How narcissistic self-construction sabotages their relationships: Accuracy and bias in partner perception

Trapped by their superordinate goal to maintain a grandiose self, narcissists navigate their relationships wishing to re-assure themselves of their specialness and superiority, using strategies bound to fail. Dyadic analyses of diary data (14 days, 83 couples) showed that narcissists focus on their partners’ shortcomings, becoming experts at detecting negative forms of support, while simultaneously minimizing their partner’s positive intentions. Partners of narcissists, in contrast, appear to have a positive bias in ongoing relationships and seem to compensate for some of the narcissists’ shortcomings. Narcissists’ focus on their own selfconstruction purposes also extends to their parenting roles. In a retrospective study, narcissistic mothers were found to demand superior performance, desiring to show-off their child, yet concurrently attributing their child’s success to themselves. They also exercise psychological control and role-reversal, requiring the child to cater to their needs, and to admire them, while simultaneously oblivious to their child’s needs and desires.

The Vacuolar H+-ATPase B1 Subunit Polymorphism p.E161K Associates with Impaired Urinary Acidification in Recurrent Stone Formers

Mutations in the vacuolar–type H+-ATPase B1 subunit gene ATP6V1B1 cause autosomal–recessive distal renal tubular acidosis (dRTA). We previously identified a single-nucleotide polymorphism (SNP) in the human B1 subunit (c.481G.A; p.E161K) that causes greatly diminished pump function in vitro. To investigate the effect of this SNP on urinary acidification, we conducted a genotype-phenotype analysis of recurrent stone formers in theDallas and Bern kidney stone registries. Of 555 patients examined, 32 (5.8%) were heterozygous for the p.E161K SNP, and the remaining 523 (94.2%) carried two wild–type alleles. After adjustment for sex, age, body mass index, and dietary acid and alkali intake, p.E161K SNP carriers had a nonsignificant tendency to higher urinary pH on a random diet (6.31 versus 6.09; P=0.09). Under an instructed low–Ca and low–Na diet, urinary pH was higher in p.E161K SNP carriers (6.56 versus 6.01; P,0.01). Kidney stones of p.E161K carriers were more likely to contain calcium phosphate than stones of wild-type patients. In acute NH4Cl loading, p.E161K carriers displayed a higher trough urinary pH (5.34 versus 4.89; P=0.01) than wild-type patients. Overall, 14.6% of wild-type patients and 52.4% of p.E161K carriers were unable to acidify their urine below pH 5.3 and thus, can be considered to have incomplete dRTA. In summary, our data indicate that recurrent stone formers with the vacuolar H+-ATPase B1 subunit p.E161K SNP exhibit a urinary acidification deficit with an increased prevalence of calcium phosphate– containing kidney stones. The burden of E161K heterozygosity may be a forme fruste of dRTA.

Response profiles of murine spiral ganglion neurons on multi-electrode arrays.

OBJECTIVE Cochlear implants (CIs) have become the gold standard treatment for deafness. These neuroprosthetic devices feature a linear electrode array, surgically inserted into the cochlea, and function by directly stimulating the auditory neurons located within the spiral ganglion, bypassing lost or not-functioning hair cells. Despite their success, some limitations still remain, including poor frequency resolution and high-energy consumption. In both cases, the anatomical gap between the electrode array and the spiral ganglion neurons (SGNs) is believed to be an important limiting factor. The final goal of the study is to characterize response profiles of SGNs growing in intimate contact with an electrode array, in view of designing novel CI devices and stimulation protocols, featuring a gapless interface with auditory neurons. APPROACH We have characterized SGN responses to extracellular stimulation using multi-electrode arrays (MEAs). This setup allows, in our view, to optimize in vitro many of the limiting interface aspects between CIs and SGNs. MAIN RESULTS Early postnatal mouse SGN explants were analyzed after 6-18 days in culture. Different stimulation protocols were compared with the aim to lower the stimulation threshold and the energy needed to elicit a response. In the best case, a four-fold reduction of the energy was obtained by lengthening the biphasic stimulus from 40 μs to 160 μs. Similarly, quasi monophasic pulses were more effective than biphasic pulses and the insertion of an interphase gap moderately improved efficiency. Finally, the stimulation with an external electrode mounted on a micromanipulator showed that the energy needed to elicit a response could be reduced by a factor of five with decreasing its distance from 40 μm to 0 μm from the auditory neurons. SIGNIFICANCE This study is the first to show electrical activity of SGNs on MEAs. Our findings may help to improve stimulation by and to reduce energy consumption of CIs and thereby contribute to the development of fully implantable devices with better auditory resolution in the future.

