A precarious avalanche threatens to put an end to Mickey and Minnie's yodeling duet. Watch brand new Disney Shorts, starring Mickey Mouse! ► https://www.youtube.com/watch?v=DwY2OqEvhS8&list=PLC6qIbU1olyXQe1WOKt8UJ4hErx3D7qt8&index=28 See more cartoons from around the world, from Disney Favorites! ► https://www.youtube.com/watch?v=Hm7s7ixJZdQ&index=24&list=PL5518FC3758234754 SUBSCRIBE to get notified when new Disney Shorts videos are posted: http://di.sn/SubscribeDisneyShorts Get more from Disney! Disney YouTube: http://di.sn/SubscribeDisney Like Disney: http://Facebook.com/Disney Follow Disney: http://Twitter.com/Disney Disney Tumblr: http://disney.tumblr.com/ Disney Google+: http://plus.google.com/+Disney/posts Disney Instagram: http://Instagram.com/Disney About Mickey Mouse: Mickey Mouse first came into our lives in 1928 with a whistle and two step in the classic Disney cartoon Steamboat Willie. He has since existed as an icon of disney, our childhoods, and the magic kingdom. Mickey has appeared in over 130 films including Brave Little Tailor (1938) and Fantasia (1940), as well as television shows like the New Mickey Mouse Club (1996)! With Minnie Mouse, Pluto, Goofy, Donald Duck, and his nemesis Pete, Mickey is back for more fun and adventures in a ton of new Disney animated shorts. Fans of all ages, new and old, are sure to enjoy. About Disney Shorts: Enjoy animated and live action Disney cartoons and short films. We have all your favorite original and new Disney characters! Enjoy new and classic cartoons starring your favorite Disney characters. And watch some of our favorite animations from other YouTube creators and across the web, curated and collected for every Disney fan to enjoy!
Mickey Mouse full episodes Cartoon Special 6 HOURS NON STOP!
When Minnie's cafe runs out of croissants, Mickey must deliver them to her fast, fighting wild traffic and other obstacles across Paris! Watch brand new Disney Shorts, starring Mickey Mouse! ► https://www.youtube.com/watch?v=dbdYBkk5PNs&list=PLC6qIbU1olyXQe1WOKt8UJ4hErx3D7qt8&index=13 See more cartoons from around the world, from Disney Favorites! ► https://www.youtube.com/watch?v=VJD3F_O_CL4&index=4&list=PL5518FC3758234754 SUBSCRIBE to get notified when new Disney Shorts videos are posted: http://di.sn/SubscribeDisneyShorts Get more from Disney! Disney YouTube: http://di.sn/SubscribeDisney Like Disney: http://Facebook.com/Disney Follow Disney: http://Twitter.com/Disney Disney Tumblr: http://disney.tumblr.com/ Disney Google+: http://plus.google.com/+Disney/posts Disney Instagram: http://Instagram.com/Disney About Mickey Mouse: Mickey Mouse first came into our lives in 1928 with a whistle and two step in the classic Disney cartoon Steamboat Willie. He has since existed as an icon of disney, our childhoods, and the magic kingdom. Mickey has appeared in over 130 films including Brave Little Tailor (1938) and Fantasia (1940), as well as television shows like the New Mickey Mouse Club (1996)! With Minnie Mouse, Pluto, Goofy, Donald Duck, and his nemesis Pete, Mickey is back for more fun and adventures in a ton of new Disney animated shorts. Fans of all ages, new and old, are sure to enjoy. About Disney Shorts: Enjoy animated and live action Disney cartoons and short films. We have all your favorite original and new Disney characters! Enjoy new and classic cartoons starring your favorite Disney characters. And watch some of our favorite animations from other YouTube creators and across the web, curated and collected for every Disney fan to enjoy!
Mickey helps Goofy by letting his Grandma stay at his house, but soon finds out that she's not the sweet old lady she appears to be. Watch brand new Disney Shorts, starring Mickey Mouse! ► https://www.youtube.com/watch?v=dbdYBkk5PNs&list=PLC6qIbU1olyXQe1WOKt8UJ4hErx3D7qt8&index=13 See more cartoons from around the world, from Disney Favorites! ► https://www.youtube.com/watch?v=VJD3F_O_CL4&index=4&list=PL5518FC3758234754 SUBSCRIBE to get notified when new Disney Shorts videos are posted: http://di.sn/SubscribeDisneyShorts Get more from Disney! Disney YouTube: http://di.sn/SubscribeDisney Like Disney: http://Facebook.com/Disney Follow Disney: http://Twitter.com/Disney Disney Tumblr: http://disney.tumblr.com/ Disney Google+: http://plus.google.com/+Disney/posts Disney Instagram: http://Instagram.com/Disney About Mickey Mouse: Mickey Mouse first came into our lives in 1928 with a whistle and two step in the classic Disney cartoon Steamboat Willie. He has since existed as an icon of disney, our childhoods, and the magic kingdom. Mickey has appeared in over 130 films including Brave Little Tailor (1938) and Fantasia (1940), as well as television shows like the New Mickey Mouse Club (1996)! With Minnie Mouse, Pluto, Goofy, Donald Duck, and his nemesis Pete, Mickey is back for more fun and adventures in a ton of new Disney animated shorts. Fans of all ages, new and old, are sure to enjoy. About Disney Shorts: Enjoy animated and live action Disney cartoons and short films. We have all your favorite original and new Disney characters! Enjoy new and classic cartoons starring your favorite Disney characters. And watch some of our favorite animations from other YouTube creators and across the web, curated and collected for every Disney fan to enjoy!
Goofy invites himself on Mickey's date with Minnie. Watch brand new Disney Shorts, starring Mickey Mouse! ► https://www.youtube.com/watch?v=DwY2OqEvhS8&list=PLC6qIbU1olyXQe1WOKt8UJ4hErx3D7qt8&index=28 See more cartoons from around the world, from Disney Favorites! ► https://www.youtube.com/watch?v=Hm7s7ixJZdQ&index=24&list=PL5518FC3758234754 SUBSCRIBE to get notified when new Disney Shorts videos are posted: http://di.sn/SubscribeDisneyShorts Get more from Disney! Disney YouTube: http://di.sn/SubscribeDisney Like Disney: http://Facebook.com/Disney Follow Disney: http://Twitter.com/Disney Disney Tumblr: http://disney.tumblr.com/ Disney Google+: http://plus.google.com/+Disney/posts Disney Instagram: http://Instagram.com/Disney About Mickey Mouse: Mickey Mouse first came into our lives in 1928 with a whistle and two step in the classic Disney cartoon Steamboat Willie. He has since existed as an icon of disney, our childhoods, and the magic kingdom. Mickey has appeared in over 130 films including Brave Little Tailor (1938) and Fantasia (1940), as well as television shows like the New Mickey Mouse Club (1996)! With Minnie Mouse, Pluto, Goofy, Donald Duck, and his nemesis Pete, Mickey is back for more fun and adventures in a ton of new Disney animated shorts. Fans of all ages, new and old, are sure to enjoy. About Disney Shorts: Enjoy animated and live action Disney cartoons and short films. We have all your favorite original and new Disney characters! Enjoy new and classic cartoons starring your favorite Disney characters. And watch some of our favorite animations from other YouTube creators and across the web, curated and collected for every Disney fan to enjoy!


Meadows of Dan is located where Route 58 crosses the Blue Ridge Parkway, near the headwaters of the Dan River. The community's motto, posted on the welcome sign, is "A simpler place in time." Meadows of Dan is located along the Crooked Road, Virginia's Heritage Music Trail, and near historic Mabry Mill on the Parkway. Meadows of Dan hosts an annual Folk Fair, in cooperation with the Virginia Peach Festival. Other festivals include Chinquapin Festival Corn Maze and Crafts in the Meadow.


4/18/18: Please welcome Mimsy! On Tuesday we found out about this sweet little girl that was at Dekalb County Animal Control. We emailed our contact and were told "Thanks for inquiring about her. She is currently a court case and is not available for rescue or adoption at this time, but I will certainly keep you all in mind if anything changes." The next day they contacted us and said she needed medical help and could be released to us now. Within a few hours she was in our hands.She has five open wounds on her body including a very large ruptured mammary tumor. We have no idea what caused the wounds. She has a dislocated hip. She has dry eye. She has a skin infection. She is heart worm positive. She is dehydrated, anemic, has a very low red blood cell count and a very very very high white blood cell count.Today we transferred her to ICU for fluids, and liquid antibiotics and liquid pain medication. We also started her on drops for her dry eye and arthritis medication. At this point she is too weak and too infected to do anything more. We need her to get stronger and give her some time for her wounds to heal. We did x rays and did not see any additional tumors. We may do an ultrasound in a few days for a second look. In the near future she will need the ruptured mammary tumor removed and she will need to be spayed. Sometime down the road she will need to be treated for heart worms and we will evaluate her hip.For now she will be spending the next few days in the ICU. Our estimated invoice for this is $1500-$2500. If you would like to donate towards Mimsy's care it would be very much appreciated.Please send positive thoughts her way!Update 4/20/18: When we spoke with the specialist this morning she said Mimsy was feeling a little better than yesterday. Her red blood cell count is up 1%, her wounds are looking a little better, she standing up on her own and she is eating!Thank you all for your donations towards her vet care!Update 4/22/18: Mimsy' condition is stable, eating a little more. Her road to recovery is going to be long.Update 4/23/18: Mimsy is off IV and out of the ICU! She's got some fresh new pink bandages too! She will be moving back to the regular vet clinic today. She is still on two antibiotics for her wounds, meds for her arthritis and meds for her pain. We will recheck all of her blood work in a few days and see when we can move forward with surgery to remove her mammary tumor.Update 4/26/18: We rechecked Mimsy's blood work and things are getting better! Her red blood cell count is going up and her white blood cell count is going down. Her wounds are looking better every day!Update 5/3/18: We recheck Mimsy's blood work and things are continuing to improve but she is still anemic therefore not ready for surgery just yet. Her wounds are looking so much better too!Update 5/9/18: We recheck Mimsy's blood work and things are continuing to improve. We are hopeful that she will be ready for surgery next week!Update 5/14/18: Mimsy was finally able to have her ultrasound today. We had to hold off because of the ruptured mammary mass. The ultrasound showed a mass or enlarged spleen as a thickened stomach wall. At this pint we know she needs to have the mammary mass removed, have her spleen removed, be spayed, have her teeth cleaned and do a biopsy of her stomach. We consulted with the specialist to decided the best way to tackle everything. Hopefully the thickened stomach lining is just secondary to all of the strong medications she has been on the past month. It has been decided that she will have her scheduled blood work done on Wednesday and if things look good enough for surgery on Thursday then we will start with the removal on the mammary mass and if there is time we will see what else can be done at that time.Update 5/17/18: Mimsy had her first surgery yesterday. She had the entire mammary mass removed, had her teeth cleaned and had one decayed tooth extracted. She was under long enough so Dr Ross felt it best to close her up and we will tackle the remaining things in a few weeks when she recovers from this surgery. She still needs to be spayed, have her spleen removed and have a biopsy done on her stomach. We will be doing a biopsy of her mammary mass now. Her leg and ear wounds are just about 100% healed up. Her arthritis is pretty severe so she does not walk all that great and she can not do steps.Update 5/24/18: We got the biopsy results back on her mammary mass and it is not cancer! We will give her a few weeks to recover from surgery then move forward with her next surgery.
Update 5/31/18: Mimsy had her staples removed and she is healing nicely. We will schedule another ultrasound in a few weeks then move forward with her next surgery. She is loving life in her foster home and she is eating a ton and has gained three more pounds! She likes dogs and young children but is not too fond of cats.Update 7/11/18: Mimsy has developed two more mammary masses that will need to be removed before she can start her heartworm treatment. She will have her surgery at the end of the month then start her heartworm treatment two weeks later.
Update 7/24/18: Mimsy had a seizure on Sunday so we decided to not put her through surgery right now to remove the mammary masses. Removing them was more of a precaution than a necessity at this time. We ran her bloodwork and everything looks fine so we will start her heartworm treatment tomorrow and watch for more seizures.
Update 8/16/18: Mimsy completed her heartworm treatment today. All went well and she is now ready for adoption!


