tbuckley/cabot-search huggingface dataset:
Miconazole as adjuvant therapy for oral lichen planus: a double-blind randomized controlled trial
Authors: G. Lodi, M. Tarozzi, A. Sardella, F. Demarosi, L. Canegallo, D. Di Benedetto, A. Carrassi
Journal: British Journal of Dermatology (2007)

Topical steroids are the first choice for the treatment of oral lichen planus (OLP). Antifungal drugs are often employed together with them, to prevent secondary oral candidosis, although it has been suggested anecdotally that they can also be beneficial for OLP itself.To compare the effect of clobetasol propionate with and without a topical antifungal drug (miconazole) on the symptoms and extension of OLP.A randomized, parallel, double-blind trial was conducted at the Unit of Oral Medicine and Pathology of the University of Milan. Thirty-five outpatients with histologically proven OLP were randomly assigned to receive either clobetasol propionate and miconazole, or clobetasol propionate and placebo for 6 weeks. Primary outcomes included symptoms and extension of lesions; adverse effects were also recorded.All the patients who concluded the study (30 of 35) showed clinical and subjective improvement within 3 weeks. The addition of miconazole did not affect in a significant way the signs and symptoms of OLP. No cases of clinical candidosis were seen in the patients taking miconazole, while one-third (five of 15) of the placebo group were affected.Although effective in preventing iatrogenic candidosis, the addition of miconazole to topical steroid treatment does not improve the efficacy of the therapy.
Systemic sarcoidosis mimicking advanced testicular cancer
Authors: Richard Woolf, Laurence Toms, Bobby Mann
Journal: Journal of the Royal Society of Medicine (2010)

Sarcoidosis is a systemic inflammatory condition characterized by non-caseating epitheloid granulomata that classically affect the chest. Extra-pulmonary granulomata occur in over 75% of cases, but genitourinary sarcoidosis (GUS) is very rare with just over 60 cases reported.1,2 We discuss an unusual presentation of GUS in a patient with known sarcoidosis who developed a testicular mass, and discrete liver and splenic lesions mimicking metastatic testicular cancer.
Phase I/II clinical study of percutaneous vertebroplasty (PVP) as palliation for painful malignant vertebral compression fractures (PMVCF): JIVROSG-0202
Authors: T. Kobayashi, Y. Arai, Y. Takeuchi, Y. Nakajima, Y. Shioyama, M. Sone, N. Tanigawa, O. Matsui, M. Kadoya, Y. Inaba
Journal: Annals of Oncology (2009)
Prolongation of the QT Interval and Ventricular Tachycardia in Patients Treated with Arsenic Trioxide for Acute Promyelocytic Leukemia
Authors: Kazunori Ohnishi
Journal: Annals of Internal Medicine (2000)

Background: Recently, arsenic trioxide has increasingly been used for relapsed acute promyelocytic leukemia. However, it is known to have several adverse effects, including acute cardiac toxicities. Objective: To determine cardiac toxicities resulting from arsenic trioxide therapy in patients with relapsed or refractory acute promyelocytic leukemia. Design: Phase II clinical prospective cohort study. Setting: A university hospital in Hamamatsu, Japan. Patients: 8 patients with relapsed acute promyelocytic leukemia. Intervention: Arsenic trioxide, 0.15 mg/kg of body weight, administered daily by 2-hour infusion for a maximum of 60 days. Measurements: Continuous monitoring with ambulatory electrocardiography. Results: Five patients (63%) achieved complete remission. During induction therapy with arsenic trioxide, prolonged QT intervals were observed in all patients. Ventricular premature contractions were noticed during 8 of 12 courses of therapy. Four patients developed nonsustained ventricular tachycardia and required treatment with antiarrhythmic agents. Conclusions: Cardiac toxicity occurs during arsenic trioxide therapy in patients with acute promyelocytic leukemia. Such patients should be monitored for prolonged QT intervals and ventricular arrhythmia.
When to leave a stone unturned ...
Authors: E. C. von Rosenvinge, C. Koh, S. M. Holland, T. Heller
Journal: Gut (2010)

