Pharmacology and Molecular Therapeutics Faculty & Staff

A.B. Smith College, Northampton, MA, USA
Ph.D. Tufts University, Boston, MA, USA

Introduction and overview:
My laboratory is dedicated to understanding normal tissue repair processes and how the repair process is altered in fibrotic remodeling. Normal tissue regeneration for wound healing is a critical focus of research for the military as well as for the medical field in general. The long term goal of my laboratory is to understand the mechanism of fibrotic repair and to identify therapeutic agents to prevent and/or treat this disease. The lung provides an excellent model system for investigation, since it is uniquely sensitive to chemicals and radiation that produce well-defined stages of injury, inflammation, attempted repair, and repair failure/remodeling. Lung fibrosis is a progressive disease with no treatments and poor prognosis. Our laboratory uses in vivo animal models and in vitro primary cell cultures to systematically elucidate the mechanisms of tissue regeneration and fibrotic remodeling at the molecular, biochemical, cellular, and tissue levels.

Radiation countermeasures for the lung and hematopoietic systems and radiation biology:
• Radiation countermeasures for both the hematopoietic and lung tissues. Radiation-induced lung injury is a late effect of radiation, whereas hematopoietic injuries are an acute radiation injury. Because of the Department of Defense’s interest in protection against both acute and delayed injuries, we were requested to develop a murine model for both the hematopoietic and pulmonary injuries, and to test radiation countermeasures in both systems. My laboratory developed an animal model system incorporating both hematopoietic and lung radiation injuries. We have determined the mechanism of action of captopril protection in both tissues, as a part of the requirement for radiation countermeasure development under the Animal Rule for the FDA. We are currently expanding our testing of captopril in the minipig model of radiation acute injuries.
• My laboratory developed a cell culture system for studying the molecular mechanisms of radiation-induced senescence in normal (non-transformed, non-immortalized) cells. Our research demonstrated for the first time that normal lung and skin cells primarily undergo accelerated senescence, and not apoptosis, in response to radiation. We identified an early cellular response to radiation is the induction of insulin-like growth factor 1 (IGF-1) and the activation of its receptor (IGF-1R). These novel and provocative observations prompted us to hypothesize that senescence is the precipitating state for radiation pathology.

Hepatocyte growth factor (HGF) signaling for tissue repair and suppression of fibrosis:
• My laboratory has identified novel signaling pathways for HGF-induced normal tissue repair mechanisms. HGF expression is required for normal tissue repair, and HGF can redirect repair away from fibrotic remodeling to induce normal tissue regrowth. To understand how HGF can accomplish this, my research team investigated signal transduction mechanisms for HGF suppression of apoptosis in epithelial and endothelial cells that is induced during fibrosis. We next investigated the mechanisms by which HGF expression is suppressed during fibrotic remodeling. We recently uncovered a novel mechanism by which miRNA regulates HGF mRNA half-life under fibrotic conditions. This research led to the identification of potential novel anti-fibrotic treatment strategies.
• My laboratory developed a synthetic peptide based on other proteins that bind the HGF receptor, MET. The structural complexity of the full length HGF structure has prevented its development as a pharmaceutical agent, and full length HGF has not been successfully produced in sufficient quantities for clinical use. A patent was submitted by the USU/HJF JOTT based on these findings. Our laboratory currently aims to improve the design of this protein, to improve stability and increase receptor affinity.

B.S & M.S., Biochemistry, Moscow State University of Education, Moscow, Russia
Ph.D., Cellular Biology, Moscow State University of Education & Ivanovsky Research Institute of Virology, Russian Academy of Medical Sciences
Postdoctoral Training, Molecular Biology of AIDS, Picower Institute for Medical Research, Manhasset, NY
Postdoctoral Training, Molecular Virology, George Washington University, Washington, DC

RESEARCH DESCRIPTION:
My laboratory studies the molecular mechanisms of innate immune response to radiation-induced stress and involvement of the endogenous retroviruses and retroelements in this response. Even mild radiation doses may induce prolonged or chronic inflammation that disrupts organ functions. This is an important factor of secondary radiation-related disorders, such as vascular abnormalities, neuronal damage, autoimmune diseases and radiation-related cancer. We consider molecular patterns associated with viral infections, such as viral RNAs and proteins as the essential factors that modulate and exacerbate radiation-induced inflammation.

