tbuckley/cabot-search huggingface dataset:
CONTROL, THROUGH THE NASAL GANGLION, OF EARACHE OF LARYNGEAL ORIGIN
Authors: Louis H. Clerf
Journal: JAMA (1924)

Patients with advanced cancer of the larynx, complaining of pain in one or both ears, are not uncommonly seen at the Bronchoscopic Clinic. Careful examination of the ears reveals no pathologic basis for the otalgia complained of. Because of its association with laryngeal cancer and pain radiating upward along the corresponding side of the neck, we have concluded that, in the presence of a normal ear, it must be of reflex origin from the larynx. Patients complain bitterly of this distressing symptom, and resort to morphin or codein is necessary to give relief. Remembering the remarkable results obtained by Dr. Greenfield Sluder, who cocainized the nasal ganglion in earache of inflammatory middle disease origin and reflex earache after tonsillectomy, Dr. Chevalier Jackson suggested that this method be tried in these cases of reflex earache of laryngeal origin. Following is a brief synopsis of the records of two of the cases,
Abstract 1244: Phosphatidylserine-targeting antibody reactivates tumor immunity and destroys tumor vasculature in mice.
Authors: Yi Yin, Xianming Huang, Dan Ye, Philip Thorpe
Journal: Cancer Research (2013)

Abstract The immunosuppressive lipid, phosphatidylserine (PS), becomes exposed on tumor blood vessels and tumor cells responding to therapy. The exposed PS contributes to the immunosuppressed tumor microenvironment. Bavituximab is a phosphatidylserine (PS)-targeting antibody that is being combined with chemotherapy in clinical trials in cancer patients. Here, we tested the hypothesis that innate immunity against cancer can be elicited by combining chemotherapy with a monoclonal antibody that indirectly binds exposed phosphatidylserine (PS). We used a murine version of bavituximab, 2aG4, plus docetaxel to treat prostate tumors in mice. Combination treatment markedly retarded tumor growth, prolonged survival times and delayed progression to androgen-independent disease. Antibody treatment reduced the presence of myeloid-derived suppressor cells (MDSCs) in the tumors and caused macrophages to repolarize from the immunosuppressive, proangiogenic M2-like state into a tumoricidal M1-like state. The reactivated macrophages destroyed antibody-coated tumor vasculature and tumor cells. Addition of 2aG4 to MDSCs in vitro caused them to differentiate into M1-like macrophages and DCs. Thus, PS-targeting antibodies appear to reactivate innate immunity in tumors resulting in tumor growth inhibition. Citation Format: Yi Yin, Xianming Huang, Dan Ye, Philip Thorpe. Phosphatidylserine-targeting antibody reactivates tumor immunity and destroys tumor vasculature in mice. [abstract]. In: Proceedings of the 104th Annual Meeting of the American Association for Cancer Research; 2013 Apr 6-10; Washington, DC. Philadelphia (PA): AACR; Cancer Res 2013;73(8 Suppl):Abstract nr 1244. doi:10.1158/1538-7445.AM2013-1244
Controlled release of vitamin B2 using mesoporous materials functionalized with amine-bearing gate-like scaffoldings
Authors: Andrea Bernardos, Elena Aznar, Carmen Coll, Ramón Martínez-Mañez, Jose Manuel Barat, Ma. Dolores Marcos, Félix Sancenón, Angel Benito, Juan Soto
Journal: Journal of Controlled Release (2008)
Milk sialyllactose influences colitis in mice through selective intestinal bacterial colonization
Authors: Andrea Fuhrer, Norbert Sprenger, Ekaterina Kurakevich, Lubor Borsig, Christophe Chassard, Thierry Hennet
Journal: The Journal of Experimental Medicine (2010)

