tbuckley/cabot-search huggingface dataset:
Fetal Hemoglobin-Containing Erythrocytes
Journal: JAMA (1963)

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
<i>QuickStats:</i> Age-Adjusted Percentage* of Adults Aged ≥65 Years,<sup>†</sup> by Number of 10 Selected Diagnosed Chronic Conditions<sup>§</sup> and Poverty Status — National Health Interview Survey, 2013–2015
Journal: MMWR Morbidity and Mortality Weekly Report (2017)

For the period 2013-2015, 13% of adults aged ≥65 years reported having none of 10 selected diagnosed chronic conditions; 25% had one, 46% had two or three, and 16% had four or more of the conditions. No differences by poverty status were observed among those who reported having two or three conditions, but those in the lowest income group (<100% of the poverty threshold) were less likely to have none or only one of the chronic conditions compared with those in the highest income group (≥400% of the poverty threshold). Those in the lowest income group also were more likely to have four or more conditions when compared with those in the highest income group (21% compared with 12%).
Abstract 4261: Upregulation of miR-34b, miR-892a and inhibition of p-glycoprotein play an important role for melatonin-induced apoptosis and autophagy in vincristine-resistant human oral cancer cells
Authors: Shun-Fa Yang, Ming-Ju Hsieh, Chiao-Wen Lin
Journal: Cancer Research (2019)

