tbuckley/cabot-search huggingface dataset:
High-Efficiency, Long-Term Cardiac Expression of Foreign Genes in Living Mouse Embryos and Neonates
Authors: Geir Christensen, Susumu Minamisawa, Peter J. Gruber, Yibin Wang, Kenneth R. Chien
Journal: Circulation (2000)

Background —The development of improved strategies for efficient and reproducible in vivo gene transfer into the murine heart will ultimately allow the intersection of somatic and germline gene transfer strategies to study complex features of cardiac biology and diseases. Methods and Results —For embryonic gene transfer, an adenovirus vector expressing β-galactosidase was injected in utero into the ventricular cavity of living embryos via microsurgical approaches. The injected embryos were developed to term, and efficient expression of the transgene was detected in all cell types in the heart. For postnatal cardiac gene transfer, adenovirus was injected into the cardiac ventricle of neonatal mice, resulting in efficient expression of the transgene in the outer layer of the myocardium as well as cardiomyocytes in the middle and inner layers of the cardiac wall. Mice examined after 3 weeks displayed a pattern of expression that completely mimicked the pattern seen after 3 days, and gene expression was also found after 6 months. The infected myocytes can be identified by coinfection of an adenovirus expressing green fluorescent protein without affecting their normal physiological function. Conclusions —We have developed a new strategy to achieve efficient and long-term foreign gene expression in both embryonic and postnatal mouse myocardium via direct intracardiac injection of recombinant adenovirus. The strategy should allow the functional assessment of the expression of dominantly acting exogenous genes, overexpression of wild-type genes, and Cre recombinase–mediated gene ablations at the single-cell level in the context of the intact adult mouse myocardium.
Prominence of the C2 Vertebra on SPECT A Normal Variant
Authors: I. P. C. MURRAY, CLAYTON J. FRATER
Journal: Clinical Nuclear Medicine (1994)

Mild preferential focal uptake of Tc-99m HDP in the spinous process of C2 was identified with SPECT of the cervical spine performed in patients in whom the indication for bone scintigraphy was suspected of lesions in the limbs. Its presence in all 21 subjects indicates that such uptake is a normal finding.
Splenosis: Rupture of Spleen, with Splenic Implants
Authors: W. J. McCann
Journal: BMJ (1956)

Autotransplantation of splenic tissue following traumatic rupture of the spleen is a rare finding, and at the time of preparation of this article I was unable to find a case report in British journals.Storsteen and Remine (1953) collected two cases and reported one of their own.Since then Wise (
Glucose and ATP levels in pancreatic islet tissue of normal and diabetic rats.
Authors: F M Matschinsky, A S Pagliara, S N Stillings, B A Hover
Journal: Journal of Clinical Investigation (1976)

It has been suggested that the hyperglucagonemia observed in diabetic animals and man may be due to an impairment of glucose uptake and metabolism by the alpha-cells resulting in a decreased production of ATP. To test this hypothesis glucose, ATP, glucagon, and insulin were measured in pancreatic islets of normal and alloxan or streptozotocin diabetic rats. Two experimental approaches were used. In the first, the pancreas was perfused in vitro for assessing insulin and glucagon release due to 10 mM amino acids with and without 5 mM glucose. These perfusions were performed in the presence and absence of insulin. After perfusion, the pancreas was frozen and processed for analysis of islet glucose, ATP, insulin, and glucagon content. The second approach was to investigate the islet sucrose, urea, and glucose spaces together with ATP, insulin, and glucagon content in vivo in normal and in insulin-treated and untreated streptozotocin diabetic rats. Perfusion of the pancreas in vitro with 5 mM glucose resulted in higher glucose content of normal islets than in alloxan and streptozotocin diabetic islets. Similarly in the in vivo studies, the intracellular glucose space of the streptozotocin diabetic islets was 30% the value found in normals. In the in vivo experiments, despite the relatively small intracellular glucose space of alpha-cell islets, the ATP content of these islets was only 15-20% lower than the ATP content of normal islets. In the in vitro experiments, perfusion with glucose resulted in ATP contents of alpha-cell islets and of normal mixed alpha-beta-cell islets which were indistinguishable. However, the ATP content of alpha-cell islets was maintained for prolonged periods in the absence of glucose in contrast to mixed islets, composed primarily of beta-cells, in which the ATP level decreased by 45% when glucose-free medium was perfused for sustained periods. Finally, insulin infused in high concentrations or administered to the diabetic animal had no effect on the glucose spaces or the ATP contents of normal or alpha-cell islets. It can be calculated that in vivo the intracellular glucose level of islets from streptozotocin treated rats is approximately 15 mM. Since in normals an extracellular glucose concentration of this magnitude inhibits stimulated glucagon release completely, it would seem unlikely that a lack of intracellular glucose is the cause of the apparent glucose "blindness" of the alpha-cells in diabetes. In fact, in perfusion studies as little as 2.5 mM free intracellular glucose was sufficient to suppress glucagon secretion from diabetic alpha-cells. The results of the ATP measurements clearly eliminate a possible energy deficit of diabetic alpha-cells as cause of the apparent glucose resistance of alpha-cells.
STUDIES ON THE CHEMISTRY AND IMMUNOCHEMISTRY OF CELL WALLS OF STAPHYLOCOCCUS AUREUS
Authors: Stephen I. Morse
Journal: The Journal of Experimental Medicine (1962)

The cell walls of an 80/81 strain of Staphylococcus aureus (NYH-6) contain alanine, glycine, glutamic acid, lysine, muramic acid, glucosamine, and ribitol phosphate. 94 per cent of the phosphorus and 41 per cent of the glucosamine are removed by extraction of the cell walls with hot 5 per cent TCA, but significant amounts of the other constituents are not extracted by this procedure. The residue after hot TCA extraction (mucopeptide) is susceptible to lysozyme whereas the intact cell walls are resistant. Staphylococcus aureus cell walls are agglutinated by S. aureus antisera. Agglutination of the cell walls of one S. aureus strain is inhibited by absorption of antisera with cell walls of other S. aureus strains but not by absorption with S. albus cell walls. The ribitol teichoic acid can be isolated from cold TCA extracts of the cell walls. This compound consists almost entirely of ribitol phosphate and glucosamine. The isolated teichoic acid of strain NYH-6 is readily fixed to tanned sheep erythrocytes and these sensitized cells are agglutinated by S. aureus antisera. Cold TCA extracts of cell walls of other strains of S. aureus inhibit hemagglutination whereas extracts of S. albus walls do not. Studies on the inhibition of both hemagglutination and precipitation indicate that the antigenic determinant of S. aureus NYH-6 teichoic acid is ß-N-acetylglucosamine.
Hereditary congenital hypopigmented and hyperpigmented macules (Westerhof syndrome) in two siblings
Authors: A. Vélez, R. Salido, V. Amorrich-Campos, G. Garnacho-Saucedo, M.A. Alvarez-López, M. Galán, J.C. Moreno-Giménez
Journal: British Journal of Dermatology (2009)

Conflicts of interest: none declared. Sir, In 1978 Westerhof et al. reported several members of a family with multiple hereditary congenital hypopigmented and hyperpigmented macules.1 Some affected members also showed retarded growth and mental deficiency. The authors suggested that this complex of symptoms represented a new neurocutaneous syndrome distinct from tuberous sclerosis complex (TSC). We report a 9‐year‐old boy who was born with multiple hypopigmented and hyperpigmented macules distributed over the trunk and extremities. The skin lesions were well defined, asymmetrical, and not confined to any dermatome (Fig. 1a). Mucous membranes were spared. Otherwise the patient was healthy. His only brother, aged 3 years, had similar congenital skin lesions (Fig. 1b). This younger child was diagnosed in utero with symmetrical retarded growth, and during his first 3 years of life has shown growth retardation at percentile < 3. Their mother had three large congenital dark brown spots on her left buttock. No other members of the family were affected.
Asymmetrical Ventricular Enlargement Secondary to Recent Cerebrovascular Accident as Demonstrated by Cisternography
Authors: ALAN SCHLESINGER, VICTOR W. LEE, EDWARD FISHER, JEROME H. SHAPIRO
Journal: Clinical Nuclear Medicine (1985)

A 65-year-old patient was admitted to Boston City Hospital because of a cerebrovascular accident. Cisternography performed three weeks afterward showed persistent ventricular filling of radiotracer. The lateral ventricles also showed an unusual pattern of asymmetrical dilatation as a result of cerebral atrophy.
25-Hydroxyvitamin D Levels and Survival in Advanced Pancreatic Cancer: Findings From CALGB 80303 (Alliance)
Authors: Katherine Van Loon, Kouros Owzar, Chen Jiang, Hedy L. Kindler, Mary F. Mulcahy, Donna Niedzwiecki, Eileen M. O’Reilly, Charles Fuchs, Federico Innocenti, Alan P. Venook
Journal: JNCI Journal of the National Cancer Institute (2014)

Data from animal and cell-line models suggest that vitamin D metabolism plays an important role in pancreatic tumor behavior. Although vitamin D deficiency has been implicated in numerous cancers, the vitamin D status of patients with advanced pancreatic cancer and the effect of baseline vitamin D levels on survival are unknown.Participants in this correlative study (CALGB 151006) were enrolled in CALGB 80303, which was a randomized trial of patients with advanced pancreatic cancer that demonstrated no difference in overall survival (OS) among patients treated with gemcitabine plus placebo vs gemcitabine plus bevacizumab. We measured baseline serum 25-hydroxyvitamin D (25[OH]D) levels and examined associations between baseline 25(OH)D levels and progression-free survival and OS using the Cox rank score test. All statistical tests were two-sided.Of 256 patients with available serum, the median 25(OH)D level was 21.7ng/mL (range 4 to 77). 44.5% of patients were vitamin D deficient (25[OH]D <20ng/mL), and 32.4% were insufficient (25[OH]D ≥20 and <30ng/mL). 25(OH)D levels were lower in black patients compared with white patients, and patients of other/undisclosed race (10.7 vs 22.4 vs 20.9ng/mL, P < .001). Baseline 25(OH)D levels were not associated with PFS (HR = 1.00, 95% CI = 0.99 to 1.01, P = .60) or OS (HR = 1.00, 95% CI = 0.99 to 1.01, P = .95).Vitamin D deficiency was highly prevalent among patients with a new diagnosis of advanced pancreatic cancer. Black patients had statistically significantly lower 25(OH)D levels than white patients. In this cohort of patients with advanced pancreatic cancer receiving gemcitabine-based chemotherapy, baseline 25(OH)D levels were not associated with PFS or OS.
Physiologic concentrations of normal human plasma lipoproteins inhibit the immortalization of peripheral B lymphocytes by the Epstein-Barr virus.
Authors: F V Chisari, L K Curtiss, F C Jensen
Journal: Journal of Clinical Investigation (1981)

Epstein-Barr virus (EBV)-induced immortalization of adult human B lymphocytes is suppressed by physiologic concentrations of human plasma lipoproteins. Several inhibitory mechanisms appear to be operative. First, low density lipoproteins (LDL) directly reduce the ability of EBV to transform human B cells. Second, LDL as well as intermediate and very low density lipoproteins modulate early inductive events rendering the B cell refractory to transforming signals from EBV. Third, LDL also selectively inhibit an EBV-inducible step that occurs within 24 h after transformation. Finally, very low density lipoproteins can abrogate the ongoing, cellular proliferation of EBV-transformed, established B cell lines. The plasma lipoproteins may therefore prevent the emergence of EBV-transformed malignant B cell clones in vivo. Conceivably, on this basis, environmental and genetic influences on plasma lipoprotein concentrations may affect the global distribution of Burkitt's lymphoma, a lymphoid malignancy putatively caused by EBV.
Chk1 Targeting Reactivates PP2A Tumor Suppressor Activity in Cancer Cells
Authors: Anchit Khanna, Otto Kauko, Camilla Böckelman, Anni Laine, Ilona Schreck, Johanna I. Partanen, Agnieszka Szwajda, Stefanie Bormann, Turker Bilgen, Merja Helenius, Yuba R. Pokharel, John Pimanda, Mike R. Russel, Caj Haglund, Kristina A. Cole, Juha Klefström, Tero Aittokallio, Carsten Weiss, Ari Ristimäki, Tapio Visakorpi, Jukka Westermarck
Journal: Cancer Research (2013)

Abstract Checkpoint kinase Chk1 is constitutively active in many cancer cell types and new generation Chk1 inhibitors show marked antitumor activity as single agents. Here we present a hitherto unrecognized mechanism that contributes to the response of cancer cells to Chk1-targeted therapy. Inhibiting chronic Chk1 activity in cancer cells induced the tumor suppressor activity of protein phosphatase protein phosphatase 2A (PP2A), which by dephosphorylating MYC serine 62, inhibited MYC activity and impaired cancer cell survival. Mechanistic investigations revealed that Chk1 inhibition activated PP2A by decreasing the transcription of cancerous inhibitor of PP2A (CIP2A), a chief inhibitor of PP2A activity. Inhibition of cancer cell clonogenicity by Chk1 inhibition could be rescued in vitro either by exogenous expression of CIP2A or by blocking the CIP2A-regulated PP2A complex. Chk1-mediated CIP2A regulation was extended in tumor models dependent on either Chk1 or CIP2A. The clinical relevance of CIP2A as a Chk1 effector protein was validated in several human cancer types, including neuroblastoma, where CIP2A was identified as an NMYC-independent prognostic factor. Because the Chk1–CIP2A–PP2A pathway is driven by DNA-PK activity, functioning regardless of p53 or ATM/ATR status, our results offer explanative power for understanding how Chk1 inhibitors mediate single-agent anticancer efficacy. Furthermore, they define CIP2A-PP2A status in cancer cells as a pharmacodynamic marker for their response to Chk1-targeted therapy. Cancer Res; 73(22); 6757–69. ©2013 AACR.
Identification and quantitation of platelet-associated fibronectin antigen.
Authors: E F Plow, C Birdwell, M H Ginsberg
Journal: Journal of Clinical Investigation (1979)

Platelet-associated fibronectin antigen has been identified by radioimmunoassay and immunofluorescent techniques. In radioimmunoassay, platelet fibronectin was immunochemically indistinguishable from plasma fibronectin. Platelet and plasma fibronectin were bound and eluted from gelatin-sepharose under similar conditions. The level of platelet fibronectin in detergent extracts of washed platelets from 12 healthy adults was 2.85 +/- 1.24 microgram/10(9) platelets. Immunofluorescence with F(ab')2 fragments of immunochemically purified antifibronectin showed that all platelets stained with a discrete punctate pattern. The identification of platelet fibronectin antigen raises the possibility that this protein may participate in platelet-platelet or platelet-surface interactions.
The scintigraphic index spleen/liver at 30 minutes predicts the success of splenectomy in persistent and chronic primary immune thrombocytopenia
Authors: Manel Roca, Eduardo Muñiz‐Diaz, Jaume Mora, Inmaculada Romero‐Zayas, Olga Ramón, Inmaculada Roig, Núria Pujol‐Moix
Journal: American Journal of Hematology (2011)

Splenectomy is considered the second-line of treatment in patients with chronic primary immune thrombocytopenia (ITP) in whom glucocorticoids have failed. Some patients do not respond to splenectomy or they have postoperative complications. Based on our previous experience using kinetic and scintigraphic parameters, we did a retrospective study with the aim of comparing all these parameters as a means of predicting the success of splenectomy in persistent and chronic primary ITP. Forty-one consecutive patients with chronic primary ITP refractory to prednisone, who had been splenectomized, were included in the study. The response to splenectomy was assessed by evaluating bleeding and platelet counts before and at different times after surgery. A complete platelet kinetic study was performed before the splenectomy using autologous (111) In-labeled platelets. The scintigraphic parameters measured included different indices between spleen/heart, liver/hearth, and spleen/liver. Thirty-six patients gave a complete response after splenectomy and five patients did not respond. A statistically significant difference between both groups was found with initial platelet recovery and with some scintigraphic indices which also showed a variable prediction value for the success of splenectomy. Among these indices, the spleen/liver at 30 minutes demonstrated a predictive value with a 100% of sensitivity and a 100% of specificity.some platelet kinetic parameters and scintigraphic indices, in particular the spleen/liver at 30 minutes, were useful to predict the outcome of splenectomy in persistent and chronic primary ITP and, therefore, they should be taken into account when deciding whether or not to perform a splenectomy.
Breaking Bad News
Authors: Rebecca Voelker
Journal: JAMA (1999)

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
Activated‐Ester‐Type Photocleavable Crosslinker for Preparation of Photodegradable Hydrogels Using a Two‐Component Mixing Reaction
Authors: Fumiki Yanagawa, Shinji Sugiura, Toshiyuki Takagi, Kimio Sumaru, Gulden Camci‐Unal, Alpesh Patel, Ali Khademhosseini, Toshiyuki Kanamori
Journal: Advanced Healthcare Materials (2014)

Photodegradable hydrogels have emerged as powerful platforms for studying and directing cellular behavior in a spatiotemporally controlled manner. Photodegradable hydrogels have previously been formed by free radical polymerizations, Michael‐type addition reactions, and orthogonal click reactions. Here, an ester‐activated photocleavable crosslinker is presented for preparing photodegradable hydrogels by means of a one‐step mixing reaction between the crosslinker and a biocompatible polymer containing amino moieties (amino‐terminated tetra‐arm poly(ethylene glycol) or gelatin). It is demonstrated that photodegradable hydrogels micropatterned by photolithography can be used to culture cells with high viability and proliferation rates. The resulting micropatterned cell‐laden structures can potentially be used to create 3D biomaterials for various tissue‐engineering applications.
A Novel Mechanism of Anode-Break Stimulation Predicted by Bidomain Modeling
Authors: Ravi Ranjan, Gordon F. Tomaselli, Eduardo Marbán
Journal: Circulation Research (1999)

Abstract —Anodal stimulation by external pacemakers has been explained on the basis of bidomain models of cardiac tissue. Bidomain models predict that anodal stimuli will hyperpolarize the underlying tissue while adjacent regions become depolarized (virtual cathodes), initiating excitation. We investigated the contribution of active cellular properties to anode-break stimulation. A bidomain model was implemented in which each cell contained realistic ionic currents, including those recruited by hyperpolarization. Simulations reveal that anode-break excitation can originate at the site of stimulation itself and not only from adjacent regions of induced depolarization. The threshold for initiating excitation at the site of stimulation is lower than that for stimulation initiating from adjacent depolarized regions. Thus, incorporation of active cellular properties into a bidomain model predicts a novel mechanism for anode-break stimulation of the heart. The results will improve our understanding of anodal pacing and its risks and benefits in patients.
Mr Waxman Went to Washington
Authors: Bridget M. Kuehn
Journal: JAMA (2014)

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
Macrophage inhibitor factor (MIF) in cutaneous lymphoproliferative diseases
Authors: PABLO UMBERT, RICHARD W. BELCHER, R.K. WINKELMANN
Journal: British Journal of Dermatology (1976)

Macrophage migration inhibitor factor (MIF) activity in the sera of patients with mycosis fungoides, Sézary syndrome, and cutaneous lymphoma was observed in the sera of eight of the ten patients with stage II (infiltrative) mycosis fungoides, but in only one of the eight patients with stage I and in neither of the two patients with stage III mycosis fungoides. Two of the three patients with Sézary syndrome had MIF in the serum. No MIF was observed in cutaneous lymphoma. These data support the concept that Sézary syndrome and mycosis fungoides are T-cell diseases, and transitional, prelymphomatous diseases.
Aristotle, the NHS, and Davie's henhouse
Authors: Colin Douglas
Journal: BMJ (2005)

In the village in which I grew up there was a little band of first world war veterans already far outnumbered by the names of their old comrades on the war memorial beside the church. Once, walking slowly past the bench on which they always sat, I overheard a conversation among them about another who had died only the week before.

“D'ye remember yon time we built Davie's henhouse?” one asked. There was a thoughtful silence. Someone nodded and …