tbuckley/cabot-search huggingface dataset:
VACCINATION PROPAGANDA AND THE MEDICAL PROFESSION
Authors: C. K. Millard
Journal: BMJ (1923)

Tza__~~~~~~~~~~~~~~~~~~~~~~~~~_ ICDICU JOWA - I gave her two injections (1.5 c.cm. and 2 c.cm.) at an interval of seven days.The rash disappeared and she has been quite free since.CASE II.A married woman, aged 24, had suffered from regular attacks of urticaria all over the body, but more pronounced where the clothing was tight (waist, etc.), for nine months.When I first saw her she had a typical urticarial rash on the legs, arms, chest, and round the waist, and at that time any scratching or irritation brought out fresh wheals.She was in a highly excited and nervous condition.I gave her 0.5 c.cm. collosol manganese by intra-
A Critical Evaluation of Glycated Protein Parameters in Advanced Nephropathy: A Matter of Life or Death
Authors: Kamyar Kalantar-Zadeh
Journal: Diabetes Care (2012)

Chronic kidney disease remains as one of the major complications for individuals with diabetes and contributes to considerable morbidity. Individuals subjected to dialysis therapy, half of whom are diabetic, experience a mortality of ∼20% per year. Understanding factors related to mortality remains a priority. Outside of dialysis units, A1C is unquestioned as the “gold standard” for glycemic control. In the recent past, however, there is evidence in large cohorts of diabetic dialysis patients that A1C at both the higher and lower levels was associated with mortality. Given the unique conditions associated with the metabolic dysregulation in dialysis patients, there is a critical need to identify accurate assays to monitor glycemic control to relate to cardiovascular endpoints. In this two-part point-counterpoint narrative, Drs. Freedman and Kalantar-Zadeh take opposing views on the utility of A1C in relation to cardiovascular disease and survival and as to consideration of use of other short-term markers in glycemia. In the narrative preceeding this counterpoint, Dr. Freedman suggests that glycated albumin may be the preferred glycemic marker in dialysis subjects. In the counterpoint narrative below, Dr. Kalantar-Zadeh defends the use of A1C as the unquestioned gold standard for glycemic management in dialysis subjects. —William T. Cefalu, MD Editor in Chief, Diabetes Care
Release of atrial natriuretic factor during selective cardiac alpha- and beta-adrenergic stimulation, intracoronary Ca2+ infusion, and aortic constriction in pigs.
Authors: G Christensen, G Aksnes, A Ilebekk, F Kiil
Journal: Circulation Research (1991)

The effects of alpha- and beta-adrenergic stimulation on release of atrial natriuretic factor (ANF) were examined in seven anesthetized, open-chest pigs. The alpha-adrenergic agonist phenylephrine (28.0 micrograms/min) and the beta-adrenergic agonist isoproterenol (0.3 micrograms/min) were infused into the proximal part of the circumflex coronary artery to stimulate the left atrial adrenoceptors without concomitant changes in left and right atrial filling pressures (v wave). Isoproterenol reduced plasma immunoreactive ANF (irANF) by 15 +/- 7 pg/ml (20%) from 76 +/- 10 pg/ml despite a rise in left atrial systolic pressure (a wave). A comparable rise in left atrial systolic pressure, induced by intracoronary infusion of calcium chloride (8.0 mg/min), increased plasma irANF by 33 +/- 10 pg/ml (53%) from 62 +/- 7 pg/ml. Phenylephrine increased plasma irANF by 9 +/- 4 pg/ml (14%) from 66 +/- 10 pg/ml without altering right and left atrial pressures. A rise in left atrial filling pressure of 3.2 +/- 0.5 mm Hg, induced by constricting the ascending aorta, increased plasma irANF by 83 +/- 35 pg/ml (141%) from 59 +/- 11 pg/ml. This increase was nine times that during phenylephrine infusion. In conclusion, alpha-adrenergic stimulation increases and beta-adrenergic stimulation inhibits ANF release by a direct action on the atrial myocytes. The direct effects of alpha- and beta-adrenergic stimulation on ANF release in vivo are small compared with the effect of a moderate rise in atrial filling pressure.
Effect of Plasmodium falciparum malaria on concentration of HIV-1-RNA in the blood of adults in rural Malawi: a prospective cohort study
Authors: James G Kublin, Padmaja Patnaik, Charles S Jere, William C Miller, Irving F Hoffman, Nelson Chimbiya, Richard Pendame, Terrie E Taylor, Malcolm E Molyneux
Journal: The Lancet (2005)
Relation between antinuclear antibodies and the autoimmune rheumatic diseases and disease type and activity in systemic lupus erythematosus using a variety of cultured cell lines.
Authors: J Sequi, I Leigh, D A Isenberg
Journal: Annals of the Rheumatic Diseases (1991)

