tbuckley/cabot-search huggingface dataset:
Diaphragmatic fatigue following voluntary hyperpnea.
Authors: J M Mador, A Rodis, J Diaz
Journal: American Journal of Respiratory and Critical Care Medicine (1996)

The purpose of this study was to determine whether diaphragmatic fatigue occurs after voluntary hyperpnea to task failure. Ten male subjects were asked to breathe at minute ventilation (V1) equal or slightly greater than 60% of their 12-s maximum voluntary ventilation (MVV) until task failure. Transdiaphragmatic pressure (Pdi) was measured during bilateral supramaximal stimulation of the phrenic nerves before and 10, 30, 60, and 120 min after hyperpnea. For the group, V1 averaged 107.1 +/- 7.1 L/min (SE) (range, 71-154 L/min), which represented 60 +/- 2% of the MVV. After voluntary hyperpnea, seven of the 10 subjects displayed at least a 10% reduction in twitch Pdi during transcutaneous stimulation, while all 10 subjects had a greater than 10% reduction in twitch Pdi during cervical magnetic stimulation. For the group, transcutaneous twitch Pdi was significantly decreased from 27.0 +/- 1.9 at baseline to 21.4 +/- 1.7 cm H2O (p < 0.0001) at 10 min posthyperpnea. Magnetic twitch Pdi was also significantly decreased from 36.0 +/- 2.1 at baseline to 28.7 +/- 1.9 cm H2O (p < 0.0001) at 10 min posthyperpnea. Twitch Pdi remained significantly decreased from baseline for at least 1 h after hyperpnea. After hyperpnea, the mean percentage decrease from baseline in twitch Pdi was virtually identical with the two stimulation techniques. The percentage fall in twitch Pdi after hyperpnea with the two techniques was not significantly correlated (r = 0.4). In conclusion, long-lasting contractile fatigue of the diaphragm reliably occurs after voluntary hyperpnea at levels sufficient to induce task failure. Cervical magnetic stimulation can detect diaphragmatic fatigue after a fatiguing task, but the results obtained with this technique may differ from those obtained with transcutaneous stimulation in individual subjects.
An unusual case of carbon monoxide poisoning.
Authors: P L Auger, B Levesque, R Martel, H Prud'homme, D Bellemare, C Barbeau, P Lachance, M Rhainds
Journal: Environmental Health Perspectives (1999)

Carbon monoxide, a gas originating from incomplete combustion of carbon-based fuels, is an important cause of human deaths. In this paper, we describe an unusual carbon monoxide poisoning in a dwelling without obvious sources of combustion gases, for which two adults had to be treated in a hyperbaric chamber. Carbon monoxide readings were taken in the house and in the neighboring homes. Methane gas and nitrogen oxide levels were also monitored in the house air. Soil samples were collected around the house and tested for hydrocarbon residues. The investigation revealed the presence of a pocket of carbon monoxide under the foundation of the house. The first readings revealed carbon monoxide levels of 500 ppm in the basement. The contamination lasted for a week. The investigation indicated that the probable source of contamination was the use of explosives at a nearby rain sewer construction site. The use of explosives in a residential area can constitute a major source of carbon monoxide for the neighboring populations. This must be investigated, and public health authorities, primary-care physicians, governmental authorities, and users and manufacturers of explosives must be made aware of this problem.
Peniscopically Controlled CO2 Laser Excision for Conservative Treatment of In Situ and T1 Penile Carcinoma: Report on 224 Patients
Authors: Gaetano Bandieramonte, Maurizio Colecchia, Luigi Mariani, Salvatore Lo Vullo, Giorgio Pizzocaro, Luigi Piva, Nicola Nicolai, Roberto Salvioni, Valentina Lezzi, Bernardina Stefanon, Giuseppe De Palo
Journal: European Urology (2008)
The gene transfection efficiency of a folate–PEI600–cyclodextrin nanopolymer
Authors: Hong Yao, Samuel S. Ng, Wesley O. Tucker, Yuk-Kai-Tiu Tsang, Kwan Man, Xiao-mei Wang, Billy K.C. Chow, Hsiang-Fu Kung, Gu-Ping Tang, Marie C. Lin
Journal: Biomaterials (2009)
ALOPECIA OF BEARD FOLLOWING PHRENICECTOMY
Authors: Fred A. Kennedy
Journal: JAMA (1933)

