRS www.fbi.gov/services/cjis/ucr/nibrs
Hate Crime Statistics
Congress passed the Hate Crime Statistics Act, 28 U.S.C. § 534, on April 23, 1990. This required the attorney general to collect data “about crimes that manifest evidence of prejudice based on race, religion, sexual orientation, or ethnicity.” Hate crime statistics may assist law enforcement agencies, provide lawmakers with justification for certain legislation, provide the media with credible information, or simply show hate crime victims that they are not alone (FBI, 2018). See the link to go to the FBI’s hate crime statistics link www.fbi.gov/services/cjis/ucr/hate-crime.
The FBI UCR Program’s Hate Crime Data Collection gathers data on the following biases:
Race/Ethnicity/Ancestry
- Anti-American Indian or Alaska Native
- Anti-Arab
- Anti-Asian
- Anti-Black or African American
- Anti-Hispanic or Latino
- Anti-Multiple Races, Group
- Anti-Native Hawaiian or Other Pacific Islander
- Anti-Other Race/Ethnicity/Ancestry
- Anti-White
Religion
- Anti-Buddhist
- Anti-Catholic
- Anti-Eastern Orthodox (Russian, Greek, Other)
- Anti-Hindu
- Anti-Islamic
- Anti-Jehovah’s Witness
- Anti-Jewish
- Anti-Mormon
- Anti-Multiple Religions, Group
- Anti-Other Christian
- Anti-Other Religion
- Anti-Protestant
- Anti-Atheism/Agnosticism/etc.
Sexual Orientation
- Anti-Bisexual
- Anti-Gay (Male)
- Anti-Heterosexual
- Anti-Lesbian
- Anti-Lesbian, Gay, Bisexual, or Transgender (Mixed Group)
Disability
- Anti-Mental Disability
- Anti-Physical Disability
Gender
- Anti-Male
- Anti-Female
Gender Identity
- Anti-Transgender
- Anti-Gender Non-Conforming
The types of hate crimes reported to the FBI are broken down by specific categories. The aggregate hate crime data collected for each incident include the following:
- Incidents and offenses by bias motivation: Includes crimes committed by and crimes directed against juveniles. Incidents may include one or more offense types.
- Victims: The types of victims collected for hate crime incidents include individuals (adults and juveniles), businesses, institutions, and society as a whole.
- Offenders: The number of offenders (adults and juveniles), and when possible, the race and ethnicity of the offender or offenders as a group.
- Location type: One of 46 location types can be designated.
- Hate crime by jurisdiction: Includes data about hate crimes by state and agency.
Law Enforcement Officers Killed and Assaulted Program LEOKA
LEOKA provides data and training that helps keep law enforcement officers by providing relevant, high quality, potentially lifesaving information to law enforcement agencies focusing on why an incident occurred as opposed to what occurred during the incident, with the hope of preventing future incidents. [4]
Exclusions from the LEOKA Program’s Data Collection
Deaths resulting from the following are not included in the LEOKA Program’s statistics:
- Natural causes such as heart attack, stroke, aneurysm, etc.
- On duty, but death is attributed to their own personal situation such as domestic violence, neighbor conflict, etc.
- Suicide
Examples of job positions not typically included in the LEOKA Program’s statistics (unless they meet the above exception) follow:
- Corrections/correctional officers
- Bailiffs
- Parole/probation officers
- Federal judges
- The U.S. and assistant U.S. attorneys
- Bureau of Prison officers
- Private security officers
All of these official statistics are a great starting point, although, recognize they are imperfect in nature. Police agencies can change their attention to certain events, which can change the overall number of arrests. For example, if police begin cracking down on domestic violence the statistics may go up. This crackdown can make it appear that the problem has increased, although it can be related to the crackdown. Just remember, if the crime is not reported, or no arrest is made it will not get captured in the data.
Bureau of Justice Statistics Exercise
The BJS is relatively user-friendly. Look at crime statistics by state, region, or city, and explore different years and crime types.
https://www.bjs.gov/index.cfm?ty=datool&surl=/arrests/index.cfm
Examine current state AND city crime trends in the past five years.
Second, pick a state AND city interested in living in and examine the crime trends for the past five years.
- U.S. Department of Justice. (2017). UCR Reports ↵
- U.S. Department of Justice. (2017). UCR Reports ↵
- Rantala, R. R. (2000). Effects of NIBRS on crime statistics. Bureau of Justice Statistics Special Report. U.S. Department of Justice, Office of Justice Programs. Washington, DC. ↵
- FBI (2017). www.fbi.gov/services/cjis/ucr/leoka ↵


3.1: Lab Foundations of Modern Cell Theory
- Explain the key points of cell theory and the individual contributions of Hooke, Schleiden, Schwann, Remak, and Virchow
- Explain the key points of endosymbiotic theory and cite the evidence that supports this concept
- Explain the contributions of Semmelweis, Snow, Pasteur, Lister, and Koch to the development of germ theory
While some scientists were arguing over the theory of spontaneous generation, other scientists were making discoveries leading to a better understanding of what we now call the cell theory. Modern cell theory has two basic tenets:
- All cells only come from other cells (the principle of biogenesis).
- Cells are the fundamental units of organisms.
Today, these tenets are fundamental to our understanding of life on earth. However, modern cell theory grew out of the collective work of many scientists.
The Origins of Cell Theory
The English scientist Robert Hooke first used the term “cells” in 1665 to describe the small chambers within cork that he observed under a microscope of his own design. To Hooke, thin sections of cork resembled “Honey-comb,” or “small Boxes or Bladders of Air.” He noted that each “Cavern, Bubble, or Cell” was distinct from the others (Figure \(\PageIndex{1}\)). At the time, Hooke was not aware that the cork cells were long dead and, therefore, lacked the internal structures found within living cells.
Despite Hooke’s early description of cells, their significance as the fundamental unit of life was not yet recognized. Nearly 200 years later, in 1838, Matthias Schleiden (1804–1881), a German botanist who made extensive microscopic observations of plant tissues, described them as being composed of cells. Visualizing plant cells was relatively easy because plant cells are clearly separated by their thick cell walls. Schleiden believed that cells formed through crystallization, rather than cell division.
Theodor Schwann (1810–1882), a noted German physiologist, made similar microscopic observations of animal tissue. In 1839, after a conversation with Schleiden, Schwann realized that similarities existed between plant and animal tissues. This laid the foundation for the idea that cells are the fundamental components of plants and animals.
In the 1850s, two Polish scientists living in Germany pushed this idea further, culminating in what we recognize today as the modern cell theory. In 1852, Robert Remak (1815–1865), a prominent neurologist and embryologist, published convincing evidence that cells are derived from other cells as a result of cell division. However, this idea was questioned by many in the scientific community. Three years later, Rudolf Virchow (1821–1902), a well-respected pathologist, published an editorial essay entitled “Cellular Pathology,” which popularized the concept of cell theory using the Latin phrase omnis cellula a cellula (“all cells arise from cells”), which is essentially the second tenet of modern cell theory. 1 Given the similarity of Virchow’s work to Remak’s, there is some controversy as to which scientist should receive credit for articulating cell theory. See the following Eye on Ethics feature for more about this controversy.
Rudolf Virchow, a prominent, Polish-born, German scientist, is often remembered as the “Father of Pathology.” Well known for innovative approaches, he was one of the first to determine the causes of various diseases by examining their effects on tissues and organs. He was also among the first to use animals in his research and, as a result of his work, he was the first to name numerous diseases and created many other medical terms. Over the course of his career, he published more than 2,000 papers and headed various important medical facilities, including the Charité – Universitätsmedizin Berlin, a prominent Berlin hospital and medical school. But he is, perhaps, best remembered for his 1855 editorial essay titled “Cellular Pathology,” published in Archiv für Pathologische Anatomie und Physiologie , a journal that Virchow himself cofounded and still exists today.
Despite his significant scientific legacy, there is some controversy regarding this essay, in which Virchow proposed the central tenet of modern cell theory—that all cells arise from other cells. Robert Remak, a former colleague who worked in the same laboratory as Virchow at the University of Berlin, had published the same idea 3 years before. Though it appears Virchow was familiar with Remak’s work, he neglected to credit Remak’s ideas in his essay. When Remak wrote a letter to Virchow pointing out similarities between Virchow’s ideas and his own, Virchow was dismissive. In 1858, in the preface to one of his books, Virchow wrote that his 1855 publication was just an editorial piece, not a scientific paper, and thus there was no need to cite Remak’s work.
By today’s standards, Virchow’s editorial piece would certainly be considered an act of plagiarism, since he presented Remak’s ideas as his own. However, in the 19 th century, standards for academic integrity were much less clear. Virchow’s strong reputation, coupled with the fact that Remak was a Jew in a somewhat anti-Semitic political climate, shielded him from any significant repercussions. Today, the process of peer review and the ease of access to the scientific literature help discourage plagiarism. Although scientists are still motivated to publish original ideas that advance scientific knowledge, those who would consider plagiarizing are well aware of the serious consequences.
In academia, plagiarism represents the theft of both individual thought and research—an offense that can destroy reputations and end careers. 2 3 4 5
- What are the key points of the cell theory?