Ongoing Projects:

Radiation-induced cellular stress and human endogenous retroviruses
Human endogenous retroviruses (HERVs) constitute 8.3% of our genome. Most of integrated HERV genomes are silenced. However, detection of high levels of HERV-K mRNA, proteins, and even viral particles in a wide range of embryonic cells and cancers suggests that some HERVs may play an essential role in cell differentiation and cancer development. Recent studies revealed transcriptional activation of some retroviral genomes in various cancers and immune cells after exposure to radiation doses. We investigate the effect of gamma radiation on the expression of human endogenous retroviruses and their impact on inflammatory response in various types of immune cells. We found that promoters of certain HERV genomes become permanently activated after the single doses of radiation. Retroviral RNA, as well as some viral proteins, particularly Env (envelope protein), affect innate immune response and can enhance radiation-induced inflammation via the activation of critical pathways. Our ultimate goal is to elucidate the retrovirus-related mechanisms that enhance radiation-induced inflammation and indirect pathogenic effect of radiation on unexposed cells. Our long term goal is to reduce the inflammatory response to ionizing radiation using reprogramming cytokine profile of radiation-activated cells from pro- to anti-inflammatory phenotype via the modulation of expression of endogenous retroelements.

Exosomes in cytopathogenesis and intercellular communications within context of radiation-induced stress.
Initially small extracellular vesicles, exosomes, were thought to be a mechanism for discarding unwanted cellular material. However, in recent years, numerous evidence has indicated the role of exosomes in intercellular communication and the progression of various pathologies, including cancer and multiple neurodegenerative disorders. Exosomes are cell-derived vesicles that are present in all biological fluids and are capable of carrying RNAs and proteins which can be exchanged from cell-to-cell. Existing data indicate that exosomes and their cargo play crucial roles in communicating of radiation-induced and bystander cells with the result related to DNA damage and cell pathogenesis. We recently demonstrated multiple pathogenic effects of exosomes from the cells containing integrated retroviral genomes, such as human T lymphotropic virus 1 (HTLV-1) and HIV-1 on naïve cells. These effects were enhanced by the exposure of producing cells to ionizing radiation. Current research in our laboratory is focused on the analysis of host-cellular and viral cargo in the exosomes released from the radiation-exposed cells. We also investigate how non radiation-exposed cells respond to exosome-mediated effect of radiation in the context of radiotherapy and environmental radiation. Potential outcomes include understanding of the functions of exosome-packaged noncoding RNAs and mRNA, viral and host proteins in recipient cells and their pathogenic impact that is related to radiation. Identification of exosome-incorporated biomarkers of radiation doses is also part of this study.

Collaborative Projects
Our laboratory is involved in collaborative projects with George Washington University (Paul Brindley Lab) and Massachusetts Institute of Technology (Kevin Esvelt Lab). These studies are related to coinfection of HIV and human blood fluke Schistosoma mansoni and S. hematobium and the use of HIV-based lentiviral vectors for delivery of gene editing tools within the context of Gene Drive strategy.

Postdoctoral, University of California, Berkeley, CA 1984-1988
Ph.D. University of California, Berkeley, CA, 1983
M.A. University of Nebraska, Omaha, NE, 1977
B.S. FuJen Catholic University, Taipei, Taiwan, ROC, 1975

Dr. Juliann Kiang is a principal investigator at Armed Forces Radiobiology Research Institute (AFRRI). She is Adjunct Professor in Department of Pharmacology and Molecular Therapeutics and in Department of Medicine, School of Medicine, Uniformed Services University of the Health Sciences (USU).

