tbuckley/cabot-search huggingface dataset:
THE NATURAL HISTORY OF THE REMITTING SCHIZOPHRENIAS
Authors: GEORGE E. VAILLANT
Journal: American Journal of Psychiatry (1963)

The lifetime clinical histories of 12 remitting schizophrenics, whose lives spanned up to 85 years, are reviewed. Such fully remitting schizoprenics constitute the 10%-15% best outcomes of an unselected schizophrenic population. After first admission 8 led independent, useful lives for 25 years or more. The clinical course of these 12 patients could be grouped into 3 patterns: i) those who remained well without further hospitalization, ii) those who were readmitted to a hospital but with a diagnosis of manic-depressive psychosis and with no reappearance of their previous schizophrenic thought disorder, iii) those who relapsed— often many years later-and remained chronically hospitalized. Six other patients are reported who fitted the syndrome of schizophrenic thought disorder, recovery, manicdepressive psychosis, and recovery. On first admission all 12 of these patients could have been predicted to have done well; all showed "reactive" features. Longterm follow-up of these patients, however, revealed that at some time during their lives 75% were again hospitalized for psychosis. Thus, there seems no justification separating remitting schizophrenics from the broader classification of " the group of schizophrenias." The findings of this study suggest that acute schizo-affective psychosis, as defined by Kasanin, is a more appropriate diagnosis for patients who recover from schizophrenic thought disorder than terms like adolescent turmoil, schizophreniform state, or reactive psychosis.
The BMJ Careers job archive
Authors: J. Connor
Journal: BMJ (2003)

<h3>Abstract</h3> Individuals with spinal cord injury (SCI) often develop debilitating neuropathic pain, which may be driven by neuronal damage and neuroinflammation. We have previously demonstrated that treatment using 670 nm (red) light irradiation alters microglia/macrophage responses and alleviates mechanical hypersensitivity at 7-days post-injury. Here, we investigated the effect of red-light on the development of mechanical hypersensitivity, neuronal markers, and glial response in the subacute stage (days 1-7) following SCI. Wistar rats were subjected to a mild T10 hemi-contusion SCI or sham surgery followed by daily red-light-treatment (30 min/day; 670 nm LED; 35 mW/cm<sup>2</sup>) or sham treatment. Mechanical sensitivity of the rat dorsum was assessed from 1-day post-injury and repeated every second day. Spinal cords were collected at 1, 3, 5 and 7-days post-injury for analysis of myelination, neurofilament protein NF200 expression, neuronal cell death, reactive astrocytes (GFAP<sup>+</sup> cells), interleukin1β (IL1β) expression, and inducible nitric oxide synthase (iNOS) production in IBA1<sup>+</sup> microglia/macrophages. Red-light treatment significantly reduced the cumulative mechanical sensitivity and the hypersensitivity incidence following SCI. This effect was accompanied by significantly reduced neuronal cell death, reduced astrocyte activation and reduced iNOS expression in IBA1<sup>+</sup> cells at the level of the injury. However, myelin and NF200 immunoreactivity and IL1β expression in GFAP<sup>+</sup> and IBA1<sup>+</sup> cells were not altered by red-light treatment. Thus, red-light therapy may represent a useful non-pharmacological approach for treating pain during the subacute period after SCI by decreasing neuronal loss and modulating the inflammatory glial response.
Interplay of matrix metalloproteinases, tissue inhibitors of metalloproteinases and their regulators in cardiac matrix remodeling
Authors: Y Li
Journal: Cardiovascular Research (2000)

Myocardial fibrosis due to maladaptive extracellular matrix remodeling contributes to dysfunction of the failing heart. Further elucidation of the mechanism by which myocardial fibrosis and dilatation can be prevented or even reversed remains of great interest as a potential means to limit myocardial remodeling and dysfunction. Matrix metalloproteinases (MMPs) are the driving force behind extracellular matrix degradation during remodeling and are increased in the failing human heart. MMPs are regulated by a variety of growth factors, cytokines, and matrix fragments such as matrikines. In the present report, we discuss the regulation of MMPs, the role of MMPs in the development of cardiac fibrosis, and the modulation of MMP activity using gene transfer and knockout technologies. We also present recent findings from our laboratory on the regulation of the extracellular MMP inducer (EMMPRIN), MMPs, and transforming growth factor-β1 in the failing human heart before and after left ventricular assist device support, as well as the possibility of preventing ventricular fibrosis using different anti-MMP strategies. Several studies suggest that such modulation of MMP activity can alter ventricular remodeling, myocardial dysfunction, and the progression of heart failure. It is therefore suggested that the interplay of MMPs and their regulators is important in the development of the heart failure phenotype, and myocardial fibrosis in heart failure may be modified by modulating MMP activity.
Endoscopic ultrasound-guided drainage of a pelvic abscess via a J-pouch
Authors: S. Varadarajulu
Journal: Endoscopy (2012)

