tbuckley/cabot-search huggingface dataset:
The Michigan Medical Legislation League. Open Letter No. 2 to the Members of the Medical Profession (regular) in Michigan.
Authors: Donald Maclean
Journal: JAMA (1896)

Detroit, Mich., Aug. 3, 1896. In response to my brief, but earnest appeal to the adherents of regular medicine and the friends of suffering humanity in this State, published in theJournalof the 23d ult., two letters appear in the issue of August 1, just received. One of these letters is signed by the President of the so-called "League," and the other by his "alter ego," J. H. Carstens. Simmered down to their ultimate elements, these communications, with apparent politeness, charge me with "illiberality" and with Phariseeism, and my attitude toward the question at issue as lacking in patriotic duty. To all such personal accusations the only answer that I have time or inclination to offer is written and can be plainly read in the quarter century record of my professional life in Michigan. Neither do I propose to condescend to recriminations or "tu quoque" charges of any kind.
Pathophysiology: Altered Regulatory Mechanisms in Disease
Authors: Harry B. Greenberg
Journal: JAMA (1972)

More than a textbook, Frohlich's<i>Pathophysiology</i>presents an up-to-the-hour view of the disordered physiologic mechanisms responsible for the signs and symptoms of disease. In the process it gives its reader a lot of current theoretical and factual information about physiology, biochemistry, and, to a lesser extent, pathology. On the other hand, its contributors (54 in all) consider treatment only briefly or indirectly, or not at all. Starting with the heart and blood vessels and ending with fascinating chapters on immunology, the contributors take up each organ system in turn. They emphasize the mechanisms that regulate or inhibit human renal, metabolic, reproductive, and other functions. Often their discussions are complex. For example, Livingston tells about neural integration and how pain disturbs vascular and other reflexes. Long-continued severe pain, he writes, becomes a physiologic juggernaut that disrupts somatic and visceral function. Events recorded in the central and autonomic nervous systems influence the
Antiguanosine Antibodies: A New Marker for Procainamide-Induced Systemic Lupus Erythematosus
Authors: RICHARD H. WEISBART
Journal: Annals of Internal Medicine (1986)

Antinuclear antibodies are present in most patients receiving procainamide. To ascertain whether IgG antiguanosine antibodies are associated with the development of the symptoms of systemic lupus erythematosus, we compared the levels of these antibodies in the sera of 65 patients receiving procainamide: 18 with procainamide-induced symptoms and 47 asymptomatic patients. Antinuclear antibodies measured by immunofluorescence were present in the 18 patients with drug-induced symptoms but also in 24 asymptomatic patients. Similarly, elevated serum levels of antibodies to single-stranded DNA were found in 15 patients with symptoms and in 20 asymptomatic patients. In contrast, levels of IgG antiguanosine antibodies were elevated in 15 patients with drug-induced symptoms, but in only 3 asymptomatic patients. Antiguanosine antibodies binding to single-stranded DNA were found primarily in patients with arthritis, pleuritis, and pericarditis. These results suggest a strong association between IgG antiguanosine antibodies and major manifestations of procainamide-induced systemic lupus erythematosus.
Noncardiac Causes of Pulmonary Edema
Authors: Joseph F. Phillips
Journal: JAMA (1975)

<h3>Common1</h3> Agonal Aspiration (eg, Mendelsohn syndrome) Cerebral (stroke, head trauma, epilepsy) Drug hypersensitivity, allergy, or poisoning Fluid overload; overtransfusion Glomerulonephritis (acute) Narcotics (heroin and others) Oxygen toxicity (shock lung) Pulmonary embolism or infarct Uremia <h3>Uncommon</h3> Hanging; suffocation High altitude Hypoproteinemia Inhalation of noxious gas Intravascular coagulation defect Liver disease [Lymphangiectasia] Malaria Mediastinal tumor with venous or lymphatic obstruction Near-drowning Pneumothorax Pregnancy Pulmonary veno-occlusive disease Radiation therapy Shock Thoracic trauma Transfusion reaction <h3>Diagnosis</h3> Pulmonary edema secondary to heroin overdose. <h3>Comment</h3> The patient was treated with endotracheal positive pressure ventilation, and sodium bicarbonate was administered to correct acidosis. The patient responded rapidly to therapy, and a roentgenogram the following day showed complete resolution of the bilateral alveolar infiltrates. Cardiovascular disease is certainly the
Prophylaxis of Hemophilus influenzae Type b Disease-Reply
Authors: Michael T. Osterholm
Journal: JAMA (1984)