Dr. Kiang serves in editorial boards of several scientific journals, NIH and VA study sections, and USU committees. She worked in Water Reed Army Institute of Research from 1989 to 2006 before joining AFRRI.

Dr. Kiang is involved in studies showing corticotrophin-releasing factor and heat shock proteins are capable of protecting against edema/inflammation and hypoxia injury, respectively. She demonstrates that overexpression of inducible form of heat shock protein 70 kDa induced by sublethal heat stress, chemical stimulation, or the gene transfer produces thermotolerance and cross-tolerance that may be related to an inhibition of changes in intracellular calcium concentrations and expression of stress-related genes and proteins such as inducible nitric oxide synthase and p38-MAPK. She has found 17-DMAG, mesenchymal stem cells, G-CSF, ghrelin, or ciprofloxacin that can make cells endure much better under circumstances of low oxygen, a way to treat heat stroke, ischemia, hemorrhage, cancer, heart attack, stroke, or ionizing radiation injury.

Dr. Kiang had made four major contributions in her research career (journal references to work are noted).

Dr. Kiang is the first to demonstrate that treatment with corticotrophin-releasing factor (CRF) inhibits neurogenic and thermally-induced protein extravasation in rats (9-14). She also found that urotensin I and sauvagine (members of the CRF superfamily) possess the same properties as CRF but with greater potency (15). She holds a patent resulting from this work. She has provided evidence that CRF and its analogs increase intracellular Ca2+ concentrations in vitro (33, 36, 50), which are correlated with capacity of these neuropeptides to inhibit thermally-induced edema (50). CRF exerts its action on CRF type 2 receptors to activate enzymes such as tyrosine kinases, phospholipase 1 and 2 to lead to a result of increases in intracellular Ca2+ concentrations (56). A patent is resulted.

Dr. Kiang’s second major contribution is that she performed extensive research to establish the effect of heat shock on components of signal transduction pathways, such as H+, Ca2+, Na+, cAMP, inositol 1,4,5-trisphosphate, and heat shock proteins in cultured cells. Her findings in this area are wide-ranging and have extended knowledge in the heat shock field (18, 19, 22, 25, 29, 40-42, 44, 46-48, 51-55, 57, 58, 60-62). Her findings provide insight to unfold the mechanisms of tolerance and cross-tolerance (64, 67). Heat shock protein 70 kDa plays a very important role in cell survival – a fine-line before occurrence of apoptosis.

Dr. Kiang’s third major contribution is that she has shown heat shock protein 70 kDa (HSP-70i) can protect the rat ileum from the ischemia/reperfusion injury (37, 66), ricin injury (47), during ileitis (57), and the mouse jejunum, lung, heart, and kidney from the hemorrhagic shock (70). She has also shown that down-regulation of inducible nitric oxide synthase inhibits the activity of caspase-3, an apoptotic protease, and overexpression of HSP-70i prevents ATP loss resulted from hemorrhage (78, 87, 91, 99, 104) or radiation-injury (106-108, 110-114). The work has resulted in a provisional patent.

Dr. Kiang’s fourth major contribution is that she has characterized radiation combined injury (110, 111, 115, 120) shown that ciprofloxacin (122, 126-128, 134), ghrelin (130, 146), and bone marrow mesenchymal stem cells (132, 140) can combat radiation injury combined with skin-wound injury. The research work is ongoing. Meanwhile, she established a new combined injury model of radiation with hemorrhage (135, 138, 142, 145) that brought her the 2016 AFRRI Research Award.

