pancreatic cells

anonymous asked:

From the prompt list: 30. The Bank for Sherlolly. Perhaps a bank hostage situation?

So, I answered this fic prompt for @mel-loves-all‘s request for a Sherlolly fic towards my 950th Sherlock fic. It’s pre-ship with them about to go out on a date at the end, but I hope you enjoy it nonetheless.

A Most Unexpectedly Eventful Day - Molly and Sherlock walk into a bank that is being robbed, and it immediately turns Molly’s day of errands into something else entirely.

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“You didn’t have to come with me, you know,” Molly said, her sentence ending in a huff as she reached for the handle to the door of her bank. Honestly, she didn’t know Sherlock was with her while she was running errands, but he seemed to be wanting to do something else instead and frankly, she’d rather have him leave than complain for one more minute.

“Well, I’m bored, and you were the only one doing anything interesting today,” he said as he followed her into the building.

“You aren’t acting like you’re finding it interesting,” Molly said, and then she stilled. Something was wrong. It only took her another minute to notice the man by the door with the gun who most certainly was not a security guard. “Sherlock…”

“Yes, I see,” he murmured. “This day certainly has become interesting.”

The man came over and motioned for Sherlock and Molly to join the other bank patrons sitting in a group by the deposit and withdrawal slips. Molly walked over slowly, doing everything Sherlock and Greg and Sally had taught her when entering a hostile situation. She had the feeling Sherlock was doing the same thing, but she doubted they would be able to converse.

Fortunately, in their boredom when Sherlock couldn’t sleep when he used her flat as a bolthole, BSL was something they were both proficient in. Sherlock had decided he needed another language to learn and that was one Mycroft hadn’t mastered, but it wasn’t easy practicing it without someone else who could translate. Molly had been proficient since she had a hearing impaired roommate in uni, someone who was still one of her best friends in the whole world, and so she taught him. It seemed as though now it would be put to good use.

They sat, hands in their laps, and Molly glanced every time she saw a quick movement of Sherlock’s hands. He would duck his head down slightly for any signs that involved touching his face, and he was careful not to do much to draw attention to him. But the message was clear: unless violence erupts, observe and do nothing.

She paid close attention to the armed man she could see. He was short and squat, not really the type of person she would envision committing such a robbery. If running from the police was involved, she barely doubted he’d make it to the end of the block, if the wheezing sound he made every time he inhaled was any indication. And she could see when he got close enough that his eyes were jaundiced. He might not even survive the end of the robbery for all she knew.

“You’re ill,” she said without thinking, getting wide eyes from Sherlock.

“Shut up,” he said in a Liverpool accent.

“I’m a doctor,” she said. “Your eyes and what skin I can see is jaundiced, and you’re wheezing. Can you breathe?”

The man swung the gun at her, but he didn’t put his finger on the trigger. “What are you talking about?”

“Your liver. You have problems with your liver. It could be cancer…pancreatic or perhaps small cell lung cancer,” Molly said.

He barked out a laugh. “Why do you think I’m robbing a bank? Even with free healthcare, it’s too expensive to die.”

“Hey!” a shout came from the back of the bank. “We’re good.”

The man nodded and then headed back to where the voice had come from. Molly looked over at Sherlock, and then the others. “Is there anyone else here?”

“Two men, in the back,” a man in a suit said. “They all had guns and they managed to get the taser off the security guard.”

“No surveillance set up?” Sherlock asked. He was answered by a round of shaken heads. “Then en masse, head to the door and leave.”

Molly watched as the group stood up, almost as one person, and ran to the doors. Sherlock was not among them. “Sherlock?”

“Just need to do one thing,” he said.

“You die today, so help me, I’ll start practicing the dark arts to resurrect you and kill you again,” she said.

He looked at her and then stood and headed towards the door with Molly close on his heels. Once outside, he pulled out his mobile and then pulled up a contact. At first, she thought it might be Greg, but then she realized it was his brother. After he finished that call, then he called Greg. Minutes later there was the sound of screeching tires coming down the alley and then a familiar black car pulled up to block the alley and two men in expensive suits got out, guns drawn. “I had assumed your usual detail was close at hand,” Sherlock said.

“I have an armed detail following me?” Molly asked, surprised.

“Ever since Jim from IT,” Sherlock said, looking at her as the sounds of sirens began to fill the air. “I did realize you were important before that Christmas, you know. You are my pathologist, and you…care.” He was quiet for a moment. “Would you really have brought me back from the dead to kill me all over again?”

