Psychology

Emma Seppala, for The Observer, has an outstanding overview of some of the health consequences and contagiousness of compassion.  Here is a portion of her article: Decades of clinical research has focused and shed light on the psychology of human suffering. That suffering, as unpleasant as it is, often also has a bright side to which research has paid less attention: compassion. Human suffering is often accompanied by beautiful acts of compassion by others wishing to help relieve it. What led 26.5 percent of Americans to volunteer in 2012 (according to statistics from the US Department of Labor)? What propels someone to serve food at a homeless shelter, pull over on the highway in the rain to help someone with a broken down vehicle, or feed a stray cat? What is Compassion? What is compassion and how is it different from empathy or altruism? The definition of compassion is often confused with that of empathy. Empathy, as defined by researchers, is the visceral or emotional experience of another person’s feelings. It is, in a sense, an automatic mirroring of another’s emotion, like tearing up at a friend’s sadness. Altruism is an action that benefits someone else. It may or may not be accompanied by empathy or compassion, for example in the case of making a donation for tax purposes. Although these terms are related to compassion, they are not identical. Compassion often does, of course, involve an empathic response and an altruistic behavior. However, compassion is defined as the emotional response when perceiving suffering and involves an authentic desire to help. Is Compassion Natural or Learned? Though economists have long argued the contrary, a growing body of evidence suggests that, at our core, both animals and human beings have what APS Fellow Dacher Keltner at the University of California, Berkeley, coins a “compassionate instinct.” In other words, compassion is a natural and automatic response that has ensured our survival. Research by APS Fellow Jean Decety, at the University of Chicago, showed that even rats are driven to empathize with another suffering rat and to go out of their way to help it out of its quandary. Studies with chimpanzees and human infants too young to have learned the rules of politeness, also back up these claims. Michael Tomasello and other scientists at the Max Planck Institute, in Germany, have found that infants and chimpanzees spontaneously engage in helpful behavior and will even overcome obstacles to do so. They apparently do so from intrinsic motivation without expectation of reward. A recent study they ran indicated that infants’ pupil diameters (a measure of attention) decrease both when they help and when they see someone else helping, suggesting that they are not simply helping because helping feels rewarding. It appears to be the alleviation of suffering that brings reward — whether or not they engage in the helping behavior themselves. Recent research by David Rand at Harvard University shows that adults’ and children’s first impulse is to help others. Research by APS Fellow Dale Miller at Stanford’s Graduate School of Business suggests that this is also the case of adults, however, worrying that others will think they are acting out of self-interest can stop them from this impulse to help. It is not surprising that compassion is a natural tendency since it is essential for human survival. As has been brought to light by Keltner, the term “survival of the fittest,” often attributed to Charles Darwin, was actually coined by Herbert Spencer and Social Darwinists who wished to justify class and race superiority. A lesser known fact is that Darwin’s work is best described with the phrase “survival of the kindest.” Indeed in The Descent of Man and Selection In Relation to Sex, Darwin argued for “the greater strength of the social or maternal instincts than that of any other instinct or motive.” In another passage, he comments that “communities, which included the greatest number of the m