While prior reports have demonstrated the usefulness of endoscopic ultrasound (EUS) for transrectal drainage of pelvic abscesses, its utility for performing drainage via an ileoanal reservoir (J-pouch) has not been reported before.
Acid-Evoked Currents in Cardiac Sensory Neurons
Authors: Christopher J. Benson, Stephani P. Eckert, Edwin W. McCleskey
Journal: Circulation Research (1999)

Sensory neurons that innervate the heart sense ischemia and mediate angina. To use patch-clamp methods to study ion channels on these cells, we fluorescently labeled cardiac sensory neurons (CSNs) in rats so that they could later be identified in dissociated primary culture of either nodose or dorsal root ganglia (DRG). Currents evoked by a variety of different agonists imply the importance of lowered pH (</=7.0) in signaling ischemia. Acidic pH evoked extremely large depolarizing current in almost all cardiac afferent neurons from the DRG (CDRGNs). In contrast, only about half of the unlabeled DRG neurons responded to acid, and their current amplitudes were much less than that in CDRGNs. In all respects tested--kinetics, selectivity, and pharmacology--the acid-evoked current was similar to that of previously described native and cloned acid-sensing ion channels. Cardiac afferents from the nodose ganglia differed from CDRGNs in having smaller acid-evoked currents but clearly larger currents evoked by ATP. Serotonin, acetylcholine, bradykinin, and adenosine elicited currents in fewer CSNs than did ATP or lowered pH, and the currents were relatively small. Capsaicin, an activator of small nociceptive sensory neurons that innervate skin, evoked only small and rare currents in CDRGNs. The extremely large amplitude and prevalent expression of acid-evoked current in CSNs imply a critical role for acidity in sensation associated with myocardial ischemia.
A prospective comparison of class IA, B, and C antiarrhythmic agents in combination with amiodarone in patients with inducible, sustained ventricular tachycardia.
Authors: L Toivonen, A Kadish, F Morady
Journal: Circulation (1991)

BACKGROUND Clinical experience suggests that combinations of antiarrhythmic agents provide more effective control of ventricular tachyarrhythmias than does therapy with single agents. METHODS AND RESULTS Antiarrhythmic and electrophysiological effects of three class I antiarrhythmic agents, one from each subclass A, B, and C, were assessed in single use and in combination with amiodarone in patients with inducible, sustained ventricular tachycardia that was not suppressed by monotherapy with these agents. Thirty-one patients underwent an electrophysiology test on four occasions: at baseline; after 2-4 days of treatment with quinidine, mexiletine, or encainide; after 2 weeks of treatment with 1,200 mg/day amiodarone; and last, after 2-4 days of treatment with both amiodarone and the previously tested class I agent. The combination of a class I agent and amiodarone prevented the induction of sustained ventricular tachycardia in only one of 31 (3%) patients. Ventricular tachycardia became hemodynamically stable in 11 of 31 (34%) patients because of a marked prolongation in the tachycardia cycle length. It increased from 323 +/- 39 to 423 +/- 84 msec (n = 11, p less than 0.01) by adding encainide to amiodarone therapy, and it showed a tendency to lengthen when quinidine was added to amiodarone (from 373 +/- 77 to 425 +/- 58 msec; n = 10, NS). Each class I agent increased amiodarone-induced depression in myocardial conduction, but the extent of the additional depression seemed to differ among the three subclasses. Ventricular refractoriness was increased by all class I agents when used in combination with amiodarone, although not by mexiletine or encainide when used alone. CONCLUSIONS Class I antiarrhythmic agents slow ventricular conduction and increase ventricular refractoriness when used in combination with amiodarone. When amiodarone and class I drugs by themselves do not suppress the induction of ventricular tachycardia, the combination of amiodarone and a class I agent seldom results in noninducibility; however, it often lengthens the ventricular tachycardia cycle length and may render the ventricular tachycardia hemodynamically stable.
Primary cutaneous cryptococcosis in an immunocompromized pigeon keeper
Authors: A.K.E. COONETILLEKE, K. KRAUSE, D.N. SLATER, D. DEV, M.L. WOOD, G.S. BASRAN
Journal: British Journal of Dermatology (1995)