Antinuclear activity was assessed in serum samples from a series of 40 patients with differing clinical subsets (including renal and neurological disease) of systemic lupus erythematosus (SLE) against a transformed keratinocyte line (SvK14)* and normal human keratinocytes. Paired serum samples were studied during disease activity and inactivity, and the effects of ultraviolet radiation on the availability of nuclear antigens in the cell substrates were assessed. Serum samples from 20 healthy controls and 40 disease controls, comprising 10 patients each with rheumatoid arthritis, Sjögren's syndrome, scleroderma, and myositis, were also studied. The keratinocytes all provided sensitive substrates for the detection of antinuclear antibodies (ANAs), and in normal keratinocytes treated with ultraviolet radiation nuclear antigens were exposed on the cell surface. There was no correlation between ANAs and disease activity or patterns so, apart from assisting diagnosis, the detection of ANAs is of little relevance to predicting disease activity.
A PSYCHIATRIC CENSUS OF THE SOUTH PACIFIC
Authors: ERIC BERNE
Journal: American Journal of Psychiatry (1960)

Figures are offered representing a psychiatric census of the South Pacific. 1. The apparent prevalence is in almost direct proportion to the ratio of practitioners with medical training in each area. 2. The apparent prevalence is related to the availability of special hospital facilities for psychiatric patients. 3. The apparent incidence (first admissions) for endogenous psychoses is approximately the same for Caucasians and Maoris (Polynesians) in New Zealand. These findings do not contradict, and tend to support, the hypotheses (a) that the reservoir of endogenous psychoses (true prevalence) maintains a constant ratio regardless of racial, cultural, geographical, and socio-economic conditions; and (b) that psychiatric hospital figures are functions of variables other than true prevalence or incidence.
Bexarotene therapy for mycosis fungoides and Sézary syndrome
Authors: R.A. Abbott, S.J. Whittaker, S.L. Morris, R. Russell-Jones, T. Hung, S.J. Bashir, J.J. Scarisbrick
Journal: British Journal of Dermatology (2009)

Bexarotene (Targretin) is a synthetic retinoid which is licensed for the treatment of advanced refractory cutaneous T-cell lymphoma (CTCL).To summarize our experience with bexarotene for patients with CTCL with the aim of assessing efficacy and safety.A retrospective study of 66 patients (44 male, 22 female) with mycosis fungoides (40 patients) or Sézary syndrome (26 patients) who were commenced on bexarotene prior to August 2007 was carried out. Nineteen patients had early-stage (IB-IIA) refractory mycosis fungoides and 47 patients had advanced-stage CTCL (IIB-IVB).Fifty-two out of 66 (79%) patients completed over 1 month of therapy with an intention-to-treat response rate of 44% (29/66). Of the patients, six (9%) had a complete response, 23 (35%) had a partial response, 15 (23%) had stable disease and eight (12%) had progressive disease. Median time to maximal response was 3 months (1-9 months). Median response duration was 8 months (1 to > 48 months). Median time to progression was 9 months (3-44 months). Fourteen patients (21%) did not complete a month of bexarotene therapy. Adverse effects of the whole group included central hypothyroidism in 100% (all grade II and managed with thyroid replacement) and hyperlipidaemia in 100% (all managed with lipid-lowering therapy +/- dose reduction). Responses were seen in all stages and were higher in advanced stages: 26% (five of 19) with early-stage and 51% (24/47) of advanced-stage disease. Responses were seen in skin, blood and lymph nodes. Twenty-eight out of 66 patients were treated with bexarotene monotherapy and the remainder were on one or more additional anti-CTCL therapies.Our data demonstrate that bexarotene is well tolerated in most patients and responses are seen in almost half of patients with all disease stages. However partial responses were not graded and would include any improvement seen in the skin, blood and lymph node.
miR-31 and its host gene lncRNA LOC554202 are regulated by promoter hypermethylation in triple-negative breast cancer
Authors: Katarzyna Augoff, Brian McCue, Edward F Plow, Khalid Sossey-Alaoui
Journal: Molecular Cancer (2012)

