tbuckley/cabot-search huggingface dataset:
Unusual distribution of punctate dysplastic keratoses and skin cancers in sunbed users: a report of three cases
Authors: F. Ismail, E.A. O'Toole, J.M. McGregor, S.M. Khorshid
Journal: British Journal of Dermatology (2005)

Conflicts of interest: none declared. Sir, We present three women (skin type II) who developed multiple dysplastic keratotic lesions and skin cancers predominantly on the plantar aspect of the feet, associated with the use of sunbeds. They have had comparatively less exposure to solar radiation and held indoor occupations. In addition, the unusual distribution and distinct histology of keratotic lesions in these patients may prove characteristic of sunbed users. Patient 1. A 42‐year‐old woman developed multiple erythematous scaly papules and small plaques on her legs and feet. She reported use of a sunbed at home since her early twenties for ∼20 min twice weekly up until the last 2 years, as well as using a commercial sunbed intermittently over a period of 6 years. She first noticed her skin lesions ∼10 years after initial sunbed exposure. Over the past 12 years she had been on six sunny holidays but prior to that had never been abroad. Examination revealed multiple discrete hyperkeratotic lesions just above the instep (Fig. 1a). Skin biopsy taken from a typical lesion on the instep showed compact hyperkeratosis with dysplasia limited to the lower part of the epidermis (Fig. 2a).
Plasma Norepinephrine, Weak Neurotransmitters, and Renin Activity During Active Tilting in Liver Cirrhosis: Relationship with Cardiovascular Homeostasis and Renal Function
Authors: Mauro Bernardi, Franco Trevisani, Costanza Santini, Giorgio Zoli, Mario Baraldini, Amedeo Ligabue, Giovanni Gasbarrini
Journal: Hepatology (1983)

Derangements in cardiovascular homeostasis are well–known features of liver failure. To evaluate the role of possible alterations in adrenergic and reninangiotensin systems in this context, tilting–induced changes in plasma norepinephrine, octopamine, β–phenylethanolamine, and plasma renin activity were related to modifications in blood pressure, heart rate, plasma volume, and renal function in 10 healthy controls and 20 patients with liver cirrhosis. After 2 hr of bed rest, the patients had higher norepinephrine (p &lt; 0.05), octopamine, β–phenyl–ethanolamine (p &lt; 0.001), plasma renin activity (0.1 ± p ± 0.05), heart rate (p &lt; 0.05), and lower mean arterial pressure (0.1 ± p ± 0.05). Renal function was characterized by reduced creatinine clearance and filtered sodium (p &lt; 0.001); tubular rejection fraction of sodium and sodium excretion were not significantly reduced. After the change in posture (observation period of 1 hr), tilting–induced tachycardia was abolished in patients who also showed a significant drop in blood pressure after a transient initial increase at 10 min, whereas a steady state was observed in normal subjects. Norepinephrine and plasma renin activity increases were greater and more prolonged in cirrhotics than in controls; octopamine and β–phenylethanolamine did not change in the latter and increased in the former, where they correlated with plasma norepinephrine in basal conditions and after tilting (r ± 0.49). Creatinine clearance, filtered sodium, and tubular rejection fraction of sodium underwent a greater decrease in cirrhotics. Although plasma volume reduction was more evident in cirrhotics, it remained steady after 10 min in both groups. In basal conditions and after tilting (60 min), plasma renin activity inversely correlated with arterial pressure (p &lt; 0.05) and creatinine clearance (p &lt; 0.01) in cirrhotic patients. In conclusion, the adrenergic system, although hyper stimulated, did not achieve an adequate cardiovascular response which could be due, at least in part, to hyperproduction of weak neurotransmitters. The renin–angiotensin system played a compensatory role and its activation appears to be mainly dependent on intrarenal mechanisms.
An economic analysis of endoscopic ablative therapy for management of nondysplastic Barrett’s esophagus
Authors: A. Das, C. Wells, H. Kim, D. Fleischer, M. Crowell, V. Sharma
Journal: Endoscopy (2009)

Background and aims: Advances have occurred in the development of safe and effective ablative therapies for Barrett's esophagus. The aim of the current study was to perform an economic analysis evaluating the cost-effectiveness of endoscopic ablation of nondysplastic Barrett's esophagus.
Russian studies on age-associated physiology, biochemistry and morphology.
Authors: J. Graham Smith
Journal: JAMA (1963)

