tbuckley/cabot-search huggingface dataset:
Factors Influencing the Restoration of Blood Flow Following Pulmonary Embolization as Determined by Angiography and Scanning
Authors: MARVIN L. MURPHY, ROBERT T. BULLOCH
Journal: Circulation (1968)

Twenty-five patients with proven pulmonary emboli were followed for at least 20 weeks with serial scans and, in select cases, angiograms to determine the factors influencing the rate of resolution. Fifteen patients showed complete resolution at some time during the observation period. Five of these 15 patients experienced recurrent embolic episodes either before or after complete resolution. The remaining 10 patients included two who died of recurrent massive emboli, three who had recurrent episodes resulting in incomplete resolution, two who showed incomplete resolution at 20 weeks without recurrent emboli, and three who were lost to follow-up. Twenty-one patients exhibited prompt resolution in single or multiple embolic episodes, and four experienced slow resolution. Recurrent embolization is the most significant event in preventing restoration of blood flow. This is most likely to occur in the patient who presents with (1) an initial field defect in excess of 35%, (2) associated heart disease, and (3) peripheral thrombophlebitis and pulmonary emboli without other disease. These factors identified the patients susceptible to recurrent embolization in this study.
Completeness of chronic disease registration in general practice.
Authors: D Mant, A Tulloch
Journal: BMJ (1987)

The completeness of chronic disease registration in four general practices was assessed by referring to the Hospital Activity Analysis. Overall, just over half (56%) of the 695 patients who had been discharged from hospital with a diagnosis of diabetes, cancer, myocardial infarction, epilepsy, hypertension, or thyroid disease were identified on the practice disease registers. Patients with diabetes were most likely to be identified (72%), and those who had had a myocardial infarct least likely (43%). If the standard of registration is to be improved general practitioners must be convinced of its value. The Hospital Activity Analysis might be used widely to audit and improve practice registers.
Enhanced alveolar macrophage-mediated antigen-induced T-lymphocyte proliferation in sarcoidosis.
Authors: A Venet, A J Hance, C Saltini, B W Robinson, R G Crystal
Journal: Journal of Clinical Investigation (1985)

Expansion of T-lymphocyte numbers is a characteristic feature of the alveolitis of pulmonary sarcoidosis. One mechanism that may influence the numbers of T-lymphocytes in the lung is the process of antigen presentation in which alveolar macrophages, in the presence of antigen, induce T-lymphocytes to replicate. To evaluate this process in sarcoidosis, alveolar macrophages were obtained by bronchoalveolar lavage, pulsed with tetanus toxoid, and co-cultured with purified autologous T cells. Strikingly, antigen-pulsed alveolar macrophages from sarcoid patients induced more than a twofold increase in autologous T-lymphocyte proliferation compared with the response seen using cells from normal or patients with idiopathic pulmonary fibrosis (P less than 0.001), all comparisons). In contrast, when monocytes were used as the antigen presenting cell, no significant differences were observed in T cell proliferation induced by antigen among the three groups. The enhanced T-lymphocyte proliferation induced by sarcoid alveolar macrophages was not dependent on the compartment from which the T cells were derived, and was independent of the specific antigen used. One possible explanation for augmented antigen presentation seen in sarcoid is that an increased percentage of sarcoid alveolar macrophages express HLA-DR or HLA-DS surface antigens. However, most normal and sarcoid alveolar macrophages express HLA-DR and HLA-DS surface antigens, and the percentage of macrophages expressing these antigens was not significantly different in the two groups. Thus, while the mechanisms of the enhanced antigen presentation in the sarcoid lung are unknown, the process of antigen-driven, alveolar macrophage-modulated lung T cell proliferation may explain, at least in part, the expansion of lung T-lymphocyte numbers that characterizes this disease.
Trombicula Irritans-Reply
Authors: Joseph H. Shaffer
Journal: JAMA (1962)

