tbuckley/cabot-search huggingface dataset:
Cope's Early Diagnosis of the Acute Abdomen
Authors: Bernard Sigel
Journal: JAMA (1979)

This is the latest edition of Sir Zachary Cope's classic on the physical diagnosis of the acute abdomen. Cope died two years after the last edition (14th) appeared in 1972. The present edition has been carefully and thoughtfully prepared by William Silen. <i>Cope's Early Diagnosis of the Acute Abdomen</i>retains the essence of the earlier editions. The outstanding feature of the book is the clear, succinct description of symptoms and signs by an astute and experienced clinician who has based the narration solidly on anatomy and pathophysiology. Dr Silen has effectively handled the difficult task of maintaining the original thrust and flavor, while updating sections in need of change. This has been done by deletions, revisions, and additions of new material. The approach has been conservative. The basic description of symptoms and signs has been preserved. Most of the deleting and rewriting has been in the description of differential diagnosis
Abstract 4331: Characterization of targeted overexpression of Claudin-1 transgenic mice
Authors: Jillian L. Pope, Ajaz Bhat, Moorthy Krishnan, R. D. Beauchamp, Amar Singh, Punita Dhawan
Journal: Cancer Research (2011)

Abstract Disruption of cell-cell junctions and changes in the expression of junctional proteins is a critical event in the progression of cancer. We have previously reported a tumor stage specific increase in the expression of a tight junction protein, Claudin-1, in colorectal cancer and its association with tumor-growth and metastasis. Furthermore, our studies have shown that in colon cancer cells, claudin-1 expression is regulated by a complex interaction between APC, Smad4 and β-catenin, three important regulators of colorectal carcinogenesis. We wanted to investigate the consequence of overexpression of claudin -1 in vivo specifically in the colon. We have generated a transgenic mouse model in which Claudin-1 is expressed under the control of the villin promoter. The villin promoter is expressed in the adult intestinal epithelium and has been frequently used for intestinal-specific overexpression of several genes of interest. Western blot analysis demonstrated a robust expression of claudin-1 in the colon, small intestine and cecum of transgenic mice while low levels of expression were present in wild type mice. These results are confirmed with immunohistochemistry analysis where claudin-1 was largely expressed on the membrane in the same tissues. Colonic permeability was assayed using FITC-dextran, however, there was no significant difference between the flux of FITC-dextran in wild-type and transgenic mice. Real-Time PCR analysis for inflammatory cytokine expression showed a decrease in IL-10 mRNA in transgenic mice compared to that of wild-type mice. Further, treatment with Dextran Sodium Sulfate (DSS) to induce colitis showed a significant decrease in body weight of claudin-1 transgenic mice as compared to wild type mice on DSS. An increase in disease severity was observed in transgenic mice as determined by histology scoring, as well as a significant difference in the ratio of colon weight to colon length. Claudin-1 expression in transgenic mice is localized to the membrane, where it maintains its normal function. Further experiments with this model include combined treatment with DSS and AOM to examine the effect of Claudin -1 overexpression in inflammation-induced-tumorigenesis as well as performing crosses with sporadic models of tumorigenesis involving mutations in the APC gene, to examine the role of claudin-1 upregulation in tumor formation and progression. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 102nd Annual Meeting of the American Association for Cancer Research; 2011 Apr 2-6; Orlando, FL. Philadelphia (PA): AACR; Cancer Res 2011;71(8 Suppl):Abstract nr 4331. doi:10.1158/1538-7445.AM2011-4331
A FATAL CASE OF SUBACUTE YELLOW ATROPHY OF THE LIVER AFTER CINCHOPHEN
Authors: T. N. Fraser
Journal: BMJ (1934)

Cases of toxic cirrhosis with jaundice following the use of cinchophen (atophan), whether fatal or non-fatal, are very infrequently met with in this country or reported in our literature.Most of our knowledge on the subject is obtained from cases reported in the American clinics.The case to be recorded is of interest owing to the fact that toxic symptomns appeared after a dose of only 377 grains had been taken during a period of five days.Weir and Comfort' published.anaccount of 117 cases of toxic cirrhosis due to cinchophen ; nineteen of the cases were seen at the Mayo Clinic, and ninety-eight were collected from the literature on this subject: of the 117 sixty-one were fatal.According to Weir and Comfort the toxic symptoms arose after doses ranging from 54 grains in five weeks to 7,200 grains in four months ; but they
Drug Screening: Rapid Prototyping of Concave Microwells for the Formation of 3D Multicellular Cancer Aggregates for Drug Screening (Adv. Healthcare Mater. 4/2014)
Authors: Ting‐Yuan Tu, Zhe Wang, Jing Bai, Wei Sun, Weng Kung Peng, Ruby Yun‐Ju Huang, Jean‐Paul Thiery, Roger D. Kamm
Journal: Advanced Healthcare Materials (2014)