- What contributions did Rudolf Virchow and Robert Remak make to the development of the cell theory?
Endosymbiotic Theory
As scientists were making progress toward understanding the role of cells in plant and animal tissues, others were examining the structures within the cells themselves. In 1831, Scottish botanist Robert Brown (1773–1858) was the first to describe observations of nuclei, which he observed in plant cells. Then, in the early 1880s, German botanist Andreas Schimper (1856–1901) was the first to describe the chloroplasts of plant cells, identifying their role in starch formation during photosynthesis and noting that they divided independent of the nucleus.
Based upon the chloroplasts’ ability to reproduce independently, Russian botanist Konstantin Mereschkowski (1855–1921) suggested in 1905 that chloroplasts may have originated from ancestral photosynthetic bacteria living symbiotically inside a eukaryotic cell. He proposed a similar origin for the nucleus of plant cells. This was the first articulation of the endosymbiotic hypothesis, and would explain how eukaryotic cells evolved from ancestral bacteria.
Mereschkowski’s endosymbiotic hypothesis was furthered by American anatomist Ivan Wallin (1883–1969), who began to experimentally examine the similarities between mitochondria, chloroplasts, and bacteria—in other words, to put the endosymbiotic hypothesis to the test using objective investigation. Wallin published a series of papers in the 1920s supporting the endosymbiotic hypothesis, including a 1926 publication co-authored with Mereschkowski. Wallin claimed he could culture mitochondria outside of their eukaryotic host cells. Many scientists dismissed his cultures of mitochondria as resulting from bacterial contamination. Modern genome sequencing work supports the dissenting scientists by showing that much of the genome of mitochondria had been transferred to the host cell’s nucleus, preventing the mitochondria from being able to live on their own. 6 7
Wallin’s ideas regarding the endosymbiotic hypothesis were largely ignored for the next 50 years because scientists were unaware that these organelles contained their own DNA. However, with the discovery of mitochondrial and chloroplast DNA in the 1960s, the endosymbiotic hypothesis was resurrected. Lynn Margulis (1938–2011), an American geneticist, published her ideas regarding the endosymbiotic hypothesis of the origins of mitochondria and chloroplasts in 1967. 8 In the decade leading up to her publication, advances in microscopy had allowed scientists to differentiate prokaryotic cells from eukaryotic cells. In her publication, Margulis reviewed the literature and argued that the eukaryotic organelles such as mitochondria and chloroplasts are of prokaryotic origin. She presented a growing body of microscopic, genetic, molecular biology, fossil, and geological data to support her claims.
Again, this hypothesis was not initially popular, but mounting genetic evidence due to the advent of DNA sequencing supported the endosymbiotic theory, which is now defined as the theory that mitochondria and chloroplasts arose as a result of prokaryotic cells establishing a symbiotic relationship within a eukaryotic host (Figure \(\PageIndex{3}\)). With Margulis’ initial endosymbiotic theory gaining wide acceptance, she expanded on the theory in her 1981 book Symbiosis in Cell Evolution . In it, she explains how endosymbiosis is a major driving factor in the evolution of organisms. More recent genetic sequencing and phylogenetic analysis show that mitochondrial DNA and chloroplast DNA are highly related to their bacterial counterparts, both in DNA sequence and chromosome structure. However, mitochondrial DNA and chloroplast DNA are reduced compared with nuclear DNA because many of the genes have moved from the organelles into the host cell’s nucleus. Additionally, mitochondrial and chloroplast ribosomes are structurally similar to bacterial ribosomes, rather than to the eukaryotic ribosomes of their hosts. Last, the binary fission of these organelles strongly resembles the binary fission of bacteria, as compared with mitosis performed by eukaryotic cells. Since Margulis’ original proposal, scientists have observed several examples of bacterial endosymbionts in modern-day eukaryotic cells. Examples include the endosymbiotic bacteria found within the guts of certain insects, such as cockroaches, 9 and photosynthetic bacteria-like organelles found in protists. 10
- What does the modern endosymbiotic theory state?
- What evidence supports the endosymbiotic theory?
The Germ Theory of Disease
Prior to the discovery of microbes during the 17 th century, other theories circulated about the origins of disease. For example, the ancient Greeks proposed the miasma theory, which held that disease originated from particles emanating from decomposing matter, such as that in sewage or cesspits. Such particles infected humans in close proximity to the rotting material. Diseases including the Black Death, which ravaged Europe’s population during the Middle Ages, were thought to have originated in this way.
In 1546, Italian physician Girolamo Fracastoro proposed, in his essay De Contagione et Contagiosis Morbis , that seed-like spores may be transferred between individuals through direct contact, exposure to contaminated clothing, or through the air. We now recognize Fracastoro as an early proponent of the germ theory of disease, which states that diseases may result from microbial infection. However, in the 16th century, Fracastoro’s ideas were not widely accepted and would be largely forgotten until the 19th century.
In 1847, Hungarian obstetrician Ignaz Semmelweis (Figure \(\PageIndex{4}\)) observed that mothers who gave birth in hospital wards staffed by physicians and medical students were more likely to suffer and die from puerperal fever after childbirth (10%–20% mortality rate) than were mothers in wards staffed by midwives (1% mortality rate). Semmelweis observed medical students performing autopsies and then subsequently carrying out vaginal examinations on living patients without washing their hands in between. He suspected that the students carried disease from the autopsies to the patients they examined. His suspicions were supported by the untimely death of a friend, a physician who contracted a fatal wound infection after a postmortem examination of a woman who had died of a puerperal infection. The dead physician’s wound had been caused by a scalpel used during the examination, and his subsequent illness and death closely paralleled that of the dead patient.
Although Semmelweis did not know the true cause of puerperal fever, he proposed that physicians were somehow transferring the causative agent to their patients. He suggested that the number of puerperal fever cases could be reduced if physicians and medical students simply washed their hands with chlorinated lime water before and after examining every patient. When this practice was implemented, the maternal mortality rate in mothers cared for by physicians dropped to the same 1% mortality rate observed among mothers cared for by midwives. This demonstrated that handwashing was a very effective method for preventing disease transmission. Despite this great success, many discounted Semmelweis’s work at the time, and physicians were slow to adopt the simple procedure of handwashing to prevent infections in their patients because it contradicted established norms for that time period.
Around the same time Semmelweis was promoting handwashing, in 1848, British physician John Snow conducted studies to track the source of cholera outbreaks in London. By tracing the outbreaks to two specific water sources, both of which were contaminated by sewage, Snow ultimately demonstrated that cholera bacteria were transmitted via drinking water. Snow’s work is influential in that it represents the first known epidemiological study, and it resulted in the first known public health response to an epidemic. The work of both Semmelweis and Snow clearly refuted the prevailing miasma theory of the day, showing that disease is not only transmitted through the air but also through contaminated items.
Although the work of Semmelweis and Snow successfully showed the role of sanitation in preventing infectious disease, the cause of disease was not fully understood. The subsequent work of Louis Pasteur, Robert Koch, and Joseph Listerwould further substantiate the germ theory of disease.
While studying the causes of beer and wine spoilage in 1856, Pasteur discovered properties of fermentation by microorganisms. He had demonstrated with his swan-neck flask experiments (link) that airborne microbes, not spontaneous generation, were the cause of food spoilage, and he suggested that if microbes were responsible for food spoilage and fermentation, they could also be responsible for causing infection. This was the foundation for the germ theory of disease.
Meanwhile, British surgeon Joseph Lister (Figure \(\PageIndex{5}\)) was trying to determine the causes of postsurgical infections. Many physicians did not give credence to the idea that microbes on their hands, on their clothes, or in the air could infect patients’ surgical wounds, despite the fact that 50% of surgical patients, on average, were dying of postsurgical infections. 11 Lister, however, was familiar with the work of Semmelweis and Pasteur; therefore, he insisted on handwashing and extreme cleanliness during surgery. In 1867, to further decrease the incidence of postsurgical wound infections, Lister began using carbolic acid (phenol) spray disinfectant/antiseptic during surgery. His extremely successful efforts to reduce postsurgical infection caused his techniques to become a standard medical practice.
A few years later, Robert Koch (Figure \(\PageIndex{5}\)) proposed a series of postulates (Koch’s postulates) based on the idea that the cause of a specific disease could be attributed to a specific microbe. Using these postulates, Koch and his colleagues were able to definitively identify the causative pathogens of specific diseases, including anthrax, tuberculosis, and cholera. Koch’s “one microbe, one disease” concept was the culmination of the 19th century’s paradigm shift away from miasma theory and toward the germ theory of disease. Koch’s postulates are discussed more thoroughly in How Pathogens Cause Disease .
- Compare and contrast the miasma theory of disease with the germ theory of disease.
- How did Joseph Lister’s work contribute to the debate between the miasma theory and germ theory and how did this increase the success of medical procedures?
After suffering a fever, congestion, cough, and increasing aches and pains for several days, Barbara suspects that she has a case of the flu. She decides to visit the health center at her university. The PA tells Barbara that her symptoms could be due to a range of diseases, such as influenza, bronchitis, pneumonia, or tuberculosis.