This is a comprehensive review of Russian theories and studies of aging, spanning the years 1761 to 1958. There is also a bibliography of 2,953 references. Unfortunately, the references are alphabetical by author without cross indexing; ready access to various subjects of interest is not possible. Excerpted from<i>Arch Derm</i><b>86:</b>95 (July) 1962.
Benign Intracranial Hypertension in an Adult After Tetracycline Therapy
Authors: Jan Koch-Weser
Journal: JAMA (1967)

BENIGN intracranial hypertension is a well-recognized complication of therapy with tetracycline and its derivatives in infants.<sup>1-9</sup>This condition manifests itself by bulging fontanelles and occasionally by spreading of sutures. Irritability, drowsiness, feeding disturbances, and vomiting are common symptoms, but the child may be asymptomatic. The results of the neurological examination are usually normal and there are no changes in the cerebrospinal fluid. The mechanism of this reaction remains quite obscure. It has not been associated with other manifestations of abnormal reactivity to tetracycline. No relationship has become apparent between the occurrence of tetracycline-induced benign intracranial hypertension and tetracycline dosage or length of therapy. The complication has appeared after five hours to four days of tetracycline treatment. Cessation of tetracycline administration has been followed by disappearance of all signs of increased intracranial pressure in a few hours to three days, and there have been no sequelae. On three occasions reexposure
Progression of autoimmune hepatitis is mediated by IL-18-producing dendritic cells and hepatic CXCL9 expression in mice
Authors: Aki Ikeda, Nobuhiro Aoki, Masahiro Kido, Satoru Iwamoto, Hisayo Nishiura, Ryutaro Maruoka, Tsutomu Chiba, Norihiko Watanabe
Journal: Hepatology (2014)

Clinical manifestations of autoimmune hepatitis (AIH) range from mild chronic to acute, sometimes fulminant hepatitis. However, it is unknown how the progression to fatal hepatitis occurs. We developed a mouse model of fatal AIH by inducing a concurrent loss of forkhead box P3(+) regulatory T cells and programmed cell death-1 (PD-1)-mediated signaling. In this model, dysregulated follicular helper T cells in the spleen are responsible for the induction, and the C-C chemokine receptor 6/C-C chemokine ligand 20 axis is crucial for the migration of these T cells into the liver. Using this fatal AIH model, we aimed to clarify key molecules triggering fatal AIH progression. During progression, T-bet together with interferon (IFN)-γ and C-X-C chemokine receptor (CXCR)3 were highly expressed in the inflamed liver, suggesting helper T (Th)1-type inflammation. T cells that dominantly expanded in the spleen and the inflamed liver were CXCR3-expressing CD8(+) T cells; depletion of these CD8(+) T cells suppressed AIH progression. Expression of one CXCR3 ligand, chemokine (C-X-C motif) ligand (CXCL)9, was elevated in the liver. CXCL9-expressing macrophages/Kupffer cells were colocalized with infiltrating T cells, and in vivo administration of anti-CXCL9 suppressed AIH progression. In addition, serum levels of interleukin (IL)-18, but not IL-1β, were elevated during progression, and dendritic cells in the spleen and liver highly produced IL-18. In vivo administration of anti-IL-18R suppressed the increase of splenic CXCR3(+) T cells and the progression to fatal AIH. Moreover, tumor necrosis factor alpha, but not IFN-γ, was involved in up-regulating CXCL9 in the liver and for increased serum levels of IL-18.These data suggest that, in our mouse model, fatal progression of AIH is mediated by IL-18-dependent differentiation of T cells into Th1 cells and effector T cells, respectively, and that CXCR3-CXCL9 axis-dependent migration of those T cells is crucial for fatal progression.
Diagnosis of Bone and Joint Disorders: With Emphasis on Articular Abnormalities
Authors: Leonard F. Peltier
Journal: JAMA (1981)

