tbuckley/cabot-search huggingface dataset:
Panic Attacks and Psychoticism
Authors: Renee D Goodwin, David M Fergusson, L John Horwood
Journal: American Journal of Psychiatry (2004)

OBJECTIVE: The authors sought to determine the association between panic attacks and psychoticism among young adults in the community. METHOD: Data were drawn from a 21-year longitudinal birth cohort study (N=1,265). Negative binomial regression models were used to determine the association between panic attacks in adolescence (age 15–21) and psychoticism during young adulthood. RESULTS: Having a panic attack in the preceding 3 years was associated with elevated rates of psychoticism at ages 18 (rate ratio=2.81, 95% CI=1.92–4.13) and 21 (rate ratio=3.01, 95% CI=2.10–4.33). These associations were adjusted for differences in previous psychoticism, comorbid anxiety, depression, and substance use disorders and a range of other potential confounding factors by using a generalized estimating equation model. This analysis showed that after adjustment for confounding factors, having a panic attack was still associated with an increased rate of psychoticism (rate ratio=1.51, 95% CI=1.14–2.02). CONCLUSIONS: Panic attacks during adolescence are associated with significantly increased levels of psychoticism among young adults in the community compared with young persons with no history of panic attacks. Much of the relationship between panic attacks and psychoticism appears to be explained by common risk factors and psychiatric comorbidity, yet these data provide evidence of an independent association between panic attacks in adolescence and psychoticism during young adulthood in the community. Replication of these findings is needed, as are future studies that further investigate the mechanism of this association.
The 'disconnect' between synovitis and erosion in rheumatoid arthritis: a result of treatment or intrinsic to the disease process itself?
Authors: F. McQueen, E. Naredo
Journal: Annals of the Rheumatic Diseases (2011)

The use of advanced imaging modalities has allowed greater understanding of the rheumatoid arthritis (RA) disease process and the links between inflammation and damage. The study by Dohn et al 1 reported in this issue of the journal ( see article on page 252. ) is the largest yet published to systematically examine responses to combination anti-tumour necrosis factor (TNF) therapy (adalimumab/methotrexate) in patients naive to biological agents using MRI, ultrasound (US), plain radiography and high-resolution CT (HRCT) scanning. The inclusion of all four imaging modalities allows important questions to be asked.

First, and most obviously, does anti-TNF therapy/methotrexate prevent the progression of bone erosion? The evidence for this is already very strong from studies using plain radiography to measure outcome,2 and is supported here at a greater level of detail using MRI and US. An earlier publication from the same study provided the same answer using CT scanning.3 There was no overall progression in erosion scores (or MRI erosion volumes) over 12 months, but individuals who were progressors or regressors could be identified and progression or regression of an erosion at individual joints over 12 months could also be studied.

The second question relates to whether changes in MRI and/or US measures of inflammation occur in parallel with changes in clinical disease activity and, by implication, whether these modalities could be used to monitor treatment response. In other words, does the detection of imaging synovitis or osteitis (MRI bone oedema) have any added value over detecting and measuring joint inflammation clinically? In this study, improvements in imaging synovitis (MRI and US) and osteitis (MRI) were concordant with reductions in C reactive protein, functional scores and joint counts, as would be expected. This is consistent with the findings of other studies which have also reported both MRI and US …
Contractile proteins in myocardial cells are regulated by factor(s) released by blood vessels.
Authors: G McClellan, A Weisberg, N S Kato, C Ramaciotti, A Sharkey, S Winegrad
Journal: Circulation Research (1992)