Abstract Multidrug-resistance was resistance of cells to a variety of drugs normally used in tumor treatment. The related mechanism of drug resistance in oral cancer has not been completely explained. Melatonin is an endogenously-produced molecule involved in active biological mechanisms including antiproliferation, oncogene expression modulation, antitumor invasion and migration, and anti-inflammatory, antioxidant, and antiangiogenic effects. Despite these numerous actions, the effect of melatonin on vincristine (VCR)-resistant human oral cancer cells still largely unknown. Present study analyzed the role of melatonin on VCR-resistant human oral cancer cells along with the underlying mechanism. We determined that melatonin induces apoptosis and autophagy of VCR-resistant oral cancer cell; these actions are mediated by AKT, p38, and JNK. Melatonin inhibits ABCB1 and ABCB4 expression in vitro/vivo. Melatonin decrease drug resistance and promotes VCR-resistant oral cancer cell execute apoptosis through upregulation of miR-892a and miR-34b-5p expression. The expression of miR-892a and miR-34b-5p are related with melatonin-induced apoptosis, but not autophagy. Thus, melatonin is a potential novel agent in chemotherapy for VCR-resistant human oral cancer cell lines. Citation Format: Shun-Fa Yang, Ming-Ju Hsieh, Chiao-Wen Lin. Upregulation of miR-34b, miR-892a and inhibition of p-glycoprotein play an important role for melatonin-induced apoptosis and autophagy in vincristine-resistant human oral cancer cells [abstract]. In: Proceedings of the American Association for Cancer Research Annual Meeting 2019; 2019 Mar 29-Apr 3; Atlanta, GA. Philadelphia (PA): AACR; Cancer Res 2019;79(13 Suppl):Abstract nr 4261.
"PULMONARY ARTERIAL HYPERTENSION ASSOCIATED WITH FENFLURAMINE EXPOSURE: REPORT OF 109 CASES". R. SOUZA, M. HUMBERT, B. SZTRYMF, X. JAIS, A. YAICI, J. LE PAVEC, F. PARENT, P. HERVE, F. SOUBRIER, O. SITBON AND G. SIMONNEAU. EUR RESPIR J 2008; 31: 343-348.
Journal: European Respiratory Journal (2008)
Computers as Allies
Authors: Michael Pugh, M -', Dorothy Coull, J Ross, Margaret Henderson, J -', A Engeset, I Omar, I Ross, G -', J Dyer, K Auchinachie, A Benzie, A Blyth, M Browne, Mary Cameron, J Davidson, Marjory Donaldson, Lesley Duffty (nee Macdonald, P Duffty, P Duffus, D Fowlie, D Franks, R Fraser, N Gavin, T Gibson, Ruth Grant, I Gray, A Grieve, M Henderson, Jean Hey, Wai Hung, T Ibiam, N Mcl, Christine Johnston, J Keating, Catherine Keeping, Sim Legg, Doris Lister, J Logie, J Lorimer, Dorothy Lunney, Elizabeth Macartney, J Mackay, D Macleod, R Macleod, Bridget Macleod, J Mcneill, Moira Miller, Rosemary Milne, R Milne, A Morrison, Mary Napper, Lesley Primrose, Joyce Prout, Linda Roberts, Susan Roddis, M Ross, F Shirreffs, G Smith, Mary Smith, E Stephen, J Tamber, P Tausjo, Irene Thom, Helen Tuttle, Elizabeth Watson, M Webster, T Whitley, Daisy Winning, H Manson, Doreen Shewan, Elizabeth Williams, G Dixon, D Panayotopoulas, D.-Sheila Morrison-Cleator, J Cormack, M Eastwood, J Ireland, Margaret Jamie
Journal: BMJ (1970)
Contents
Authors: Jeremy Guggenheim, Cathy Williams, Yinon Shapira, Michael Mimouni, Yossy Machluf, Yoram Chaiter, Haitam Saab, Eedy Mezer, Sonia Phene, R Dunn, Naama Hammel, Yun Liu, Jonathan Krause, Naho Kitade, Mike Schaekermann, Rory Sayres, Derek Wu, Ashish Bora, Christopher Semturs, Anita Misra, Abigail Huang, Arielle Spitze, Felipe Medeiros, April Maa, Monica Gandhi, Greg Corrado, Lily Peng, Dale Webster, Tiarnan Keenan, B Bch, Henry Wiley, Elvira Agrón, Mary Aronow, Eleonora Lad, Amitha Domalpally, Jeong Ma, Tiarnan Pak, B Keenan, Fredrick Bch, Traci Ferris, Emily Clemons, Marco Nassisi, Jianqin Lei, Saleh Abdelfattah, Ayesha Karamat, Siva Balasubramanian, Wenying Fan, Akihito Uji, Kenneth Marion, Kirstie Baker, Xiwen Huang, Elizabeth Morgenthien, Srinivas Sadda, Zihan Sun, Fangyao Tang, Raymond Wong, Jerry Lok, Simon Szeto, Jason Chan, Carmen Chan, Clement Tham, Danny Ng, Carol Cheung, Aude Couturier, Pierre-Antoine Rey, Ali Erginay, Carlo Lavia, Sophie Bonnin, Bénédicte Dupas, Alain Gaudric, Ramin Tadayoni, Evan Chen, Ravi Parikh, Dan Reply, Stanley Gong
Journal: Ophthalmology (2019)
Immature Rat Uterotrophic Assay of Bisphenol A
Authors: Kanji Yamasaki, Masakuni Sawaki, Mineo Takatsuki
Journal: Environmental Health Perspectives (2000)

We used the immature rat uterotrophic assay to determine the estrogenicity of bisphenol A (BPA). We administered BPA (in sesame oil) to rats subcutaneously (sc; 0, 8, 40, and 160 mg/kg/day) or orally (0, 40, 160, and 800 mg/kg/day) for 3 days beginning on postnatal day (PND) 18; rats were sacrificed 24 hr after the last administration. Uterine wet, blotted, and relative weights increased in all groups given BPA sc. After oral administration, uterine relative weight increased in 160 and 800 mg/kg BPA groups, and wet and blotted weights increased in the 800 mg/kg BPA group. Plasma concentrations of BPA at 1 hr after the last administration were detected in all groups given BPA sc and in groups given 160 and 800 mg/kg BPA orally, with a dose-response effect. The study was then reproduced under the same conditions. After sc injections, uterine wet and blotted weights increased in the 40 and 160 mg/kg BPA groups, and relative weight increased in all groups given BPA sc. By contrast, uterine wet, blotted, and relative weights increased only in the 160 and 800 mg/kg oral BPA groups. Also, to examine time-course changes in uterine weight, we administered BPA (in sesame oil) sc from PND 18 to PND 20 for 3 days at doses of 0, 8, 40, and 160 mg/kg/day; uterine weights were then measured at 6, 12, 18, and 24 hr after the last administration. Uterine wet, blotted, and relative weights increased in all BPA groups at 6 and 24 hr and in 40 and 160 mg/kg BPA groups at 12 hr. By contrast, at 18 hr, uterine wet, blotted, and relative blotted weights increased in all BPA groups and relative wet weight increased in 40 and 160 mg/kg BPA groups. The percentage increases in uterine wet and relative weights of 40 and 160 mg/kg BPA groups at 6 hr were higher than those at 24 hr relative to the controls, but the coefficient of variation in these weights in the group given 8 mg/kg BPA at 24 hr was smaller than that at 6 hr. These findings demonstrate BPA-induced uterotrophy in the immature uterotrophic assay in rats administered 8 mg/kg/day sc and in rats given 160 mg/kg/day orally, and suggest that the autopsy at 24 hr after the last administration is suitable.
Highlights
Journal: JAMA Psychiatry (2018)

