tbuckley/cabot-search huggingface dataset:
Children in motor vehicles. Never too young to die
Authors: J. J. Karwacki
Journal: JAMA (1979)

In a series of 89 children less than 15 years old who were killed as motor vehicle occupants, children under 1 year of age were greatly overrepresented. Only three children were using child restraint systems or seat belts. Eight were traveling on their parents' laps. Head injuries predominated and were most common in the youngest children. Children under age 1 were the most likely to have reached the hospital alive. The high death rate for very young children was not explained by the circumstances of the crashes or by the age distribution of children involved in all crashes. (<i>JAMA</i>242:2848-2851, 1979)
WHY PROHIBITION FAILS.
Journal: JAMA (1902)

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
Intravenous Lidocaine in the Treatment of Convulsions
Authors: Lloyd J. Lemmen, Marilyn Klassen, Barbara Duiser
Journal: JAMA (1978)

LIDOCAINE, combined with other anticonvulsant medications, often dramatically halts repetitive convulsions. The addition of lidocaine to the anticonvulsant medication program may afford control of seizures without heavy sedation. While high blood levels of local anesthetic can themselves induce convulsions, there is a lower dosage range wherein lidocaine exerts pronounced antiepileptogenic effects in man and animal. Experimental and clinical studies indicate that in higher dosages, lidocaine activates limbic structures, eg, hippocampus and amygdala.<sup>1</sup>Single doses of lidocaine, 2 to 3 mg/kg or 6 to 10 mg/kg/hr, have been suggested along with a barbiturate given at 3 mg/hr, for the control of status epilepticus in man.<sup>2</sup> The Table lists the four patients, with ages ranging from 15 to 61 years and with weights ranging from 52 to 70 kg, we treated by various modes of administration of intravenous (IV) lidocaine. Complete seizure control was attained in each instance. <h3>Complications</h3> Lidocaine
Signaling through CD28 and CTLA-4 controls two distinct forms of T cell anergy
Authors: Andrew D. Wells, Matthew C. Walsh, Jeffrey A. Bluestone, Laurence A. Turka
Journal: Journal of Clinical Investigation (2001)

Primary T cell proliferative responses to TCR ligation plus CD28 costimulation are surprisingly heterogeneous. Many cells that enter G1 fail to progress further through the cell cycle, and some of these cells subsequently fail to divide upon restimulation, even in the presence of IL-2. Such IL-2–refractory anergy is distinct from the IL-2–reversible anergy induced by TCR occupancy in the absence of CD28 costimulation. Here, we focus on the contributions of cell cycle progression and costimulatory (CD28/CTLA-4) signals in the regulation of anergy. We show that CD28 costimulation is not sufficient for anergy avoidance and that activated T cells must progress through the cell cycle in order to escape anergy. Induction of this “division-arrest” form of anergy requires CTLA-4 signaling during the primary response. Also, cell division per se is not sufficient for anergy avoidance: the few T cells that undergo multiple rounds of cell division during overt CD28 costimulatory blockade do not escape the ultimate induction of clonal anergy. Anergy avoidance by primary T cells is thus a multistep process: in order to participate in a productive immune response, an individual T cell activated through its antigen receptor must receive CD28 costimulation and progress through the cell cycle. Anergy may be induced either through a combination of CTLA-4 signaling and the failure of cell cycle progression, or through a proliferation-independent mechanism in which TCR ligation occurs in the absence of CD28.
International J Fertility, Springfield, Mass
Journal: JAMA (1964)

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
Network television news. A resource for medical education
Authors: W. A. Gardner
Journal: JAMA (1982)

THE ALMOST ubiquitous television monitors and playback facilities in classrooms and conference rooms attest to the widespread use of television as an instructional medium.<sup>1</sup>A less widely acknowledged instructional approach but one that has been shown to be effective, especially in the social sciences, is the incorporation of news reports into the classroom.<sup>2,3</sup>This communication describes the use of network television news coverage of health-related events as a supplemental audiovisual resource in medical education. <h3>Resource</h3> "Clearly, an improved awareness of what sources are open to the academic user is almost as important as insuring that future sources are even more complete and easily acceptable."<sup>4</sup> In August 1968, Vanderbilt University, Nashville, Tenn, began videotaping weekday evening network news programs. This project has continued and expanded to produce one of the largest archival resources in the United States. The collection includes the evening news broadcasts of the three major
Source Affiliation and Title Incorrect
Journal: JAMA (1992)

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
AID TO RUSSIAN PHYSICIANS
Journal: JAMA (1921)

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
Therapeutics.
Journal: JAMA (1901)

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
Antecedents and Correlates of Improved Cognitive Performance in Children Exposed in Utero to Low Levels of Lead
Authors: David Bellinger, Alan Leviton, Jone Sloman
Journal: Environmental Health Perspectives (1990)

Up to 2 years of age, children with umbilical cord blood lead levels of 10 to 25 micrograms/dL achieve significantly lower scores on tests of cognitive development than do children with lower prenatal exposures. By age 5 years, however, they appear to have recovered from, or at least compensated for, this early insult. Change in performance between 24 and 57 months of age was examined in relation to level of postnatal lead exposure and various sociodemographic factors. Among children with high prenatal lead exposure, greater recovery of function was associated with lower blood level at 57 months, higher socioeconomic status, higher Home Observation for Measurement of the Environment scores, higher maternal IQ, and female gender. The difference between the scores at 57 months of children with optimal and less optimal values on these variables generally exceed 1/2 standard deviation. Higher prenatal lead exposure is associated with an increased risk of early cognitive deficit. Furthermore, the risk that a deficit will persist through the preschool years is increased among children with high prenatal exposure and either high postnatal exposure or less optimal sociodemographic characteristics.
Obstetrics Illustrated
Authors: John W. Huffman
Journal: JAMA (1970)

The distinguishing characteristic of this undergraduate textbook is its illustrations. Several fine line drawings are found on almost every page. They should simplify the student's introduction to obstetrics. The arrangement of the subject matter is similar to that of most other obstetrical texts. Emphasis is placed on the physiology of reproduction and gestation, obstetric anatomy, prophylactic prenatal care, the early diagnosis of diseases concurrent with and peculiar to pregnancy, and the mechanism of normal labor. There are excellent chapters on malpositions, malpresentations, and anomalies and complications of labor and the puerperium. An exceptionally good chapter on vaginal bleeding during pregnancy presents the subject in a novel and refreshing fashion. Axis traction forceps are unknown to the many modern obstetricians, or, if known, are derided. It will, therefore, be gratifying to those who knew Frederick Irving to note that the authors state that Milne Murry's axis traction forceps (somewhat similar to
5. Oral Carbenicillin
Journal: JAMA (1977)

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 Podcasts Clinical Reviews Editors' Summary Medical News Author Interviews More 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) 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
A phase I and biodistribution study of ABT-806i, an <sup>111</sup>indium-labeled conjugate of the tumor-specific anti-EGFR antibody ABT-806.
Authors: Hui Kong Gan, Matthew E. Burge, Benjamin J. Solomon, Kyle D. Holen, Yumin Zhang, Marika Ciprotti, Thomas Merdan, Wijith Munasinghe, Michelle Pedersen, Patricia F. Hintzman, Gerard B. Fox, Rod A. Humerickhouse, Andrew Mark Scott
Journal: Journal of Clinical Oncology (2013)

2520 Background: ABT-806 is a humanized antibody targeting a conformationally exposed epitope only available when tumor Epidermal Growth Factor Receptor (EGFR) is overexpressed or (EGFRvIII) mutated. A prior trial treated 8 patients (pts) with a chimeric homologue (single-dose 5-40 mg/kg), with a minor response in one squamous cell carcinoma of skin pt. A prior phase 1A study of ABT-806 treated 26 pts (2-24 mg/kg IV q2w), with prolonged SD in one head and neck (H&amp;N) cancer pt. No pt had a typical EGFR-inhibitor rash. The current study gathers further ABT-806 clinical data, assesses ABT-806i dosimetry in normal and malignant tissues and examines its relationship to clinical and PK/PD data. Methods: Pts with advanced tumors likely to express EGFR, ECOG 0-2, measurable disease and adequate organ function were enrolled. ABT-806i scans comprised ABT-806i 5-7mCi injection followed by whole body and regional SPECT scans over one week. Cohort (C) 1 pts (n=6) had ABT-806i scans alone. C2 pts (n=12) had ABT-806i scans at baseline and at week 6 (after 3 fortnightly doses of ABT-806; 6 pts at 18 mg/kg and 6 at 24 mg/kg). Subjects with PR/SD could receive ABT-806 on an extension study until progression. Results: 18 pts (M:F 11:7; median age 57 yrs) with tumors of H&amp;N (6), colon (3), lung (2), brain (2), bladder (1), cervical (1) and other (3) were treated. An H&amp;N pt had a confirmed PR whilst 5 pts had SD (lasting 37 and 24 wks in an adrenal carcinoma and H&amp;N pt respectively). Two potential toxicities were seen at 24mg/kg on the extension study: equivocal rash (G1; three transient lesions on nose) and allergic reaction (Sweet’s syndrome, G2). Dosimetry in C1 pts confirmed safe radiation exposure levels to normal tissues. Many pts showed high, specific tumor uptake of ABT-806i, including 1 pt with an intracranial tumor. ABT-806i uptake was not significantly affected by concurrent ABT-806 treatment. Ongoing analyses of how ABT-806i uptake correlates with tumor EGFR and clinical response may inform the recommended phase 2 dose of ABT-806. Conclusions: The high therapeutic index and specificity of ABT-806 merits further investigation as monotherapy or an antibody-drug conjugate. ABT-806i may have utility as a bioimaging agent. Clinical trial information: NCT01472003.
Medicine, Baltimore
Journal: JAMA (1964)

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
Abstract 14: Pim-1 Preserves Mitochondrial Morphology by Inhibiting Drp1 Translocation
Authors: Shabana Din, Matt Mason, Mirko Volkers, Bevan Johnson, Mathias Konstandin, Pearl Quijada, Jodi Nunnari, Mark A Sussman
Journal: Circulation Research (2012)

Rationale: Mitochondrial morphological dynamics affect the outcome of ischemic heart damage. Mitochondrial fission protein Dynamin Related Protein 1 (Drp1) is a mediator of mitochondrial morphological changes and cell death during ischemic injury. Mitochondrial integrity is maintained by cardioprotective kinase Pim1, which enhances resistance to apoptotic challenge and ischemia reperfusion injury. In this study we examine the relationship between Pim1 activity and Drp1 regulation of mitochondrial morphology in cardiomyocytes challenged by ischemia. Objective: To demonstrate that Pim1 inhibits Drp1 translocation to the mitochondria in response to ischemic injury. Methods and Results: Simulated ischemia and simulated ischemia reperfusion (sI &amp; sI/R) induced mitochondrial fragmentation and cell death in neonatal rat cardiac myocytes (NRCM), respectively. Mitochondrial fragmentation accompanied Drp1 translocation to the mitochondria in NRCM. Inhibition of Drp1 by mdivi1 preserved mitochondrial reticular morphology and inhibited apoptotic cell death. Mice subjected to sI/R injury displayed Drp1 mitochondrial localization, while exposure to mdivi1 led to reduced infarct size. Interestingly, transgenic hearts overexpressing Pim1 decreased total Drp1 levels, increased phosphorylation of Drp1 at serine 637, and inhibited Drp1 localization to mitochondria while preserving reticular morphology after sI. In contrast, Pim1 dominant negative (PDN) transgenic hearts and NRCM exhibit increased Drp1 translocation to mitochondria and fragmented mitochondria. PDN hearts exhibit decreased phosphorylation of serine 637 and upregulation of BH3 protein PUMA, inducing Drp1 accumulation at mitochondria and increased sensitivity to apoptotic stimuli. In PDN NRCMs, overexpression of Puma dominant negative (PumaDN) attenuated localization of Drp1 to mitochondria and inhibited cell death during sI. Conclusion: Pim1 activity prevents Drp1 compartmentalization to the mitochondria and preserves reticular mitochondrial morphology in response to simulated ischemia. Therefore, selective manipulation of Pim1 should be pursued as a therapeutic target to maintain mitochondrial morphology for cardioprotection.
In Reply:
Authors: William D. Figg, Avi Retter, Seth M. Steinberg, William L. Dahut
Journal: Journal of Clinical Oncology (2005)

In the July 15, 2004, issue of the Journal of Clinical Oncology, Dahut et al 1 showed that the addition of thalidomide to docetaxel resulted in an encouraging prostatespecific antigen decline and overall median survival rate in patients with metastatic androgen-independent prostate cancer.In this study, low-molecular-weight heparin (LMWH) was offered to patients in the combination arm for median 6 months, but not offered to patients in the control arm. 1 Preclinical evidence suggests that angiogenesis is important for tumor progression in prostate cancer. 2,3LMWH inhibits angiogenesis, and this effect seems to be independent of the anticoagulant actions. 4,5In a recent randomized study, we tested the effect on patient mortality of a prophylactic dose of LMWH (dalteparin; 5,000 U/d subcutaneously) given in combination with chemotherapy versus chemotherapy alone in patients with small-cell lung cancer (42 patients per group).This trial demonstrated an improvement in overall survival for those patients randomly assigned to receive LMWH. 6 In another recent randomized study, the FAMOUS (Fragmin Advanced Malignancy Outcome Study) Trial, 385 patients with advanced solid cancers were randomly assigned to receive a prophylactic dose of the dalteparin or placebo for up to 1 year.There was suggestion of a marked survival advantage for patients with a better prognosis receiving LMWH therapy. 7 We think that LMWH could provide a therapeutic and survival advantage for patients in the thalidomide arm in the Dahut et al study.To understand whether this survival advantage is depending on thalidomide, the authors should have used LMWH on the control arm as well.