The importance of perfusion of the coronary vasculature in the regulation of ATPase activity of myosin in rat myocardial cells has been studied. Quantitative histochemistry was used to determine the activity of the enzyme among cells in tissues that had been either perfused through the coronary system or superfused over the surface of the tissue. Enzymatic activity was measured in cryostatic sections from three different preparations: 1) hearts frozen immediately after removal from the animal; 2) isolated hearts frozen after they had been perfused through the coronary circulation; and 3) isolated papillary muscles or trabeculae that had been superfused after dissection and then frozen. ATPase activity was measured in the isolated tissues at different times after dissection. Both calcium- and actin-activated myosin ATPase activities were uniform among cells in both the ventricles of the hearts frozen immediately after dissection and those that had been perfused through the coronary system. In the superfused tissues, although calcium-activated myosin ATPase activity was uniform, actin-activated ATPase activity was not uniform for about 90 minutes after the dissection, the period required for stabilization of the contraction. The pattern of nonuniformity was complex. In all bundles the lowest enzymatic activity was found in the most superficial cells. In very thin bundles, the cells in the center had the highest activity. In the medium and thicker bundles, there were three concentric zones of actin-activated ATPase activity, the superficial zone with the lowest activity, an intermediate zone with high activity, and a central zone with lower activity. Within each zone, the activity was often greatest in myocardial cells immediately next to blood vessels even though the blood vessels had not been perfused. The transverse distribution of ATPase activity of myosin could be explained by a mechanism in which cells in blood vessels (presumably endothelium) release a substance that upregulates myosin ATPase activity, with the rate of release being related to the local oxygen tension. A downregulating substance may also be produced. The period of stabilization of the contraction coincides with the time during which the pattern of actomyosin ATPase activity is nonuniform. These data suggest that the contractile proteins are regulated by a substance produced by blood vessels in proportion to the local PO2, and possibly in relation to shear force on the vascular endothelium.
Nur77 converts phenotype of Bcl-B, an antiapoptotic protein expressed in plasma cells and myeloma
Authors: Frederic Luciano, Maryla Krajewska, Paulina Ortiz-Rubio, Stan Krajewski, Dayong Zhai, Benjamin Faustin, Jean-Marie Bruey, Beatrice Bailly-Maitre, Alan Lichtenstein, Siva Kumar Kolluri, Arnold C. Satterthwait, Xiao-Kun Zhang, John C. Reed
Journal: Blood (2007)
Chronic hepatitis B infection in adolescents who received primary infantile vaccination
Authors: Tzu-Wei Wu, Hans Hsienhong Lin, Li-Yu Wang
Journal: Hepatology (2012)

Hepatitis B virus (HBV) infection is a global health issue. Universal infantile hepatitis B (HB) vaccination is very efficacious. However, HBV infections among those immunized subjects have been reported. The long-term efficacy of postnatal passive-active HB vaccination in high-risk subjects is not well explored. A total of 8,733 senior high school students who were born after July 1987 were assayed for hepatitis B surface antigen (HBsAg) and antibodies to HBsAg (anti-HBs). The overall HBsAg and anti-HBs-positive rates were 1.9% and 48.3%, respectively. The HBsAg-positive rate was 15% in HB immunoglobulin (HBIG) recipients (adjusted odds ratio [OR]: 15.63; 95% confidence interval [CI]: 10.99-22.22). Among students who did not receive HBIG, there was a significantly negative association between HB vaccination dosage and HBsAg-positive rate (P for trend = 0.011). Adjusted ORs for those who received 4, 3, and 1 to 2 doses were 1.00, 1.52 (95% CI: 0.91-2.53), and 2.85 (95% CI: 1.39-5.81), respectively. Among HBIG recipients, the HBsAg-positive rate was significantly higher in subjects with maternal hepatitis B e antigen (HBeAg) positivity and who received HBIG off-schedule. A booster dose of HB vaccination was administered to 1974 HBsAg- and anti-HBs-negative subjects. Prebooster and a postbooster blood samples were drawn for anti-HBs quantification. The proportions of postbooster anti-HBs titer <10 mIU/mL was 27.9%. Subjects with prebooster anti-HBs titers of 1.0-9.9 mIU/mL had significantly higher postbooster anti-HBs titers than those with prebooster anti-HBs titers of <1.0 mIU/mL (P < 0.0001).Having maternal HBeAg positivity is the most important determinant for HBsAg positivity in adolescents who received postnatal passive-active HB vaccination 15 years before. A significant proportion of complete vaccinees may have lost their immunological memories against HBsAg.
Le Beau Doc Sans Merci
Authors: L. Farrell
Journal: BMJ (2001)

I met a young lady in the meads. Her hair was long, her step was light; she had intended to go to medical school, she said, but she had visited the local hospital and the junior doctors had discouraged her, and she was starting dentistry instead.

I set her on my pacing steed and all day long extolled the virtues of medical life.

