tbuckley/cabot-search huggingface dataset:
Pancreas divisum: opinio divisa
Authors: L QUEST
Journal: Gut (2000)

“Pancreas divisum” describes the congenital anomaly in which the dorsal and ventral pancreatic glands drain separately into the duodenum. It occurs due to failure of fusion of the dorsal and ventral ducts during the seventh week of gestation and is characterised not only by the anatomical configuration but also by the physiology of duct drainage—that is, predominant drainage through the dorsal duct of Santorini.1 The pancreas gland arises during the fifth week of gestation from three outgrowths of the primitive duodenum.2 3 The dorsal pancreatic bud grows at first posteriorly in the midline and later comes to lie in the concavity of the duodenum. Two ventral buds develop slightly caudal to the dorsal bud and the left bud later atrophies but rarely persists to become an annular pancreas. The right ventral bud develops in association with the primitive bile duct. Later the ventral pancreas rotates posteriorly until it comes to lie on the left of the duodenum, caudal to the dorsal pancreas. The duct systems then usually fuse together, the dorsal duct forming the main duct of the body and tail while the ventral duct (Wirsung's duct) becomes the main conduit for pancreatic secretion coursing through the head and opening into the major papilla in the duodenum. The dorsal duct usually also continues to drain along its original course in the duct of Santorini through the minor or accessory papilla which opens in the duodenum proximal to the major papilla.

The discovery of pancreas divisum is usually attributed to Joseph Hyrtl (anatomist, 1810–1894), although it had been described previously in the seventeenth century. Three variants have been described1 4: type 1 or classical divisum in which there is total failure of fusion; type 2 in which dorsal drainage is dominant in the absence of Wirsung's duct; …
A case of hereditary angio-oedema type III presenting with C1-inhibitor cleavage and a missense mutation in the F12 gene
Authors: L. Bouillet, D. Ponard, H. Rousset, S. Cichon, C. Drouet
Journal: British Journal of Dermatology (2007)

Journal Article A case of hereditary angio‐oedema type III presenting with C1‐inhibitor cleavage and a missense mutation in the F12 gene Get access L. Bouillet, L. Bouillet Département de Médecine Interne and *Laboratoire d'Immunologie, Université Joseph Fourier, CHU de Grenoble, BP 217, 38043 Grenoble cedex 09, France †Département de Médecine Interne, Hospices Civils de Lyon, Lyon, France ‡Institut für Humangenetik, Universität Bonn, Bonn, Germany E‐mail: LBouillet@chu‐grenoble.fr Search for other works by this author on: Oxford Academic Google Scholar D. Ponard, D. Ponard Département de Médecine Interne and *Laboratoire d'Immunologie, Université Joseph Fourier, CHU de Grenoble, BP 217, 38043 Grenoble cedex 09, France †Département de Médecine Interne, Hospices Civils de Lyon, Lyon, France ‡Institut für Humangenetik, Universität Bonn, Bonn, Germany E‐mail: LBouillet@chu‐grenoble.fr Search for other works by this author on: Oxford Academic Google Scholar H. Rousset, H. Rousset Département de Médecine Interne and *Laboratoire d'Immunologie, Université Joseph Fourier, CHU de Grenoble, BP 217, 38043 Grenoble cedex 09, France †Département de Médecine Interne, Hospices Civils de Lyon, Lyon, France ‡Institut für Humangenetik, Universität Bonn, Bonn, Germany E‐mail: LBouillet@chu‐grenoble.fr Search for other works by this author on: Oxford Academic Google Scholar S. Cichon, S. Cichon Département de Médecine Interne and *Laboratoire d'Immunologie, Université Joseph Fourier, CHU de Grenoble, BP 217, 38043 Grenoble cedex 09, France †Département de Médecine Interne, Hospices Civils de Lyon, Lyon, France ‡Institut für Humangenetik, Universität Bonn, Bonn, Germany E‐mail: LBouillet@chu‐grenoble.fr Search for other works by this author on: Oxford Academic Google Scholar C. Drouet C. Drouet Département de Médecine Interne and *Laboratoire d'Immunologie, Université Joseph Fourier, CHU de Grenoble, BP 217, 38043 Grenoble cedex 09, France †Département de Médecine Interne, Hospices Civils de Lyon, Lyon, France ‡Institut für Humangenetik, Universität Bonn, Bonn, Germany E‐mail: LBouillet@chu‐grenoble.fr Search for other works by this author on: Oxford Academic Google Scholar British Journal of Dermatology, Volume 156, Issue 5, 1 May 2007, Pages 1063–1065, https://doi.org/10.1111/j.1365-2133.2007.07778.x Published: 01 May 2007
The Care of Patients With AIDS: Don't Ignore the Family Practitioner
Authors: Margaret Dolan
Journal: JAMA (1989)