“If you did something as idiotic as getting yourself killed, yes,” she said with an emphatic nod. “You’re important to me too.”

He reached over for her hand, surprising her. “Perhaps when we’re done giving our statements, we can postpone the rest of your errands for lunch? A lunch…date, I suppose.”

Molly moved closer, squeezing his hand. The day had taken a strange and sudden turn but, perhaps, it was for the best. “Lunch would be wonderful, Sherlock.” The smile on his face told him he saw the situation the same way.

Tunneling nanotubes

Cancer patients are often treated with chemotherapy that kills rapidly dividing cells. Some cancers, however, can mutate and become resistant to chemotherapy, causing the cancer to recur much more aggressively later in life. In this microscopic image, two pancreatic cancer cells “communicate” with a tunneling nanotube, a thin bridge between which two cells transfer molecules and information, including instructions for becoming drug resistant. Research is underway to understand how these bridges form and function, providing a new avenue for treatments that can halt cancer communication and progression.

Image by Matthew J. Ware and Biana Godin Vilentchouk, Houston Methodist Research Institute.

So. The urgent care thinks I may have pancreatitis. My white cell count is SLIGHTLY elevated (like it’s barely over the line) and they’re doing an enzyme test but won’t know the results till tomorrow

i’m incredibly woozy and the pain comes and goes. I do not have a fever. They gave me a couple medications to help a couple issues I’m having. 

I have a CT on Wednesday (something unrelated, but it’s full body so it’d get my abdomen) and best case I can wait until then and if anything is wrong, they’ll tell me, if not, then maybe this is just a passing painful infection

And my lovely parents keep reminding me that the hospital is expensive so please do not have to go to the hospital

yeah I’ll do my best

I’m just making a point here that really grinds my gears. 

I am a type 1 diabetic, and have been since my pancreas failed at the age of 6. There are several theories for why this happens, but the most widely accepted is that juveniles contract a virus, and for whatever reason, this virus confuses your immune system, and instead of killing the virus, it attacks pancreatic cells as if they are the enemy. They don’t know why certain children this happens to, and others it doesn’t. Some are genetically inclined, because T1 AND T2 diabetes are hereditary, but I have no history of it in my family. 

So, my pancreas is dead, just floating around in there like a lazy unemployed roommate that doesn’t pay rent. Without insulin, which is what healthy pancreases produce, I would die. It wouldn’t take long. 

This all brings me to the point. This is a picture of my most recent pharmacy receipt, just for two vials of insulin. A 30 day supply. $467.99 for one month of my life. 

Narcotics will barely put a dent in your wallet, by the way. Insulin has ZERO street value. It will only inevitably kill anyone who doesn’t need to use it. 

I have been unable to get medical insurance before, many times, and many diabetics I know have to try to find a way to keep themselves alive. It’s part of the reason the nerves are fucked in my feet now; trying to stretch insulin, going without, having to go to an ER begging. 

Can you see why this would piss me off?

New technology enables us to "chart" all cells in the brain

The human brain is made up of hundreds of millions of cells. Many of these cells and their functions are as yet unknown. This is about to change with a new technology that is being used for the first time at the Center for Brain Research at MedUni Vienna and Karolinska Institutet in Stockholm. By combining traditional methods of identifying cells under a microscope and so-called “single-cell RNA sequencing”, it is possible to identify every building block of any given excitable cell. “We are well on the way to being able to map many, if not all, neurons and their functions before too long,” explains lead investigator Tibor Harkany, Head of the Department of Molecular Neurosciences at MedUni Vienna.

So far, we have only been able to study neurons based on a set of scientific premises and to determine or “search for” their function on the basis of a priori knowledge on their morphology (what does the cell look like?), biochemistry (what does it contain?) and what partners a cell might communicate with. “This has hindered the analysis of new types of neurons for which we do not have any anatomical, biochemical or electrophysiological markers. Neuroscience therefore needs radically new approaches to chart the identity of all neurons and other types of non-neuronal cells in the brain,” explains Harkany. “Any new method that helps us to gain a better understanding of the brain and its cellular components has direct relevance to our search for new therapies to treat neuropsychiatric and age-related diseases.”

Catalogue and family tree of all mRNAs
Using the new technology, which is being jointly applied for the first time in the world in a collaboration between MedUni Vienna and Karolinska Institutet, it is now possible to screen each cell and to compile an exact list of its constituents without any prior knowledge – and at the same time to assess its activity and function in the brain in relation to specific behaviors. Thousands of genes are active at any given time in a single neuron. “This will enable us to compile a representative catalogue of mRNA molecules in the neurons and we can use this, for example, to differentiate various neuronal subtypes and to compare healthy and diseased cells or young neurons with old. This technology is a revolutionary breakthrough, because it enables us to record molecular determinants of neuronal identity,” says Harkany. mRNA molecules are single-stranded ribonucleic acids that carry the code for all proteins that a cell produces. 