Milk oligosaccharides contribute to the development of the intestinal environment by acting as decoy receptors for pathogens and as prebiotics, which promote the colonization of commensal bacteria. Here, using α2,3- and α2,6-sialyltransferase-deficient mice, we investigated the role of the sialylated milk oligosaccharides sialyl(α2,3)lactose and sialyl(α2,6)lactose on mucosal immunity. The exposure of newborn mice to milk containing or deficient in sialyllactose had no impact on the development of mucosal leukocyte populations. However, when challenged by dextran sulfate sodium (DSS) in drinking water, adult mice that had been fostered on sialyl(α2,3)lactose-deficient milk were more resistant to colitis compared with mice fostered on normal milk or sialyl(α2,6)lactose-deficient milk. Analysis of intestinal microbiota showed different colonization patterns depending on the presence or absence of sialyl(α2,3)lactose in the milk. Germ-free mice reconstituted with intestinal microbiota isolated from mice fed on sialyl(α2,3)lactose-deficient milk were more resistant to DSS-induced colitis than germ-free mice reconstituted with standard intestinal microbiota. Thus, exposure to sialyllactose during infancy affects bacterial colonization of the intestine, which influences the susceptibility to DSS-induced colitis in adult mice.
Abstract 2816: Low-carbohydrate diets and prostate cancer growth: How low is “low enough”
Authors: Elizabeth M. Masko, Jean A. Thomas, Jodi A. Antonelli, Jessica C. Lloyd, Tameika E. Phillips, Susan H. Poulton, Salvatore V. Pizzo, Stephen J. Freedland
Journal: Cancer Research (2010)

Abstract Introduction: Previous dietary studies indicate carbohydrate intake may influence prostate cancer biology, as LAPC-4 and LNCaP xenograft mice fed a no-carbohydrate ketogenic diet (NCKD; 84% fat-0% carbohydrate-16% protein kcal) had significantly smaller tumors and longer survival times compared to mice fed a Western diet (40% fat-44% carbohydrate-16% protein kcal). The NCKD mice were also found to have higher levels of circulating IGFBP-3 and the lowest levels of insulin, IGF-1, and IGF-1:IGFBP-3 ratio despite consuming more calories than the Western group. As it is nearly impossible for a human to consume and maintain a no-carbohydrate diet similar to that in the previous xenograft studies, we sought to determine whether diets containing 10% or 20% kcal from carbohydrates could slow tumor growth in a similar manner to the NCKD in a xenograft model. METHODS: A total of 150 male SCID mice were injected with LAPC-4 cells and placed on a Western diet (35% fat-49% carbohydrate-16% protein kcal) ad libitum. Two weeks post-injection, all mice were randomized to one of three arms: NCKD, 10% carbohydrate, or 20% carbohydrate. Ten mice not injected with tumor were fed an ad libitum low-fat diet (12% fat-72% carbohydrate-16% protein kcal) and served as the reference group in a modified-paired feeding protocol for the other three groups. Calorie intake and body weights were measured thrice weekly and tumor volumes twice per week. Mice were sacrificed when tumors reached 1,000mm3. RESULTS: Despite consuming 5-10% extra calories on average, all mice receiving low-carbohydrate diets were significantly lighter than the mice consuming the low-fat diet (p&amp;lt;0.04). Overall, the mice fed a NCKD were significantly lighter than the other two arms at multiple time points (p&amp;lt;0.05). There were no significant differences in tumor volumes among groups at any time except at Day 52 and 59, where 10% carbohydrate mice had larger tumors (p&amp;lt;0.05). However, after adjusting for the fact that tumor volumes were compared at multiple time points (i.e. multiple comparisons), these were no longer significant. Dietary treatment did not impact overall survival (p=0.34). NCKD mice had significantly higher glucose levels at sacrifice compared to the mice fed 10% and 20% carbohydrates (p=0.001), but similar levels of urinary ketones (p=0.37). CONCLUSIONS: LAPC-4 xenograft mice fed a low-carbohydrate diet (10-20% carbohydrate kcal) had similar survival to mice consuming a NCKD (0% carbohydrate kcal). Thus, the survival benefit of a NCKD may be achievable with less restrictive low-carbohydrate diets. 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 2816.
Inhibition of intestinal epithelial DNA synthesis and adaptive hyperplasia after jejunectomy in the rat by suppression of polyamine biosynthesis.
Authors: G D Luk, S B Baylin
Journal: Journal of Clinical Investigation (1984)

