tbuckley/cabot-search huggingface dataset:
Stress inoculation training to control anxiety in sport: two case studies in squash.
Authors: R Mace, D Carroll
Journal: British Journal of Sports Medicine (1986)

This study arose as a result of two squash players, one male one female, seeking advice on how to improve their mental approach to playing. They both felt that their game suffered badly through too much anxiety. After preliminary interviews it was decided to use a programme of stress inoculation training to help them learn to control their anxiety. In order to obtain baseline measures of anxiety, both subjects completed a state anxiety questionnaire on five occasions, immediately prior to playing important league or team matches. They were then given eight training sessions. On completion of the training, subjects were asked to complete a further five state anxiety tests immediately prior to analogous matches. There was a considerable decrease in self-reported anxiety levels and both players reported that their performance had improved. It is argued that stress inoculation training is potentially very useful as a technique for controlling anxiety in certain competitive sports.
Comparison between maximal inspiratory pressures measured by unidirectional valve method and conventional method in healthy subjects without artificial airway
Authors: Wellington Yamaguti, Marina Lança, Karen Kimoto, Elen Oliveira, André Albuquerque, Christina Brito
Journal: European Respiratory Journal (2012)

The most used method to evaluate maximal inspiratory pressure (MIP) is by maintaining maximum negative pressure forced against an occluded airway (MIPsta). To eliminate the need for collaboration, a new technique was developed using a unidirectional expiratory valve (MIPuni) in patients undergoing invasive mechanical ventilation. The aim of this study was to compare these two methods of measurement in patients with spontaneous breathing without artificial airway. We also tested the intra- and inter-observer reproducibility of MIPuni. The study had a crossover design and twelve healthy volunteers performed the evaluation of MIP of each method in a randomized order. A digital manometer was attached to a mouthpiece (MIPsta) or facemask (MIPuni) and the maximal value in each method was considered. The MIPuni was evaluated by two independent observers (A and B), at two different times (1 st  and 2 nd  tests) with an interval of at least one week. MIPuni displayed significantly larger values than MIPsta (106.1+/-29.3 and 98.4+/-25.8, respectively; p=0.01). The MIPuni obtained by observer A was not different from that obtained by observer B for both the 1 st  test (105.9+/-30.4 and 104.3+/-26.1, respectively; p=0.32) and the 2 nd  test (105.5+/-30.1 and 102.6+/-31.7, respectively; p=0.24). The MIPuni obtained in the 1 st  and 2 nd  tests was not different for both observer A (105.9+/-30.4 and 105.5+/-30.1, respectively; p=0.13) and observer B (104.3+/-26.1 and 102.6+/-31.7, respectively; p=0,21). MIPuni is the better method for measuring MIP in individuals without artificial airway. The inter- and intra-observer measurements were similar.
MicroRNA-30 family members regulate calcium/calcineurin signaling in podocytes
Authors: Junnan Wu, Chunxia Zheng, Xiao Wang, Shifeng Yun, Yue Zhao, Lin Liu, Yuqiu Lu, Yuting Ye, Xiaodong Zhu, Changming Zhang, Shaolin Shi, Zhihong Liu
Journal: Journal of Clinical Investigation (2015)

Calcium/calcineurin signaling is critical for normal cellular physiology. Abnormalities in this pathway cause many diseases, including podocytopathy; therefore, understanding the mechanisms that underlie the regulation of calcium/calcineurin signaling is essential. Here, we showed that critical components of calcium/calcineurin signaling, including TRPC6, PPP3CA, PPP3CB, PPP3R1, and NFATC3, are the targets of the microRNA-30 family (miR-30s). We found that these 5 genes are highly expressed as mRNA, but the level of the proteins is low in normal podocytes. Conversely, protein levels were markedly elevated in podocytes from rats treated with puromycin aminonucleoside (PAN) and from patients with focal segmental glomerulosclerosis (FSGS). In both FSGS patients and PAN-treated rats, miR-30s were downregulated in podocytes. In cultured podocytes, PAN or a miR-30 sponge increased TRPC6, PPP3CA, PPP3CB, PPP3R1, and NFATC3 expression; calcium influx; intracellular Ca2+ concentration; and calcineurin activity. Moreover, NFATC3 nuclear translocation, synaptopodin degradation, integrin β3 (ITGB3) activation, and actin fiber loss, which are downstream of calcium/calcineurin signaling, were induced by miR-30 reduction but blocked by the calcineurin inhibitor FK506. Podocyte-specific expression of the miR-30 sponge in mice increased calcium/calcineurin pathway component protein expression and calcineurin activity. The mice developed podocyte foot process effacement and proteinuria, which were prevented by FK506. miR-30s also regulated calcium/calcineurin signaling in cardiomyocytes. Together, our results identify miR-30s as essential regulators of calcium/calcineurin signaling.
The Coronary Risk Personality: Psychological and Psychophysiological Aspects
Authors: L.J.P van Doornen
Journal: Psychotherapy and Psychosomatics (1980)