A 16-year-old, 41 kg boy with chronic granulomatous disease presented with fever, chills, and diaphoresis. CT showed necrotising mediastinal lymphadenitis and a contracted but otherwise normal gallbladder (figure 1A). The patient was started on intravenous antibiotics and clinically improved. Culture of the lymphadenitis obtained by CT-guided aspiration grew Granulibacter bethesdensis. …
Atrial natriuretic factor inhibits vasopressin-stimulated osmotic water permeability in rat inner medullary collecting duct.
Authors: H Nonoguchi, J M Sands, M A Knepper
Journal: Journal of Clinical Investigation (1988)

The inner medullary collecting duct (IMCD) has been proposed to be a site of atrial natriuretic factor (ANF) action. We carried out experiments in isolated perfused terminal IMCDs to determine whether ANF (rat ANF 1-28) affects either osmotic water permeability (Pf) or urea permeability. In the presence of a submaximally stimulating concentration of vasopressin (10(-11) M), ANF (100 nM) significantly reduced Pf by an average of 46%. Lower concentrations of ANF also significantly inhibited vasopressin-stimulated Pf by the following percentages: 0.01 nM ANF, 18%; 0.1 nM, 46%; 1 nM, 48%. Addition of exogenous cyclic GMP (0.1 mM) mimicked the effect of ANF, decreasing Pf by an average of 48%. ANF also inhibited cyclic AMP-stimulated Pf by an average of 31%. ANF did not affect urea permeability, nor did it alter vasopressin-stimulated cyclic AMP accumulation. We conclude that ANF at physiological concentrations causes a large inhibition of vasopressin-stimulated Pf in the rat terminal IMCD, and that cyclic GMP is the second messenger mediating the effect. ANF appears to act at a site distal to cyclic AMP generation in the chain of events linking vasopressin receptor binding to an increase in osmotic water permeability.
Activation of T cells recognizing self 60-kD heat shock protein can protect against experimental arthritis.
Authors: S M Anderton, R van der Zee, B Prakken, A Noordzij, W van Eden
Journal: The Journal of Experimental Medicine (1995)

Lewis rats are susceptible to several forms of experimental arthritis-induced using heat-killed Mycobacterium tuberculosis (adjuvant arthritis, or AA), streptococcal cell walls, collagen type II, and the lipoidal amine CP20961. Prior immunization with the mycobacterial 65-kD heat shock protein (hsp65) was reported to protect against AA, and other athritis models not using M. tuberculosis, via a T cell-mediated mechanism. Hsp65 shares 48% amino acid identity with mammalian hsp60, which is expressed at elevated levels in inflamed synovia. Several studies have reported cross-reactive T cell recognition of mycobacterial hsp65 and self hsp60 in arthritic and normal individuals. We previously described nine major histocompatibility complex class II-restricted epitopes in mycobacterial hsp65 recognized by Lewis rat T cells. Of these only one, covering the 256-270 sequence, primed for cross-reactive T cell responses to the corresponding region of rat hsp60. Here we have tested each hsp65 epitope for protective activity by immunizing rats with synthetic peptides. A peptide containing the 256-270 epitope, which induced cross-reactive T cells, was the only one able to confer protection against AA. Similarly, administration of a T cell line specific for this epitope protected against AA. Preimmunization with the 256-270 epitope induced T cells that responded to heat-shocked syngeneic antigen-presenting cells, and also protected against CP20961-induced arthritis, indicating that activation of T cells, recognizing an epitope in self hsp60 can protect against arthritis induced without mycobacteria. Therefore, in contrast to the accepted concept that cross-reactive T cell recognition of foreign and self antigens might induce aggressive autoimmune disease, we propose that cross-reactivity between bacterial and self hsp60 might also be used to maintain a protective self-reactive T cell population. This discovery might have important implications for understanding T cell-mediated regulation of inflammation.
The renin-angiotensin system in streptozotocin-induced diabetes mellitus in the rat.
Authors: J E Kalinyak, L A Sechi, C A Griffin, B R Don, K Tavangar, F B Kraemer, A R Hoffman, M Schambelan
Journal: Journal of the American Society of Nephrology (1993)