Disease evolution and outcomes in familial AML with germline CEBPA mutations

In-depth molecular investigation of familial leukemia has been limited by the rarity of recognized cases. This study examines the genetic events initiating leukemia and details the clinical progression of disease across multiple families harboring germ-line CEBPA mutations. Clinical data were collected from 10 CEBPA-mutated families, representing 24 members with acute myeloid leukemia (AML). Whole-exome (WES) and deep sequencing were performed to genetically profile tumors and define patterns of clonal evolution. Germline CEBPA mutations clustered within the N-terminal and were highly penetrant, with AML presenting at a median age of 24.5 years (range, 1.75-46 years). In all diagnostic tumors tested (n = 18), double CEBPA mutations (CEBPAdm) were detected, with acquired (somatic) mutations preferentially targeting the C-terminal. Somatic CEBPA mutations were unstable throughout the disease course, with different mutations identified at recurrence. Deep sequencing of diagnostic and relapse paired samples confirmed that relapse-associated CEBPA mutations were absent at diagnosis, suggesting recurrence was triggered by novel, independent clones. Integrated WES and deep sequencing subsequently revealed an entirely new complement of mutations at relapse, verifying the presentation of a de novo leukemic episode. The cumulative incidence of relapse in familial AML was 56% at 10 years (n = 11), and 3 patients experienced ≥3 disease episodes over a period of 17 to 20 years. Durable responses to secondary therapies were observed, with prolonged median survival after relapse (8 years) and long-term overall survival (10-year overall survival, 67%). Our data reveal that familial CEBPA-mutated AML exhibits a unique model of disease progression, associated with favorable long-term outcomes.

What’s the best method? Comparison of different short forms oft he Pathological Narcissism Inventory

Recent research emphasizes the various facets of narcissism. As a consequence, newly developed questionnaires for narcissism have a large number of subscales and items. However, for the daily use in research and practice, short measures are crucial. In this study we compare different short forms of the Pathological Narcissism Questionnaire, a 54 item measure with seven subscales. In different samples (total N>2000) we applied different theoretical models to construct short forms of approximately 20 items. In particular, we compared IRT, item-total correlation, and factor loading based short forms and versions based on content validity and random selection. In all versions the original subscale structure was preserved. Results show that the short forms all have high correlations with the original version. Furthermore, correlations with criterion validation measures were comparable. We conclude that the item number can be reduced substantially without loosing information. Pros and cons of the different reduction methods are discussed.

How to measure Narcissism – an ongoing discussion

Over the last decades, research on narcissism was dominated with a focus on grandiose narcissism as measured by the NPI (Raskin & Terry, 1988), however, recent discussions emphasize the broad range of manifestations of narcissism, in particular more vulnerable aspects. As a result, new questionnaires were developed to cover the full range of these aspects. One example is the Pathological Narcissism Scale (PNI, Pincus et al. 2009), a 52 item questionnaire with seven subscales covering both grandiose and vulnerable aspects. Validation studies show that narcissism as measured with the PNI differs substantially from narcissism as measured with the NPI. Moreover, a discussion concerning the composition of grandiose and vulnerable narcissism has evolved from these data. In our study we demonstrate how scores on narcissism and narcissism subtypes are associated with a broad variety of personality and clinical measures. In a sample of 1837 participants (1240 female, 597 male; mean age 26.8 years) we investigated the correlation patterns of both PNI and NPI subscales with constructs like FFM, aggression, emotions, clinical symptoms, and well-being. Results show that the assignment of subscales to grandiose and vulnerable subtypes are not unambiguous. We therefore conclude that the decision of how to measure narcissism needs further investigation.

Hepatitis B Infection, Viral Load and Resistance in HIV-Infected Patients in Mozambique and Zambia.