The arrival of these three volumes, weighing 25 pounds and numbering 3,300 pages, calls for more than casual comment. First of all, the typography, drawings, tables, and the reproductions of roentgenograms and photographs are outstanding. In a work of this size, a comprehensive index is essential, and one is not lacking here. The usefulness of many of the bibliographies would be improved if the references were listed alphabetically. The book purports to be a correlation of the roentgenographic findings with the gross and microscopic pathological abnormalities in diseases of the bones and joints. The editors, one a radiologist, the other a pathologist, are well qualified to do this, and they have had at their disposal a wealth of clinical and pathological material. Their collaborators are well chosen, and each makes a contribution to the whole. There is no question, however, that the major burden has fallen on the editors, which
Long-term survival and preservation of natural killer cell activity in a xeroderma pigmentosum patient with spontaneous regression and multiple deposits of malignant melanoma
Authors: A.V. ANSTEY, C.F. ARLETT, J. COLE, P.G. NORRIS, A.S. HAMBLIN, G.A. LIMB, A.R. LEHMANN, J.D. WILKINSON, M. TURNER
Journal: British Journal of Dermatology (1991)

Journal Article Long‐term survival and preservation of natural killer cell activity in a xeroderma pigmentosum patient with spontaneous regression and multiple deposits of malignant melanoma Get access A.V. ANSTEY, A.V. ANSTEY Department of Dermatology, Wycombe General Hospital, High Wycombe. U.K. Dr A.V.Anstey, Department of Dermatology, St Bartholomews Hospital. West Smithfield. London EClA 7BE, U.K. Search for other works by this author on: Oxford Academic Google Scholar C.F. ARLETT, C.F. ARLETT MRC Cell Mutation Unit, University of Sussex, Brighton. U.K. Search for other works by this author on: Oxford Academic Google Scholar J. COLE, J. COLE MRC Cell Mutation Unit, University of Sussex, Brighton. U.K. Search for other works by this author on: Oxford Academic Google Scholar P.G. NORRIS, P.G. NORRIS Photobiology Unit, St Thomas's Hospital, London, U.K. Search for other works by this author on: Oxford Academic Google Scholar A.S. HAMBLIN, A.S. HAMBLIN Department of Immunology, St Thomas's Hospital, London, U.K. Search for other works by this author on: Oxford Academic Google Scholar G.A. LIMB, G.A. LIMB Department of Immunology, St Thomas's Hospital, London, U.K. Search for other works by this author on: Oxford Academic Google Scholar A.R. LEHMANN, A.R. LEHMANN MRC Cell Mutation Unit, University of Sussex, Brighton. U.K. Search for other works by this author on: Oxford Academic Google Scholar J.D. WILKINSON, J.D. WILKINSON Department of Dermatology, Wycombe General Hospital, High Wycombe. U.K. Search for other works by this author on: Oxford Academic Google Scholar M. TURNER M. TURNER Department of Histopathology, Wycombe General Hospital, High Wycombe. U.K. Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 125, Issue 3, 1 September 1991, Pages 272–278, https://doi.org/10.1111/j.1365-2133.1991.tb14754.x Published: 01 September 1991
My first week at Guy's 40 years ago
Authors: A. Abrahams
Journal: BMJ (1996)

The dean of Guy's must have had a sense of humour. He divided the clinical intake of 1956 into two. The Guy's preclinicals were put into an intensive induction class. The Cambridge and Oxford intake, who had never seen a patient, were put on clinical firms. We exchanged roles three months later.

On my first day at Guy's I was put in the surgical on take firm for a week as a junior dresser—not that I ever did or could have done a dressing. Our main duty was to wheel patients from ward to …
A blistering eruption after a holiday in India
Authors: F. S. Worsnop, E. E. Craythorne, A. W. P. du Vivier
Journal: BMJ (2011)

A 33 year old woman presented with an intensely itchy, erythematous, blistering eruption bilaterally on the distal upper and lower limbs a week after coming back from a holiday in India. The rash was associated with oedema. She had attended a friend’s wedding while in India, and as part of the festivities she took part in the ritual of “mehndi,” which involved having an intricate henna design painted on her hands and feet. Five days after this ritual she developed a sharply demarcated erythematous, itchy, papulovesicular swelling in the proximal distribution of the tattoo design, which spread distally (figure⇓). Other than the skin irritation, she had no other symptoms and was systemically well.





