Tinykcafe

words:

계절 (gyejeol) - season

봄 (bom) - spring

봄비 (bombi) - spring rain

태양 (taeyang) / 해 (hae) - sun 

무지개 (mujigae) - rainbow 

벚꽃 (beojkkoch) - cherry blossom

벚꽃 놀이 (beojkkoch noli) - cherry blossom viewing

나무 (namu) - tree 

소풍 (sopung) - picnic 

행복한 (haengbokhan) - happy 

화창한 (hwachanghan) - sunny

개강 (geagang) - beginning of a new semester in a university

황사 (hwangsa) - yellow dust

questions & answers:

이번주 날씨 어때요? (ebeonju nalsshi eoddaeyo?) - how’s the weather this week?

내일 날씨가 어떨까요? (naeil nalssiga eotteolkkayo) - what’s the weather going to be like tomorrow?

습해요 (seubhaeyo) - it’s humid

따뜻해요 (ddaddeuthaeyo) - it’s warm

비 온대요 (bi ondaeyo) - it’s going to rain

phrases:

꽃이 피고 있어요 (kkochi pigo isseoyo) - the flowers are blooming 

오늘 황사가 심해서 밖에 나가면 안 돼요 (oneul hwangsaga simhaeseo bakke nagamyeon an dwaeyo) - you shouldn’t go outside today because the yellow dust is bad

날씨가 따뜻해지고 있어요 (nalssiga ttatteushaejigo isseoyo) - the weather is getting warmer

구름이 그쳤어요 (guleumi geuchyeosseoyo) - the clouds cleared up

봄소풍 가자 (bomsopung gaja) -  let’s go on a spring picnic

verbs:

피다 (pida) - for a flower to bloom

지다 (jida) - for the sun to set

뜨다 (tteuda) - for the sun to rise 

호랑이 굴에 잡혀가도 정신만 차리면 산다 = Even if you are caught by a tiger, you will survive if you keep your cool. 

다그치다 to push someone to do something

애정행각을 하다 to be physically affectionate w/someone

기겁하다 to freak out

~에 구애받다 to be limited by ~

문란하다 to be sexually promiscuous/have a dirty mind

아이를 기르다 to raise a child

보듬다 to embrace someone

상처를 보듬다 to lick one’s wounds

사랑의 결실 the fruit of love

무지하다 ignorant

수긍하다 agree/accept something

무안하다 to be embarrassed/humiliated

눈물 또르르 하다 to shed tears

muji in taipei ❤️📔📌📝🖊📂🖇📐

In a small pilot study of men with schizophrenia, researchers at Johns Hopkins Medicine and Sheppard Pratt Health System say they have evidence that adding probiotics — microorganisms, such as bacteria found in yogurts — to the patients’ diets may help treat yeast infections and ease bowel problems. Probiotics may also decrease delusions and hallucinations, but in the study, these psychiatric benefits mostly affected those without a history of yeast infections. 

The findings, published in the May 1 issue of Brain, Behavior, and Immunity, support growing evidence of close links between the mind and the gut.

The investigators caution that larger and more rigorous studies are needed to validate their findings and determine if women with schizophrenia respond similarly to probiotics before this fairly simple and cost-effective treatment strategy should be recommended widely to people with schizophrenia.

“The mental health field is in desperate need of new treatments for psychiatric disorders, yet there’s been very little progress toward this goal for too long a time. The tiny living organisms that make up the human microbiome and the overwhelming evidence for a gut-brain axis together represent a new frontier for schizophrenia research,” says Emily Severance, Ph.D., assistant professor of pediatrics and part of the Stanley Division of Developmental Neurovirology at the Johns Hopkins University School of Medicine. “We need to rethink how we study brain disorders such as schizophrenia by looking at clues offered by a whole-body approach and identifying and understanding the basis for dysfunctions that are occurring outside the brain.”

In an initial study published in 2014, the researchers looked at whether probiotics could treat general psychiatric symptoms and bowel function in people with schizophrenia. They did notice bowel improvement but didn’t notice any effect on total psychiatric symptoms. Also, in a recent publication from this year, the group observed greater memory problems in people with schizophrenia who also had Candida yeast infections.

This new analysis included 56 adult participants with an average age of 46. Nineteen participants were women, and 61 percent were white. At the start of the trial, each participant gave a blood sample and completed the Positive and Negative Syndrome Scale (PANSS) exam used for measuring a standard set of symptoms of schizophrenia.