BACKGROUND Few data on the virological determinants of hepatitis B virus (HBV) infection are available from southern Africa. METHODS We enrolled consecutive HIV-infected adult patients initiating antiretroviral therapy (ART) at two urban clinics in Zambia and four rural clinics in Northern Mozambique between May 2013 and August 2014. HBsAg screening was performed using the Determine® rapid test. Quantitative real-time PCR and HBV sequencing were performed in HBsAg-positive patients. Risk factors for HBV infection were evaluated using Chi-square and Mann-Whitney tests and associations between baseline characteristics and high level HBV replication explored in multivariable logistic regression. RESULTS Seventy-eight of 1,032 participants in Mozambique (7.6%, 95% confidence interval [CI]: 6.1-9.3) and 90 of 797 in Zambia (11.3%, 95% CI: 9.3-13.4) were HBsAg-positive. HBsAg-positive individuals were less likely to be female compared to HBsAg-negative ones (52.3% vs. 66.1%, p<0.001). Among 156 (92.9%) HBsAg-positive patients with an available measurement, median HBV viral load was 13,645 IU/mL (interquartile range: 192-8,617,488 IU/mL) and 77 (49.4%) had high values (>20,000 UI/mL). HBsAg-positive individuals had higher levels of ALT and AST compared to HBsAg-negative ones (both p<0.001). In multivariable analyses, male sex (adjusted odds ratio: 2.59, 95% CI: 1.22-5.53) and CD4 cell count below 200/μl (2.58, 1.20-5.54) were associated with high HBV DNA. HBV genotypes A1 (58.8%) and E (38.2%) were most prevalent. Four patients had probable resistance to lamivudine and/or entecavir. CONCLUSION One half of HBsAg-positive patients demonstrated high HBV viremia, supporting the early initiation of tenofovir-containing ART in HIV/HBV-coinfected adults.

Allogeneic haematopoietic stem cell transplantation for mitochondrial neurogastrointestinal encephalomyopathy.

Haematopoietic stem cell transplantation has been proposed as treatment for mitochondrial neurogastrointestinal encephalomyopathy, a rare fatal autosomal recessive disease due to TYMP mutations that result in thymidine phosphorylase deficiency. We conducted a retrospective analysis of all known patients suffering from mitochondrial neurogastrointestinal encephalomyopathy who underwent allogeneic haematopoietic stem cell transplantation between 2005 and 2011. Twenty-four patients, 11 males and 13 females, median age 25 years (range 10-41 years) treated with haematopoietic stem cell transplantation from related (n = 9) or unrelated donors (n = 15) in 15 institutions worldwide were analysed for outcome and its associated factors. Overall, 9 of 24 patients (37.5%) were alive at last follow-up with a median follow-up of these surviving patients of 1430 days. Deaths were attributed to transplant in nine (including two after a second transplant due to graft failure), and to mitochondrial neurogastrointestinal encephalomyopathy in six patients. Thymidine phosphorylase activity rose from undetectable to normal levels (median 697 nmol/h/mg protein, range 262-1285) in all survivors. Seven patients (29%) who were engrafted and living more than 2 years after transplantation, showed improvement of body mass index, gastrointestinal manifestations, and peripheral neuropathy. Univariate statistical analysis demonstrated that survival was associated with two defined pre-transplant characteristics: human leukocyte antigen match (10/10 versus <10/10) and disease characteristics (liver disease, history of gastrointestinal pseudo-obstruction or both). Allogeneic haematopoietic stem cell transplantation can restore thymidine phosphorylase enzyme function in patients with mitochondrial neurogastrointestinal encephalomyopathy and improve clinical manifestations of mitochondrial neurogastrointestinal encephalomyopathy in the long term. Allogeneic haematopoietic stem cell transplantation should be considered for selected patients with an optimal donor.