### 1 What is the diagnosis?

#### Short answer

The diagnosis is contact dermatitis to paraphenylenediamine (PPD). This chemical is widely used in hair dye and is an ingredient in many other products, including black henna, which is used in temporary tattooing.

#### Long answer

PPD is an aromatic amine compound that is primarily used as a hair colouring agent. It is also found in a variety of products including textile dyes, photography development agents, certain local anaesthetics, cosmetics, and printing inks. It is becoming increasingly used in temporary tattoos as an addition to henna.1

Henna is a greenish brown vegetable colouring from the leaves of the plant Lawsonia inermis or L alba , which grows in India, North Africa, and Sri Lanka.2 The active ingredient is lawsone (2-hydroxy-1,4-naphthoquinone). On its own, …
Human erythroid burst-forming units. Growth in vitro is dependent on monocytes, but not T lymphocytes.
Authors: K S Zuckerman
Journal: Journal of Clinical Investigation (1981)

The roles of monocytes and T lymphocytes in the regulation of human peripheral blood erythroid burst-forming units (BFU-E) were studied in erythropoietin-containing plasma clot cultures of subpopulations of human blood mononuclear cells. BFU-E growth was decreased significantly after depletion of monocytes alone (mean 11% of expected, range 0 to 42% of expected) or depletion of both monocytes and T cells (mean 6.5% of expected, range 0.5 to 12% of expected) from mononuclear cells. T cell depletion did not impair BFU-E growth in vitro. Using 10(5) monocyte- and T lymphocyte-depleted mononuclear cells as target cells (less than 1% monocytes, less than 5% T cells), BFU-E growth was restored to 40% of expected by addition of 10(4) monocytes, and to 96% of expected by 10(5) monocytes alone. Addition of as many as 2 X 10(5) T cells but no monocytes resulted in stimulation to only 34% of expected BFU-E growth. Addition of 2 X 10(4) T cells, which alone did not affect BFU-E growth, could augment significantly the stimulatory effect of 5-20 X 10(3) monocytes on BFU-E growth. Thus, monocytes alone appear to be capable of stimulating BFU-E growth in vitro in the presence of erythropoietin. T cells also may make small quantities of BFU-E stimulators. However, it seems more likely that the most important role of T lymphocytes in BFU-E regulation in vitro is a result of interactions with monocytes and augmentation of monocyte production of stimulators of BFU-E growth.
Metabolic correlates of nonalcoholic fatty liver in women and men
Authors: Gloria Lena Vega, Manisha Chandalia, Lidia S. Szczepaniak, Scott M. Grundy
Journal: Hepatology (2007)

Nonalcoholic hepatic steatosis associates with a clustering of metabolic risk factors and steatohepatitis. One risk factor for hepatic steatosis is obesity, but other factors likely play a role. We examined metabolic concomitants of hepatic steatosis in nonobese and obese men and women. Sixty-one obese women and 35 obese men were studied; both those with and without hepatic steatosis were compared against each other and against nonobese controls (17 women and 32 men) without hepatic steatosis. Obesity (defined as ≥25% body fat in men and ≥35% in women), was identified by x-ray absorptiometry, whereas hepatic steatosis (≥5.5% liver fat) was detected by magnetic resonance spectroscopy. The primary endpoint was a difference in insulin sensitivity. Obese groups with and without steatosis had similar body fat percentages. Compared with obese women without hepatic steatosis, those with steatosis were more insulin resistant; the same was true for men, although differences were less striking. Obese subjects with hepatic steatosis had higher ratios of truncal-to-lower body fat and other indicators of adipose tissue dysfunction compared with obese subjects without steatosis. Conclusion : These results support the concept that obesity predisposes to hepatic steatosis; but in addition, insulin resistance beyond that induced by obesity alone and a relatively high ratio of truncal-to-lower body fat usually combined with obesity to produce an elevated liver fat content. (Hepatology 2007.)
Effect of flutamide on survival in patients with pancreatic cancer: results of a prospective, randomised, double blind, placebo controlled trial
Authors: B. A Greenway
Journal: BMJ (1998)