The hypothesis was tested that psychophysiological features of the Coronary Risk Personality (CRP) already are clearly discernable before myocardial infarction (MI). Psychological test assessments were obtained from a group of 46 male MI patients, and a group of 78 'Healthy' controls, which were classified as either 'High risk' or 'Low risk' on blood pressure, serum cholesterol, and/or smoking. Psychophysiological measurements were also taken. The crucial features of the CRP appear to be: the impatience and activity dimensions of type A behavior, and depression; the mediating physiological mechanism with regard to infarction risk possibly is sympathetic reactivity.
Tumor-Derived Chemokine CCL5 Enhances TGF-β–Mediated Killing of CD8+ T Cells in Colon Cancer by T-Regulatory Cells
Authors: Li-Yuan Chang, Yung-Chang Lin, Jayashri Mahalingam, Ching-Tai Huang, Ten-Wen Chen, Chiao-Wen Kang, Hui-Min Peng, Yu-Yi Chu, Jy-Ming Chiang, Avijit Dutta, Yuan-Ji Day, Tse-Ching Chen, Chau-Ting Yeh, Chun-Yen Lin
Journal: Cancer Research (2012)

Abstract Chemokine CCL5/RANTES is highly expressed in cancer where it contributes to inflammation and malignant progression. In this study, we show that CCL5 plays a critical role in immune escape in colorectal cancer. We found that higher levels of CCL5 expression in human and murine colon tumor cells correlated with higher levels of apoptosis of CD8+ T cells and infiltration of T-regulatory cells (Treg). In mouse cells, RNA interference (RNAi)-mediated knockdown of CCL5 delayed tumor growth in immunocompetent syngeneic hosts but had no effect on tumor growth in immunodeficient hosts. Reduced tumor growth was correlated with a reduction in Treg infiltration and CD8+ T-cell apoptosis in tumors. Notably, we found that CCL5 enhanced the cytotoxicity of Treg against CD8+ T cells. We also found tumor growth to be diminished in mice lacking CCR5, a CCL5 receptor, where a similar decrease in both Treg cell infiltration and CD8+ T-cell apoptosis was noted. TGF-β signaling blockade diminished apoptosis of CD8+ T cells, implicating TGF-β as an effector of CCL5 action. In support of this concept, CCL5 failed to enhance the production of TGF-β by CCR5-deficient Treg or to enhance their cytotoxic effects against CD8+ T cells. CCR5 signaling blockade also diminished the in vivo suppressive capacity of Treg in inhibiting the antitumor responses of CD8+ T cells, in the same way as CCL5 signaling blockade. Together, our findings establish that CCL5/CCR5 signaling recruits Treg to tumors and enhances their ability to kill antitumor CD8+ T cells, thereby defining a novel mechanism of immune escape in colorectal cancer. Cancer Res; 72(5); 1092–102. ©2012 AACR.
Shape Differences in the Corpus Callosum in First-Episode Schizophrenia and First-Episode Psychotic Affective Disorder
Authors: Melissa Frumin, Polina Golland, Ron Kikinis, Yoshio Hirayasu, Dean F. Salisbury, John Hennen, Chandlee C. Dickey, Mark Anderson, Ferenc A. Jolesz, W. Eric L. Grimson, Robert W. McCarley, Martha E. Shenton
Journal: American Journal of Psychiatry (2002)