During her physical examination, the PA notes that Barbara’s heart rate is slightly elevated. Using a pulse oximeter, a small device that clips on her finger, he finds that Barbara has hypoxemia—a lower-than-normal level of oxygen in the blood. Using a stethoscope, the PA listens for abnormal sounds made by Barbara’s heart, lungs, and digestive system. As Barbara breathes, the PA hears a crackling sound and notes a slight shortness of breath. He collects a sputum sample, noting the greenish color of the mucus, and orders a chest radiograph, which shows a “shadow” in the left lung. All of these signs are suggestive of pneumonia, a condition in which the lungs fill with mucus (Figure \(\PageIndex{6}\)).
What kinds of infectious agents are known to cause pneumonia?
Lab: The Cell Theory Journal
BACKGROUND INFORMATION
Imagine life before the discovery of cells, when diseases attacked the human population, unseen and undetected by doctors and scientists of the time. Diseases like the Black Plague, caused by a bacterium, brought about one of the greatest pandemics in human history. The Irish Potato Famine was caused by a unicellular fungus that infected potatoes, thereby destroying one of the country's main food sources and resulting in mass starvation.
The invention of the microscope allowed for the discovery of cells and unicellular organisms, opening scientists' eyes to a whole other world - the world of microorganisms. The study of microorganisms is known as microbiology. The microscope opened the doors to many modern fields of science, including:
Microscopy - the study and use of microscopes
Bacteriology - the study of bacteria Mycology - the study of fungi Parasitology - the study of parasites Virology - the study of viruses Botany - the study of plants Cytology - the study of cells
In the nearly four hundred years since Robert Hooke identified the cell, the work of other scientists led to the development of the Cell Theory.
The Cell Theory states three points:
1. All living things are made up of cells.
2. Cells are the basic unit of structure and function in living things.
3. All cells come from pre-existing cells.
By studying these early scientists and their discoveries, you will be taking a scientific journey back in time. As you view each slide, imagine that what you see is what each of the scientists saw through the ocular lenses of their primitive microscopes!
This activity consists of 8 stations. Find the following materials at each station:
MATERIALS:
· Microscope
· Slide
PROCEDURE:
1. Go to the station for your group, as designated by the instructor.
2. Once at the station, find the write-up for that station number on your Lab Report.
At each station:
1. The historian should read the narrative for that station. Take turns reading so that each member of your group is the historian at least twice.
2. Listen carefully to the narrative, as it sets the stage for that scientist's work.
3. Write the scientist's name on the blank line, next to the date of the discovery.
4. Have each person in your group take a turn looking through the microscope at the station. When it is your turn, look through the microscope and then, in the circle for the appropriate station number on the worksheet, sketch what you see. In the space below the circle, record the
magnification used.
5. In your own words, describe what you see, under 'written observations'. In your description, be sure to note the name of the slide you are observing.
Your instructor will give you a designated amount of time at each station. When time is up, proceed to the next numbered station. For example, if your group began at station #6, your group should now proceed to station #7. The group at station #8 should proceed to station #1
Use this format for completing the write ups:
|
1978 |
Scientist: Their name |
Magnification: 40x, 100x, or 400x |
|
Written Observations: |
Describe what you see here and be as detailed as possible |
Draw your slide here: Label as needed |
Station #1:
Narrative: An English scientist named made a primitive microscope and used it to look at a thin piece of cork (a piece of bark from a cork oak tree). He described the structures that he saw as cells, coming from the Latin word 'cella', meaning "small rooms". He wrote about what he saw in a book called Micrographia, published in 1665. In your sketch of the cork cells that you observe at this station, label one of the "small rooms" that you see "cell".
|
1665 |
Scientist: |
Magnification: |
|
Written Observations: |
Draw your slide here: |
Station #2:
Narrative: was a fabric merchant from Holland. He was interested in lenses and used them to count threads in woven cloth. He became so interested in lenses that he learned how to make his own
by grinding and polishing pieces of glass. He noticed that if he made smaller lenses with greater arcs, the lenses produced greater magnification. Although he did not invent the microscope, he improved the microscopes of his day by increasing the magnification. His microscopes were able to magnify over 200 times what the unaided eye could observe and Leeuwenhoek was able to see things that no one had seen before. In 1674, he observed algae and many swimming 'animalcules' (tiny animals or as we know them, protists) in a drop of water. Because of his discoveries, he is often referred to as the father of microbiology. The long string of cells you will view at this station are called Spirogyra. Spirogyra are green algae that are often found in pond water. Count how many cells appear in your field of view and note that number in your observations. Hint: The individual cells may be easier to see in some strings than in others.
|
1674 |
Scientist: |
Magnification: |
|
Written Observations: |
Draw your slide here: |
Station #3:
Narrative: was a French botanist (a scientist who studies plants). In 1809, he observed that plants are made up of cells that form a continuous membrane. For this and other observations concerning plant and animal cells, he is known as the founder of cytology (the study of cells). The cells you will view at this station are generalized plant cells. Because these are plant cells, you will see a box- like structure surrounding each cell. This structure is known as the cell wall. In your sketch, label the "cell wall".
|
1809 |
Scientist: |
Magnification: |
|
Written Observations: |
Draw your slide here: |
Station #4:
Narrative: was a French soldier and professor. Lamarck observed that all living things (plant or animal) are made up of cellular tissue. Lamarck is much better known for his work in evolution, but is no doubt a contributor to the Cell Theory by making the above observation. In the slide of a general animal cell that you will observe at this station, notice that all of the cells that make up this tissue are very similar. In your sketch, label one of these cells as an "animal cell".
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1810 |
Scientist: |
Magnification: |
|
Written Observations: |
Draw your slide here: |
Station #5:
Narrative: was a Scottish botanist. He named the cell nucleus while viewing orchid epidermal cells. The word "nucleus" is Latin for "kernel" or "little nut." He also discovered the movement of certain cells suspended in a liquid. This motion is called Brownian movement, named after him. In the allium or onion epidermal cells that you will view at this station, notice the small dark structures near the center of each cell. This is the nucleus of the cell. In your sketch, label one of these structures "nucleus".
|
1831 |
Scientist: |
Magnification: |
|
Written Observations: |
Draw your slide here: |
Station #6:
Narrative: was a German botanist. During his studies, he began to formulate the Cell Theory for plants. In his published paper of 1838, Schleiden proposed that all plants are composed of cells and that the cell is the most basic unit of plant life. He also forecasted that plant growth takes place by the generation of new cells somehow involving the nucleus. Although his idea of how cell division took place was not correct, he was definitely on the right track! In the slide of tilia (basswood) root cells that you will observe at this station, notice the cell wall surrounding each cell. In your sketch, label one of the cells "plant cell of plant tissue".
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1838 |
Scientist: |
Magnification: |
|
Written Observations: |
Draw your slide here: |
Station #7:
Narrative: was a German physiologist (a scientist who studies living organisms). He discovered cells that surround and protect the axons of nerve cells. (An axon is the part of a nerve cell where impulses travel away from the cell body.) Today these cells are named after him. He took the work of Matthias Schleiden one step further and applied the Cell Theory to plants and animals. In his publication of 1839, he stated that cells are organisms, all organisms consist of one or more cells, and the cell is the basic unit of structure for all organisms (plants and animals). He further discussed cell origin, organization, and differentiation. At this station, you will be viewing a slide of frog skin. Notice that the skin is made of many similar epidermal cells. In your sketch, label one of the cells "animal cell of animal tissue".
|
1839 |
Scientist: |
Magnification: |
|
Written Observations: |
Draw your slide here: |
Station #8:
Narrative: was a German doctor. His many discoveries include being the first to recognize leukemia, He also recognized the cell as the basic unit of structure and function in all living things and is known for his theory of 1858, "Omnis cellula e cellula" (Latin for "every cell originates from another existing cell like it"). The slide that you will view at this station is an allium or onion root tip undergoing cell division. You may be able to distinguish other stages of the cell cycle. In your sketch, find an area where one cell is clearly dividing into two and label that area "cell division".
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1858 |
Scientist: |
Magnification: |
|
Written Observations: |
Draw your slide here: |
CONCLUSIONS:
Referring to the instructions online, list the three points of the Cell Theory, below.
1.
2.
3.
After the name of each scientist, note which point(s) of the Cell Theory (1, 2 and or 3) is/are supported by that scientist's work.
|
Robert Hooke |
|
|
Antony Leeuwenhoek |
|
|
Charles-Francois Brisseau de Mirbel |
|
|
Jean-Baptiste Lamarck |
|
|
Robert Brown |
|
|
Matthias Schleiden |
|
|
Theodor Schwann |
|
|
Rudolf Virchow |
EXTENSION ACTIVITY:
Create a time line to summarize the development of the Cell Theory.
Key Concepts and Summary
- Although cells were first observed in the 1660s by Robert Hooke, cell theory was not well accepted for another 200 years. The work of scientists such as Schleiden, Schwann, Remak, and Virchow contributed to its acceptance.
- Endosymbiotic theory states that mitochondria and chloroplasts, organelles found in many types of organisms, have their origins in bacteria. Significant structural and genetic information support this theory.
