NY Colored Orphan Asylum 1836 to 1863

Pardon my political incorrectness! This is my entry for Black History Month, February 1018, about a unique part of African-American history yn New York City at the 19th Century – the 1800’s.

In the 18th and 19th centuries, the city of New York used outer areas to house orphans, sick, and unwanted. It kept the peace stable. Most people lived in what is now the financial center and Tribeca. Farms gave way to establishing a city in lower Manhattan. One key question, how were “Negro” orphans treated in the segregated 19th century?

Orphans are and have been a reality for centuries. Churches have tried to camouflage it but there were orphanages in most western civilized societies. If you were black, Afro-American, or Negro in New York City’s 19th-century, and an orphan, you had a safe place to stay. The NY Colored Orphan Asylum was a secure, racist-free orphanage on Fifth Avenue, between 42nd and 43rd Streets. The Colored Orphan Asylum provided home services for about 233 children.

The New York City Colored Orphan Asylum was at this location from 1836 to 1863. Actually, the idea began in 1834 when three Quakers decided to create a safe haven for negro orphans. In 1836 they purchased a house on 12th Street between Fifth and Sixth Avenues. The purchase was necessary because no property owner would lease to a group housing black children. With the house ready to receive orphans, three Quaker women headed to the almshouse. They rescued 11 children who were being housed in the cellar there.

In 1836, New York City barely resembled how it appears today. Most New York City residents lived south of 14th Street. Actually, south pf Canal Street. The infamous 5-Points neighborhood wasn’t built yet toward the now trendy lower east-side.

42nd Street and Fifth Avenue was undeveloped land and a socially acceptable area to build asylums, particularly a Colored Orphan Asylum. People didn’t need to see, hear, or think about the wayward, the sick, and the orphans. As a matter, one main reservoir from the original Croton Reservoir (1843) was on 42nd Street, where Bryant Park is today. That’s how remote the current midtown hub was in 1836. It remained there until 1863 when it was destroyed and burned.

White racism among the poor and immigrant people reacted to the Civil War military draft imposed by President Abraham Lincoln. A key problem focused that the advantaged wealthy were able to pay for exemption. The poor and new immigrants from Germany and Ireland would be drafted.

The poor Irish and German immigrants had a particular focal point at targeting the African-Americans of New York as scapegoats. The Irish usually had to compete with the “Negroes” for jobs and grunt labor, particularly in building tunnels, such as the water tunnels and sewage tunnels. In addition, “Negroes” were pretty much exempt from being drafted due to a lack of military opportunities.

The riots were a three-day orgy of violence towards Afro-American owned businesses, Afro-Americans, and Native Americans. They marched upwards to the shanty areas where those “minorities” lived. And, by the third day, the Colored Orphan Asylum was burned to the ground. Most of the children were rescued by the Fire and Police department.

The asylum would relocate to 144th Street and Amsterdam Avenue, in the new village of Harlem, at Sugar Hill. Later it moved to Riverdale in the Bronx. Though attractive, the Riverdale site was the most upper, out-of-the-way area of the Bronx, on West 261 Street bordering Yonkers. It was larger and considered one of the best orphanages in New York City. In the 1960’s, the site was sold to the Hebrew Home for the Aged.

Dr. James McCune Smith, an African-American physician, provided medical services for about 20 years to the orphans at Colored Orphan Asylum in New York. As there were absolutely no opportunities for Africans to enter medical schools in the United States, Dr. McCune received his medical education at the University of Glasgow in Scotland. In addition, he was the founder of the American Geographic Society.

It is difficult to put yourself in the shoes of those who are not seen as being on par with tour status. Many minorities are viewed under different scopes. This included blacks and the poor. The conceptualization of race (or gender) moved from the biological to the sociological sphere with the march of science. The atmosphere created by racial inferiority theories and stereotypes, 246 years of black chattel slavery, along with biased educational processes, almost inevitably led to medical and scientific abuse, unethical experimentation, and over-utilization of African-Americans as subjects for teaching and training purposes. Stricter ethical controls became issues only in the late 1970’s.

With no acceptance to the American Medical Society, most 19th-century African medical doctors received training in Africa, Europe, or very segregated schools in the Americas. Thus it is important to understand how influential the Quakers were in providing medical care to those residing at the New York City Colored Orphan Asylum.

In contrast to what happened in Manhattan in 1863, There was a Home for Colored Aged in Crown Heights in 1863, supported by many philanthropists of that area. These African Americans had lived in a Brooklyn area called Weeksville. This area had one of the largest (one of three) “Colored” communities.

Unwanted or orphaned children continues to be a society-wide dilemma, often debated. Fortunately, segregation is no longer legally valid. Despite strides toward the American Dream of equal opportunity, people are still separated by race, ethnic, religious and gender issues. As Senator Patrick Moynihan may have said, New York (and the USA) is less of a melting pot but more like a tossed salad. There are still many strides and challenges to overcome.

Alzheimer disease and neurostimulation pacemaker

The powers of cognition (the ability to recognize people, places, things and relationships) are believed to take place in the frontal lobe areas of the brain. Some theorists believe that when certain areas of the frontal lobe degrade, so do the rapid access to the entire brain’s cognitive networks. New research seems to be emerging on creating digital pacemakers to stimulate those tissues of the frontal cerebral cortex that otherwise might develop Alzheimer Disease.

Cognition is about thinking and interpreting sensory perceptions – touch, see, hear, smell, and taste. We create emotional attachments to these senses and the viability of those senses off significant contributions to survival and growth. These begin at birth. Some say before birth, as evolutionary genetic markers pass along to generations.

Many people get frightened when they seem forgetful or get stuck on that tip-of-tongue phenomenon. Some fear these are signs of Alzheimer Disease. Other causes for memory problems can include aging, medical conditions, emotional problems, mild cognitive impairment, or another type of dementia.

Alzheimer Disease was once exclusively attributed to aging. It is the degradation of the ability to develop and access cognitive networks. Simply put, it isn’t. Many adults maintain cognition throughout their entire lifespans. Alzheimer disease may also form at much earlier ages. Cognition is a very lively, experimented topic. The development of Alzheimer disease and cognitive research are part of a mutually cohesive network with many branches. Can brain stimulation of certain areas improve chances of reducing or avoiding the effects of Alzheimer disease?

The use and research of brain pacemakers is less than a decade old and was originally developed to help treat Parkinson’s disease. A significant research sponsor is Michael J. Fox, a popular TV actor who was diagnosed with Parkinson’s.

When it comes to Alzheimer Disease, there are many memory disorders. Currently research theorists on the development of Alzheimer disease debate inferences of causality.

The problem has been that as it emerged beyond the aged norm of senility, Alzheimer’s disease was diagnosed with complete accuracy only after death, when microscopic examination of the brain reveals the characteristic plaques and tangles. This leads to questions as to why so many living people are being diagnosed with Alzheimer disease?

There has been much evidence that has shown how mice kept in a stimulated environment (vs mice in a non-stimulated environment) developed more brain tissue and neuron networks. Neurologists have been discussing that physical exercise produces BDNF or Brain-derived neurotrophic factors. BDNF, it is believed, promotes the survival of nerve cells (neurons) by playing a role in the growth, maturation (differentiation), and maintenance of these cells. It may play a role in building new neuron networks. Some studies support that BDNF increases as a result of physical exercise, aiding neuronal health. The presence of BDNF acts as a natural stimulant for certain brain areas. Since BDNF is genetic, can the reduction or absence of BDNF be behind some cognitive declines?

Cardio-exercise, REM Sleep, Antioxidants found in Coffee or Tea and Meditation help produce BDNF. Subsequently, stress, sugar, and social isolation may reduce BDNF. As such, some that are immobile or old (lacking social networks) might be developing some cognitive impairment because of lower BDNF levels.

According to BBC News,Doctors have known for some time that loneliness is bad for the mind. It leads to mental health problems like depression, stress, anxiety, and a lack of confidence. But there’s growing evidence that social isolation is connected with an increased risk of physical ill health as well. Again, stimulation helps cognitive wellness.

Use of brain pacemakers to help prevent cognitive decline is relatively new and few agree where they should be implanted. Nonetheless, Nanobioelectronics represents a rapidly developing field with broad-ranging opportunities in fundamental biological sciences, biotechnology, and medicine. Instead of referring to these as pacemakers, I prefer neuroprosthetics for monitoring and treating neurological diseases that may help resolve some of those cognitive pathologies that we only are beginning to fathom. Be it Parkinson’s, dementia (there are 4 types of dementia), aphasia, or Alzheimer disease symptoms, there are futures to behold.

There are many things that disrupt access to memories. Finding the seat to how memories are retrieved, processed and accessed is very complex and often to broad to even consider. Normal memory function involves many parts of the brain. Any disease or injury that affects the brain can interfere with memory. Amnesia, for example, might result from a physical trauma from an injury or accident. It may also develop from other causes, often undefined. Dissociative amnesia is organic and may results from a medical or psychological cause as opposed to direct damage to the brain.

There are two types of amnesia:

Anteror Grade Amnesia – Anterograde amnesia is a loss of the ability to create new memories after the event that caused the amnesia, leading to a partial or complete inability to recall the recent past, while long-term memories from before the event remains intact. In a sense, one with Anteror Grade amnesia has no short-term memory.

RetroGrade is a loss of memory-access to events that occurred, or information that was learned, before an injury or the onset of a disease. … It is not to be confused with antero-grade amnesia, which deals with the inability to form new memories following the onset of an injury or disease. One with retrograde may create new memories.

While neuroscience has made inroads at understanding the locations of where memories are stored and, possible treating amnesia. Yet, as result of research, amnesia – particularly antero-grade amnesia – was medically induced. This happened in the case of H.M.

The high incidences of cognitive loss and Alzheimer disease continue despite vast experimentation and research. Are more people being diagnosed with Alzheimer’s than before. There is a genetic marker, APOe-4, that seems to cite some evidence. Yet there are clean genes, dirty genes, and mutated genes. And nutritionists believe that this gene could be influence by dietary factors.

But is APOe-4 the only gene behind Alzheimer onset? Is there more research necessary? In the complex universe of the brain, there is obviously a vast network of questions covering nutrition, neurotransmitters, neurotransmission co factors, and infinite variables from environment and activity.

How would positive results of an APOe-4 test and scale influence one’s life, career, and state of living?

Are we dealing with Alzheimer disease, micro-stroke with cognitive decline, or other cognitive issues?

Of course many of the research experiments aren’t well funded. Perhaps some corporate donors might want to sponsor the research. Elon Musk, of Tesla and Space-X, is developing Neuralink that connects brains with computers. While Neuralink shows no ambitions to treat Parkinson or Alzheimer disease, it may stimulate other business leaders to consider possible investments.

I supported and studied frontal lobe dementia. Frontal lobe dementia does not cause memory loss, but it can exhibit cognitive and neurological problems similar to those caused by Alzheimer’s disease or stroke. The particular area of atrophy is not dissimilar between schizophrenia and dementia. Similar theorists believe that long-term memory storage may have been disaffected due to biochemical deficiencies in REM sleep. On either level, there are no clear etiologies that indicate or predetermine any causal effect of alzheimer disease type symptoms. Yet schizophrenic symptoms and dementia symptoms share some similarities that may be from a missing link between the cortex and the mid-brain memiry centers.

Genetics, diet, smoking, alcohol, substance abuse might be not highly associative to dementia. The problems involve neurotransmitters, catalysts, inhibitors, proteins, peptides, enzymes and a host of variability make us wonder ever more how this prefrontal lesion originated and its effects on memory and organized thinking.

A neurostimulation implant pacemaker therapy may be one significant approach to help suppress cognitive deficits. Using nano-electronic intervention for cognitive decline and avoiding Alzheimer disease, is a promising exploration into helping patients and families deal with cognitive decline. Whether a brain pacemaker will be a benefit is really up to further research as to where they could best stimulate possible reduction in Alzheimer disease decline. Yet, the pot of gold at the end of the rainbow may still require a series of quixotic games, puzzles, and questions to conclusively answer. We still don’t know what lies ahead. Do you?