The corpus callosum, the largest white matter tract in the brain, is a midline structure associated with the formation of the hippocampus, septum pellucidum, and cingulate cortex, which have been implicated in the pathogenesis of schizophrenia. Corpus callosum shape deformation, therefore, may reflect a midline neurodevelopmental abnormality.Corpus callosum area and shape were analyzed in 14 first-episode psychotic patients with schizophrenia, 19 first-episode psychotic patients with affective disorder, and 18 normal comparison subjects.No statistically significant corpus callosum area differences between groups were found, but there were differences in the structure's shape between the patients with schizophrenia and the comparison subjects. A correlation between width and angle of the corpus callosum was found in patients with affective disorder.Corpus callosum shape abnormalities in first-episode psychotic patients with schizophrenia may reflect a midline neurodevelopmental abnormality.
Enhanced Contractile Mechanisms in Vasospasm
Authors: Kathryn G. Lamping
Journal: Circulation (2002)

he importance of the endothelium in regulating vascular tone and reactivity is well recognized.The endothelium produces a variety of substances including nitric oxide (NO), prostaglandins, endothelin-1, and an unidentified hyperpolarization factor that control vascular tone, thrombus formation, platelet and leukocyte adhesion and aggregation, and cellular proliferation.Alterations in the synthesis or activity of these substances appear to play a major role in the pathogenesis of a variety of diseases.Emphasis has been placed on alterations in the generation and function of NO as an underlying mechanism for abnormal vascular reactivity in atherosclerosis and other vascular diseases.Studies in both animal models and humans demonstrate that NO-mediated responses are decreased in atherosclerosis, diabetes, and a wide variety of vascular diseases.But measurements of NO in atherosclerosis have produced variable results with decreases 1 and increases 2 in the levels of NO reported.Inactivation of NO by reactive oxygen species may account for the decrease in NO-mediated responses.
FURTHER INVESTIGATIONS ON THE ORIGIN OF TUMORS IN MICE
Authors: A. E. C. Lathrop, Leo Loeb
Journal: The Journal of Experimental Medicine (1915)

1. In crossing strains known to diner in their tumor rates, the hybrids show in a considerable number of cases a tumor rate corresponding to the parent with a high tumor incidence; in some cases the offspring have the tumor rate of the parent with the low tumor incidence; in certain cases the tumor rate of the offspring is intermediate between those of the parents. That these results are not accidental follows from the fact that we could show in some cases that two sisters crossed with the same strains or with the same male give similar offspring, and in other cases we could show that the same individual crossed successively with two strains that behave similarly produces hybrids with a similar tumor incidence. 2. There exists some evidence for the conclusion that different strains in being crossed with other strains differ in their power to impress their tumor rate upon the crosses. Thus the English strain and the I and II daughters of No. 10 have the tendency to transmit to the offspring a high tumor rate, while Cream, Silver, and some European other than 151 have a tendency to transmit a low tumor rate. While crosses of these daughters of No. 10 with European 151 or with No. 8(1/2) show the high tumor rate of the mothers, the crosses of one of the same females with Cream or Silver show an intermediate tumor rate. 3. We find further evidence for our conclusion previously stated that age class, of the tumors and tumor rate are not dependent on the same factor. The age class enters into the crosses as a factor independent of the tumor rate. Thus we find in the crosses between the first daughter of No. 10 and Cream, and in the crosses between the same female and English Silver a similar tumor rate, but the age classes differ in conformity with the difference in the age classes of the parents. We find, furthermore, that while in some cases a tumor rate and an age class that correspond to each other (high tumor rate, early tumors-low tumor rate, late tumors) are transmitted to the offspring, in other cases tumor rate and age class transmitted to the crosses diverge. 4. It seems that certain strains with very late tumors if mated with strains with earlier tumors have a tendency to transmit to the offspring their own tendency to very late tumors. With a certain strain lateness of the tumors seems to be dominant, while a low tumor rate is not necessarily dominant in the same crosses. This was noticeable in the crosses into which the strain European +/- 102 or 103 entered as one of the parents. 5. If both parents have a similar tumor rate the offspring have usually a similar tumor rate. There was, however, one exception to this rule in the case of the German +/- Carter mice, in which the offspring showed a much lower tumor rate and higher age class than either of the parent strains.
Alteration of Balance between Myeloid Dendritic Cells and Plasmacytoid Dendritic Cells in Peripheral Blood of Patients with Asthma
Authors: Hiroyuki Matsuda, Takafumi Suda, Hideo Hashizume, Koushi Yokomura, Kazuhiro Asada, Kenichiro Suzuki, Kingo Chida, Hirotoshi Nakamura
Journal: American Journal of Respiratory and Critical Care Medicine (2002)

