An embryo is actually a human; it should be valued as highly as a human life.

The reasoning can be summed up by the fact that, once an egg is fertilized, unless inhibited, it will develop into a fully-developed adult. This opinion is often related to religious doctrines which assert that conception marks the beginning of human life or the presence of a soul.

Viability is another standard under which embryos and fetuses have been regarded as human lives. In the United States, the 1973 Supreme Court case of Roe v. Wade concluded that viability determined the permissibility of abortions performed for reasons other than the protection of the woman's health, defining viability as the point at which a fetus is "potentially able to live outside the mother's womb, albeit with artificial aid."

The point of viability was 24 to 28 weeks when the case was decided and has since moved to about 22 weeks due to advancement in medical technology.

If further technological advances allow a sperm and egg to be combined and fully developed completely outside of the womb, an embryo will be viable as soon as it is conceived, and under the viability standard, life will begin at conception.

Embryonic stem cells should be abandoned in favor of alternatives, such as those involving adult stem cells.

This argument is used by opponents of embryonic destruction as well as researchers specializing in adult stem cell research. It is often claimed by pro-life supporters that the use of adult stem cells from sources such as umbilical cord blood has consistently produced more promising results than the use of embryonic stem cells.

Furthermore, adult stem cell research may be able to make greater advances if less money and resources were channeled into embryonic stem cell research. Adult stem cells have already produced therapies, while embryonic stem cells have not.

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Arguments Against Embryonic Stem Cell Research - Stem ...

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Stem cells have the potential to treat a wide range of diseases. Here, discover why these cells are such a powerful tool for treating diseaseand what hurdles experts face before new therapies reach patients.

How can stem cells treat disease? What diseases could be treated by stem cell research? How can I learn more about CIRM-funded research in a particular disease? What cell therapies are available right now? When will therapies based on embryonic stem cells become available? What about the therapies that are available overseas? Why does it take so long to create new therapies? How do scientists get stem cells to specialize into different cell types? How do scientists test stem cell therapies? Can't stem cell therapies increase the chances of a tumor? Is there a risk of immune rejection with stem cells? How do scientists grow stem cells in the right conditions?

When most people think about about stem cells treating disease they think of a stem cell transplant.

In a stem cell transplant, embryonic stem cells are first specialized into the necessary adult cell type. Then, those mature cells replace tissue that is damaged by disease or injury. This type of treatment could be used to:

But embryonic stem cell-based therapies can do much more.

Any of these would have a significant impact on human health without transplanting a single cell.

In theory, theres no limit to the types of diseases that could be treated with stem cell research. Given that researchers may be able to study all cell types via embryonic stem cells, they have the potential to make breakthroughs in any disease.

CIRM has created disease pages for many of the major diseases being targeted by stem cell scientists. You can find those disease pages here.

You can also sort our complete list of CIRM awards to see what we've funded in different disease areas.

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The Power of Stem Cells | California's Stem Cell Agency

The extracellular matrix covers the entire nervous system and is necessary to ensure the survival of the glial cells that wrap, insulate and protect the nerves. Photo: Vanessa Auld

Sockeye salmon (Oncorhynchus nerka) school together in Scotch Creek, BC. Tony Farrell's lab is investigating how cardiac performance limits the ability of salmon to tolerate high temperatures. Photo: M. Casselman

A scanning electron micrograph of two pulsating gregarines copulating within the coelomic space of a bamboo worm. Brian Leander's lab studies these enigmatic parasites, which inhabit the extracellular cavities of marine invertebrates. Photo: B. Leander

Pisaster ochraceus is the original keystone predator, and controls biodiversity on rocky shores. The Harley lab studies how the impacts of this sea star may change with climate change. Photo: Chris Harley

Tony Farrell's lab is investigating how cardiac performance limits the ability of salmon to tolerate high temperatures. Photo: M. Casselman

Long-tailed Jaeger on Herschel Island, Yukon, site of an International Polar Year project. Photo: Alistair Blachford

Photo: W.K. Milsom

Whelk laying egg capsules, for study of biopolymers. Photo: Shadwick Lab

The brain of a fruit fly, Drosophila melanogaster, stained to visualize a set of approximately 50 neurons. Among the visualized neurons is a pair that controls a specific component of feeding behaviour. Photo: M. Gordon

Rosie Redfield used candy to make a stop-motion movie of DNA uptake by a Haemophilus influenzae bacterium. Photo: R. Redfield

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Department of Zoology, UBC

Environmental or genetic factors may be responsible for individual susceptibility to LSCC. A genetic predisposition for the development of LSCC is highly probable. Genetic polymorphisms of carcinogen-metabolizing enzymes have been found in tobacco smoke and there is evidence that they are associated with the risk of cancer development of the aerodigestive tract. Polymorphisms of genes encoding for arylamine N-acetyltransferases, human OGG1 DNA repair enzyme, CYP1A1, XRCC and glutathione S-transferases have been evaluated in relation to the risk LSCC development, however with controversial results.