text:
Autism in Africa
1 year ago VIRGINIA HUGHES
Mental illness is the leading cause of disability in the world, according to the World Health Organization. Even more troubling: Four out of five people with psychiatric disorders live in developing countries, where they have few opportunities for treatment.
That's certainly the case for autism in Africa, though, like in other resource-poor areas of the world, awareness is beginning to improve. In the past few years, a handful of researchers in various African countries have investigated children with autism. A new review of these reports finds that these children tend to be diagnosed much later than their counterparts in the U.S., and are more likely to be nonverbal.
The review, published in the December issue of the South African Journal of Psychiatry, analyzes six studies: three from Nigeria, the most populous country in Africa, and one each from Tunisia, Tanzania and Kenya.
The studies, published between 1982 and 2010, each identified only a few dozen children with autism, from clinics thousands of miles apart. Yet the cases are strikingly similar. Nearly all of the children were diagnosed relatively late: many at around 8 years old and some into their teenage years. Two of the studies reported nonverbal rates among children with autism of 51 and 71 percent, respectively, compared with around 25 percent in the U.S.
There are many factors that could account for these numbers, not least of which is a weak medical infrastructure and lack of resources. For example, compared with the rest of the world, the prevalence of treatable disease — malaria, tuberculosis, HIV — is high, while the number of doctors and medical facilities is low. Cultural and educational factors may play a role, too.
The authors cite research showing that autism awareness is low not only in the general African population, but also in the medical community.
One survey asked Nigerian nurses who specialize in psychiatry or pediatrics about the causes of autism. Some 40 percent fingered preternatural or supernatural causes, such as ancestral spirits, enemies, sinning or the action of the devil.
These attitudes, the researchers suggest, mean that when a child has a mental or neurodevelopmental problem, help may first be sought from traditional healers or religious leaders, rather than from a medical clinic, which could account for the late diagnoses. These lost years may also contribute to the lack of language in many of the children with autism, perhaps because they did not have access to early interventions or speech therapy.
The good news is that mental health issues in Africa are starting to get more attention.
For example, in 2005, the World Health Organization launched the Mental Health and Poverty Project, which aims to bring psychiatric care to poor communities in Ghana, South Africa, Uganda and Zambia. And just last week, a large group of public health experts called on the United Nations General Assembly to host a special session on the issue of global mental health.
This article was originally published on Autism in Africa
Previous Virtual games teach real-world skills to kids with autism
Next In Chinese newspapers, stories on autism neglect science