Summary We report the case of a pigeon keeper with CD4 lymphopenia, not associated with human immunodeficiency virus infection, who developed primary cutaneous cryptococcosis at the site of a pigeon peck.
Prevention of Lithotripsy-Induced Renal Injury by Pretreating Kidneys with Low-Energy Shock Waves
Authors: Lynn R. Willis, Andrew P. Evan, Bret A. Connors, Rajash K. Handa, Philip M. Blomgren, James E. Lingeman
Journal: Journal of the American Society of Nephrology (2006)

Lithotripsy shock waves (SW) to one renal pole damage that pole but protect the opposite pole from the damage inflicted by another, immediate application of SW. This study investigated whether the protection (1) occurs when the first treatment causes no injury, (2) is caused by SW or injury, (3) exhibits a threshold, and (4) occurs when the same pole receives both treatments. Six- to 7-wk-old anesthetized female pigs were studied. The following groups were studied: group 1 (n=4), 2000 SW at 12 kV to one pole and 2000 SW at 24 kV (standard) to the opposite pole; group 2 (n=6), same as group 1 except 500 12-kV SW pretreatment; group 3 (n=8), 500 12-kV, 2000 standard SW, all to the same pole; and group 4 (n=8), same as group 3 except 100 12-kV SW pretreatment. Mean+/-SD lesion size in group 1, first pole treated, was 0.66+/-0.82% of functional renal volume (FRV; P<0.05 versus 5.22+/-3.6% FRV with no pretreatment [NP]; 95% confidence interval [CI] -7.0 to -2.1) and 0.50+/-0.68% FRV in the opposite pole after 2000 standard SW (P<0.05 versus NP; 95% CI -9.4 to -0.08). Mean lesion size (first pole) in group 2 was 0.020+/-0.028% FRV (P<0.01 versus NP; 95% CI -9.2 to -1.2) and 0.43+/-0.54% FRV in the opposite pole after 2000 standard SW (P<0.05 versus NP; 95% CI -8.8 to -0.82). Same-pole SW (groups 3 and 4) also protected. Mean lesion sizes were 0.28+/-0.33% (P<0.01 versus NP; 95% CI -8.0 to -1.9) in group 3 and 0.39+/-0.48% FRV (P<0.01 versus NP; 95% CI -8.2 to -1.7) in group 4. It is concluded that the pretreatment protocol substantially limits the renal injury that normally is caused by SWL and occurs when the pretreatment and standard SW are applied to the same pole. The threshold for the protection may be <100 SW.
Abstract P4-11-03: Effect of tamoxifen and raloxifene on proliferative activity of breast epithelium in premenopausal women
Authors: R Freitas-Junior, MT Lucato, MA Moreira, JM Bernardes-Junior, SA Pinto, RR Paulinelli, LR Soares
Journal: Cancer Research (2013)

Abstract Background: Both Tamoxifen and raloxifene have been demonstrated to be effective to reduce the incidence of breast cancer among women. Objective: To compare the effects of raloxifene (60 mg/day) and tamoxifen (20 mg/day) on the proliferative activity of normal human breast epithelium, during the luteal phase of the menstrual cycle, by means of the immunoexpression of Ki-67/MIB-1. Patients and Methods: Forty-eight women presenting benign breast nodules with an indication for lesion excision took part in this study. These women were randomized to use tamoxifen or raloxifene for 22 days. They underwent surgery after using the medication, and a one-centimeter fragment of normal breast tissue was removed to study the immunoexpression of Ki-67. For this, the frequency of cells immunolabeled for Ki-67/MIB-1 per thousand epithelial cells was quantified. Results: The mean percentage ratios between immunolabeled and non-labeled cells were 2.02 (±1.09) and 3.13 (±3.23) for the tamoxifen and raloxifene groups, respectively. There was no statistically significant difference between the two groups, tamoxifen (n = 16) and raloxifene (n = 14), in relation to the immunoexpression of Ki-67 (p = 0.205). The mean of progesterone level was 19.62 (±17.67) for the tamoxifen group and 14.59 (±8.98) for the raloxefene group (p = 0.32). The plasma levels of estradiol, the values found were: 355.72 (± 337.98) and 171.02 (± 119.83) for groups of tamoxifen e raloxifene groups, respectively (p = 0.055). Conclusion: In this study, we observed that there was no difference in the potential for reducing the proliferative activity of normal breast epithelium between tamoxifen and raloxifene in premenopausal women. Citation Information: Cancer Res 2013;73(24 Suppl): Abstract nr P4-11-03.
BMA meeting: BMA rejects attempt to lower upper time limit for abortion
Authors: M. Limb
Journal: BMJ (2011)

The BMA annual meeting defeated a motion calling for the legal limit for termination of pregnancy, in the absence of fetal abnormality, to be reduced from 24 to 20 weeks gestation.