<h3>To the Editor:—</h3> Dr. Flake is a careful and critical reader who knows his entomology. Insects are a class of<i>Arthropoda</i>and include: (1) Hemiptera (bugs and lice which pierce and suck), (2) Diptera (2-winged insects, such as flies, gnats, and mosquitos), and (3) Siphonaptera (fleas and bloodsuckers). Chiggers (<i>Trombicula irritans</i>) are not bugs or insects, but are mites and ticks. I appreciate Dr. Flake's calling this to my attention.
Doctors and the Social Trend
Authors: H. S. Gaskell
Journal: BMJ (1945)

Pradaxa (dabigatran) is a direct thrombin inhibitor approved for prevention of stroke and systemic embolism in patients with non-valvular atrial fibrillation. We describe a case of esophageal ulceration associated with Pradaxa administration in a 75-year-old man. The patient reported difficulty swallowing and a burning sensation after taking his first dose of Pradaxa. An esophagogastroduodenoscopy (EGD) revealed linear ulcerations in the mid-esophagus. Pradaxa was held beginning the day before the EGD. The patient reported that his pain and difficulty swallowing resolved on stopping Pradaxa. Pradaxa is formulated with a tartaric acid excipient to reduce variability in absorption. We hypothesise that the capsule lodged in the patient9s esophagus and the tartaric acid may have caused local damage resulting in an esophageal ulcer. It is important to educate patients on proper administration of Pradaxa, to decrease the risk of this rare, but potentially serious adverse event.
Oesophageal lichen planus
Authors: R.A. SHEEHAN-DARE, J. A. COTTERILL, A. V. SIMMONS
Journal: British Journal of Dermatology (1986)

A 50-year-old woman with severe oral lichen planus complained of painful dysphagia. Fiberoptic endoscopy revealed erosive lichen planus of the oesophagus which responded to treatment with systemic corticosteroids.
The Case Identification Challenge in Measuring Quality of Cancer Care
Authors: Marjorie L. Pearson, Patricia A. Ganz, Kimberly McGuigan, Jennifer R. Malin, John Adams, Katherine L. Kahn
Journal: Journal of Clinical Oncology (2002)

The delivery of quality care to all patients with cancer has been named as a national priority within the American health care system. This article addresses the issues critical to case identification in cancer quality measurement and recommends possible strategies for accurately identifying a population of cancer patients.We present the measurement issues associated with the basic challenges of case identification strategies for quality measurement. We discuss two basic challenges: (1) accurately identifying all patients with the defining characteristics (eg, a diagnosis of breast cancer), and (2) identifying only patients with these characteristics.Possible options for identifying newly diagnosed patients include using claims or other administrative data, cancer registries, cancer registry rapid case ascertainment, pathology laboratories, and physicians' offices. In the published literature, the sensitivity of claims varies from 75% to 95%, whereas central registries must have a 90% completeness rate to be certified. Most of these approaches, however, involve limitations to obtaining valid and comparable data across multiple settings.Using an existing data collection system staffed by skilled data collectors and managers should result in substantially more accurate and timely data. Registry officials and the government agencies that provide their support should be encouraged to adopt quality-of-care analyses as an important purpose of the registry system and to enhance their capacity to rapidly ascertain cases, collect the appropriate identifying information needed for patient contact, and verify stage at diagnosis. In order to meet the growing demand for timely, accurate information about quality of care, registries are likely to require additional support so they can enhance their capacity to rapidly ascertain cases, collect the appropriate identifying information needed for patient contact, and verify stage at diagnosis.
Academic Medicine as a Public Trust
Authors: Steven A. Schroeder
Journal: JAMA (1989)

Academic medicine is entrusted by society with the responsibility to undertake several important social missions toward improving the health of the public, including education, patient care, and research. This trust is given implicit authority by generous public funding and considerable autonomy. Medical academia can take pride in its successes, manifested by a premier scientific establishment, the development and use of sophisticated medical technologies and drugs, and the recent dramatic declines in death rates from heart disease and stroke. Academic medicine, however, has been relatively unresponsive to a number of vexing public problems, including skyrocketing expenditures for medical care, substandard indexes of population health, uneven quality of care, an unfavorable geographic and specialty mix of physicians, and widespread disability from long-term medical and psychiatric problems. Although there are many cogent reasons why academic medicine has chosen to define its task relatively narrowly (the nature of its funding successes, the intractability of the social problems, and the attractiveness of the biomedical model), the central issue is how well academic medicine is fulfilling its responsibilities to the public. To the degree that academic medicine defines its central mission narrowly, it may violate its implicit social contract and jeopardize its primary source of financial support. Alternatively, in recognition of its public responsibilities, academic medicine can choose to expand its current activities to be more responsive to the health concerns of the general population.
P57. Activation of RIG-I induces immunogenic cell death
Authors: S Bek, D Kreppel, M Bscheider, CC Lin, T Haas, H Poeck
Journal: Journal for ImmunoTherapy of Cancer (2014)

