tbuckley/cabot-search huggingface dataset:
Perinatal changes in lung surfactant calcium measured in situ.
Authors: R G Eckenhoff
Journal: Journal of Clinical Investigation (1989)

Calcium ion is thought to play a role in the structure and function of pulmonary surfactant after secretion into the alveolar space. Since fetal lung liquid calcium concentration is inadequate for this hypothesized role, at a time when optimal surfactant function is necessary for survival, we speculated that the necessary calcium is secreted with the surfactant material, i.e., in the lamellar body. Lungs from rat fetuses at 20, 21, and 22 d gestation, and also from newborn rats at 3-5 h, 1 and 3 d, were rapidly frozen, sectioned, freeze-dried, and examined cold (-100 degrees C) in a transmission electron microscope equipped with a fully quantitative energy-dispersive x-ray detector and analyzer. X-ray spectra were collected from the lamellar bodies and cytoplasm of type II cells at each time point. Lamellar body calcium concentration in the fetus was approximately twice that of the adult (70 +/- 4 vs. 37 +/- 2 mmol/kg dry wt +/- SEM, P less than 0.01), and it decreased rapidly after birth to adult levels. Apically located lamellar bodies in the fetus have a significantly higher calcium concentration than those in a perinuclear position (76 +/- 4 vs. 52 +/- 3, P less than 0.01). There is significant correlation of calcium and chloride concentrations in lamellar bodies, suggesting that factors responsible for the distribution of chloride, i.e., pH, may also be responsible for the accumulation of calcium by these organelles. These results show that mature calcium transport in lamellar bodies is achieved prenatally in the rat, and suggest that the calcium required for normal surfactant function at birth is secreted with the lamellar body.
Effects of Mineralocorticoids, Altered Sodium Intake, and Adrenalectomy on Urinary Kallikrein in Rats
Authors: RONALD G. GELLER, HARRY S. MARGOLIUS, JOHN J. PISANO, HARRY R. KEISER
Journal: Circulation Research (1972)

The urinary excretion of kallikrein was examined in rats whose mineralocorticoid level was increased by the administration of deoxycorticosterone or a low-sodium diet and decreased by adrenalectomy. Administration of deoxycorticosterone by injection or by subcutaneous implantation of pellets resulted in a threefold increase in kallikrein excretion after 10-30 days ( P &lt;0.01). Low-sodium intake produced a twofold increase in kallikrein excretion after 2 and 4 weeks ( P &lt;0.01). Urine volume and blood pressure were normal and unchanged throughout the study. Sodium excretion was unaltered by deoxycorticosterone but was essentially zero during low-sodium intake. Adrenalectomized rats excreted less than half the kallikrein of shamoperated control rats ( P &lt;0.01). These data show a direct relationship between mineralocorticoids and kallikrein excretion and suggest that mineralocorticoids are a primary factor regulating the urinary excretion of kallikrein in rats.
Sirtuins and the hepatic regulation of energy homeostasis
Authors: Puneet Puri, Arun J. Sanyal
Journal: Hepatology (2009)

The fasting-activated longevity protein sirtuin 1 (SirT1) promotes gluconeogenesis in part, by increasing transcription of the key gluconeogenic genes pepck1 and g6pase, through deacetylating PGC-1α and FOXO1. In contrast, signal transducer and activator of transcription 3 (STAT3) inhibits glucose production by suppressing expression of these genes. It is not known whether the inhibition of gluconeogenesis by STAT3 is controlled by metabolic regulation. Here we show that STAT3 phosphorylation and function in the liver were tightly regulated by the nutritional status of an animal, through SirT1-mediated deacetylation of key STAT3 lysine sites. The importance of the SirT1-STAT3 pathway in the regulation of gluconeogenesis was verified in STAT3-deficient mice in which the dynamic regulation of gluconeogenic genes by nutritional status was disrupted. Our results reveal a new nutrient sensing pathway through which SirT1 suppresses the inhibitory effect of STAT3, while activating the stimulatory effect of PGC-1α and FOXO1 on gluconeogenesis, thus ensuring maximal activation of gluconeogenic gene transcription. The connection between acetylation and phosphorylation of STAT3 implies that STAT3 may have an important role in other cellular processes that involve SirT1.
Calpromotin, a cytoplasmic protein, is associated with the formation of dense cells in sickle cell anemia
Authors: R. Blaine Moore, Stephanie K. Shriver, Lucy D. Jenkins, Vipul N. Mankad, Arvind K. Shah, Gordon A. Plishker
Journal: American Journal of Hematology (1997)

We have tested the hypothesis that dense cell formation in sickle cell disease is associated with increased binding of calpromotin to the membrane, an event that occurs during the activation of calcium-dependent potassium transport. By SDS polyacrylamide gel electrophoresis, we found that sickle cell membranes contained more calpromotin than did normal membranes when stained with Coomassie brilliant blue or when transferred to nitrocellulose paper and immunostained with horseradish peroxidase. Also, the membranes from dense sickle cells contained significantly (P = 0.00055) higher levels of calpromotin, 2.62 ± 1.59 μg/mg membrane protein, compared to light sickle cells, 1.40 ± 0.70 μg/mg membrane protein, when measured by an enzyme-linked immunosorbent assay. The ratio of calpromotin associated with dense cell membranes to light cell membranes was significantly greater than 1.0 (P < 0.00005). Transmission electron micrographs of immunogold-labelled membranes supported the increase in calpromotin binding in dense sickle cell membranes. In addition, the immunogold probe demonstrated clustering, which was not observed in light sickle cell membranes nor in normal membranes. Finally, we incubated HbSS cells in vitro using a repetitive deoxygenation/reoxygenation procedure to produce dense cells and then measured the levels of calpromotin associated with their membranes. As expected, the levels of calpromotin bound to the membrane doubled during the procedure relative to the basal levels at the beginning of the incubation. The correlation coefficient, calculated between the increase in dense cell formation and the increase in calpromotin associated with the membrane, was statistically significant (P = 0.038). The results demonstrate that an increase in calpromotin binding to the membrane is associated with dense cell formation presumably through the activation of the calcium-dependent potassium channel. Am. J. Hematol. 56:100–106, 1997. © 1997 Wiley-Liss, Inc.
Pressure to Publish and Fraud in Science
Authors: PATRICIA K. WOOLF
Journal: Annals of Internal Medicine (1986)

Pressure to publish is an overworked and ill-used phrase that encompasses at least two meanings: the pressure an individual scientist may feel, and the pressure exerted by the institutions of science. It is important not to confuse the two. A modest level of institutional pressure is legitimate and healthy for science. Persons who respond to these pressures by publishing extravagantly may be doing a disservice to impressionable young colleagues and to the notions of responsible authorship.
DECREASED MYOCARDIAL DENDRITIC CELLS IS ASSOCIATED WITH IMPAIRED REPARATIVE FIBROSIS AND DEVELOPMENT OF CARDIAC RUPTURE AFTER MYOCARDIAL INFARCTION IN HUMANS
Authors: Toshiyuki Nagai, Satoshi Honda, Yasuo Sugano, Taka-aki Matsuyama, Keiko Ohta-Ogo, Yasuhide Asaumi, Yoshihiko Ikeda, Kengo Kusano, Masaharu Ishihara, Hisao Ogawa, Satoshi Yasuda, Hatsue Ishibashi-Ueda, Toshihisa Anzai
Journal: Journal of the American College of Cardiology (2014)
An American Text-book of Gynecology, Medical and Surgical, for Practitioners and Students.
Authors: Henry T. Byford M.D., J.M. Baldy, Edwin B. Cragin M.D., J.H. Etheridge M.D., William Goodell M.D., Howard A. Kelly M.D., Florian Krug M.D., E.E. Montgomery M.D., William R. Pryor M.D., George M. Tuttle M.D.
Journal: JAMA (1898)

Our website uses cookies to enhance your experience. By continuing to use our site, or clicking "Continue," you are agreeing to our Cookie Policy | Continue JAMA HomeNew OnlineCurrent IssueFor Authors Publications JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry (1919-1959) Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More JN Learning / CMESubscribeJobsInstitutions / LibrariansReprints & Permissions Terms of Use | Privacy Policy | Accessibility Statement 2023 American Medical Association. All Rights Reserved Search All JAMA JAMA Network Open JAMA Cardiology JAMA Dermatology JAMA Forum Archive JAMA Health Forum JAMA Internal Medicine JAMA Neurology JAMA Oncology JAMA Ophthalmology JAMA Otolaryngology–Head & Neck Surgery JAMA Pediatrics JAMA Psychiatry JAMA Surgery Archives of Neurology & Psychiatry Input Search Term Sign In Individual Sign In Sign inCreate an Account Access through your institution Sign In Purchase Options: Buy this article Rent this article Subscribe to the JAMA journal
Prevention of infective endocarditis.
Authors: C M Oaklay
Journal: Thorax (1979)

A series of layered peripheral checkpoints maintain self-reactive B cells in an unresponsive state. Autoantibody production occurs when these checkpoints are breached; however, when and how this occurs is largely unknown. In particular, how self-reactive B cells are restrained during bystander inflammation in otherwise healthy individuals is poorly understood. A weakness has been the unavailability of methods capable of dissecting physiologically relevant B cell responses without the use of an engineered BCR. Resolving this will provide insights that decipher how this process goes awry during autoimmunity or could be exploited for therapy. In this study, we use a strong adjuvant to provide bystander innate and adaptive signals that promote B cell responsiveness in conjunction with newly developed B cell detection tools to study in detail the ways that peripheral tolerance mechanisms limit the expansion and function of self-reactive B cells activated under these conditions. We show that although self-reactive B cells are recruited into the germinal center, their development does not proceed, possibly because of rapid counterselection. Consequently, differentiation of plasma cells is blunted, and Ab responses are transient and devoid of affinity maturation. We propose this approach, and these tools can be more widely applied to track Ag-specific B cell responses to more disease-relevant Ags, without the need for BCR transgenic mice, in settings where tolerance pathways are compromised or have been genetically manipulated to drive stronger insights into the biology underlying B cell–mediated autoimmunity.
Interaction Between Soluble Thrombomodulin and Intercellular Adhesion Molecule-1 in Predicting Risk of Coronary Heart Disease
Authors: Kenneth K. Wu, Nena Aleksic, Christie M. Ballantyne, Chul Ahn, Harinder Juneja, Eric Boerwinkle
Journal: Circulation (2003)

Background— Results from previous ARIC (Atherosclerosis Risk In Communities) analyses indicate that soluble intercellular adhesive molecule-1 (sICAM) and soluble thrombomodulin (sTM) levels are associated with risk of coronary heart disease (CHD) in an opposite direction. A high sICAM level increases the risk of CHD, whereas a high level of sTM has a lower risk of CHD. It was unclear whether there was an interaction between sTM and sICAM. Methods and Results— Using a nested case-cohort design, we measured sTM and sICAM in 317 incident CHD cases and 726 non-cases from the ARIC participants. Consistent with our previous reports, sICAM values in the upper versus the lower tertile increased the risk of CHD event by ≈2-fold (95% confidence interval [CI], 1.46 to 2.87) whereas sTM values in the lower versus the upper tertile increased CHD risk by ≈4-fold (95% CI, 2.80 to 5.74). Interaction between these 2 parameters was determined by weighted Cox proportional hazard regression. A significant interaction ( P =0.038) was noted. Combinatorial analysis shows a significant increase in CHD risk ratio (RR) (4.66, 95% CI, 1.89 to 11.46) of the lower sTM/upper sICAM group versus the upper sTM/lower sICAM group. Individuals whose sTM values were in the upper tertile had a RR below 1, even when sICAM were in the upper tertile. The RR of lower tertile sTM was increased by sICAM in a tertile-dependent manner. Conclusion— Weighted Cox proportional hazard analysis shows a significant interaction between sTM and sICAM in predicting risk of CHD event. Combinatorial analysis reveals that an upper tertile sICAM had a significant increase in the risk of a CHD event only when sTM was in the lower tertile.
Dipeptidyl peptidase-4 inhibitor, vildagliptin, inhibits pancreatic beta cell apoptosis in association with its effects suppressing endoplasmic reticulum stress in db/db mice
Authors: Yan-ju Wu, Xin Guo, Chun-jun Li, Dai-qing Li, Jie Zhang, Yiping Yang, Yan Kong, Hang Guo, De-min Liu, Li-ming Chen
Journal: Metabolism (2014)

AimsVildagliptin promotes beta cell survival by inhibiting cell apoptosis. It has been suggested that chronic ER (endoplasmic reticulum) stress triggers beta cell apoptosis. The objective of the study is to explore whether the pro-survival effect of vildagliptin is associated with attenuation of endoplasmic reticulum stress in islets of db/db mice.MethodsVildagliptin was orally administered to db/db mice for 6 weeks, followed by evaluation of beta cell apoptosis by caspase3 activity and TUNEL staining method. Endoplasmic reticulum stress markers were determined with quantitative RT-PCR, immunohistochemistry and immunoblot analysis.ResultsAfter 6 weeks of treatment, vildagliptin treatment increased plasma active GLP-1 levels (22.63 ± 1.19 vs. 11.69 ± 0.44, P < 0.001), inhibited beta cell apoptosis as demonstrated by lower amounts of TUNEL staining nuclei (0.37 ± 0.03 vs. 0.55 ± 0.03, P < 0.01) as well as decreased caspase3 activity (1.48 ± 0.11 vs. 2.67 ± 0.13, P < 0.01) in islets of diabetic mice compared with untreated diabetic group. Further, vildagliptin treatment down-regulated several genes related to endoplasmic reticulum stress including TRIB3 (tribbles homolog 3) (15.9 ± 0.4 vs. 33.3 ± 1.7, ×10−3, P < 0.001), ATF-4(activating transcription factor 4) (0.83 ± 0.06 vs. 1.42 ± 0.02, P < 0.001) and CHOP(C/EBP homologous protein) (0.07 ± 0.01 vs. 0.16 ± 0.01, P < 0.001).ConclusionsVildagliptin promoted beta cell survival in db/db mice in association with down-regulating markers of endoplasmic reticulum stress including TRIB3, ATF-4 as well as CHOP.
Interesting Presentation of Renal and Adjacent Rib Infection on Bone Scintigraphy: The Additive Value of Tissue Phase Images
Authors: Nir Hod, Tifha Horne
Journal: Clinical Nuclear Medicine (2004)

Apart from being an extremely sensitive diagnostic tool for various skeletal abnormalities, bone scintigraphy not infrequently provides valuable information on many urinary tract abnormalities. Although the exact cause of the abnormality may not be apparent on bone scanning, the abnormal findings should be noted for further workup. The authors present a child with severe renal infection, which initially had an interesting presentation on the tissue phase of bone scintigraphy. Late-phase images revealed findings that were compatible with an adjacent rib osteomyelitis caused by contiguous spread of infection from an underlying perinephric abscess.
Rat atrial myocyte plasmalemmal caveolae in situ. Reversible experimental increases in caveolar size and in surface density of caveolar necks.
Authors: L Kordylewski, G E Goings, E Page
Journal: Circulation Research (1993)

The structure, size, and surface density of the conspicuous flask-shaped structures called caveolae that are located under the plasma membrane of cardiac myocytes in intact rat atria were studied by electron microscopy after physiological perturbations designed to examine whether caveolae and/or their necks are fixed or mobile and whether the caveolar lumen is always open or can close off from the interstitial space. We showed that, in stretched and unstretched atria, horseradish peroxidase could enter or be washed out of caveolae at 37 degrees, 18 degrees, and 4 degrees C, but this finding does not rule out that caveolae and/or their necks can cycle rapidly between states closed and open to the interstitial space. Electron microscopy of thin sections revealed that exposure of atria at 37 degrees or 18 degrees C to physiological salt solutions made hypertonic by adding 150 mM sucrose or mannitol resulted in a striking enlargement of caveolar profiles within 1 to 5 minutes. Caveolar enlargement was rapidly reversible on return to control saline. After freeze fracture of atria exposed to these hypertonic solutions, quantitative analysis of electron micrographs of the fracture faces revealed statistically significant increases in cross-sectional diameter of cross-fractured caveolar necks and in mean number of caveolar necks penetrating per unit area of plasmalemmal fracture face. These results suggest that atrial myocyte caveolae are dynamic structures whose necks may be reversibly inserted into and withdrawn from the plasmalemma, possibly (but not necessarily) corresponding to states in which caveolae are, respectively, open and closed to the interstitial spaces.
A multicenter cross-sectional study of circulating soluble urokinase receptor in Japanese patients with glomerular disease
Authors: Takehiko Wada, Masaomi Nangaku, Shoichi Maruyama, Enyu Imai, Kumi Shoji, Sawako Kato, Tomomi Endo, Eri Muso, Kouju Kamata, Hitoshi Yokoyama, Keiji Fujimoto, Yoko Obata, Tomoya Nishino, Hideki Kato, Shunya Uchida, Yoshie Sasatomi, Takao Saito, Seiichi Matsuo
Journal: Kidney International (2014)
Comparison of outcome measures in patients with COPD
Authors: M. FERRER, J. ALONSO, L. PRIETO, J. M ANTO;, R. HARPER, J. BRAZIER, J. WATERHOUSE
Journal: Thorax (1998)

Harper et al 1 found completion rates and success scaling rates of the St George’s Respiratory Questionnaire (SGRQ) lower than those observed in other questionnaires completed by patients with COPD attending an outpatient clinic. Readers may infer from this finding that the SGRQ is a less useful instrument than the Chronic Respiratory Questionnaire (CRQ), but an alternative explanation may lie on some methodological limitations of the study.

Firstly, the CRQ was administered only to an opportunistic subsample and, unfortunately, the authors provide insufficient information to rule out systematic differences with the rest of the patients. Secondly, the claim that SGRQ had lower completion rates may reflect the local condition in which it was applied rather than a general limitation. The CRQ was administered by an interviewer while the SGRQ …
Treatment of Recurrent Symptomatic Ventricular Tachycardia
Authors: ROGER A. WINKLE
Journal: Annals of Internal Medicine (1976)

Eleven consecutive patients with recurrent ventricular arrhythmias were treated by an aggressive protocol and followed up prospectively. Arrhythmias, symptoms, and cardiac lesions were defined. Antiarrhythmic drugs were given on schedule, with blood levels determining dose; success or failure was defined by elimination or recurrence of symptomatic arrhythmias. When drug therapy failed, left ventricular aneurysmectomy was done when appropriate. Recurrent ventricular tachycardia was most frequently responsible for symptoms; coronary artery disease was the most frequent underlying disease. Symptomatic arrhythmias were eliminated in 8 of 11 patients (5 with drugs and 3 with aneurysmectomies), with a 16.5-month symptom-free average follow-up. An average of 2.9 therapeutic trials per patient was needed to control symptomatic arrhythmias. The average time from entry into the study until the start of ultimately effective therapy was 18 days. Therapy that eliminated symptoms did not eliminate all premature ventricular contractions, and occasionally even brief asymptomatic episodes of ventricular tachycardia persisted. Recurrent symptomatic ventricular arrhythmias can be controlled in many patients by rigorous application of current therapies.
Bioavailability and biotransformation of benzo(a)pyrene in an isolated perfused In situ catfish intestinal preparation.
Authors: K M Kleinow, M O James, Z Tong, C S Venugopalan
Journal: Environmental Health Perspectives (1998)

In the aquatic environment, diet is an important route of exposure for the common contaminant and procarcinogen benzo(a)pyrene (BaP). Dietary organisms vary in their BaP content and in contaminated areas often contain other xenobiotics including cytochrome P4501A inducers. This study examined the effect of dose and previous dietary exposure to the inducer ss-naphthoflavone (BNF) upon the intestinal metabolism of BaP and the systemic bioavailability of BaP-derived products in catfish. BaP was administered at 2 and 20 microM into in situ-isolated perfused intestines of control and BNF-pretreated catfish. The intestine formed an array of metabolites in all treatments including potentially hazardous metabolites such as BaP-7,8 and 9,10 dihydrodiols and 6-methyl-BaP. BNF treatment disproportionally increased the contribution of BaP-7,8 and 9,10 dihydrodiols relative to the contributions of other metabolites. A greater percentage of metabolites was evident as conjugates in 2 microM controls, whereas a greater percentage of unconjugated metabolites was evident for 20 microM controls and BNF treatments of both dosages. BNF pretreatment and the higher 20 microM BaP dosage resulted in greater bioavailability, with 2.6-5.5-fold and 3.0-6. 3-fold increases in systemically available BaP products, respectively. Metabolites represented 10.2-23.1% of the increased bioavailability with BNF treatment, suggesting that mechanisms, in addition to induced metabolism, may be operative. These results indicate that intestinal bioavailability, level of biotransformation, and the metabolic profile of BaP-derived products entering the blood from the intestine may be altered by dose and dietary BNF pretreatment.
PLASTIC BAG FOR URETHRAL LEAKAGE CONTROL AFTER PROSTATECTOMY
Authors: Thomas S. Cullen
Journal: JAMA (1952)

In March, 1950, Dr. Howard C. Smith removed the central lobe of my prostate at the Church Home and Hospital. He described it as the largest central lobe he had ever encountered in surgery; the weight was 254 gm. The posterior incision healed by first intention; nevertheless, there was a great amount of leakage from the urethral orifice, evidently due to laxness after removal of the large tumor. As soon as I was well enough, Mrs. Cullen, a graduate of the Johns Hopkins Hospital School of Nursing, undertook control of the leakage. She selected a waterproof plastic,<sup>1</sup>so soft that it could hardly be felt. She made a round bag of this material sufficiently large to contain the genitalia, with a wide hem through which to draw tapes. Two absorbent pads were placed in the bag, the bag was placed around the genitalia, and the tapes were drawn tight
STUDY OF ACUTE TYPE A AORTIC DISSECTION PATIENTS WITH UNDILATED AORTAS
Authors: Benjamin Froehlich, Santi Trimarchi, Eduardo Bossone, Toru Suzuki, Alan Braverman, Eva Kline-Rogers, Jehangir Appoo, Marco Di Eusanio, Thomas Gleason, Khaled Abdul-Nour, Teng Lee, Daniel Montgomery, Eric Isselbacher, Christoph Nienaber, Kim Eagle
Journal: Journal of the American College of Cardiology (2014)