ADA 32 at the White House

Me shaking hands with the President

It's an honor to get invited to the White House and get to shake hands with the President of the United States, more so for 32nd anniversary of the Americans with Disabilities Act.

I am of the post-ADA generation, born after ADA was passed in 1990. Undoubtedly, it is laws like ADA that the allow the doors of opportunity to open to the possibility of me, and in President's Biden's words, "to work, to study, to make connections."  

It is a reason I can, with some measure of confidence, say - So what if I am significantly disabled, I too can pursue a PhD. I too can aspire to higher education, to employment (that's next), to inclusion, and aspire to go toe to toe with my non disabled peers. Perchance, I too can change the world. 

It is because of laws like ADA that Lady Liberty turns her torch towards folks like me, so we too get the opportunity to pursue our version of the American Dream.

I am extremely grateful and in deep admiration of all stalwarts who laid groundwork that folks in my generation and beyond can now build on. In her speech, First Lady, Dr Jill Biden, spoke of 8 year old Jennifer Keelan who cast aside her wheelchair and crawled up the steps of the Capitol Hill in March 1990; "acts of protest," (widely televised) which spurred the signing of the law in July 1990. The then Senator Joe Biden has been a co-sponsor of the bill, sponsored by Sen Harkin and signed into law by President George HW Bush.

Thank you, thank you, to all those tireless stalwarts, (including living legends like my hero, Judy Heumann), in Dr Biden's words, for "refusing to be silent about indignities... faced" and for "holding on to the hope of a better way."

Thank you Mr President for acknowledging this momentous occasion for all of us disabled folks and being part if its journey right from inception. 

In his speech at the Rose Garden of the White House, President Biden referred to the ADA as "one of the most important civil rights laws ever," as he recalled the words of Justin Dart Jr. (regarded as the godfather of ADA) - "ADA is only the beginning, its not the solution, Its the center foundation on which solutions will be constructed." 

Indeed, ADA is a starting point that was crafted 32 years ago and it is up to our generation to continually shape it to meet the changing needs of today and tomorrow. 

I feel, the fact of ADA being a work in progress needs to be highlighted, as it seems especially relevant to the wide diversity in autism, which means building in flexibility and open-mindedness, as there is not going to be a clear one-solution-fits-all. 

“For our country, the ADA is a testament to the character of our people, to the country... It’s proof we can work together and keep moving closer to realizing the promise of America for all Americans,” Biden said.

(President's full remarks, fact sheet)  

We have to continue to look for solutions and workarounds on many many fronts; this is a humankind issue. There is a reason for the word "kind" in the word humankind; "kind-ness" is a fundamental but oft forgotten character trait of people, that has carried us through the troubling periods of human history from time immemorial. 

I want to believe Charles Darwin’s take on the human species as one of “survival of the kindest,” and not just “survival of the fittest.” I want to believe our human society has great capacity for goodness and compassion for all its members.

My generation has to carry this torch forward and demand not just a seat at the table of solutions, but perhaps redefine the table itself, and not just in this country but worldwide for humankind. 

Blind jazz pianist, Jose Andre Montano, prior to his mesmerizing performance that day, gave some very good and practical advice which was very relevant to our mental health - "life is more wonderful if you love your differences and you love who you are... [otherwise] life would not make sense." We often forget the toll of mental health that accompanies the fact of disability as we are constantly in this race to catch up or meet the ever moving target of what society considers acceptable.

On a personal note, too thrilling to get invited to the White House and get to shake hands with the President. The White House is truly magnificent both inside and out. And to be where such laws were signed.... In total awe.

Cal 1973

What a contrast to the developed and bustling Cal campus of today. 

https://twitter.com/CalBearsHistory

 

Violators Toad

Interesting word play at yesterday's Nelson Andrews Leadership retreat site for the Vanderbilt Neuroscience Retreat. 

Have to wonder what the toads (Bufonidae) there think?