Jean Paul Thiery, Roger D. Kamm, and co-workers demonstrate a rapid (in minutes), low-cost prototyping method of a conventional untreated culture dish to create concave microwells. On page 609, controllable size of three-dimensional lung cancer aggregates can be uniformly grown in microwells. Preclinical anti-cancer drug screening reveals considerable functional differences between 2D and 3D assay types.
The future of health care in Africa
Authors: Lola Dare, Eric Buch
Journal: BMJ (2005)

Depends on making commitments work in and outside Africa 

A s the group of eight leading industrialised nations (G8) meets for its summit at Gleneagles, Scotland, next week Africa is at a crossroads. It faces a double edged crisis: its healthcare workforce is rapidly depleting, and its health systems are weak, fragile, and hanging on a precipice. A direct consequence of this is that the indicators for health development in the continent are dismal. About one in six African children die before their fifth birthday, with half of these dying from diseases preventable by vaccines; and one woman dies every two minutes from complications of pregnancy and delivery.1 From all such indications and current evidence, it would appear that very few countries in the continent will achieve the millennium development goals.2 The goal to reduce deaths among children aged under 5 (figure) is just one example.



Progress in reducing mortality in children aged under 5 years, comparing sub-Saharan Africa with low and middle income countries in the rest of the world. Red represents sub-Saharan Africa, blue low income countries, green middle income countries (with solid lines indicating path to goal, dotted lines progress to date, and dashed lines projected progress at current rate)



Chronic underinvestment, interventions by global partnerships that focus only on single diseases, and sporadic financing by both national governments and their partners have left African health systems prostrate. They are unable to deliver drugs, tools, and …
Doxycycline in enteric fever and brucellosis.
Authors: A Z Shafei, W S Luka
Journal: BMJ (1973)

this effect is unknown and findings are the opposite to those on serum corticosteroids in immobilized patients, which are significantly raised.2There may be either reduced testicular response to gonadotrophins or decreased hypothalamus-pituitary gland activity.It would seem that both extremes of physical activity have significant effects on serum androgens in men.-We are, etc.,
Preventing Infectious Diseases during and after International Adoption
Authors: Lin H. Chen, Elizabeth D. Barnett, Mary E. Wilson
Journal: Annals of Internal Medicine (2003)

Families of internationally adopted children face risks associated with travel if they pick up their children overseas. Unlike other travelers, they also face risks because of close contact with a child with uncertain infection and vaccination status. Tuberculosis organisms, hepatitis A virus, hepatitis B virus, and measles virus have been transmitted from adopted children to family and community members. Intestinal parasites, Bordetella pertussis, and other infectious disease agents can also be transmitted. Some of these infections may be inapparent or may not manifest in adopted children until many years after the adoption. Increased attention to preventive measures for family members and early diagnosis of infectious diseases in adopted children can reduce transmission of the organisms causing these infections. Those providing health care to families planning international adoption should know about standard pretravel advice, as well as the spectrum of possible infections in adopted children, so that they can protect the health of the travelers and family members and close friends who will welcome the new child into the home.
Impact of gene expression profiling-based risk stratification in patients with myeloma receiving initial therapy with lenalidomide and dexamethasone
Authors: Shaji K. Kumar, Hajime Uno, Susanna J. Jacobus, Scott A. Van Wier, Greg J. Ahmann, Kimberly J. Henderson, Natalie S. Callander, Jessica L. Haug, David S. Siegel, Philip R. Greipp, Rafael Fonseca, S. Vincent Rajkumar
Journal: Blood (2011)
PLASTIC RADIOGRAPHY.A PRELIMINARY COMMUNICATION.
Authors: WALTER G. STERN
Journal: JAMA (1907)