This article from YourTango was written by Julie Orlov. Words are powerful. They can cut you, heal you, inspire you, and stop you from certain actions. Learning the language of a strong, healthy relationship or marriage takes time and diligence, but saying some words regularly may cause irreparable damage. Here are five words that are destined to cause damage to your relationship or marriage. 1.  “Never.”  “Never” implies a sense of hopelessness and finality. When you use “never,” you’re telling your spouse that they are no good, will never be any good and that there’s no hope for change. It’s an all-or-nothing phrase that does not lend itself to listening, compromising and creating good will. 2. ”Always.”  “Always” implies a sense of rigidity and righteousness. When you use “always,” you’re telling your spouse that they are wrong, you are right, and that there’s nothing that can be done about it. It’s also an all-or-nothing phrase, and it does not lend itself to understanding, learning, or healing. 3. ”But.”  “But” implies a sense of manipulation and a lack of integrity. When you use “but,” you negate whatever was said before. It invalidates your message and turns a positive statement into a negative one. It’s a conjunction that does not lend itself to building trust, credibility and intimacy. Similar words to avoid include “however” and “although.” 4. ”*#%&.”  Use your imagination and fill in the blanks and what you’re left with is a vulgar, obscenity-laced attack. Any way you look at it, attacking your spouse by name-calling will cause irreparable damage. Doing this regularly will surely destroy your spouse’s soul and kill the marriage. Outright contempt has no place in a marriage. 5. ”Divorce” or “Breakup.”  Threatening to divorce or break-up, suggesting divorce as an option, or accusing your spouse of destroying the marriage will lead to just that. A divorce is a very serious decision, and using it as a weapon or method of control creates anxiety and despair. It’s not conducive for effective communication, conflict resolution, problem solving, or intimacy. Take the time to think about the impact of your words before you speak to your spouse. Consider what you want to create with the communication. Create a powerful and loving intention rather than one that is meant to hurt, control, scare or push away the person youlove. Find words that are conducive to creating intimacy. These might include phrases like, “I notice that when I [blank], you react by [blank]. When you do [blank], I feel [blank]. It would mean a lot to me if you would [blank], because when you do, I feel [blank].” And: “I want our marriage to feel good to both of us. How can we approach things in a way that makes us both feel heard, appreciated, accepted, and loved?” Learning new ways of communicating and relating to each other is not easy. Couples get trapped into certain ways of relating that have been established early on in the relationship.

Because men who are cultural minorities make up the majority of the population with HIV, prevention/intervention programs must adjust to address minority ethnic groups....

No, this isn't about the Cincinnati IRS holding up applications for non-profit status filed by certain conservative organizations. This is about the employees in a different department at the IRS Cincinnati office. You may recall that the IRS sent us a huge bill for an issue stemming from a supposed paperwork error that we believe occurred on their end. It was all about a missing one-page form that they said wasn't filed, but we have a copy and say it...

by Anthony M. Buckley, Janice Spencer, Lindsay M. Maclellan, Denise Candlish, June J. Irvine, Gillian R. Douce Clostridium difficile is the most commonly associated cause of antibiotic associated disease (AAD), which caused ?21,000 cases of AAD in 2011 in the U.K. alone. The golden Syrian hamster model of CDI is an acute model displaying many of the clinical features of C. difficile disease. Using this model we characterised three clinical strains of C. difficile, all differing in toxinotype; CD1342 (PaLoc negative), M68 (toxinotype VIII) & BI-7 (toxinotype III). The naturally occurring non-toxic strain colonised all hamsters within 1-day post challenge (d.p.c.) with high-levels of spores being shed in the faeces of animals that appeared well throughout the entire experiment. However, some changes including increased neutrophil influx and unclotted red blood cells were observed at early time points despite the fact that the known C. difficile toxins (TcdA, TcdB and CDT) are absent from the genome. In contrast, hamsters challenged with strain M68 resulted in a 45% mortality rate, with those that survived challenge remaining highly colonised. It is currently unclear why some hamsters survive infection, as bacterial & toxin levels and histology scores were similar to those culled at a similar time-point. Hamsters challenged with strain BI-7 resulted in a rapid fatal infection in 100% of the hamsters approximately 26 hr post challenge. Severe caecal pathology, including transmural neutrophil infiltrates and extensive submucosal damage correlated with high levels of toxin measured in gut filtrates ex vivo. These data describes the infection kinetics and disease outcomes of 3 clinical C. difficile isolates differing in toxin carriage and provides additional insights to the role of each toxin in disease progression.