“It was an enormous challenge to overcome existing technical difficulties, especially to preserve RNA in a state that allows high-quality and reproducible quantitative and qualitative analyses even when first assessing more than hundred parameters of neuronal activity” adds Janos Fuzik, the study’s lead author. As such, the novel technology allows to categorise how neurons might be related to each other, which subsets function in a similar way, what essentially differentiates them, and to predict their roles in neuronal networks and response patterns at unprecedented precision.

Harkany: “Then we will be able to compile a family tree for individual neurons and have a better understanding of their specific contributions to their networks, for example during emotional or learning processes or in memory formation.” Initial study findings included the discovery of five subtypes of neurons that have previously been impossible to research because of their diverse nature. The study also offers another important potential for analysing other types of brain cells, such as astrocytes or microglia (parts of the immune system) in greater detail than was previously possible.

The successful application of the new technology opens up new possibilities for research and clinical practice: entry points for new drugs can be identified more quickly, thus speeding up the development of medicines. At the same time, the new method can also be used for identifying and analysing excitable cells in pancreatic and cardiac tissues, or even in brain tumours. “In this way we will be able to detect both accurately and relatively quickly which cell is not working correctly or is damaged and, more specifically, what is going wrong in the cell,” say the MedUni Vienna brain researchers.

Pancreatic Cancer

Palladin Expression in Primary Cultures of Pancreatic Ductal Cells Derived from Increasingly Neoplastic Samples. Expression of Palladin RNA increases relative to the degree of precancer to cancer: normal to PanIN 1 (hyperplasia) to PanIN 3 (carcinoma in situ) to cancer. Each bar represents epithelial cell cultures from one person. The PanIN 1 and PanIN 3 lesions (lower left photomicrograph) were purified from two affected members of Family X. The pancreatic cancer epithelial cells (lower right photomicrograph) were purified from a sample of sporadic adenocarcinoma.


The pancreas is comprised of separate functional units that regulate two major physiological processes: digestion and glucose metabolism.

The exocrine pancreas consists of acinar and duct cells. The acinar cells produce digestive enzymes and constitute the bulk of the pancreatic tissue. They are organized into grape-like clusters that are at the smallest termini of the branching duct system. The ducts, which add mucous and bicarbonate to the enzyme mixture, form a network of increasing size, culminating in main and accessory pancreatic ducts that empty into the duodenum.

The endocrine pancreas, consisting of four specialized cell types that are organized into compact islets embedded within acinar tissue, secretes hormones into the bloodstream. The - and -cells regulate the usage of glucose through the production of glucagon and insulin, respectively. Pancreatic polypeptide and somatostatin that are produced in the PP and -cells modulate the secretory properties of the other pancreatic cell types.

a | Gross anatomy of the pancreas.

b | The exocrine pancreas.

c | A single acinus.

d | A pancreatic islet embedded in exocrine tissue.

anonymous asked:

I read your post and your right! I don't use birth control, pain pills etc. I just eat a Vegan diet and don't need any of those. BEFORE I was VEGAN I tried to use pain killers and my body overrides them after the 3rd try of taking them. It literally STOPS working. NEED proof of NOT taking insulin? Look up rawfor30days website, watch the video. I don't believe in using anything synthetic. Nature has a way of preventing disease and having a strong immune system naturally like breastfeeding yr baby



Well. I’ll be waiting in the ED with all my evil synthetic medicine in case that plan doesn’t work out for you. Good luck!

Spoiler: if you have type 1 diabetes you literally need exogenous insulin to live because your body has destroyed the pancreatic cells that make it and no amount of raw food is goona bring those guys back, sorry.

A touch of biochem in morning rounds

Intern V doing a short presentation on sulfonylurea drugs: sulfonylureas block ATP sensitive potassium channels in pancreatic Beta cells … blahty blah…which then affects the Krebs cycle… blahty blah

Attending Dr. B: Ok, too much detail!

External image

Sassy Wayfaring, now post-24 hour call: I’m sorry Dr. B but I’m going to need a detailed refresher on the Krebs Cycle from V if I’m going to be able to prescribe sulfonylureas properly in the future.  Now V, from what I remember, the Krebs Cycle is circular, correct?