Bubliography

Peer-reviewed publications (149)
1. Kiang JG, Dewey WL, and Wei ET. Tolerance to morphine bradycardia in the rat. J. Pharmacol Exp. Ther. 226:187 192, 1983.
2. Kiang JG and Wei ET. Inhibition of an opiate-induced vagal reflex in rats by naloxone, SMS 201 995 and ICI 154, 129. Regulatory Peptides 6:255 262, 1983.
3. Dashwood MR, Kiang JG, and Wei ET. An etorphine-evoked reflex in rats is inhibited by naloxone, N-methylnaloxone, and SMS 201 995. Arch. Int. Pharmacodyn. Ther. 266:77 82, 1983.
4. Kiang JG and Wei ET. Sensitivity to morphine-evoked bradycardia in rats is modified by dynorphin (1 13), (Leu)enkephalin and (Met)enkephalin. J. Pharmacol. Exp. Ther. 229:469 473, 1984.
5. Kiang JG and Wei ET. Peripheral opioid receptors influencing heart rate in rats: evidence for endogenous tolerance. Regulatory Peptides 8:297 303, 1984.
6. Tang J, Webber RJ, Chang D, Chang JK, Kiang JG, and Wei ET. Depressor and natriuretic activities of several atrial peptides. Regulatory Peptides 9:543 549, 1984.
7. Wei ET and Kiang JG. Peripheral opioid receptors influencing heart rate in rats. In: Opioid Peptides in the Periphery. (Eds, F. Fraioli, A. Isidori and M. Mazzetti) Developments in Neuroscience 18:95 101, 1984, Amsterdam, Elsevier.
8. Kiang JG and Wei ET. CRF-evoked bradycardia in urethane-anesthetized rats is blocked by naloxone. Peptides 6:409 413, 1985.
9. Kiang JG and Wei ET. CRF: an inhibitor of neurogenic plasma extravasation produced by saphenous nerve stimulation. Eur. J. Pharmacol. 114:111 112, 1985.
10. Wei ET, Kiang JG, Buchan P, and Smith T. Corticotropin-releasing factor (CRF) inhibits neurogenic plasma extravasation in the rat paw. J. Pharmacol. Exp. Ther. 238:783 787, 1986.
11. Kiang JG and Wei ET. Corticotropin-releasing factor (CRF) inhibits thermal injury. J. Pharmacol. Exp. Ther. 243:517- 520, 1987.
12. Wei ET and Kiang JG. Inhibition of protein exudation from the trachea by corticotropin-releasing factor. Eur. J. Pharmacol. 140:63-67, 1987.
13. Wei ET, Kiang JG, and Tien JQ. Anti-inflammatory activity of corticotropin-releasing factor: I. Efficacy studies. Proc. West. Pharmacol. Soc. 30:59 62, 1987.
14. Kiang JG, Poree L, and Wei ET. Anti-inflammatory activity of corticotropin-releasing factor: II. Mechanisms of action. Proc. West. Pharmacol. Soc. 30:63 65, 1987.
15. Wei ET and Kiang JG. Peptides of the corticoliberin superfamily attenuate thermal and neurogenic inflammation in rat paw skin. Eur. J. Pharmacol. 168:81 86, 1989.
16. Kiang JG and Colden-Stanfield M. Morphine induces an intracellular alkalinization in bovine aortic endothelial cells (BAECs), In: International Narcotic Research Conference (INRC) '89. (Eds. R. Quirion, K. Jhamandas and C. Gianoulakis) Alan Liss Press, N.Y., Prog. Clin. Biol. Res. 328:137 140, 1989.
17. Wei ET, Wong JC, and Kiang JG. Decreased inflammatory responsiveness of hypophysectomized rats to heat is reversed by a CRF antagonist. Regulatory Peptides 27:317 323, 1990.
18. Kiang JG, McKinney LC, and Gallin EK. Heat induces an intracellular acidification in human A 431 cells: role of Na+/H+ exchanger and metabolism. Am. J. Physiol., 259(Cell Physiol. 28):C727-C737, 1990.