This case is reported because of the unusual complications following a phrenicectomy. A Horner's syndrome followed an attempt to cause paralysis of the diaphragm on the right side, as manifested by a narrowing of the palpebral aperture and miosis. This was later followed by an alopecia of the beard along the submaxillary space.  A white man, aged 36, a farmer, who had had spinal meningitis in infancy, without complications or sequels, stated that in 1918 he caught cold easily, had a persistent cough with increased sputum, weakness and dyspnea on exertion, and lost 20 pounds (9 Kg.). In 1920 he had pleurisy on the left side. A diagnosis of colitis with some evidence of ulceration, possibly tuberculosis, was made in 1930, after examination with the sigmoidoscope. Previously he had been in and out of many government hospitals for treatment of pulmonary tuberculosis.  In October, 1930, Dr. E. J. O'Brien did
An abnormal triglyceride-rich lipoprotein containing excess sialylated apolipoprotein C-III.
Authors: G Holdsworth, J Stocks, P Dodson, D J Galton
Journal: Journal of Clinical Investigation (1982)

An abnormal triglyceride-rich lipoprotein has been isolated from some patients with chronic renal failure or severe hypertriglyceridemia. The abnormal lipoprotein was characterized by an increased content of apolipoprotein (apo) C-III-2 (57.5% of total apo C-III peptides compared with 35.5% for controls, P less than 0.001) as characterized by isoelectric focusing and scanning densitometry. As determined by a substrate competition assay, the abnormal lipoprotein was a less efficient substrate for purified bovine milk lipoprotein lipase than control lipoproteins. Neuraminidase digestion of abnormal or control lipoprotein resulted in a reduction of the apo C-III-2 band with a corresponding increase in the region of apo C-III-0, which suggests that the increased content of apo C-III-2 in the abnormal is due to excessive sialylation of the C-III peptide. Limited incubation of the abnormal lipoproteins with neuraminidase caused a partial loss of sialic acid and resulted in a triglyceride-rich lipoprotein with a normal C-III-2:C-III-1 ratio. This preparation displayed normal substrate interaction with lipoprotein lipase. Three severely hypertriglyceridemic patients with the abnormal lipoprotein showed a marked reduction in serum triglyceride concentration, which is associated with a reversion to a normal C-peptide profile after dietary therapy. The results suggest that the extent of sialylation of the apo C-III peptide carried on triglyceride-rich lipoproteins may be critical for their interaction with lipoprotein lipase.
Hypertransaminasaemia with heparin treatment: effect of regular haemodialysis.
Authors: J G Salway, G S Walker
Journal: BMJ (1976)

Comparison of intravenous and aerosol salbutamolAerosol salbutamol has a prolonged bronchodilator effect' and is more potent than an equal intravenous dose.2We have studied both routes of administration in asthmatic patients to compare their length of action. Patients, methods, and resultsFive patients with well controlled asthma were studied.Their asthma showed no significant diurnal variation.All were being treated with salbu- tamol by regular inhalation, and three took prednisone.They were studied on two consecutive mornings, having stopped bronchodilator drugs for 12 hours. CommentThese results indicate that routine heparin treatment during standard haemodialysis three times a week caused no significant acute change in the SGPT activity.Moreover, the range of SGPT values was not significantly different from that of the normal population, suggesting that chronic, intermittent heparin treatment does not cause on 12 August
Poetry and medicine. "To waken an old lady."
Authors: J. Mukand
Journal: JAMA (1988)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Drug Thieves at the Doctor's Office
Authors: Carol Barrett
Journal: JAMA (1991)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Treatment of Advanced Hormone-Sensitive Breast Cancer in Postmenopausal Women With Exemestane Alone or in Combination With Celecoxib
Authors: Luc Yves Dirix, Jorge Ignacio, Shona Nag, Poonamally Bapsy, Henry Gomez, Digumarti Raghunadharao, Robert Paridaens, Stephen Jones, Silvia Falcon, Marina Carpentieri, Antonello Abbattista, Jean-Pierre Lobelle
Journal: Journal of Clinical Oncology (2008)