“Asking a junior doctor what it's like to be a doctor is like asking a tadpole what it's …
Episodic memory, amnesia, and the hippocampal–anterior thalamic axis
Authors: John P. Aggleton, Malcolm W. Brown
Journal: Behavioral and Brain Sciences (1999)

By utilizing new information from both clinical and experimental (lesion, electrophysiological, and gene-activation) studies with animals, the anatomy underlying anterograde amnesia has been reformulated. The distinction between temporal lobe and diencephalic amnesia is of limited value in that a common feature of anterograde amnesia is damage to part of an "extended hippocampal system" comprising the hippocampus, the fornix, the mamillary bodies, and the anterior thalamic nuclei. This view, which can be traced back to Delay and Brion (1969), differs from other recent models in placing critical importance on the efferents from the hippocampus via the fornix to the diencephalon. These are necessary for the encoding and, hence, the effective subsequent recall of episodic memory. An additional feature of this hippocampal-anterior thalamic axis is the presence of projections back from the diencephalon to the temporal cortex and hippocampus that also support episodic memory. In contrast, this hippocampal system is not required for tests of item recognition that primarily tax familiarity judgements. Familiarity judgements reflect an independent process that depends on a distinct system involving the perirhinal cortex of the temporal lobe and the medial dorsal nucleus of the thalamus. In the large majority of amnesic cases both the hippocampal-anterior thalamic and the perirhinal-medial dorsal thalamic systems are compromised, leading to severe deficits in both recall and recognition.
Acute intratubular crystal deposition causing permanent renal damage in the pig.
Authors: P J Hatfield, H A Simmonds, D A Farebrother, A S Jones
Journal: Annals of the Rheumatic Diseases (1973)

Heberden Society 393 because we are missing the diagnosis.You did not comment on two particular diagnostic features.One is the menstrual irregularities affecting women, and the second is tenosynovitis especially around the wrist and ankle.DR. S EIFERT Three of the patients had tenosynovitis in the region of the wrist.Seven patients presented with symptoms within a few days of a menstrual period, and one was pregnant.PROF.E. G. L. BY WATERS (London) The histology of the skin lesions is very much like that of an Osler's node taken in the acute stage.
Proximal subungual onychomycosis caused by<i>Fusarium falciforme</i>successfully cured with posaconazole
Authors: A.M.S. Al-Hatmi, A. Bonifaz, L. Calderón, I. Curfs-Breuker, J.F. Meis, A.D. van Diepeningen, G.S. de Hoog
Journal: British Journal of Dermatology (2015)

Funding sources: The work of A.M.S.A. was financially supported by the Ministry of Health, Oman. Conflicts of interest: J.F.M. has received grants from Astellas, Basilea and Merck; has been a consultant to Astellas, Basilea and Merck; and has received speaker's fees from Merck and Gilead. Dear Editor, Proximal subungual onychomycosis (PSO) is a fungal infection of the inner layer of the nail plate, which starts from the eponychium and nail matrix.1 Onychomycosis can be caused by a variety of dermatophytes, yeasts and nondermatophyte moulds (NDMs), including species of Aspergillus, Acremonium, Scopulariopsis, Chaetomium and Fusarium.2 Fusarium and Acremonium spp. require special attention because of their intrinsically low susceptibility to most common antifungal agents and their ability to disseminate in severely compromised hosts, using the nail as a potential source of infection.3 4 Since the application of molecular methods to the taxonomy of Fusarium, a large hidden diversity has been found. At least 71 molecularly identified species have been reported to be involved in mycoses of humans and animals; all of these species belong to eight species complexes. Members of the Fusarium solani species complex (FSSC) are phenotypically indistinguishable and rely on multilocus sequence analysis for identification.5 Summerbell and Schroers showed that several FSSC species do not display typical F. solani morphology.6 Consequently, species consistently lack characteristic morphology; nevertheless, with a phylogenetic relationship to Fusarium, they were accepted as members of the genus. One of these is Fusarium falciforme, an increasingly recognized species within the FSSC, recovered from superficial infections such as onychomycosis. PSO has been reported in immunocompromised patients, specifically those with HIV, but also with other immunodeficiencies. Here, we report a rare case of PSO caused by F. falciforme, successfully treated with posaconazole, in a patient with HIV/AIDS.
The identification of novel targets of miR-16 and characterization of their biological functions in cancer cells
Authors: Xin Yan, Hongwei Liang, Ting Deng, Kegan Zhu, Suyang Zhang, Nan Wang, Xueyuan Jiang, Xueliang Wang, Rui Liu, Ke Zen, Chen-Yu Zhang, Yi Ba, Xi Chen
Journal: Molecular Cancer (2013)