3. The best means of accomplishing the last-named object is a few buried sutures in the apex of the axilla and a properly adjusted compressive dressing held in place by adhesive plaster. DISCUSSION.Dr. William L. Rodman, Philadelphia, agreed with Dr. Por- ter as to the necessity of the free removal of the overlying skin, even in such cases as show that we can not get primary union.He inclined to the belief that possibly the greatest mistake that is made in practice generally is to subordinate the probabilities of a radical cure to securing primary union in every case.He said that we should keep constantly before us that Gross and Pancoast and the older surgeons reached 10 and 15 per cent, of cures, but only by very freely removing the skin.A complete axillary dissection was never done, and muscles were not destroyed.Whatever good was in these operations must have been in the free removal of skin.There- fore, he thinks that we should not accentuate the necessity for getting primary union, even in a majority of the cases.It is all very well if it can be done and without making too much tension, and this, he said, can be done, as Dr. Porter says, by undermining the skin, or by skin grafting, which can always be resorted to to cover in any defect that may exist.
Toll-like Receptor 2 Senses β-Cell Death and Contributes to the Initiation of Autoimmune Diabetes
Authors: Hun Sik Kim, Myoung Sook Han, Kun Wook Chung, Sunshin Kim, Eunshil Kim, Myoung Joo Kim, Eunkyeong Jang, Hyun Ah Lee, Jeehee Youn, Shizuo Akira, Myung-Shik Lee
Journal: Immunity (2007)
Sine-Wave Pattern Arrhythmia and Sudden Paralysis That Result From Severe Hyperkalemia
Authors: Maurice J.H.M. Pluijmen, Ferry M.R.J. Hersbach
Journal: Circulation (2007)

A 54-year-old man with a history of end-stage renal disease treated with hemodialysis presented to the emergency department because of a sudden inability to move his limbs.Physical examination revealed a complete quadriplegia.Blood pressure was 145/90 mm Hg, with a regular pulse of 45 beats per minute.Initial 12-lead electrocardiography showed a sinus bradycardia with atrial, atrioventricular, and intraventricular conduction delay (Figure 1).Subsequently, the patient developed several episodes of a nonsustained widecomplex tachycardia with a right bundle-branch block configuration that gradually evolved into and from a "sinewave" pattern (Figures 2 and3).Remarkably, the patient remained hemodynamically stable.Because hyperkalemia was suspected, serum potassium was determined in venous as well as arterial blood samples to be 9.9 mmol/L.Calcium gluconate was administered, and emergency hemodialysis was performed.After normalization of the serum potassium concentration, sinus rhythm was maintained, the cardiac conduction times returned to normal (Figure 4), and the quadriplegia resolved completely.This case illustrates some typical features of severe hyperkalemia.Initial characteristic electrocardiographic abnormalities in hyperkalemia are tall and peaked T waves, followed by an increasing cardiac conduction delay.As demonstrated in this case, this results in flattened and broadened P waves, an atrioventricular block of first or higher degrees, and widening of the QRS complex.In rare instances, ST-segment elevation may occur, which leads to a "pseudoinfarction"
Activation of the PI3K/mTOR pathway by BCR-ABL contributes to increased production of reactive oxygen species
Authors: Jeong H. Kim, Stephanie C. Chu, Jessica L. Gramlich, Yuri B. Pride, Emily Babendreier, Dharminder Chauhan, Ravi Salgia, Klaus Podar, James D. Griffin, Martin Sattler
Journal: Blood (2004)
Effect of maximal coronary vasodilation on transmural myocardial perfusion during tachycardia in dogs with left ventricular hypertrophy.
Authors: R J Bache, T R Vrobel, C E Arentzen, W S Ring
Journal: Circulation Research (1981)