- The miasma theory of disease was widely accepted until the 19th century, when it was replaced by the germ theory of disease thanks to the work of Semmelweis, Snow, Pasteur, Lister, and Koch, and others.
Footnotes
- 1 M. Schultz. “Rudolph Virchow.” Emerging Infectious Diseases 14 no. 9 (2008):1480–1481.
- 2 B. Kisch. “Forgotten Leaders in Modern Medicine, Valentin, Gouby, Remak, Auerbach.” Transactions of the American Philosophical Society 44 (1954):139–317.
- 3 H. Harris. The Birth of the Cell . New Haven, CT: Yale University Press, 2000:133.
- 4 C. Webster (ed.). Biology, Medicine and Society 1840-1940 . Cambridge, UK; Cambridge University Press, 1981:118–119.
- 5 C. Zuchora-Walske. Key Discoveries in Life Science . Minneapolis, MN: Lerner Publishing, 2015:12–13.
- 6 T. Embley, W. Martin. “Eukaryotic Evolution, Changes, and Challenges.” Nature Vol. 440 (2006):623–630.
- 7 O.G. Berg, C.G. Kurland. “Why Mitochondrial Genes Are Most Often Found in Nuclei.” Molecular Biology and Evolution 17 no. 6 (2000):951–961.
- 8 L. Sagan. “On the Origin of Mitosing Cells.” Journal of Theoretical Biology 14 no. 3 (1967):225–274.
- 9 A.E. Douglas. “The Microbial Dimension in Insect Nutritional Ecology.” Functional Ecology 23 (2009):38–47.
- 10 J.M. Jaynes, L.P. Vernon. “The Cyanelle of Cyanophora paradoxa : Almost a Cyanobacterial Chloroplast.” Trends in Biochemical Sciences 7 no. 1 (1982):22–24.
- 11 Alexander, J. Wesley. “The Contributions of Infection Control to a Century of Progress” Annals of Surgery 201:423-428, 1985.


5.28: Reading- Product Liability
Introduction
Product liability is the legal liability a manufacturer or trader incurs for producing or selling a faulty product.
There is not a single federal law or code that covers all product liability. Fourteen states have adopted the Uniform Commercial Code, which governs business transactions between states. Specifically, Article 2 of the code includes the requirements for contract formation and breach, which are important in many product liability cases. In general, product liability laws come about as a result of civil court cases being prosecuted at the state level.
The courts are increasingly holding sellers responsible for the safety of their products. The U.S. courts generally maintain that the producer of a product is liable for any product defect that causes injury in the course of normal use. Liability can even result if a court or a jury decides that a product’s design, construction, or operating instructions and safety warnings make the product unreasonably dangerous to use.
Types of Product Defects
There are three types of product defects that incur product liability: design defects, manufacturing defects, and defects in marketing.
Design Defects
Design defects exist before the product is manufactured. There is something in the design of the product that is inherently unsafe, regardless of how well it is manufactured. Since “product” is one of the primary elements of the marketing mix, the marketer bears responsibility for ensuring that the design results in a product that is safe and that the product will fulfill the promises of the other aspects of the marketing mix such as promotional commitments.
Let’s look at a current example of a product design going awry. One of the hottest holiday gift items in 2015 is the hoverboard self-balancing scooter. The premium models often cost more than $1,000, but several companies have created less expensive versions by using lower-cost board components. One expensive component that has been downgraded in the cheaper models is the rechargeable lithium-ion battery. Many less expensive boards use a lower-quality (and lower-priced) mass-produced battery cell. These cheaper batteries are more likely to have quality issues that might cause them to break and burst into flame when they are repeatedly bumped, which is a regular occurrence during the normal use of the scooter. After more than ten reported fires, the U.S. Consumer Product Safety Commission opened a case to investigate the hoverboard fires.
Manufacturing Defects
Manufacturing defects occur while a product is being constructed, produced, or assembled. Specifically, when a product departs from its intended design, even though all possible care was exercised in the preparation and marketing of the product [1] , it is a manufacturing defect. The manufacturer may be very careful with the design, the material selection, the development of the manufacturing process, and the quality-assurance guidelines. Nevertheless, if a poorly manufactured product leaves the manufacturers facility and causes injury when used for any of its intended purposes, then there is a defect in manufacturing.
It might seem that manufacturing defects occur only in product sales and not in the service industry, but there’s a very well-known case in this category: the McDonald’s coffee case.
On February 27, 1992, a seventy-nine-year-old woman named Stella Liebeck went to McDonald’s with her grandson, Chris. They got the coffee, and Chris pulled into a parking space so that Stella could add cream and sugar. Since the car had a curved dash and lacked cup holders, Stella put the cup between her knees and removed the lid. When she did, the cup fell backward, burning her groin, thighs, genitalia, and buttocks. Liebeck was taken to the hospital, where it was discovered that she had third-degree burns on 6 percent of her body and other burns on 16 percent of her body. She required multiple skin grafts and was in the hospital for eight days. Liebeck spent two years recovering from the injury, lost 20 percent of her bodyweight after the accident, and was left permanently scarred by the ordeal.
Liebeck wrote a letter to McDonald’s asking them to pay her medical bills, which totaled around $10,500 in 1992 (approximately $16,110 today). The company offered her $800. Liebeck and McDonald’s exchanged several more letters, but the company refused to increase their $800 offer, so Liebeck hired a law firm.
Liebeck’s lawyers conducted a study of coffee temperatures. They discovered that coffee brewed at home is usually served at 135–145°F and coffee served at most fast-food restaurants is in the 160–175°F range. McDonald’s, however, served its coffee at 190°F, which can cause third-degree burns on human skin after two to seven seconds of contact. No safety study of any kind was undertaken by either McDonald’s or the consultant who recommended the hotter temperature.
Moreover, Liebeck’s lawyers also discovered more than seven hundred other burn claims—many of them for third-degree burns—from McDonald’s customers between February 1983 and March 1992. In court, McDonald’s quality-control manager, Christopher Appleton, testified that McDonald’s served around 20 million cups of coffee a year and that seven hundred incidents during nine years was statistically insignificant. While this was factually accurate, the jury did not like to hear that McDonald’s considered seven hundred burned customer to be insignificant.
The jury found in Liebeck’s favor. They awarded her $200,000 in compensatory damages, but that amount was later reduced to $160,000 because they felt that the spill was 20 percent Liebeck’s fault. The jury made headlines when it came to the punitive damages, however, which they settled at $2.7 million. The jurors defended the amount, saying that it was to punish the company for its callous attitude toward Ms. Liebeck and the 700+ other McDonald’s customers who had suffered burns. Although it sounds like a lot, $2.7 million represented only two days’ worth of McDonald’s coffee sales, and the jurors felt that was fair.
The judge agreed, accusing McDonald’s of “willful, wanton, and reckless behavior” for ignoring all the customer complaints.
McDonald’s process for making coffee constituted a manufacturing defect, which resulted in many customer injuries and generated significant product liability for the company.
Marketing Defects
Marketing defects result from flaws in the way a product is marketed. Examples include improper labeling, poor or incomplete instructions, or inadequate safety warnings. Often marketing defects are referred to as a “failure to warn.” It is important for the marketer to think not only about the warnings that the user might need when using the product as intended but also about other, potentially dangerous uses for which the product was not intended.
For example, fabric used in children’s sleepwear must meet certain flammability requirements to prevent the risk of injury from fires. Certain comfortable children’s clothing that does not meet the flammability requirement can be confused with sleepwear. For this reason, such clothing will often contain a warning label that reads, “Not intended for sleepwear.”
Over time, product liability has shifted more to the side of the injured product user. Consumer advocates like Ralph Nader argue that, for too long, product liability favored producers at the expense of the product user. They assert that it’s the threat of lawsuits and huge settlements and restitutions that force companies to make safe products. While a discussion of all aspects of product liability is beyond the scope of this course, it is clear that liability has and will continue to have a tremendous impact on consumers and manufacturers alike. These two groups are not the only ones affected, either. Retailers, franchises, wholesalers, sellers of mass-produced homes, and building-site developers and engineers are all subject to liability legislation.
- Restatement of Torts, Third, Apportionment of Liability (2000) ↵
Contributors and Attributions
- Manufacturing Defects. Authored by : Jim Cofer. Located at : jimcofer.com/personal/2012/01/19/righting-the-wrongs-the-mcdonalds-coffee-case/. Project : Righting the Wrongs: The McDonald's Coffee Case. License : CC BY-NC-SA: Attribution-NonCommercial-ShareAlike
- Chapter 5: External Considerations in Marketing, from Introducing Marketing. Authored by : John Burnett. Project : Global Text. License : CC BY: Attribution
- Hoverboard. Provided by : Soar Boards. Located at : https://en.Wikipedia.org/wiki/Self-balancing_two-wheeled_board#/media/File:Red_self-balancing_two-wheeled_board_with_a_person_standing_on_it.png . License : CC BY: Attribution
- Lawsuits Welcome. Authored by : Chris Tengi. Located at : https://www.flickr.com/photos/cjtengi/2022308688/ . License : CC BY-NC-ND: Attribution-NonCommercial-NoDerivatives


5.2: Principles
The air we breathe is made up of various gases, 21% of which is oxygen. Therefore, a patient who is receiving no supplemental oxygen therapy is still receiving oxygen from the air. This amount of oxygen is adequate provided that the patient’s airway is not compromised and there is sufficient hemoglobin in the blood. The cardiovascular system must also be intact and able to circulate blood to all body tissues. If any of these systems fail, the patient will require supplemental oxygen to increase the likelihood that adequate levels of oxygen will reach all vital body tissues necessary to sustain life.