In Reply.—  We welcome the new analysis by Band and colleagues of data from the collaborative study to determine the efficacy of rifampin prophylaxis for prevention of secondaryH influenzaedisease. With the new analysis, statistical significance (P=.028) is achieved by combining data from children receiving the regimens of 10 mg/kg per dose and 20 mg/kg per dose. The authors changed their protocol during the study because the regimen of 10 mg/kg per dose proved unreliable in eradication ofH influenzaecolonization. Thus, it would seem inappropriate at this time to combine results from the regimen of 10 mg/kg per dose with those from children in the second phase of their study, during which the regimen of 20 mg/kg per dose was used. Was the decision to combine these data made before it was known to which group subsequent cases had been assigned and before analysis began? Would a
Not much legislation, but plenty of argument
Authors: W. Russell
Journal: BMJ (1984)

It looks like a fallow year for legislation on health and medical matters.That is no bad thing, given the interest that politicians have shown in recent years.It is possible to argue that now is a time for a breathing space, especially as the modifications to the structure of the National Health Service required by the implementation of the Griffiths report have still to be carried through.The likelihood is that in the Queen's speech at the opening of parliament on 6 November there will be a promise of action on the controversial subject of fluoridation.The promise was made last year after the decision by Lord Jauncey in the case brought by Mrs Catherine McColl against Strathclyde regional council that the council had no power under the 1980 Water (Scotland) Act to add fluoride to the water supply.But he also added that fluoride was likely to reduce considerably the incidence of dental decay and rejected allegations that it could cause cancer or damage to patients with kidney disease.In England and Wales it is unclear where the responsibility for adding fluoride lies, and the legislation will make clear that the onus is with the health authorities.A lot ofargument is inevitable, since it is an issue that rouses passions and there is a vocal and powerful antifluoride lobby.Fluoridation is costly to carry out, however, and given the restraints on public spending those who oppose it may well be able to at least stave off the day.Action on the Warnock committee's report will have to wait until the 1985 Queen's speech as the consultation process is still under way and will take up the rest of the year.That is not to say that some MP may not attempt a small Bill on the specific issue of surrogate motherhood as a business.That, however, will depend on the luck of the draw in the ballot for private member's time, and while Mrs Anna McCurley, Conservative MP for Renfrew West and Inverclyde, who has taken up the issue, was convinced towards the end of the summer that she would, if she was lucky, get a fair wind, it now looks as if ministers have had second thoughts.No obstacles will be put in anybody's way, but it seems that they would far rather, should a MP do well in the ballot and wish to take up a health topic, that it should be female circumcision.A Bill on that was lost in the Lords in the session just ended.The feeling seems to be that so far as Warnock is concerned a piecemeal approach would be wrong and it is better to wait and come up with a major Bill based on extensive consultation.
Investigation of a Truncated Cardiac Troponin T That Causes Familial Hypertrophic Cardiomyopathy
Authors: Charles Redwood, Karin Lohmann, Wu Bing, Giovanna M. Esposito, Kathryn Elliott, Hassan Abdulrazzak, Adam Knott, Ian Purcell, Steven Marston, Hugh Watkins
Journal: Circulation Research (2000)