redpajama_set_name: RedPajamaCommonCrawl


text:
5.4: Summary- Organelles - Biology
Describe the basic composition of cytoplasm
Describe the structure and function of the nucleus and nuclear membrane
Describe the structure, function, and components of the endomembrane system
Describe the structure and function of ribosomes
Describe the structure and function of mitochondria
Describe the structure and functions of vesicles
Describe the structure and function of peroxisomes
Demonstrate familiarity with various components of the cytoskeleton
Describe the structure and functions of flagella and cilia
Explain the structure and function of cell membranes
Identify key organelles present only in plant cells, including chloroplasts and vacuoles
Identify key organelles present only in animal cells, including centrosomes and lysosomes
Table 1 provides the components of prokaryotic and eukaryotic cells and their respective functions.
Table 1. Components of Prokaryotic and Eukaryotic Cells and Their Functions
Cell Component
Present in Prokaryotes?
Present in Animal Cells?
Present in Plant Cells?
Plasma membrane Separates cell from external environment; controls passage of organic molecules, ions, water, oxygen, and wastes into and out of the cell Yes Yes Yes
Cytoplasm Provides structure to cell; site of many metabolic reactions; medium in which organelles are found Yes Yes Yes
Nucleoid Location of DNA Yes No No
Nucleus Cell organelle that houses DNA and directs synthesis of ribosomes and proteins No Yes Yes
Ribosomes Protein synthesis Yes Yes Yes
Mitochondria ATP production/cellular respiration No Yes Yes
Peroxisomes Oxidizes and breaks down fatty acids and amino acids, and detoxifies poisons No Yes Yes
Vesicles and vacuoles Storage and transport; digestive function in plant cells No Yes Yes
Centrosome Unspecified role in cell division in animal cells; source of microtubules in animal cells No Yes No
Lysosomes Digestion of macromolecules; recycling of worn-out organelles No Yes No
Cell wall Protection, structural support and maintenance of cell shape Yes, primarily peptidoglycan in bacteria but not Archaea No Yes, primarily cellulose
Chloroplasts Photosynthesis No No Yes
Endoplasmic reticulum Modifies proteins and synthesizes lipids No Yes Yes
Golgi apparatus Modifies, sorts, tags, packages, and distributes lipids and proteins No Yes Yes
Cytoskeleton Maintains cell's shape, secures organelles in specific positions, allows cytoplasm and vesicles to move within the cell, and enables unicellular organisms to move independently Yes Yes Yes
Flagella Cellular locomotion Some Some No, except for some plant sperm.
Cilia Cellular locomotion, movement of particles along extracellular surface of plasma membrane, and filtration No Some No
Like a prokaryotic cell, a eukaryotic cell has a plasma membrane, cytoplasm, and ribosomes, but a eukaryotic cell is typically larger than a prokaryotic cell, has a true nucleus (meaning its DNA is surrounded by a membrane), and has other membrane-bound organelles that allow for compartmentalization of functions. The plasma membrane is a phospholipid bilayer embedded with proteins. The nucleolus within the nucleus is the site for ribosome assembly. Ribosomes are found in the cytoplasm or are attached to the cytoplasmic side of the plasma membrane or endoplasmic reticulum. They perform protein synthesis. Mitochondria perform cellular respiration and produce ATP. Peroxisomes break down fatty acids, amino acids, and some toxins. Vesicles and vacuoles are storage and transport compartments. In plant cells, vacuoles also help break down macromolecules.
Animal cells also have a centrosome and lysosomes. The centrosome has two bodies, the centrioles, with an unknown role in cell division. Lysosomes are the digestive organelles of animal cells.
Plant cells have a cell wall, chloroplasts, and a central vacuole. The plant cell wall, whose primary component is cellulose, protects the cell, provides structural support, and gives shape to the cell. Photosynthesis takes place in chloroplasts. The central vacuole expands, enlarging the cell without the need to produce more cytoplasm.
The endomembrane system includes the nuclear envelope, the endoplasmic reticulum, Golgi apparatus, lysosomes, vesicles, as well as the plasma membrane. These cellular components work together to modify, package, tag, and transport membrane lipids and proteins.
The cytoskeleton has three different types of protein elements. Microfilaments provide rigidity and shape to the cell, and facilitate cellular movements. Intermediate filaments bear tension and anchor the nucleus and other organelles in place. Microtubules help the cell resist compression, serve as tracks for motor proteins that move vesicles through the cell, and pull replicated chromosomes to opposite ends of a dividing cell. They are also the structural elements of centrioles, flagella, and cilia.
Animal cells communicate through their extracellular matrices and are connected to each other by tight junctions, desmosomes, and gap junctions. Plant cells are connected and communicate with each other by plasmodesmata.
Practice Question
In the context of cell biology, what do we mean by form follows function? What are at least two examples of this concept?
[practice-area rows="4″][/practice-area]
[reveal-answer q="596885″]Show Answer[/reveal-answer]
[hidden-answer a="596885″]"Form follows function" refers to the idea that the function of a body part dictates the form of that body part. As an example, organisms like birds or fish that fly or swim quickly through the air or water have streamlined bodies that reduce drag. At the level of the cell, in tissues involved in secretory functions, such as the salivary glands, the cells have abundant Golgi.[/hidden-answer]
All cells, whether they are prokaryotic or eukaryotic, have some common features. These common features are:
DNA, the genetic material contained in one or more chromosomes and located in a nonmembrane bound nucleoid region in prokaryotes and a membrane-bound nucleus in eukaryotes
Plasma membrane, a phospholipid bilayer with proteins that separates the cell from the surrounding environment and functions as a selective barrier for the import and export of materials
Cytoplasm, the rest of the material of the cell within the plasma membrane, excluding the nucleoid region or nucleus, that consists of a fluid portion called the cytosol and the organelles and other particulates suspended in it
1. The genetic material (DNA) is localized to a region called the nucleoid which has no surrounding membrane.
2. The cell contains large numbers of ribosomes that are used for protein synthesis.
3. At the periphery of the cell is the plasma membrane. In some prokaryotes the plasma membrane folds in to form structures called mesosomes, the function of which is not clearly understood.
4. Outside the plasma membrane of most prokaryotes is a fairly rigid wall which gives the organism its shape. The walls of bacteria consist of peptidoglycans. Sometimes there is also an outer capsule. Note that the cell wall of prokaryotes differs chemically from the eukaryotic cell wall of plant cells and of protists.
Much of what you will need to know applies to the structure of eukaryotic cells. They are characterised by having membrane-bound organelles.
Cytosol and Endoplasmic Reticulum (ER)
Cytoplasm refers to the jelly-like material with organelles in it.
If the organelles were removed, the soluble part that would be left is called the cytosol. It consists mainly of water with dissolved substances such as amino acids in it.
Also present in the cytosol are larger proteins and enzymes used in reactions within the cell. Running through the cytosol is endoplasmic reticulum (ER), a system of flattened cavities lined by a thin membrane. It is the site of the synthesis of many substances in the cell and so provides a compartmentalised area in which this takes place. The cavities also function as a transporting system whereby substances can move through them from one part of the cell to another.
There are 2 types of ER - rough (RER) and smooth (SER). SER obviously looks as though it has a smooth surface. It is where lipids and steroids are made so you would expect there to be a lot of SER in liver cells where lipid is metabolised.
RER looks rough on the surface because it is studded with very small organelles called ribosomes. Ribosomes are made of RNA and protein and are the site of protein synthesis (see DNA and Genetic Code).
There may be free ribosomes in the cytoplasm as well, which also are the site of protein synthesis. The proteins (which include enzymes) that are synthesised then move into the cavities of the RER to be transported.
The Golgi apparatus is a series of flattened layers of plate-like membranes.
The proteins that are made by the RER for export from the cell are pinched off at the end of the cavity of the RER, so that a layer of membrane surrounds them. The whole structure is called a vesicle. This vesicle will move through the cytosol and fuse with the membrane of the Golgi apparatus.
In the cavity of the Golgi apparatus, the vessel proteins are modified for export - for example, by having a carbohydrate added to the protein. At the end of a Golgi cavity, the secretory product is pinched off so that the vesicle containing the substance can move through the cytosol to the cell surface membrane.
The vesicle will fuse with this membrane and so release the secretory product. If the vesicle contains digestive enzymes, it is called a lysosome. Lysosomes may be used inside the cell during endocytosis, or to break-down old, redundant organelles.
A typical cell may contain 1,000 mitochondria, though some will contain many more. Generally, they are sausage-shaped organelles whose walls consist of 2 membranes.
The inner membrane is folded inwards to form projections called cristae. Inside this is the matrix.
Most of the reactions for aerobic respiration take place in the mitochondria so it is an incredibly important organelle.
During respiration, ATP is produced, which is used to provide energy for the cells' reactions. Most of the ATP is produced on the inner mitochondrial membrane.It is highly folded so there is maximum surface area available.
Cell wall and chloroplasts
These are only found in plant cells.
Chloroplasts will be discussed in photosynthesis - but, like the mitochondria - they have an envelope of two membranes making up the outer "wall".
They have pairs of membranes called thylakoids arranged in stacks, each stack being called a granum. Connecting different grana together are inter-granal thylakoids. Surrounding the internal membranes, inside the envelope is the stroma.
The reactions of photosynthesis take place in the membranes and stroma of the chloroplast.
The cell wall is rigid and made of cellulose fibres running through a mixture of other polysaccharides (more complex sugars) such as pectins and hemicelluloses.
The sticky middle lamella that holds next-door cells together is made of calcium pectate and magnesium pectate.
In young cells, the cellulose fibrils of the primary cell wall run parallel to each other. In older cells, a secondary cell wall may be laid down where the fibres are all parallel to each other, but at a different angle to those of the primary cell wall.
The cell wall is fully permeable unless a substance called lignin is deposited in the cellulose layers. Lignin makes the cell wall very strong and resistant to strain but it also makes it impermeable. If all the gaps between the fibres are filled in, the wall becomes completely impermeable and the cell will die.
The nucleus is separated from the surrounding cytoplasm by the double membrane around it, the nuclear envelope. This regulates the flow of substances into and out of the nucleus.
At some points around the nucleus, the 2 membranes fuse to create nuclear pores - these are channels through which substances can move. The outer of the 2 membranes is continuous with the ER.
Within the nuclear envelope is the nucleoplasm. In this are suspended thread-like chromosomes (for chromosome structure see DNA and Genetic Code).
Another structure within the nucleus is the nucleolus. The RNA, which will be made into ribosomes, is synthesised in the nucleolus.
Other organelles
Vacuole: a fluid-filled space in the cytoplasm surrounded by a membrane called the tonoplast. It contains a solution of sugars and salts called the cell sap.
Microtubules: hollow rod-like structures with walls of tubulin protein. They provide the structural support of cells and can aid transport through the cell.
Microfilaments: rod-like structures made of contractile protein. Again, like microtubules, provide support and aid movement.
Centrioles: a pair of short hollow cylinders, usually found near the nucleus of an animal cell. They are involved in the formation of spindle fibres used in mitosis (see Reproduction and Cell Cycle Learn-it).
Cilia: hollow tubes extending outside some cells. They move fluid, which is outside the cell - for example, ciliated cells lining the respiratory tract move mucus, away from the lungs.
Flagella: similar to cilia, though longer. Used in the movement of the whole cell. The only structure like this in humans is the tails of the sperm.
Investigating the function of cell organelles
To obtain reliable information about the activity of an organelle, it is necessary to isolate it and test it individually.
First the cells are broken open or cell fractionation occurs to produce a homogenate or suspension. This is done using a blender with the cells in an isotonic, cold solution. Because the solution is isotonic, the organelles neither gain, or loose water by osmosis and as it is cold, the action of enzymes, which might damage the organelles, is prevented.
Differential centrifugation of the suspension is then carried out. A tube containing the suspension is spun in a centrifuge at a speed, which causes the heaviest organelles to be thrown to the bottom, forming a sediment. The other lighter organelles remain floating in the clear supernatant fluid above the sediment.
The sediment may be removed and the activity of the heaviest organelles such as the nucleus, determined. The supernatant may then be spun at a faster speed so that lighter organelles like the mitochondria sediment out.
Sperm Are Highly Adapted for Delivering Their DNA to an Egg