To the Editor. —  I strongly disagree with the contention of Dr Cotton in her article  Impact of AIDS on the Medical Care System that a new acquired immunodeficiency syndrome (AIDS) specialty needs to be established. This is just not an acceptable way to provide basic health care services for patients with AIDS. It will only lead to increased fragmentation of health care provision. There are just too many patients who have HIV infections, and their problems crossover many of the traditional specialty lines.  These individuals deserve the skills of a primary care physician who can call on the expertise of specialists, both medical and nonmedical, to coordinate their care.  The good news is that this specialty already exists and it is called family practice. Family physicians are trained to care for individuals of all ages and to do so in the context of their families and communities. It
Progression of Chronic Kidney Disease: The Role of Blood Pressure Control, Proteinuria, and Angiotensin-Converting Enzyme Inhibition: A Patient-Level Meta-Analysis
Authors: Tazeen H. Jafar, Paul C. Stark, Christopher H. Schmid, Marcia Landa, Giuseppe Maschio, Paul E. de Jong, Dick de Zeeuw, Shahnaz Shahinfar, Robert Toto, Andrew S. Levey
Journal: Annals of Internal Medicine (2003)

Background: Angiotensin-converting enzyme (ACE) inhibitors reduce blood pressure and urine protein excretion and slow the progression of chronic kidney disease. Purpose: To determine the levels of blood pressure and urine protein excretion associated with the lowest risk for progression of chronic kidney disease during antihypertensive therapy with and without ACE inhibitors. Data Sources: 11 randomized, controlled trials comparing the efficacy of antihypertensive regimens with or without ACE inhibitors for patients with predominantly nondiabetic kidney disease. Study Selection: MEDLINE database search for English-language studies published between 1977 and 1999. Data Extraction: Data on 1860 nondiabetic patients were pooled in a patient-level meta-analysis. Progression of kidney disease was defined as a doubling of baseline serum creatinine level or onset of kidney failure. Multivariable regression analysis was performed to assess the association of systolic and diastolic blood pressure and urine protein excretion with kidney disease progression at 22 610 patient visits. Data Synthesis: Mean duration of follow-up was 2.2 years. Kidney disease progression was documented in 311 patients. Systolic blood pressure of 110 to 129 mm Hg and urine protein excretion less than 2.0 g/d were associated with the lowest risk for kidney disease progression. Angiotensin-converting enzyme inhibitors remained beneficial after adjustment for blood pressure and urine protein excretion (relative risk, 0.67 [95% CI, 0.53 to 0.84]). The increased risk for kidney progression at higher systolic blood pressure levels was greater in patients with urine protein excretion greater than 1.0 g/d (P < 0.006). Conclusion: Although reverse causation cannot be excluded with certainty, a systolic blood pressure goal between 110 and 129 mm Hg may be beneficial in patients with urine protein excretion greater than 1.0 g/d. Systolic blood pressure less than 110 mm Hg may be associated with a higher risk for kidney disease progression. *For members of the AIPRD Study Group, see the Appendix.
Is the M probe really necessary to measure liver stiffness by FibroScan?
Authors: Praveen Sharma, Anil Arora
Journal: Hepatology (2012)

