tbuckley/cabot-search huggingface dataset:
Wegener's Granulomatosis and Gangrene in the Feet
Authors: ROBERT W. PHILLIPS
Journal: Annals of Internal Medicine (1983)

Letters and Corrections1 October 1983Wegener's Granulomatosis and Gangrene in the FeetROBERT W. PHILLIPS, M.D., MELVIN W. TWIEST, M.D.ROBERT W. PHILLIPS, M.D.Search for more papers by this author, MELVIN W. TWIEST, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-99-4-571_1 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: We have seen a patient with Wegener's granulomatosis who had gangrene in the feet.A 68-year-old white man was referred with purulent sinusitis of 2 years duration. He had had several surgical procedures. He had also had an episode of renal failure that resolved spontaneously, although blood chemical indicators of renal functions remained slightly elevated. Two months previously, a right peroneal neuropathy and several small, tender, purple, pretibial nodules were noted. Results of a sural nerve biopsy showed vasculitis with secondary demyelination. A short course of steroids resolved both problems. The patient's medical history included hypertension controlled...References1. REEDJENSENKONWALERHUNTER WABD. The cutaneous manifestations in Wegener's granulomatosis. Acta Derm Venereol. 1963;43:250-64. MedlineGoogle Scholar2. FAUCIHAYNESKATZWOLFF ABPS. Wegener's granulomatosis: prospective clinical and therapeutic experience with 85 patients for 25 years. Ann Intern Med. 1983;98:76-85. LinkGoogle Scholar3. FAUCIWOLFF AS. Wegener's granulomatosis: studies in 18 patients and a review of the literature. Medicine. 1973;52:535-61. CrossrefMedlineGoogle Scholar4. LEGGATWALTON PE. Wegener's granulomatosis. Thorax. 1956;11:94-100. CrossrefMedlineGoogle Scholar5. MATSUDAMITSUKAWAISHIISHIRAI SSNM. A case of Wegener's granulomatosis with necrosis of the penis. Tohoku J Exp Med. 1976;118:145-51. CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: ROBERT W. PHILLIPS, M.D.; MELVIN W. TWIEST, M.D.Affiliations: Lovelace Medical Center Albuquerque, NM 87108 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics Cited byDigital Necrosis in Granulomatosis with PolyangiitisSensory-Motor Polyneuropathy and Digital Ischemia: A Rare Presentation of Granulomatosis with PolyangiitisA rare case of digital ischemia and gangreneUpper-Extremity Digital Ischemia in Granulomatosis With PolyangiitisUpper limb ischemia in a patient with Wegener's granulomatosisWegener's granulomatosis and acute upper limb digital ischemiaWWegener’s granulomatosis presenting during pregnancy with acute limb ischemia 1 October 1983Volume 99, Issue 4Page: 571-571KeywordsBiopsyBloodHypertensionNervesNeuropathyRenal failureSteroidsVasculitisWegener granulomatosis ePublished: 1 December 2008 Issue Published: 1 October 1983 PDF downloadLoading ...
Sebaceous gland suppression in female acne patients by combined glucocorticoid-oestrogen therapy*
Authors: E. M. SAIHAN, J. L. BURTON
Journal: British Journal of Dermatology (1980)

Women with severe acne were treated with a combination of oestrogen and a low dose of glucocorticoid daily in order to suppress their androgen production. This combination therapy reduced their sebum production by 50%, with a concomitant improvement in their acne.
The Link between Reiter's Syndrome and Psoriatic Arthritis
Authors: V. Wright, W. B. Reed
Journal: Annals of the Rheumatic Diseases (1964)