Violators, a new species of toad?

A wider picture

Along with the science talks, there was also an Unconscious Bias workshop at yesterday's Vanderbilt Brain Institute retreat

Paying attention - Very applicable for the highly distracted ADHD person like me, with a thousand thoughts running through my head. 

Rest of message very relevant too, for all.  "notice the patterns and treatments of experiences of members of both privileged and marginalized groups"

I was also very appreciative that there was mention of (dis)ability as an identity and often overlooked as a marginalized group along with race/ethnicity etc. It is good to hear such conversations at Vanderbilt. 

I think back to what Arlene Mayerson of DREDF had once said at my Autism Class at UC Berkeley - Civil rights for Disability mean that you not just take away the sign so you can sit anywhere on the bus,  but also giving the disabled person a way to get on the bus in the first place.  

This is really the bigger/wider view for Disability Inclusion. It's not just about allowing disabled people to occupy the same space but also about the accommodations (to get on the bus), supports (to stay seated on the bus) and making disabled people feel they belong, a sense of community, so that they can SUCCEED in that environment. 

 @VanderbiltU #VanderbiltBrainInstitute

Image Description. Text on large screen reads, PAN. Pay Attention Now. Just as a movie camera pans the environment to see the whole picture, we need to continuously pan all around us as we increase our ability to notice the patterns and treatments of experiences of members of  both privileged and marginalized groups. Awareness. While this was at a Neuroscience retreat, this so applies to disability. 

Neuroscience Retreat

Vanderbilt Neuroscience Graduate Program retreat. 

Day started with Hippocampal Place Cells and included a walk by Percy Priest Lake

Autistic Mice

What is a Mouse Model 

The goal of developing mouse models of autism is to gain a better understanding of its genetic and neurobiological basis, and to identify potential targets for therapeutic interventions.

Mouse models of autism are developed using a variety of genetic engineering techniques; the goal of these modifications is to mimic the genetic alterations that have been associated with human autism, and to study the resulting effects on behavior, brain function, and development.

• Knockout mice: insertion of specific gene or gene sequences eg: mouse that expresses a mutated version of the gene that causes alterations in protein function.
• Knock-in mice: insertion of gene eg: mouse lacks particular gene that has been linked to human autism,.
• Viral-vectors:  introduce specific genetic modifications into the mouse brain. This allows researchers to study the effects of altering gene expression or protein function in specific brain regions or cell types.

Once the mouse model has been developed, researchers can use a variety of behavioral, physiological, and molecular techniques to study the effects of the genetic modifications on brain function and behavior. This might involve measuring social behavior, communication, repetitive behaviors, or other autism-like symptoms in the mice, as well as examining brain structure, gene expression, or neurotransmitter function.

Some examples of autism mouse models:

• BTBR T+ Itpr3tf/J mice: These mice exhibit several behaviors seen in human autism, including repetitive behaviors, social deficits, and decreased communication.
• Engrailed-2 (En2) knockout mice: The En2 gene has been linked to autism in some studies. They exhibit reduced social behavior, increased repetitive behaviors, and atypical brain development.
• Neuroligin-3 (NLGN3) knockout mice: The NLGN3 gene, which has been associated with human autism. They exhibit deficits in social behavior and communication, as well as increased repetitive behaviors.
• Fragile X 1 (Fmr1) knockout mice:  Fmr1 gene is associated with fragile X syndrome, a genetic condition that may co-occur with autism. They exhibit deficits in social behavior, communication, and learning.
• Shank3 knockout mice: The Shank3 gene has been implicated in autism development. They exhibit deficits in social behavior, communication, and synaptic function.
• 16p11.2 deletion mouse model: This model is designed to mimic the human 16p11.2 microdeletion, a genetic variation that has been associated with a range of neurodevelopmental disabilites including autism. Mice with this deletion exhibit several autism-like behaviors, including reduced social interaction, repetitive behaviors, and altered vocalizations.
• Tsc2 heterozygous knockout mouse model: Tuberous sclerosis complex (TSC) is a genetic condition associated with autism. This mouse model mimics a TSC-related mutation, in which one copy of the Tsc2 gene is deleted. These mice exhibit social deficits, increased repetitive behaviors, and altered brain connectivity.
• Methyl CpG binding protein 2 (MeCP2) R306C knock-in mouse model: Mutations in the MECP2 gene have been linked to Rett syndrome, a genetic condition that shares some features with autism. This mouse model introduces a specific R306C mutation into the MeCP2 gene, leading to deficits in social interaction and communication.
• Contactin-associated protein-like 2 (Cntnap2) knockout mouse model: CNTNAP2 is a gene that has been associated with autism and language challenges. This mouse model lacks the Cntnap2 gene and exhibits social and communication deficits, as well as alterations in brain development and function.
• Oxtr -/- mouse model: Oxytocin is a hormone that plays a key role in social bonding and has been investigated as a potential treatment for autism. This mouse model lacks the gene for the oxytocin receptor and exhibits deficits in social behavior and communication.
• CNTNAP2-deficient mouse model: CNTNAP2 is a gene that has been associated with human autism. Researchers have developed a mouse model in which the Cntnap2 gene is selectively deleted, resulting in autism-like behaviors, such as reduced social interaction, altered communication, and repetitive behaviors.
• En2-deficient mouse model: En2 is a gene that is involved in the development of the cerebellum, a brain region that is known to be involved in motor coordination and cognitive processing. Mutations in the EN2 gene have been linked to human autism. Researchers have developed a mouse model in which the En2 gene is selectively deleted, resulting in autism-like behaviors, such as altered social interaction and communication.

Researchers often use multiple models to gain a more comprehensive understanding of the complex genetics and neurobiology of autism.

A Vandy welcome to Nashville

 

A Vandy welcome to Nashville at the airport. 

A WW2 Veteran at 101

Met a 101 year old World War 2 veteran on the plane from DC to Nashville. 

Thank you and Oh wow. What changes you must have seen.

101 years, a life so long 

Witness to change, a never-ending song. 

From war to peace, and back again

Through trials and triumphs, and joys and pain.

You've seen the world shift, and the people too

From black and white, to a vivid hue

Technology soaring, and time ticking by

And through it all, you've stayed the course, never shy.

Your stories are treasures, a glimpse of the past

A time machine of memories that will forever last

You are a hero, a symbol of resilience and might

A living reminder of a world we can make right.

Has anyone dropped this?

 

On my recent flight:
Flight Attendant (from front of plane): "Has anyone dropped this?"

All the passengers looked up.

Flight Attendant:
It works everytime!! (smiling).
Now that we have your attention, we'll start the safety announcements.

Be intentional with your interactions

Good tip at Diversity and Inclusion talk today at Vandy

Image shows lecture hall screen with words "Be intentional with your interactions" which inspired a poem. 

Be intentional with your interactions, 

word, gesture, every reaction, 

in these small moments... connections are made

impact on others, never understated.

Choose your words with care, 

filled with kindness and empathy, 

power of words can hurt or heal, 

And can shape the way others see you.

Be present in every interaction, 

Listen with an open heart and mind, 

For in truly hearing others, 

We can learn, grow, and be kind.

Let your interactions be intentional, 

Watch them ripple out, 

Making a positive impact, 

On all those around about.

Flat Effect in Autism

Flat affect, sometimes referred to as "flat effect," is characterized by reduced emotional expressiveness. This manifests through limited facial expressions, a lack of prosodic variation in speech, and minimal gestural communication that typically conveys emotions during social interactions. Flat affect is common among some autistic individuals, presenting unique challenges in social communication and interaction. 