It has been hypothesized that the renin-angiotensin system plays a pathophysiologic role in the renal hemodynamic abnormalities that occur in diabetes mellitus and thereby contributes to the development of diabetic nephropathy. In this study, the tissue-specific regulation of renin and angiotensinogen mRNA levels and the abundance of glomerular angiotensin II receptors were examined in male Sprague-Dawley rats (160 to 240 g) made diabetic with streptozotocin. One subgroup of diabetic rats remained untreated, whereas a second diabetic subgroup received twice-daily doses of insulin to ameliorate hyperglycemia. Animals were euthanized 2 wk after the induction of diabetes. Mean plasma glucose levels at the time of euthanasia were significantly elevated in the untreated diabetic animals when compared with controls or insulin-treated diabetic rats. Weight gain was similar in control and insulin-treated diabetic rats, whereas the untreated diabetic rats gained significantly less. Plasma renin concentration did not differ between control, diabetic, and insulin-treated diabetic groups. In the kidney, no significant differences were found in either angiotensinogen or renin mRNA levels in diabetic animals, whereas glomerular angiotensin II receptors were significantly less abundant in untreated rats as compared with control or insulin-treated diabetic subgroups. Angiotensinogen mRNA levels were significantly lower in the livers and adrenals of diabetic rats in comparison to those in controls and insulin-treated diabetic rats, whereas angiotensinogen mRNA levels in the brain remained unaltered.(ABSTRACT TRUNCATED AT 250 WORDS)
Foot Muscle Energy Reserves in Diabetic Patients Without and With Clinical Peripheral Neuropathy
Authors: Thanh Dinh, John Doupis, Thomas E. Lyons, Sarada Kuchibhotla, Walker Julliard, Charalambos Gnardellis, Barry I. Rosenblum, Xiaoen Wang, John M. Giurini, Robert L. Greenman, Aristidis Veves
Journal: Diabetes Care (2009)

OBJECTIVE To investigate changes in the foot muscle energy reserves in diabetic non-neuropathic and neuropathic patients. RESEARCH DESIGN AND METHODS We measured the phosphocreatinine (PCr)/inorganic phosphate (Pi) ratio, total 31P concentration, and the lipid/water ratio in the muscles in the metatarsal head region using MRI spectroscopy in healthy control subjects and non-neuropathic and neuropathic diabetic patients. RESULTS The PCr/Pi ratio was higher in the control subjects (3.23 ± 0.43) followed by the non-neuropathic group (2.61 ± 0.36), whereas it was lowest in the neuropathic group (0.60 ± 1.02) (P &amp;lt; 0.0001). There were no differences in total 31P concentration and lipid/water ratio between the control and non-neuropathic groups, but both measurements were different in the neuropathic group (P &amp;lt; 0.0001). CONCLUSIONS Resting foot muscle energy reserves are affected before the development of peripheral diabetic neuropathy and are associated with the endothelial dysfunction and inflammation.
Evidence for a Functional Role of Angiotensin II Type 2 Receptor in the Cardiac Hypertrophic Process In Vivo in the Rat Heart
Authors: Zoltán Lakó-Futó, István Szokodi, Balázs Sármán, Gábor Földes, Heikki Tokola, Mika Ilves, Hanna Leskinen, Olli Vuolteenaho, Réka Skoumal, Rudolf deChâtel, Heikki Ruskoaho, Miklós Tóth
Journal: Circulation (2003)