been demonstrated that Reiter's syndrome has features of an inflammatory arthritis distinct from rheumatoid arthritis (Harkness, 1950;Ford, 1958;Murray, Oates, and Young, 1958; Csonka, 1960;Catterall and Perkins, 1961;Wright, 1963).We have observed, from our total experi- ence of patients with psoriasis and arthritis, twelve who seem to form a very definite link between "psoriatic arthritis" and "Reiter's syndrome".Although various authors have hinted at such a possibility, we have been unable to find any report in the literature of a similar series.It seemed desirable therefore to report our findings in these patients in some detail.The genito-urinary and ocular manifestations of the patients are sum-Conjunctivitis and Iritis appeared that both attacks responded to penicillin. 11months previously, after a 24-year remission of arthritis, he had an acute exacerbation.10 days later a rash appeared on the abdominal wall and spread to involve the feet, knees, genitalia, anterior aspect of the thighs, chest, and back between the scapulae (Figs 1 and2).The patient had lost 30 lb. in the month before admission.Case 1, a 26-year-old man, was admitted to hospital with an exacerbation of arthritis.He had developed polyarthritis 5 years previously with involvement of the spine indicating ankylosing spondylitis.He had episodes of urethritis 3 years and 18 months before.No bacterio- logical diagnosis was made on these occasions, but it Fig.1.-Case 1, showing keratoderimia blennorrhagica on sole.
Löffler's Syndrome as a Complication of Bipedal Lymphangiography
Authors: David A. Bray
Journal: JAMA (1970)

Löffler's syndrome was a complication of lymphangiography in two cases. A review of 88 consecutive bipedal lymphangiograms demonstrates that fever and pulmonary microemboli are the most common aftermath of lymphangiography. These appear of little clinical significance by themselves. Severe pulmonary complications are relatively uncommon.
Hyponatremia in cirrhosis: Results of a patient population survey
Authors: Paolo Angeli, Florence Wong, Hugh Watson, Pere Ginès
Journal: Hepatology (2006)

Low serum sodium concentration is an independent predictor of mortality in patients with cirrhosis, but its prevalence and clinical significance is unclear. To evaluate prospectively the prevalence of low serum sodium concentration and the association between serum sodium levels and severity of ascites and complications of cirrhosis, prospective data were collected on 997 consecutive patients from 28 centers in Europe, North and South America, and Asia for a period of 28 days. The prevalence of low serum sodium concentration as defined by a serum sodium concentration < or =135 mmol/L, < or =130 mmol/L, < or =125 mmol/L, and < or =120 mmol/L was 49.4%, 21.6%, 5.7%, and 1.2%, respectively. The prevalence of low serum sodium levels (<135 mmol/L) was high in both inpatients and outpatients (57% and 40%, respectively). The existence of serum sodium <135 mmol/L was associated with severe ascites, as indicated by high prevalence of refractory ascites, large fluid accumulation rate, frequent use of large-volume paracentesis, and impaired renal function, compared with normal serum sodium levels. Moreover, low serum sodium levels were also associated with greater frequency of hepatic encephalopathy, spontaneous bacterial peritonitis, and hepatorenal syndrome, but not gastrointestinal bleeding. Patients with serum sodium <130 mmol/L had the greatest frequency of these complications, but the frequency was also increased in patients with mild reduction in serum sodium levels (131-135 mmol/L). In conclusion, low serum sodium levels in cirrhosis are associated with severe ascites and high frequency of hepatic encephalopathy, spontaneous bacterial peritonitis, and hepatorenal syndrome.
Abstract 2502: Next-generation sequencing: Integrated exotome analysis in human multiple neuroblastoma
Authors: Eiso Hiyama, Keiko Hiyama
Journal: Cancer Research (2012)