Identification of tumour suppressor genes and proto-oncogenes may be critical for an understanding of the biological initiation and progression of laryngeal cancer. Knowledge about the time course of a single molecular alteration may be helpful in its clinical use for molecular epidemiology, diagnostics or characterisation of laryngeal cancer.

The perfect marker for molecular characterisation of LSCC should have the following properties: 1. not be constantly present in malignant cells, 2. associated with precise biological features and predictable clinical behaviour and, 3. easily detected by a standard, simple and reliable method on a small tissue sample. Unfortunately, no such marker yet exists.

Alterations of p53 protein expression and mutations of the p53 gene have been proposed as independent predictors of recurrence in LSCC, however with controversial prognostic value.

p53 protein overexpression has been detected in a high percentage of LSCC correlating well with p53 gene mutation.

p53 gene mutation has been suggested more reliably than p53 protein overexpression for characterisation, predicting also the response to radiotherapy in LSCC patients. This observation is in accordance with the biological role of p53, which mediates apoptosis associated with DNA damage.

Alterations in p53 status have been evaluated in healthy mucosa, precancerous lesions and tumour cells in order to predict the development of LSCC and secondary primary tumours. Mutations of p53 have also been evaluated to detect whether multiple primary tumours have a mono- or polyclonal origin, without however, definitive conclusions.

In LSCC, degradation mediated by other cellular proteins, such as MDM2 or by human papillomavirus (HPV) E6 oncoprotein may represent alternative pathways leading to loss of p53 function.

A p53 gene therapy approach has already been shown to induce apoptosis, radio- and chemosensitisation in cell lines and this, in combination with radiotherapy or chemotherapy, is a rational possibility. Another potential application considered the treatment of dysplastic lesions, as p53 mutations seem to occur early in laryngeal carcinogenesis.

EGFR is frequently and early overexpressed in LSCC, mainly by post-translational mechanisms. EGFR expression retains a strong predictive value independently of treatment (surgery, chemotherapy and radiation) and adversely influences overall relapse-free and metastasis-free survival in LSCC. At present, EGFR is the most reliable biological marker for molecular characterisation, aggressiveness and invasiveness of LSCC.

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Laryngeal Tumors: an overview - Atlas of Genetics and ...

Neurons, Receptors, Neurotransmitters, and Alcohol David M. Lovinger, Ph.D.

David M. Lovinger, PH.D., is chief of the Laboratory for Integrative Neuroscience at the National Institute on Alcohol Abuse and Alcoholism, Bethesda, Maryland.

Nerve cells (i.e., neurons) communicate via a combination of electrical and chemical signals. Within the neuron, electrical signals driven by charged particles allow rapid conduction from one end of the cell to the other. Communication between neurons occurs at tiny gaps called synapses, where specialized parts of the two cells (i.e., the presynaptic and postsynaptic neurons) come within nanometers of one another to allow for chemical transmission. The presynaptic neuron releases a chemical (i.e., a neurotransmitter) that is received by the postsynaptic neurons specialized proteins called neurotransmitter receptors. The neurotransmitter molecules bind to the receptor proteins and alter postsynaptic neuronal function. Two types of neurotransmitter receptors existligand-gated ion channels, which permit rapid ion flow directly across the outer cell membrane, and G-proteincoupled receptors, which set into motion chemical signaling events within the cell. Hundreds of molecules are known to act as neurotransmitters in the brain. Neuronal development and function also are affected by peptides known as neurotrophins and by steroid hormones. This article reviews the chemical nature, neuronal actions, receptor subtypes, and therapeutic roles of several transmitters, neurotrophins, and hormones. It focuses on neurotransmitters with important roles in acute and chronic alcohol effects on the brain, such as those that contribute to intoxication, tolerance, dependence, and neurotoxicity, as well as maintained alcohol drinking and addiction. KEY WORDS: Alcohol and other drug effects and consequences; brain; neurons; neuronal signaling; synaptic transmission; neurotransmitter receptors; neurotrophins; steroid hormones; -aminobutyric acid (GABA); glutamate; dopamine; adenosine; serotonin; opioids; endocannabinoids