Typical sperm are "stripped-down" cells, equipped with a strong flagellum to propel them through an aqueous medium but unencumbered by cytoplasmic organelles such as ribosomes, endoplasmic reticulum, or Golgi apparatus, which are unnecessary for the task of delivering the DNA to the egg. Sperm, however, contain many mitochondria strategically placed where they can most efficiently power the flagellum. Sperm usually consist of two morphologically and functionally distinct regions enclosed by a single plasma membrane: the tail, which propels the sperm to the egg and helps it to burrow through the egg coat, and the head, which contains a condensed haploid nucleus (Figure 20-25). The DNA in the nucleus is extremely tightly packed, so that its volume is minimized for transport, and transcription is shut down. The chromosomes of many sperm have dispensed with the histones of somatic cells and are packed instead with simple, highly positively charged proteins called protamines.
Figure 20-25
A human sperm. It is shown in longitudinal section.
In the head of most animal sperm, closely apposed to the anterior end of the nuclear envelope, is a specialized secretory vesicle called the acrosomal vesicle (see Figure 20-25). This vesicle contains hydrolytic enzymes that may help the sperm to penetrate the egg's outer coat. When a sperm contacts an egg, the contents of the vesicle are released by exocytosis in the so-called acrosome reaction in some sperm, this reaction also exposes or releases specific proteins that help bind the sperm tightly to the egg coat.
The motile tail of a sperm is a long flagellum, whose central axoneme emanates from a basal body situated just posterior to the nucleus. As described in Chapter 16, the axoneme consists of two central singlet microtubules surrounded by nine evenly spaced microtubule doublets. The flagellum of some sperm (including those of mammals) differs from other flagella in that the usual 9 + 2 pattern of the axoneme is further surrounded by nine outer dense fibers (Figure 20-26). These dense fibers are stiff and noncontractile, and it is not known what role they have in the active bending of the flagellum, which is caused by the sliding of adjacent microtubule doublets past one another. Flagellar movement is driven by dynein motor proteins, which use the energy of ATP hydrolysis to slide the microtubules, as discussed in Chapter 16. The ATP is generated by highly specialized mitochondria in the anterior part of the sperm tail (called the midpiece), where the ATP is needed (see Figures 20-25 and 20-26).
Drawing of the midpiece of a mammalian sperm as seen in cross section in an electron microscope. The core of the flagellum is composed of an axoneme surrounded by nine dense fibers. The axoneme consists of two singlet microtubules surrounded by nine microtubule (more. )
What Are the Parts of the Cell?
Have you ever wondered what the inside of a cell looks like? If you think about the rooms in our homes, the inside of any animal or plant cell has many similar room-like structures called organelles. Each organelle is a place where specific jobs are done.
Plant and animal cells have many of the same organelles. But in some cases, the organelles in cells are different. For example, in plant cells, there are more types of organelles than are found in animal cells. And fungal cells have organelles not found in any other cell type. Below are some names and descriptions of organelles commonly found in certain cells. There is also an interactive cell viewer and game that can be used to learn about the parts of animal, plant, fungal, and bacterial cells. Archaea cells are very similar to bacterial cells, so have not been included separately.
Plasma membrane - The membrane enclosing a cell is made up of two lipid layers called a "bilipid" membrane. The lipids that are present in the plasma membrane are called "phospholipids."
These lipid layers are made up of a number of fatty acid building blocks. The fatty acid that makes up this membrane has two different parts to it- a small water loving head- hydrophilic head. Hydro stands for water and philic means liking or loving. The other part of this fatty acid is a long water-repelling or water hating tail.
This tail is hydrophobic- Hydro stands for water and phobic means fear. The plasma membrane is arranged in such a way so that the tails face each other on the inside and the heads face towards the outside of the membrane.
Channels/pores- A channel in the cell's plasma membrane. This channel is made up of certain proteins that control the movement of molecules, including food and water, into the cell.
Cell wall and plasmodesmata - In addition to cell membranes, plants have cell walls. Cell walls provide protection and support for plants. In land plants, the cell wall is mostly made of cellulose.
Unlike cell membranes, materials cannot get through cell walls. This would be a problem for plant cells if not for special openings called plasmodesmata.
These openings are used to communicate and transport materials between plant cells because the cell membranes are able to touch and therefore exchange needed materials.
Cell wall septum and pores - Fungal cells have both cell membranes and cell walls, like plant cells. Cell walls provide protection and support. Fungal cell walls are largely made of chitin, which is the same substance in insect exoskeletons.
Because materials cannot get through cell walls, fungal cells have special openings called pores. Materials can be moved between fungal cells through the pores.
Some fungal cells also have a septum (plural is septa) that are special internal walls between cells that are found in long tube-shaped strings or strands called hyphae.
Yeast strain construction
Standard methods were used throughout. All strains used in this study were congenic w303 (MATa his3-11,15 trp1-1 leu2-3 ura3-1 ade2-1). All anchor genes were cloned from the genome directly and tagged with PhyB (aa 1–908) and mCherry at the N-terminus with a 15-aa linker (EFDSAGSAGSAGGSS) between the PhyB and mCherry and a 10-aa linker (SAGSAGKASG) between mCherry and anchor gene. Endogenous GAL80 and CLB2 were tagged with mCitrine and PIF at the C-terminus with an 11-aa linker (AAAGDGAGLIN) between GAL80/CLB2 and mCitrine. CLB1 was deleted by using the KanMX2 fragment. Endogenous SPC42 was tagged with GFP at the C-terminus with an 11-aa linker (AAAGDGAGLIN). All strains were characterized by sequencing PCR products.
Time-lapse microscopy
Cells growing exponentially in synthetic liquid medium were seeded onto thin 1.5–2% agarose slabs of the same medium. For titration and spatial control experiments, cells were seeded onto concanavalin A–coated well plates with 0.17-µm coverglass bottoms. Multiple different positions were followed simultaneously. For most experiments, stacks of nine images were acquired every 3 min at 30°C, with 30-ms exposure for green channel and 50 ms for red channel. For reversibility experiments, only one image was acquired for each time point. For light control experiments, PCB was added to cells 2 h before imaging with a final concentration of 27 μM (stock, 5.4 mM in dimethyl sulfoxide). PCB was purified according to Toettcher et al. (2011b) or purchased from ChemPep (Wellington, FL). Because room light activates the system, cells were kept in the dark once PCB was added.
For most experiments, fluorescence and phase microscopies were performed in the University of California, San Francisco (UCSF), Nikon Imaging Center using a TE2000U inverted microscope (Nikon, Melville, NY) with Yokogawa CSU22 spinning-disk confocal illumination (Solamere Technology Group, Salt Lake City, UT) and a Cascade II CCD Camera (Photometrics, Tucson, AX). Images were acquired using Micromanager software (http://micromanager.org/) and analyzed using ImageJ (National Institutes of Health, Bethesda, MD) with the SpotTracker2D plug-in (http://bigwww.epfl.ch/sage/soft/spottracker/gasser.html). Potential toxicity of PCB and fluorescence illumination was evaluated in control experiments (Supplemental Figure S1).
Titration and spatial control experiments were performed on a Nikon Eclipse Ti inverted microscope using a 100× PlanApo total internal reflection fluorescence, 1.49 numerical aperture objective, a xenon arc-lamp (Sutter Instrument, Novato, CA), and an Evolve electron-multiplying charge-coupled device camera (Photometrics). For these experiments, the microscope, dichroic positions, filters, shutters, and camera were controlled using the open-source Micromanager software package with additional custom Matlab code (Toettcher et al., 2011a). Epifluorescence images were computationally denoised in collaboration with John Sedat (UCSF), using an algorithm built into the Priism image analysis package (Kervrann and Boulanger, 2006).
For fully activating and inactivating light control experiments, we used one 650- and one 750-nm light-emitting diode (LED Lightspeed Technologies, Campbell, CA), which are directly attached on the microscope condenser. For the titration and spatial control experiments, we used one 650-nm LED and two 750-nm LEDs (Lightspeed Technologies). Light intensity was controlled by changing the applied voltage (0–5 V). Voltage was controlled using custom Matlab code by connecting the LEDs to the analogue outputs of a DT9812 board (Data Translation, Marlboro, MA). For spatial control, user-defined patterns of LED light were projected on the sample using a custom dual-input digital micromirror device (DMD Andor, Belfast, United Kingdom). Pixels on this device can be in two states, ON or OFF ON pixels are illuminated with both 650- and 750-nm light, and OFF pixels are illuminated by the second 750-nm light source with a constant voltage. Sample exposure to DMD light was controlled using a 620-nm short-pass filter (Chroma Technology, Brattleboro, VT). In addition, we used a 625-nm sputtered short-pass emission filter (Chroma) to block DMD light from reaching the camera during imaging, allowing us to keep the 620-nm short-pass filter in place (and thus continue exposing the sample to 650- and 750-nm light) while images were collected.
Image analyses
Image segmentation and fluorescence quantification were performed using custom Matlab software and ImageJ with Image5D plug-in. Maximum-intensity projections of z-stacks were reported for most experiments, except for plasma membrane images. For the plasma membrane, the middle plane was used.
For assaying the concentration increase/decrease measurements as the system is turned ON and OFF (Figure 5, C and D), PhyB library strains were mixed wild-type cells that do not contain fluorescence labeling. Nonfluorescent cells were used to subtract cell autofluorescence, and the anchor images were used to define the desired position. Average fluorescence intensity per pixel was used to calculate the decrease/increase. Typically, 50–100 cells were used for each anchor strain.
The health of a cell requires proper functioning, regulation, and quality control of its organelles, the membrane-enclosed compartments inside the cell that carry out its essential biochemical tasks. Aging commonly perturbs organelle homeostasis, causing problems to cellular health that can spur the initiation and progression of degenerative diseases and related pathologies. Here, we discuss emerging evidence indicating that age-related defects in organelle homeostasis stem in part from dysfunction of the autophagy-lysosome system, a pivotal player in cellular quality control and damage clearance. We also highlight natural examples from biology where enhanced activity of the autophagy-lysosome system might be harnessed to erase age-related organelle damage, raising potential implications for cellular rejuvenation.
In eukaryotic cells, molecular waste and damaged materials can be delivered to lysosomes for enzymatic degradation via autophagy [1]. During this process, autophagic vesicles, termed autophagosomes, form around select cargo, then subsequently fuse with the lysosome to allow for targeted degradation. Though autophagosomes were first observed by electron microscopy in the mid-1950s [2], it was not until nearly 40 years later that the first autophagy genes were identified in yeast [3–5]. Since then, breakthroughs in live-cell imaging have enabled sophisticated, real-time imaging of the autophagic process in several eukaryotic species, including animals [6,7]. In addition, an expanding pharmacological toolkit of molecules that modify autophagic activity in vivo (Table 1) has facilitated manipulation of this system in live organisms and raised exciting therapeutic prospects.
A defining feature of the autophagy-lysosome system is its unique ability to recalibrate cellular homeostasis in response to a cell's needs. If a cell is under intrinsic or extrinsic stress, activation of autophagy can help to erase molecular damage and to recycle material needed to support basic biological functions [1]. When these mechanisms fail, the stress can amplify, leading to an irreparable collapse in cellular homeostasis. Notably, aging is accompanied by several molecular signs of stress. As cells get older, genetic instability increases, proteins cluster into non-functional aggregates, and organelles, the cellular mini-factories that execute distinct signaling and metabolic functions, become damaged and inefficient [8]. Is this age-related collapse in cellular health and homeostasis linked to defects in autophagy?
Remarkably, researchers have found that an early-age decrease in lysosome and autophagic activity may be an initiating "domino" in age-related cellular deterioration [9,10]. Consistent with this model, modifying autophagic activity has profound effects on the aging process experimental inhibition of lysosomal and/or autophagic factors accelerates aging in various organisms [11–14], whereas interventions that boost autophagic activity delay the appearance of cellular signs of aging and extend lifespan [15–17]. Even human centenarians [18], like long-lived mutant animals [19], have been reported to display exceptionally high levels of autophagic activity. These and other findings highlight the autophagy-lysosome system as an emerging nexus in the control of aging and longevity (Figure 1). Still, molecular details of this regulation remain obscure.