19. Kiang JG, Wu YY, and Lin M. Hyperthermia elevates cAMP levels in human epidermoid A 431 cells. Biochem. J. 276:683 689, 1991.
20. Kiang JG. Effect of intracellular pH on cytosolic free [Ca2+]i in A-431 cells. Eur. J. Pharmacol. 207(Molecular Pharmacol. Section):287-296, 1991.
21. Lin W-W, Kiang JG, and Chuang D-M. Pharmacological characterization of endothelin-stimulated phosphoinositides breakdown and cytosolic Ca2+ rise in C6 rat glioma cells. J. Neurosci., 12:1077 1085, 1992.
22. Kiang JG, Koenig ML, and Smallridge RC. Heat shock increases cytosolic free Ca2+ concentration via the Na+/Ca2+ exchange in human epidermoid A 431 cells. Am. J. Physiol. 263(Cell Physiol. 32):C30-38, 1992.
23. Smallridge RC, Gist ID, and Kiang JG. Na+-H+ antiport and monensin effects on cytosolic pH and iodide transport in FRTL 5 rat thyroid cells. Am. J. Physiol. 262(Endocrinol. Metab.) 25:E834-E839, 1992.
24. Smallridge RC, Kiang JG, Gist ID, Fein HG, and Galloway R. U 72133 inhibits TRH-induced activities in GH3 cells. Endocrinol. 131:1883 1888, 1992.
25. Kiang JG and McClain DE. Effect of heat shock, Ca2+, and cAMP on inositol 1,4,5-trisphosphate in human epidermoid A 431 cells. Am. J. Physiol. 264 (Cell Physiol. 33):C1561-C1569, 1993.
26. Aloj SM, Liguoro D, Kiang JG, and Smallridge RC. Purinergic (P2) receptor -operated calcium entry into rat thyroid cells. Biophy. Biochim. Res. Comm. 195:1-7, 1993.
27. Kiang JG. Corticotropin-releasing factor increases cytosolic free calcium via receptor-mediated Ca2+ channels. Eur. J. Pharmacol. (Molecular Pharmacol. Section) 267:135-142, 1994.
28. Kiang JG and Smallridge RC. Sodium cyanide increases cytosolic free calcium: Evidence of activation of the reversed mode of Na+/Ca2+ exchanger and Ca2+ mobilization from inositol trisphosphate-insensitive pools. Toxicol. Appl. Pharmacol., 127:173-181, 1994.
29. Kiang JG, Carr FE, Burns MR, and McClain DE. HSP-72 synthesis is promoted by increase in [Ca2+]i or activation of G proteins but not pHi or cAMP. Am. J. Physiol. 267 (Cell Physiol. 36):C104-C114, 1994.
30. Tang T, Kiang JG, and Cox BM. Opioids acting through delta-receptors increase the intracellular free calcium concentration in the dorsal root ganglion neuroblastoma hybrid ND8-47 cells. J. Pharmacol. Exptl. Ther., 270:40-46, 1994.
31. Wang X, Kiang JG, and Smallridge RC. U-73122 inhibits increases in inositol trisphosphates and cytosolic free [Ca2+] induced by TSH in FRTL-5 cells. Bioph. Biochim. Acta, 1223:101-106, 1994.
32. Poola I and Kiang JG. The estrogen inducible transferrin receptor-like membrane glycoprotein is related to stress regulated proteins. J. Biol. Chem. 269:1-8, 1994.
33. Kiang JG, Wang XD, and McClain DE. Corticotropin-releasing factor increases protein kinase C activity by elevating isoforms  and  at the membrane. Chin J. Physiol. 37:105-110, 1994.
34. Wang XD, Kiang JG, and Smallridge RC. Identification of protein kinase C and its multiple isoforms in Frtl-5 thyroid cells. Thyroid 5:137-140, 1995.
35. Tang T, Kiang JG, Cote T, and Cox BM. Opioid-induced increase [Ca2+]i in ND8-47 neuroblastoma X DRG hybrid cells is mediated through G protein-coupled delta opioid receptors and desensitized by chronic exposure to opioid. J. Neurochem. 65:1612-1621, 1995.
