Jonah McIntyre

University of South Alabama

Author Statistics

Papers

Citation

H-Index

i-10 index

Research Trends

Author Order

Document Type

Co-Authors

Steven R. Goodman

University of Tennessee Health Science Center

Arvind Shah

National Academy of Medical Sciences

Archil Shartava

Breakthrough

Naomi F. Campbell

Jackson State University

Carlos A. Monteiro

Escola Superior de Saúde Egas Moniz

Xunda A. Gibson

University of South Alabama

Yalin Zhang

Hainan Center for Disease Control & Prevention

Keith R Hill

Max Bayard

East Tennessee State University

Jack R. Woodside

East Tennessee State University

Cooperative Institutions

University of South Alabama

East Tennessee State University

University of Tennessee Health Science Center

University of Leeds

Case Western Reserve University

Cornell University

SUNY Upstate Medical University

Association of American Medical Colleges

Health Affairs

Pacific Northwest University of Health Sciences

Author Statistics

Papers

Citation

H-Index

i-10 index

Research Field

The Efficacy of Reducing Agents or Antioxidants in Blocking the Formation of Dense Cells and Irreversibly Sickled Cells In Vitro

Blood (1998)

Xunda A. Gibson Archil Shartava Jonah McIntyre Carlos A. Monteiro Yalin Zhang

Cysteamine

Dimercaprol

10.1182/blood.v91.11.4373.411k37_4373_4378

Cite

Citations (10)

The Gardos channel is responsible for CDNB‐induced dense sickle cell formation

American Journal of Hematology (2000)

Archil Shartava Jonah McIntyre Arvind Shah Steven R. Goodman

The red blood cells (RBCs) derived from blood taken from homozygous sickle cell (SS) patients demonstrate densities that are inversely proportional to the intracellular reduced glutathione (GSH) content. Addition of 1 mM 1-chloro-2,4-dinitrobenzene (CDNB) to low-density sickle cells (LDSS), at 4°C, results in a shift of LDSS erythrocytes to high-density sickle cells (HDSS), with corresponding decreases in GSH. We have previously demonstrated that this CDNB effect was due to increased K+ leakage and that dense cell formation could be inhibited by clotrimazole (specific for the Gardos channel) but not DIOA (specific for the K+–Cl− co-transport system) at pH 7.4 (Shartava et al. Am. J. Hematol. 1999;62:19–24). Here we demonstrate that clotrimazole (10 μM) inhibits dense cell formation at pH 7.1 and 6.8, while DIOA (1 mM) has no effect. As pH 6.8 is the optimal pH for the K+–Cl− co-transport system, we can now reasonably conclude that damage to the Gardos channel is responsible for CDNB-induced dense cell formation. Am. J. Hematol. 64:184–189, 2000. © 2000 Wiley-Liss, Inc.

Clotrimazole

Red Cell

10.1002/1096-8652(200007)64:3<184::aid-ajh8>3.3.co;2-v

Cite

Citations (1)

The Gardos channel is responsible for CDNB-induced dense sickle cell formation

American Journal of Hematology (2000)

Archil Shartava Jonah McIntyre Arvind Shah Steven R. Goodman

The red blood cells (RBCs) derived from blood taken from homozygous sickle cell (SS) patients demonstrate densities that are inversely proportional to the intracellular reduced glutathione (GSH) content. Addition of 1 mM 1-chloro-2,4-dinitrobenzene (CDNB) to low-density sickle cells (LDSS), at 4 degrees C, results in a shift of LDSS erythrocytes to high-density sickle cells (HDSS), with corresponding decreases in GSH. We have previously demonstrated that this CDNB effect was due to increased K(+) leakage and that dense cell formation could be inhibited by clotrimazole (specific for the Gardos channel) but not DIOA (specific for the K(+)-Cl(-) co-transport system) at pH 7.4 (Shartava et al. Am. J. Hematol. 1999;62:19-24). Here we demonstrate that clotrimazole (10 microM) inhibits dense cell formation at pH 7.1 and 6.8, while DIOA (1 mM) has no effect. As pH 6.8 is the optimal pH for the K(+)-Cl(-) co-transport system, we can now reasonably conclude that damage to the Gardos channel is responsible for CDNB-induced dense cell formation.

Clotrimazole

Red Cell

10.1002/1096-8652(200007)64:3<184::aid-ajh8>3.0.co;2-3

Cite

Citations (16)

Alcohol Withdrawal Syndrome

CRC Press eBooks (2000)

Max Bayard Jonah McIntyre Keith R Hill Jack R. Woodside

The spectrum of alcohol withdrawal symptoms ranges from such minor symptoms as insomnia and tremulousness to severe complications such as withdrawal seizures and delirium tremens. Although the history and physical examination usually are sufficient to diagnose alcohol withdrawal syndrome, other conditions may present with similar symptoms. Most patients undergoing alcohol withdrawal can be treated safely and effectively as outpatients. Pharmacologic treatment involves the use of medications that are cross-tolerant with alcohol. Benzodiazepines, the agents of choice, may be administered on a fixed or symptom-triggered schedule. Carbamazepine is an appropriate alternative to a benzodiazepine in the outpatient treatment of patients with mild to moderate alcohol withdrawal symptoms. Medications such as haloperidol, beta blockers, clonidine, and phenytoin may be used as adjuncts to a benzodiazepine in the treatment of complications of withdrawal. Treatment of alcohol withdrawal should be followed by treatment for alcohol dependence.

Delirium tremens

Alcohol withdrawal syndrome

Lorazepam

Withdrawal syndrome

10.1201/9781420036961-14

Cite

Citations (241)

The Efficacy of Reducing Agents or Antioxidants in Blocking the Formation of Dense Cells and Irreversibly Sickled Cells In Vitro

Blood (1998)

Xunda A. Gibson Archil Shartava Jonah McIntyre Carlos A. Monteiro Yalin Zhang

Cysteamine

10.1182/blood.v91.11.4373

Cite

Citations (67)