We tested the hypothesis that a functional abnormality may contribute to impaired myocardial perfusion during tachycardia in the chronically pressure-overloaded hypertrophied left ventricle.Left ventricular hypertrophy (LVH) was produced by banding the ascending aorta of seven young dogs, 5-6 weeks of age, and studies were carried out after the animals reached adulthood when the mean left ventricular: body weight ratio was 91% greater than in seven control dogs.Myocardial blood flow was measured with radioactive microspheres during ventricular pacing at 100, 200, and 250 beats/min in the presence of normal coronary vasomotor activity and during maximum coronary vasodilation (adenosine, iv).At a heart rate of 100 beat«/min, there was no difference in myocardial blood flow between control and LVH dogs either during normal conditions or during adenosine infusion.However, since mean coronary perfusion pressure was higher in the dogs with aortic banding, minimum coronary resistance was greater in the dogs with LVH [22.7 ± 2.5 (mean ± BE)] than in the control dogs (14.5 ± 1.4 mm Hg/min per g per ml; P < 0.05).In the presence of intact coronary vasomotor tone, pacing at 2S0 beats/min resulted in transmural redistribution of perfusion away from the subendocardium in the dogs with LVH [subendocardial: subepicardial blood flow ratio (endoiepi) -0.68 ± 0.09], but not in the control dogs (endo: epi = 1.05 ± 0.03; P < 0.02).This relative reduction of subendocardial flow In the dogs with LVH resulted from extravascular factors since blood flow to the inner half of the left ventricular wall failed to increase in response to adenosine infusion during pacing at 250 beats/min.Thus, both an anatomic abnormality of coronary perfusion, marked by impaired minimum coronary resistance at a heart rate of 100 beats/min, and a functional abnormality of perfusion resulting in redistribution of blood flow away from the subendocardium at a heart rate of 250 beats/min were demonstrated in this model of LVH.
Chronic Illness Behavior and Noncompliance with Treatment: Pathways to an Interactional Approach
Authors: Walter Vandereycken, Rolf Meermann
Journal: Psychotherapy and Psychosomatics (1988)

The increasing cost of medical overconsumption is partially due to the physicians' neglect in everyday clinical practice of the intrinsic gratification of the sick role in our society. Many health care providers do not seem to realize that their intervention as experts in the patient's personal life inevitably implies they are becoming part of the ongoing learning history of that individual. Chronic somatic complaining and partial or complete refusal to follow therapeutic advice have to be viewed, first and foremost, as a symptom of a dysfunctional interaction between the patient and his/her immediate environment of which the clinician became a significant member. Management of chronic illness behavior and non-compliance with treatment requires both a functional analysis and a strategy inspired by an interactional perspective on the attitudes and behaviors of at least three parties involved in health care: doctor, patient, and family.
Factor VII deficiency rescues the intrauterine lethality in mice associated with a tissue factor pathway inhibitor deficit
Authors: Joyce C.Y. Chan, Peter Carmeliet, Lieve Moons, Elliot D. Rosen, Zhong-Fu Huang, George J. Broze, Désiré Collen, Francis J. Castellino
Journal: Journal of Clinical Investigation (1999)

Mice doubly heterozygous for a modified tissue factor pathway inhibitor (TFPI) allele (tfpiδ) lacking its Kunitz-type domain-1 (TFPI+/δ) and for a deficiency of the factor VII gene (FVII+/–) were mated to generate 309 postnatal and 205 embryonic day 17.5 (E17.5) offspring having all the predicted genotypic combinations. Progeny singly homozygous for the tfpiδ modification but with the wild-type fVII allele (FVII+/+/TFPIδ/δ), and mice singly homozygous for the fVII deficiency and possessing the wild-type tfpi allele (FVII–/–/TFPI+/+), displayed previously detailed phenotypes (i.e., a high percentage of early embryonic lethality at E9.5 or normal development with severe perinatal bleeding, respectively). Surprisingly, mice of the combined FVII–/–/TFPIδ/δ genotype were born at the expected mendelian frequency but suffered the fatal perinatal bleeding associated with the FVII–/– genotype. Mice carrying the FVII+/–/TFPIδ/δ genotype were also rescued from the lethality associated with the FVII+/+/TFPIδ/δ genotype but succumbed to perinatal consumptive coagulopathy. Thus, the rescue of TFPIδ/δ embryos, either by an accompanying homozygous or heterozygous FVII deficiency, suggests that diminishment of FVII activity precludes the need for TFPI-mediated inhibition of the FVIIa/tissue factor coagulation pathway during embryogenesis. Furthermore, the phenotypes of these combined deficiency states suggest that embryonic FVII is produced in mice as early as E9.5 and that any level of maternal FVII in early-stage embryos is insufficient to cause a coagulopathy in TFPIδ/δ mice.
Fortnightly review: Treatment of gastro-oesophageal reflux disease in adults
Authors: J. P. Galmiche, E. Letessier, C. Scarpignato
Journal: BMJ (1998)