36. Kiang JG. Mystixin-7 and Mystixin-11 increase [Ca2+]i and inositol trisphosphates in human A-431 cells. Eur. J. Pharmacol. (Mol. Pharmacol. Section) 291:107-113, 1995.
37. Stojadinovic A, Kiang JG, Smallridge RC, Galloway RL, and Shea-Donahue T. Heat shock protein 72 kD induction protects rat intestinal mucosa from ischemia/reperfusion injury. Gastroenterol. 109:505-515, 1995.
38. Tang T, Kiang JG, Cote T, and Cox BM. Antisense oligodeoxynucleotide to Gái2 protein á-subunit sequence inhibits an opioid-induced increase in intracellular free calcium in ND8-47 neuroblastoma x DRG hybrid cells. Mol. Pharmacol. 48:189-193, 1995.
39. Ding XZ, Smallridge RC, Galloway RJ, and Kiang JG. Rapid assay of HSF1 and HSF2 gene expression by reverse transcriptase PCR. Mol. Cell Biochem. 158: 48-51, 1996.
40. Ding XZ, Smallridge RC, Galloway RJ, and Kiang JG. Increases in HSF1 translocation and synthesis in human epidermoid A-431 cells: role of protein kinase C and [Ca2+]i. J. Investig. Med. 44:144-153, 1996.
41. Kiang JG, Ding XZ, and McClain DE. Thermotolerance attenuates heat-induced increases in [Ca2+]i and HSP-72 synthesis but not heat-induced intracellular acidification in human A-431 cells. J. Investig. Med. 44:189-192, 1996.
42. Kiang JG, Wang XD, Ding XZ, Gist I, and Smallridge RC. Heat shock inhibits the hypoxia-induced effects on iodide uptake and signal transduction and enhances cell survival in rat thyroid FRTL-5 cells. Thyroid, 6:475-483, 1996.
43. Wang XD, Kiang JG, Atwa MA, and Smallridge RC. Evidence for the involvement of protein kinase C isoforms in á-1 adrenergic activation of phospholipase A2 in Frtl-5 thyroid cells, J. Investig. Med. 44:566-574, 1996.
44. Kiang JG and Koenig ML. Characterization of intracellular calcium pools in thermotolerant and their desensitization in thermotolerant cells. J. Investig. Med. 44:352-361, 1996.
45. Kiang JG and Tsokos GC. Signal transduction and heat shock protein expression. J. Biomed. Sci. 3:379-388, 1996.
46. Ding XZ, Tsokos GC, Smallridge RC, and Kiang JG. Heat shock gene expression in HSP-70 and HSF1 gene-transfected human epidermoid A-431 cells. Mol. Cell. Biochem. 167:145-152, 1997.
47. Stojadinovic A, Kiang JG, Smallridge RC, Galloway RL, and Shea-Donahue T. Induction of the heat shock response limits tissue injury during acute inflammation of the rat ileum. Critical Care Medicine 25:309-317, 1997.
48. Ding XZ, Tsokos GC, and Kiang JG. Heat shock factor 1 protein in heat shock factor 1 gene-transfected human epidermoid A-431 cells requires phosphorylation prior to inducing heat shock protein-70 production. J. Clin. Investig. 99:136-143, 1997.
49. Liossis S-N, Ding XZ, Kiang JG, and Tsokos GC. Overexpression of HSP70 offers thermoprotection but enhances the TCR/CD3- and Fas-induced apoptotic death in Jurkat T-cells. J. Immunol. 158:5668-5675, 1997.
50. Kiang JG. Corticotropin-releasing factor-like peptides increase cytosolic free calcium in human epidermoid A-431 cells. Eur. J. Pharmacol. (Molecular Pharmacology Section), 329:237-244, 1997.
51. Kiang JG, Gist ID, and Tsokos GC. 17-Estradiol-induced increases in glucose-regulated proteins protect human breast cancer T47-D cells from thermal injury. Chin. J. Physiol. 40:213-219, 1997.