We read with interest the article by Myers et al.1, who concluded that compared with the M probe, the FibroScan XL probe reduces transient elastography (TE) failure and facilitates reliable liver stiffness measurement (LSM) in obese patients. In an ongoing prospective study in chronic liver disease patients in our department, the initial 100 cases (male:female [M:F] ratio 70:30; hepatitis B, n = 26; hepatitis C, n = 12; nonalcoholic fatty liver [NAFL], n = 32; alcohol, n = 30; median body mass index [BMI] 26 kg/m2) were done using the M probe and reliable stiffness measured in 82%; in the remaining 18% we used the XL probe and could perform reliable measurement in all except two patients. Subsequently, we started using the XL probe in the next consecutive 200 patients (M:F 160:40; hepatitis B, n = 46; hepatitis C, n = 32; NAFL, n = 76; alcohol, n = 46; median BMI 25 kg/m2) and obtained reliable LSM in 98%; we used the M probe in patients in whom the XL probe failed without any success. In all six patients in whom we could not measure LSM the BMI was >35 kg/m2. Myers et al.1 concluded that the XL probe reduces failure compared to the M probe (1.1% versus 16%) and facilitates reliable LSM (73% versus 50%). Reliable results were obtained in 61% of patients by the XL probe in whom the M probe was unreliable. This is an important issue considering the high prevalence of obesity in Western as well as Eastern countries and the relationship between BMI and frequency of LSM unreliability in these patients. A study by de Lédinghen et al.2 found a reliable LSM using the M probe in 79.7% of cases. In the other 21.3%, LSM using the XL probe was obtained in 56.9% of patients. A strong correlation was found between the M and XL values, regardless of BMI. A recent study3 concluded a 11% rate of discordance between LSM and liver biopsy by the XL probe and this figure is consistent with the literature regarding the standard M probe (11%-14%) and the FibroTest (16%-19%).4 Disagreement is mainly in patients with severe obesity (BMI >40 kg/m2), but these are the patients who will have TE failure using the M probe and were less likely to have >10 valid shots, and a success rate <60% even using the FibroScan XL probe.3 Hence, we believe that the XL probe should be used and validated in future trials. Praveen Sharma MD, DM*, Anil Arora MD, DM*, * Department of Gastroenterology, Sir Ganga Ram Hospital, Rajender Nagar, New Delhi, India.
Left Ventricular Function in Acute Myocardial Infarction Evaluated by Gated Scintiphotography
Authors: P. RIGO, M. MURRAY, H. W. STRAUSS, D. TAYLOR, D. KELLY, M. WEISFELDT, B. PITT
Journal: Circulation (1974)

Ten normal volunteers and 38 patients with acute myocardial infarction were evaluated by biplane gated blood pool scanning. The mean left ventricular end-diastolic volume in those with infarction was 125 ± 41 ml/m 2 compared to 82 ± 10 ml/m 2 in the normals. The left ventricular end-systolic volume was 82 ± 35 ml/m 2 compared to 35 ± 4 ml/m 2 , and the left ventricular ejection fraction 36 ± 8% compared to 56 ± 3% in the normals. Thirty-six of the 38 patients with infarction had an area of akinesis which ranged from 15 to 59% of the left ventricular wall. Patients with acute myocardial infarction were found to have a significant increase in left ventricular end-systolic volume and decrease in ejection fraction compared to normals. The end-diastolic volume was, however, increased only in those with an elevated left ventricular filling pressure or decreased cardiac index. Follow-up studies obtained in 20 patients between one week and three months following infarction showed that in the 14 who improved clinically, left ventricular ejection fraction significantly increased from 38 to 45% ( P &lt; 0.001) while in six who failed to show clinical improvement or worsened, left ventricular ejection fraction remained at 30%. Left ventricular ejection fraction was significantly greater and the extent of akinesis significantly less in the patients who survived compared to those who died.
Clinical relevance of mutations in the precore genome of the hepatitis B virus.
Authors: H Tillmann, C Trautwein, D Walker, K Michitaka, S Kubicka, K Boker, M Manns
Journal: Gut (1995)

A stop codon in the precore genome of the hepatitis B virus (HBV) in anti-HBe positive HBV carriers may be associated with a more progressive form of HBV infection. Earlier studies, however, were mainly performed in patients from the Mediterranean area who had severe infection. The aim of this study was to evaluate the prevalence of precore mutants in an unselected population living in northern Europe. Twenty of 42 of these patients are infected predominantly with a virus strain, which has the typical stop codon in the precore genome, characterised by a mutation at base 83. In six patients there was an additional G to A mutation at base 86 of the precore genome. Statistical analysis showed no difference between the patients with or without a stop codon in the precore genome. When patients with a double mutation at base 83 and 86 of the precore genome were compared with the other anti-HBe positive HBV carriers, however, the corresponding clinical data were worse. Therefore we suggest, that it is not the stop codon in the precore gene itself, but the occurrence of a double mutation at bases 83 and 86, which is associated with a more severe course of disease in anti-HBe positive HBV carriers.
Abstract 923: Interrelations between roles of phospholipase C-gamma 1 inhibition, mTOR and glycolytic enzymes in growth and survival of glioblastoma cells
Authors: Aditi Jain, James C.K. Lai, Golam MI Chowdhury, Kevin Behar, Alok Bhushan
Journal: Cancer Research (2012)