The precise function of angiotensin II type 2 receptor (AT2-R) in the mammalian heart in vivo is unknown. Here, we investigated the role of AT2-R in cardiac pressure overload.Rats were infused with vehicle, angiotensin II (Ang II), PD123319 (an AT2-R antagonist), or the combination of Ang II and PD123319 via subcutaneously implanted osmotic minipumps for 12 or 72 hours. Ang II-induced increases in mean arterial pressure, left ventricular weight/body weight ratio, and elevation of skeletal alpha-actin and beta-myosin heavy chain mRNA levels were not altered by PD123319. In contrast, AT2-R blockade resulted in a marked increase in the gene expression of c-fos, endothelin-1, and insulin-like growth factor-1 in Ang II-induced hypertension. In parallel, Ang II-stimulated mRNA and protein expression of atrial natriuretic peptide were significantly augmented by AT2-R blockade. Moreover, PD123319 markedly increased the synthesis of B-type natriuretic peptide. Furthermore, the expression of vascular endothelial growth factor and fibroblast growth factor-1 was downregulated by Ang II only in the presence of AT2-R blockade.Our results provide evidence that AT2-R plays a functional role in the cardiac hypertrophic process in vivo by selectively regulating the expression of growth-promoting and growth-inhibiting factors.
P21WAF1, P27KIP1, TP53 and C-MYC analysis in 204 ovarian carcinomas treated with platinum-based regimens
Authors: J. Plisiecka-Hałasa, G. Karpińska, T. Szymańska, I. Ziółkowska, R. Mądry, A. Timorek, J. Dębniak, M. Ułańska, M. Jędryka, A. Chudecka-Głaz, M. Klimek, A. Rembiszewska, E. Kraszewska, B. Dybowski, J. Markowska, J. Emerich, A. Płużańska, M. Goluda, I. Rzepka-Górska, K. Urbański, J. Zieliński, J. Stelmachów, M. Chrabowska, J. Kupryjańczyk
Journal: Annals of Oncology (2003)
Impaired lung function and health status in adult survivors of bronchopulmonary dysplasia
Authors: Aisling Gough, Mark Linden, Dale Spence, Chris C. Patterson, Henry L. Halliday, Lorcan P.A. McGarvey
Journal: European Respiratory Journal (2013)

More infants with bronchopulmonary dysplasia (BPD) now survive to adulthood, but little is known regarding persisting respiratory impairment. We report respiratory symptoms, lung function and health-related quality of life (HRQoL) in adult BPD survivors compared with preterm (non-BPD) and full-term controls. Respiratory symptoms (European Community Respiratory Health Survey) and HRQoL (EuroQol (EQ)-5D) were measured in 72 adult BPD survivors (mean± sd study age 24.1±4.0 years; mean± sd gestational age 27.1±2.1 weeks; and mean± sd birth weight 955±256 g) cared for in the regional neonatal intensive care unit, Royal Maternity Hospital, Belfast, UK (between 1978 and 1993). These were compared with 57 non-BPD controls (mean± sd study age 25.3±4.0 years; mean± sd gestational age 31.0±2.5 weeks; and mean± sd birth weight 1238±222 g) and 78 full-term controls (mean± sd study age 25.7±3.8 years; mean± sd gestational age 39.7±1.4 weeks; and mean± sd birth weight 3514±456 g) cared for at the same hospital. Spirometry was performed on 56 BPD, 40 non-BPD and 55 full-term participants. BPD subjects were twice as likely to report wheeze and three times more likely to use asthma medication than controls. BPD adults had significantly lower forced expiratory volume in 1 s and forced expiratory flow at 25–75% of forced vital capacity than both the preterm non-BPD and full-term controls (all p&lt;0.01). Mean EQ-5D was 6 points lower in BPD adults compared to full-term controls (p&lt;0.05). BPD survivors have significant respiratory and quality of life impairment persisting into adulthood.
Continuous nasal positive airway pressure with a mouth leak: effect on nasal mucosal blood flux and nasal geometry.
Authors: M J Hayes, F B McGregor, D N Roberts, R C Schroter, N B Pride
Journal: Thorax (1995)