by Asier González, Carlos Casado, Joaquín Ariño, Antonio Casamayor Ptc6 is one of the seven components (Ptc1-Ptc7) of the protein phosphatase 2C family in the yeast Saccharomyces cerevisiae. In contrast to other type 2C phosphatases, the cellular role of this isoform is poorly understood. We present here a comprehensive characterization of this gene product. Cells lacking Ptc6 are sensitive to zinc ions, and somewhat tolerant to cell-wall damaging agents and to Li+. Ptc6 mutants are sensitive to rapamycin, albeit to lesser extent than ptc1 cells. This phenotype is not rescued by overexpression of PTC1 and mutation of ptc6 does not reproduce the characteristic genetic interactions of the ptc1 mutation with components of the TOR pathway, thus suggesting different cellular roles for both isoforms. We show here that the rapamycin-sensitive phenotype of ptc6 cells is unrelated to the reported role of Pt6 in controlling pyruvate dehydrogenase activity. Lack of Ptc6 results in substantial attenuation of the transcriptional response to rapamycin, particularly in the subset of repressed genes encoding ribosomal proteins or involved in rRNA processing. In contrast, repressed genes involved in translation are Ptc6-independent. These effects cannot be attributed to the regulation of the Sch9 kinase, but they could involve modulation of the binding of the Ifh1 co-activator to specific gene promoters.

by Isabel Fofana, Fei Xiao, Christine Thumann, Marine Turek, Laetitia Zona, Rajiv G. Tawar, Fritz Grunert, John Thompson, Mirjam B. Zeisel, Thomas F. Baumert Background and Aims Hepatitis C virus (HCV) infection is a challenge to prevent and treat because of the rapid development of drug resistance and escape. Viral entry is required for initiation, spread, and maintenance of infection, making it an attractive target for antiviral strategies. Methods Using genetic immunization, we produced four monoclonal antibodies (mAbs) against the HCV host entry factor CD81. The effects of antibodies on inhibition of HCV infection and dissemination were analyzed in HCV permissive human liver cell lines. Results The anti-CD81 mAbs efficiently inhibited infection by HCV of different genotypes as well as a HCV escape variant selected during liver transplantation and re-infecting the liver graft. Kinetic studies indicated that anti-CD81 mAbs target a post-binding step during HCV entry. In addition to inhibiting cell-free HCV infection, one antibody was also able to block neutralizing antibody-resistant HCV cell-cell transmission and viral dissemination without displaying any detectable toxicity. Conclusion A novel anti-CD81 mAb generated by genetic immunization efficiently blocks HCV spread and dissemination. This antibody will be useful to further unravel the role of virus-host interactions during HCV entry and cell-cell transmission. Furthermore, this antibody may be of interest for the development of antivirals for prevention and treatment of HCV infection.

by Martin J. Larsen, Torben A. Kruse, Qihua Tan, Anne-Vibeke Lænkholm, Martin Bak, Anne E. Lykkesfeldt, Kristina P. Sørensen, Thomas v. O. Hansen, Bent Ejlertsen, Anne-Marie Gerdes, Mads Thomassen Pathogenic germline mutations in BRCA1 or BRCA2 are detected in less than one third of families with a strong history of breast cancer. It is therefore expected that mutations still remain undetected by currently used screening methods. In addition, a growing number of BRCA1/2 sequence variants of unclear pathogen significance are found in the families, constituting an increasing clinical challenge. New methods are therefore needed to improve the detection rate and aid the interpretation of the clinically uncertain variants. In this study we analyzed a series of 33 BRCA1, 22 BRCA2, and 128 sporadic tumors by RNA profiling to investigate the classification potential of RNA profiles to predict BRCA1/2 mutation status. We found that breast tumors from BRCA1 and BRCA2 mutation carriers display characteristic RNA expression patterns, allowing them to be distinguished from sporadic tumors. The majority of BRCA1 tumors were basal-like while BRCA2 tumors were mainly luminal B. Using RNA profiles, we were able to distinguish BRCA1 tumors from sporadic tumors among basal-like tumors with 83% accuracy and BRCA2 from sporadic tumors among luminal B tumors with 89% accuracy. Furthermore, subtype-specific BRCA1/2 gene signatures were successfully validated in two independent data sets with high accuracies. Although additional validation studies are required, indication of BRCA1/2 involvement (“BRCAness”) by RNA profiling could potentially be valuable as a tool for distinguishing pathogenic mutations from benign variants, for identification of undetected mutation carriers, and for selecting patients sensitive to new therapeutics such as PARP inhibitors.

