tbuckley/cabot-search huggingface dataset:
THE ESTIMATION OF UREA BY MERCURIC NITRATE.
Authors: J. H. LONG
Journal: JAMA (1903)

Since the original publications of Liebig on the use of a solution of mercuric nitrate in the urea estimation several attempts have been made to so modify the process as to render it more perfectly accurate for the purpose. Liebig himself recognized the variable character of the precipitate formed when a solution of mercuric nitrate is added to one of urea, even when the latter has a mean concentration of 2 gm. to 100 c.c. and the mercuric solution is dilute, with 1 c.c. about equivalent to 10 mg. of urea. This irregularity depends in part on the liberation of free nitric acid in the operation, and Rautenberg and others<sup>1</sup>attempted to correct for this by the gradual addition of alkali in the form of calcium carbonate. In this paper the authors recommend to correct the direct result of the titration by subtracting 0.06 c.c. of mercury solution for
Epidemiologic and Public Health Aspects of Insulin-treated Diabetes in Denmark
Authors: Anders Green
Journal: Diabetes Care (1985)

The epidemiology, mortality, and use of hospital services of insulin-treated diabetes mellitus have been studied in Fyn County, Denmark (450,000 inhabitants). The overall prevalence rate was 3.6 and 3.3 per 1000 for men and women, respectively, and overall annual incidence rates have been estimated to be 15 and 11 per 100,000, respectively. Based on a mortality analysis, it is estimated that the overall mortality rate in this patient population is 4–5% per year. During follow-up, hospital admission rates were estimated to be 0.47 and 0.53 per patient person-yr for men and women, respectively; corresponding values for estimated number of hospital bed days used by the patients were 7.2 and 9.6 per person-yr. Only 26% of the patients (74% in the age class 0–9 yr) attended a diabetes outpatient clinic at the prevalence date (1 July 1973); the remaining patients were supervised by their general practitioner. Based on these figures, an epidemiologic model for insulin-treated diabetes has been formulated, and it is concluded that this disease represents a major public health problem.
A distal single nucleotide polymorphism alters long-range regulation of the PU.1 gene in acute myeloid leukemia
Authors: Ulrich Steidl, Christian Steidl, Alexander Ebralidze, Björn Chapuy, Hye-Jung Han, Britta Will, Frank Rosenbauer, Annegret Becker, Katharina Wagner, Steffen Koschmieder, Susumu Kobayashi, Daniel B. Costa, Thomas Schulz, Karen B. O’Brien, Roel G.W. Verhaak, Ruud Delwel, Detlef Haase, Lorenz Trümper, Jürgen Krauter, Terumi Kohwi-Shigematsu, Frank Griesinger, Daniel G. Tenen
Journal: Journal of Clinical Investigation (2007)

Targeted disruption of a highly conserved distal enhancer reduces expression of the PU.1 transcription factor by 80% and leads to acute myeloid leukemia (AML) with frequent cytogenetic aberrations in mice. Here we identify a SNP within this element in humans that is more frequent in AML with a complex karyotype, leads to decreased enhancer activity, and reduces PU.1 expression in myeloid progenitors in a development-dependent manner. This SNP inhibits binding of the chromatin-remodeling transcriptional regulator special AT-rich sequence binding protein 1 (SATB1). Overexpression of SATB1 increased PU.1 expression, and siRNA inhibition of SATB1 downregulated PU.1 expression. Targeted disruption of the distal enhancer led to a loss of regulation of PU.1 by SATB1. Interestingly, disruption of SATB1 in mice led to a selective decrease of PU.1 RNA in specific progenitor types (granulocyte-macrophage and megakaryocyte-erythrocyte progenitors) and a similar effect was observed in AML samples harboring this SNP. Thus we have identified a SNP within a distal enhancer that is associated with a subtype of leukemia and exerts a deleterious effect through remote transcriptional dysregulation in specific progenitor subtypes.
Nonabandonment: Medical Ethics
Authors: Gregory B. Patrick
Journal: Annals of Internal Medicine (1995)

Letters15 September 1995Nonabandonment: Medical EthicsGregory B. Patrick, MDGregory B. Patrick, MDSewickley Medical Association; Sewickley, PA 15143Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-123-6-199509150-00023 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail TO THE EDITOR:Quill and Cassel's concept of nonabandonment [1] is a worthwhile ethical obligation inherent in the physician–patient relationship. However, this concept is largely irrelevant in today's economic climate.The relationship may be ripped asunder if the patient's employer chooses to change insurance companies. If the physician is not part of the panel, the patient may not be permitted to see the physician at all. Within the network, if the relationship is between a patient and a specialist, the “gatekeeper” must agree to maintain the relationship. Note that the gatekeeper might not have any choice either. Insurance plans actively ...References1. Quill TE, Cassel CK. Nonabandonment: a central obligation for physicians. Ann Intern Med. 1995; 121:368-74. Google Scholar Author, Article, and Disclosure InformationAffiliations: Sewickley Medical Association; Sewickley, PA 15143 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 15 September 1995Volume 123, Issue 6Page: 473KeywordsMedical ethics Issue Published: 15 September 1995 Copyright & PermissionsCopyright © 1995 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
5 P53 DELETION INDUCES PROLONGED SURVIVAL OF BIPOTENT LIVER STEM CELLS AND THE EVOLUTION OF BI-DIFFERENTIATED HEPATO-CHOLANGIOCELLULAR CARCINOMA
Authors: S.-F. Katz, A. Lechel, Y. Begus-Nahrmann, D. Hartmann, P. Schirmacher, K.L. Rudolph
Journal: Journal of Hepatology (2010)
Two of Them
Authors: Jack Coulehan
Journal: Annals of Internal Medicine (1997)

Ad Libitum15 October 1997Two of ThemJack Coulehan, MDJack Coulehan, MDSetauket, NY 11733Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-127-8_Part_1-199710150-00016 SectionsAboutFull TextPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail The old Russian couplein adjoining chairsteeter toward each otherand tell me everything.She demonstrates the joltat the edge of sleepby jabbing a finger at me,vindicatively.He shows his scalp-it crawlswith emptiness at nightand keeps him up. There,he bats it behind his ear.I think he sold diamondsfor a living, enoughto convince himself, hesaid once, it's not muchof a life. At the endof her list is Need sleepunderlined twice, and Whathappened to my eyes? Author, Article, and Disclosure InformationAffiliations: Setauket, NY 11733Corresponding Author: Jack Coulehan, MD, 4 Townsend Court, Setauket, NY 11733. Previousarticle Advertisement FiguresReferencesRelatedDetails Metrics 15 October 1997Volume 127, Issue 8_Part_1Page: 651 ePublished: 15 August 2000 Issue Published: 15 October 1997 Copyright & PermissionsCopyright © 1997 by American College of Physicians. All Rights Reserved.PDF downloadLoading ...
Critical role for classical PKC in activating Akt by phospholipase A<sub>2</sub>-modified LDL in monocytic cells
Authors: Stefan Preiß, Dmitry Namgaladze, Bernhard Brüne
Journal: Cardiovascular Research (2006)

Modification of low density lipoprotein (LDL) by phospholipases confers pro-atherogenic properties, although signalling pathways of phospholipase-modified LDL (PLA-LDL) remain obscure. We questioned whether members of the protein kinase C (PKC) family are involved in PLA-LDL-induced Akt phosphorylation and survival of THP-1 monocytic cells.Akt phosphorylation in THP-1 cells was monitored by Western analysis. To modulate PKC expression cells were transfected with dominant-negative enhanced green fluorescent protein linked PKCalpha (PKCalpha-EGFP K368R) and PKCbeta (PKCbeta-EGFP K371M) constructs or with siRNA specific for PKCalpha/PKCbeta using nucleofection technology. Cell survival was assessed by Annexin V/propidium iodide staining or mitochondrial membrane potential measurement with 3,3'-dihexyloxacarbocyanine iodide (DiOC(6)) using flow cytometry.Inhibitors of phospholipase C (PLC) or classical PKCs as well as PKC depletion following phorbol ester treatments, blocked Akt phosphorylation in response to PLA-LDL. In contrast, phosphatidylinositol 3-kinase (PI3K) activation by PLA-LDL was insensitive to PKC inhibition. Using RNA interference to knockdown PKCalpha and overexpression of dominant-negative PKCalpha as well as PKCbeta drastically lowered Akt phosphorylation after PLA-LDL. Moreover, inhibition of PKC attenuated a PLA-LDL-induced survival response towards oxidative stress in THP-1 cells.We show that PKCalpha and PKCbeta are critical for PLA-LDL-induced Akt phosphorylation and survival in THP-1 monocytic cells.
Regulation of Insulin-Gene Expression
Authors: Jeffrey S. Flier, Lisa H. Underhill, Richard F. Selden, Marek J. Skośkiewicz, Paul S. Russell, Howard M. Goodman
Journal: New England Journal of Medicine (1987)

DURING the past decade, the focus of mammalian molecular biology has evolved from the characterization of gene structure to the regulation of gene expression. In parallel, the ability to manipulate isolated DNA in vitro has led to the development of methods for the modification of the genomes of both individual cells and whole animals. These technological leaps have now made it worthwhile to consider new remedies for human genetic diseases as well as for some deficiency states that are not genetically determined. In this review, we examine the regulation of mammalian gene expression and several approaches to gene therapy, using . . .
Enhancer Stimulation Unmasks Latent Gene Transfer After Adenovirus-Mediated Gene Delivery Into Human Vascular Smooth Muscle Cells
Authors: Gerald J. Clesham, Helena Browne, Stacey Efstathiou, Peter L. Weissberg
Journal: Circulation Research (1996)

Recombinant adenoviral vectors are being used increasingly for gene transfer studies in mammalian cells and gene therapy protocols in humans. High adenoviral titers are often required for successful transduction of vascular smooth muscle cells (VSMCs), defined as uptake and detectable expression of the foreign gene, but the relative contributions of efficiency of viral uptake and control of transcription are poorly understood. To explore the extent to which a lack of detectable gene expression may be due to inefficient transcription of a successfully transferred gene, we have used a replication-deficient adenovirus expressing β-galactosidase (RAd35β-Gal), under the control of the human cytomegalovirus major immediate-early promoter (CMV-IEP), which contains cAMP and nuclear factor-κB response elements, to investigate constitutive and inducible gene expression after gene transfer into human VSMCs. Histochemical staining with 5-bromo-4-chloro-3-indolyl β- d -galactopyranoside (X-gal), a quantitative spectrophotometric assay, SDS-PAGE, Western blotting, and Northern analysis were used to evaluate β−galactosidase expression in infected cells. After infection with RAd35β-Gal at 30, 100, and 1000 plaque-forming units per cell (pfu/cell), expression of β-galactosidase was augmented up to 17-, 19-, and 23-fold, respectively, in human VSMCs treated with forskolin and phorbol ester compared with unstimulated cells. After infection, the proportion of detectably transduced cells was increased by enhancer stimulation from 58% to 100% at 100 pfu/cell and from 9% to 62% at 10 pfu/cell, indicating quiescent viral DNA in unstimulated cells. At high adenoviral titers (1000 pfu/cell), the recombinant gene became the most abundant protein in cell extracts. These findings demonstrate that in human VSMCs, limited constitutive expression from the CMV-IEP, rather than failure of translocation of adenoviral DNA, may be responsible for the apparent failure of transduction at a low multiplicity of infection.
Abstract 3454: Integrin-linked kinase and proximal signaling contributes to the cisplatin resistance of ovarian cancer cells
Authors: Daniel Soto, Fatima Valiyeva, Ileabett Echevarria, Jeyshka Reyes, Pablo E. Vivas-Mejia
Journal: Cancer Research (2014)

Abstract Platinum-based chemotherapy has been used for more than four decades for ovarian cancer patients. Although initially most ovarian tumors respond well to cisplatin treatment, many of the tumors become resistant to chemotherapy. Several drug resistant-associated genes have been identified by gene expression arrays in drug sensitive and drug resistant cells. Recent evidence indicates that posttranscriptional and posttranslational regulation of gene expression governs the function of several proteins associated with cancer initiation, progression and drug resistance. To reveal additional proteins associated with cisplatin resistance, we performed a proteomic analysis in cisplatin sensitive (A2780) and cisplatin resistant (A2780CP20) ovarian cancer cells. Forty-seven, out of 148 identified proteins, were differentially abundant in A2780CP20 compared with A2780 cancer cells. Western blot analysis was used to confirm the proteomic results. Particularly, the Integrin-Linked Kinase-Associated Serine/Threonine Phosphatase 2C (ILKAP) was decreased in A2780CP20 compared with A2780 cells. The phosphorylation levels of the Integrated-Linked Kinase ILK (the major ILKAP effector), protein kinase B (AKT), and glycogen synthase kinase 3β (GSK3β) (two ILK downstream effectors) were higher in A2780CP20 compared with A2780 cells. Small-interference RNA (siRNA)-targeted ILK, reduced the phosphorylation levels of AKT and GSK3β; and reduced cell proliferation and invasion of the A2780CP20 cells. Most important, combination of inactive ILK-targeted siRNA doses plus inactive cisplatin doses reduced cell growth in a synergistic-like way. These results indicate that protein phosphorylation of the ILK/AKT/GSK3β cascade play a vital role in cisplatin resistance, and propose ILK as a therapeutic target for advanced and drug resistant ovarian cancer. Citation Format: Daniel Soto, Fatima Valiyeva, Ileabett Echevarria, Jeyshka Reyes, Pablo E. Vivas-Mejia. Integrin-linked kinase and proximal signaling contributes to the cisplatin resistance of ovarian cancer cells. [abstract]. In: Proceedings of the 105th Annual Meeting of the American Association for Cancer Research; 2014 Apr 5-9; San Diego, CA. Philadelphia (PA): AACR; Cancer Res 2014;74(19 Suppl):Abstract nr 3454. doi:10.1158/1538-7445.AM2014-3454
Neurologic Abnormalities of Lyme Disease: Successful Treatment with High-Dose Intravenous Penicillin
Authors: ALLEN C. STEERE
Journal: Annals of Internal Medicine (1983)

Twelve patients were treated with high-dose intravenous penicillin for neurologic abnormalities of Lyme disease. Headache, stiff neck, and radicular pain usually began to subside by the second day of therapy and were often gone by 7 to 10 days. Five of the 12 patients continued to have intermittent mild headache for several more weeks, but no patient relapsed after therapy was stopped. Compared to 15 previous patients treated with prednisone alone, the duration of meningitic syndrome was significantly shorter in those given penicillin (mean duration, 1 versus 29 weeks, p less than 0.000001). However, in both groups, a mean of 7 to 8 weeks was required for complete recovery of motor deficits. Despite antibiotic therapy, 3 of the 12 patients treated with penicillin continued to have frequent arthralgias, musculoskeletal pain, and fatigue. We conclude that high-dose intravenous penicillin is effective therapy for neurologic abnormalities of Lyme disease.
A woman with acute myelopathy in pregnancy: case outcome
Authors: R. Reuss, P. S Rommer, W. Bruck, F. Paul, M. Bolz, S. Jarius, T. Boettcher, A. Grossmann, A. Bock, F. Zipp, R. Benecke, U. K Zettl
Journal: BMJ (2009)

Before inserting a chest drain, individual doctors should always ask themselves:• Do I need to do this?(The presence of a pneumothorax or pleural effusion does not automatically require insertion of a chest drain.)• Does it need to be done as an emergency or can it wait?(There are few indications for chest drain insertion as an emergency "out of hours.")• Have I had enough training to feel confident to do this?Are senior staff to hand? • Am I familiar with this equipment?• Is ultrasound available, with trained staff, to enable me to position the drain safely?And if something were to go wrong (for example, if no portable ultrasound machine is available on the ward) the doctor should always report this as a patient safety incident so that local action can be taken and others can learn. What else do we need to know?Queries from clinicians after the issue of the NPSA's RRR highlighted further areas of uncertainty: competencies and training (such as the minimum number of procedures required before a clinician is safe to practise, and the use of manikins for simulation); relative safety and effectiveness of different techniques (small versus large bore drains; Seldinger technique versus blunt dissection); appropriate use of thoracic ultrasonography and, if this is performed by physicians, the minimum amount of training required. 4 These areas of uncertainty will be clarified by the British Thoracic Society, which is currently updating its guidelines on pleural procedures and has also published guidance to help clinicians implement the recommendation in the RRR. 5 How will we know when practice has become safer?No national baseline data on pleural procedures are available, but in a survey of 99 UK trusts in 2008, two thirds had encountered major complications associated with chest drain insertion (including 17 deaths) in the preceding five years, suggesting higher rates of harm than indicated by incident reporting.Only 11 trusts had a formal training policy for chest drain insertion, and only a fifth routinely sought written patient consent.Chest drains were commonly inserted by junior trainees.
Management of Foreign Bodies in the Esophagus
Authors: Martin S. Kleinman
Journal: JAMA (1976)

<h3>To the Editor.—</h3> I should like to comment on Dr Palmer's discussion of the management of foreign bodies in the esophagus ("Backyard Barbecue Syndrome," 235:2637, 1976). As Dr Palmer suggests, we tend to approach the impacted bolus of meat endoscopically with expedition. Contrary to his experience, we have had excellent success using fiberoptic endoscopic equipment in this procedure. We have found that endoscopes used in conjunction with available special service biopsy forceps and polypectomy snares provide an excellent method for removing food that has become impacted in the distal esophagus. In general, a bolus of food can be removed with the polypectomy snare. To do this, one "lassos" the bolus and then pulls it and the gastroscope out together, thus removing the food bolus. Since the bolus is liable to fragment, this often takes three to six passages of the gastroscope. Often, the food bolus is sufficiently modified in size
Acute Psychiatric Services in the General Hospital: III. Statistical Survey
Authors: JAMES J. MULLER, MORRIS E. CHAFETZ, HOWARD T. BLANE
Journal: American Journal of Psychiatry (1967)

From the point of view of community mental health, the critical aspect of the acute psychiatric admission to a general hospital service lies in the opportunity to establish a needed treatment relationship during the brief interval the patient (who is often chronic) is motivated to accept it. There is evidence that lower-class, chronic patients follow through on long-range treatment programs when such programs are actively promoted in the emergency service.
The Frequency and Determinants of Metabolic Syndrome in Patients with Operable Stage I-III Breast Cancer.
Authors: S. Aksoy, [. Dizdar, D. Dede, C. Arslan, E. Dogan, [. Tapan, [. Özkan, S. Hesenov, M. Cinel, S. Yaman, M. Kizilarslan, Y. Özisik, K. Altundag
Journal: Cancer Research (2009)

Abstract Background: Metabolic syndrome is a cluster of multiple risk factors including obesity, insulin resistance, hypertriglyceridemia, low HDL (high density lipoprotein), and hypertension. Metabolic syndrome is associated with an increased risk of breast cancer. We evaluated the frequency and determinants of metabolic syndrome in patients with operable stage I-III breast cancer.Methods: In this cross-sectional study we analyzed the frequency and determinants of metabolic syndrome in patients with stage I-III breast cancer. Metabolic syndrome was defined according to NCEP (National Cholesterol Education Program) definitions. Data on metabolic syndrome criteria were collected along with demographic data, tumor size, grade, lymph node, estrogen, progesterone, HER2 status, grade and history of chemotherapy/endocrine therapy.Results: A total of 331 patients were analyzed. Median age was 50.0 years (range 20-84 years). Eighty-five patients were using tamoxifen, 98 patients were using aromatase inhibitors and the remaining 148 patients were not receiving hormonal therapy (newly diagnosed and/or triple-negative patients). According to the NCEP criteria 48.0% of the patients had metabolic syndrome. More patients receiving aromatase inhibitors had metabolic syndrome than those receiving tamoxifen (60.2% vs. 37.6%, p = 0.008). The frequency of MS among those not taking any hormonal therapy was 45.9%. Additionally, post-menopausal patients had higher rate of MS compared to pre-menopausal ones (53.4% vs. 25.0% p=&amp;lt;0.001). Patients with HER2 positive tumors and patients who had a history of oral contraceptive use had lower rates of metabolic syndrome than those with HER2 negative tumors and no oral contraceptive use, respectively (40,0% vs. 53,7% for HER2, p=0.028 and 32,6% vs. 50,3% for oral contraceptive use, p=0.034).There was no significant correlation between the presence of metabolic syndrome and estrogen/progesterone receptor status, tumor size, nodal status, stage, grade, adjuvant chemotherapy, hormone replacement therapy, smoking history.Conclusions: Nearly half of the patients with stage I-III breast cancer had metabolic syndrome. Adjuvant aromatase inhibitor therapy was found to be associated with higher rate of metabolic syndrome whereas history of oral contraceptive use and HER2 positivity were associated with lower rate. Whether the aromatase inhibitors contribute the development of metabolic syndrome or not needs to be elucidated by future prospective studies. Citation Information: Cancer Res 2009;69(24 Suppl):Abstract nr 5121.
Cobalamin as coenzyme: A twisting trail of research
Authors: William S. Beck
Journal: American Journal of Hematology (1990)

Abstract Cobalamin derivatives serve as coenzymes for the body's two cobalamin‐dependent enzymes—adenosylcobalamin‐dependent methylmalonyl CoA mutase, and methylcobalamin‐dependent methionine methyltransferase. This essay reviews, in brief form and in personal terms, the history, beginning in the mid‐1950s, of how these enzymes and coenzymes were discovered and what has been learned of their reaction mechanisms. It is clear that because of the fragility of the unique carbon‐cobalt bond in Cobalamin coenzymes, they serve primarily as free radical formers. This accounts for their efficiency in abstracting hydrogen from substrate molecules and for a subsequent chain of events that results in the isomerization of methylmalonyl CoA, the transfer of methyl groups, and (in certain bacteria) the reduction of ribonucleotides. Some thoughts are offered on the possible evolutionary significance of these facts.
Telephony remains useful in medical informatics
Authors: B W Lloyd, M A Rossiter, D Gurtin
Journal: BMJ (1995)

EDITOR,—Enrico Coiera1 and Paul McLaren and C J Ball2 point out that even in the midst of recent technological advances the telephone remains a valuable tool for doctors. We have recently shown that, in north London at least, the telephone's potential for improving communication between consultants and general practitioners has not been realised.

We sent a questionnaire to …