Abstract Background: Although multifocal neuroblastoma (NBL) is rare, its susceptibility is due to germline aberration and this predisposition gene may also be involved in sporadic neuroblastoma tumorigenesis. Sequence capture enrichment strategies and massively parallel next generation sequencing (NGS) were used for gene discovery because of their alterations. Methods: Out of approximately 500 NBL samples, 10 samples derived from 5 multifocal neuroblastoma cases were analyzed by a method for whole-exome sequencing coupling Agilent whole-exome capture to the Illumina DNA-sequencing platform. Using this technology, we investigated consistent point-mutations and insertions-deletions in these cases. Then, we analyzed the expression levels of these candidate genes in 298 sporadic NBL samples. Results: Among these 5 cases, one case showed ALK mutation in both of his multifocal tumors and germline mutation of ALK exon 23 (F1174L) was identified. The remaining 4 cases showed 57 candidate loci with consistent point-mutations and insertions-deletions including NBPF family genes and cell division cycle protein (CDC) genes. The expression levels of these candidate genes revealed that two genes were significantly decreased in these multifocal NBL tumors, except for one ALK mutated case. Then, we examined the expression levels of these two genes in sporadic NBL tumors. The expression levels of these candidate genes were significantly low in 34 and 59 NBL tumors, respectively but the low expression of both genes were detected in only two NBL tumors.Conclusions: Whole-exome sequencing using NGS in multifocal neuroblastoma revealed several candidate germline-mutated genes including ALK in such NBL-susceptibility cases. The expression levels of these genes also indicated that heterogeneous subtypes exist in sporadic NBLs. NGS can be used in research and diagnostic settings to screen for mutations and deletion/insertion in number of loci in genetically heterogeneous neuroblastoma. Further NGS analysis provided important candidates of indicators for diagnostic and therapeutic targets for NBLs. Citation Format: {Authors}. {Abstract title} [abstract]. In: Proceedings of the 103rd Annual Meeting of the American Association for Cancer Research; 2012 Mar 31-Apr 4; Chicago, IL. Philadelphia (PA): AACR; Cancer Res 2012;72(8 Suppl):Abstract nr 2502. doi:1538-7445.AM2012-2502
Phosphatidylinositol Ether Lipid Analogues Induce AMP-Activated Protein Kinase–Dependent Death in LKB1-Mutant Non–Small Cell Lung Cancer Cells
Authors: Regan M. Memmott, Joell J. Gills, Melinda Hollingshead, Margaret C. Powers, Zhiping Chen, Bruce Kemp, Alan Kozikowski, Phillip A. Dennis
Journal: Cancer Research (2008)

Abstract Loss of function of the tumor suppressor LKB1 occurs in 30% to 50% of lung adenocarcinomas. Because LKB1 activates AMP-activated protein kinase (AMPK), which can negatively regulate mTOR, AMPK activation might be desirable for cancer therapy. However, no known compounds activate AMPK independently of LKB1 in vivo, and the usefulness of activating AMPK in LKB1-mutant cancers is unknown. Here, we show that lipid-based Akt inhibitors, phosphatidylinositol ether lipid analogues (PIA), activate AMPK independently of LKB1. PIAs activated AMPK in LKB1-mutant non–small cell lung cancer (NSCLC) cell lines with similar concentration dependence as that required to inhibit Akt. However, AMPK activation was independent of Akt inhibition. AMPK activation was a major mechanism of mTOR inhibition. To assess whether another kinase capable of activating AMPK, CaMKKβ, contributed to PIA-induced AMPK activation, we used an inhibitor of CaMKK, STO-609. STO-609 inhibited PIA-induced AMPK activation in LKB1-mutant NSCLC cells, and delayed AMPK activation in wild-type LKB1 NSCLC cells. In addition, AMPK activation was not observed in NSCLC cells with mutant CaMKKβ, suggesting that CaMKKβ contributes to PIA-induced AMPK activation in cells. AMPK activation promoted PIA-induced cytotoxicity because PIAs were less cytotoxic in AMPKα−/− murine embryonic fibroblasts or LKB1-mutant NSCLC cells transfected with mutant AMPK. This mechanism was also relevant in vivo. Treatment of LKB1-mutant NSCLC xenografts with PIA decreased tumor volume by ∼50% and activated AMPK. These studies show that PIAs recapitulate the activity of two tumor suppressors (PTEN and LKB1) that converge on mTOR. Moreover, they suggest that PIAs might have utility in the treatment of LKB1-mutant lung adenocarcinomas. [Cancer Res 2008;68(2):580–8]
Adolescent Alcohol Use and Violence
Authors: Richard Saitz, Timothy S. Naimi
Journal: JAMA (2010)

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
Tamoxifen may increase the risk of later tumours being more aggressive
Authors: S. Gottlieb
Journal: BMJ (2001)

If a woman who takes tamoxifen for breast cancer develops a cancer in her other previously healthy breast, the risk is higher that it will be of a more dangerous type than a contralateral cancer in a woman who has never taken the drug.

Researchers collected data on 8981 women with primary unilateral breast cancer aged at least 50 who had received adjunctive hormonal therapy but not chemotherapy (tamoxifen users) or had received neither hormonal therapy nor chemotherapy (tamoxifen non-users) ( Journal of the National Cancer Institute 2001;93:1008-12).