The 24 week time limit in England, Wales, and Scotland was approved by parliament in 1990, and MPs voted to retain it in 2008. The BMA’s annual meeting last debated abortion time limits …
Abstract 5698: MicroRNA-31 acts as an oncomir in lung cancer by repressing specific tumor suppressors
Authors: Xi Liu, Lorenzo F. Sempere, Haoxu Ouyang, Vincent A. Memoli, Angeline S. Andrew, Yue Luo, Eugene Demidenko, Murray Korc, Wei Shi, Meir Preis, Konstantin H. Dragnev, Hua Liu, James DiRenzo, Mads Bak, Sakari Kauppinen, Sarah J. Freemantle, Ethan Dmitrovsky
Journal: Cancer Research (2010)

Abstract MicroRNAs (miRNAs) encode small RNAs that regulate gene expression. The expression profiles of miRNAs have proven useful to improve classification, diagnostic and prognostic information for human cancers. We sought to uncover miRNAs preferentially over-expressed in lung cancers versus adjacent normal lung tissues. We comprehensively interrogated miRNA array expression profiles conducted on lung cancers versus adjacent normal lung tissues isolated from murine transgenic cyclin E models that were engineered. Notably, miR-136, miR-376a and miR-31 were each significantly over-expressed in murine lung cancers as compared to adjacent normal lung tissues. Real-time RT-PCR and in situ hybridization assays independently confirmed these miRNA expression profiles in paired normal-malignant lung tissues from transgenic mice as well as from a well characterized panel of paired human normal-malignant lung tissues. Knock-down of miR-31, but not other highlighted miRNAs, using a synthetic antagonist significantly repressed lung cancer cell growth and in vivo tumorigenicity. Bioinformatically predicted miR-31 target genes were identified and studied. These included two tumor suppressors: large tumor suppressor 2 (LATS2) and PP2A regulatory subunit B alpha isoform (PPP2R2A) that were each substantially increased by miR-31 knock-down and repressed by miR-31 over-expression. Engineered repression of either LATS2 or PPP2R2A significantly antagonized miR-31-mediated growth inhibition. Luciferase binding assays confirmed that miR-31 directly suppressed LATS2 and PPP2R2A through binding to their respective 3′-untranslated regions (UTRs). Interestingly, miR-31 was inversely expressed relative to these identified target genes in both murine and human lung cancers. Clinical relevance was uncovered using miR-31 in situ hybridization and cyclin E immunohistochemistry assays performed on tissue arrays from the population-based New Hampshire Lung Cancer Registry. As expected, cyclin E expression was significantly associated with miR-31 levels. Real-time RT-PCR assays validated LATS2 and PPP2R2A repression in lung cancers versus adjacent normal lung tissues. Thus, these findings implicate miR-31 as an oncogenic miRNA (oncomir) that exerts its effects by repressing specific tumor suppressors. Taken together, miR-31 is proposed as a novel molecular target for lung cancer therapy and chemoprevention. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 5698.
Body surface potential mapping in patients with Brugada syndrome: right precordial ST segment variations and reverse changes in left precordial leads
Authors: H Bruns
Journal: Cardiovascular Research (2002)

Objective: The aim of this study was to perform quantitative signal analysis of high-resolution body surface potential mapping (BSPM) recordings to assess its usefulness for the electrocardiographic characterization of patients with Brugada syndrome. The diagnostic value of the QRS integral and of the gradient of the ST segment have not been elucidated in Brugada syndrome. Methods: In 27 subjects (16 with Brugada syndrome and 11 healthy subjects), 120-lead BSPMs were recorded at baseline and after pharmacological provocation with intravenous administration of ajmaline (1 mg/kg). The recordings were analyzed for two regions outside the positions of the standard ECG leads: the right precordial leads (RPL) on the second and third intercostal space (high RPL) and the left precordial leads (LPL) between the fifth and seventh intercostal space (low LPL). Results: At baseline, in high RPL regions, patients with Brugada syndrome showed more positive QRS integrals (−5±8 vs. −16±8 mV ms) and a steeper negative ST segment gradient (−0.62±0.41 vs. −0.29±0.40 mV/s) compared to healthy subjects, P<0.001. In contrast, in low LPL regions, reduced QRS integrals and positive ST segment gradients were observed. These ECG signs were even more pronounced after intravenous ajmaline and showed a better discrimination for patients with Brugada syndrome than differences in RPL or LPL during baseline, respectively. Conclusions: In the left precordial leads, patients with Brugada syndrome showed ECG changes which were reversed in relation to the ECG changes observed in right precordial leads. BSPM measurement is a useful tool to improve the understanding of the electrocardiographic changes in the Brugada syndrome.
Normal versus Decinormal Salt Solution.
Authors: R. H. Harper
Journal: JAMA (1901)