GLUCAGON GENE EXPRESSION: ANALYSIS OF PREPROGLUCAGON

Glucagon is a 29 amino acid polypeptide hormone produced in the (alpha) cells of the pancreatic islets. The purpose of this research was to understand better the role of glucagon in the regulation of metabolic processes. As with other polypeptide hormones, the synthesis of glucagon is thought to involve a larger precursor, which is then enzymatically cleaved to the functional form. The specific research objectives were to obtain cloned copies of the messenger RNA (mRNA) for pancreatic glucagon, to determine their primary sequences, and from this coding information to deduce the amino acid sequence of the initial glucagon precursor. From this suggested preproglucagon sequence and prior information on possible proglucagon intermediate processing products, the overall objective of this research is to propose a possible pathway for the biosynthesis of pancreatic glucagon.^ Synthetic oligodeoxynucleotide probes of 14-nucleotides (14-mer) and 17-nucleotides (a 17-mer) complementary to codons specifying a unique sequence of mature glucagon were synthesized. The ('32)P-labeled-14-mer was hybridized with size-fractionated fetal bovine pancreatic poly(A('+))RNA bound to nitrocellulose. RNA fractions of (TURN)14S were found to hybridize specifically, resulting in an (TURN)10-fold enrichment for these sequences. These poly(A('+))RNAs were translated in a cell-free system and the products analyzed by gel electrophoresis. The translation products were found to be enriched for a protein of the putative size of mammalian preproglucagon ((TURN)21 kd). These enriched RNA fractions were used to construct a complementary DNA (cDNA) library is plasmid pBR322.^ Screening of duplicate colony filters with the ('32)P-labeled-17-mer and a ('32)P-labeled-17-mer-primed cDNA probe indicated 25 possible glucagon clones from 3100 colonies screened. Restriction mapping of 6 of these clones suggested that they represented a single mRNA species. Primary sequence analysis of one clone containing a 1200 base pair DNA insert revealed that it contained essentially a full-length copy of glucagon cDNA.^ Analaysis of the cDNA suggested that it encoded an initial translation product of 180 amino acids with an M(,r) = 21 kd. The first initiation codon (ATG, methionine) followed by the longest open reading frame of 540 nucleotides was preceded by a 5'-untranslated region of 90 nucleotides, and was followed by a longer 3'-untranslated region of 471 nucleotides, resulting in a total of 1101 nucleotides. . . . (Author's abstract exceeds stipulated maximum length. Discontinued here with permission of author.) UMI ^

Physician adoption of a practice guideline: Effect on the cost of medical care for adult patients with diabetes

In the demanding environment of healthcare reform, reduction of unwanted physician practice variation is promoted, often through evidence-based guidelines. Guidelines represent innovations that direct change(s) in physician practice; however, compliance has been disappointing. Numerous studies have analyzed guideline development and dissemination, while few have evaluated the consequences of guideline adoption. The primary purpose of this study was to explore and analyze the relationship between physician adoption of the glycated hemoglobin test guideline for management of adult patients with diabetes, and the cost of medical care. The study also examined six personal and organizational characteristics of physicians and their association with innovativeness, or adoption of the guideline. ^ Cost was represented by approved charges from a managed care claims database. Total cost, and diabetes and related complications cost, first were compared for all patients of adopter physicians with those of non-adopter physicians. Then, data were analyzed controlling for disease severity based on insulin dependency, and for high cost cases. There was no statistically significant difference in any of eight cost categories analyzed. This study represented a twelve-month period, and did not reflect cost associated with future complications known to result from inadequate management of glycemia. Guideline compliance did not increase annual cost, which, combined with the future benefit of glycemic control, lends support to the cost effectiveness of the guideline in the long term. Physician adoption of the guideline was recommended to reduce the future personal and economic burden of this chronic disease. ^ Only half of physicians studied had adopted the glycated hemoglobin test guideline for at least 75% of their diabetic patients. No statistically significant relationship was found between any physician characteristic and guideline adoption. Instead, it was likely that the innovation-decision process and guideline dissemination methods were most influential. ^ A multidisciplinary, multi-faceted approach, including interventions for each stage of the innovation-decision process, was proposed to diffuse practice guidelines more effectively. Further, it was recommended that Organized Delivery Systems expand existing administrative databases to include clinical information, decision support systems, and reminder mechanisms, to promote and support physician compliance with this and other evidence-based guidelines. ^

The role of LMX1B and PITX2 in anterior segment development and adult ocular function