Preclinical data showed that the combination of exemestane and celecoxib has synergistic effects. Therefore, a study was undertaken to explore the efficacy and tolerability of this combination in postmenopausal patients with advanced, hormone-sensitive breast cancer.A randomized phase II study was conducted in postmenopausal patients with hormone-sensitive breast cancer and measurable disease who had progressive disease after treatment with tamoxifen. Patients were randomly assigned to either exemestane 25 mg daily or the combination of exemestane 25 mg daily with celecoxib 400 mg twice daily. Response Evaluation Criteria in Solid Tumors Group criteria were used to determine antitumor efficacy. Primary end point was the rate of clinical benefit. Secondary end points were tolerability, objective response rate, time to progression (TTP), and duration of clinical benefit. A pharmacodynamic and a pharmacokinetic study were conducted in parallel.One hundred eleven patients (exemestane, n = 55; combination, n = 56) were enrolled in 2002. The demographic characteristics and prognostic factors were similar in both arms. In the assessable population, 24 of 51 patients in the combination arm and 24 of 49 patients in the exemestane arm achieved clinical benefit. TTP was similar in both groups. Duration of clinical benefit was longer in the combination group (median, 96.6 v 49.1 weeks). The addition of celecoxib did not change the tolerability profile of exemestane alone.Similar rates of clinical benefit were achieved in both groups.
ON ANKYLOSTOME INFESTATION: THE CHANGING PROBLEM
Authors: C. Lane
Journal: BMJ (1923)

TJ 55'tlhe generally accepted view.After reviewing the conditions in which an increased blood pressure is generally regarded as responsible for the vascular lesion, lhe remarks that "the factor of increased content of mnetabolites in the blood is also involved," and he expresses the opinion that an increased blood pressure cannot be excluded from the etiology of arterio-sclerosis, and that " it is witlhout doubt an accessory factor in the production of arterio-sclerosis provoked by other causes."For a full discussion of this subject reference should be made to Allbutt, Andrewes, Thorel, MacCallum, and Moschcowitz.Whetlher, however, a degenerative or proliferative lesion results from the action of a toxin on the vessel wall, ma,y depend on the one lhand on the nature of the pathogenic agent.On the other hand, tlle power of resistance of vascular tissues to the pathogenic agent must be an important deter- nmining factor, and it is possible that whether diffuse hyper- plastic sclerosis or senile arterio-sclerosis result depends rather on the vitalitv of the tissues affected than on the nature of the pathogenic agent.There is some evidence in favour of this view, and factors such as age and inheritance find their due place in the tangle of causation in the extent to Yvhich they undermine and modify the reaction of vascular tissues to insult.Thus there is no reason to believe that age in itself is the cause of arterio-sclerosis, and Ophuls"2 has slhown that the curve of incidence of arterio-sclerosis does not correspond with what would be expected if the lesion were the direct result of it and of the senile deterioration associated with it.3. Monckeberg's Sclerosis.Mnckeberg's sclerosis illustrates this aspect of the problem from another point of view.The form of sclerosis that he describes is often included in the senile form of arterio-sclerosis; it does indeed often occur in old age, and it is like senilearteriosclerosis in the fact that it is apparently a primary affection of -the media and is characterized by calcification, In a sense it is more senile than senile-arterio- sclerosis, for the intima often fails to proliferate, and when it occurs it is often late in the evolution of the lesion as a tardy process of repair.But it is -not age'that has weakened the vessel walls and prevented their reaction to insult-it is disease, not local but general; thus of the 12 pure cases described in M6nckeberg's original paper,2n 4 died of cancer, 4 died of phthisis, 1 of advanced morbus cordis, and 3 of cachexia due to chronic infection.I think it is here that diabetes mellitus sometimes finds its place in the etiology of arterio-sclerosis.SUMMARY.
Relationship between daily dose of oral medications and idiosyncratic drug-induced liver injury: Search for signals
Authors: Craig Lammert, Stefan Einarsson, Chandan Saha, Anna Niklasson, Einar Bjornsson, Naga Chalasani
Journal: Hepatology (2008)