Abstract Glioblastoma multiforme (GBM) is a deadly and a frequently occurring brain tumor in humans. Patients with this disease survive on an average for 12-14 months after diagnosis. Conventional approaches to treat the cancer are not effective in improving patient survival. Thus, it is imperative to seek new drug targets and therapies that could effectively treat brain tumors and enhance patient survival. Phospholipase C-gamma 1 (PLCα1) plays an important role in regulating intracellular calcium stores and acts as a point of convergence in several cell signaling cascades. Inhibition of PLCα1 is known to decrease cell differentiation, invasion and motility in several cancers. We previously demonstrated inhibition of PLCα1 blocks invasion of glioma cells. In this study, we investigated the effects of PLCα1 inhibition on cell viability, cell signaling and metabolism in brain tumor (U-87 MG) cells. We investigated the hypothesis that inhibition of PLCα1 blocks cellular progression of U-87 MG. U73122, an inhibitor of PLCα1, induced a dose-related decrease in survival of U-87 MG cells, with a maximal effect at 2 µM: this finding correlated with the U73122-induced decrease in expression of lactate dehydrogenase, a protein important in U-87 MG cell survival and metabolism. Moreover, U73122 was effective in enhancing the cytotoxic potential of temozolomide, a modestly effective drug used currently for the treatment of glioblastoma. Western blot analysis of U-87 MG cells treated with U73122 at concentrations between 0.5 and 2 µM showed biphasic effects on expression of phospho-ERK and mTOR, proteins involved in PLCα1 signaling as well as hexokinase II, an important glycolytic enzyme. Employing 1H-[13C]-NMR spectroscopy, we noted that treatment with 2 µM U73122 for 72 hours induced increased glycolytic flux in U-87 MG cells. Thus, our results suggest important mechanistic interrelations between PLCα1 signaling and roles of mTOR and glycolytic enzymes in regulating survival of brain tumor cells. Furthermore, our results also suggest that inhibition of PLCα1 may be exploited in combination with conventional therapies in treating patients with glioblastoma to improve their outcome. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 923. doi:1538-7445.AM2012-923
Travels and travails
Authors: S Miller
Journal: BMJ (1994)

A year ago I was in India. Not on holiday, you understand, but travelling. I base the distinction on time and money. On holiday you have little time and plenty of money. Travelling requires lots of time and that stretches finances. We were definitely travelling.

We started our odyssey in Australia, where we also worked for a while. There we found that time out to roam the planet is often actively encouraged, whereas in Britain many people still consider it to be an exercise in work avoidance. I will not defend it merely because I did it for six months, but rather on the basis that, like any great undertaking, travelling teaches you about all those things that diploma courses cannot.

I have just decided to take another six months off. Not yet - perhaps not for another 18 months - but I am already trying to decide what to do; learn another language, for example, or join an expedition. …
Induction of antibodies to nuclear antigens in rabbits by immunization with hydralazine-human serum albumin conjugates.
Authors: Y Yamauchi, A Litwin, L Adams, H Zimmer, E V Hess
Journal: Journal of Clinical Investigation (1975)

The antihypertensive drug hydralazine can induce in man a syndrome similar to spontaneous systemic lupus erythematosus (SLE). The pathogenesis of this drug-induced syndrome is not understood. In this investigation, five groups of rabbits were studied: group I, 10 rabbits hyperimmunized with hydralazine conjugated to human serum albumin (HSA) in complete Freund's adjuvant (CFA); group II, four rabbits with HSA in CFA; group III, four rabbits with CFA alone; group IV, five rabbits with hydralazine conjugated to rabbit serum albumin (RSA); and group V, four rabbits with a major metabolite of hydralazine conjugated to HSA. The rabbits immunized with hydralazine-HSA developed rising titers of antibodies to hydralazine and progressively increasing amounts of antibodies to both single-stranded and native DNA. The antibodies to DNA were cross-reactive with hydralazine as determined by inhibition of DNA binding and DNA hemagglutination tests. Similar results were obtained in rabbits immunized with the metabolite-HSA compound except the major hapten antibody response was to the metabolite. The DNA antibodies in this group were also capable of being absorbed by metabolite-HSA as well as hydralazine-HSA, indicative of the cross-reactivity between hydralazine and its metabolite. Immunization with hydralazine-RSA caused rabbits to produce antibodies to hydralazine but not to DNA, indicating the requirement for an immune response to the carrier protein in order for antibodies reactive with DNA to be produced. Thus, hyperimmunization of rabbits with hydralazine-protein conjugates may provide a useful animal model of SLE. The data suggests that an immune response to hydralazine may be important in human hydralazine-induced SLE.
mTOR Complex 2 Is Required for the Development of Prostate Cancer Induced by Pten Loss in Mice
Authors: David A. Guertin, Deanna M. Stevens, Maki Saitoh, Stephanie Kinkel, Katherine Crosby, Joon-Ho Sheen, David J. Mullholland, Mark A. Magnuson, Hong Wu, David M. Sabatini
Journal: Cancer Cell (2009)
What is a good GP?
Authors: R M Berrington
Journal: BMJ (1987)

Honour a physician with the honour which is due unto him.In the current debate on the future of primary health care GPs may recall this familiar exhortation.Unfortunately, in contrast to recent statements it provides no clue as to how we attain high esteem nor does it mention any reward other than "honour"-but then it is apocryphal.The government's discussion paper on primary health care suggests that performance indicators for general practice might include personal availability, range ofservices, preventive activities, attendance at postgraduate courses, and "those aspects of practice indicative of high quality work."'Prescribing patterns and hospital referral rates are mentioned in relation to high quality.Defining a good GP is a dynamic process that takes in patients, government, and the health professions.Government inclines towards hard measurements of effectiveness, efficiency, and economy, the performance related contract, and measurable indicators that are determined outside the profession.Most GPs would prefer self regulation using criteria based on personal care and clinical standards, though many acknowledge the need for accountability on basic standards, such as premises and equipment, staffing levels, accessibility, records, repeat prescription, and range ofservices.Such features have, ofcourse, been assessed for the past 15 years before the appointment of general practitioner vocational trainers.This might be acceptable to GPs generally if it was carried out by experienced GPs visiting practices, perhaps accompanied by a family practitioner committee representative.injuries.Surprisingly, only 9% were back injuries.The non- attendance rate was 2-2%, and only 7% of patients failed to complete treatment.Nearly all the patients were able to attend the clinic, only 4% requiring home treatment.By March 1986, 90 treatments a week were being carried out at a cost of £6-11 per patient.Compared with official hospital figures, this represents a savings of £21 500 a year for a practice of 12 000 patients.
Anti–IFN-γ autoantibodies in adults with disseminated nontuberculous mycobacterial infections are associated with HLA-DRB1*16:02 and HLA-DQB1*05:02 and the reactivation of latent varicella-zoster virus infection
Authors: Chih-Yu Chi, Chen-Chung Chu, Jing-Pei Liu, Chia-Hao Lin, Mao-Wang Ho, Wen-Jyi Lo, Po-Chang Lin, Hung-Jen Chen, Chia-Huei Chou, Jia-Yih Feng, Chang-Phone Fung, Yuh-Pyng Sher, Chi-Yuan Li, Jen-Hsien Wang, Cheng-Lung Ku
Journal: Blood (2012)
Primary anti-viral cytotoxic T-cell responses in semiallogeneic chimeras are not absolutely restricted to host H-2 type.
Authors: R V Blanden, M E Andrew
Journal: The Journal of Experimental Medicine (1979)

Chimeras produced by reconstitution of 950 rads irradiated type A or type B host mice with (AXB)F1 fetal liver stem cells were examined in primary (in vivo) and secondary (in vitro) Tc-cell responses to ectromelia virus infection. Of 33 individual chimeras which gave primary responses, 26 produced significant specific lysis of infected targets of both A and B type, though host type targets were invariably lysed more efficiently (host bias). The other 7 chimeras gave lysis of infected host type targets only (absolute restriction). 12 individual chimeras were used in secondary responses. Nine showed host bias, and three showed absolute restriction. Whether an individual chimera showed host bias or absolute restriction seemed to be unrelated to whether the response was primary or secondary, to the time after reconstitution (ranging from 4 to 22 wk), to strain of mouse, or to the batch of fetal liver stem cells used.
TCTAP C-172 Fibrinous Pleuritis and Necrotizing Pericarditis: Unique and Serious Complications of Degos Disease
Authors: Muhammad Anis Haider, Maria Karas, Evelyn Horn, James Horowitz, Francine Garrett, Cynthia Magro, Maria DeSancho, Harsimran Singh
Journal: Journal of the American College of Cardiology (2014)