Transient increases in the activity of ornithine decarboxylase (ODC), the first and rate-limiting enzyme in polyamine biosynthesis, may be critical to initiation of cell growth. We previously reported such increases in ODC activity, and the polyamines, putrescine, and spermidine in rat ileal mucosa between days 1 and 4 after intestinal resection. During this time, there is initiation of mucosal cell hyperplasia, as measured morphologically and biochemically. Intestinal weight and mucosal thickness increase, as do mucosal DNA content and DNA synthesis. In the present study, we gave rats the specific irreversible ODC inhibitor, alpha-difluoromethyl ornithine (DFMO), beginning 3 d before jejunectomy. DFMO completely suppressed the increases in ODC activity and polyamine content in the intestinal mucosa. The suppression in ODC activity was associated with an 87% suppression of DNA synthesis, and resulted in a complete abolition of intestinal adaptation, as manifested by the absence of intestinal weight gain, increase in mucosal thickness, or increase in crypt cell production. Our results indicate that the increases in ODC activity and polyamine biosynthesis are critical for adaptive postresectional crypt cell proliferation in vivo, and that the critical step mediated by polyamines in this adaptive process is the onset of new DNA synthesis.
ASSOCIATION OF APICAL LONGITUDINAL ROTATION WITH TRICUSPID ANNULAR PLANE SYSTOLIC EXCURSION IN PATIENTS WITH PULMONARY HYPERTENSION
Authors: Yoshiki Motoji, Hidekazu Tanaka, Yuko Fukuda, Keiko Ryo, Hiromi Toki, Hiroyuki Shimoura, Junichi Ooka, Hiroyuki Sano, Takuma Sawa, Yoshiki Yamadori, Junichi Imanishi, Tatsuya Miyoshi, Yasuhide Mochizuki, Kazuhiro Tatsumi, Kensuke Matsumoto, Toshiro Shinke, Noriaki Emoto, Ken-ichi Hirata
Journal: Journal of the American College of Cardiology (2014)
REPORT OF TWO CASES OF INTESTINAL OBSTRUCTION CAUSED BY ROUNDWORMS FOLLOWING DOSAGE OF SANTONIN
Authors: Thomas H. Watkins
Journal: JAMA (1924)

The cases reported here were in children less than 5 years of age, members of the same family. They occurred within a period of two weeks. The patients were brought in to us by Dr. Crawford, a colleague practicing in a nearby town, with a diagnosis of acute intestinal obstruction. <h3>Case 1.</h3> —E. Y., a child, aged 3 years, in whose family history there was nothing of note, had had whooping cough one year before admission, lasting seven weeks and leaving the throat in bad condition. The general health was poor. The child had always been thin and pale. The appetite was poor, the bowels were in good condition; the diet consisted of ordinary table food. February 28, the child was taken sick with cramps in the abdomen, but became better and was up playing all day. That evening it became worse. Dr. C. was called and found the child
Clevudine myopathy in patients with chronic hepatitis B
Authors: Byung Kook Kim, Jeeyoung Oh, So Young Kwon, Won Hyeok Choe, Soon Young Ko, Kyoung Hoon Rhee, Tae Ho Seo, So Dug Lim, Chang Hong Lee
Journal: Journal of Hepatology (2009)

Clevudine (L-FMAU) is a thymidine l-nucleoside analogue that was recently introduced for the treatment of chronic hepatitis B virus infection. Previous studies showed that clevudine has potent and sustained antiviral activity without causing viral resistance. No severe adverse event occurred during clinical trials. We describe two cases of drug-induced myopathy during long-term treatment of chronic hepatitis B with clevudine.
S105 The Effects Of Real-world Exposures To Diesel Traffic Emissions On Cardio-respiratory Outcomes In Copd : 'oxford Street 2'
Authors: R. Sinharay, B. Barratt, J. Gong, C. Goward, J. Rocha, F. Kelly, J. Zhang, P. Cullinan, K. Chung
Journal: Thorax (2014)