Meeting abstracts The interaction between the immune system and cancer cells has become a focus of recent cancer therapy research. Immunogenic cell death, short ICD, was described as a cell death modality that stimulates an immune response against dead-cell antigens, in particular when they derive
Delayed generalized inflammatory psoriasis flare during efalizumab treatment
Authors: B. Martin, J.L. Sánchez-Carazo, A. Pérez-Ferriols, V. Oliver, V. Alegre
Journal: British Journal of Dermatology (2009)

Conflicts of interest: none declared. Sir, Efalizumab has shown a good efficacy and safety profile in multiple studies,1 although serious adverse events may occur during the treatment of psoriasis. These events include clinical worsening or the development of new forms of psoriasis during or following therapy.2 The most severe of these events is the so‐called generalized inflammatory flare that has been defined as the development of a flare of inflammatory, widespread psoriasis lesions characteristically appearing during the first 4–6 weeks of treatment. This entity typically affects patients who are not responding to efalizumab, and in some cases can be solved by adding a short course of classic psoriasis systemic therapy to the biologic agent.3 Worsening or de novo psoriatic arthritis during or following efalizumab therapy has also been reported.4, 5 Bang and Gniadecki6 suggested that this phenomenon could be explained by the mechanism of action of the drug, which impairs T‐lymphocyte trafficking to sites of cutaneous inflammation. Thus T cells would be redistributed and increased in other compartments such as the joints, provoking the articular response. A previous history of arthropathy and poor clinical response seem to increase the possibility of developing articular symptoms.7
Abstract CT-05: A phase II trial of selumetinib in women with recurrent low-grade serous carcinoma of the ovary or peritoneum
Authors: John H. Farley, William E. Brady, Michael J. Birrer, Heather Lankes, Robert Coleman, Mark Morgan, Robert Mannel, Diane Yamada, David Mutch, William H. Rodgers, David M. Gershenson
Journal: Cancer Research (2012)

Abstract Background: This study evaluated selumetinib (AZD6244, ARRY-142866), an inhibitor of MEK-1/2, and explored associations between RAS/RAF mutations with clinical outcome. Methods: Women with recurrent low-grade serous ovarian or peritoneal carcinoma were eligible and received selumetinib at 100 mg orally BID until progression or toxicity. Adverse events were assessed with CTCAE v 3.0. Primary measure of efficacy was tumor response by RECIST v 1.0. BRAF, KRAS, and NRAS mutational analysis was performed. Results: Between December 2007 and November 2009, 52 patients were enrolled. Fifty-eight percent of patients had received at least 3 prior chemotherapy regimens. Eight patients (15.4%) had complete (1) or partial (7) responses, and 34 (65%) had stable disease. The median PFS was 11.0 months. The median number of cycles received was 4.5, and 33% of patients received at least 12 cycles of selumetinib. Sixty-three percent of patients (33/52) had PFS&amp;gt; 6 months. Grade 4 toxicities included cardiac (1 patient), pulmonary (1), and pain (1). The most common grade 3 toxicities were gastrointestinal (13), and dermatologic (9). Thirty-four patients had sufficient DNA for mutational analysis: 6% BRAF, 41% KRAS, 15% NRAS mutations were found, and 38% had no detectable mutation. There were no statistically significant differences in the proportion of responses by any mutation. Conclusions: Selumetinib is well tolerated and is active in the treatment of recurrent low-grade serous carcinoma. In exploratory analyses, response to selumetinib did not appear to be related to RAS/RAF mutational status, however the sample size was small. The 81% disease control rate is encouraging and worthy of further evaluation of MEK inhibitors in this population. 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 CT-05. doi:1538-7445.AM2012-CT-05
THE INFLUENCE OF MOUSE-RAT PARABIOSIS ON THE GROWTH IN RATS OF A TRANSPLANTABLE MOUSE SARCOMA
Authors: R. A. Lambert
Journal: The Journal of Experimental Medicine (1911)

The results in these experiments seem to justify us in concluding that the growth of mouse tumors in rats is very definitely promoted by mouse-rat parabiosis, the percentage of " takes" being markedly increased, the rate of growth accelerated, and the duration of active growth extended to at least seventeen days. These findings are in accord with Ehrlich's hypothesis, although, on account of the complexity of the factors involved in such experiments, other explanations may be advanced.
Scanning electron microscopy of the normal epidermis and the epidermis in vitro
Authors: R. MARKS, B. BHOGAL
Journal: British Journal of Dermatology (2006)

A simplified technique has been used to examine the epidermis in five skin biopsies and in eight cultured skin specimens by scanning electron microscopy. Paraffin or cryostat sections of the tissue were cut and prepared according to routine histological methods and then given an electrically conducting coating before examination in the scanning electron microscope. The epidermis was easily identified and a particularly good view was obtained of intercellular bridges at high magnifications. Intra‐epidermal and basal layer dendritic cells were also easily located and their relationships to surrounding keratinocytes by long intercellular processes are described. The scanning electron microscopic appearance of epidermal cells in cultured explains of skin showed a strong resemblance to other cells and tissues in culture and also demonstrated the presence of a unicellular or subcellular membrane at the leading edge similar in appearance to the undulating membrane of fibroblasts in culture. It is stressed that the method is of particular use in the examination of intercellular relationships within the epidermis and in the inspection of histological material at higher magnifications than are possible by light microscopy.
DABIGATRAN VERSUS WARFARIN IN ATRIAL FIBRILLATION PATIENTS WITH LOW, MODERATE AND HIGH CHADS2 SCORE: A RE-LY SUBGROUP ANALYSIS
Authors: Jonas Oldgren, Marco Alings, Harald Darius, John Eikelboom, Michael Ezekowitz, Amit Parekh, Janice Pogue, Paul Reilly, Salim Yusuf, Lars Wallentin, Stuart Connolly
Journal: Journal of the American College of Cardiology (2010)
Prevention and management of pressure ulcers in primary and secondary care: summary of NICE guidance
Authors: G. Stansby, L. Avital, K. Jones, G. Marsden
Journal: BMJ (2014)

Pressure ulcers are serious and distressing, and they can affect people of any age. Not only do they increase mortality, result in extended hospital stays, and consume substantial healthcare resources, they are often an example of avoidable harm. Reported prevalence rates range from 4.7% to 32.1% in hospital populations and as much as 22% in nursing home populations.1 Prevention of this devastating condition must be a priority for the NHS. Stage 1 pressure ulcers (see box for definition of stages) can be reversible if identified promptly, and most stage 2 and 3 ulcers can be healed with appropriate care, but all require a multidisciplinary approach for effective management. It is hoped that this guideline will help reduce pressure ulcers nationally and improve care when pressure ulcers do occur.

#### Pressure ulcer categories/stages2

##### Category/stage 1: Non-blanchable redness of intact skin

Intact skin with non-blanchable erythema of a localised area, usually over a bony prominence. Discoloration of the skin, warmth, oedema, hardness, or pain may also be present. Darkly pigmented skin may not have visible blanching.

The area may be painful, firm, soft, and warmer or cooler than adjacent tissue. This category may be difficult to detect in people with dark skin tones. It may indicate that the person is “at risk.”

##### Category/stage 2: Partial thickness skin loss or blister

Partial thickness loss of dermis presenting as a shallow open ulcer with a red-pink wound bed, without slough. May also present as an intact or open (or ruptured) blister filled with serum or sero-sanguinous fluid.

Presents as a shiny or dry shallow ulcer without slough or bruising. This category should not be used to describe skin tears, tape burns, incontinence associated dermatitis, maceration, or excoriation.

##### Category/stage 3: Full thickness skin loss (fat visible)

Full thickness tissue loss. Subcutaneous fat may be visible but bone, tendon, or muscle is not exposed. Some slough may be present, as may undermining, where the ulcer extends under the surface.

The depth of …
Activation of the unfolded protein response and autophagy after hepatitis C virus infection suppresses innate antiviral immunity in vitro
Authors: Po-Yuan Ke, Steve S.-L. Chen
Journal: Journal of Clinical Investigation (2010)

Autophagy, a process for catabolizing cytoplasmic components, has been implicated in the modulation of interactions between RNA viruses and their host. However, the mechanism underlying the functional role of autophagy in the viral life cycle still remains unclear. Hepatitis C virus (HCV) is a single-stranded, positive-sense, membrane-enveloped RNA virus that can cause chronic liver disease. Here we report that HCV induces the unfolded protein response (UPR), which in turn activates the autophagic pathway to promote HCV RNA replication in human hepatoma cells. Further analysis revealed that the entire autophagic process through to complete autolysosome maturation was required to promote HCV RNA replication and that it did so by suppressing innate antiviral immunity. Gene silencing or activation of the UPR-autophagy pathway activated or repressed, respectively, IFN-β activation mediated by an HCV-derived pathogen-associated molecular pattern (PAMP). Similar results were achieved with a PAMP derived from Dengue virus (DEV), indicating that HCV and DEV may both exploit the UPR-autophagy pathway to escape the innate immune response. Taken together, these results not only define the physiological significance of HCV-induced autophagy, but also shed light on the knowledge of host cellular responses upon HCV infection as well as on exploration of therapeutic targets for controlling HCV infection.
Evolution of the reasoning hominid brain
Authors: Herman T. Epstein
Journal: Behavioral and Brain Sciences (2002)

Cognition is readily seen to be connected to evolution through plots of the ratio of cranial capacity to body size of hominids which show two regions of sharply increasing ratios beginning at 2.5 and 0.5 million years ago – precisely the critical times inferred by the author from his study of tools. A similar correlation exists between current human brain growth spurts and the onsets of the Piagetian stages of reasoning development. The first goal of the author's target article is stated to be “to make a case for the relevance of archeological contributions to studies of the evolution of cognition” (sect. 1, Introduction). His analysis focuses on spatial cognition.
Hyperoxia: A Stereologic Ultrastructural Examination of Its Influence on Cytoplasmic Components of the Pulmonary Granular Pneumocyte
Authors: Gloria D. Massaro, Donald Massaro
Journal: Journal of Clinical Investigation (1973)

We used the technique of lineal analysis to study the influence of 48 h of hyperoxia on cytoplasmic organelles of pulmonary granular pneumocytes with particular reference to their lamellar bodies. We undertook this study because lamellar bodies are considered to be storage granules for pulmonary surfactant and because we had found that hyperoxia decreased [(14)C]leucine incorporation into protein of a surface-active lung fraction. We found that for lamellar bodies the percent cytoplasmic volume was 12.8+/-1.5 (mean+/-SEM) and 8.4+/-2.2, the organelle area (mum(2)) per organelle was 0.98+/-0.13 and 0.62+/-0.10 and the organelle volume (mum(2)) was 0.35+/-0.04 and 0.18+/-0.01, for air- and oxygen-exposed rats, respectively, (P=<0.05). The surface density of the lamellar body membrane was 7.05+/-0.47 and 9.36+/-0.96 (P=<0.05) for air- and oxygen-exposed rats. There were no differences in lamellar body number per cytoplasmic area or per pneumocyte between air- and oxygen-exposed rats. There were no statistical differences in these parameters between mitochondria of air- or oxygen-exposed rats. The surface density of the rough endoplasmic reticulum was the same in both groups. This study indicates that granular pneumocytes of rats exposed to hyperoxia have the same number of lamellar bodies as control rats but the lamellar bodies are smaller. This findings in consistent with the hypothesis that the hyperoxia-induced decrease in protein synthesis by lung represents at least in part a decreased synthesis of the secretory lipoprotein-pulmonary surfactant.