The behavioral effects of alcohol are produced through its actions on the central nervous system (CNS) and, in particular, the brain. Synaptic transmissionthe process by which neurons in the CNS communicate with one anotheris a particular target for alcohol actions that alter behavior. Intoxication is thought to result from changes in neuronal communication taking place while alcohol is present in the brain. Tolerance to alcohol involves cellular and molecular adaptations that begin during alcohol exposure; the adaptations develop and diversify with repeated episodes of exposure and withdrawal and are linked to the environment present during exposure. Alcohol dependence develops after several exposure/withdrawal cycles and involves neuroadaptive changes brought about by both the exposure and withdrawal processes. Neurotoxicity produced by alcohol ingestion involves a number of cellular and molecular processes, and neurotransmitters can participate inand modulatemany of these mechanisms. The actions of alcohol on synaptic transmission also contribute to alcohol-seeking behavior, excessive drinking, and alcoholism. Thus, understanding all of these behavioral actions of alcohol requires some knowledge of neuronal signaling in the brain and, especially, the process of synaptic transmission. This article will focus on the basic processes underlying neuronal communication and review the neuronal actions of several neurotransmitters, neurotrophic factors, and hormones thought to be involved in the neural actions of alcohol. This information, although admittedly incomplete, will provide a foundation for the detailed information on alcohol actions provided in subsequent articles in this issue and in Part 2.

Neurons are the cells within the brain that are responsible for rapid communication of information. Although similar to other cells in the body, neurons are specialized in ways that set them apart from other cells and endow them with the properties that allow them to carry out their unique role in the nervous system. The neurons shape is one such unique feature. In addition to the cell body, or soma, which is much like that of other cells, neurons have specialized thin branches know as dendrites and axons. Neurons receive chemical input from other neurons through dendrites and communicate information to other cells through axons. Neurons also are excitable cells. The neuronal surface membrane contains an abundance of proteins known as ion channels that allow small charged atoms to pass through from one side of the membrane to the other. Some of these channels are opened when the voltage across the cell membrane changes. One subtype of these voltage-gated channels allows the neuron to produce a rapid signal known as the action potential, which is the fastest form of intracellular electrical signal conduction in biology (see figure 1).

Individual neurons usually are completely separated from one another by their outer cell membranes and thus cannot directly share electrical or chemical signals. The exception to this situation is the so-called electrical synapse, in which ion-conducting pores made from proteins called connexins connect the intracellular compartments of adjacent neurons, allowing direct ion flow from cell to cell (Kandel et al. 2000). This form of interneuronal communication is much less common in the mammalian CNS than chemical transmission and will not be discussed any further. Rather, the focus will be on chemical interneuronal communication involving the release of a neurotransmitter from one neuron, which alters the activity of the receiving neuron. This chemical communication usually occurs at a specialized structure called a synapse, where parts of the two cells are brought within 20 to 50 nanometers of one another (see figure 2). The neuron that releases the chemical is called the presynaptic neuron. A specialized structure at the tip of the axon of the presynaptic neuron, termed the axon terminal, contains small packets known as vesicles, which are filled with neurotransmitter molecules. When an action potential reaches the axon terminal and stimulates a rise in the concentration of calcium, this ion stimulates the vesicle to fuse with the cell membrane and release the neurotransmitter into the small synaptic gap between cells.

The neuron that is acted upon by the chemical is termed the postsynaptic neuron. The neurotransmitter molecules released from the presynaptic vesicles traverse the synaptic gap and bind to proteins, termed neurotransmitter receptors, on the surface membrane of the postsynaptic neuron.

Figure 1. Schematic drawing of a neuron showing dendrites, where neurons receive chemical input from other neurons; soma (cell body); and axon terminal, where neurons communicate information to other cells. Voltage-gated sodium channels in the membrane of the soma, axon, and axon terminal allow positively charged sodium ions to enter the neuron and produce rapid (in milliseconds) conduction of the excitatory action potential to the terminal. This signal stimulates neurotransmitter release at the axon terminal.

Neurotransmitter receptors are divided into two major classes: ligand-gated ion channel (LGIC) receptors and G-proteincoupled receptors (GPCRs). LGIC receptors are proteins specialized for rapid transduction of the neurotransmitter chemical signal directly into an electrical response (Brunton et al. 2005; Kandel et al. 2000) (see figure 3A). One part of the protein is specialized to bind the neurotransmitter molecule. This binding site is on the extracellular side of the protein. The part of the protein that is buried within the cell surface membrane forms an ion pore, which is basically a fluid-filled hole in the membrane through which the Figure 1 Schematic drawing of a neuron showing dendrites, where neurons receive chemical input from other neurons; soma (cell body); and axon terminal, where neurons communicate information to other cells. Voltage-gated sodium channels in the membrane of the soma, axon, and axon terminal allow positively charged sodium ions to enter the neuron and produce rapid (in milliseconds) conduction of the excitatory action potential to the terminal. This signal stimulates neurotransmitter release at the axon terminal. charged ions can pass (ions cannot pass through lipids or other solid membrane constituents). The time between neurotransmitter binding and opening of the ion pore is on the order of microseconds to milliseconds. Thus, at synapses using ligand-gated channels, the time between action potential depolarization1 (1For a definition of this and other technical terms, see the Glossary, pp. 279283.) of the axon terminal and the beginning of the current flowing through the postsynaptic LGIC is a matter of 1 to 2 milliseconds. This type of synaptic transmission produces a rapid and strong influence on postsynaptic neuron function.

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NIAAA Publications

Ralph Nelson and Victoria Connaughton

1. Introduction.

Retinal ganglion cells are typically only two synapses distant from retinal photoreceptors, yet ganglion cell responses are far more diverse than those of photoreceptors. The most direct pathway from photoreceptors to ganglion cells is through retinal bipolar cells. Thus, it is of great interest to understand how bipolar cells transform visual signals.

Werblin and Dowling (1) were among the first to investigate light-evoked responses of retinal bipolar cells. Based on these studies using penetrating microelectrodes, they proposed that retinal bipolar cells lacked impulse activity, and that they processed visual signals through integration of analogue signals, that is synaptic currents and non-spike-generating voltage-gated membrane currents.

Frank Werblin and John Dowling discovered the ON or OFF light-evoked physiology of retinal bipolar cells (1). They characterized these neurons as processors of analogue visual signals that did not use impulse generation. The work was done at Johns Hopkins University as a part of Frank Werblins doctoral dissertation under John Dowlings mentorship.

Werblin and Dowing also proposed that retinal bipolar cells come in two fundamental varieties: ON-center and OFF-center (Fig. 1). Both types displayed a surround region in their receptive field that opposed the center, similar to the classic, antagonistic center-surround organization earlier described for ganglion-cell receptive fields (2). Ganglion cell receptive field organization is further reviewed in the Webvision chapter on ganglion cells. ON-center bipolar cells are depolarized by small spot stimuli positioned in the receptive field center. OFF-center bipolar cells are hyperpolarized by the same stimuli. Both types are repolarized by light stimulation of the peripheral receptive field outside the center (Fig. 1). Bipolar cells with ON-OFF responses were not encountered (1). ON-OFF responses, excitation at both stimulus onset and offset, first occur among amacrine cells, neurons postsynaptic to bipolar cells.

The Werblin and Dowling characterization of bipolar-cell physiology has proved quite durable over many decades. The notion that bipolar cells do not spike has found exception for some bipolar types. Dark-adapted Mb1 (rod bipolar cells) of goldfish generate light-evoked calcium spikes. These spikes originate in bipolar-cell axon terminals (3, 4). Through genetic imaging techniques this finding has been extended to the axon terminals of many zebrafish bipolar-cell types. In these studies bipolar terminals were labeled transgenically with the Ca2+ reporter protein SyGCaMP2 and light-induced fluctuations in Ca2+ were followed by 2-photon photometry. Fully 65% of the terminals delivered a spiking Ca2+ signal (4). In the cb5b bipolar-cell type of ground squirrel retina Na+ action potentials are driven by light. Other bipolar types in this retina do not exhibit spiking (5). These results suggest that bipolar cells are responsible for significantly more of the encoding of visual signals than had been previously supposed, and that axon-terminal spiking is actively involved. Impulse generation in bipolar cells is further discussed in the section on Voltage-gated currents.

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Bipolar Cell Pathways in the Vertebrate Retina by Ralph ...