<h3>Introduction and objectives</h3> We studied the changes in lung function and cardiovascular responses in healthy volunteers and patients with COPD exposed to the high pollution levels in a busy London street. <h3>Methods</h3> Using a cross-over design, 37 healthy volunteers and 37 COPD patients (walked along Oxford Street (diesel only traffic) and, on a separate occasion, in Hyde Park (low or little traffic), London for two hours. Cardio-respiratory measurements were performed at baseline, and during and after each exposure, alongside personal particulate and gaseous exposure measurements. <h3>Findings</h3> Compared to Hyde Park, mean exposures on Oxford Street had higher levels of black carbon (10.4 μm/m<sup>3</sup> vs. 1.2 μm/m<sup>3</sup>, p &lt; 0.001) and ultrafine particle counts (25472/cm<sup>3</sup> vs 5709/cm<sup>3</sup>, p &lt; 0.001). In comparison with Hyde Park the healthy subjects had a mean fall in FEV<sub>1</sub> from baseline of6.05% (p = 0.01) 6 h and a fall of 4.17% (p = 0.01) 24 h after arrival in Oxford St. There was no associated drop in FVC. Arterial stiffness measured by pulse wave velocity (PWV) increased 24 h after arriving on Oxford Street. In volunteers with COPD, there was a mean fall in FEV<sub>1</sub> of 4% (p = 0.01) with an associated drop in FVC of 3.4% (p = 0.02) one hour after the start of exposure on Oxford Street, compared to Hyde Park. Measurement of impulse oscillometry in volunteers with COPD demonstrated increased airway resistance at 5 Hz of 0.05 kPa/l/s (p = 0.01) four hours and at 20 Hz of 0.02 (p = 0.04) 24 h after exposure began on Oxford Street. PWV increased by 0.8 m/s and 0.5 m/s three hours and six hours after exposure started on Oxford street respectively. There were no changes in FeNO in either group between the two sites. Preliminary multivariate analysis has so far found no associations with individual particulate measurements. <h3>Conclusions</h3> These findings show that airways obstruction occurred in both the healthy volunteers and COPD patients exposed to ambient levels of diesel pollution on a busy London Street. The associated vascular dysfunction was more prominent in COPD patients. Further analyses of markers of inflammation in the collected samples are now needed to ascertain the mechanistic cause of the pathophysiological findings.
Toxicity of combustion products from burning polymers: development and evaluation of methods
Authors: P. L. Wright, C. H. Adams
Journal: Environmental Health Perspectives (1976)

Laboratory and room-scale experiments were conducted with natural and synthetic polymers: cotton, paper, wood, wool, acetate, acrylic, nylon, and urethane. Smoke and off-gases from single materials were generated in a dual-compartment 110-liter exposure chamber. Multicomponent, composite fuel loads were burned within a 100 m3 facility subdivided into rooms. In chamber experiments, mortality depended on the amount of material burned, i.e., fuel consumption (FC). Conventional dose (FC)/mortality curves were obtained, and the amount of fuel required to produce 50% mortality (FC50) was calculated. With simple flame ignition, cotton was the only material that produced smoke concentrations lethal to rats; FC50 values for cotton ranged from 2 g to 9 g, depending on the configuration of the cotton sample burned. When supplemental conductive heat was added to flame ignition, the following FC50 values were obtained; nylon, 7 g; acrylic, 8 g; newsprint, 9 g; cotton, 10 g; and wood, 11 g. Mortality resulting from any given material depended upon the specific conditions employed for its thermal decomposition. Toxicity of off-gasses from pyrolysis of phosphorus-containing trimethylol propane—polyurethane foams was markedly decreased by addition of a flame ignition source. Further studies are needed to determine the possible relevance of single-material laboratory scale smoke toxicity experiments. Room-scale burns were conducted to assess the relative contributions of single materials to toxicity of smoke produced by a multicomponent self-perpetuating fire. Preliminary results suggest that this approach permits a realistic evaluation of the contribution of single materials to the toxicity of smoke from residential fires.
Cephalopelvic disproportion and caesarean section.
Authors: G J Jarvis
Journal: BMJ (1980)

However, it seems relevant to refer now to the incidence of vomiting in paracetamol poison- ing.In total, we have records of 392 patients who ingested analgesic overdoses which included paracetamol; 120 took paracetamol alone, 44 took Distalgesic (dextropropoxyphene and paracetamol) alone, 157 took paracetamol combined with other drugs, and 71 took Distalgesic combined with other drugs.Among these patients only 46 (11-7 %) had vomited or were vomiting at the time of admission; and of the 63 who were treated with oral methionine, vomiting occurred in only 13.Further examination of these cases shows that all vomited before the treatment began but that this symptom did not persist during treatment.Obviously further analysis of these data is required, but it is already appaient that the difference in the incidence of vomiting with this type of poisoning as reported from Edinburgh (77 %)1 and London (16 %)2 cannot be explained simply by the fact that many of the latter data are collected indirectly through the Poisons Information Service inquiries.
TCT-471 Comparison of Bivalirrudin and Heparin use for Acute Myocardial Infarction: a Meta-Analysis of the Randomized Trials
Authors: Mohammad M. Ansari, Daniel C. Garcia, Josef L. Toussaint, Cesar Mendoza, Carlos Alfonso, Mauricio G. Cohen, Alam Schob
Journal: Journal of the American College of Cardiology (2014)
Campylobacter fetus bacteraemia in a healthy individual: clinical and therapeutical implications
Authors: Dimitrios I. Zonios, Georgios D. Panayiotakopoulos, Eleytherios O. Kabletsas, Eystathia L. Tzima, Ioanna Stefanou, Athanasios J. Archimandritis
Journal: Journal of Infection (2004)
Androgenetic alopecia in children: report of 20 cases
Authors: A. Tosti, M. Iorizzo, B.M. Piraccini
Journal: British Journal of Dermatology (2005)