Oxygen in the Blood
Hemoglobin (Hgb) holds oxygen in reserve until the metabolic demands of the body require more oxygen. The Hgb then moves the oxygen to the plasma for transport to the tissues. The body’s demand for oxygen is affected by activity, metabolic status, temperature, and level of anxiety. The ability of Hgb to move the oxygen to the tissues depends on a number of factors, such as oxygen supply, ventilatory effectiveness, nutrition, cardiac output, hemoglobin level, smoking, drug use, and underlying disease. Any one of these factors can potentially impede the supply and transport of oxygen to the tissues.
Measurement of Oxygen in the Blood
The vast majority of oxygen carried in the blood is attached to hemoglobin and can be assessed by monitoring the oxygen saturation through pulse oximetry (SpO 2 ).The target range for oxygen saturation as measured by blood analysis (SaO 2 ), such as arterial blood gas, is 92% to 98% for a normal adult. Arterial blood gas (ABG) is the analysis of an arterial blood sample to evaluate the adequacy of ventilation, oxygen delivery to the tissues, and acid-base balance status (Simpson, 2004). For patients with COPD, the target SaO 2 range is 88% to 92% (Alberta Health Services, 2015; British Thoracic Society, 2008; Kane et al., 2013). Only about 3% of the oxygen carried in the blood is dissolved in the plasma, which can be assessed by looking at the partial pressure of oxygen in the blood through blood gas analysis (PaO 2 ). The normal PaO 2 of a healthy adult is 80 to 100 mmHg. The SpO 2 is more clinically significant than the PaO 2 in determining the oxygen content of the blood.
Oxygen is considered a medication and therefore requires continuous monitoring of the dose, concentration, and side effects to ensure its safe and effective use (Alberta Health Services, 2015). Oxygen therapy may be indicated for hypoxemia and hypoxia.
Understanding Hypoxemia and Hypoxia
Although the terms hypoxemia and hypoxia are often used interchangeably, they do not mean the same thing. Hypoxemia is a condition where arterial oxygen tension or partial pressure of oxygen (PaO 2 ) is below normal (<80 mmHg). Hypoxemia is the inadequate supply of oxygen in the arterial blood. Hypoxia is the reduction of oxygen supply at the tissue level, which is not measured directly by a laboratory value (Metrovic, 2014), but by pulse oximetry and SpO 2 (British Thoracic Society, 2008).
Generally, the presence of hypoxemia suggests that hypoxia exists. However, hypoxia may not be present in a patient with hypoxemia if the patient is able to compensate for a low PaO 2 by increasing oxygen supply. This is usually achieved by increasing cardiac output (by raising the heart rate) or by decreasing tissue oxygen consumption. Conversely, patients who do not show signs of hypoxemia may be hypoxic if oxygen delivery to the tissues is diminished or if the tissues are unable to adequately use the oxygen.
Hypoxemia is the most common cause of tissue hypoxia, and if the correct diagnosis is made, it is readily treatable.
The Vancouver Coastal Health Authority (2015) lists three causes of hypoxemia: deadspace and shunts, low inspired oxygen tension, and alveolar hypoventilation.
Deadspace and Shunts
Ventilation and perfusion are not always equal between the alveoli and pulmonary capillaries. There is sometimes too much perfusion and not enough ventilation in some areas of the lungs, causing a shunt where the blood is unable to pick up oxygen and unload carbon dioxide. In other areas of the lungs, there may be too much ventilation and not enough perfusion, causing deadspace where oxygen is unable to diffuse into the blood.
Low Inspired Oxygen Tension
Hypoxemia can be caused by breathing air at pressures less than atmospheric pressure, such as at high altitudes or in an enclosed space with inadequate ventilation. The enclosed space may be especially hazardous if there is a low concentration of oxygen or if it contains toxic gases.
Alveolar Hypoventilation
If a patient hypoventilates, the level of oxygen in the alveoli will fall, and the level of carbon dioxide will increase. Hypoxemia occurs because less oxygen is moved into the pulmonary blood flow.
Examples of medical conditions that cause hypoxemia include:
- Asthma
- COPD
- Heart failure
- Pleural effusions
- Pneumonia
- Pneumothorax
- Pulmonary edema
- Pulmonary emboli
With hypoxia, there is inadequate transport of oxygen to the cells or tissues, either because of obstruction, secretions, or tumours in the lungs; hypoventilation due to disease, injury to the respiratory system, or medications; or poor blood flow due to a compromised circulatory system (British Thoracic Society, 2008). Hypoxia related to anemia or circulatory system compromise, such as decreased cardiac output, will respond poorly to oxygen therapy, and other appropriate interventions should be considered.
Hypoxia is a medical emergency (Alberta Health Services, 2015). Oxygen therapy will:
- Decrease the work of breathing in patients with respiratory or cardiovascular conditions, which may prevent respiratory and muscle fatigue (Jardins & Burton, 2011).
- Decrease cardiopulmonary workload by reducing high cardiopulmonary demand (Perry et al., 2014). For example, patients with left ventricular failure benefit from additional oxygen to the tissues because the heart cannot provide enough oxygen to the tissues due to decreased cardiac output.
- Support post-operative recovery, and may be ordered for a specific time frame at a specific rate while the patient recovers from the surgical procedure.
Critical Thinking Exercises
- How do you know if your patient is hypoxic or hypoxemic? Please explain.
- Why would the post-surgical patient require supplemental oxygen?


11.11: Summary
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- Last updated
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- A one sample t-test is used to compare a single sample mean against a hypothesised value for the population mean. (Section 13.2)
- An independent samples t-test is used to compare the means of two groups, and tests the null hypothesis that they have the same mean. It comes in two forms: the Student test (Section 13.3 assumes that the groups have the same standard deviation, the Welch test (Section 13.4) does not.
- A paired samples t-test is used when you have two scores from each person, and you want to test the null hypothesis that the two scores have the same mean. It is equivalent to taking the difference between the two scores for each person, and then running a one sample t-test on the difference scores. (Section 13.5)
- Effect size calculations for the difference between means can be calculated via the Cohen’s d statistic. (Section 13.8).
- You can check the normality of a sample using QQ plots and the Shapiro-Wilk test. (Section 13.9)
- If your data are non-normal, you can use Wilcoxon tests instead of t-tests. (Section 13.10)
References
Student, A. 1908. “The Probable Error of a Mean.” Biometrika 6: 1–2.
Box, J. F. 1987. “Guinness, Gosset, Fisher, and Small Samples.” Statistical Science 2: 45–52.
Welch, B. L. 1947. “The Generalization of ‘Student’s’ Problem When Several Different Population Variances Are Involved.” Biometrika 34: 28–35.
Cohen, J. 1988. Statistical Power Analysis for the Behavioral Sciences . 2nd ed. Lawrence Erlbaum.
McGrath, R. E., and G. J. Meyer. 2006. “When Effect Sizes Disagree: The Case of r and d.” Psychological Methods 11: 386–401.
Hedges, L. V. 1981. “Distribution Theory for Glass’s Estimator of Effect Size and Related Estimators.” Journal of Educational Statistics 6: 107–28.
Hedges, L. V., and I. Olkin. 1985. Statistical Methods for Meta-Analysis . New York: Academic Press.
Shapiro, S. S., and M. B. Wilk. 1965. “An Analysis of Variance Test for Normality (Complete Samples).” Biometrika 52: 591–611.
- We won’t cover multiple predictors until Chapter 15
- Informal experimentation in my garden suggests that yes, it does.  Nutrients to European plants are poison to Australian ones. There’s probably a joke in that, but I can’t figure out what it is.
- Actually this is too strong. Strictly speaking the z test only requires that the sampling distribution of the mean be normally distributed; if the population is normal then it necessarily follows that the sampling distribution of the mean is also normal. However, as we saw when talking about the central limit theorem, it’s quite possible (even commonplace) for the sampling distribution to be normal even if the population distribution itself is non-normal. However, in light of the sheer ridiculousness of the assumption that the true standard deviation is known, there really isn’t much point in going into details on this front!
- Well, sort of. As I understand the history, Gosset only provided a partial solution: the general solution to the problem was provided by Sir Ronald Fisher.
- More seriously, I tend to think the reverse is true: I get very suspicious of technical reports that fill their results sections with nothing except the numbers. It might just be that I’m an arrogant jerk, but I often feel like an author that makes no attempt to explain and interpret their analysis to the reader either doesn’t understand it themselves, or is being a bit lazy.  Don’t annoy them if you can help it.
- Although it is the simplest, which is why I started with it.