Abstract —Familial hypertrophic cardiomyopathy (HCM) is caused by mutations in at least 8 contractile protein genes, most commonly β myosin heavy chain, myosin binding protein C, and cardiac troponin T. Affected individuals are heterozygous for a particular mutation, and most evidence suggests that the mutant protein acts in a dominant-negative fashion. To investigate the functional properties of a truncated troponin T shown to cause HCM, both wild-type and mutant human cardiac troponin T were overexpressed in Escherichia coli , purified, and combined with human cardiac troponins I and C to reconstitute human cardiac troponin. Significant differences were found between the regulatory properties of wild-type and mutant troponin in vitro, as follows. (1) In actin-tropomyosin–activated myosin ATPase assays at pCa 9, wild-type troponin caused 80% inhibition of ATPase, whereas the mutant complex gave negligible inhibition. (2) Similarly, in the in vitro motility assay, mutant troponin failed to decrease both the proportion of actin-tropomyosin filaments motile and the velocity of motile filaments at pCa 9. (3) At pCa 5, the addition of mutant complex caused a greater increase (21.7%) in velocity of actin-tropomyosin filaments than wild-type troponin (12.3%). These data suggest that the truncated troponin T prevents switching off of the thin filament at low Ca 2+ . However, the study of thin filaments containing varying ratios of wild-type and mutant troponin T at low Ca 2+ indicated an opposite effect of mutant troponin, causing enhancement of the inhibitory effect of wild-type complex, when it is present in a low ratio (10% to 50%). These multiple effects need to be taken into account to explain the physiological consequences of this mutation in HCM. Further, these findings underscore the importance of studying mixed mutant:wild-type preparations to faithfully model this autosomal-dominant disease.
Recurrent neutrophilic eccrine hidradenitis
Authors: E.F. BERNSTEIN, R.L. SPIELVOGEL, D.L. TOPOLSKY
Journal: British Journal of Dermatology (1992)

Neutrophilic eccrine hidradenitis (NEH) is a neutrophilic dermatosis primarily affecting the eccrine glands, and most commonly seen in patients undergoing chemotherapy for treatment of a malignancy. Rapid diagnosis may avert unnecessary changes in therapy to treat conditions which clinically mimic NEH. We describe a patient who developed NEH on three separate occasions provoked by two different chemotherapeutic agents—cytarabine and mitoxantrone. The lesions were morphologically distinct and differed in their anatomical distribution during each episode. The response to intravenous corticosteroids was dramatic, but lesions recurred after their withdrawal. This case illustrates the potential diversity of clinical lesions in a single patient with NEH, and its response to systemically administered corticosteroids.
Accelerated Approval for Pertuzumab in the Neoadjuvant Setting: Winds of Change?
Authors: Laura J. Esserman, Angela DeMichele
Journal: Clinical Cancer Research (2014)

Accelerated approval for agents that improve the frequency of complete pathologic response in the primary breast cancer setting heralds a broadening of the opportunities to get effective agents to the market more quickly. However, these new pathways will require identifying the signature or subtype for which the agent is most effective, and evidence of enrollment of patients to a trial that enables the ascertainment of event-free survival. The recent approval of pertuzumab for use in the neoadjuvant setting is evidence that the FDA is committed to supporting the accelerated approval pathway. The situations in which approval is likely to be granted are discussed.
Competency of the Mentally Retarded to Stand Trial: New Rules from the Supreme Court
Authors: William J. Curran
Journal: New England Journal of Medicine (1972)

ONE of the continuing fallacies in the law of most American jurisdictions is the assumption that mental retardation and mental illness are the same thing for legal purposes. The fallacy is reinforced by the location in many states of retardation programs in state agencies for mental health operated by psychiatrists.An impressive and influential blow was struck for a more specific examination of legal issues in mental retardation in a recent decision of the United States Supreme Court. In Jackson vs. Indiana1 a retarded 27-year-old deaf mute was charged with two minor robberies. A question of his mental competency to . . .
Uterine Inversion and Cord Traction
Authors: C. J. Dewhurst
Journal: BMJ (1964)

form.Juvenile diabetes mellitus with optic atrophy but without diabetes insipidus has been repeatedly reported in the past as a familial recessive syndrome.`'In most of these individuals profound perceptive hearing loss and in some an automatic bladder developed subsequently.Furthermore, the familial association of Friedreich's ataxia with diabetes mellitus of early onset has been recorded far too fre- quently to be fortuitous.
Left ventricular diastolic performance at rest and during exercise in patients with coronary artery disease. Assessment with first-pass radionuclide angiography.
Authors: L A Reduto, W J Wickemeyer, J B Young, L A Del Ventura, J W Reid, D H Glaeser, M A Quinones, R R Miller
Journal: Circulation (1981)