BACKGROUND--Obstructive sleep apnoea is a common condition. Treatment with nasal continuous positive airway pressure (CPAP), while effective and safe, causes nasal congestion and stuffiness in some patients. The hypothesis that this study aimed to test was that nasal CPAP with a mouth leak and subsequent unidirectional airflow across the nasal mucosa causes an increase in nasal mucosal blood flux and a fall in both nasal volume and minimal cross sectional area. A secondary aim was to study if this could be prevented by humidifying the air inspired with nasal CPAP. METHODS--Nasal CPAP was applied to eight normal subjects who kept their mouths open until they had expired 500 litres. The effect of this on nasal mucosal blood flux and nasal geometry was studied with and without humidification using a laser Doppler blood flowmeter and acoustic rhinometer. In addition, nasal mucosal blood flux was measured in four of the eight subjects before and after nasal CPAP with the mouth closed. RESULTS--Nasal CPAP using room air with the mouth closed did not result in any change in nasal mucosal blood flux; with a mouth leak nasal CPAP using room air was associated with a 65% increase in nasal mucosal blood flux. There was no change in nasal geometry. Nasal CPAP using humidified air with a mouth leak did not cause any change in nasal mucosal blood flux or nasal geometry. CONCLUSION--Nasal CPAP used with an open mouth leads to an increase in nasal mucosal blood flux. This can be prevented by humidifying the air inspired with nasal CPAP.
Book: When Smoke Ran Like Water: Tales of Environmental Deception and the Battle Against Pollution
Authors: B. Brunekreef
Journal: BMJ (2003)

Devra Davis The Perseus Press, £14.99, pp 316 http://www.theperseuspress.com/ Rating: ![Graphic][1]</img>![Graphic][2]</img> ISBN 1 903985 50 1 This book begins by describing the air pollution disasters that occurred in Donora, Pennsylvania, in 1948 and in London in 1952, along with accounts of the health effects of more current conditions. Then follows a look at scientific uncertainties in the environmental health field, and how commercial interests sometimes exploit these to postpone or derail environmental regulations. There are chapters on breast cancer and male reproductive health in relation to environmental factors, and a look at environmental health problems in developing countries and … [1]: /embed/inline-graphic-1.gif [2]: /embed/inline-graphic-2.gif
Anticancer activity of cationic porphyrins in melanoma tumour-bearing mice and mechanistic in vitro studies
Authors: Valentina Rapozzi, Sonia Zorzet, Marina Zacchigna, Emilia Della Pietra, Susanna Cogoi, Luigi E Xodo
Journal: Molecular Cancer (2014)

Porphyrin TMPyP4 (P4) and its C14H28-alkyl derivative (C14) are G-quadruplex binders and singlet oxygen (1O2) generators. In contrast, TMPyP2 (P2) produces 1O2 but it is not a G-quadruplex binder. As their photosensitizing activity is currently undefined, we report in this study their efficacy against a melanoma skin tumour and describe an in vitro mechanistic study which gives insights into their anticancer activity. Uptake and antiproliferative activity of photoactivated P2, P4 and C14 have been investigated in murine melanoma B78-H1 cells by FACS, clonogenic and migration assays. Apoptosis was investigated by PARP-1 cleavage and annexin-propidium iodide assays. Biodistribution and in vivo anticancer activity were tested in melanoma tumour-bearing mice. Porphyrin binding and photocleavage of G-rich mRNA regions were investigated by electrophoresis and RT-PCR. Porphyrin effect on ERK pathway was explored by Western blots. Thanks to its higher lipophylicity C14 was taken up by murine melanoma B78-H1 cells up to 30-fold more efficiently than P4. When photoactivated (7.2 J/cm2) in B78-H1 melanoma cells, P4 and C14, but not control P2, caused a strong inhibition of metabolic activity, clonogenic growth and cell migration. Biodistribution studies on melanoma tumour-bearing mice showed that P4 and C14 localize in the tumour. Upon irradiation (660 nm, 193 J/cm2), P4 and C14 retarded tumour growth and increased the median survival time of the treated mice by ~50% (P <0.01 by ANOVA), whereas porphyrin P2 did not. The light-dependent mechanism mediated by P4 and C14 is likely due to the binding to and photocleavage of G-rich quadruplex-forming sequences within the 5′-untranslated regions of the mitogenic ras genes. This causes a decrease of RAS protein and inhibition of downstream ERK pathway, which stimulates proliferation. Annexin V/propidium iodide and PARP-1 cleavage assays showed that the porphyrins arrested tumour growth by apoptosis and necrosis. C14 also showed an intrinsic light-independent anticancer activity, as recently reported for G4-RNA binders. Porphyrins P4 and C14 impair the clonogenic growth and migration of B78-H1 melanoma cells and inhibit melanoma tumour growth in vivo. Evidence is provided that C14 acts through light-dependent (mRNA photocleavage) and light-independent (translation inhibition) mechanisms.
The Pathophysiology of IgA Nephropathy
Authors: Hitoshi Suzuki, Krzysztof Kiryluk, Jan Novak, Zina Moldoveanu, Andrew B. Herr, Matthew B. Renfrow, Robert J. Wyatt, Francesco Scolari, Jiri Mestecky, Ali G. Gharavi, Bruce A. Julian
Journal: Journal of the American Society of Nephrology (2011)