Objectives: To assess whether flutamide (Drogenil), a pure androgen receptor blocking agent, improves survival in patients with pancreatic carcinoma and thus whether testosterone is a major growth factor for this tumour. Design: A prospective, randomised, double blind placebo controlled trial. Subjects: 49 patients with a clinical diagnosis of pancreatic carcinoma. Interventions: 24 patients received flutamide and 25 received placebo. Main outcome measures: Death of the patient. Results: Analysis of all patients at 6 months and 1 year showed 14 and eight patients alive, respectively, in the flutamide group compared with 10 and one in the placebo group. After exclusion of those patients in both groups who received less than 6 weeks' treatment because of advanced disease and early death the comparable results were 14 (88%) and eight (50%) alive in the flutamide group compared with 10 (50%) and one (5%) in the placebo group. Median survival for all patients was 8 months in the flutamide group compared with 4 months in the placebo group. With the 6 week exclusions median survival was 12 months compared with 5 months, respectively. Conclusions: This study supports the concept that testosterone is a growth factor for pancreatic carcinoma and that blockade of androgen receptors offers an appropriate new approach to treatment. #### Key messages
Personal views of the NHS--warts and all.
Authors: J. Petrie, C. Harris, G. Williams, S. V. Patel, S. Jeavons, M. Pringle, P. M. Oppenheimer, C. Goodhead, G. Irwin
Journal: BMJ (1988)

training experience than her general house jobs.When the midwives got into trouble she set off on her bicycle with emergency bag and lamp-many of the houses had no electricity-and applied the forceps or whatever was necessary.Both of them commonly had to act as anaesthetist and obstetrician in a routine that sounds deceptively simple.Don two pairs of gloves, go to the head end and give a light chloroform anaesthetic, rush to the other to do a forceps delivery.Most breeches were delivered vaginally in those days. Innovations preceded the NHSIn Oxford we were in a unique position though, for in 1938, £2m was given to create the Nuffield department of obstetrics, together with the corres- ponding departments of medicine, surgery, and anaesthetics.Before taking up my post as first assistant to the new department I spent three months in Vienna studying under Professor Fraenkel.At this time, in marked contrast to England and America, colposcopy was a routine procedure in the teaching hospitals in Vienna, Leipzig, and Berlin, and indeed in much of Europe, and after the war we imported a colposcope and started a colposcopy service.Gradually we took over the gynaecology from the general surgeons and built up our department.We also took over responsibility for the maternity home and built up outpatient clinics in all the outlying hospitals in the Oxford region, with a back up consultancy service for general practitioner obstetricians working in cottage hospitals as well.I was on call all the time, and it was rare to have an unbroken night.But such was the spirit in the hospital that no one resented the hours they put in.One of the innovations with the most impact was the weekly departmental meetings we started to discuss difficult cases and clinical, research, and training policies.Registrars from as far afield as London, Bristol, and Birmingham came for, amazingly enough, at this time such meetings were actively discouraged because they were "not conducive to good departmental discipline."We also, in 1938 on the advice of Professor Chassar Moir, set up a flying squad for it was not uncommon for women with serious obstetric complications to be dead on arrival by the time the ambulance had reached hospital from villages 30-40 miles away.
Whatever Became of That Old-Fashioned Patient?
Authors: Charles L. Hudson
Journal: JAMA (1968)

A question frequently asked somewhat wistfully is, "Whatever became of the old-fashioned doctor?" By the tone of the question, the impression is left that the old-fashioned doctor is no more and that he has been succeeded by someone or something that, to a significant degree, is inferior. In response to these implications of "failure" on the doctors' part, I would like to turn the question around and ask, "Whatever became of the oldfashioned patient?" Actually, there still are among us today many "old-fashioned" doctors and many "old-fashioned" patients. But the pertinent fact is that the conditions of medical practice have changed, and this situation has modified the actions of both patients and doctors. It is fashionable today to speak of people or organizations as projecting an image. The doctors are said to worry about their image. At regular intervals the public press reports that the American Medical Association is concerned
Vascular PPARγ Controls Circadian Variation in Blood Pressure and Heart Rate through Bmal1
Authors: Ningning Wang, Guangrui Yang, Zhanjun Jia, Hui Zhang, Toshinori Aoyagi, Sunhapas Soodvilai, J. David Symons, Jurgen B. Schnermann, Frank J. Gonzalez, Sheldon E. Litwin, Tianxin Yang
Journal: Cell Metabolism (2008)