Figure 1. Changes to autophagy of cellular organelles during the aging process. Lysosomes in young, healthy cells (on the left) are acidic and effectively degrade cellular waste, including organelles when necessary. This maintains robust homeostasis, which supports proper functioning not only of a cell but of a whole organism. However, in an old cell (on the right), lysosome dysfunction jeopardizes autophagic turnover, causing a build-up of damaged organelles along with protein aggregates this leads to several age-related disease pathologies and brings about changes to organismal physiology. Re-establishing the correct dynamics of organelle turnover at lysosomes in old cells might provide one entry point to trigger a rejuvenation of cellular health and homeostasis. AP, autophagosome.
For one, how is different autophagic cargo handled in aging cells, and do changes to cargo turnover directly contribute to the aging process? Many studies have investigated how defective autophagy impedes protein-aggregate clearance in old cells [20]. This is an important line of research, given that impaired protein homeostasis ('proteostasis') is characteristic of many age-related diseases, including Alzheimer's [21]. Yet, defective organelles are also common to age-related diseases [22–24], and their turnover is likewise sensitive to lysosome dysfunction [1,25]. To date, surprisingly little is known about the dynamics and control of organelle turnover in aging cells. Clarifying the regulation of organelle-specific autophagy during aging could provide novel clues on the biological basis of age-related disease, and might also hint at therapies for fighting the aging process.
Perhaps the most information is currently known regarding the age-related regulation of mitochondria, the energetic hubs of a cell. With age, mitochondrial function and homeostasis break down. Several proteins involved in oxidative phosphorylation and fatty-acid metabolism, two key cellular processes that occur at mitochondria, have been reported to decrease in abundance in old animals [26–28]. These molecular alterations, combined with other age-induced changes to mitochondrial protein levels and stoichiometry [29], are thought to impair mitochondrial activity and destabilize cellular bioenergetics and metabolism. As a consequence of this dysfunction, fragmented, oxidatively-damaged mitochondria are commonly seen in old cells of diverse eukaryotic species, ranging from yeasts to mammals [8,9,30–32]. Though healthy cells can effectively eliminate dysfunctional mitochondrial fragments by mitochondrial autophagy, or 'mitophagy' [33], mitochondrial-clearance mechanisms show signs of failure in old age [34,35]. This disrupts the balance between mitochondrial biogenesis and degradation, causing an age-dependent increase in damaged mitochondria that further exacerbates cell stress [34]. Mitophagy defects can predispose humans to degenerative disease indeed, dysfunction of mitophagy factors, including Parkin and PINK1, is commonly seen in Parkinson's disease patients [36,37]. Thus, impaired turnover of damaged organelles is at least partly to blame for some of the classic aging pathologies commonly seen in the clinic.
Importantly, impaired turnover with age does not appear to be limited to mitochondria. In cells, lysosomes are responsible for degrading additional types of organelles, including portions of the endoplasmic reticulum (ER), peroxisomes, and even other lysosomes. Like mitochondrial damage, ER stress accumulates in old cells [38]. Strikingly, genetic inhibition of ER-phagy causes progeric phenotypes and shortened lifespan in mice [39], hinting that ER turnover might be required to slow the pace of aging. Additionally, peroxisomes and lysosomes have been reported to increase in abundance in late age in some species and cell types [40,41]. In fact, uncleared lysosomes generate a non-degradable, autofluorescent 'age pigment', which has been used as a visual readout for biological age in multiple systems [42–44]. It will be important to clarify how directly these age-related changes in organelle number reflect impairment of the autophagy-lysosome system, and whether these changes bring about physiological effects on metabolic functioning in old animals.
While the general trend is that organelle turnover appears to decline with advanced age due to autophagy-lysosome dysfunction (Figure 1), this may not be true of all organelles, or for all stages of the aging process. For example, pieces of the nucleus are degraded at lysosomes in aging worms, even in the healthiest of individuals [45]. How nuclear autophagy ('nucleophagy') regulates organismal physiology, particularly during aging, is unclear, but it may be protective, as suggested in mouse models of laminopathies [46]. It remains to be seen whether other organelles likewise undergo regulated, active turnover in aging animals. Some organelles may even be degraded in early aging but start to accumulate later once lysosomes become dysfunctional. Understanding the dynamics and timing of organelle turnover at different stages of aging could reveal complexities that affect aging rate and/or stochasticity among different individuals in a population.
If organelle damage is generally characteristic of very old age, could harnessing organelle-specific autophagy help an old cell to regain its vitality and youthfulness? Germ (reproductive) cells provide a unique opportunity to study cellular rejuvenation, because age is naturally reset across generations. We and others have shown that cellular damage, including defective mitochondria, can be rapidly reversed as oocytes prepare for fertilization [47,48]. Removal of dysfunctional molecules and organelles is also seen during gametogenesis in single-celled yeast [49]. These findings imply that damage-clearance mechanisms may function centrally to the biological mechanisms of transgenerational rejuvenation. In support of this interpretation, lysosomes are activated in maturing oocytes prior to fertilization [47], and, once active, they could conceivably clear various forms of cellular damage, including dysfunctional organelles, to reset cellular health and homeostasis across generations. Though the specific cargo received by oocyte lysosomes awaits full description, identification of natural mechanisms that renew organelle health in the immortal germ-cell lineage could point the way to new strategies to counteract organelle damage in old somatic cells.
Lysosome induction has been reported to also occur during stem-cell activation and differentiation [50–52]. In these contexts, as in oocyte maturation, lysosome activation is linked to a developmental rewiring of cellular metabolism. Though, again, much attention has been paid to the role of lysosome activity in stem-cell proteostasis, there is recent evidence that organelle-specific autophagy plays a fundamental role in stem-cell and regenerative biology [53–57]. For one, impaired mitophagy leads to muscle stem-cell quiescence in old mice, and re-establishing autophagic flux is sufficient for old muscle stem cells to exit quiescence and regain stemness [58]. Importantly, defective mitophagy appears to cause oxidative stress and stem-cell depletion in other cell types as well [59,60]. These findings hint that mitochondrial turnover might be a pivotal determinant of regenerative capacity.
Notably, mitophagy also appears important in the generation of induced pluripotent stem cells (iPSCs) [57,61]. A number of rejuvenating events, including telomere re-lengthening and organelle renewal, have been associated with iPSC generation from differentiated cells [62–64]. Inhibiting mitochondrial fission, one of the early steps in mitophagy induction [33,65], prevents the conversion of fibroblasts to iPSCs [61]. Thus, it is exciting to speculate that organelle-specific autophagy may be integrated with other rejuvenating events involved in iPSC reprogramming, and that enhancing these activities might provide an entry point to improve the efficiency of this process.
Beyond mitophagy, other forms of organelle-specific autophagy are only beginning to be studied in the context of cellular regeneration and rejuvenation. Interestingly, elevated ER stress has been linked to iPSC death [66], and significant ER remodeling occurs as part of iPSC reprogramming [67]. In principle, ER quality control mechanisms, including ER-phagy, could aid regenerative capacity, particularly in old animals where persistent ER stress abounds [38]. As a compelling corollary, the ER has been shown to undergo dramatic rearrangements coincident with oocyte maturation and lysosome activation in the C. elegans germline [68]. How the ER and lysosomes are functionally and/or mechanically linked to support cellular rejuvenation is an important open question moving forward, as is the involvement of other organelle-turnover events in cellular-rejuvenation mechanisms.
In summary, dynamic changes to the landscape of the cell occur during aging, and several of these age-related changes can be traced to alterations in organelle homeostasis and turnover (Figure 1). Harnessing the natural rejuvenating capacities of the autophagy-lysosome system provides one possible means to reverse age-related organelle damage and re-establish a more youthful cellular environment (Figure 1). In fact, pharmacological tools that boost lysosome function (Table 1) are currently being tested as potential anti-aging therapies in old animals and humans [69,70]. Looking forward, it seems likely that growing knowledge on the mechanistic principles that govern organelle turnover at lysosomes, and the specific parts of these systems that fail with old age, will open new doors for aging-biology researchers in the quest to promote healthy aging, particularly at a cellular level.
Structure of Cell Nucleus
Would you like to write for us? Well, we're looking for good writers who want to spread the word. Get in touch with us and we'll talk.
The cell nucleus consists of a nuclear membrane (nuclear envelope), nucleoplasm, nucleolus and chromosomes. Nucleoplasm, also known as karyoplasm, is the matrix present inside the nucleus. Let's discuss in brief about the several parts of a cell nucleus.
Nuclear Membrane
The nuclear membrane is a double-layered structure that encloses the contents of the nucleus. The outer layer of the membrane is connected to the endoplasmic reticulum. A fluid-filled space or perinuclear space is present between the two layers of a nuclear membrane.
The nucleus communicates with the remaining of the cell or the cytoplasm through several openings called nuclear pores. Such nuclear pores are the sites for exchange of large molecules (proteins and RNA) between the nucleus and cytoplasm.
Chromosomes are present in the form of strings of DNA and histones (protein molecules) called chromatin. The chromatin is further classified into heterochromatin and euchromatin based on the functions. The former type is a highly condensed, transcriptionally inactive form, mostly present adjacent to the nuclear membrane. On the other hand, euchromatin is a delicate, less condensed organization of chromatin, which is found abundantly in a transcribing cell.
Nucleolus
The nucleolus (plural nucleoli) is a dense, spherical-shaped structure present inside the nucleus. Some of the eukaryotic organisms have nucleus that contains up to four nucleoli. The nucleolus plays an indirect role in protein synthesis by producing ribosomes. These ribosomes are cell organelles made up of RNA and proteins they are transported to the cytoplasm, which are then attached to the endoplasmic reticulum.
Ribosomes are the protein-producing organelles of a cell. Nucleolus disappears when a cell undergoes division and is reformed after the completion of cell division.
What Are the Three Organelles Involved in Protein Synthesis?
There are four organelles that are involved in protein synthesis. These include the nucleus, ribosomes, the rough endoplasmic reticulum and the Golgi apparatus, or the Golgi complex. All four work together to synthesize, package and process proteins.
Protein synthesis begins with DNA. The DNA in an organism creates the RNA that then codes for and synthesizes the proteins. DNA is found in the cell's nucleus and makes the RNA in the nucleus as well. The RNA then exits the nucleus and is translated by the cell's organelles into amino acids. These small subunits are then put together in the ribosomes that are attached to the membrane of the rough endoplasmic reticulum. Then, the proteins exit the ribosomes and exit the rough endoplasmic reticulum to enter the Golgi apparatus. The Golgi apparatus packages the proteins and sends them out of the cell.
Cell Fractionation [back to top]
This means separating different parts and organelles of a cell, so that they can be studied in detail. All the processes of cell metabolism (such as respiration or photosynthesis) have been studied in this way. The most common method of fractionating cells is to use differential centrifugation:
1. Cut tissue (e.g. liver, heart, leaf, etc) in ice-cold isotonic buffer. Cold to stop enzyme reactions, isotonic to stop osmosis, and buffer to stop pH changes.
2. Grind tissue in a blender to break open cells.
3. Filter. This removes insoluble tissue (e.g. fat, connective tissue, plant cell walls, etc). This filtrate is not called a cell-free extract, and is capable of carrying out most of the normal cell reactions.
4. Centrifuge filtrate at low speed
5. Centrifuge supernatant at medium speed
6. Centrifuge supernatant at high speed
7. Centrifuge supernatant at very high speed
8. Supernatant is now organelle-free cytoplasm
A more sophisticated separation can be performed by density gradient centrifugation. In this, the cell-free extract is centrifuged in a dense solution (such as sucrose or caesium chloride). The fractions don't pellet, but instead separate out into layers with the densest fractions near the bottom of the tube. The desired layer can then be pipetted off. This is the technique used in the Meselson-Stahl experiment (module 2) and it is also used to separate the two types of ribosomes. The terms 70S and 80S refer to their positions in a density gradient
Watch the video: 11. Η Αντιγραφή του DNA. Δράση DNA πολυμεράσης 1 2ο κεφ. - Βιολογία Γ λυκείου. (January 2022).
Why mammals don't have renal portal system
Adam's Apple and Voice box
Where does this equation in the electrophysiology literature form come from?
Botany Course
Are there nuclei with "real" interneurons?
Could Cyanobacteria farms help dilute pollutants in the atmosphere
23.1: Case Study: How Our Bodies Change Throughout Life - Biology
Why is the food we consume right from birth not immunogenic to elicit an immune response?
Incestual Reproduction in Animals
Copyright 2022 \ 5.4: Summary- Organelles - Biology...