Asthma, a well-known helper T cell Type 2 (Th2)-mediated disease, has a polarized immune response toward a Th2 phenotype. However, the factors causing the Th2 polarization remain to be fully determined in this disease. Dendritic cells (DCs) are the most potent antigen-presenting cells that play a central role in initiating the primary immune response. In human blood, two functional distinct subsets of DCs, myeloid DCs and plasmacytoid DCs, have been identified. Myeloid DCs (mDCs) and plasmacytoid DCs (pDCs) are also called Type 1 DCs (DC1) and Type 2 DCs (DC2), respectively, because mDCs and pDCs were shown to preferentially differentiate naive T cells into Th1 and Th2 cells, respectively. In asthma, it can thus be speculated that an altered balance of mDCs to pDCs toward pDCs may contribute to the Th2 polarization. To clarify this, we examined the numbers of mDCs and pDCs in the peripheral blood of 44 patients with asthma and 38 normal subjects, using multicolor flow cytometry. We found that the patients with asthma had a significantly higher number of pDCs, resulting in a significant decrease in the ratio of mDCs to pDCs compared with normal subjects. These data indicate that the patients with asthma had a polarization of the mDC:pDC balance toward pDCs, which may be involved in producing the Th2-dominant immune phenotype in asthma.
Serum amyloid A is a chemoattractant: induction of migration, adhesion, and tissue infiltration of monocytes and polymorphonuclear leukocytes.
Authors: R Badolato, J M Wang, W J Murphy, A R Lloyd, D F Michiel, L L Bausserman, D J Kelvin, J J Oppenheim
Journal: The Journal of Experimental Medicine (1994)

Serum amyloid A (SAA) is an acute phase protein that in the blood is bound to high density lipoproteins; SAA is secreted mainly by hepatocytes, and its concentration increases in the blood up to 1000 times during an inflammatory response. At present, its biological function is unclear. Since some forms of secondary amyloidosis are caused by deposition in tissues of peptides derived from the SAA and leukocytes seem to be involved in this process, we investigated the effect of human SAA on human monocytes and polymorphonuclear cells (PMN). When recombinant human SAA (rSAA) was used at concentrations corresponding to those found during the acute phase (&amp;gt; 0.8 microM), it induced directional migration of monocytes and polymorphonuclear leukocytes. Preincubation of rSAA with high density lipoproteins blocked this chemoattractant activity for both monocytes and PMN. rSAA also regulated the expression of the adhesion proteins CD11b and leukocyte cell adhesion molecule 1 and induced the adhesion of PMN and monocytes to umbilical cord vein endothelial cell monolayers. When subcutaneously injected into mice, rSAA recruited PMN and monocytes at the injection site. On the basis of these data, we suggest that SAA may participate in enhancing the migration of monocytes and PMN to inflamed tissues during an acute phase response.
THE PROSTAGLANDINS: A FAMILY OF BIOLOGICALLY ACTIVE LIPIDS
Authors: SUNE BERGSTRÖM, LARS A. CARLSON, JAMES R. WEEKS
Journal: Pharmacological Reviews (1968)

The prostaglandins are a family of lipids, originally discovered over 30 years ago in human seminal fluid, which have since been found not only to have a wide variety of striking pharmacological actions, but also to be present in many if not all mammalian tissues. They have an unusual chemical structure, being 20-carbon fatty acids derived enzymically from the essential fatty acids by cyclization and oxidation. Converting enzymes have been demonstrated in many tissues; they are especially active in the vesicular glands of the sheep, which are used for a practical method of biosynthesis.

The individual prostaglandins differ among themselves both qualitatively and quantitatively. Prostaglandins have a wide spectrum of biological action: They are smooth muscle stimulants, depressor peripheral vasodilators (except the PGFs which are pressor and venoconstrictor in dogs), and inhibitors of lipolysis, platelet aggregation and gastric secretion. In these areas, they are among the most potent compounds known, activity being present in some systems at concentrations of 0.01 ng/ml in vitro , and activity of 10 ng/kg in vivo . Prostaglandin formation and release is brought about by nerve activity, both central and peripheral. Their presence in biologically large concentrations in menstrual fluid and amniotic fluid at term is intriguing.