Urbanicity and Psychosis in Low-and Middle-Income Countries 678Urban residence is a well-established risk factor for psychosis, but most evidence comes from high-income countries.Using World Health Survey data from 215 682 adults residing in 42 low-and middle-income countries, DeVylder and colleagues found that urban residence was not significantly associated with psychotic experiences or psychotic disorder in either low-or middle-income countries.These results indicate that urbanicity may be a risk factor for psychosis in high-income countries only.In an Invited Commentary, Plana-Ripoll and colleagues discusses implications of these findings for our understanding of psychotic disorders.
Abstract 18131: Canadian Multi-center Experience With WATCHMAN for Percutaneous Left Atrial Appendage Closure
Authors: Jacqueline Saw, Peter Fahmy, Lorenzo Azzalini, Jean-Francois Marquis, Benjamin Hibbert, Carlos Morillo, Aldo Carrizo, Reda Ibrahim
Journal: Circulation (2015)

Background: There is limited data with WATCHMAN for left atrial appendage (LAA) closure in patients with nonvalvular atrial fibrillation (AF) and contraindications to anticoagulation. The purpose of this study was to evaluate the safety and efficacy of WATCHMAN in our early Canadian experience. Methods: We report our consecutive series of patients who underwent WATCHMAN implantation at 4 Canadian centers (Vancouver General Hospital, Montreal Heart Institute, Hamilton General Hospital and Ottawa Heart Institute). Indications for LAA closure were CHADS2≥1, and contraindication/intolerance to or failure on anticoagulation. All cases were done under general anesthesia and TEE guidance. Majority of patients received dual antiplatelet therapy (DAPT) for 3-6 months after implant. Follow-up TEE was typically performed at 1-6 months post-procedure. Results: Ninety patients underwent LAA closure with WATCHMAN from May 2013 to June 2015. The mean age was 75.0 ± 7.9. The mean CHADS2 score was 2.9 ± 1.2, CHADS-VASc score was 4.4 ± 1.5, and HASBLED score was 3.2 ± 1.2. Permanent AF was present in 66.7% and paroxysmal AF in 33.3%. Indications for LAA closure were prior bleeding in 81 patients (90.0%; 74 major bleeding, and 7 minor bleeding), 9 were deemed high-risk for bleeding (renal failure, cirrhosis, labile INR, esophageal ulcers, on DAPT), and 1 with recurrent strokes on warfarin. Procedural success was 97.8% (88/90), with one device embolization (snared percutaneously) and one implant failure due to inadequate LAA depth. There was no procedural stroke/TIA, death, MI, or cardiac tamponade. There were 3 major bleeding that required transfusions. Mean hospital stay was 1.4 ± 1.8 days. Antithrombotic therapy post-implant included DAPT in 66/90 (73.3%), anticoagulant in 21/90 (5 warfarin, 16 direct anticoagulant), and aspirin alone in 3/90. Follow-up TEE was available in 53 patients, there was 1 device-associated thrombus (treated successfully with anticoagulation), and 18 peri-device leaks (all &lt;5mm). Mean follow-up was 173.8 ± 117.3 days, with no stroke or death, but there was 1 TIA and 3 major bleeding. Conclusion: In our early Canadian experience, WATCHMAN for LAA closure in patients contraindicated to anticoagulation is safe and effective.
Nitrated Polycyclic Aromatic Hydrocarbons: A Risk Assessment for the Urban Citizen
Authors: Lennart Moller, Ingemar Lax, Lennart C. Eriksson
Journal: Environmental Health Perspectives (1993)