Gastro-oesophageal reflux disease is caused by retrograde flow of gastric contents through an incompetent gastro-oesophageal junction. The disease encompasses a broad spectrum of clinical disorders from heartburn without oesophagitis to severe complications such as strictures, deep ulcers, and intestinal metaplasia (Barrett's oesophagus).1 The prevalence of heartburn, the most typical symptom of gastro-oesophageal reflux disease, is extremely high,2 but most people with reflux do not seek medical help for this condition and treat themselves with over the counter preparations. Oesophagitis (defined by mucosal breaks) is less frequent, occurring in less than half of patients undergoing endoscopy for reflux symptoms. Symptoms and severity of oesophagitis are poorly correlated. Although reflux may remain silent in patients with Barrett's oesophagus, heartburn can severely affect the quality of life of patients with negative endoscopy results. The natural course of the disease also varies considerably.2 Patients with gastro-oesophageal reflux disease seen by gastroenterologists usually have a chronic condition with frequent relapses, whereas those who rely on general practitioners' help usually have less severe disease, consisting of intermittent attacks with prolonged periods of remission.

#### Summary points

Most patients with dominant heartburn have no signs of oesophagitis at endoscopy. However, chronic relapsing gastro-oesophageal reflux disease can severely affect quality of life

In primary care many patients can be successfully treated by intermittent courses of drugs on demand

Alginate-antacids and H2 receptor antagonists are useful in patients with mild disease

Cisapride is as effective as H2 receptor antagonists in short term treatment and can prevent relapse in mild oesophagitis

Proton pump inhibitors relieve symptoms and heal oesophagitis more completely and faster than other drugs. They are effective throughout the disease spectrum, and maintenance therapy prevents recurrences

The principles of laparoscopic and open antireflux surgery are the same. In skilled hands, similarly good results have been reported …
A New and Simple Antipyretic
Authors: L. Aitken
Journal: BMJ (1884)

TItE BRITISH MEDICAL JOURNAL6 653 as one suggesting a new line of investigation in cases of the sort, and as likely to lead to a clearer explanation of the origin of some of these cases.The rarity of such cases, which the antiseptic system of surgery has done so much to produce, must be my excuse for having brought so short a record before the Association; but I do so in the belief that, if observations in the direction indicated be made on the isolated cases which do occur, much of interest may be found out, and valuable indications may be established on which to base a system of treatment.
[541] CONFIRMATION OF THE ACCURACY OF FIB-4, A SIMPLE MARKER OF FIBROSIS IN HCV PATIENTS WITH AND WITHOUT HIV CO-INFECTION
Authors: J.A. Galeras, M. Timeno, C. Tural, I. Cirera, A. Panades, A. Seoane, C. Barranco, M.D. Gimenez, C. Marquez, I. Ojanguren, B. Clotet, R. Sola
Journal: Journal of Hepatology (2007)
Dynamic changes in Mcl-1 expression regulate macrophage viability or commitment to apoptosis during bacterial clearance
Authors: Helen M. Marriott, Colin D. Bingle, Robert C. Read, Karen E. Braley, Guido Kroemer, Paul G. Hellewell, Ruth W. Craig, Moira K.B. Whyte, David H. Dockrell
Journal: Journal of Clinical Investigation (2005)

Macrophages are critical effectors of bacterial clearance and must retain viability, despite exposure to toxic bacterial products, until key antimicrobial functions are performed. Subsequently, host-mediated macrophage apoptosis aids resolution of infection. The ability of macrophages to make this transition from resistance to susceptibility to apoptosis is important for effective host innate immune responses. We investigated the role of Mcl-1, an essential regulator of macrophage lifespan, in this switch from viability to apoptosis, using the model of pneumococcal-associated macrophage apoptosis. Upon exposure to pneumococci, macrophages initially upregulate Mcl-1 protein and maintain viability for up to 14 hours. Subsequently, macrophages reduce expression of full-length Mcl-1 and upregulate a 34-kDa isoform of Mcl-1 corresponding to a novel BH3-only splice variant, Mcl-1Exon-1. Change in expression of Mcl-1 protein is associated with mitochondrial membrane permeabilization, which is characterized by loss of mitochondrial inner transmembrane potential and translocation of cytochrome c and apoptosis-inducing factor. Following pneumococcal infection, macrophages expressing full-length human Mcl-1 as a transgene exhibit a delay in apoptosis and in bacterial killing. Mcl-1 transgenic mice clear pneumococci from the lung less efficiently than nontransgenic mice. Dynamic changes in Mcl-1 expression determine macrophage viability as well as antibacterial host defense.