Abstract Background microRNAs have been established as powerful regulators of gene expression in normal physiological as well as in pathological conditions, including cancer progression and metastasis. Recent studies have demonstrated a key role of miR-31 in the progression and metastasis of breast cancer. Downregulation of miR-31 enhances several steps of the invasion-metastasis cascade in breast cancer, i.e., local invasion, extravasation and survival in the circulation system, and metastatic colonization of distant sites. miR-31 exerts its metastasis-suppressor activity by targeting a cohort of pro-metastatic genes, including RhoA and WAVE3. The molecular mechanisms that lead to the loss of miR-31 and the activation of its pro-metastatic target genes during these specific steps of the invasion-metastasis cascade are however unknown. Results In the present report, we identify promoter hypermethylation as one of the major mechanisms for silencing miR-31 in breast cancer, and in the triple-negative breast cancer (TNBC) cell lines of basal subtype, in particular. miR-31 maps to the intronic sequence of a novel long non-coding (lnc)RNA, LOC554202 and the regulation of its transcriptional activity is under control of LOC554202. Both miR-31 and the host gene LOC554202 are down-regulated in the TNBC cell lines of basal subtype and over-expressed in the luminal counterparts. Treatment of the TNBC cell lines with either a de-methylating agent alone or in combination with a de-acetylating agent resulted in a significant increase of both miR-31 and its host gene, suggesting an epigenetic mechanism for the silencing of these two genes by promoter hypermethylation. Finally, both methylation-specific PCR and sequencing of bisulfite-converted DNA demonstrated that the LOC554202 promoter-associated CpG island is heavily methylated in the TNBC cell lines and hypomethylated in the luminal subtypes. Conclusion Loss of miR-31 expression in TNBC cell lines is attributed to hypermethylation of its promoter-associated CpG island. Together, our results provide the initial evidence for a mechanism by which miR-31, an important determinant of the invasion metastasis cascade, is regulated in breast cancer.
Intravascular Coagulation in Liver Disease
Authors: M Verstraete, J Vermylen, D Collen
Journal: Annual Review of Medicine (1974)

Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), the cause of coronavirus disease 2019 (COVID-19), emerged in China in December 2019 and quickly spread around the globe, killing more than 4 million people and causing a severe economic crisis. ...Read More
Substantial Increase in Incidence of Severe Hypoglycemia Between 1997–2000 and 2007–2010
Authors: Andreas Holstein, Olaf M. Patzer, Kathrin Machalke, Judith D. Holstein, Michael Stumvoll, Peter Kovacs
Journal: Diabetes Care (2012)

To compare the incidences of severe hypoglycemia and corresponding clinical circumstances in a German population between 2007-2010 and 1997-2000.A screening for severe hypoglycemia was performed in the Lippe-Detmold area in Germany to sensitively detect severe hypoglycemia. This was defined as a symptomatic event requiring treatment with intravenous glucose and being confirmed by a blood glucose measurement of <50 mg/dL.Severe hypoglycemia increased considerably from 264 events in 1997-2000 to 495 events in 2007-2010, which translated into an increase in frequency of severe hypoglycemia among all emergency admissions from 0.68 to 0.83% (P = 0.015). This was mostly related to intensification of antihyperglycemic therapy, particularly in the increasingly morbid group of hypoglycemic patients with type 2 diabetes indicated by lower HbA(1c), more comedication (3.3 vs. 7.7 drugs), and more concomitant diseases (3.6 vs. 4.4) (all P values <0.001).Within a 10-year period, there was an intensification of antihyperglycemic therapy in increasingly comorbid subjects, leading to a considerably higher incidence of severe hypoglycemia.
LPS-induced lung inflammation is linked to increased epithelial permeability: role of MLCK
Authors: H. Eutamene, V. Theodorou, F. Schmidlin, V. Tondereau, R. Garcia-Villar, C. Salvador-Cartier, M. Chovet, C. Bertrand, L. Bueno
Journal: European Respiratory Journal (2005)

The respiratory system is directly exposed to low levels of lipopolysaccharide (LPS), present as a contaminant on airborne particles. In cystic fibrosis, the prevailing data identify structural changes of the airway epithelium, as well as tight junction dilatation. This study was aimed at determining the contribution of myosin light chain kinase to maintaining airway epithelium barrier integrity in the lung inflammatory response to LPS in rats. The effects of the selective myosin light chain kinase inhibitor, 5-iodonaphthalene-1-sulphonyl-homopiperazine (ML-7), were evaluated: 1) on pulmonary inflammation and airway epithelium barrier permeability alterations induced by intra-tracheal LPS from Pseudomonas aeruginosa ; and 2) on levels of the phosphorylated form of the myosin light chain, which is increased in a human airway epithelial cell line (NCI-H292) and tracheal tissue after LPS exposure. The results show that LPS increased airway epithelium barrier paracellular permeability and lung inflammation, and that pre-treatment with ML-7 inhibited both effects. This effect of ML-7 was associated with the inhibition of phosphorylated myosin light chain in both NCI-H292 cells and tracheal tissue. The data, obtained using in vivo and in vitro approaches, demonstrate a key role for myosin light chain kinase in lung inflammation, and suggest that myosin light chain kinase could be a potential target for novel drugs intended for relief of lung injury.
Chemotherapy in advanced bladder cancer: current status and future
Authors: Nabil Ismaili, Mounia Amzerin, Aude Flechon
Journal: Journal of Hematology & Oncology (2011)