- A funny question almost always pops up at this point: what the heck is the population being referred to in this case? Is it the set of students actually taking Dr Harpo’s class (all 33 of them)? The set of people who might take the class (an unknown number) of them? Or something else? Does it matter which of these we pick? It’s traditional in an introductory behavioural stats class to mumble a lot at this point, but since I get asked this question every year by my students, I’ll give a brief answer. Technically yes, it does matter: if you change your definition of what the “real world” population actually is, then the sampling distribution of your observed mean ¯X changes too. The t-test relies on an assumption that the observations are sampled at random from an infinitely large population; and to the extent that real life isn’t like that, then the t-test can be wrong. In practice, however, this isn’t usually a big deal: even though the assumption is almost always wrong, it doesn’t lead to a lot of pathological behaviour from the test, so we tend to just ignore it.
- Yes, I have a “favourite” way of thinking about pooled standard deviation estimates. So what?
- A more correct notation will be introduced in Chapter 14.
- Well, I guess you can average apples and oranges, and what you end up with is a delicious fruit smoothie. But no one really thinks that a fruit smoothie is a very good way to describe the original fruits, do they?
- This design is very similar to the one in Section 12.8 that motivated the McNemar test. This should be no surprise. Both are standard repeated measures designs involving two measurements. The only difference is that this time our outcome variable is interval scale (working memory capacity) rather than a binary, nominal scale variable (a yes-or-no question).
- At this point we have Drs Harpo, Chico and Zeppo. No prizes for guessing who Dr Groucho is.
- This is obviously a class being taught at a very small or very expensive university, or else is a postgraduate class. I’ve never taught an intro stats class with less than 350 students.
-
The
sortFrame()
function sorts factor variables likeid
in alphabetical order, which is why it jumps from “student1” to “student10” - This is a massive oversimplification.
-
Either that, or the Kolmogorov-Smirnov test, which is probably more traditional than the Shapiro-Wilk, though most things I’ve read seem to suggest Shapiro-Wilk is the better test of normality; although Kolomogorov-Smirnov is a general purpose test of distributional equivalence, so it can be adapted to handle other kinds of distribution tests; in R it’s implemented via the
ks.test()
function. - Actually, there are two different versions of the test statistic; they differ from each other by a constant value. The version that I’ve described is the one that R calculates.


10.7: Gyroscopic Effects- Vector Aspects of Angular Momentum
Learning Objectives
By the end of this section, you will be able to:
- Describe the right-hand rule to find the direction of angular velocity, momentum, and torque.
- Explain the gyroscopic effect.

Angular momentum is a vector and, therefore, has direction as well as magnitude . Torque affects both the direction and the magnitude of angular momentum. What is the direction of the angular momentum of a rotating object like the disk in Figure ? The figure shows the right-hand rule used to find the direction of both angular momentum and angular velocity. Both \(L\) and \(\omega\) are vectors—each has direction and magnitude. Both can be represented by arrows. The right-hand rule defines both to be perpendicular to the plane of rotation in the direction shown. Because angular momentum is related to angular velocity by \(L = I\omega\), the direction of \(L\) is the same as the direction of \(\omega\). Notice in the figure that both point along the axis of rotation.
Now, recall that torque changes angular momentum as expressed by
\[net \, \tau = \dfrac{\Delta L}{\Delta t}.\]
This equation means that the direction of \(\Delta L\) is the same as the direction of the torque \(\tau\) that creates it. This result is illustrated in Figure , which shows the direction of torque and the angular momentum it creates.
Let us now consider a bicycle wheel with a couple of handles attached to it, as shown in Figure . (This device is popular in demonstrations among physicists, because it does unexpected things.) With the wheel rotating as shown, its angular momentum is to the woman's left. Suppose the person holding the wheel tries to rotate it as in the figure. Her natural expectation is that the wheel will rotate in the direction she pushes it—but what happens is quite different. The forces exerted create a torque that is horizontal toward the person, as shown in Figure (a). This torque creates a change in angular momentum \(L\) in the same direction, perpendicular to the original angular momentum \(L\), thus changing the direction of \(L\) but not the magnitude of \(L\). Figure shows how \(\Delta L\) and \(L\) add, giving a new angular momentum with direction that is inclined more toward the person than before. The axis of the wheel has thus moved perpendicular to the forces exerted on it , instead of in the expected direction.
This same logic explains the behavior of gyroscopes. Figure shows the two forces acting on a spinning gyroscope. The torque produced is perpendicular to the angular momentum, thus the direction of the torque is changed, but not its magnitude. The gyroscope precesses around a vertical axis, since the torque is always horizontal and perpendicular to \(L\). If the gyroscope is not spinning, it acquires angular momentum in the direction of the torque (\( L = \Delta L\)), and it rotates around a horizontal axis, falling over just as we would expect.
 Its angular momentum is along its axis and points at Polaris, the North Star. But Earth is slowly precessing (once in about 26,000 years) due to the torque of the Sun and the Moon on its nonspherical shape.
Exercise \(\PageIndex{1}\)
Rotational kinetic energy is associated with angular momentum? Does that mean that rotational kinetic energy is a vector?
- Answer
-
No, energy is always a scalar whether motion is involved or not. No form of energy has a direction in space and you can see that rotational kinetic energy does not depend on the direction of motion just as linear kinetic energy is independent of the direction of motion.
Section Summary
- Torque is perpendicular to the plane formed by \(\tau\) and \(F\) and is the direction your right thumb would point if you curled the fingers of your right hand in the direction of \(F\). The direction of the torque is thus the same as that of the angular momentum it produces.
- The gyroscope precesses around a vertical axis, since the torque is always horizontal and perpendicular to \(L\). If the gyroscope is not spinning, it acquires angular momentum in the direction of the torque (\(L = \Delta L\)), and it rotates about a horizontal axis, falling over just as we would expect.
 Its angular momentum is along its axis and points at Polaris, the North Star.
Glossary
- right-hand rule
- direction of angular velocity ω and angular momentum L in which the thumb of your right hand points when you curl your fingers in the direction of the disk’s rotation


6.4: Organizing Forces - Collections and Scales
Folk, pop, classical, and modern composers often organize pitch materials using scales other than major and minor. Some of these scales, like the various diatonic modes and the pentatonic collection, are relatively familiar to most listeners. Others — such as octatonic, whole-tone, and acoustic collections/scales — are more novel, and usually (but not always) found in twentieth- and twenty-first-century compositions.
When characterizing many of these new musical resources, the word “collection” is often more appropriate than “scale.” A collection is a group of notes — usually five or more. Imagine a collection as a source from which a composer can draw musical material — a kind of “soup” within which pitch-classes float freely. Collections by themselves do not imply a tonal center. But in a composition a composer may establish a tonal center by privileging one note of the collection, which we then call a scale .
Diatonic Collection (modes)
The diatonic collection is any transposition of the 7 white keys on the piano. Refer to these collections by the number of sharps and flats they contain: the “0-sharp” collection, the “1-sharp” collection, and so on. The “2-flat” collection, for example, contains the pitch classes {F, G, A, B-flat, C, D, E-flat}.
When these collections gain a tonic note, they morph into scales, which by tradition we name according to the “modal” system established in centuries ago. (Note that while these modes share their names with the modes of the Medieval Christian church, they function quite differently. The similarity is principally one of name.)
One way to look at these “modes” is to think of the seven white keys of the piano {C, D, E, F, A, B}. These notes, when starting on different pitches, create the different modal scales. By taking each note of the seven-white-key collection, and treating it as as the tonic, all seven modal scales can be played. Ionian treats C as tonic, Dorian treats D as tonic, Phrygian treats E as tonic, Lydian treats F as tonic, Mixolydian treats G as tonic, Aeolian treats A as tonic, and Locrian treats B as tonic:
Ionian mode (major scale): do re mi fa sol la ti do
Dorian mode: do re me fa sol la te do
Phrygian mode: do ra me fa sol le te do
Lydian mode: do re mi fi sol la ti do
Mixolydian mode: do re mi fa sol la te do
Aeolian mode (natural-minor scale): do re me fa sol le te do
Locrian mode (uncommon outside jazz): do ra me fa se le te do
Like the major and minor scales, these intervallic relationships can be transposed to any tonic pitch.
Pentatonic Collection
Pentatonic collections are five-note subsets of the diatonic collection. Here’s a quick way to create a pentatonic collection: (1) List the notes of a major scale. (2) Remove scale degress 4 and 7. (E.g., the pentatonic collection {C,D,E,G,A} corresponds to scale degrees 1,2,3,5,6 of the C major scale.)
Removing scale degrees 4 and 7 results in a collection with no half steps. As a result of its “halfsteplessness”, any member of the collection easily functions as a tonal center. For example, given the 0-sharp pentatonic collection, there are five unique scales formed when each of the collection’s pitch classes become a tonic: C pentatonic (C,D,E,G,A), D pentatonic (D,E,G,A,C), E pentatonic (E,G,A,C,D), and so on.
The black keys on the piano also form a pentatonic collection:
Whole Tone Collection
This is a group of notes generated entirely by whole tones: {0,2,4,6,8,10}, for example.