by Sae-Won Han, Hwang-Phill Kim, Jong-Yeon Shin, Eun-Goo Jeong, Won-Chul Lee, Kyung-Hun Lee, Jae-Kyung Won, Tae-Yong Kim, Do-Youn Oh, Seock-Ah Im, Yung-Jue Bang, Seung-Yong Jeong, Kyu Joo Park, Jae-Gahb Park, Gyeong Hoon Kang, Jeong-Sun Seo, Jong-Il Kim, Tae-You Kim Recent advance in sequencing technology has enabled comprehensive profiling of genetic alterations in cancer. We have established a targeted sequencing platform using next-generation sequencing (NGS) technology for clinical use, which can provide mutation and copy number variation data. NGS was performed with paired-end library enriched with exons of 183 cancer-related genes. Normal and tumor tissue pairs of 60 colorectal adenocarcinomas were used to test feasibility. Somatic mutation and copy number alteration were analyzed. A total of 526 somatic non-synonymous sequence variations were found in 113 genes. Among these, 278 single nucleotide variations were 232 different somatic point mutations. 216 SNV were 79 known single nucleotide polymorphisms in the dbSNP. 32 indels were 28 different indel mutations. Median number of mutated gene per tumor was 4 (range 0–23). Copy number gain (>X2 fold) was found in 65 genes in 40 patients, whereas copy number loss (APC in 35 patients (58%), TP53 in 34 (57%), and KRAS in 24 (40%). Altered gene list revealed ErbB signaling pathway as the most commonly involved pathway (25 patients, 42%). Targeted sequencing platform using NGS technology is feasible for clinical use and provides comprehensive genetic alteration data.

by Atsushi Yasukawa, Koa Hosoki, Masaaki Toda, Yasushi Miyake, Yuki Matsushima, Takahiro Matsumoto, Daniel Boveda-Ruiz, Paloma Gil-Bernabe, Mizuho Nagao, Mayumi Sugimoto, Yukiko Hiraguchi, Reiko Tokuda, Masahiro Naito, Takehiro Takagi, Corina N. D'Alessandro-Gabazza, Shigeru Suga, Tetsu Kobayashi, Takao Fujisawa, Osamu Taguchi, Esteban C. Gabazza Eosinophilic inflammation and remodeling of the airways including subepithelial fibrosis and myofibroblast hyperplasia are characteristic pathological findings of bronchial asthma. Epithelial to mesenchymal transition (EMT) plays a critical role in airway remodelling. In this study, we hypothesized that infiltrating eosinophils promote airway remodelling in bronchial asthma. To demonstrate this hypothesis we evaluated the effect of eosinophils on EMT by in vitro and in vivo studies. EMT was assessed in mice that received intra-tracheal instillation of mouse bone marrow derived eosinophils and in human bronchial epithelial cells co-cultured with eosinophils freshly purified from healthy individuals or with eosinophilic leukemia cell lines. Intra-tracheal instillation of eosinophils was associated with enhanced bronchial inflammation and fibrosis and increased lung concentration of growth factors. Mice instilled with eosinophils pre-treated with transforming growth factor(TGF)-?1 siRNA had decreased bronchial wall fibrosis compared to controls. EMT was induced in bronchial epithelial cells co-cultured with human eosinophils and it was associated with increased expression of TGF-?1 and Smad3 phosphorylation in the bronchial epithelial cells. Treatment with anti-TGF-?1 antibody blocked EMT in bronchial epithelial cells. Eosinophils induced EMT in bronchial epithelial cells, suggesting their contribution to the pathogenesis of airway remodelling.