Bladder cancer occurs in the majority of cases in males. It represents the seventh most common cancer and the ninth most common cause of cancer deaths for men. Transitional cell carcinoma is the most predominant histological type. Bladder cancer is highly chemosensitive. In metastatic setting, chemotherapy based on cisplatin should be considered as standard treatment of choice for patients with good performance status (0-1) and good renal function-glomerular filtration rate (GFR) > 60 mL/min. The standard treatment is based on cisplatin chemotherapy regimens type MVAC, HD-MVAC, gemcitabine plus cisplatin (GC) or dose dense GC. In unfit patients, carboplatin based regimes; gemcitabine plus carboplatin or methotrexate plus carboplatin plus vinblastine (MCAVI) are reasonable options. The role of targeted therapies when used alone, or in combination with chemotherapy, or in maintenance, was evaluated; targeting angiogenesis seem to be very promising. The purpose of this literature review is to highlight the role of chemotherapy in the management of advanced transitional cell carcinoma of the bladder.
Respiratory Control in Neonatal Rats Exposed to Prenatal Cigarette Smoke
Authors: Jonathan D. Pendlebury, Richard J. A. Wilson, Shehr Bano, Kathleen J. Lumb, Jennifer M. Schneider, Shabih U. Hasan
Journal: American Journal of Respiratory and Critical Care Medicine (2008)

Prenatal cigarette smoke (CS) exposure, increased environmental temperature, and hypoxic episodes have been postulated as major risk factors for sudden infant death syndrome.To test the hypothesis that maternal CS exposure disrupts eupneic breathing and depresses breathing responses of neonatal rats to thermal and hypoxic challenges.Experiments were performed on 1-week-old rat pups exposed prenatally to CS (n = 39) or room air (sham; n = 30). Breathing patterns were recorded by whole-body plethysmography during thermoneutral or hyperthermic states under normoxic and hypoxic conditions.Mean pup weight, breaths per minute, and gasping respiratory patterns were measured for both smoke- and sham-exposed groups during thermoneutral and hyperthermic states under normoxic and hypoxic conditions. Under thermoneutral conditions, hypoxia caused gasping in CS-exposed animals but not in sham-exposed animals. Furthermore, under hyperthermic conditions, whereas hypoxia induced gasping in both groups, only CS-exposed animals exhibited a pronounced and longer lasting respiratory depression after the termination of hypoxia.We show that prenatal CS exposure increases the likelihood of gasplike respiration and provide the first experimental evidence that the combined effects of prenatal CS exposure and hyperthermia dramatically prolong the time required for neonates to return to eupneic breathing after hypoxia. These observations provide important evidence of how prenatal CS exposure, hypoxic episodes, and hyperthermia might place infants at higher risk for sudden infant death syndrome.
A phase II trial of primary temozolomide in patients with grade III oligodendroglial brain tumors
Authors: Hui K Gan, Mark Andrew Rosenthal, Anthony J. Dowling, Renate Kalnins, Elizabeth Algar, Nicholas Wong, Angela Benson, Anne Marie Woods, Lawrence Cher
Journal: Neuro-Oncology (2010)