Manifestations of Flat Affect

Flat affect can be identified by several observable behaviors:

• Facial Expressions: Autistic individuals with flat affect might not exhibit the typical range of facial expressions, such as smiling or frowning.
• Prosodic Variation: Their speech might lack the usual variations in tone, often sounding monotone or emotionally flat.
• Gestural Communication: They might use fewer hand movements or other gestures while speaking, which are typically used to convey emotions and emphasis.

Emotional Experience vs. Expression

It's crucial to understand that flat affect does not imply a reduction in the intensity or frequency of experienced emotions. Autistic individuals with flat affect experience emotions similarly to others; however, their outward presentation of these affective states is muted. This can lead to misunderstandings in social interactions, where others might perceive them as uninterested or disengaged, even when they are emotionally involved.

Challenges in Social Interactions

The muted emotional expressiveness associated with flat affect can complicate social interactions. Nonverbal cues, such as facial expressions and tone of voice, play a significant role in how we communicate and understand each other. When these cues are diminished, it becomes harder for others to interpret the emotional states and intentions of individuals with flat affect, potentially leading to social isolation and miscommunication.

Neuroscientific Insights

From a neuroscientific standpoint, flat affect in autism can be understood through the lens of atypical neural processing and connectivity. Research suggests that autistic individuals may exhibit differences in the activation and connectivity of brain regions involved in emotion processing and expression. Key areas implicated include:

• Amygdala: The amygdala plays a crucial role in processing emotions. Studies have shown that autistic individuals may have differences in amygdala activation and connectivity, contributing to atypical emotional responses and expressions (Baron-Cohen et al., 2000; Tottenham et al., 2014).
• Prefrontal Cortex: The prefrontal cortex is involved in regulating emotional responses and social behavior. Atypical activity in this region may influence the ability to modulate and express emotions effectively (Di Martino et al., 2009).
• Mirror Neuron System: The mirror neuron system is believed to be involved in understanding and mimicking the emotions and actions of others. Differences in the functioning of this system in autistic individuals may impact their ability to express emotions through gestures and facial expressions (Dapretto et al., 2006).

Implications for Understanding and Support

Understanding flat affect and its underlying mechanisms is essential for improving social interactions and support for autistic individuals. Here are some practical steps:

• Education and Awareness: Educating peers, educators, and healthcare providers about flat affect can foster a more empathetic and supportive environment. Awareness can help mitigate misunderstandings and reduce social isolation.
• Communication Strategies: Developing alternative communication strategies, such as using clear verbal cues and seeking explicit feedback, can enhance interactions with individuals exhibiting flat affect.
• Supportive Interventions: Therapeutic interventions, such as social skills training and emotion recognition exercises, can help autistic individuals navigate social situations more effectively.

References

• Baron-Cohen, S., Ring, H. A., Wheelwright, S., Bullmore, E. T., Brammer, M. J., Simmons, A., & Williams, S. C. (2000). The amygdala theory of autism. Neuroscience & Biobehavioral Reviews, 24(3), 355-364.
• Di Martino, A., Ross, K., Uddin, L. Q., Sklar, A. B., Castellanos, F. X., & Milham, M. P. (2009). Functional brain correlates of social and nonsocial processes in autism spectrum disorders: An activation likelihood estimation meta-analysis. Biological Psychiatry, 65(1), 63-74.
• Dapretto, M., Davies, M. S., Pfeifer, J. H., Scott, A. A., Sigman, M., Bookheimer, S. Y., & Iacoboni, M. (2006). Understanding emotions in others: Mirror neuron dysfunction in children with autism spectrum disorders. Nature Neuroscience, 9(1), 28-30.
• Tottenham, N., & Gabard-Durnam, L. (2014). The developing amygdala: A student of the world and a teacher of the cortex. Current Opinion in Psychology, 17, 55-60.

At the Frist Center

 

Grandparents and the Queen

Grandparents and the Queen
Late grandpa Raghavan and grandma Pushpa got invited to.meet the queen on her yacht. then also got a card from her 35 years later.