52. Kiang JG, Ding XZ, and McClain DE. Overexpression of HSP-70 attenuates increases in [Ca2+]i and protects human epidermoid A-431 cells after chemical hypoxia. Toxicol. Appl. Pharmacol. 149:185-194, 1998.
53. Ding XZ, Tsokos GC, and Kiang JG. Overexpression of HSP-70 inhibits the phosphorylation of HSF1 by activating protein phosphatase and inhibiting protein kinase C activity. FASEB. J. 12:451-459, 1998.
54. Kiang JG, Gist ID, and Tsokos GC. Cytoprotection and regulation of heat shock proteins induced by heat shock in human breast cancer T47-D cells: role of [Ca2+]i and protein kinases. FASEB J. 12: 1571-1579, 1998.
55. Kiang JG and Tsokos GC. Heat shock protein 70 kD family: Molecular Biology, Biochemistry, and Physiology. Pharmacol.Ther. 80:183-201, 1998.
56. Kiang JG, Ding XZ, Gist ID, and Tsokos GC. Corticotropin-releasing factor increases phosphotyrosine of phospholipase C- at tyrosine residues via its receptor 2 in human epidermoid A-431 cells. Eur. J. Pharmacol. 363:203-210, 1998.
57. Goldhill JM, Stojadinovic A, KiangJG, Smallridge RC, and Shea-Donohue T. Hyperthermia prevents functional, histological and biochemical abnormalities induced during ileitis. Neurogastroenterol. Mot. 11:69-76, 1999.
58. Kiang JG, Gist ID, and Tsokos GC. Biochemical requirement of heat shock protein 72 kD expression in human breast cancer MCF-7 cells. Mol. Cell. Biochem.199: 179-188, 1999.
59. Wang XD, Kiang JG, Scheibel LW, and Smallridge RC. Phospholipase C activation by Na+/Ca2+ exchange is essential for monensin-induced Ca2+ influx and arachidonic release in FRTL-5 thyroid cells. J. Investig. Med., 47:388-396, 1999.
60. Kiang JG and McClain DE. N-nitro-L-arginine decreases resting cytosolic [Ca2+] and enhances heat stress-induced increase in cytosolic [Ca2+] in human colon carcinoma T84 cells. Chin. J. Physiol. 42: 153-160, 1999.
61. Smallridge RC, Gist ID, Tsokos GC, and Kiang JG. Characterization of distinct heat shock and thapsigargin-induced cytoprotective proteins in FRTL-5 cells. Thyroid, 9: 1041-1047, 1999.
62. Kiang JG, Gist ID, and Tsokos GC. Heat shock induces expression of heat shock protein 72 kD and 90 kD in human breast cancer MDA-231 cells. Mol. Cell. Biochem. 204: 169-178, 2000.
63. Kiang JC and Lu PY. Biological effects of qigong and an overview of research design and methodology. Proceedings: The Science and Spirituality of Healing, 1: 99-121, 2000.
64. Kiang JG, Kiang SC, Juang Y-T, and Tsokos GC. Nω-nitro-L-arginine inhibits the inducible heat shock protein 70 kDa via Ca2+, PKC, and PKA. Am. J. Physiol. 282:G415-G423, 2002.
65. Kiang JG, Marotta D, Wirkus M, Wirkus M, and Jonas WB. External bioenergy increases intracellular free calcium concentrations and reduces cellular response to heat stress. J. Investig. Med., 50: 38-45, 2002.
66. Fleming SD, Starnes BW, Kiang JG, Stojadinovic A, Tsokos GC, and Shea-Donohue T. Heat stress protection against mesenteric ischemia/reperfusion-induced alteration in intestinal mucosa in rats. J. Appl. Physiol. 92:2600-2607, 2002.
67. Kiang JG. Genistein inhibits herbimycin A-induced inducible heat shock protein 70 kDa. Mol Cell Biochem, 245:191-199, 2003.