We used first-pass radionuclide angiocardiography to assess filling fraction during the first third of diastole, peak filling rate and peak filling rate during the first third of diastole as indexes of left ventricular diastolic performance at rest and after upright bicycle exercise in 32 normal patients and 68 patients with coronary artery disease. The mean filling fraction was unchanged from rest to exercise in normal patients (47+/- 15% vs 46 +/- 13%; NS). Even in 49 coronary patients with normal (greater than or equal to 50%) ejection fraction at rest, filling fraction was less than that in normal patients at rest (35 +/- 11% vs 47 +/- 15%, p less than 0.001). Despite similar resting heart rates, patients with coronary disease had lower (p less than 0.001) peak filling rate and peak filling rate during the first third of diastole than normal patients. With exercise, filling fraction decreased (p less than 0.001) from the resting value in coronary patients. These data suggest that (1) indexes of diastolic performance can be noninvasively assessed at rest and during exercise using first-pass radionuclide angiocardiography, (2) abnormalities in early diastolic performance are often present at rest in patients with coronary artery disease despite normal systolic performance, and (3) exercise-induced ischemia results in increased early diastolic dysfunction in patients with coronary disease.
Inhibition of plasma-mediated adherence of sickle erythrocytes to microvascular endothelium by conformationally constrained RGD-containing peptides
Authors: Anjali Kumar, James R. Eckman, Timothy M. Wick
Journal: American Journal of Hematology (1996)

Adherence of sickle erythrocytes to vascular endothelium likely initiates or participates in microvascular occlusion, leading to ischemic tissue and organ damage characteristic of sickle-cell pain episodes. In vitro, sickle-cell adherence to endothelium involves adhesive plasma proteins and integrin and nonintegrin receptors on sickle cells and endothelial cells. The involvement of arginine-glycine-aspartic acid (RGD) sequences in adhesive plasma proteins and integrin receptors suggests that RGD-containing peptides may inhibit sickle-cell/endothelial-cell adherence. In the present study, inhibition of plasma-mediated sickle-erythrocyte adherence to endothelium using conformationally constrained RGD-containing peptides was quantified in vitro under continuous flow at a shear stress of 1.0 dyn/cm2. Two conformationally constrained RGD peptides were investigated: 6Z (which has high affinity for alpha5beta1, alpha(V)beta3, and alpha(IIIb)beta3 integrin receptors), and TP9201 (which preferentially binds to alpha(IIb)beta3). Peptide 6Z at 50 microM inhibited plasma-mediated sickle-cell adherence to microvascular endothelium 70% when incubated with sickle red cells, and 63% when incubated with endothelium. Under similar conditions, peptide TP9201 inhibited plasma-mediated sickle-cell adherence up to 85% at concentrations from 250 to 500 microM TP9201. The inhibition of plasma-mediated adherence by conformationally constrained RGD peptides, but not by linear or circular constructs, suggests that the tertiary structure of the peptide containing the binding sequence is important. Inhibition of plasma-mediated sickle-cell adhesion with these peptides in vitro suggests that such conformationally constrained RGD peptides could provide therapeutic interventions in the course of the disease by inhibiting receptor-ligand interactions.
THE INTERFERENCE OF INACTIVE SERUM AND EGG-WHITE IN THE PHENOMENON OF COMPLEMENT FIXATIONS
Authors: Hideyo Noguchi, J. Bronfenbrenner
Journal: The Journal of Experimental Medicine (1911)