Glial tumors with oligodendroglial components are considered chemo-responsive. Forty newly diagnosed patients (11 anaplastic oligodendrogliomas [OD] and 29 anaplastic oligoastrocytomas [OA]) were enrolled into this multicenter, open-label, single-arm Phase II trial of first-line temozolomide (200 mg/m(2) on days 1-5 every 4 weeks for 6 cycles). The primary endpoint was 6-month progression-free survival (PFS) with response rate (RR), median PFS, and median overall survival (OS) as secondary endpoints. Of 39 evaluable patients at the 6-month time point (median follow-up, 34 months), 6-month PFS was 77% (95% confidence interval [CI], 74.5%-79.3%). There were 15 complete responses (CRs, 38%), 6 partial responses (PRs, 15%), and 9 disease stabilization (23%). The median PFS was 21 months (95% CI, 3-39 months), and the median OS was 43 months (95% CI, 20-66 months). Chromosome 1p/19q codeletions were seen in 47% (18 of 38) of the patients, and O-6-methylguanine-DNA-methyltransferase (MGMT) methylation was seen in 48% (10 of 21) of the patients. All patients with OD showed MGMT methylation and most (71%) had chromosome 1p/19q codeletions. Conversely, fewer patients with OA showed MGMT methylation (23%) or had chromosome 1p/19q codeletions (31%). The presence of either 1p/19q codeletion or MGMT methylation was associated with increased RR at 6 months but not with improved PFS or OS. Only 18% of the patients (7 of 40) experienced treatment-related grade 3/4 toxicities. This regimen was active and well tolerated. These data add to the growing body of data showing that primary chemotherapy may be an acceptable alternative to radiotherapy for patients with gliomas containing oligodendroglial histology.
On the course of low back pain in general practice: a one year follow up study
Authors: H. J M van den Hoogen, B. W Koes, J. T. M van Eijk, L. M Bouter, W. Deville
Journal: Annals of the Rheumatic Diseases (1998)

<h3>OBJECTIVES</h3> Knowledge on the clinical course of low back pain presented in general practice is poor. Preceding studies offer a fragmentary view only, whereas further knowledge is important to enable the assessment of the prognosis. The object of this study is to investigate the course of low back pain presented in general practice to enable the assessment of the prognosis. <h3>METHODS</h3> A one year follow up study on the clinical course of low back pain in consecutive cases receiving usual care in general practice. During a period of two years 15 general practitioners from Amsterdam and surrounding areas included consecutive patients with both chronic and recent onset low back pain. After the initial visit, each patient was monitored for a period of 12 months. The follow up consisted of monthly postal questionnaires on the course of the low back pain and the related disability. <h3>RESULTS</h3> A total of 443 of 605 patients identified were included in the follow up, which was fully completed by 269 patients. In general, patients with less serious low back pain participated less often or did not complete the follow up. At 12 weeks 35% and at the end of the follow up 10% of the population, respectively, still suffered from low back pain. Both the pain and the disability seemed to diminish quickly after the initial visit, and both seemed to stabilise at a lower level if the low back pain did not disappear completely. About three of four patients, whose pain disappeared before the end of the follow up, endured one or more relapses within a year. The median time to a relapse was about seven weeks, and its median duration about six weeks. Both the pain and the disability turned out to be less severe during relapses. The median time to recovery for patients whose low back pain developed more than seven weeks before the initial visit, was four weeks longer than for patients with more recently developed low back pain at the initial visit. <h3>CONCLUSIONS</h3> The clinical course of low back pain presented in general practice, for the most patients, clearly is less favourable than expected. It takes more than just a few weeks to recover, and relapses occur within a year in most cases. Fortunately, both the pain and the disability quickly diminish, even if the low back pain does not resolve within a few weeks.
History of Multiple Suicide Attempts as a Behavioral Marker of Severe Psychopathology
Authors: Evan M. Forman, Michele S. Berk, Gregg R. Henriques, Gregory K. Brown, Aaron T. Beck
Journal: American Journal of Psychiatry (2004)

OBJECTIVE: Individuals with a differing number of past suicide attempts are generally considered a homogeneous group, despite emerging evidence to the contrary. The current study aimed to test the hypothesis that multiple suicide attempters would exhibit a more severe clinical profile than single suicide attempters. METHOD: A series of self-report batteries and clinical interviews was administered to 39 single attempters and 114 multiple attempters who came to an urban hospital emergency room after a suicide attempt. The participants were predominantly poor and nonwhite. RESULTS: Multiple suicide attempters versus single attempters exhibited a greater degree of deleterious background characteristics (e.g., a history of childhood emotional abuse, a history of family suicide), increased psychopathology (e.g., depression, substance abuse), higher levels of suicidality (e.g., ideation), and poorer interpersonal functioning. Profile differences existed even after control for borderline personality disorder. CONCLUSIONS: Results indicate that multiple attempters display more severe psychopathology, suicidality, and interpersonal difficulties and are more likely to have histories of deleterious background characteristics than single attempters. Moreover, these differences cannot be explained by the diagnosis of borderline personality disorder. Results suggest that the identification of attempt status is a simple, yet powerful, means of gauging levels of risk and psychopathology.