68. Kiang JG, McClain DE, Warke VG, Krishnan S, and Tsokos GC. Constitutive NO synthase regulates the Na+/Ca2+ exchanger in human Jurkat T cells: role of [Ca2+]i and tyrosine phosphorylation. J. Cellular Biochem., 89:1030-1043, 2003.
69. Kiang JG, Warke VG, and Tsokos GC. NaCN-induced chemical hypoxia is associated with altered gene expression. Mol Cell Biochem 254:211-216, 2003.
70. Kiang JG, Bowman DP, Wu BW, Hampton N, Kiang AG, Zhao B, Juang Y-T, Atkins JL, and Tsokos GC. Geldanmaycin inhibits hemorrhage-induced increases in caspase-3 activity, KLF6, and iNOS expression in unresuscitated organs of mice: Role of inducible HSP-70. J Appl Phsiol 97:564-569, 2004.
71. Kiang JG, Bowman PD, Zhao B, Atkins JL, and Tsokos GC. Heat shock protein-70 inducers and iNOS inhibitors as therapeutics to ameliorate hemorrhagic shock. NATO-HFM-109-P28:1-11, 2004.
72. Fleming SD, Kiang JG, and Tsokos GC. Targeting complement in treatment of ischemia/reperfusion-induced injury. NATO-HFM-109-P24:1-13, 2004.
73. Bowman PD, Zhao B, Bynum JA, Sondeen JL, Kiang JG, Dubick MA, and Atkins JL. Application of gene expression analysis with microarrays and proteinomics to the problem of hemorrhagic shock and resuscitation. NATO-HFM-109-P29:1-15, 2004.
74. Kiang JG. Inducible heat shock protein 70 kD and inducible nitric oxide synthase in hemorrhage/resuscitation-induced injury. Cell Res 14:450-459, 2004.
75. Kiang JG, Ives JH, and Jonas WB. External bioenergy-induced increases in intracellular free calcium concentrations are mediated by the Na+/Ca2+ exchanger and L-type calcium channel. Mol Cell Biochem 271:51-59, 2005.
76. Kiang JG. Lu X, Tabaku LS, Bentley TB, Atkins JL, and Tsokos GC. Resuscitation with lactated Ringers solution limits the expression of molecular events associated with lung injury after hemorrhage. J Appl Physiol 98:550-556, 2005.
77. Krishnan S, Kiang JG, Fisher CU, Nambiar MP, Nguyen HT, Kyttaris VC, Chowdhury B, Rus V, Tsokos GC. Increased caspase-3 expression and activity contributes to reduced CD3 expression in Systemic Lupus Erythematosus T cells. J Immunol 175:3417-3423, 2005.
78. Kiang JG, Bowman DP, Lu X, Li Yansong, Ding XZ, Zhao B, Juang YT, Atkins JL, Tsokos GC. Geldanmaycin treatment prevents hemorrhage-induced ATP loss in mouse organs by overexpressing HSP-70 and activating pyruvate dehydrogenase. Am J Physiol 291:G117-G127, 2006.
79. Tsen KT, Tsen SWD, Kiang JG. Lycopene is more potent than bata carotene in the neutralization of singlet oxygen: role of energy transfer probed by ultrafast Raman spectroscopy. J Biomed Optics 11:064025 (6 pages), 2006.
80. Tsen KT, Kiang JG, Ferry DK, Morkoc H. Subpicosecond time-resolved Raman studies of LO phonons in GaN: Dependence on the injected carrier density. App Physics Lett 89:11211 (3 pages), 2006.
81. Tsen KT, Kiang JG, Ferry DK, Kochelap VA, Komirenko SM, Kim KW, Morkoc H. Subpicosecond Raman studies of electric-field-induced optical phonon instability in an In0.53Ga0.47As-based semiconductor nanostructure. J Phys: Condens Matter 18:7961-7974, 2006.
82. Kiang JG, Tsen KT. Biology of hypoxia. Chin J Physiol 49:223-233, 2006.
83. Tsen KT, Dykeman E, Sankey OF, Tsen S-WD, Lin N-T, Kiang JG. Observation of the low frequency vibrational modes of bacteriophage M13 in water by Raman spectroscopy. Virology J 3:79 (11 pages), 2006.
84. Tsen KT, