Monthly Archives: February 2012

Shahram Shiva, blogger on, is a leading Rumi translator, author, scholar and performer. Shiva’s translations of Rumi have been published in several books and are available in a CD “Rumi: Lovedrunk.”

I am gone,
lost any sense of wanting the wine
of the nowhereness ask me,
I don’t know where I am.
At times I plunge
to the bottom of the sea,
at times, rise up
like the Sun.

At times, the universe is pregnant by me,
at times I give birth to it.
The milestone in my life
is the nowhereness,
I don’t fit anywhere else.
This is me:
a rogue and a drunkard,
easy to spot
in the tavern of Lovers.
I am the one shouting hey ha.

They ask me why I don’t
behave myself.
I say, when you
reveal your true nature,
then I will act my age.

Last night, I saw Goodness getting drunk.
He growled and said,
I am a nuisance, a nuisance.
A hundred souls cried out, but
we are yours, we are yours, we are yours.
You are the light
that spoke to Moses and said
I am God, I am God, I am God.
I said Shams-e Tabrizi, who are you?
He said, I am you, I am you, I am you.

Brain and Cognitive Sciences MIT Lecture Notes

Lecture 1: From Neurons to Neural Networks

The Liu Lab at MIT, where we are working to elucidate the biophysical mechanisms of plasticity in synapses, cells and networks. We are particularly interested in innovating new techologies that permit conclusive experiments – to understand the rules of plasticity in terms of their functional logic as well as their biological implementations. Ultimately we attempt to examine how rules at different functional levels (from synapse to network) interact. We believe that this integrative approach will eventually lead to a coherent general framework for neural plasticity.
A Culture System for Direct Neuronal Manipulation

We have perfected a culture system that allows us to grow dissociated neurons in a dish where they can be directly observed. The neurons form connections and self-assemble into functional networks, allowing us access to the same phenomena of plasticity that occur in vivo. The system is also amenable to genetic transfections, and provides a very short incubation period for studying the role of various genes. Best of all, the cultured cells can be viewed, measured and manipulated without dissection, providing what is perhaps the most convenient preparation for plasticity studies.
Synaptic Staining and Functional Visualization

The lab incorporates a wide variety of staining and dynamical imaging techniques for locating synapses and characterizing their functional capabilities. Functional dyes such as FM1-43 and FM4-64 are used in nearly all of our experiments to depict which synapses on a given cell or network are functional, as well as providing some index of the synapses’ strengths. We have also been experimenting with methods for using the exchange of these dyes to visualize synaptic activity, and have recently fostered collaborations to develop new staining molecules for better functional assays. These methods can combine with calcium-sensitive fluorescence and immunostaining to provide a visual description of the synapses along a cultured cell or neural network.
Stimulation and Recording of Single Synapses

A major challenge in studying the synapse is how to tell what observed effects are due to presynaptic factors and which to postsynaptic ones. A large proportion of the lab’s efforts have gone towards finding a technique to directly control the behavior of one side of the synapse – the presynaptic one – by replacing it with an artificial terminal under our control. By using a carefully optimized form of iontophoresis, we are able to deliver specified profiles of neurotransmitter directly to single synapses.

A slight holding potential can retain transmitter inside a quartz micropipette that can then be robotically positioned directly alongside a single synapse (located using dyes such as those described above). A specialized amplifier and software program then delivers an iontophoretic current to eject transmitter from the pipette, generating a time course that exactly mimics that observed during real synaptic transmission. A patch-clamped electrode on the receiving cell can then record any post-synaptic activity that results from this simulated presynaptic release. This method therefore allows the researcher to study the synapse one side at a time, by effectively replacing the presynaptic terminal with an artificial “terminal” capable of delivering arbitrary profiles of neurotransmitter.
Functional Mapping of Dendritic Trees

One of our recent techniques is to provide a complete functional description of a given neuron’s dendrites. After labeling functional synapses with FM1-43, automated computer software drives robotic manipulators to guide iontophoresis pipettes to synaptic sites. Applying iontophoretic pulses while patch clamping the postsynaptic cell then yields a functional description of each synapse’s strength. After approximately five minutes a dendritic tree of many synapses can be precisely mapped, giving information that can be useful for describing poly-synaptic interactions within a given neuron.
Confocal and Two-photon Microscopy

The use of cultured neurons permits direct visualization that we try to realize via the best optical equipment. The lab is equipped with three confocal microscopes, many with muiltiple lasers, that provide high-resolution imaging of cells and fluorscent markers during recording and stimulation. The lab has also recently gained access to a two-photon microscope setup, as well as acquired our own high-resolution digital video microcamera for rapid, real-time visualization of network activity.
Genetic Manipulations in Cultured Cells and Animal Models

We are also equipped with full facilities for transfecting our cell cultures with inserted genes, with up to 50% of all cells within a culture successfully transfected. Also, thanks to a collaboration with Prof. Susumu Tonegawa, we are able to probe questions of synaptic plasticity in vivo at the physiological and behavioral levels, by creating mice overexpressing or deficient in particular genes.
Computational Analysis and Biologically-inspired Modeling

The lab is unusual among groups working at a similar level of experimental biology in the number of students with computational backgrounds that we employ. Our group has numerous members with degrees in computer science and engineering, and we hope to continue to attract more. Modeling studies are currently underway to predict the transmitter release and binding kinetics at single synapses, while other models seek to discern equations governing the homeostasis of synaptic input. We especially hope to require computational analysis in the coming years as our cultured neural network technology matures. Towards this end, collaborations are currently underway with students in the Seung Lab for Theoretical Neurobiology.
Multi-electrode Arrays for Observing Cultured Neural Networks

One of our recent acquisitions is a 64-channel multi-electrode array, which supports recording and inducing the electrical activity of many cultured neurons. The system can be used in conjunction with patch clamp and iontophoresis, as well as our visualization protocols. Commercial software allows for in-depth analysis of network activity in real time, and stimulation protocols that automatically respond to the system’s observations. We have been working on ways to deploy this system in an incubator to extend our interface with the cells from hours to days.
Lecture 2 Prefrontal Cortex and the Neural Basis of Cognitive Control

Our research interests center around the neural mechanisms for voluntary, goal-directed, behavior. Much effort is directed at the prefrontal cortex, a brain region associated with the highest levels of cognitive function. We combine a sophisticated behavioral methodology with techniques for examining the activity of groups of neurons.

The prefrontal cortex (PFC), a cortical region at the anterior end of the brain, has long been known play a central role in orchestrating complex thoughts and actions. Its damage or dysfunction seems to result in a loss of the brain’s “executive”. It disrupts our ability to ignore distractions, hold important information “in mind”, plan behavior, and control impulses.

Results from our laboratory suggests that the PFC provides an infrastructure for the rapid synthesis of the diverse information. Its major function may be to acquire and implement our internal representations of the “rules of the game” needed to achieve a given goal in a given situation. This could lay the foundation for the complex and elaborate forms of behavior observed in primates, in whom this structure is most elaborate.
Lecture 3: Hippocampal Memory Formation and the Role of Sleep

Research in the Wilson laboratory focuses on the study of information representation across large populations of neurons in the mammalian nervous system, as well as on the mechanisms that underlie formation and maintenance of distributed memories in freely behaving animals. To study the basis of these processes, the lab employs a combination of molecular genetic, electrophysiological, pharmacological, behavioral, and computational approaches. Using techniques that allow the simultaneous activity of ensembles of hundreds of single neurons to be examined in freely behaving animals, the lab examines how memories of places and events are encoded across networks of cells within the hippocampus ­ a region of the brain long implicated in the processes underlying learning and memory.

These studies of learning and memory in awake, behaving animals have led to the exploration of the nature of sleep and its role in memory. Previous theories have suggested that sleep states may be involved in the process of memory consolidation, in which memories are transferred from short to longer-term stores and possibly reorganized into more efficient forms. Recent evidence has shown that ensembles of neurons within the hippocampus, which had been activated during behavior are reactivated during periods of dreaming. By reconstructing the content of these states, specific memories can be tracked during the course of the consolidation process.
Lecture 4: The Formation of Internal Modes for Learning Motor Skills

In this talk, I will discuss a new perspective on how the central nervous system (CNS) represents and solves some of the most fundamental computational problems of motor control. In particular, I will discuss the task of transforming a planned limb movement into an adequate set of motor commands. To carry out this task the CNS must solve a complex inverse dynamic problem. This problem involves the trans-formation from a desired motion to the forces that are needed to drive the limb. The inverse dynamic problem is a hard computational challenge because of the need to coordinate multiple limb segments and because of the continuous changes in the mechanical properties of the limbs and of the environment with which they come in contact. A number of studies of motor learning have provided support for the idea that the CNS creates, updates and exploits internal representations of limb dynamics in order to deal with the complexity of inverse dynamics. In the talk I will discuss how such internal representations are likely to be built by combining the modular primitives in the spinal cord as well as other building blocks found in higher brain structures. Experimental studies on spinalized frogs and rats have led to the conclusion that the premotor circuits within the spinal cord are organized into a set of discrete modules. Each module, when activated, induces a specific force field and the simultaneous activation of multiple modules leads to the vectorial combination of the corresponding fields. I regard these force fields as computational primitives that are used by the CNS for generating a rich grammar of motor behaviors.
Lecture 5: Look and See: How the Brain Selects Objects and Directs the Eyes
Purpose of the Research

To determine how visual perception is processed by the brain and how visually guided eye movements are generated.

The methods used in the Schiller lab are:

Physiological studies in non-human primates that utilize single-cell recordings, microstimulation, pharmacological manipulation, tissue inactivation and ablation.
Behavioral studies in normal human subjects, in patients with brain infarcts, and in non-human primates that examine visual and oculomotor capacities.

Lecture 6: How the Brain Wires Itself
Plasticity and Dynamics in the Developing and Adult Cerebral Cortex

Plasticity, or the adaptive response of the brain to changes in inputs, is essential to brain development and function. The developing brain requires a genetic blueprint but is also acutely sensitive to the environment. The adult brain constantly adapts to changes in stimuli, and this plasticity is manifest not only as learning and memory but also as dynamic changes in information transmission and processing. The goal is to understand long-term plasticity and short-term dynamics in networks of the developing and adult cortex.

Brain Anatomy

Annotated histology sections of developing mouse is a digital atlas of mouse development and a database resource for spatially mapped data such as in situ gene expression and cell lineage. The 3D Mouse atlas (MRI based) site allows visitors to query cerebral structures of a 13.5 dpc mouse embryo and view 3-D reconstructions of those structures as well as reconstructions of the entire embryo. Cranial nerve tutorial. Fundamental information about the cranial nerves. Neuroanatomy online at University of Utah. This site contains interactive multimedia which allows the learner to move between diagrams, gross anatomy, microscopic specimens, definitions, and atlases in a manner tailored to the student’s needs. Loyola University. Online neuroanatomy course information and content.

Instructors: Prof. Peter H. Schiller
MIT Course Number: 9.95-A

Readings on Neurology, Neuropsychology, and Neurobiology of Aging:

1 Introduction: The Aging Brain, Corkin Lecture Squire, L. “Memory systems of the brain: A brief history and current perspective.” Neurobiology of Learning and Memory 82 (2004): 171-177.

Hof, P. R., and J. H. Morrison. “The aging brain (includes Alzheimer’s): morphomolecular senescence of cortical circuits.” Trends in Neurosci 27 (2004): 607-613.


Piguet, O., and S. Corkin. “The aging brain.” In Learning and the Brain: An Encyclopedia. Edited by S. Feinstein. Westport, CT: Greenwood Publishing Group. (In press)

2 Imaging the Aging and Demented Brain Jack, C. R., B. A. Shiung, J. L. Gunter, et al. “Comparison of different MRI brain atrophy rate measures with clinical disease progression in AD.” Neurology 62 (2004): 591-600.

Karas, G. B., O. Scheltens, S. A. R. B. Rombouts, et al. “Global and local gray matter loss in mild cognitive impairment and Alzheimer’s disease.” NeuroImage 23 (2004): 708-716.

Salat, D., D. Tuch, D. Greve, et al. “Age-related alterations in white matter microstructure measured by diffusion tensor imaging.” Neurobiology of Aging. (In press)

Den, Heijer T., M. Oudkerk, L. J. Launder, et al. “Hippocampal, amygdalar, and global brain atrophy in different apolipoprotein E genotypes.” Neurology 59 (2002): 746-748.

Klunk, W., H. Engler, A. Nordberg, et al. “Imaging brain amyloid in Alzheimer’s disease with Pittsburgh compound-B.” Annals of Neurology 55 (2004): 306-319.


Petersen, R. “Mild cognitive impairment as a diagnostic entity.” Journal of Internal Medicine 256 (2004): 183-194.

3 Working Memory in Aging and Alzheimer’s Bowles, R. P., and T. A. Salthouse. “Assessing the age-related effects of proactive interference on working memory tasks using the Rasch model.” Psychology and Aging 18 (2003): 608-615.

Lamar, M., D. M. Yousem, and S. M. Resnick. “Age differences in orbitofrontal activation: an fMRI investigation of delayed match and nonmatch to sample.” Neuroimage 21 (2004): 1368-1376.

Park, D. C., R. C. Welsh, C. Marshuetz, et al. “Working memory for complex scenes: age differences in frontal and hippocampal activations.” JOCN 15 (2003): 1122-1134.

Cabeza, R., S. M. Daselaar, F. Dolcos, et al. “Task-independent and taskspecific age effects on brain activity during working memory, visual attention and episodic retrieval.” Cereb Cortex 14 (2004): 364-375.

Baddeley, A. D., S. Bressi, Sala S. Della, R. Logie R, and H. Spinnler. “The decline of working memory in Alzheimer’s disease. A longitudinal study.” Brain 114 (1991): 2521-2542.


Salthouse, T. “The aging of working memory.” Neuropsychology 8 (1994): 353-543.

4 Recollection and Familiarity in Healthy Aging Naveh-Benjamin, M., J. Guez, A. Kilb, and S. Reedy S. “The associative memory deficit of older adults: further support using face-name associations.” Psychology and Aging 19 (2004): 541-546.

Glisky, E. L., S. R. Rubin, and P. S. Davidson. “Source memory in older adults: an encoding or retrieval problem?” JEP: LMC 27 (2001): 1131-1146.

Castel, A. D., and F. I. Craik. “The effects of aging and divided attention on memory for item and associative information.” Psychology and Aging 18 (2003): 873-885.

Clarys, D., M. Isingrini, and K. Gana. “Mediators of age-related differences in recollective experience in recognition memory.” Acta Psychologica 109 (2002): 315-329.

Vandenbroucke, M. W., R. Goekoop, E. J. Duschek, et al. “Interindividual differences of medial temporal lobe activation during encoding in an elderly population studied by fMRI.” Neuroimage 21 (2004): 173-180.


Naveh-Benjamin, M. “Effects of divided attention on encoding and retrieval processes: assessment of attentional costs and a componential analysis.” JEP: LMC 26 (2000): 1170-1187.

5 Emotional Memory in Aging and Age-related Disease Leigland, L., L. Schulz, and J. Janowsky. “Age related changes in emotional memory.” Neurobiology of Aging 25 (2004): 1117-1124.

Kensinger, E., A. Anderson, J. Growdon, and S. Corkin. “Effects of Alzheimer disease on memory for verbal emotional information.” Neuropsychologia 42 (2004): 791-800.

Denburg, N., T. Buchanan, D. Tranel, and R. Adolphs. “Evidence for preserved emotional memory in normal older persons.” Emotion 3 (2003): 239-253.

Charles, S. T., M. Mather, and L. Cstensen. “Aging and emotional memory: The forgettable nature of negative images for older adults.” JEP: General 132 (2003): 310-324.

Kensinger, E. “Memory for contextual details: Effects of emotion and aging.” Psychology and Aging. (In press)

6 Midterm Exam (1 Hour)

Implicit Memory

Woodruff-Pak, D. S., and R. G. Finkbiner. “Larger nondeclarative than declarative deficits in learning and memory in human aging.” Psychol Aging 10, no. 3 (1995): 416-26.

Light, L. L., and A. Singh. “Implicit and explicit memory in young and older adults.” J Exp Psychol Learn Mem Cogn 13, no. 4 (1987): 531-41.

7 Alzheimer’s Disease: Natural History, Genetics, and Pathophysiology
(Guest Lecture: Michael C. Irizarry, M. D., Alzheimer Disease Research Unit, Massachusetts General Hospital)

Ingelsson, M., H. Fukumoto, K. L. Newell, J. H. Growdon, E. T. Hedley-Whyte, M. P. Frosch, M. S. Albert, B. T. Hyman, and M. C. Irizarry. “Early Aß accumulation and progressive synaptic loss, gliosis, and tangle formation in AD brain.” Neurology 62 (2004): 925-31.

8 Alzheimer’s Disease: Early Molecular Biology, Genetics, Animal Models Nestor, P. J., P. Scheltens, and J. R. Hodges. “Advances in the early detection of Alzheimer’s disease.” Nature Medicine 10 Suppl. (2004): S34-S41.

Melov, S. “Modeling mitochondrial function in aging neurons.” Trends in Neurosci 27 (2004): 601-606.

Mattson, M. P., S. Maudsley, and B. Martin. “BDNF and 5-HT: a dynamic duo in age-related neuronal plasticity and neurodegenerative disorders.” Trends in Neurosci 27 (2004): 589-594.

Toescu, E. C., A. Verkhrasky, and P. W. Landfield. “Ca++ regulation and gene expression in normal brain aging.” Trends in Neurosci 27 (2004): 614-620.

9 Alzheimer’s Disease (cont.) Glenner, G. “Amyloid ß protein and the basis for Alzheimer’s disease.” In Progress in Clinical and Biological Research. Edited by N. Back, G. Brewer, V. Eijsvoogel, R. Grover, K. Hirschhorn, et al. Vol. 317, Alzheimer’s Disease and Related Disorders, edited by K. Iqbal, H. Wisniewski, and B. Winblad. New York, NY: Alan R. Liss, Inc., 1989, pp. 857-868.

Schenk, D., R. Barbour, W. Dunn, et al. “Immunization with amyloid-ß attenuates Alzheimer-disease-like pathology in the PDAPP mouse.” Nature 400, no. 6740 (1999): 173-7.

Selkoe, D. J., and D. Schenk. “Alzheimer’s Disease: Molecular understanding predicts amyloid-based therapeutics.” Annu Rev Pharmacol Toxicol 43 (2003): 545-584.

10 Alzheimer’s Disease: ß-amyloid and LTP, Distribution of AD Target Tissues, Tauopathies Teter, B. and C. E. Finch. “Caliban’s heritance and the genetics of neuronal aging.” Trends in Neurosci 27 (2004): 627-632.

Citron, M., T. Oltersdorf, C. Haass, et al. “Mutation of the ß-amyloid precursor protein in familial Alzheimer’s disease increases bprotein production.” Nature 360 (1992): 672-4.

Schenk, D., M. Hagen, and P. Seubert. “Current progress in ß-amyloid immunotherapy.” Curr Opin Immunol 16 (2004): 599-606.

Hock, C., U. Konietzko, J. R. Streffer, et al. “Antibodies against betaamyloid slow cognitive decline in Alzheimer’s disease.” Neuron 38, no. 4 (2003): 547-54.

Blanchard, B. J., A. Chen, L. M. Rozeboom, K. A. Stafford, P. Weigele, and V. M. Ingram. “Efficient reversal of Alzheimer’s disease fibril formation and elimination of neurotoxicity by a small molecule.” Proc Natl Acad Sci U S A 101 (2004): 14326-32.

Ye, C., D. M. Walsh, D. J. Selkoe, and D. M. Hartley. “Amyloid ß-protein induced electrophysiological changes are dependent on aggregation state: N-methyl-D-aspartate (NMDA) versus non-NMDA receptor/channel activation.” Neurosci Letters 366 (2004): 320-325.

11 Parkinson’s Disease/Huntington’s Disease: Molecular, Genetic Mechanisms, Memory Gilbert, B., S. Belleville, L. Bherer, and S. Chouinard. “Study of verbal working memory in patients with Parkinson’s disease.” Neuropsychology 19 (2005): 106-14.

Ross, C. A., and M. A. Poirier. “Protein Aggregation and neurodegenerative disease.” Nature Medicine 10 Suppl. (2004): S10-S17.

Lemiere, J., M. Decruyenaere, G. Evers-Kiebooms, et al. “Cognitive changes in patients with Huntington’s disease (HD) and asymptomatic carriers of the HD mutation-a longitudinal followup study.” J Neurol 251 (2004): 935-42.

12 Parkinson’s Disease/Huntington’s Disease: Molecular, Genetic Mechanisms, Memory (cont.) Bossy-Wetzel, E., R. Schwarzenbacher, and S. A. Lipton. “Molecular pathways to neurodegeneration.” Nature Medicine 10 Suppl. (2004): S2-S9.

Castner, S., and P. Goldman-Rakic P. “Enhancement of working memory in aged monkeys by a sensitizing regimen of dopamine D1 receptor stimulation.” J Neurosci 24, no. 6 (2004): 1446-50.

Knopman, D. S., B. F. Boeve, and R. C. Petersen. “Essentials of the proper diagnoses of mild cognitive impairment, dementia, and major subtypes of dementia.” Mayo Clin Proc 78, no. 10 (2003): 1290-308.

Final Exam

Prof. Suzanne Corkin
Prof. Vernon M. Ingram
MIT Course Number: 9.110J / 7.92J

Indigenous cultures of peace is an International conference hosted in Turin, Italy, on March 16th-18th 2012.

Indigenous cultures of peace offers three days of speeches, workshops and events to bare witness of and exchange views with today’s societies of peace. These societies are living instances of egalitarian communities without any form of violence against women or children, let alone warfare.

With the participation of: Women from the Moso (Cina) and Khoesan (South Africa) communities; Heide Goettner Abendroth (Germany); Bernedette Muthien (South Africa); Peggy Reeves Sanday (USA); Diarmuid O’Murchu (Ireland); Luciana Percovich, Genevieve Vaughan, Mario Bolognese, Francesca Freeman, Iole Natoli, Daniela Degan, Alberto Castagnola, Cerchio di Luna Turino, Gruppo Italiano Dakini, Ass. Argiope, Ass. Talanith, Rodolfo Brun and Cerchio Guerrieri Altrove, Ass. Stregatocacolor, Barbara Zanoni, Monica di Bernardo, Francesca Colombini, Aldon Silvestri.

For registration and more information, please visit:

The Storm Before the Calm is the first book of Neale Donald Walsch’s “Conversations with Humanity Series”.

These are some excerpts, as shared by the CWG Foundation. You can order your copy of The Storm Before the Calm on

“You have come here–to physical form, to this place called Earth, at this particular and critical time in history–to participate in the evolution of our species.

“I realize that this may sound grandiose, yet I believe deeply that it’s true. But a lot of people just don’t know what they can do, and so they assume there is nothing they can do. That’s just not true. There is a gentle assistance that Life invites you to provide right now. If you are willing to offer it, you could truly help to change the world.

“Please don’t allow yourself to be ‘scared off” by that big agenda. You won’t have to perform verbal somersaults or career back flips or relationship jumping jacks or financial miracles or whatever else you might think you’d have to do to get peoples’ attention or to make a difference on the planet. You don’t have to be a good speaker or a fabulous writer or a workshop presenter or any of that.

“Nothing that might involve you will be too much for you. And, as I have said now a couple of times, you will not be alone in this process. Thousands–many thousands–will be joining with you…and I shall be one of them. Yes? Okay? We’ll be doing this together!

“So here’s the scoop: Your participation in the evolution of our species will be achieved through the work you do with your own Soul.

“Humanity could be just one conversation from paradise. That conversation begins with a talk that you have with yourself. It involves you questioning the prior assumption–about yourself, about who you are and why you are here.

“Now for some of you this idea of “working with your soul” may feel like a new concept. “How do you work with your soul?”, you may ask. It’s a fair question. No one teaches this stuff in high school. Very little is written about it. Churches don’t even get very deeply into it.

“As I have already done some of this work, I can tell you that it is the most exciting work you could ever imagine; the most fulfilling work in which you could ever engage; the most powerful work you could ever do. It is powerful enough to shift the reality of your person–and of a planet.

“In your conversation with your Soul you will ask the Four Fundamental Questions of Life: Who am I? Where am I? Why am I where I am? What do I intend to do about that? And when you finish asking yourself these questions (and answering them), I will invite you to ask them of others. Indeed, I am inviting all of humanity to ask these questions of all of humanity.

“I am inviting people everywhere to start a conversation with other people everywhere, asking the same questions they are asking themselves. I want to encourage people to engage other people at the same level at which they engage their own Soul. Because when they engage other people at this level, they will experience that they are engaging their own Soul. For this is the level at which we all experience that We are all One.

“When we speak to each other from that place of Oneness, we take a huge step in our evolution. So let us talk with one another. Let us have a conversation with humanity. Let us lead each other back home, by reminding each other of who we really are — in the aggregate, and in our individual expression.”

1. What is the difference between a concept and Reality? 
a. A concept is a thought of a separate object together with a name or identifier of the object.
 b. Thoughts begin to arise in early childhood. The infant’s mind contains few concepts whereas the sage’s mind sometimes may contain many thoughts but the sage always sees directly that separation is an illusion.
 c. Without thoughts, there are no objects (e.g., in dreamless sleep, under anesthesia, or in samadhi) because, by definition, an object is the thought of it.
 d. Reality is not a thought. Rather, It is absence of separation.

2. What is meant by true and untrue concepts?
a. A belief is a concept which contains the concept of attachment.
b. A belief that cannot be verified by direct seeing is always subject to attack by a counter-belief. Therefore, it must be constantly reinforced by repetition of the belief.
c. Since Reality is absence of separation, It cannot be perceived. Therefore, concepts cannot describe Reality (but they can be true, see g and h below).
d. Example: A material object by definition is separate from other material objects. Therefore, material objects are not real. The belief that material objects are real is constantly reinforced by materialistic culture, and is sustained only by a failure to see the distinction between objects and Reality.
e. Although concepts cannot describe Reality, they can point to Reality. 
f.  A pointer is an invitation to see directly the distinction between an object and Reality. 
g. If a concept asserts or implies the reality of any object, it is untrue. If it negates the reality of an object, it is true (but not a description of Reality). A true concept can be a useful pointer to Reality.
h. Example: The concept that material objects are not real is true, and is a pointer to Reality.

3. What is the world (the universe)? 
a. The world (the universe) is the collection of objects consisting of the body-mind and all other objects. The world appears to exist in time and space.
b. However, time and space are nothing but concepts. They are not real.
c. Time is the concept of change. Since all objects change, all objects are temporal concepts.
d. Space is the concept of extension (size and shape). Since all objects are extended in space, all objects are spatial concepts.

4. What are polar, or dual, pairs of concepts?
a. Thought always results in inseparable pairs of concepts (dual pairs) because every thought has an opposite.
b. Reality is apparently split into dual pairs by thought. However, no thought is real since Reality cannot be split.
c. The result of apparently splitting Reality into dual pairs of concepts is called duality. 
d. The two concepts of a pair are always inseparable because the merger of the opposites will cancel the pair.
e. Example: “I”/not-“I” is a dual pair of concepts. If the “I” and not-“I” merge, neither concept remains. 

5. What is Awareness/Presence?
a. Awareness/Presence is not a concept or object. It is what is aware of all concepts and objects.
b. It does not change and It has no extension so It is time-less and space-less.
c. However, It is said to be space-like because all concepts and objects are said to appear in It.
d. The terms “Awareness/Presence” and “Reality” are equivalent conceptual pointers.

6. What are We? 
a. We are not a concept or object because We are what is aware of all concepts and objects.
b. Therefore, We are Awareness/Presence.
c. Because the body-mind and the world are objects, they appear in Us–We do not appear in them.
d. We do not appear in the body so We are not contained or restricted by it.

7. What is existence? 
a. An object is said to exist if it is believed to be separate from Awareness/Presence. It then also appears to be separate from other objects.
b. Existence is only apparent because Awareness/Presence always remains unsplit.
c. The apparently real existence of objects is called illusion (Maya).
d. The sage, being only Awareness/Presence and knowing only Awareness/Presence, knows that he/she is not separate from anything.

8. What is the “I”-object?
a. When an “I”-concept is believed to be separate from Awareness/Presence, it is said to exist as an “I”-object.
b. However, clear seeing shows that there is no “I”-object.
c. We are not objects and We do not exist as objects. We are Reality (Awareness/Presence). 

9. What is it that makes other objects seem to exist?
a. Whenever the “I”-object appears to arise, the not-“I” object also appears to arise.
b. Then, desire for completion also arises, including the desire for the not-“I” object.
c. But, because fear/desire form a dual pair, whenever desire arises, fear also arises, including the fear of the not-“I” object.
d. Thus, the not-“I” object seems real.
e. Thoughts also splits the apparent not-“I” object into a multitude of apparent objects, and fear/desire makes them all seem real.

10.  What is the true nature of all objects?
a. All apparent objects arise in Awareness/Presence.
b. Because physical space and time are apparent objects, they also arise in Awareness/Presence.
c. No apparent object is separate from Awareness/Presence. Thus, all apparent objects consist of Awareness/Presence.
d. Objects are not real as objects but they are real as Awareness/Presence.
e. Awareness/Presence welcomes/loves all apparent objects that appear in It.

11. What is the personal sense of doership? 
a. Along with illusory “I”-object, arises also the sense of personal doership.
b. However, since there is no “I”-object, there is no doer, no thinker, no chooser, and no observer.
c. Therefore, “we” have no control. Thus, whatever happens, happens. Whatever doesn’t happen, doesn’t happen.

12. If there is no doer, how do things happen? 
a. Everything that happens is only an arising in Awareness/Presence.
b. Only one arising is present at any moment. No other arisings are ever present to affect the arising that is present.
c. Since no arising is present to affect the arising that is present, there can be no law of cause-and-effect.
d. The concept of causality, i.e., that one event causes another event, is only an arising in Awareness/Presence.
e. Since causality is only a concept, “I” can never do anything.
f. Because “I” can do nothing, neither can “I” choose. Thus, free will is nothing but an empty concept.

13. What is suffering? 
a. The feeling of being separate is an arising that carries with it a sense of shame for feeling isolated, alienated, lonely, and disconnected.
b. The sense of free will is an arising that carries with it the feeling of personal responsibility for “my” past and “my” future.
c. The sense of personal responsibility is an arising that carries with it guilt and regret for “my” past and worry and anxiety for “my” future.

14. What is awakening (enlightenment)? 
a. Awakening is the realization that I am not separate and I have never been separate. Therefore there is no shame.
 b. Awakening carries with it the realization that I do nothing and I have never done anything. Therefore, there is no regret, guilt, worry, or anxiety.
 c. Awakening is the awareness that Reality, which is what I am, has never been affected by any concepts.
 d. Awakening is the awareness that my true nature includes a sense of Welcoming/Love. 

15. What can we do to awaken?
a. Since direct seeing shows that there is no doer, there is nothing that the “individual” can do to awaken.
b. Since awakening transcends time, no practice that occurs in time can bring about awakening. Thus most practices do not bring about awakening.
c. However, direct seeing can bring about awakening because direct seeing is timeless seeing.

16. Does this mean that there is no hope for the sufferer? 
a. Definitely not. There are many practices that will lead to less suffering. However, like all other actions, they are never done by a doer since there is no doer. Therefore, “we” cannot do them. If they happen, they happen. If not, they don’t.
 b. Example: To see that there is no “I”, look inward for it and see that there is none. See also that everything that happens, including all thoughts and feelings, happens spontaneously so there can be no doer.
 c. Example: To see that no object exists, look and see that all objects are nothing but arisings in Awareness/Presence. Then, look and see that no object could ever bring “you” peace. Finally, see that nothing can affect You who are Awareness/Presence/Presence Itself.

17.  What else can we do?
a. We can go inward and downward and feel the breath. This takes us out of the head and the thinking mind and puts us in the body and the senses.
b. We can practice mindfulness and see that our attachments and aversions are nothing but arisings in Awareness/Presence.
c. We can become aware that all objects are nothing but arisings in Awareness/Presence and therefore cannot affect Us.
d. We can see that there can be no suffering in pure Awareness/Presence.
e. We can trust Awareness/Presence, which is our true nature.
f. We can rest in Awareness/Presence, which is our home

Courtesy of Stanley Sobottka, Emeritus Professor of Physics, University of Virginia, Charlottesville, VA 22904-4714. Source:

The Carbon Footprint of a Shrimp Cocktail – by Erik Stokstad Source:

In many parts of Latin America and Asia, large swaths of coastal mangrove forests have been cut down and turned into shrimp farms. Not only does this deforestation destroy habitat for birds and cause other ecological problems, but it also releases a large amount of the carbon stored in mangrove soil—so much, in fact, that the shrimp end up having a sizable carbon footprint, according to calculations presented here today at the annual meeting of the American Association for the Advancement of Science (which publishes ScienceNOW).

To get a handle on how much carbon dioxide is represented by shrimp, ecologist Boone Kauffman of Oregon State University in Corvallis made some estimates based on typical shrimp farms in southeast Asia. He looked at farms that are relatively large and not particularly productive, with harvests yielding 50 to 500 kilograms of shrimp per hectare. These farms, which make up about half of those in the world, only last for 5 years or so before the buildup of sludge in the ponds and the acid sulfate soil renders them unfit for shrimp. “It’s the equivalent of slash-and-burn agriculture,” Kauffman said. (Other types of shrimp farms are more efficient and not located in mangrove forests.)

Drawing on other studies, Kauffman estimated that 401 metric tons of carbon are emitted to the atmosphere when a hectare of mangrove is converted to a shrimp farm, which is equivalent to 1472 tons of carbon dioxide. Over the average 5-year life span of a farm, a farmer will typically harvest about 1659 kilograms of shrimp. So a 100-gram shrimp cocktail represents an “astonishing” 198 kilograms of carbon dioxide from the loss of the mangrove, Kauffman said, the equivalent of burning 90 liters of gasoline. The carbon intensity of shrimp from deforested mangroves is 10 times greater than that of beef grown in deforested Amazonian rain forest, according to other unpublished calculations Kauffman has made. The calculations don’t include the energy involved in feeding, processing, and transporting the shrimp.

“The shrimp cocktail is a good example of how carbon cost associated with mangrove degradation way outweighs the actual product that is produced,” Emily Pidgeon of Conservation International told the audience at a session entitled “Blue Carbon, Green Opportunities: Innovative Solutions To Protect Coastal Ecosystems.” So, how much would it cost to prevent mangroves from being turned into shrimp farms? Based on his calculations, Kauffman says that compensating farmers for not growing shrimp would mean that each ton of carbon kept intact in mangrove soil would cost about $4.50. “That’s well within the range of carbon markets,” Kauffman said.

At the moment, these carbon markets only trade in credits for terrestrial ecosystems; for example, keeping a certain amount of forest intact in order to offset a ton of carbon dioxide emitted by burning fossil fuels. At the session, Carolyn Ching of the VCS Association—a firm that creates accounting standards for carbon credits—described progress in devising the first carbon credit program for mangroves and other wetlands, which could provide funds for their conservation and restoration. Ching suggested the system could be finalized and running as early as September: “We see carbon finance as one of the potential mechanisms for addressing wetlands conservation.”

Wonderful example of Ernst Chladni plates, to see the sounds:

Chladni repeated the pioneering experiments of Robert Hooke of Oxford University who, on July 8, 1680, had observed the nodal patterns associated with the vibrations of glass plates. Hooke ran a bow along the edge of a plate covered with flour, and saw the nodal patterns emerge.

Chladni’s technique, first published in 1787 in his book, Entdeckungen über die Theorie des Klanges (“Discoveries in the Theory of Sound”), consisted of drawing a bow over a piece of metal whose surface was lightly covered with sand. The plate was bowed until it reached resonance and the sand formed a pattern showing the nodal regions. Since the 20th century it has become more common to place a loudspeaker driven by an electronic signal generator over or under the plate to achieve a more accurate adjustable frequency.

Variations of this technique are commonly used in the design and construction of acoustic instruments such as violins, guitars, and cellos.

Anima & Animus: Bridge to the Soul is offered by the Carl Jung Society of Vancouver on March 23rd. The speaker is Dr. Karen Evers-Fahey, based in Victoria. Dr. Karen Evers-Fahey is a Zurich trained Jungian analyst and a training & supervising analyst with the Association of Graduate Analytical Psychologists.

In this lecture I would like to ask the audience to forget everything they have learned about anima/animus, and to re-introduce these concepts as a way to connect to ourselves and to others.

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