Each participant took a placebo pill once per day with a meal for the next two weeks and then were split into groups so that neither the researchers nor the participants could tell who would be given a real probiotic or the placebo for the next 14 weeks.

The commercially available probiotic contained over 1 billion colony-forming units of Lactobacillus rhamnosus and Bifidobacterium animalis in each pill. PANSS scores were reassessed every two weeks, and the participants self-reported on the ease of their bowel movements weekly on a scale of 0 to 4. At the end of the study, the researchers collected another blood sample.

Using the blood samples, the researchers measured antibody levels to yeast Saccharomyces cerevisiae, known as brewer’s yeast, and Candida albicans, known to cause yeast infections, before and after the probiotic treatment. Both types of yeast are elevated in people with schizophrenia.

The researchers found Candida antibody levels decreased by 43 percent over time in the 22 men taking probiotics but saw only a 3 percent decrease of antibodies in the 15 men receiving the placebo. Eighteen men responded to the treatment with reduced antibody levels; four men didn’t respond to the treatment. Antibody levels for the brewer’s yeast didn’t change over the course of the study in the participants after probiotic treatment. A treatment effect wasn’t detected in the women because their starting Candida antibody levels were already much higher in those on the placebo than in those taking the probiotics, which the researchers attributed to the small sample size of the trial.

For the next analysis, the researchers focused on the men who had evidence of a yeast infection due to elevated Candida antibodies. The five men in the placebo group with Candida had more difficulty with bowel movements over time, with an average bowel score of 0.74, compared to the 10 men without evidence of infection, who had an average score of 0.19. Severance says these results are consistent with the group’s earlier 2014 analysis of bowel function, but the current study reinforces that Candida yeast contribute to bowel difficulties in men with schizophrenia.

Severance next analyzed whether PANSS psychiatric symptom scores varied between those males with schizophrenia if they had a Candida infection or not. The PANSS exams measure symptoms on three scales: the positive symptoms, such as delusions, hostility, grandiosity and hallucinations; negative symptoms, like social withdrawal and poor socialization; and general psychological symptoms, such as guilt, anxiety and depression. For this analysis, the researchers examined previous data from a larger study of schizophrenia and found that 165 men with Candida infections had higher levels of positive symptoms, like delusions and hostility, with an average PANSS score of 19.5 out of 24, compared to those 219 men without Candida infections who scored on average less than 18.5. In patients treated with probiotics, PANSS scores on positive symptoms improved the most — from an average of 18 down to 14.6 on their PANSS score after 13 weeks — in those who didn’t have a Candida infection to begin with.

“The biggest change in psychiatric symptoms over time by probiotics in men without elevated Candida levels suggests that introduced bacteria via probiotics might shift the resident bacterial community dynamics more easily to a balanced state when fungal competitors such as Candida are not present,” says Severance. “Compared to the bacterial microbiome, relatively little is known about the fungal community in the gut and how it interacts with other classes of microbiota.”

“We hope that with additional studies, we can show that something as cost-effective and easy to access as probiotics would be a way to lessen some symptoms of schizophrenia,” says Severance.

(Image caption: An MIT study of the neural circuits that underlie memory process reveals, for the first time, that memories are formed simultaneously in the hippocampus and the long-term storage location in the brain’s cortex. This image shows memory engram cells (green and red) which are crucial for permanent memory storage in the prefrontal cortex. Credit: Takashi Kitamura)

Neuroscientists identify brain circuit necessary for memory formation

When we visit a friend or go to the beach, our brain stores a short-term memory of the experience in a part of the brain called the hippocampus. Those memories are later “consolidated” — that is, transferred to another part of the brain for longer-term storage.

A new MIT study of the neural circuits that underlie this process reveals, for the first time, that memories are actually formed simultaneously in the hippocampus and the long-term storage location in the brain’s cortex. However, the long-term memories remain “silent” for about two weeks before reaching a mature state.

“This and other findings in this paper provide a comprehensive circuit mechanism for consolidation of memory,” says Susumu Tonegawa, the Picower Professor of Biology and Neuroscience, the director of the RIKEN-MIT Center for Neural Circuit Genetics at the Picower Institute for Learning and Memory, and the study’s senior author.

The findings, which appear in Science on April 6, may force some revision of the dominant models of how memory consolidation occurs, the researchers say.