There are only two unique whole-tone collections. WT0 contains pitch classes {0,2,4,6,8,10}, while WT1 contains pitch classes {1,3,5,7,9,11}. In other words, WT0 contains the pitch classes {C, D, E, F-sharp, G-sharp, B-flat}, while WT1 contains pitch classes {C-sharp, D-sharp, F, G, A, B}.
Octatonic Collection
Called octatonic because it has eight pitch classes, the octatonic collection is full of compositional potential and has been used by many composers to a variety of ends. An octatonic collection is easily generated by alternating half steps and whole steps. Using pitch class numbers, one example is {0,1,3,4,6,7,9,10}.
The interval content of this collection is very homogenous, and this intervallic consistency leads to one of its most interesting properties. When we transpose the above collection by 3—adding 3 to each of the integers in the collection—{0,1,3,4,6,7,9,10} becomes {3,4,6,7,9,10,0,1}. Comparing the two shows that these collections are exactly the same! In fact, you would come up with the same collection if you transposed it by 6 or 9 as well.
Olivier Messiaen called such collections “modes of limited transposition.” (The whole-tone scale is also a mode of limited transposition.) And as a result of the property, there are only three unique octatonic collections. We name these arbitrarily as OCT(0,1), OCT(1,2), and OCT(2,3). The numbers to the right of “OCT” are pitch classes within that scale. (E.g., the {0,1,3,4,6,7,9,10} collection I discussed above is OCT(1,2).) We can also call them C–C♯ octatonic, C♯–D octatonic, and D–E♭ octatonic.
Other Collections and Scales
There are many, many other collections and scales used by composers and musicians in the twentieth- and twenty-first centuries. Messiaen, for example, described five more modes of limited transposition , and there are other smaller collections that have the same property. Acoustic scales , formed from the first seven unique partials of the overtone series, are common in the music of Debussy, Bartok, and Crumb — ocassionally as a representation of nature. Jazz musicians have an entire set of scales used for improvisation. Non-Western musics often have unique systems of scales and collections, such as the rāgas used in Indian classical music.
More generally, any large set of pitch classes that form the basis for a passage may function as a collection, even if it has no familiar name. Most often, music theorists refer to these collections with pitch-class set notation.
This resource was created by Brian Moseley and contains contributions from Meredith Cahill, Elise Campbell, and Kris Shaffer.


12.3: Reading- Third-Party Sales
Introduction
Throughout the channel structure there are a number of points where sales may occur.
The most straightforward of these is the direct channel, in which the producer sells directly to the consumer. In every other structure, multiple sales occur—from producer to wholesaler, from wholesaler to retailer, from retailer to buyer. In cases involving an intermediary, there is a third-party sale. Third-party sales are sales conducted by anyone other than the producer. Even when there are four or five parties involved, we refer to all of them as third parties.
Third-party sales are often vexing for marketers. When a company uses a direct sales approach, the marketer can devise a sales compensation structure that creates the right incentives for the sales team to sell the right products to the right customers at the right price. In a third-party sales situation, it is much more difficult to understand and influence the sales process. Let’s look at a direct sales situation and a third-party sales situation to understand the differences.
Direct Sales Incentives
Nanette Lepore is a high-end clothing designer who has created a personal brand. Nanette sells direct to consumers both online and through her boutique stores across the U.S. Through the direct channel, Nanette’s marketing team owns every aspect of the sales experience. When customers enter a store or land on her Web page, they see a complete outfit that is designed to sell the look that Nanette most wants them to buy. This includes clothing, shoes, and accessories all designed and sold by Nanette Lepore.
Nanette Lepore’s blog and social media presence drive interest in the products that are available in stores and online, with an emphasis on those that are targeted for immediate sale.
When she completes drawings for next season’s looks, Nanette provides digital copies of her drawings to her sales associates, who have been cultivating a list of their most fashion-forward customers. These customers can review drawings and preorder clothing before it is available to the public. These customers pay top dollar for Nanette Lepore’s most current creations.
In the store, sales associates are not equally compensated for all sales. Once a line of clothing goes on sale, the price is reduced. From the perspective of a sales associate, instead of earning a 5 percent commission ($40) on an $800 dress, the associate will earn a 5 percent commission ($10) on a discounted $200 dress. The associate may earn no commission or a reduced commission on clearance items.
The sales staff is preparing customers in advance and in the moment to pay top dollar for Nanette Lepore’s hottest fashions. They do this because there is an entire sales system and compensation structure that centers on Nanette Lepore. They also do this because they have become part of the Nanette Lepore brand and feel a commitment to Nanette Lepore and to the women for whom she is designing.
Third-Party Sales Incentives
Many retailers sell the Nanette Lepore line, including Neiman Marcus, Saks Fifth Avenue, Nordstrom, Zappos, Gilt, Shopbop, and 6pm.com.
The Neiman Marcus sales associate in the dress department is paid a flat commission regardless of the brand she sells. A strong sales associate will identify shoppers with an affinity for Nanette’s designs and present them in the changing room or call to let them know that new Nanette Lepore designs have arrived. If a dress from Diane von Furstenberg or Kate Spade is more likely to make the sale, the dress by Nanette Lepore will not be suggested. The sales associate has incentives to make the largest possible sale—regardless of brand.
If the customer buys a Nanette Lepore dress and heads to the shoe department or accessory department to complete her outfit, she won’t have Nanette Lepore brands as an option. Each department carries the most popular brands, and Nanette Lepore bags and shoes are a new, unproven brand.
In a more extreme example, 6pm.com is the online bargain outlet for Zappos. There is no sales associate, and little effort is made to feature or present any particular brand or clothing. Customers come searching for rock-bottom pricing. Nanette Lepore’s fashions sell at a discount of 60 percent to 70 percent off the manufacturers’ suggested retail price.
If this example doesn’t seem like something that you have experienced, walk into BestBuy and look for a phone, camera, or computer. Ask a sales associate to help you. You will quickly find that the store’s sales compensation structure is driving what is available to you—and what is recommended.
What about something as simple as breakfast cereal in a grocery store? Which products are at eye level? Which are difficult to find? Which are not available? Sales incentives are determining the answers to each of these questions.
Approaches to Support Third-Party Sales Success
If the marketer works for the producer—in our example, Nanette Lepore—he will lose significant control and influence in the third-party sale, while the Neiman Marcus marketing team will gain control or power. How can a marketer approach third-party sales most effectively? The following approaches can be used:
- Understand and align incentives. A good marketer must understand why each channel partner buys and sells, how they are compensated, and what objectives they are hoping to achieve. In third-party sales, the marketer must optimize an existing structure rather than creating the structure.
- Provide exceptional sales support. While the Nanette Lepore sales associates only needs to learn about her line, the Neiman Marcus sales associates must learn thirty or more. Make it very easy for the third-party sales team to become expert in your product.
- Create demand for your product. Often marketers blame channel partners for a marketing mix that doesn’t deliver value to the customer. While it is trite to say that a good product sells itself, it is true that the right product is easier to sell. When the distribution channel—”place,” in the marketing mix—creates a lot of complexity, it is even more important to get the other three elements of the marketing mix just right.
Contributors and Attributions
- Third-Party Sales. Provided by : Lumen Learning. License : CC BY: Attribution
- Nanette Lepore. Authored by : Amber Karnes. Located at : www.flickr.com/photos/ambernussbaum/2850735703/. License : CC BY-NC-ND: Attribution-NonCommercial-NoDerivatives


1.6: Summary
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We’ve now seen that the field of linguistics approaches the study of language from a scientific point of view. As linguists, we seek to make systematic, descriptive observations about human language behaviour. From these empirical observations, linguists have learned that every speaker of every human language has a mental grammar. And the mental grammar of every language includes systematic principles for how sounds (or hand signs, in a signed language) are made, for how these sounds or signs are organized into words, for how words and smaller pieces of words are combined to form phrases and sentences, and for how we assign meaning to words and sentences. When we speak our language, we use our mental grammar to generate new phrases and sentences, and the people who listen to us use their mental grammar to understand us.


23.1: Introduction
Organisms are classified into three domains: Archaea, Bacteria, and Eukarya. The first two lineages comprise all prokaryotic cells, and the third contains all eukaryotes. A very sparse fossil record prevents us from determining what the first members of each of these lineages looked like, so it is possible that all the events that led to the last common ancestor of extant eukaryotes will remain unknown. However, comparative biology of extant (living) organisms and the limited fossil record provide some insight into the evolution of Eukarya.
The earliest fossils found appear to be those of domain Bacteria, most likely cyanobacteria. They are about 3.5 to 3.8 billion years old and are recognizable because of their relatively complex structure and, for prokaryotes, relatively large cells. Most other prokaryotes have small cells, 1 or 2 µm in size, and would be difficult to pick out as fossils. Fossil stromatolites suggest that at least some prokaryotes lived in interactive communities, and evidence from the structure of living eukaryotic cells suggests that it was similar ancestral interactions that gave rise to the eukaryotes. Most living eukaryotes have cells measuring 10 µm or greater. Structures this size, which might be fossilized remains of early eukaryotes, appear in the geological record in deposits dating to about 2.1 billion years ago.
