jtotheizzoe:

Chocolate skulls! A delicious crani-nom. Unfortunately only available to those lucky folks who order them from Two Little Cats Bakery in the UK.
Sigh. that would have made my Halloween.
(via EAT YOUR HEART OUT)

I’m moving to the UK in a week. Oh yes.

jtotheizzoe:

Chocolate skulls! A delicious crani-nom. Unfortunately only available to those lucky folks who order them from Two Little Cats Bakery in the UK.

Sigh. that would have made my Halloween.

(via EAT YOUR HEART OUT)

I’m moving to the UK in a week. Oh yes.

biomedicalephemera:

Ways To Die: Amoebic Dysentery and Amoebiasis

First off, let’s get this out of the way - dysentery is not always amoebic, and the term “dysenteryrefers only to the condition of having bloody diarrhea (bloody flux), caused by an infectious pathogen in the large intestine.

There are viral, protozoan, and bacillary dysenteries, in addition to the amoebic dysentery that shows up so often in tropical medicine. As a side-note, the dysentery that reared its ugly head in Oregon Trail (and on the real Oregon trail) would have been either bacillary (Shigellosis) or amoebic, depending upon the season and the location.

Amoebic dysentery and amoebiasis are caused by the amoebic pathogen Entamoeba histolytica. This single-celled organism is hardy, and able to spread easily, especially in environments where proper sanitation is not practiced.

Infection occurs by fecal-oral transmission, and begins when an encysted parasite is ingested by an individual, due to improper handling of food, water, fecal matter, or poor hand-washing practices. When the organism reaches the stomach, the acid dissolves the tough cyst surrounding the amoeba, and the now-active trophozoite (bottom) moves into the small intestine.

There are several paths that E. histolytica is known to take from here; for 90% of those infected, they’ll experience no symptoms, but will still spread encysted amoebas in their feces, possibly infecting others. Of course, acute amoebic dysentery (center left) is a possibility, and occurs in approximately 10% of infected patients. Many times, the amoebas will lie dormant in the mucosal wall of the small intestine, and not cause dysenteric symptoms until months or years later. Sometimes, chronic, long-term infection can occur (center right), especially when there is no or inadequate treatment. However, that is much more common in bacillary dysentery than amoebic dysentery. Of the 10% who become symptomatic, only 16% will experience severe ulceration and long-term damage of the intestine, and that number is much lower with proper anti-amoebic treatment.

In some people, the amoeba makes its way through the intestinal wall, and into the bloodstream. From there, it can cause amoebic liver abscesses (top), compromising liver function, and sometimes mistaken for cancers. With some Latin American strains of E. histolytica, the semi-dormant amoebae will burrow into the lining of the ascending colon or rectum, and cause a long-lasting cellular response, which eventually can end up forming a large granulomatous mass. Other strains of this amoeba can cause severe swelling and flask-shaped ulcers in the lining of the large intestine.

The most important part of treating amoebic dysentery is continuous rehydration therapy - the rapid loss of fluids severely hinders the activity of the immune system and the body at large. Amoebicides (anti-amoebic medications) are also used these days, to speed recovery. In a typical amoebic dysentery case, the patient will recover within one week, assuming a basic standard of care.

Images:
Top: Large amoebic liver abscess protruding from the epigastrum.
Center left: Intestines affected by acute amoebic dysentery.
Bottom: Entamoeba histolytica in the mucosa of the small intestine.
Center right: Intestines affected by chronic amoebic dysentery. 
Source: Dysenteries; their differentiation and treatment. Leonard Rogers, 1913.

Read more:
Diseases of the Oregon Trail at APHL, by Michelle Forman
Dysentery in the Bad Bug Book, United States FDA

biomedicalephemera:

Top: Cranial Nerve I (Olfactory Nerve) Branches in the Nasal Cavity
Bottom: Base of Brain - Olfactory Nerve and Optic Chiasma Emphasized

Ever wonder why you don’t think of an event or memory for years at a time, but the unexpected whiff of a familiar smell can bring it all flooding back?

The olfactory (smell-processing) nerve is the first (I) of the cranial nerves, and is, like the other cranial nerves, directly connected to the brain. However, unlike the others, the cortex of the brain where scent is processed is not near the back of the brain. It is between the frontal and temporal lobe, very close to the long-term memory centers, and the optic olfactory nerve passes directly below the optic nerve. As such, smells can often trigger strong visual and emotional memories that had a unique scent involved, even if you didn’t notice the scent at the time.

Despite the human’s relatively weak and somewhat-insignificant sense of smell, it’s still considered the sense most closely associated with all episodic (event) long-term memories. Certain smells have been known to bring back memories more than half a century after the event occurred.

Anatomy, Descriptive and Surgical. Henry Gray, 1911.

psydoctor8:

Brains in jars still remain in this abandoned Russian neuroscience laboratory

There are few details on this abandoned neuroscience lab, so we’ll have to take the photographer’s word that it’s the real deal. Supposedly, this former Soviet laboratory sits in Moscow, where it was operated by the army. Some time after the lab was hastily abandoned, it was sealed off. But civilians who venture inside will see skinned animal heads, slides depicting brain cross-sections, and lots and lots of actual brains amidst the more mundane dirty dishes and glassware. Head over to the Russian blog brusnichka for more macabre photos from the lab. [via]

соответствующие.

jtotheizzoe:

infinity-imagined:

Each kidney contains thousands of glomeruli, tiny knots of blood vessels that filter large molecules out of urine.

This puts the “pee” in pretty.

For her Tissue Series, artist Lisa Nilsson constructs anatomical cross sections of the human body using rolled pieces of Japanese mulberry paper, a technique known as quilling or paper filigree. Each piece takes several weeks to assemble and begins with an actual photograph of a lateral or mid-sagittal cross section to which she begins pinning small rolls of paper. Depending on its function she rolls the paper on almost anything small and cylindrical including pins, needles, dowels, and drill bits (she even attempted using some of her husband’s 8mm film editing equipment but to no avail). Lastly she even builds the wooden boxes containing the cross-sections by hand. A graduate of RISD, Nilsson now lives and works in Massachusetts and you can learn more about her process in this pair of interviews on All Things Paper and ArtSake.

(via scinerds)

medicalstate:

Magic Arms

Two-year-old Emma wanted to play with blocks, but a condition called arthrogryposis meant she couldn’t move her arms. So researchers at a Delaware hospital 3D printed a durable custom exoskeleton with the tiny, lightweight parts she needed.

This is a heart-warming video that showcases the power of technology to facilitate - in medicine and beyond - the latest discoveries and advances of our time, our world, and our human nature. It is that relationship that powers the frontiers to a better tomorrow.

(Source: youtube.com)

mothernaturenetwork:

If you win or lose by a very small margin, you imagine that the opposite could also have happened — and that can be a very motivating, says a professor who studies the causes and consequences of rivalry.

mothernaturenetwork:

If you win or lose by a very small margin, you imagine that the opposite could also have happened — and that can be a very motivating, says a professor who studies the causes and consequences of rivalry.

(via scinerds)

ucsdhealthsciences:

Alzheimer’s Cognitive Decline Slows in Advanced Age
The greatest risk factor for Alzheimer’s disease (AD) is advancing age. By age 85, the likelihood of developing the dreaded neurological disorder is roughly 50 percent. But researchers at the University of California, San Diego School of Medicine say AD hits hardest among the “younger elderly” – people in their 60s and 70s – who show faster rates of brain tissue loss and cognitive decline than AD patients 80 years and older.
The findings, reported online in the August 2, 2012 issue of the journal PLOS One, have profound implications for both diagnosing AD – which currently afflicts an estimated 5.6 million Americans, a number projected to triple by 2050 – and efforts to find new treatments. There is no cure for AD and existing therapies do not slow or stop disease progression.
“One of the key features for the clinical determination of AD is its relentless progressive course,” said Dominic Holland, PhD, a researcher at the Department of Neurosciences at UC San Diego who led the study and is the paper’s first author. “Patients typically show marked deterioration year after year. If older patients are not showing the same deterioration from one year to the next, doctors may be hesitant to diagnose AD, and thus these patients may not receive appropriate care, which can be very important for their quality of life.”
Holland and colleagues used imaging and biomarker data from participants in the Alzheimer’s Disease Neuroimaging Initiative, a multi-institution effort coordinated at UC San Diego. They examined 723 people, ages 65 to 90 years, who were categorized as either cognitively normal, with mild cognitive impairment (an intermediate stage between normal, age-related cognitive decline and dementia) or suffering from full-blown AD.
“We found that younger elderly show higher rates of cognitive decline and faster rates of tissue loss in brain regions that are vulnerable during the early stages of AD,” said Holland. “Additionally cerebrospinal fluid biomarker levels indicate a greater disease burden in younger than in older individuals.”
Holland said it’s not clear why AD is more aggressive among younger elderly.
“It may be that patients who show onset of dementia at an older age, and are declining slowly, have been declining at that rate for a long time,” said senior author Linda McEvoy, PhD, associate professor of radiology. “But because of cognitive reserve or other still-unknown factors that provide ‘resistance’ against brain damage, clinical symptoms do not manifest till later age.”
Another possibility, according to Holland, is that older patients may be suffering from mixed dementia – a combination of AD pathology and other neurological conditions. These patients might withstand the effects of AD until other adverse factors, such as brain lesions caused by cerebrovascular disease, take hold. At the moment, AD can only be diagnosed definitively by an autopsy. “So we do not yet know the underlying neuropathology of participants in this study,” Holland said.
Clinical trials to find new treatments for AD may be impacted by the differing rates, researchers said. “Our results show that if clinical trials of candidate therapies predominately enroll older elderly, who show slower rates of change over time, the ability of a therapy to successfully slow disease progression may not be recognized, leading to failure of the clinical trial,” said Holland. “Thus, it’s critical to take into account age as a factor when enrolling subjects for AD clinical trials.”
The obvious downside of the findings is that younger patients with AD lose more of their productive years to the disease, Holland noted. “The good news in all of this is that our results indicate those who survive into the later years before showing symptoms of AD will experience a less aggressive form of the disease.”

ucsdhealthsciences:

Alzheimer’s Cognitive Decline Slows in Advanced Age

The greatest risk factor for Alzheimer’s disease (AD) is advancing age. By age 85, the likelihood of developing the dreaded neurological disorder is roughly 50 percent. But researchers at the University of California, San Diego School of Medicine say AD hits hardest among the “younger elderly” – people in their 60s and 70s – who show faster rates of brain tissue loss and cognitive decline than AD patients 80 years and older.

The findings, reported online in the August 2, 2012 issue of the journal PLOS One, have profound implications for both diagnosing AD – which currently afflicts an estimated 5.6 million Americans, a number projected to triple by 2050 – and efforts to find new treatments. There is no cure for AD and existing therapies do not slow or stop disease progression.

“One of the key features for the clinical determination of AD is its relentless progressive course,” said Dominic Holland, PhD, a researcher at the Department of Neurosciences at UC San Diego who led the study and is the paper’s first author. “Patients typically show marked deterioration year after year. If older patients are not showing the same deterioration from one year to the next, doctors may be hesitant to diagnose AD, and thus these patients may not receive appropriate care, which can be very important for their quality of life.”

Holland and colleagues used imaging and biomarker data from participants in the Alzheimer’s Disease Neuroimaging Initiative, a multi-institution effort coordinated at UC San Diego. They examined 723 people, ages 65 to 90 years, who were categorized as either cognitively normal, with mild cognitive impairment (an intermediate stage between normal, age-related cognitive decline and dementia) or suffering from full-blown AD.

“We found that younger elderly show higher rates of cognitive decline and faster rates of tissue loss in brain regions that are vulnerable during the early stages of AD,” said Holland. “Additionally cerebrospinal fluid biomarker levels indicate a greater disease burden in younger than in older individuals.”

Holland said it’s not clear why AD is more aggressive among younger elderly.

“It may be that patients who show onset of dementia at an older age, and are declining slowly, have been declining at that rate for a long time,” said senior author Linda McEvoy, PhD, associate professor of radiology. “But because of cognitive reserve or other still-unknown factors that provide ‘resistance’ against brain damage, clinical symptoms do not manifest till later age.”

Another possibility, according to Holland, is that older patients may be suffering from mixed dementia – a combination of AD pathology and other neurological conditions. These patients might withstand the effects of AD until other adverse factors, such as brain lesions caused by cerebrovascular disease, take hold. At the moment, AD can only be diagnosed definitively by an autopsy. “So we do not yet know the underlying neuropathology of participants in this study,” Holland said.

Clinical trials to find new treatments for AD may be impacted by the differing rates, researchers said. “Our results show that if clinical trials of candidate therapies predominately enroll older elderly, who show slower rates of change over time, the ability of a therapy to successfully slow disease progression may not be recognized, leading to failure of the clinical trial,” said Holland. “Thus, it’s critical to take into account age as a factor when enrolling subjects for AD clinical trials.”

The obvious downside of the findings is that younger patients with AD lose more of their productive years to the disease, Holland noted. “The good news in all of this is that our results indicate those who survive into the later years before showing symptoms of AD will experience a less aggressive form of the disease.”

NIGHTNIGHT by DEDDY