The fixing property of a specific precipitate and of syphilitic serum in the presence of certain antigenic lipoids, can be removed by adding certain non-complementary proteins of blood serum or hen's egg. This disappearance of the complementary activity in the syphilis reaction, as well as in the true Bordet-Gengou reaction, is a phenomenon which incidentally accompanies the fixation of certain serum constituents, some of which possess a complementary activity. The presence or absence of the complementary property in these protein components does not influence fixation. Whether the disappearance of the complementary activity during the phenomenon of so-called fixation is due to a mechanical precipitation of the molecules through absorption or whether it is due to a physico-chemical alteration of the active molecules, is unknown. It is more probable that a chemical interaction takes place in the case of the syphilis reaction. Certain sera, for example, those derived from man and goat, show a low fixability. It is interesting to note that the fixability is gradually diminished when these sera and egg-white are heated to a temperature above 56 degrees C., and totally disappears at 85 degrees C. The coagulation of proteins with absolute alcohol or by boiling, destroys their interfering property. The fact that the fixation is not selectively directed towards complement, has a very important meaning for exact serology. The one-sided accuracy as to the complementary unity is no longer sufficient for quantitative work. Both the complementary and the volumetric unity of a serum serving as the source of complement should be taken into consideration. Besides, the fixability of the sera of various species of animals must also be considered. From these facts a formula may be derived for deciding the degree of suitableness of a serum. see PDF for Equation X is the degree of suitableness; K, the species constant for the fixability; P, the complementary activity; and V, the volume of serum. It will be seen that the suitableness is proportional to the fixability constant and the complementary unity, and inversely proportional to the volume of serum employed. As to what species yields the largest value for X, we refer the reader to our studies published elsewhere.
AI-15 * EPIDERMAL GROWTH FACTOR-LIKE MODULE CONTAINING MUCIN-LIKE HORMONE RECEPTOR 2 ROLE IN PREDICTING SURVIVAL IN INVASIVE GLIOMAS
Authors: M. Ivan, M. Safaee, T. Oh, A. Clark, M. Sun, J. Kim, O. Bloch, A. Jahangiri, M. Aghi, A. Parsa
Journal: Neuro-Oncology (2014)

Epidermal growth factor (EGF) module-containing mucin-like receptor 2 (EMR2) is a member of the seven span transmembrane adhesion G-protein coupled receptor subclass. This protein is expressed in a subset of glioblastoma (GBM) cells and associated with an invasive phenotype. The expression pattern and functional significance of EMR2 in low grade or anaplastic astrocytomas is unknown and our goal was to expand and further define EMR2's role in gliomas with an aggressive invasive phenotype. Using the TCGA survival data we describe EMR2 expression patterns across histologic grades of gliomas and demonstrate an association between increased EMR2 expression and poor survival (p < 0.05). We support this data with qPCR of EMR2 expression in 3 separate tumor grades from our own brain tumor research center showing increase in EMR2 expression correlates with tumor grade (p < 0.05). This data supports our prior functional data depicting that EMR2-positive neoplasms possess a greater capacity for infiltrative and metastatic spread. Genomic analysis suggests that EMR2 overexpression is associated with the mesenchy mal GBM subtype(p < 0.0001). We also demonstrate that immunohistorchemistry (IHC) is a feasible method for screening GBM patients for EMR2 expression. Protein and mRNA analysis demonstrated variable expression of all isoforms of EMR2 in all glioma grades, however GBM displayed the most diverse isoforms expression pattern as well as the highest expression of the EGF1-5 isoform of EMR2. Finally, a correlation of an increase in EMR2 expression after bevacizumab treatment in glioma cells lines as well as in an animal model is identified (P < 0.05). This observation should serve as the impetus for future studies to determine if this up-regulation of EMR2 plays a role in the observation of the diffuse and increasingly invasive recurrence patterns witnessed in a subset of GBM patients after bevacizumab treatment.