text:
A United Village Against Anti-terror law
Posted bytonylavina August 19, 2020 November 5, 2020 Leave a comment on A United Village Against Anti-terror law
We often hear and say the African proverb: "It takes a village to raise a child." One can understand it merely from the point of view of the 'child'. But a step back and a turn towards the 'village' could lead us to a fuller understanding of the proverb, which means that the 'child' symbolizes the very future of the village; and that it requires the village's collective effort – a united village – to chart that future.
This is why many have united against The Anti-Terrorism Act of 2020 (also known as Anti-Terror Law or ATL) or Republic Act No. 11479.
The ATL is particularly dangerous for those of us who live and work in Mindanao where development aggression has persisted since our colonial history and where resistance to outside domination and oppression by political and economic elites are automatically labelled as terrorists. That is why many of us have filed petitions against this law in the Supreme Court.
United front against ATL
Despite the pandemic, we saw petition after petition filed before the Supreme Court to an extent that has never been seen in the country's history. At the time of writing, there are 27 petitions (25 consolidated and 2 still to be consolidated) filed challenging the law's constitutionality. I know of a few more petitions that will be filed in the next few days.
To give context, two of the highly contested laws in the last ten years, R.A. No. 10175 or the Cybercrime Prevention Act of 2012 and R.A. No. 10354 or the Responsible Parenthood and Reproductive Health Act of 2012 faced 15 and 14 petitions, respectively.
Interestingly, the petitioners come from diverse sectors of society transcending barriers of profession, generation, and ethnicity.
Either acting as petitioners themselves or as legal counsels, luminaries of the legal profession lead the pack: Senior Associate Justice Antonio Carpio and former Associate Justice and Ombudsman Conchita Carpio-Morales; former Senator Rene Saguisag, former Vice President Jojo Binay, and former UP Law Dean Pacifico Agabin representing the Concerned Lawyers for Civil Liberties (CLCL) of which I too am a member. Framers of the 1987 Constitution, Christian Monsod, Felicitas Arroyo, Florangel Braid, and Ed Garcia, are also challenging the law. Various law groups are have also stepped up, such as Alternative Law Groups, Center for International Law (CenterLaw), Ateneo Human Rights Center, National Union of Peoples' Lawyers (NUPL), professors from FEU Law (with Dean Mel Sta. Maria), UP Law, Ateneo Law, Lyceum Law (with Dean Soledad Mawis) and Xavier Law; and private practitioners led by Atty. Howard Calleja.
Former and incumbent lawmakers Sen. Francis Pangilinan, Sen. Leila de Lima, Sen. Serge Osmeña, Albay Rep. Edcel Lagman, Quezon City Rep. Kit Belmonte, Quezon Rep. Erin Tañada, Basilan Rep. Mujiv Hataman, and Makabayan Bloc Reps. Zarate, Gaite, Cullamat, Brosas, Castro, and Elago also join.
Labor groups SENTRO, Federation of Free Workers, Center for Trade Union and Human Rights; progressive groups Sanlakas, Bagong Alyansang Makabayan, Gabriela, Bayan Muna, ACT Teachers, and Anakpawis have always been at the forefront of government excesses.
Journalists Maria Ressa, Chay Hofileña, John Nery, National Union of Journalists of the Philippines (NUJP), VERA Files, and Foundation for Media Alternatives will be one of the most affected by the chilling effect that the law is set to spread.
Prominent members of civil society such as Brother Armin Luistro, FSC, former CHR Chair Etta Rosales, journalist Ces Drilon, and former UP Dean Luis Teodoro; religious groups led by Apostolic Administrator of the Archdiocese of Manila Broderick Pabillo also organized their sectors.
It is a refreshing sight to see youth groups from University of the Philippines, Ateneo de Manila University, De La Salle University, and University of Santo Tomas; Cebu student leaders; and concerned online netizens, who may be gravely affected if the Anti-Terror Law crosses to new media, as petitioners as well.
Three petitions have so far been filed filed by Mindanao based groups. These include the Anak Mindanao (Amin) party-list and a group of Moro politicians and lawmakers, human rights lawyers, journalists, and Lumad leaders and advocates have petitioned the high court for a temporary restraining order. These include, among others, personalities like Hataman, former Vice Governor of the Autonomous Region in Muslim Mindanao Haroun Alrashid Alonto Lucman, journalist Leonardo Vicente Corrales of Cagayan de Oro City, and Dean Manuel Quibod of Ateneo de Davao University College of Law.
Leaders of indigenous peoples groups (Igorot, Aeta, Lumad, etc.) and Moros such as KATRIBU, SANDUGO, AkoBakwit, Moro-Christian Peoples Alliance, Save Our Schools Network, Sabokahan, Moro Consensus Group, Bai Indigenous Women's Network in the Philippines, ALCADEV, LILAK also seek protection. They are represented by myself and other colleagues. I am proud to say that most of the petitioners in this case, which was filed two days ahead of the World Indigenous Peoples' Day, are women.
IP and Moro as the most vulnerable
Of all the petitioners and all the soon-to-be suspected terrorists under the Anti-Terror Law, I argue that it is our indigenous peoples and Moros who are most vulnerable. Not to in any way discredit the possible dangers to other petitioners such as lawyers, politicians, activists, and journalists, but it is a reality that when the eyes of the Anti-Terror Law see our indigenous and Moro peoples, they are the most defenseless and live at greatest risk.
The historical position of disadvantage, most evident in the Supreme Court cases Cariño v. Insular Government (Joanna Cariño, co-petitioner in the present case, is the great granddaughter of Mateo Cariño), Rubi v. Provincial Board of Mindoro, and Cruz v. DENR, among others, along with the government's neglect to respect and recognize indigenous peoples' rights through red-baiting or red-tagging, an act of labelling persons as terrorists, would amount to a violation of the right to self-determination.
The essence of the right to self-determination is for indigenous peoples to freely assert their identity, culture, heritage, and ancestral domain without fear of reprisal. The anti-terror law violates that right.
Villagers, stand up
The anti-terror law petition we filed on behalf of indigenous and Moro peoples from the Cordillera to Mindanao – took a lot of work. I have already mentioned the petitioners; I would also recognize the lawyers I collaborated with in that case.
I start with Atty Mai Taqueban, Executive Director of the Legal Rights and Natural Resources Center (LRC). Mai is my fellow Mindanawon from Cagayan de Oro and fellow alumna from Xavier University (her law degree is from XU where I also teach) and Ateneo de Manila (we are both philosophy majors!). Helping Mai in LRC and responsible for putting together the first draft of the petition is Atty Ryan Roset. An Ateneo de Manila law graduate, Ryan had worked in the Supreme Court and is familiar with the in and outs of filing petitions of this nature. Thanks also to LRC colleagues Maya Quirino, Jean Marie Ferraris and Noemi Librella for their indispensable help.
I also acknowledge Atty Joy Reyes, a recent graduate from UP Law, for her indispensable role. She actually helped in two of the anti-terror petitions as she also helped with that filed by the Concerned Lawyers for Civil Liberties. Jayvy Gamboa, a UP Law student, assisted in the research while Denise Galias helped us with the visual aspects of this advocacy.
We also had volunteer lawyers and under bar people, graduates of the colleges of law of University of the Philippines, Ateneo de Manila, San Beda, De La Salle University, and San Sebastian, helping us with the petition. Thank you Francis "Kiko" del Valle, Carmela Chua, Jesse Santos, Jonnah Morado, Elainne Encila, Ivan Valcos, Dan Ramos, Kylie Dado, and others who preferred to remain anonymous.
Finally, most of our petitioners are outside Manila and so aside from lawyers in Quezon City and Makati, colleagues from Baguio City, Cagayan de Oro City, Cotabato City, Koronodal City, Malaybalay City, Marawi City, Iba (Zambales), Tandag City (Surigao del Sur), and Davao City also assisted in the verifications and certifications necessary for this type of petition.
In my constitutional and political law, environmental law, public international law, and legal philosophy classes, where my students do moot court exercises, I teach them to always work as teams. I tell them that it takes a village to get big things accomplished. For sure, we practiced that here.
United for the children of our village
What we see here is a broad coalition across sectors of society – a united front – against a law that may authorize possible government abuses. This only shows the far-reaching fears that the law instills to the Filipino citizens of whatever stature.
The united front against the Anti-Terror Law of course goes beyond the village's action to protect the Filipino citizens, journalists, legitimate dissenters and critics, and indigenous peoples of today. It is best understood as a way to protect the village's children; to protect their future. For we cannot bear to see that future with the Anti-Terror Law in effect; not today and not tomorrow.
Posted bytonylavina August 19, 2020 November 5, 2020 Posted inLegal Issues, OpinionTags: MindaNews, The Riverman's Vista
Marathon Run in the Mud
The Rains of August


text:
Q: resource IDs in VC++ I define resource IDs as below:

    #define _RESOURCE_ID             150
    #define IDR_OPBUTTON            _RESOURCE_ID + 10

When I use below code to change the text of button, it doesn't work:

    SetDlgItemText(hWnd, IDR_OPBUTTON, _T("-"));

But if I give it a number directly, it does work:

    #define IDR_OPBUTTON            160

Can anybody tell me why? Thanks in advance!
Also, I tried function GetDlgItemInt for a textbox, it has the same behavior.

A: Did you try to put parenthesis?
#define IDR_OPBUTTON (_RESOURCE_ID + 10)

redpajama_set_name: RedPajamaStackExchange


E saiu a tão esperada versão 0.84 do GLPI. Mas não se animem tanto assim, esta é apenas a versão BETA para testes.
Eis a mensagem original do grupo de e-mails do GLPI.
We enter in the beta-test period of the 0.84 version of GLPI.
On this occasion, we invite you to install and thoroughly test the betaversion of GLPI 0.84 in participating in the Game "bug hunter".
Each bug report validated by the development team gives you a chance towin a mysterious gift. Everyone has a chance!
We remind you that this version is not a stable release and should notbe used in production.
The lucky winners will be drawn at the end of the period of beta testingscheduled for february. This deadline may be postponed if necessary.
Thank you for your cooperation and good hunting!
Documentação parcial em inglês:https://forge.indepnet.net/daily-doc/ (Quem quiser ajudar com essa tradução é bem vindo.
OBSERVAÇÃO IMPORTANTE: ESSAS VERSÕES NÃO DEVEM SER USADAS EM PRODUÇÃO. APENAS TESTES POR SEREM VERSÕES BETA DO GLPI 0.84.


Trump is trying to rewrite history on preexisting conditions.
The president is tweeting blatant falsehoods yet again.
This statement bears absolutely no relation to reality. As president, Donald Trump has repeatedly tried—and so far failed—to end the rules that ensure that people with preexisting conditions have access to health insurance.
Trump spent much of the 2016 campaign talking about how once he was president, he was going to repeal the Affordable Care Act (also known as Obamacare), the law that made it illegal for insurance companies to deny coverage or charge higher rates because someone has a preexisting medical condition. But, he reassured people, that would not mean ending those protections.
Then Trump spent much of 2017 boosting congressional Republicans' efforts to repeal the ACA. While initial versions of the bill would have left many of the preexisting condition protections untouched, in order to win over the more conservative elements of their caucus, House Republicans tacked on a provision that would in fact have allowed states to opt out of a key protection—the ban against insurers charging sick people higher rates—rendering any preexisting condition measures meaningless. When that bill passed the House, the president summoned party leaders for a celebration on the White House lawn.
Even after the GOP failed to overturn Obamacare in the Senate, Trump got busy whittling away at the law from the White House. Earlier this summer, his administration gave its support to a lawsuit filed by Republican state attorneys general, which, if successful, would explicitly overturn Obamacare's preexisting condition protections. When Attorney General Jeff Sessions announced that decision in a letter in June, he started off by stating that he was acting "with the approval of the President of the United States." That case is still ongoing, and the Trump administration hasn't changed its stance.
Now in the throes of campaigning for reelection, Republicans across the country have been trying to rewrite their health care stances, and for good reason: Health care is a top concern among voters. A poll from the Kaiser Family Foundation released Thursday found that voters ranked health care as the most important factor in the election.
Looks like Trump owes McConnell a phone call.


In 1949, Gertrude Stafford Burnison, of Red Oak, Iowa, constructed a chart listing a large number of Stafford descendants. We compiled this information and it is available in downloadable PDF format from Descendants of John Stafford & Elizabeth Wainscott of North Carolina and Indiana.
To take our Stafford line further back than John Stafford of North Carolina is speculative. Family tradition states that this line descends from William Stafford (b.1606 - d. bef. 3 March, 1643/44) of Warwickshire, England. William immigrated to Virginia, in 1622, on the ship Furtherance when he was 16 years old. He was married to Anne Mason whose parents were Francis Mason and Mary Dickman of Virginia. The weak link in the Stafford genealogy is between John Stafford of North Carolina, and William Stafford, his possible grandfather. John's parents are unknown. His connection to any other Staffords is very tenuous at this point.
John and Elizabeth Stafford had 14 children. Of these, three are of special interest to us. Leodica was their ninth child. Her daughter was Mary Dorcas Irwin whose youngest son was Floyd M. Grasz of Nappanee, Indiana. Floyd was the grandfather of Eugene Field (co-author with his daughter Lucie, of this web site.) Sarah was the fourth child. She married George W. Julian and they immigrated to the gold fields of California and their descendants are in and around Dutch Flats, Rocklin and Manteca, California. The thirteenth child of the family was William (an older son was also William. He was killed by Indians in Franklin County, Indiana, in March of 1812, when he was just 15 years old.) The younger William married Priscilla Jane Ramsay.
William and Jane immigrated west over the Oregon Trail. First to Washington state and then to Lane County, Oregon. They were accompanied by friends and family; on the Stafford side as well as the Ramsay side. They arrived in Washington in 1852. By 1853 they had acquired 360 acres of the Mohawk Valley outside of present Eugene, Oregon. In March of 1853, William and Priscilla Jane's son, Henry Newell, eight years old, got erysipelas (an infection) in his ankle and died. His death led to the establishment of the Stafford Pioneer Cemetery. It is a plot of ground on what was originally Stafford Family property that is 100 by 100 feet. It is a well maintained cemetery and still in use today. In 2009 Robert R. Stafford was buried there.
The people buried in the Stafford Pioneer Cemetery are the descendants of William and Priscilla Jane Ramsey Stafford, members of other families that married into the Stafford family and friends of the family. William Stafford is not buried here but in Tacoma, Washington.
The Oregon Trail began for many at Independence, Missouri. The trail was originally only suited for foot and horse travel. By 1836 it was passable for wagons. It is estimated that more than 400,000 hearty pioneers emmigrated over the trail to the valleys of Oregon between the years of 1846 and 1869. In 1852 William and Priscilla Ramsey Stafford with their family and other relatives made the trek. William (1814-1888) was a son of John (abt 1768-) and Elizabeth Wainscott Stafford (abt 1780-) of North Carolina. One of William's sisters was Leodicia Stafford Irwin (1809-). Leodicia is the great grandmother of Miriam Grasz Field to whom this website is dedicated.
Lucie and Gene Field visited the cemetery in August of 2004 and again in April of 2012. The cemetery is being looked after by Cynthia Stafford Crawford a third great granddaughter of William and Priscilla. Our original Stafford Pioneer Cemetery web page listed tombstones by row. To see that page click here.
This cemetery begins at a point one rod east & 2½ rods south of this stone running thence forth 100 ft. north 100 ft. thence west 100 ft. & south 100 ft. thence east 100 ft. to place of beginning. DONATED BY J. M. STAFFORD TO HIS HEIRS to hold forever for said purposes.
William M. Stafford was born to John and Elizabeth "Betsy" Stafford on 14 March 1814. William was born in Franklin County, Indiana. He died 30 June 1888 in Tacoma, Pierce County, Washington. Priscilla Jane Ramsey was a daughter of Samuel (1777-1843) and Elizabeth Boyles (-1835). Priscilla was born in Pennsylvania and died 23 January 1903 in the Mohawk Valley, Lane County, Oregon.
"My grandfather Stafford came to Oregon in 1852. The train reached the Willamette Valley in May, 1853, having been delayed on the road by the Cholera. Some of the party were almost drowned on the way while crossing the Platte River. Grandfather started for Oregon with three span of oxen and one pony. On the plains they had to burn two of the wagons for fuel and to kill most of the poor bony oxen for food. They finally reached Oregon with only one wagon and one team. (The wagons were all new when they started.)"
"Grandmother was a very timid person and she, herself often laughed at some of the 'crazy' things that she did when frightened. I have often heard her tell how she kept the Indians from stealing her many children. She and the children traveled in a wagon which was also used for carrying the bedding. Grandmother had an old, useless, rusty pistol. The old thing would not shoot even had grandmother possessed sufficient courage to shoot it. The Indians would come to the side of the wagon and try secretly to reach under the cover and take a child away. Grandmother, when she heard a movement along the side would point her old rusty pistol at them and her eyes were so big and blue and she looked so serious that it would scare them. She got all of her children safely through to Oregon but later one died of Erysipelas and one by snake bite." --Lena Stafford Finley, from the Linn Genealogical Society, Linn County Oregon, 2 April 1940.
According to her third-great-granddaughter Cynthia Stafford Crawford, Priscilla held her newborn son Bethel in her arms all the way from the Midwest, with a pistol under her skirt. She was terrified that the Indians would steal her baby.
Matilda Alice "Allie" Stafford Burkhart was born in 1860 and she died in 1878. Matilda was a daughter of Albert and Rosanne. She married Alonzo P. Turner in 1858 and a man named Burkhart after Alonzo's death. Matilda is buried in Albany, Linn County, Oregon.
Priscilla's large tombstone lists all the children of her and William Stafford. Not all of them are buried in the cemetery. There are other grave markers that specifically mark the burial location of those that are.
Wilson McClure Stafford was the fifth child of William and Priscilla. He was also born in Missouri, 14 May 1848. In 1867 he married Melissa Jane Pugh of whom we no nothing more. He died in California in 1932.
The seventh child of William and Priscilla was Bethel Allen Stafford. Bethel was the baby Priscilla carried across the country in the covered wagon with her rusty gun as "protection" against the Indians. Bethel was born in Missouri, 2 December 1851 and died in Pendleton, Umatilla County, Oregon, 20 October 1933. He married Mary Jane "Jennie" Thompson, the daughter of Mercer Thompson.
Barnet Ramsay Stafford was born in Oregon, 15 August 1853 soon after the family arrived. He married Eva Gilbert in Linn County, Oregon, in 1875. He was named after one of Priscilla's brothers who also emigrated to Oregon and became a potter.
Alice May Stafford, the twin of Elizabeth Levina Stafford, was born in Oregon, 4 may 1857. She married Ben. E. Hervey in 1878. She died in 1914 and is buried in Tacoma, Pierce County, Washington.
Henry Newell Stafford was the fourth child of William and Priscilla. He was born in Missouri, 12 January 1845. He died in Oregon of erysipelas 31 March 1853.
John Bird Stafford was the fifth child of William and Priscilla. He was born in Missouri, 19 November 1849. He died 4 June 1855 in the Mohawk Valley Oregon after being bitten by a rattlesnake.
Betty May/Dau of Wm. & P. J./Stafford/Died/Sept. 6, 1858/Aged/1y. 4m. 2d.
Levina Elizabeth ""Betty" Stafford was the twin of Alice May Stafford Harvey, daughters of William and Priscilla Stafford. Elizabeth and Alice were born on 4 May 1857. Elizabeth died just over a year later 6 September 1858 in Oregon.
Fred J. Stafford was born 7 February 1882 and died 8 November 1896. He was a son of the Hon. James Madison and Sarah Ellen Hardman Stafford.
Hon. James M. Stafford (1842-1909) was a son of William and Priscilla Stafford. He was ten years old when the family migrated along the Oregon Trial from Missouri to Oregon. From 1872 to 1874 he was a Justice of the Peace for Mohawk, Lane County. He served in the Oregon Legislature House of Representatives between 1885 and 1889.
Sarah Ellen Hardman (1848-1905) was a daughter of Samuel Hardman who immigrated with her family from Indiana to Oregon in 1850. She was born in South Bend, St. Joseph County, Indiana, 21 February 1878. She married James Stafford 25 October 1866 in Linn County, Oregon. Sarah died 17 September 1848, likely in Lane County, Oregon.
Rose Ann Pell Stafford Price was born 23 February 1842 and died 25 March 1920. She was the Daughter of Calvin and Mary McCarren Pell. After Albert's death she married a man named Price.
Albert Marion Stafford, the oldest son of William and Priscilla, was born in Indiana, 5 February 1837. He married Rosanne Pell in June of 1859 in Linn County, Oregon. He died in the Mohawk Valley of Lane County, Oregon on 24 May 1900.
Clive Pell Stafford was born 26 December 1879 and died 30 March 1926. He was the son of Albert Marion and Rose Ann Pell Stafford. He married Franklyn "Frankie" Dean about 1911.
We have no other information on Mary Clark.
Marion Franklin "Frank" Stafford was born 17 July 1869 and died 11 August 1943. He was a son of the Hon. James Madison and Sarah Ellen Hardman Stafford. He married Mollie M. Baxter 21 August 1889. Marion was born and died in the Mohawk Valley of Lane County, Oregon.
Mollie M. Baxter was born 21 June 1868 in Helena, Lewis and Clark County, Montana. She died in the Mohawk Valley, Lane County, Oregon, 20 March 1834.
Clara May Stafford Haines was a daughter of the Hon. James Madison Stafford and Sarah Ellen Hardman. She was born 23 February 1874 and died 7 November 1965. She married John A Haines.
Walter Eugene Stafford was born in the Mohawk Valley of Oregon 1 November 1885. His parents were the Hon. James Madison Stafford and Sarah Ellen Hardman. He married Agnes Belle Vanduyn 22 December 1910. He died 26 February 1922.
Agnes Belle Vanduyn was born in Coburg, Lane County, Oregon in December of 1844. She died in Lane County 11 February 1935. Her parents were William Malone (1843-1923) and Mary A. Withers (1855-1909) Vanduyn.
Virginia Belle Stafford was born 10 September 1911 and died 30 May 2003. She was a daughter of Walter Eugene Stafford and Agnes Belle Vanduyn. She married Ben Simpson, son of Helena Leota Rooney.
Lloyd Edgar Stafford was a son of the Hon. James and Sarah Hardman Stafford. He was born in the Mohawk Valley, 13 August 1889. He married Margaret Rhodes 5 March 1913 in Eugene, Oregon. He died 10 May 1966 in Lane County, Oregon.
Virginia has a very interesting connection to us. Being a Stafford she is related to us on Gene's mother's side of the family.
Virginia's grandmother was Mary A. Withers (1855-1919) and her grandfather was John Evan Price Withers (1830-1912) of Nicholasville, Jessamine County, Kentucky. Continuing back on the Wither's side, Virginia's 3rd great grandparents were James Withers (1681-1746) and Elizabeth Keene (abt 1682-1769) of Stafford County, Virginia. Two of the children of James and Elizabeth Keene Withers were Elizabeth (1706-1760) and John (1714-1794).
Elizabeth married Capt. Abraham Field (bef 1699-1744) the 7th great grandfather of Gene. John is the ancestor of Virginia Stafford Simpson.
This makes Virginia Stafford Simpson Gene's 3rd cousin once removed on the Stafford Family side and his 6th cousin 3 times removed on the Field Family side.
Click here for a document showing both relationships between Lucie Field and Virginia Stafford Simpson.
"When my father [the Hon. James Stafford] was ten years old-the first year that he was in Oregon, he and his brother [Albert] Marion were sent by their father to get some pigs from a settler named Vandine living near present Coburg. To reach Coburg it was necessary to go directly over the high mountain visible from the highway east of that place. Uncle Marion was at that time about fifteen years old. By the time they got to Coburg with their slow ox team, and got the hogs loaded, it was almost night. Under the circumstances they hoped that Mr. Vandine [William Vanduyn] would ask them to stay over until morning but he did not, so the boys started back on their long wild trip very late in the day. There was no real road, only a trace through the scattered timber. It was a black night and when they had reached the top of the mountain they could go no further. They had no lantern, it was freezing cold, and bears and wolves were then very common. Uncle Marion had a coat but father had none. At the top of the mountain they unhitched their oxen and tied them to the trees. The two boys raked fallen leaves into a pile in a hollow and burrowed into them for the night. Uncle Marion gave my father his coat. Father always thought that was so wonderful of him. He never got over his gratitude to his older brother and all his life he considered Uncle Marion a wonderful man."
Esther Belle Stafford was a daughter of the Hon. James Madison and Sarah Ellen Hardman Stafford. She was born 5 February 1893 and died 6 August 1962. She married George Moznette 16 May 1917 in Benton County, Oregon.
George Franklin Moznette was a son of Roman F. (abt 1864-) and Antonie M. Moznette (abt 1865-). George was born 21 December 1889 in St. Paul, Ramsey Couty, Minnesota and died 14 October 1968 in Multnomah County, Oregon.
Harry Raymond "Ray" Stafford was a son of Marion Franklin and Mollie Baxter Stafford. He was born in Springfield, Lane County, Oregon,, 14 August 1890. He was owner and operator of a lumber company in the Mohawk Valley. He married Ida R. Sunderman, daughter of Simon and Henrietta Sunderman. Harry died 30 August 1967.
Beldon Robert Stafford was a son of Harry Raymond and Ida R. Sunderman Stafford. He was born in Oregon, 25 August 1918 and died 6 April 2008.
Lyle Raymond Stafford was a son of Harry Raymond and Ida R. Sunderman Stafford. With his father and brother Beldon he ran a lumber company. He was born 24 December 1921 and died 18 November 2003. When Lucie and Gene visited the Stafford Pioneer Cemetery in the summer of 2004 his grave monument had just been put in place that same day.
Robert R. Stafford was born 14 May 1920 and died 10 September 2009. He was a son of Lloyd Edgar and Margaret Rhodes Stafford.
Wendel Stafford Spence was a son of Dr. Harry Yandall Spence and Effie Pearl Stafford (1880-1957). He was born 5 April 1914 and died 7 January 1983.
Richard Henry Stafford was born 19 February 1924 and died 14 September 2004, He was a son of Lloyd Edgar and Margaret Rhodes Stafford.
William, Mary, John and Sarah Rader are the children of Archibald Rader and Drucilla Simmons. Drucilla's mother was Martha Stafford. Their maternal great-grandparents were John Stafford (abt 1768-) and Elizabeth "Betsy" Wainscott (abt 1780). Their grandfather, William Simmons, migrated to Oregon in 1846 but we do not know from where. Martha Stafford was a sister to William M. Stafford who was one of the early Stafford pioneers in Land County, Oregon. Martha died in 1841 and William Simmons then married Catherine Rader, sister to Archibald. It was with Catherine that William Simmons emigrated to Oregon in 1847.
Drucilla Simmons married Archibald M. Rader 24 May 1849 in Marion County, Oregon. They had six children. By 1870 Archibald had been sentenced to three years in the State Penitentiary at Salem, Oregon. We have not been able to uncover the crime Archibald committed to merit his incarceration. Drucilla divorced him in 1871. On 22 June 1871 Drucilla married Jacob Wigle. At some point she moved to Seattle, King County, Washington, where she died on 13 March 1915 and was buried in the Evergreen Washelli Memorial Park in Seattle.
John Barnard Robertson was the son of William and Mary Zumwalt Robertson. Rama C. Miller was his wife. She was born in Missouri on 18 March 1882, and was married to John Bernard Robertson at Portland, Oregon, on 18 November 18 1907. They lived in Eugene, Lane County, Oregon. John's mother Mary Zumwalt was a sister of Sarah Francis Zumwalt Hammitt. They were both the daughters of Solomon Zumwalt.
William Guillford was the second husband of Ellen, last name unknown, the second wife of the Hon. James Madison Stafford. His name is spelled several different ways.
Norman Peter Hammitt was born 1 July 1828 in Ohio. He died in Marcola, Lane County, Oregon 2 June 1901. He married Sarah Frances Zumwalt 17 February 1857 in Eugene, Lane County, Oregon. His parents were Benjamin George Hammitt and Ruth Van Meter. Norman and Sarah had 18 children.
Sarah Francis Zumwalt was the daughter of Solomon Zumwalt and Nancy Groce. She was born in Flint Hill, St. Charles County, Missouri and died in Marcola, Lane County, Oregon.
Benjamin Clay Hammitt was born in Eugene, Oregon to Norman Peter Hammet and Sarah Frances Zumwalt. He was their first child. He was born 20 September 1859 and died 17 March 1924 in Donna, Lane County, Oregon, on the Mohawk River.
His wife was India Taylor Reynolds, daughter of Curtis Otwell Reynolds and Eliza Ellen White. She was born 6 July 1877 in Wayne County Georgia and died 18 December in Lane County, Oregon.
George M. Hammitt. was a son of Norman and Sarah Frances Zumwalt Hammitt. He was born in Lane County, Oregon. He was born 20 June 1864 and died in Marcola, Lane County, Oregon, 30 September 1909. In the 1870s he resided in Eugene, Lane County, Oregon.
Paul Hammitt was born 10 September 1968 in Oregon. His parents were Norman and Sarah Frances Zumwalt Hammitt. He residedin Eugene, Oregon in the 1870s. He died 31 June 1901 in Marcola, Oregon.
Marvin Lee Hammitt was the ninth child of Norman and Sarah Zumwalt Hammitt. He was born in Oregon, 30 October 1871 and died in Marcola, Lane County, Oregon, 21 September 1951.
Kathleen Alice Campbell was the daughter of John Campbell and Martha Thompson. She was born 7 June 1877 in Iowa and died 26 May 1915 in Donna, Oregon.
Robert Norman Hammitt was the first child of Marvin and Kathleen Hammitt. He was born 21 October 1903 and died 9 February 1984 in Eugene, Lane County, Oregon.
Zella Irene Evans Hammitt was the wife of Robert Norman Hammitt.
Andrew Jerry Hammitt was the third child of Marvin and Kathleen Hammitt. He was born 6 August 1910 in Portland, Oregon and died in Marcola, Lane County, Oregon.
Rachael Bierig was born in Okeene, Oklahoma, to Isaac and Elizabeth Bierig. She married Andrew Jerry Hammitt in California on 4 November 1933.
Carol Lee Hammitt Perkins was a daughter of Robert Norman Hammitt. She married James Randolph Ventgen on 7 September 1968.
Harry Victor Hammitt was born in Eugene, Lane County, Oregon, September, 1876 and died in Marcola, Lane County, Oregon in 1960. He was the the thirteenth child of Norman P. Hammitt and Sarah F. Zumwalt.
Dorcas E. Hammitt Teter was the sister of Norman Peter Hammitt and the daughter of Benjamin Hammitt. She married Samuel Coiner on 26 May 1853 in Wapello County, Iowa and later married Dr. John E. Teter on 7 June 1866 in Iowa.
John B. Thompson is the brother of Carrie McGee below. He is the son of Johnson Thompson and was born in Kansas.
P. E. Hayfield was a son of F. T. and Martha A. Hayfield. They were neighbors of Hon. James M. Stafford in 1880.
John E. George was born in Wisconsin and died in Lane County, Oregon. He was born February 1856 and died 8 July 1927. His parents were Eli George (1829-1893) and Elizabeth Parkin (1828-1899). John married Elizabeth Barbara Brown in 1881. He resided in Cheever, Dickinson County, Kansas and Camp Creek, Mohawk Valley, Lane County, Oregon. He also lived in Long Tom, Lane County, Oregon.
Binger George died 7 July 1901 at eight year old.
Harriet Cowgill was born about 1876 in New York. Her husband was Timothy Cowgill born in Ohio. She was a resident of the Mohawk Valley, Lane County, Oregon. She died as a result of injuries sustained in a buggy accident. She had a daughter, Mrs. N. M. Van Buren, living in the Mohawk Valley at the time of her death.
Elizabeth Bonner was born about 1807 and died April 2, 1891. Her tombstone has her death as April 4. In the 1880 census for Mohawk, Lane County, Oregon, she is listed as "mother" in the household of F. T. Hayfield. The census also states she was born in England. If she was F. T. Hayfield's mother the possibly her husband died and remarried a man named Bonner. The Hayfield family lives next door to the E. L. Warren family in which Soloman Zumwalt is listed as the "father-in-law" and the Norman Hammitt family.
Carrie Rankin Thompson was the wife of James Robert McGee and the daughter of Johnson Thompson. She was born in Kansas on September 26, 1877. She died on Sept. 15, 1916. Her brother is Johh B. Thompson (above).
Doris was the 17th month old daughter of Mr. and Mrs. Harold Conner of Yarnel, Oregon.
This plaque describes the actual location of the cemetery. A transcription of the description is under the first picture of this web page.
Albert Bierstadt's painting of an evening camp on the Oregon Trail.
Information on the Hammitt Family: DeVore7-1 Owner: DHarrisonWeaver.
This is an update of our original web page on the Stafford Pioneer Cemetery. The original page has all of the graves listed by row and plot location. Click here to go to the original page for this cemetery. Use back button to return to this page.


Swift codes, which are also known as BIC codes, are used when you want to make an International Wire Transfer. While routing numbers in the USA are used for domestic wire transfers, Swift codes are only used for making international transfers. Before you can make a wire transfer payment to BANK SPOLDZIELCZY W KROSNIEWICACH, you'll need the appropriate Swift code..
Notice: These Swift/BIC codes for BANK SPOLDZIELCZY W KROSNIEWICACH are only used for international wire transfer payments.