Afton, Ind. Ter., June 20, 1901. <h3>To the Editor:</h3> —InThe Journalof June 15 is a communication from Dr. C. S. Minnich on normal salt solution; he concludes that the solution meant is the "decinormal," not "normal." "Normal" means "the rule," the general average; if a man, a horse, or a cow has the normal number of teeth, it has the number which is the rule for the species; if a man has in his blood-serum sodium chlorid to the amount of 0.6 to 0.8 per cent., then he has the normal amount; normal for a chemist's test solution or reagent, and normal for human blood are two wholly different "normals;" universal agreement could be made whereby the normal and dccinormal of the chemist could be changed; but environment has been unable to change the blood serum of terrestrial animals very much from the sea water, which was their
Abstract 5195: Shh/Gli signaling pathway promotes tumor metastasis and lymphangiogenesis via activation of PI3K/Akt and Erk pathway in gastric cancer
Authors: Young-A Yoo, Myoung-Hee Kang, Han-Na Kang, Jung-Lim Kim, Jae-Hong Seo, Jun-Suk Kim, Sang-Cheul Oh
Journal: Cancer Research (2010)

Abstract The activation of Sonic hedgehog (Shh)/Gli signaling is involved in the progression and invasion of various tumors types, including gastric carcinoma. Epithelial-mesenchymal transition (EMT) and matrix metalloproteinases (MMPs) have been implicated in facilitating the invasion and metastatsis. Herein, we investigated the impact of phosphoinositide 3-kinase (PI3K)/Akt and Erk pathway and MMPs activity on the Shh/Gli-mediated EMT and invasion of gastric cancer cells. We found that overexpression of Shh significantly enhanced cellular motility/invasiveness, lymphangiogenesis, and metastatic ability of tumor cells in gastric cancer cell lines and mice. Stimulation of Shh in gastric cancer cells also induced a full EMT process (characterized by Snail induction and E-cadherin down-regulation) and expression and activity of MMP-9. Meanwhile, blockade of Shh/Gli signaling by Cyclopamine (a Shh signaling inhibitor), anti-Shh neutralizing antibodies, or Gli siRNA inhibited Shh-induced motility/invasiveness and lymphangiogenesis in gastric cancer by subsequently restoring these changes of EMT markers and activity of MMP-9. The phosphorylation of Akt and Erk was also enhanced by treatment with Shh, but not cyclopamine, anti-Shh neutralizing antibodies, or Gli siRNA. Blockade of the Akt and MEK kinase using kinase-dead Akt, LY294002, or PD98059 significantly inhibited the Shh-induced EMT, activity of MMP-9, lymphangiogenesis, and metastasis in tumor cell lines and mice over-expressing Shh. Furthermore, knock-down of MMP-9 by its siRNA results in an decrease in invasiveness of gastric cancer cells treatment with Shh. Immunohistochemistry on gastric tumor biopsies showed that the levels of Gli, E-cadherin, MMP-9, D2-40 (lymphangiogenic factor), and phospho-Akt expression were enhanced in cases of metastatic gastric cancer than in cases of primary gastric cancer. Moreover, the strong correlation between Gli and E-cadherin, MMP-9, D2-40, phospho-Akt, or phospho-Erk expression was also observed in lymph node metastasis specimens. These data indicate that Shh/Gli signaling pathway promotes tumor metastasis in gastric cancer through activation of PI3K/Akt and Erk pathway followed by up-regulation of EMT, MMP-9, and lymphangiogenesis, which results in the stimulation of invasiveness of tumor cells. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 101st Annual Meeting of the American Association for Cancer Research; 2010 Apr 17-21; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2010;70(8 Suppl):Abstract nr 5195.
Mitochondrial myopathy caused by arsenic trioxide therapy
Authors: Andoni Echaniz-Laguna, Aurélien Benoilid, Stéphane Vinzio, Luc-Matthieu Fornecker, Béatrice Lannes, Jean-Pierre Goullé, Frank Broly, Bénédicte Mousson de Camaret
Journal: Blood (2012)