tbuckley/cabot-search huggingface dataset:
Treatment of Acute Osteomyelitis
Authors: G. A. B. Walters
Journal: BMJ (1939)

Cholinergic neuromodulation is pivotal for arousal, attention, and cognitive processes. Loss or dysregulation of cholinergic inputs leads to cognitive impairments like those manifested in Alzheimer9s disease. Such dysfunction can be at least partially restored by an increase of acetylcholine (ACh). In animal studies, ACh selectively facilitates long-term excitability changes induced by feed-forward afferent input. Consequently, it has been hypothesized that ACh enhances the signal-to-noise ratio of input processing. However, the neurophysiological foundation for its ability to enhance cognition in humans is not well documented. In this study we explore the effects of rivastigmine, a cholinesterase inhibitor, on global and synapse-specific forms of cortical plasticity induced by transcranial direct current stimulation (tDCS) and paired associative stimulation (PAS) on 10–12 healthy subjects, respectively. Rivastigmine essentially blocked the induction of the global excitability enhancement elicited by anodal tDCS and revealed a tendency to first reduce and then stabilize cathodal tDCS-induced inhibitory aftereffects. However, ACh enhanced the synapse-specific excitability enhancement produced by facilitatory PAS and consolidated the inhibitory PAS-induced excitability diminution. These findings are in line with a cholinergic focusing effect that optimizes the detection of relevant signals during information processing in humans.
Doxorubicin plus docetaxel as neoadjuvant treatment in patients with large (T&gt;5cm), locally advanced carcinoma of the breast
Authors: S.-H. Lee, J. Y. Lee, Y.-H. Im, J. Park, H. Y. Kim, Y. S. Park, J. H. Kim, S. J. Nam, J. H. Yang, K. Park
Journal: Journal of Clinical Oncology (2004)

746 Background: The objective of this study was to evaluate the activity and toxicity of doxorubicin plus docetaxel as neoadjuvant chemotherapy for women with locally advanced (tumor size > 5 cm) or metastatic breast carcinoma confined to ipsilateral supraclavicular lymph node. Methods: In this single-center, open-label, phase II trial, neoadjuvant chemotherapy consisted of doxorubicin (50 mg/m2; 15-min intravenous infusion) followed by docetaxel (75 mg/m2; 1-hour intravenous infusion) on day 1 of each cycle and repeated every 3 weeks. After 3 cycles, the patients received surgical treatment and adjuvant chemotherapy with/without radiation according to pathologic status. Results: Thirty-six patients were entered between Jul 2001 and Jun 2003. Median age of them was 41 years (range, 25–67). Four of 36 patients (11%) had inflammatory breast carcinoma, and another two patients (6%) had pathologically confirmed metastasis to ipsilateral supraclavicular lymph node. Median size of tumor was 7.0 cm (range, 5.1–12.0 cm) by physical examination. All 36 patients received three cycles of neoadjuvant chemotherapy. Thirty-three patients (92%; 95% confidence interval, 83–100%) had a clinical objective response. Thirty-five patients (97%) underwent surgery, nine patients (25%) of whom underwent breast conserving surgery. One pathologic CR was achieved. Grade 3–4 neutropenia was recorded in 18 patients (50%) and febrile neutropenia in 15 patients (42%), and no treatment-related mortality was recorded. The non-hematologic toxicities greater than grade 2 were stomatitis, nausea, vomiting, fatigue and diarrhea. With median follow-up duration of 18.9 months, median overall survival and time to progression did not reach yet. Conclusions: Neoadjuvant chemotherapy with doxorubicin plus docetaxel was a feasible treatment and was active in an unfavorable series of patients with locally advanced breast carcinoma including inflammatory breast carcinoma or metastatic breast carcinoma confined to ipsilateral supraclavicular lymph node. No significant financial relationships to disclose.
Handbuch der sozialen Hygiene und Gesundheitsfürsorge.
Journal: JAMA (1926)

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
Soluble VEGF isoforms are essential for establishingepiphyseal vascularization and regulating chondrocyte development and survival
Authors: Christa Maes, Ingrid Stockmans, Karen Moermans, Riet Van Looveren, Nico Smets, Peter Carmeliet, Roger Bouillon, Geert Carmeliet
Journal: Journal of Clinical Investigation (2004)