The researchers identified contralateral breast cancers in 89 …
Allgemeine und experimentelle Immunologie und Immunopathologie sowie ihre klinische Anwendung
Authors: Max Samter
Journal: JAMA (1969)

Experimental and clinical immunology is a discipline of startling advances and increasing complexity. I have wondered whether its measure could still be taken by a single author, in a single volume. Professor Steffen and his new textbook have almost succeeded, although, of course, not everywhere and not without paying a price. The scope of the volume is encyclopedic; it not only covers, in sequence, fundamentals, pathogenicity of various forms of sensitization, and the serological diagnosis of immunological diseases, but it includes an informative manual of immunological experimentation. The author dominates the book; his disagreements are clearly stated. He is concerned with semantics, and with good reason: he argues that hypersensitivity suggests quantitative rather than qualitative changes. Yet, we have become more philosophical about terms. Many have tried in vain to replace the objectional term "autoimmune disease" with something more meaningful. We are lucky that von Pirquet's genius coined a surprisingly
Plasma-cell Mastitis
Authors: B. N. Colabawalla
Journal: BMJ (1957)

MEDICAL MEMORANDAThe case described presented with pyrexia, enlargement of the spleen, and profound depression of both red and white cells.The bone marrow was markedly hypoplastic.There was no clinical or radiological evidence of disseminated tuberculosis, and no glands were available for biopsy.Culture and guinea-pig inoculation of material obtained by bone-marrow aspiration might have confirmed a tuberculous infection during life, as might examination of bone marrow for miliary tubercles (Schleicher, 1946).This case was treated with streptomycin for 10 days without any beneficial effect.I thank Dr. J.
Carmustine and Myelodysplasia
Authors: STUART M. LICHTMAN
Journal: Annals of Internal Medicine (1985)

Letters and Corrections1 December 1985Carmustine and MyelodysplasiaSTUART M. LICHTMAN, M.D., PHILIP SCHULMAN, M.D.STUART M. LICHTMAN, M.D.Search for more papers by this author, PHILIP SCHULMAN, M.D.Search for more papers by this authorAuthor, Article, and Disclosure Informationhttps://doi.org/10.7326/0003-4819-103-6-964_3 SectionsAboutPDF ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareFacebookTwitterLinkedInRedditEmail ExcerptTo the editor: A recent editorial (1) has discussed the complexities of the myelodysplastic syndromes. Although the cause of most cases is unknown, the occurrence of myelodysplastic syndromes after treatment of a primary malignancy with chemotherapy has been increasingly recognized (1). These syndromes are commoner after treatment of hematologic disorders, but their occurrence after solid tumors is also occurring in greater frequency. Recently, Boice and colleagues (2) have reported the leukemogenic effect of semustine (methyl-CCNU). We now report a case of carmustine (BCNU)-induced myelodysplasia.A 64-year-old white man had evaluation of the right eye for ocular melanoma in March 1982,...References1. LARSON R. Management of the myelodysplastic syndromes [Editorial]. Ann Intern Med. 1985;103:136-8. LinkGoogle Scholar2. BOICEGREENEKILLEN JMJ. Leukemia and preleukemia after adjuvant treatment of gastrointestinal cancer with semustine (methyl-CCNU). N Engl J Med. 1983;309:1079-84. CrossrefMedlineGoogle Scholar3. COHENWIERNIKWALKER RPM. Acute nonlymphocytic leukemia associated with nitrosourea chemotherapy: report of two cases. Cancer Treat Rep. 1976;60:1257-61. MedlineGoogle Scholar4. VOGL S. Acute leukemia complicating treatment of glioblastoma multiforme. Cancer. 1978;41:333-6. CrossrefMedlineGoogle Scholar5. GENOTKRULIKPOISSON JMM. Two cases of acute leukemia following treatment of malignant glioma. Cancer. 1983;52:222-6. CrossrefMedlineGoogle Scholar This content is PDF only. To continue reading please click on the PDF icon. Author, Article, and Disclosure InformationAuthors: STUART M. LICHTMAN, M.D.; PHILIP SCHULMAN, M.D.Affiliations: North Shore University Hospital Cornell University Medical College Manhasset, NY 11030 PreviousarticleNextarticle Advertisement FiguresReferencesRelatedDetails Metrics 1 December 1985Volume 103, Issue 6_Part_1Page: 964-965KeywordsChemotherapyMelanomaMyelodysplastic syndromes ePublished: 1 December 2008 Issue Published: 1 December 1985 PDF downloadLoading ...
FDG-Avid Venous Malformation Could Mimic Malignancy on 18F-FDG PET/CT
Authors: Alireza Mojtahedi, Ravinder K. Grewal, Gary A. Ulaner
Journal: Clinical Nuclear Medicine (2013)