Physiological roles for these recently rediscovered compounds are yet to be established, but whenever substances are found in tissues which in very small doses can affect the function of these tissues, there is the possibility that they are regulators of physiological activity. Each effect of one or another prostaglandin suggests a corresponding physiological role, whether stimulatory or inhibitory, on such systems as smooth muscle, nerves, the circulation, and the reproductive organs. In the last named, roles in relation to fertilityand coitus and later possible action in relation to labor and postpartum uterine contraction have been proposed. Prostaglandins liberated by nerve stimulation, which then have actions opposite to that of the nerve stimulation, suggests a role as feed-back inhibitors. Thus, sympathetic nerve stimulation to adipose tissue induces both lipolysis and the release of antilipolytic prostaglandins, and vagal stimulation to the stomach, both secretion and the release of prostaglandins with powerful antisecretory actions. On the other hand, the ability of minute amounts of certain prostaglandins, inactive in their own right, to potentiate other agonists, suggests a more general role on ion transport or membrane function.
Absence of the calcium-binding protein, S100A1, confers pulmonary hypertension in mice associated with endothelial dysfunction and apoptosis
Authors: Krystyna Teichert-Kuliszewska, James N. Tsoporis, Jean-Francois Desjardins, Jun Yin, Liming Wang, Wolfgang M. Kuebler, Thomas G. Parker
Journal: Cardiovascular Research (2014)

S100A1, a 10-kDa, Ca2+-binding protein, is expressed in endothelial cells (ECs) and binds eNOS. Its absence is associated with impaired production of nitric oxide (NO) and mild systemic hypertension. As endothelial dysfunction contributes to clinical and experimental pulmonary hypertension (PH), we investigated the impact of deleting S100A1 in mice, on pulmonary haemodynamics, endothelial function, NO production, associated signalling pathways, and apoptosis. Compared with wild-type (WT), S100A1-knock-out mice (KO) exhibited increased right ventricular (RV) weight/body weight ratio and elevated RV pressure in the absence of altered left ventricular filling pressures, accompanied by increase in wall thickness of muscularized pulmonary arteries and a reduction in microvascular perfusion. In isolated lung preparations, KO revealed reduced basal NO, blunted dose-responsiveness to acetylcholine, and augmented basal and angiotensin (AII)-induced pulmonary vascular resistance (R0) compared with WT. Pre-treatment of KO lungs with S100A1 attenuated the AII-induced increase in pulmonary arterial pressure and R0. S100A1-induced phosphorylation of eNOS, Akt, and ERK1/2 is attenuated in pulmonary EC of KO compared with WT. Basal and TNF-α-induced EC apoptosis is greater in KO vs. WT, and cell survival is enhanced by S100A1 treatment. Our data demonstrate that the absence of S100A1 results in PH by disruption of its normal capacity to (i) enhance pulmonary EC function by induction of eNOS activity and NO levels via Akt/ERK1/2 pathways and (ii) promote EC survival. The ability of exogenously administered S100A1 to rescue this phenotype makes it an attractive therapeutic target in the treatment of PH.
The complex pattern of cytokines in serum from patients with meningococcal septic shock. Association between interleukin 6, interleukin 1, and fatal outcome.
Authors: A Waage, P Brandtzaeg, A Halstensen, P Kierulf, T Espevik
Journal: The Journal of Experimental Medicine (1989)

Serum samples from patients with meningococcal disease were examined for the presence of IL-6, TNF-alpha, and LPS. Median serum concentration of IL-6 was 1,000 times higher in patients with septic shock (189 ng/ml) than in patients with bacteriaemia, meningitis, or combined septic shock and meningitis. 11 of 21 patients with serum levels greater than 3.0 ng/ml died, whereas all 58 patients with serum levels at less than or equal to 3.0 ng/ml, survived. All four patients with serum IL-6 levels greater than 750 ng/ml, died. IL-1 was detected in serum from three patients who also had high serum levels of IL-6, TNF-alpha, and LPS, and rapidly fatal courses. IL-6 appeared to be released into serum later than TNF-alpha, and was detected in serum for up to 36 h. The half-life of IL-6 and TNF-alpha was calculated to be 103 +/- 27 min and 70 +/- 11 min, respectively. These data indicate that a complex pattern of cytokines exists in serum from patients with meningococcal septic shock, and that the release of IL-6 and IL-1, in addition to TNF-alpha, is associated with fatal outcome.