VEGF is crucial for metaphyseal bone vascularization. In contrast, the angiogenic factors required for vascularization of epiphyseal cartilage are unknown, although this represents a developmentally and clinically important aspect of bone growth. The VEGF gene is alternatively transcribed into VEGF120, VEGF164, and VEGF188 isoforms that differ in matrix association and receptor binding. Their role in bone development was studied in mice expressing single isoforms. Here we report that expression of only VEGF164 or only VEGF188 (in VEGF188/188 mice) was sufficient for metaphyseal development. VEGF188/188 mice, however, showed dwarfism, disrupted development of growth plates and secondary ossification centers, and knee joint dysplasia. This phenotype was at least partly due to impaired vascularization surrounding the epiphysis, resulting in ectopically increased hypoxia and massive chondrocyte apoptosis in the interior of the epiphyseal cartilage. In addition to the vascular defect, we provide in vitro evidence that the VEGF188 isoform alone is also insufficient to regulate chondrocyte proliferation and survival responses to hypoxia. Consistent herewith, chondrocytes in or close to the hypoxic zone in VEGF188/188 mice showed increased proliferation and decreased differentiation. These findings indicate that the insoluble VEGF188 isoform is insufficient for establishing epiphyseal vascularization and regulating cartilage development during endochondral bone formation.
Cyclamate sweeteners
Authors: T. H. Jukes
Journal: JAMA (1976)

ON OCT 18, 1969, the Secretary of Health, Education, and Welfare, Mr Robert Finch, announced that "the artificial sweetener cyclamate was removed from the list of substances generally recognized as safe (GRAS) for use in food." In so doing, he invoked the "so-called Delaney amendment which states that any food additive must be removed from the market if it has been shown to cause cancer when fed to humans or animals." This announcement caused surprise and consternation both in the United States and other countries, for cyclamates had been in steadily increasing use since the early 1950s, and in 1959 had been put on the safe list for addition to foods. The ban is still making news. The discovery by Sveda in 1937 of a sweet substance lacking the aftertaste of saccharin started a train of research and development that led to the introduction of Sucaryl sodium, C<sub>6</sub>H
Hepatitis A Vaccination Coverage Among Children Aged 24-35 Months—United States, 2003
Journal: JAMA (2005)

After the licensure of hepatitis A vaccine in 1995 for children aged > or =24 months, the Advisory Committee on Immunization Practices (ACIP) incrementally expanded the proportion of children for whom it recommended the vaccine. In 1996, ACIP recommended vaccinating children in communities that had high rates of hepatitis A virus (HAV) infection, including American Indian/Alaska Native (AI/AN) communities and selected Hispanic and religious communities. In 1999, ACIP extended the recommendation to include routine vaccination for all children living in states, counties, and communities with incidence rates twice the 1987-1997 national average of 10 cases per 100,000 population (i.e., > or =20 cases per 100,000 population); ACIP also recommended considering vaccination for children living in states, counties, and communities with incidence rates exceeding the 1987-1997 national average (i.e., >10 to <20 cases per 100,000 population). National estimates of hepatitis A vaccination coverage were first made available through the 2003 National Immunization Survey (NIS), which indicated an overall national 1-dose coverage level of 16.0% (range: 6.4%-72.7%) among children aged 24-35 months. The estimates in this report update those findings by including 2 additional years of data (2004 and 2005). National 1-dose vaccination-coverage levels among children aged 24-35 months increased from 17.6% in 2004 to 21.3% in 2005. Coverage in states where vaccination was recommended (overall in 2005: 56.5%; range: 12.9%-71.0%) was below those for other recommended childhood vaccinations, such as varicella (87.5% in 2004). Despite low hepatitis A vaccination-coverage levels compared with other recommended childhood vaccinations, incidence of acute HAV infections have declined to the lowest level ever recorded. The 2005 licensure of the hepatitis A vaccine for use in younger children (aged > or =12 months) and the 2006 ACIP guideline for routine hepatitis A vaccination of all children aged > or =12 months should result in improved vaccination coverage and further reductions in disease incidence.
Erratum: Chronic idiopathic myelofibrosis expressing a novel type of TEL-PDGFRB chimaera responded to imatinib mesylate therapy
Authors: K Tokita, K Maki, J Tadokoro, Y Nakamura, Y Arai, K Sasaki, M Eguchi-Ishimae, M Eguchi, K Mitani
Journal: Leukemia (2008)
ENGLAND AND THE OPIUM TRADE.
Journal: JAMA (1900)

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
Intensive Care Unit Opens for Shock Patients
Journal: JAMA (1966)

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
Woman's Hospital Medical College of Chicago.
Journal: JAMA (1884)

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
The carbonate affair: chalk one up
Authors: C. B. Clayman
Journal: JAMA (1980)

Aluminum magnesium antacids have achieved widespread acceptance over the past 15 to 20 years. Before that, the Sippy regimen of milk and calcium magnesium antacids were the primary agents used in the treatment of acid-peptic disorders. Today, cimetidine has the spotlight. Comparing antacids with cimetidine in the treatment of peptic ulcer has not produced a clear-cut choice, but it has reawakened the present generation of physicians to the effectiveness of antacids.<sup>1,2</sup> The clinical choice of a therapeutic agent, as always, is one that is individualized and balances benefits with adverse effects. In comparing the side effects of these agents, we note the low level of toxicity with the short-term use of cimetidine. Agranulocytosis, diminished sperm counts, and other antiandrogenic effects, as well as confusional states in the elderly (some with renal impairment), have been reported infrequently. We cannot yet speak of the potential adverse effects of cimetidine over the
Differential Expression of Human Metallothionein Isoform I mRNA in Human Proximal Tubule Cells Exposed to Metals
Authors: Scott H. Garrett, Seema Somji, John H. Todd, Mary Ann Sens, Donald A. Sens
Journal: Environmental Health Perspectives (1998)

In contrast to the single metallothionein (MT)-1 gene of the mouse, the human MT-1 gene family is composed of seven active genes and six pseudogenes. In this study, the expression of mRNA representing the seven active human MT-1 genes was determined in cultured human proximal tubule (HPT) cells under basal conditions and after exposure to the metals Cd2+, Zn2+, Cu2+, Hg2+, Ag2+, and Pb2+. Basal expression of MT-1X and MT-1E mRNA in HPT cells was similar to expression of the housekeeping gene glyceraldehyde 3-phosphate dehydrogenase. In contrast, mRNAs representing the basal expression of MT-1A and MT-1F were a minor transcript in HPT cells. Treatment of HPT cells with Cd2+, Zn2+, or Cu2+ increased the levels of MT-1E and MT-1A mRNA, but not the levels of MT-1X or MT-1F mRNA. The increase in MT-1E mRNA appeared to be influenced mainly by exposure to the various metals, whereas the increase in MT-1A mRNA was influenced more by exposure to a metal concentration eliciting a loss of cell viability. Treatment of HPT cells with the metals Hg2+, Ag2+, and Pb2+ was found to have no effect on the level of MT-1 mRNA at either sublethal or lethal concentrations. Using HPT cells as a model, these results suggest that new features of MT gene expression have been acquired in the human due to the duplication of the MT-1 gene.
EPEN-23. MOLECULAR HETEROGENEITY AMONG PEDIATRIC POSTERIOR FOSSA EPENDYMOMA
Authors: Kristian W Pajtler, Ji Wen, Martin Sill, Tong Lin, Jens M Hübner, Vijay Ramaswamy, Chandanamali Punchihewa, David T W Jones, Hendrik Witt, Lukas Chavez, Ruth G Tatevossian, Richard Grundy, Thomas E Merchant, Arzu Onar-Thomas, Michael D Taylor, Stefan M Pfister, Andrey Korshunov, Marcel Kool, David W Ellison
Journal: Neuro-Oncology (2018)

Previously, we have identified nine distinct molecular groups of ependymoma across all age groups, three in each major anatomical compartment of the CNS: spinal, posterior fossa, and supratentorial. These groups are genetically, epigenetically, transcriptionally, and clinically distinct. The commonest pediatric intracranial ependymomas belong to the posterior fossa type-A (PFA) molecular group. Observing distinct outcomes among children with PFA ependymomas, we tested the hypothesis that further molecular diversity with clinical utility, including possible novel genetic alterations, may exist among these tumors. Genome-wide DNA methylation profiles of 675 pediatric PFA ependymomas were analyzed by unsupervised consensus hierarchical clustering and t-distributed stochastic neighbor embedding. These analyses revealed two major subgroups and nine subtypes of PFA ependymoma. Two major subgroups, PFA-1 and PFA-2, demonstrated distinct gene expression profiles suggesting an independent histogenesis, while nine subtypes were characterized by significant differences in age at diagnosis, gender ratio, pathologic grade, outcome, and frequency of genetic alterations, including chromosome 1q gain and H3 K27M mutations. Specifically, one subtype, PFA-1c, was enriched for 1q gain and had a very poor outcome, while PFA-2c tumors showed an overall survival at 5 years of >90% and elevated levels of OTX2 expression, a potential biomarker for this subtype. We conclude that further molecular refinement of pediatric PFA ependymomas has clinical utility and the potential for enhanced risk assessment or therapeutic stratification. In addition, identification of PFA subgroups and further molecular heterogeneity within these subgroups may help to identify the drivers of PFA ependymomas, which are currently unknown.
[612] Withdrawn
Authors: C-J Liu', P-J Chen', J-H Kao', M-Y Lai', C-L Chen', C-H Liu', D-S Chen', M-L Yu', C-Y Dai', Y-Z Lin', W-L Chuang', S-N, J-H Lu3, T-H Wang3, C-H Hu3, C-M Hung3, W-W Lee3, S-S Su4, C-L Wu4, L-Y Lin', H-T Liao', H-D Kuo', Y-C Tung6, S-Y Chao7, S-S Tug', Tuiwan Nutional, Uniuer~xity Hospitul, Chung Gung, Memoriul Hospitul- Kuohsiung
Journal: Journal of Hepatology (2007)
Centrilobular hepatic fibrosis following acetaminophen-induced hepatic necrosis in an alcoholic
Authors: J. R. O'Dell
Journal: JAMA (1986)

ACETAMINOPHEN ingested acutely in amounts of 10 g or more can cause centrilobular hepatic necrosis, which may be fatal.<sup>1</sup>Chronic liver disease secondary to acetaminophen has been described (three cases) and is said to be histologically similar to chronic active hepatitis.<sup>2-4</sup>Alcoholics seem unusually sensitive to acute acetaminophen liver injury and can develop hepatic necrosis at lower doses of acetaminophen.<sup>5-7</sup>We describe a patient who, while consuming alcohol, experienced repeated episodes of acute centrilobular necrosis secondary to doses of acetaminophen usually not considered to produce toxic reactions. An unusual aspect of this case is the development, over a short period of time, of extensive fibrosis in the areas of acetaminophen-induced centrilobular necrosis. We speculate that while alcohol may have potentiated acetaminophen hepatotoxicity, the combination of acetaminophen-induced centrilobular necrosis and alcohol may have caused the development of centrilobular fibrosis. <h3>Report of a Case</h3> A 38-year-old woman was admitted
Nederlands Tijdschrift Geneeskunde, Amsterdam
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
苏金单抗治疗化脓性汗腺炎
Authors: L. Thorlacius, P. Theut Riis, G.B.E. Jemec
Journal: British Journal of Dermatology (2018)

化脓性汗腺炎(HS)是一种严重的皮肤疾病。HS的病因尚不清楚,但有人认为免疫系统的反应受到干扰在其中发挥重要作用。研究发现,HS皮肤中被称为细胞因子的小分子蛋白的水平会升高。细胞因子是免疫系统细胞用于相互交流的信号分子。某些细胞因子会增加皮肤炎症,另一些则会减少皮肤炎症。IL‐17A是引起炎症的细胞因子之一,研究发现,HS皮肤中的该细胞因子会升高。如果您从皮肤组织中去除IL‐17A,炎症便会减少,甚至可能会消失。苏金单抗是一种结合并破坏IL‐17A的抗体。由于HS患者的皮肤中有许多IL‐17A,我们已尝试采用这种新型疗法来治疗病重患者。我们的患者是一位47岁的男性老人,患有严重HS。他已经接受多年治疗,从尝试的许多其他疗法中仅能暂时受益。我们认真记录了该患者的治疗经历,将治疗开始时的结果与治疗12周后的结果作了对比。在使用苏金单抗治疗后,该患者的脓疖数减少(从23个减少到7个);疼痛减轻(以10分为标准,从5分降低到3分)且疼痛/效用损失/障碍降低(以10分为标准,从7分降低到4分)。此结果可用于说明IL‐17A靶向药物可能为未来治疗HS提供一种可能的方法。
Title Change
Journal: JAMA (1979)

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