Characteristics of Eukaryotes
Data from these fossils, as well as from the study of living genomes, have led comparative biologists to conclude that living eukaryotes are all descendants of a single common ancestor. Mapping the characteristics found in all major groups of eukaryotes reveals that the following characteristics are present in at least some of the members of each major lineage, or during some part of their life cycle, and therefore must have been present in the last common ancestor .
- Cells with nuclei surrounded by a nuclear envelope with nuclear pores : This is the single characteristic that is both necessary and sufficient to define an organism as a eukaryote. All extant eukaryotes have cells with nuclei.
- Mitochondria : Most extant eukaryotes have "typical" mitochondria, although some eukaryotes have very reduced mitochondrial “remnants” and a few lack detectable mitochondria.
- Cytoskeleton of microtubules and microfilaments : Eukaryotic cells possess the structural and motility components called actin microfilaments and microtubules . All extant eukaryotes have these cytoskeletal elements.
- Flagella and cilia : Organelles associated with cell motility. Some extant eukaryotes lack flagella and/or cilia, but their presence in related lineages suggests that they are descended from ancestors that possessed these organelles.
- Chromosomes organized by histones : Each eukaryotic chromosome consists of a linear DNA molecule coiled around basic (alkaline) proteins called histones. The few eukaryotes with chromosomes lacking histones clearly evolved from ancestors that had them.
- Mitosis : A process of nuclear division in which replicated chromosomes are divided and separated using elements of the cytoskeleton. Mitosis is universally present in eukaryotes.
- Sexual reproduction : A meiotic process of nuclear division and genetic recombination unique to eukaryotes. During this process, diploid nuclei at one stage of the life cycle undergo meiosis to yield haploid nuclei, which subsequently fuse together (karyogamy) to create a diploid zygote nucleus.
- Cell walls : It might be reasonable to conclude that the last common ancestor could make cell walls during some stage of its life cycle, simply because cell walls were present in their prokaryote precursors. However, not enough is known about eukaryotes’ cell walls and their development to know how much homology exists between those of prokaryotes and eukaryotes. If the last common ancestor could make cell walls, it is clear that this ability must have been lost in many groups.
In the span of several decades, the Kingdom Protista has been disassembled because sequence analyses have revealed new genetic (and therefore evolutionary) relationships among these eukaryotes. Moreover, protists that exhibit similar morphological features may have evolved analogous structures because of similar selective pressures—rather than because of recent common ancestry. This phenomenon, called convergent evolution, is one reason why protist classification is so challenging. The emerging classification scheme groups the entire domain Eukarya into six “supergroups” that contain all of the protists as well as animals, plants, and fungi that evolved from a common ancestor (Figure 23.1.1). Each of the supergroups is believed to be monophyletic, meaning that all organisms within each supergroup are believed to have evolved from a single common ancestor, and thus all members are most closely related to each other than to organisms outside that group. There is still evidence lacking for the monophyly of some groups. Each supergroup can be viewed as representing one of many variants on eukaryotic cell structure. In each group, one or more of the defining characters of the eukaryotic cell—the nucleus, the cytoskeleton, and the endosymbiotic organelles—may have diverged from the "typical" pattern.
Keep in mind that the classification scheme presented here represents just one of several hypotheses, and the true evolutionary relationships are still to be determined. The six supergroups may be modified or replaced by a more appropriate hierarchy as genetic, morphological, and ecological data accumulate. When learning about protists, it is helpful to focus less on the nomenclature and more on the commonalities and differences that illustrate how each group has exploited the possibilities of eukaryotic life.
Archaeplastida
Molecular evidence supports the hypothesis that all Archaeplastida are descendents of an endosymbiotic relationship between a heterotrophic protist and a cyanobacterium. The protist members of the group include the red algae and green algae. It was from a common ancestor of these protists that the land plants evolved, since their closest relatives are found in this group. The red and green algae include unicellular, multicellular, and colonial forms. A variety of algal life cycles exists, but the most complex is alternation of generations, in which both haploid and diploid stages are multicellular. A diploid sporophyte contains cells that undergo meiosis to produce haploid spores. The spores germinate and grow into a haploid gametophyte, which then makes gametes by mitosis. The gametes fuse to form a zygote that grows into a diploid sporophyte. Alternation of generations is seen in some species of Archaeplastid algae, as well as some species of Stramenopiles. In some species, the gametophyte and sporophyte look quite different, while in others they are nearly indistinguishable. We will cover the non-protist Archaeplastids (land plants) in a later lab.
Amoebozoa
Like the Archaeplastida, the Amoebozoa include species with single cells, species with large multinucleated cells, and species that have multicellular phases. Amoebozoan cells characteristically exhibit pseudopodia that extend like tubes or flat lobes. These pseudopods project outward from anywhere on the cell surface and can anchor to a substrate. The protist then transports its cytoplasm into the pseudopod, thereby moving the entire cell. This type of motion is similar to the cytoplasmic streaming used to move organelles in the Archaeplastida, and is also used by other protists as a means of locomotion or as a method to distribute nutrients and oxygen. The Amoebozoa include both free-living and parasitic species.
Opisthokonta
The Opisthokonts are named for the single posterior flagellum seen in flagellated cells of the group. The flagella of other protists are anterior and their movement pulls the cells along, while the opisthokonts are pushed. Protist members of the opisthokonts include the animal-like choanoflagellates, which are believed to resemble the common ancestor of sponges and perhaps, all animals. Choanoflagellates include unicellular and colonial forms (Figure 23.1.4), and number about 244 described species. In these organisms, the single, apical flagellum is surrounded by a contractile collar composed of microvilli. The collar is used to filter and collect bacteria for ingestion by the protist. A similar feeding mechanism is seen in the collar cells of sponges, which suggests a possible connection between choanoflagellates and animals.
The Mesomycetozoa form a small group of parasites, primarily of fish, and at least one form that can parasitize humans. Their life cycles are poorly understood. These organisms are of special interest, because they appear to be so closely related to animals. In the past, they were grouped with fungi and other protists based on their morphology. We will cover the non-protist Opisthokonts (animals and fungi) in later labs.
The previous supergroups are all the products of primary endosymbiontic events and their organelles—nucleus, mitochondria, and chloroplasts—are what would be considered "typical," i.e., matching the diagrams you would find in an introductory biology book. The next three supergroups all contain at least some photosynthetic members whose chloroplasts were derived by secondary endosymbiosis. They also show some interesting variations in nuclear structure, and modification of mitochondria or chloroplasts.
Rhizaria
The Rhizaria supergroup includes many of the amoebas with thin threadlike, needle-like or root-like pseudopodia (Figure 23.1.5), rather than the broader lobed pseudopodia of the Amoebozoa. Many rhizarians make elaborate and beautiful tests—armor-like coverings for the body of the cell—composed of calcium carbonate, silicon, or strontium salts. Rhizarians have important roles in both carbon and nitrogen cycles. When rhizarians die, and their tests sink into deep water, the carbonates are out of reach of most decomposers, locking carbon dioxide away from the atmosphere. In general, this process by which carbon is transported deep into the ocean is described as the biological carbon pump, because carbon is “pumped” to the ocean depths where it is inaccessible to the atmosphere as carbon dioxide. The biological carbon pump is a crucial component of the carbon cycle that maintains lower atmospheric carbon dioxide levels. Foraminiferans are unusual in that they are the only eukaryotes known to participate in the nitrogen cycle by denitrification, an activity usually served only by prokaryotes.
Foraminiferans
Foraminiferans, or forams, are unicellular heterotrophic protists, ranging from approximately 20 micrometers to several centimeters in length, and occasionally resembling tiny snails (Figure 23.1.6). As a group, the forams exhibit porous shells, called tests that are built from various organic materials and typically hardened with calcium carbonate. The tests may house photosynthetic algae, which the forams can harvest for nutrition. Foram pseudopodia extend through the pores and allow the forams to move, feed, and gather additional building materials. Typically, forams are associated with sand or other particles in marine or freshwater habitats. Foraminiferans are also useful as indicators of pollution and changes in global weather patterns.
Radiolarians
A second subtype of Rhizaria, the radiolarians, exhibit intricate exteriors of glassy silica with radial or bilateral symmetry (Figure 23.1.7). Needle-like pseudopods supported by microtubules radiate outward from the cell bodies of these protists and function to catch food particles. The shells of dead radiolarians sink to the ocean floor, where they may accumulate in 100 meter-thick depths. Preserved, sedimented radiolarians are very common in the fossil record.


10.15: Postpartum Depression
Having a baby is usually one of the happiest times in a woman's life, but for some women, it can include times of sadness and depression. More women actually suffer from postpartum depression than we really know. Women usually ignore the emotional and physical signs, dealing with their feelings on their own.
Postpartum depression affects approximately 10 to 15 percent of new mothers. It often causes anxiety and obsession about caring for the baby or the cleanliness of the home. It may cause changes in sleep patterns and affect relationships, including the ability to form a bond with the baby and other family members. Some mothers with postpartum depression have thoughts of wanting to die or of hurting the baby. If the symptoms are so severe that they keep the mother from being able to function, medical treatment is necessary.
Baby blues are common due to rapid hormonal changes but resolve after 1-2 weeks. Postpartum depression is characterized by persisting symptoms, and the mother should notify her provider immediately.