Androgenetic alopecia (AGA) is the most common type of hair loss in adults. Although there are differences in the age at onset, the disease starts after puberty when enough testosterone is available to be transformed into dihydrotestosterone. We report 20 prepubertal children with AGA, 12 girls and eight boys, age range 6-10 years, observed over the last 4 years. All had normal physical development. Clinical examination showed hair loss with thinning and widening of the central parting of the scalp, both in boys and girls. In eight cases frontal accentuation and breach of frontal hairline were also present. The clinical diagnosis was confirmed by pull test, trichogram and dermoscopy in all cases, and by scalp biopsy performed in six cases. There was a strong family history of AGA in all patients. The onset of AGA is not expected to be seen in prepubertal patients without abnormal androgen levels. A common feature observed in our series of children with AGA was a strong genetic predisposition to the disease. Although the pathogenesis remains speculative, endocrine evaluation and a strict follow-up are strongly recommended.
The language bioprogram hypothesis
Authors: Derek Bickerton
Journal: Behavioral and Brain Sciences (1984)

Abstract It is hypothesized that creole languages are largely invented by children and show fundamental similarities, which derive from a biological program for language. The structures of Hawaiian Pidgin and Hawaiian Creole are contrasted, and evidence is provided to show that the latter derived from the former in a single generation. A realistic model of the processes of Creole formation shows how several specific historical and demographic factors interacted to restrict, in varying degrees, the access of pidgin speakers to the dominant language, and hence the nature of input to the children of those speakers. It is shown that the resulting similarities of Creole languages derive from a single grammar with a restricted list of categories and operations. However, grammars of individual Creoles will differ from this grammar to a varying extent: The degree of difference will correlate very closely with the quantity of dominant-language input, which in turn is controlled by extralinguistic factors. Alternative explanations of the above phenomena are surveyed, in particular, substratum theory and monogenesis: Both are found inadequate to account for the facts. Primary acquisition is examined in light of the general hypothesis, and it is suggested that the bioprogram provides a skeletal model of language which the child can then readily convert into the target language. Cases of systematic error and precocious learning provide indirect support for the hypothesis. Some conjectures are made concerning the evolutionary origins of the bioprogram and what study of Creoles and related topics might reveal about language origins.
Differential activation of transcription factors NF-ϰB and AP-1 in rat liver macrophages
Authors: Thuy-Anh Tran-Thi, Karl Decker, Patrick A. Baeuerle
Journal: Hepatology (1995)

Liver macrophages (Kupffer cells) respond to many stimulations with the production of bioactive substances including cytokines, eicosanoids, and inorganic radicals. In this study the activation of transcription factors by substances inducing cytokine gene expression or superoxide formation in rat Kupffer cells was examined. Using primary cultures of rat Kupffer cells the role of NF-κB and activator protein 1 (AP-1) in the expression of the tumor necrosis factor-alpha (TNF-α) gene by lipopolysaccharide (LPS) was investigated. Both transcription factors were strongly activated but with different kinetics. Maximal DNA-binding activity was induced with 50 ng of LPS/mL of medium and persisted for at least 24 hours. At that time, NF-κB- as well as AP-1-DNA complexes decreased their mobilities in native gels. Among the cytokines tested only TNF-α and macrophage colony-stimulating factor (M-CSF) were able to activate NF-κB in Kupffer cells. Phorbol ester and zymosan activated AP-1 but not NF-κB; the treatment of zymosan yielding a modified form of AP-1. Of all substances found to interfere with TNF-α production by Kupffer cells (pyrrolidine dithiocarbamate, dexamethasone, prostaglandin E 2 , interleukin [IL]-4, IL-10, and transforming growth factor-beta [TGF-β]) only pyrrolidine dithiocarbamate was able to completely inhibit the activation of NF-κB by LPS. Although not abrogating the LPS activation of NF-κB, dexamethasone inhibited that of AP-1. The results indicate a direct participation of NF-κkB in the regulation of TNF-α synthesis and a differential effect of LPS on NF-κB and AP-1, respectively. (Hepatology 1995; 22:613-619.)