Nitrated polycyclic aromatic hydrocarbons (nitro-PAHs) are formed during incomplete combustion.Sources include emissions from vehicles (mainly diesel vehicles), heating, smoking, certain types of food processing, and incomplete combustion in general.Nitro-PAHs are direct-acting mutagens, and a number of them have been shown to be carcinogens. 2-Nitrofluorene (NF) represents a model substance for the nitro-PAHs.An attempt has been made to calculate the human cancer risk due to exposure to nitro-PAHs by two different models.In the first model, genotoxic lesions were transferred to units of Gray (y-irradiation), and in the second model a mega study (24,000 animals) on the carcinogenicity of one metabolite of NF was used to elucidate the risk.Gamma-irradiation of the rat liver gave rise to preneoplastic foci in a dose-dependent manner.which was statistically significant.The Gray-equivalents of chemically (NF) induced foci were calculated, and from the human nitro-PAH exposure, expressed in Sievert, a human risk estimate was calculated.In the second model, an extrapolation from laboratory animals to man was performed because tumor data on 2-acety- laminofluorene (AAF), a major metabolite of NF, were available in the literature.The tumor dose-response data on AAF was linear for tested lifetime doses.The results ofboth models agreed, with a risk range of 0.15-49x 10 -i on human cancer risk for an urban citizen.
A phase II study of oral enzastaurin in patients with metastatic breast cancer previously treated with an anthracycline and a taxane-containing regimen: HOG BRE05–97
Authors: I. E. Krop, K. D. Miller, R. T. Zon, S. Isakoff, C. J. Schneider, M. Yu, C. Johnson, L. G. Vaughn, O. O. Shonukan, G. W. Sledge
Journal: Journal of Clinical Oncology (2008)

1004 Background: Enzastaurin is a potent, serine-threonine kinase inhibitor which selectively targets PKCβ and PI3K/AKT signaling pathways. By blocking these key pathways, enzastaurin suppresses tumor cell proliferation, induces tumor cell death, and inhibits tumor-induced angiogenesis. As PKCβ and PI3K/AKT signaling are both involved in breast cancer pathogenesis, we hypothesized that enzastaurin would be active in metastatic breast cancer (MBC). Methods: This multicenter phase II single-arm study of enzastaurin monotherapy in MBC utilized a 2-stage design with 21 patients (pts) planned in stage 1 and 20 pts in stage 2. The primary objective was to assess antitumor activity of enzastaurin, as measured by clinical benefit response (CR, PR, or SD ≥6 months). Eligible pts had locally recurrent or MBC, had 0–2 prior chemotherapy regimens in the metastatic setting, had received prior therapy with an anthracycline and a taxane, and if HER2+, had progressed on trastuzumab. Pts received orally a loading dose of enzastaurin 1,125 mg, followed by continuous daily dosing of enzastaurin 500 mg. Pts were restaged every 8 weeks. Results: A total of 21 pts were enrolled. Mean age was 52.9 years (range: 33- 67). ECOG performance status scores were 0 (11 pts), 1 (8 pts), 2 (2 pts). Nine pts (43%) were ER+ and 2 pts (10%) were HER2+. Prior history of MBC chemotherapy included 1 regimen (7 pts), 2 regimens (7 pts), and 3 regimens (1 pt). In general, enzastaurin therapy was well tolerated. Drug-related grade 3 toxicities were musculoskeletal chest pain (1 pt, 5%), dyspnea (1 pt, 5%), fatigue (1 pt, 5%), hypoxia (1 pt, 5%), pulmonary hemorrhage (1 pt, 5%), and pneumonitis (1 pt, 5%). There were no objective responses and no pts had SD ≥6 months. As protocol-specified efficacy stopping rules were not exceeded, the trial was stopped after the initial 21 pts. Pharmacodynamic studies to determine extent of target inhibition are underway. Conclusions: Enzastaurin monotherapy was well tolerated, but had no activity in a pretreated population of pts with MBC. Based on preclinical data, phase II studies are ongoing to evaluate the combination of enzastaurin with chemotherapy or hormone therapy. Author Disclosure Employment or Leadership Consultant or Advisory Role Stock Ownership Honoraria Research Expert Testimony Other Remuneration Eli Lilly Eli Lilly
&lt;I&gt;SETA&lt;/I&gt;: A novel SH3 domain-containing adapter molecule associated with malignancy in astrocytes
Authors: Oliver Bögler, Frank B. Furnari, Andrea Kindler-Roehrborn, Virginia W. Sykes, Richard Yung, H.-J. Su Huang, Webster K. Cavenee
Journal: Neuro-Oncology (2000)