Abstract Background In eukaryotes, miR-16 is an important microRNA (miRNA) that is involved in numerous biological processes. However, it is not fully understood how miR-16 executes its physiological functions. In the present study, we aimed to identify novel miR-16 targets and study their biological functions. Methods Candidate target genes of miR-16 were screened by microarray analysis of mRNA levels in several cancer cell lines with enhanced miR-16. Three bioinformatics algorithms, including TargetScan, PicTar, and miRanda, were used in combination to calculate the miR-16 targets. The expression levels of miR-16 and target mRNA were examined by relative quantification RT-PCR, and the expression levels of target protein were detected by Western blot. Luciferase reporter plasmids were constructed to confirm direct targeting. The effect of miR-16 and target gene on cell viability was evaluated using MTT assays. The effects of miR-16 and target gene on apoptosis and cell cycle distribution were evaluated by flow cytometry analysis. Results By overexpressing miR-16 in several cancer cell lines and measuring global mRNA levels using microarray analysis, we identified 27 genes that may be regulated by miR-16. After the bioinformatics filtering process, 18 genes were selected as candidate miR-16 targets. Furthermore, we experimentally validated three of these candidates, MAP7 (microtubule-associated protein 7), PRDM4 (PR domain containing 4) and CDS2 (CDP-diacylglycerol synthase 2), as direct targets of miR-16. Finally, we demonstrated that miR-16 targeting MAP7 played a critical role in regulating proliferation but not apoptosis and cell cycle progression in cancer cells. Conclusion In summary, the present study identifies several novel miR-16 targets and illustrates a novel function of miR-16 targeting MAP7 in modulating proliferation in cancer cells.
Elastase and matrix metalloproteinase inhibitors induce regression, and tenascin-C antisense prevents progression, of vascular disease
Authors: Kyle Northcote Cowan, Peter Lloyd Jones, Marlene Rabinovitch
Journal: Journal of Clinical Investigation (2000)

Increased expression of the glycoprotein tenascin-C (TN) is associated with progression of clinical and experimental pulmonary hypertension. In cultured smooth muscle cells (SMCs) TN is induced by matrix metalloproteinases (MMPs) and amplifies the proliferative response to growth factors. Conversely, suppression of TN leads to SMC apoptosis. We now report that hypertrophied rat pulmonary arteries in organ culture, which progressively thicken in association with cell proliferation and matrix accumulation, can be made to regress by inhibiting either serine elastases or MMPs. This effect is associated with reduced TN, suppression of SMC proliferation, and induction of apoptosis. Selective repression of TN by transfecting pulmonary arteries with antisense/ribozyme constructs also induces SMC apoptosis and arrests progressive vascular thickening but fails to induce regression. This failure is related to concomitant expansion of a SMC population, which produces an alternative cell survival αvβ3 ligand, osteopontin (OPN), in response to pro-proliferative cues provided by a proteolytic environment. OPN rescues MMP inhibitor–induced SMC apoptosis, and αvβ3 blockade induces apoptosis in hypertrophied arteries. Our data suggest that proteinase inhibition is a novel strategy to induce regression of vascular disease because this overcomes the pluripotentiality of SMC-matrix survival interactions and induces coordinated apoptosis and resorption of matrix.
A role for the nasal cycle in respiratory defence
Authors: R Eccles
Journal: European Respiratory Journal (1996)

This review describes the phenomenon of the nasal cycle, which consists of periodic congestion and decongestion of the nasal venous sinusoids. The hypothesis is put forward that the nasal venous sinusoids participate in respiratory defence by generation of plasma exudate. This hypothesis is based on recent studies, which have shown that the nasal venous sinusoids have a fenestrated endothelium and that the nasal cycle is increased during periods of nasal infection; and also on a series of older observations in the literature, which link the generation of nasal fluid to the decongestion of nasal venous sinusoids. It is proposed that the periodic congestion and decongestion of nasal venous sinusoids may provide a pump mechanism for the generation of plasma exudate, and that this mechanism is an important component of respiratory defence.
CLINICAL AND BIOCHEMICAL ABNORMALITIES IN COPPERSMITHS EXPOSED TO CADMIUM
Authors: R. Scott, P.J. Paterson, E.A. Mills, A. Mckirdy, G.S. Fell, J.M. Ottoway, F.E.R. Husain, O.P. Fitzgerald-Finch, A.J. Yates, A. Lamont, S. Roxburgh
Journal: The Lancet (1976)
Primary Epstein-Barr virus infection does not erode preexisting CD8+ T cell memory in humans
Authors: Oludare A. Odumade, Jennifer A. Knight, David O. Schmeling, David Masopust, Henry H. Balfour, Kristin A. Hogquist
Journal: The Journal of Experimental Medicine (2012)

Acute Epstein-Barr virus (EBV) infection results in an unusually robust CD8+ T cell response in young adults. Based on mouse studies, such a response would be predicted to result in attrition of preexisting memory to heterologous infections like influenza A (Flu) and cytomegalovirus (CMV). Furthermore, many studies have attempted to define the lymphocytosis that occurs during acute EBV infection in humans, but it is unclear whether bystander T cells contribute to it. To address these issues, we performed a longitudinal prospective study of primary EBV infection in humans. During acute EBV infection, both preexisting CMV- and Flu-specific memory CD8+ T cells showed signs of bystander activation, including up-regulation of granzyme B. However, they generally did not expand, suggesting that the profound CD8+ lymphocytosis associated with acute EBV infection is composed largely of EBV-specific T cells. Importantly, the numbers of CMV- and Flu-specific T cells were comparable before and after acute EBV infection. The data support the concept that, in humans, a robust CD8+ T cell response creates a new memory CD8+ T cell niche without substantially depleting preexisting memory for heterologous infections.
The Identification of Ligands at Orphan G-Protein Coupled Receptors
Authors: Alan Wise, Steven C. Jupe, Stephen Rees
Journal: The Annual Review of Pharmacology and Toxicology (2004)

The completion of the human genome sequencing project has identified approximately 720 genes that belong to the G-protein coupled receptor (GPCR) superfamily. Approximately half of these genes are thought to encode sensory receptors. Of the remaining 360 receptors, the natural ligand has been identified for approximately 210 receptors, leaving 150 so-called orphan GPCRs with no known ligand or function. The identification of ligands active at orphan GPCRs has been achieved through the development of a number of experimental approaches, including the screening of putative small molecule and peptide ligands, reverse pharmacology, and the use of bioinformatics to predict candidate ligands. In this review, we discuss the methodologies developed for the identification of ligands at orphan GPCRs and include examples of their successful application.
Hepatitis C virus NS2 protein triggers endoplasmic reticulum stress and suppresses its own viral replication
Authors: Annette von dem Bussche, Raiki Machida, Ke Li, Gideon Loevinsohn, Amrin Khander, Jianguo Wang, Takaji Wakita, Jack R. Wands, Jisu Li
Journal: Journal of Hepatology (2010)
Distinct Roles for Basal and Induced COX-2 in Podocyte Injury
Authors: Huifang Cheng, Xiaofeng Fan, Youfei Guan, Gilbert W. Moeckel, Roy Zent, Raymond C. Harris
Journal: Journal of the American Society of Nephrology (2009)

Transgenic mice that overexpress cyclooxygenase-2 (COX-2) selectively in podocytes are more susceptible to glomerular injury by adriamycin and puromycin (PAN). To investigate the potential roles of COX-2 metabolites, we studied mice with selective deletion of prostanoid receptors and generated conditionally immortalized podocyte lines from mice with either COX-2 deletion or overexpression. Podocytes that overexpressed COX-2 were virtually indistinguishable from wild-type podocytes but were significantly more sensitive to PAN-induced injury, produced more prostaglandin E(2) and thromboxane B(2), and had greater expression of prostaglandin E(2) receptor subtype 4 (EP(4)) and thromboxane receptor (TP). Treatment of COX-2-overexpressing podocytes with a TP antagonist reduced apoptosis, but treatment with an EP(4) antagonist did not. In contrast, podocytes from COX-2-knockout mice exhibited increased apoptosis, markedly decreased cell adhesion, and prominent stress fibers. In vivo, selective deletion of podocyte EP(4) did not alter the increased sensitivity to adriamycin-induced injury observed in mice overexpressing podocyte COX-2. In contrast, genetic deletion of TP in these mice prevented adriamycin-induced injury, with attenuated albuminuria and foot process effacement. These results suggest that basal COX-2 may be important for podocyte survival, but overexpression of podocyte COX-2 increases susceptibility to podocyte injury, which is mediated, in part, by activation of the thromboxane receptor.