The paper’s lead authors are research scientist Takashi Kitamura, postdoc Sachie Ogawa, and graduate student Dheeraj Roy. Other authors are postdocs Teruhiro Okuyama and Mark Morrissey, technical associate Lillian Smith, and former postdoc Roger Redondo.

Long-term storage

Beginning in the 1950s, studies of the famous amnesiac patient Henry Molaison, then known only as Patient H.M., revealed that the hippocampus is essential for forming new long-term memories. Molaison, whose hippocampus was damaged during an operation meant to help control his epileptic seizures, was no longer able to store new memories after the operation. However, he could still access some memories that had been formed before the surgery.

This suggested that long-term episodic memories (memories of specific events) are stored outside the hippocampus. Scientists believe these memories are stored in the neocortex, the part of the brain also responsible for cognitive functions such as attention and planning.

Neuroscientists have developed two major models to describe how memories are transferred from short- to long-term memory. The earliest, known as the standard model, proposes that short-term memories are initially formed and stored in the hippocampus only, before being gradually transferred to long-term storage in the neocortex and disappearing from the hippocampus.

A more recent model, the multiple trace model, suggests that traces of episodic memories remain in the hippocampus. These traces may store details of the memory, while the more general outlines are stored in the neocortex.

Until recently, there has been no good way to test these theories. Most previous studies of memory were based on analyzing how damage to certain brain areas affects memories. However, in 2012, Tonegawa’s lab developed a way to label cells called engram cells, which contain specific memories. This allows the researchers to trace the circuits involved in memory storage and retrieval. They can also artificially reactivate memories by using optogenetics, a technique that allows them to turn target cells on or off using light.

In the new Science study, the researchers used this approach to label memory cells in mice during a fear-conditioning event — that is, a mild electric shock delivered when the mouse is in a particular chamber. Then, they could use light to artificially reactivate these memory cells at different times and see if that reactivation provoked a behavioral response from the mice (freezing in place). The researchers could also determine which memory cells were active when the mice were placed in the chamber where the fear conditioning occurred, prompting them to naturally recall the memory.

The researchers labeled memory cells in three parts of the brain: the hippocampus, the prefrontal cortex, and the basolateral amygdala, which stores memories’ emotional associations.

Just one day after the fear-conditioning event, the researchers found that memories of the event were being stored in engram cells in both the hippocampus and the prefrontal cortex. However, the engram cells in the prefrontal cortex were “silent” — they could stimulate freezing behavior when artificially activated by light, but they did not fire during natural memory recall.

“Already the prefrontal cortex contained the specific memory information,” Kitamura says. “This is contrary to the standard theory of memory consolidation, which says that you gradually transfer the memories. The memory is already there.”

Over the next two weeks, the silent memory cells in the prefrontal cortex gradually matured, as reflected by changes in their anatomy and physiological activity, until the cells became necessary for the animals to naturally recall the event. By the end of the same period, the hippocampal engram cells became silent and were no longer needed for natural recall. However, traces of the memory remained: Reactivating those cells with light still prompted the animals to freeze.

In the basolateral amygdala, once memories were formed, the engram cells remained unchanged throughout the course of the experiment. Those cells, which are necessary to evoke the emotions linked with particular memories, communicate with engram cells in both the hippocampus and the prefrontal cortex.

Theory revision

The findings suggest that traditional theories of consolidation may not be accurate, because memories are formed rapidly and simultaneously in the prefrontal cortex and the hippocampus on the day of training.

“They’re formed in parallel but then they go different ways from there. The prefrontal cortex becomes stronger and the hippocampus becomes weaker,” Morrissey says.

“This paper shows clearly that from the get-go, engrams are formed in the prefrontal cortex,” says Paul Frankland, a principal investigator in the Neurobiology Laboratory at the Hospital for Sick Children in Toronto, who was not involved in the study. “It challenges the notion that there’s a movement of the memory trace from the hippocampus to the cortex, and makes the point that these circuits are engaged together at the same time. As the memories age, there’s a shift in the balance of which circuit is engaged as a memory is recalled.”

Further studies are needed to determine whether memories fade completely from hippocampal cells or if some traces remain. Right now, the researchers can only monitor engram cells for about two weeks, but they are working on adapting their technology to work for a longer period.

Kitamura says he believes that some trace of memory may stay in the hippocampus indefinitely, storing details that are retrieved only occasionally. “To discriminate two similar episodes, this silent engram may reactivate and people can retrieve the detailed episodic memory, even at very remote time points,” he says.