Differential display poymerase chain reaction analysis was used to compare ve differentiation states of the O-2A progenitor-like cell line CG4: progenitor cells and cells at 12 h or 4 days after the induction of differentiation into oligodendrocytes or astrocytes.This led to the identication of 52 sequence tags that were expressed differentially with cellular phenotype.One sequence was upregulated during differentiation of CG4 cells and represented a novel gene that we named SETA (SH3 domaincontaining gene expressed in tumorigenic astrocytes).This gene encodes an SH3 domain-containing adapter protein with sequence similarity to the CD2AP (CD2 adapter protein) and CMS (Cas ligand with multiple Src homology) genes.SETA mRNA was expressed at high levels in the developing rat brain but was barely detectable in the normal adult rat or human brain.However, SETA mRNA was found in approximately one half of the human gliomas tested, including astrocytomas grades II, III, and IV, as well as oligodendrogliomas, mixed oligoastrocytomas, and human glioma-derived cell lines.A rat glioma generated by treatment with the alkylating carcinogen ethylnitrosourea on postnatal day 1 and a derived cell line also expressed SETA mRNA.Furthermore, in an in vitro model of astrocytoma progression based on p53 -/-astrocytes, expression of SETA was restricted to cells that are tumorigenic.
Pulmonary Tuberculosis. Its Modern Prophylaxis and the Treatment in Special Institutions and at Home. Alvarenga Prize Esasy of the College of Physicians of Philadelphia for the Year 1898. Revised and Enlarged.
Journal: JAMA (1899)

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
WILLIAM HEWSON— FRIEND OF BENJAMIN FRANKLIN
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
Lidocaine-cimetidine interaction can be toxic
Journal: JAMA (1982)

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
β‐thalassemia intermedia caused by compound heterozygosity for Hb Malay (β codon 19 AAC→AGC; Asn→Ser) and codons 41/42 (‐CTTT) β0‐thalassemia mutation
Authors: S.K. Ma, Eudora Y.D. Chow, Amy Y.Y. Chan, Nelson N.S. Kung, John S. Waye, L.C. Chan, David H.K. Chui
Journal: American Journal of Hematology (2000)

We report a case of β-thalassemia intermedia caused by compound heterozygosity for hemoglobin (Hb) Malay and codon 41/42 (-CTTT) β0-thalassemia mutation in a 38-year-old Chinese woman. This patient has long-standing anemia with a baseline Hb level of around 70 g/L. She worked as a full-time cashier and had not required regular blood transfusions. Nevertheless, she had splenomegaly necessitating splenectomy, cholelithiasis, and iron overload. This case illustrates the varied phenotypic expression associated with compound heterozygosity for Hb Malay and other β-thalassemia mutations. Since Hb Malay migrates as Hb A on electrophoresis and chromatography, this variant Hb mutation ought to be included in the differential diagnosis for β-thalassemia major or intermedia patients of Southeast Asian descent who are reported to have Hb A on the basis of Hb analysis. The possible presence of this mutation should also be considered in appropriate cases for genetic counseling in couples at risk of conceiving fetuses with β-thalassemia major or intermedia. Am. J. Hematol. 64:206–209, 2000. © 2000 Wiley-Liss, Inc.