Idiosyncratic drug-induced liver injury (DILI) is traditionally thought not to be dose-related. However, it has been pointed out that most medicines that were withdrawn from marketing or received a black-box warning because of hepatotoxicity were prescribed at daily doses greater than 50 mg/day. To examine the relationship between daily dose of medications and idiosyncratic DILI, we conducted a study with two aims. First, using two pharmaceutical databases, we examined the relationship between daily dose of commonly prescribed medicines in the United States and reported frequency of their selected hepatic adverse events. Second, we examined serious DILI cases reported to the Swedish Adverse Drug Reactions Advisory Committee (1970-2004) for any signals supporting the relationship between daily dose and idiosyncratic DILI. Medications were categorized into ≤10 mg/day, 11-49 mg/day, and ≥50 mg/day groups. Among US prescription medicines, a statistically significant relationship was observed between daily dose of oral medicines and reports of liver failure ( P = 0.009), liver transplantation ( P &lt; 0.001), and death caused by DILI ( P = 0.004) but not alanine aminotransferase (ALT) &gt; 3 × upper limit of normal ( P = 0.10) or jaundice ( P = 0.16). Of 598 eligible Swedish DILI cases, 9% belonged to the ≤10 mg/day group, 14.2% to the 11-49 mg/day group, and 77% of cases were caused by medications given at dose ≥50 mg/day. A statistically significant relationship was noted between daily dose and poor outcome (death or liver transplantation) of Swedish DILI cases (2%, 9.4%, and 13.2% in ≤10, 11-49, and ≥50 mg/day groups, respectively, P = 0.03). Conclusion: These data suggest a relationship between daily doses of oral prescription medications and idiosyncratic DILI. More studies are needed to validate these observations and to explore their implications.
The Role of Data Audits in Detecting Scientific Misconduct-Reply
Authors: Drummond Rennie
Journal: JAMA (1990)

<h3>In Reply.—</h3> Wyllie et al<sup>1</sup>believed that the bioavailability of generic primidone was deficient. They may well have been right about the bioavailability: I do not pretend to know. This issue is addressed in the response above from Nightingale and colleagues. As Dr Conomy indicates, I did not address the issue of bioavailability in my editorial,<sup>2</sup>which was certainly not written to "acknowledge or address" all the points they made in their article, far less to pronounce on their correctness. The editorial question that the article by Wyllie et al posed, and the question I addressed, was not the correctness of the data, but the provision of all relevant data. The reason that Wyllie et al looked into the question of bioavailability of primidone in the first place was, I believe, because the patient's seizures increased in frequency. If, shortly afterward (and well before submittal of the
EPA: airing on the side of caution or pulling standards out of thin Air?
Authors: K Breslin
Journal: Environmental Health Perspectives (2000)

In May 1999, a federal appeals court ruled that the U.S. Environmental Protection Agency (EPA) had violated the Constitution when it strengthened regulations for ground-level ozone and particulate matter (PM). Although the court did not question the validity of the EPA's scientific basis for establishing the PM and ozone standards, it did challenge how the EPA selected the particular levels since the scientific record in both rules did not indicate unequivocally where the standards should be set. The agency failed to identify an "intelligible principle" that would guide such choices, the court said, and thereby exceeded the power it was granted by Congress. Because scientific uncertainty attends so much rule making, the ruling leaves open the question of when the EPA may make what is essentially a policy determination versus when those determinations must be made by Congress. For this reason, observers consider the ruling to have potentially significant implications beyond just the ozone and PM standards that may affect other EPA regulations and regulations by other agencies.
Use of digitalis in general practice.
Authors: R Krakauer
Journal: BMJ (1978)

The Department understands that in general the shortage is not expected to be troublesome but may cause difficulties in some fields of surgical or medical practice where alternative drugs are less satisfactory.The decision as to the most appropriate treatment for particular patients rests, of course, with the doctor responsible.I believe, however, that in the circumstances all doctors will wish to do all that they can to preserve the limited stocks of cocaine by using alternative drugs wherever possible.
Defective insulin response of phosphorylase phosphatase in insulin-resistant humans.
Authors: Y Kida, I Raz, R Maeda, B L Nyomba, K Stone, C Bogardus, J Sommercorn, D M Mott
Journal: Journal of Clinical Investigation (1992)

Insulin-stimulated glycogen synthase activity in human muscle is reduced in insulin-resistant subjects. Insulin regulation of human muscle glycogen synthase may require activation of a type-1 protein phosphatase (PP-1). We investigated the change of phosphorylase phosphatase and glycogen synthase activities in muscle biopsies obtained during a 2-h hyperinsulinemic euglycemic clamp in 12 insulin-sensitive (group S) and 8 insulin-resistant (group R) subjects. Fasting phosphorylase phosphatase activity was lower in group R than in group S, and did not increase significantly with insulin infusion in group R until 20 min. In group S, phosphorylase phosphatase was significantly stimulated by 10 min, remaining significantly higher than in group R at all time points. The insulin-mediated changes in phosphatase activities were not decreased by 3 nM okadaic acid but were completely inhibited by 1 microM okadaic acid, thereby verifying that insulin-stimulated phosphorylase phosphatase is accounted for by a PP-1. Subcellular fractionation demonstrated reduced fasting PP-1 activities in both the glycogen and cytosolic fractions of muscle obtained from subjects in group R compared to those in group S. These results suggest that insulin activation of PP-1 could contribute to the stimulation of glycogen synthase by this hormone in human muscle. Lower fasting PP-1 activity in cytosol and glycogen fractions plus lower insulin-stimulated PP-1 activity could explain, in part, reduced insulin-stimulated glycogen synthase in skeletal muscle of insulin-resistant subjects.
Abstract 2110: Comparing detection of EGFR mutations in lung cancer patients
Authors: Takaya Ikeda, Katsumi Nakatomi, Hiroyuki Yamaguchi, Yoichi Nakamura, Taiki Ogawara, Hiroaki Senju, Nanae Tomonaga, Seiji Doi, Tetsuya Iida, Tsukasa Igawa, Takeshi Nagayasu, Kazuhiro Tsukamoto, Shigeru Kohno
Journal: Cancer Research (2010)

Abstract INTRODUCTION: Epidermal growth factor receptor (EGFR) mutations are a strong determinant factor of response to EGFR tyrosine kinase inhibitors in non-small cell lung cancer (NSCLC). Now some methods have been used to detect EGFR mutations and they have approximately the same sensitivity and specificity. In a case, we experienced unmatched results from two methods of detecting EGFR mutations. In this study, we compared data from three methods of detecting mutations. METHODS: We obtained 30 samples of operation, transbronchial lung biopsy, bronchoscopic brushing, pleural effusion and lymph nodes from NSCLC patients. EGFR mutation status was determined by two or three methods (mutant-enriched PCR method, PNA-LNA PCR Clamp method and PCR invader method). RESULTS:method (n=31)mutation positive2 method (n=20)m.e./Clamp (n=10)4/4 m.e./invader (n=2)1/0 Clamp/invader (n=8)4/33 method (n=10)m.e./Clamp/invader (n=10)3/2/3m.e.: mutant-enriched PCR, Clamp: PNA-LNA PCR Clamp, invader: PCR invader EGFR mutations were detected in 12 samples. Mutation statuses of two or three methods were matched in 9 samples, but 3 samples were unmatched. CONCLUSIONS: EGFR mutation statuses were unmatched in same samples. EGFR gene status is essential information for NSCLC patients. We need to take false negative into consideration in the clinical setting and need father deliberation about detecting methods of EGFR mutations. 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 2110.