A 49-year-old female patient with melanoma underwent FDG PET/CT for surveillance. PET/CT demonstrated multiple mildly FDG-avid soft tissue attenuation lesions in the pelvis of unknown etiology. MRI was performed for further evaluation. MRI demonstrated multiple dilated vascular structures measuring up to 2.5 cm consistent with venous malformation. Follow-up PET/CT 1 and 2 years later demonstrated stable FDG-avid soft-tissue densities in the pelvis representing venous malformation. No recurrence or distant metastases were identified. This case demonstrates how a benign FDG-avid vascular malformation on PET/CT could have been misinterpreted as malignancy. Biopsy of a vascular malformation could have had dire consequences.
Cardiac Nitric Oxide Synthase 1 Regulates Basal and β-Adrenergic Contractility in Murine Ventricular Myocytes
Authors: Euan A. Ashley, Claire E. Sears, Simon M. Bryant, Hugh C. Watkins, Barbara Casadei
Journal: Circulation (2002)

Background — Evidence indicates that myocardial NO production can modulate contractility, but the source of NO remains uncertain. Here, we investigated the role of a type 1 NO synthase isoform (NOS1), which has been recently localized to the cardiac sarcoplasmic reticulum, in the regulation of basal and β-adrenergic myocardial contraction. Methods and Results — Contraction was assessed in left ventricular myocytes isolated from mice with NOS1 gene disruption (NOS1 −/− mice) and their littermate controls (NOS1 +/+ mice) at 3 stimulation frequencies (1, 3, and 6 Hz) in basal conditions and during β-adrenergic stimulation with isoproterenol (2 nmol/L). In addition, we examined the effects of acute specific inhibition of NOS1 with vinyl- l - N -5-(1-imino-3-butenyl)- l -ornithine (L-VNIO, 500 μmol/L). NOS1 −/− myocytes exhibited greater contraction at all frequencies (percent cell shortening at 6 Hz, 10.7±0.92% in NOS1 −/− myocytes versus 7.21±0.8% in NOS1 +/+ myocytes; P &lt;0.05) with a flat frequency-contraction relationship. Time to 50% relaxation was increased in NOS1 −/− myocytes at all frequencies (at 6 Hz, 26.53±1.4 ms in NOS1 −/− myocytes versus 21.27±1.3 ms in NOS1 +/+ myocytes; P &lt;0.05). L-VNIO prolonged time to 50% relaxation at all frequencies (at 6 Hz, 21.28±1.7 ms in NOS1 +/+ myocytes versus 26.45±1.4 ms in NOS1 +/+ +L-VNIO myocytes; P &lt;0.05) but did not significantly increase basal contraction. However, both NOS1 −/− myocytes and NOS1 +/+ myocytes treated with L-VNIO showed a greatly enhanced contraction in response to β-adrenergic stimulation (percent increase in contraction at 6 Hz, 25.2±10.8 in NOS1 +/+ myocytes, 68.2±11.2 in NOS1 −/− myocytes, and 65.1±13.2 in NOS1 +/+ +L-VNIO myocytes; P &lt;0.05). Conclusions — NOS1 disruption enhances basal contraction and the inotropic response to β-adrenergic stimulation in murine ventricular myocytes. These findings indicate that cardiac NOS1-derived NO plays a significant role in the autocrine regulation of myocardial contractility.
Escitalopram, Problem-Solving Therapy, and Poststroke Depression
Authors: Jeffrey Lacasse
Journal: JAMA (2008)

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
Scavenging effect of nicorandil on free radicals and lipid peroxide in streptozotocin-induced diabetic rats
Authors: Toshiki Mano, Rikio Shinohara, Akio Nagasaka, Hifumi Nakagawa, Keiko Uchimura, Ritsuko Hayashi, Itsuko Nakano, Toru Tsugawa, Fumiko Watanabe, Takako Kobayashi, Kentaro Fujiwara, Akira Nakai, Mitsuyasu Itoh
Journal: Metabolism (2000)