Several congenital syndromes associated with anterior segment (AS) anomalies can lead to impaired vision and glaucoma, such as nail-patella syndrome (NPS), caused by mutations in the LIM homeodomain transcription factor LMX1B and Axenfeld-Rieger's syndrome (ARS), caused by mutations in the bicoid-related homeodomain transcription factor PITX2. Targeted mutations in lmx1b and pitx2 and RNA in situ analysis reveal that both genes are required for AS development and are co-expressed within the periocular mesenchyme, suggesting they participate in a shared genetic pathway. Lmx1b homozygous mutants display iris and corneal stroma hypoplasia, and defects in ciliary body formation. In contrast, pitx2 homozygous mutants exhibit a more severe phenotype: the AS chamber, corneal endothelium, and extraocular muscles (EOM) fail to develop. The absence of EOM in pitx2 mutants suggests pitx2 acts upstream of lmx1b, or that other lmx1b family members, such as lmx1a, can compensate for lmx1b function. Lmxla/lmx1b double homozygous mutants have a reduced capacity to generate EOM, implying that lmx1 gene products have a redundant function in EOM development and that lmx1 family members may act downstream of pitx2. However, analysis of pitx2 expression in the AS tissues of lmx1b mutants and reciprocal studies of lmx1b expression in pitx2 mutants indicate that these genes do not function in a simple linear pathway. Instead, lmx1b and pitx2 may regulate a shared set of downstream targets or both genes may work in parallel transcribing unique targets required for a common biological process. Ultrastructural analysis of lmx1b and pitx2 mutant corneas indicates that collagen fibrillogenesis is perturbed, revealing a common role for both genes in the deposition of extracellular matrix. Furthermore, lmx1b/pitx2 double heterozygotes develop corneal opacities not observed in single heterozygotes demonstrating that lmx1b and pitx2 genetically interact. Data suggests that defects in the basement membrane of the corneal endothelium underlie the opacities observed in double heterozygotes. Additionally, double heterozygotes develop anterior synechias that occlude the trabecular meshwork, potentially blocking aqueous humor drainage. These data suggest that lmx1b and pitx2 are responsible for ECM deposition in multiple cell types and imply that such defects may contribute to the glaucomas observed in NPS and ARS patients. ^

Na 1 Nachlass Max Horkheimer, 563 - Korrespondenzen u.a. mit Alice H. Maier und Leo Löwenthal (p. VI 27, 1-253)

Briefwechsel zwischen Max Horkheimer und Alice H. Maier; 5 Briefe an Maurice und Carolyn Tumarkin von Max Horkheimer, 1957/1964; 1 Brief von Max Horkheimer an Charles Gorman, 27.04.1957; 1 Brief von Alice H. Maier an die Marquis Company (Chicago), 06.05.1957; 2 Briefe an H. P. Edelman von Max Horkheimer, 1964; 3 Briefe zwischen Alice H. Maier und H. P. Edelman, 1957/1963; 1 Brief von Margot von Mendelssohn an Alice H. Maier, 01.04.1957; 1 Brief an Richard Corwine Stevenson von Max Horkheimer, 16.03.1957; 1 Brief von Max Horkheimer an Inge Aicher-Scholl, 26.02.1957; 1 Brief an Herman Strasburger von Max Horkheimer, 21.01.1957; 1 Brief von Elisabeth Richter an Alice H. Maier, [1957]; 1 Brief an den Director of International Operations (Washington) von Chauncy D. Harris, 05.02.1957; 1 Brief von Alice H. Maier an Comptroller of Customs (New York), 11.01.1957; 1 Brief an Herbert Marcuse von Alice H. Maier, 14.01.1957; 2 Briefe zwischen Alice H. Maier und The Saturday Evening Post (Philadelphia), Oktober 1956; 1 Brief an die Staats-Herold Corporation (Woodside) von Alice H. Maier, 24.09.1956; 2 Briefe zwischen Alice H. Maier und Werner Thönnessen, 1956; 2 Briefe zwischen dem National Better Business Bureau (New York) und Alice H. Maier, 1956; 2 Briefe zwischen Alice H. Maier und Herman L. Filene, Januar 1956; 5 Briefe zwischen Max Horkheimer und Edwin J. Lukas, 1962 - 1963; 7 Briefe zwischen Monroe Karasik und Max Horkheimer, 1963; 1 Brief von Max Horkheimer an James Conant, 30.05.1963; 1 Brief an John J. McCloy von Max Horkheimer, 30.05.1963; 3 Briefe an Herman S. Klein von Alice H. Maier, 1960/1963; 1 Brief von Max Horkheimer an Hartley Chemists (New York), 06.02.1962; 1 Brief an Columbia Chemists (New York) von Max Horkheimer, 06.02.1962; 1 Brief von Max Horkheimer an A. P. Bersohn, 06.06.1962; 1 Brief an A. P. Bersohn von Alice H. Maier, 20.04.1962; 1 Brief an Alice H. Maier von Paul Kind, 22.05.1962; 1 Brief an Cyrus C. Hoffman von Alice H. Maier, 23.03.1961; 2 Briefe von Alice H. Maier an Friedrich Pollock, 1960/1966;