Here we discuss recent advances in understanding the biochemical, immunologic, and genetic pathogenesis of IgA nephropathy, the most common primary glomerulonephritis. Current data indicate that at least four processes contribute to development of IgA nephropathy. Patients with IgA nephropathy often have a genetically determined increase in circulating levels of IgA1 with galactose-deficient O-glycans in the hinge-region (Hit 1). This glycosylation aberrancy is, however, not sufficient to induce renal injury. Synthesis and binding of antibodies directed against galactose-deficient IgA1 are required for formation of immune complexes that accumulate in the glomerular mesangium (Hits 2 and 3). These immune complexes activate mesangial cells, inducing proliferation and secretion of extracellular matrix, cytokines, and chemokines, which result in renal injury (Hit 4). Recent genome-wide association studies identify five distinct susceptibility loci--in the MHC on chromosome 6p21, the complement factor H locus on chromosome 1q32, and in a cluster of genes on chromosome 22q22--that potentially influence these processes and contain candidate mediators of disease. The significant variation in prevalence of risk alleles among different populations may also explain some of the sizable geographic variation in disease prevalence. Elucidation of the pathogenesis of IgA nephropathy provides an opportunity to develop disease-specific therapies.
Keratodermia blenorrhagica, arthritis, and polymyositis with cardiopulmonary complications.
Authors: S Jalava, L Paljarvi, H Isomaki
Journal: Annals of the Rheumatic Diseases (1983)

A patient is described who had polymyositis with arthritis, keratodermia blenorrhagica, pulmonary fibrosis, and cardiac failure with a right bundle branch block. The cutaneous lesions on his palms and soles, considered to be specific for Reiter9s syndrome, pointed to an overlapping of polymyositis with features of this syndrome. Findings typical of myositis were present. In addition a muscle biopsy showed sarcolemmal and endomysial deposits of IgG and IgM, and the serum level of IgM was elevated. Because skin lesions appeared at the height of symptoms in other organs, the possibility is raised that both might stem from a common immune process.
Binary oppositions and what focuses in focal attention
Authors: Cyril Latimer
Journal: Behavioral and Brain Sciences (1999)

Pylyshyn makes a convincing case that early visual processing is cognitively impenetrable, and although I question the utility of binary oppositions such as penetrable/impenetrable, for the most part I am in agreement. The author does not provide explicit designations or denotations for the terms penetrable and impenetrable, which appear quite arbitrary. Furthermore, the use of focal attention smacks of an homunculus, and the account appears to slip too easily between the perceptual, the cognitive, and the neurophysiological.
The MAGUK Family Protein CARD11 Is Essential for Lymphocyte Activation
Authors: Hiromitsu Hara, Teiji Wada, Chris Bakal, Ivona Kozieradzki, Shinobu Suzuki, Nobutaka Suzuki, Mai Nghiem, Emily K Griffiths, Connie Krawczyk, Birgit Bauer, Fulvio D'Acquisto, Sankar Ghosh, Wen-Chen Yeh, Gottfried Baier, Robert Rottapel, Josef M Penninger
Journal: Immunity (2003)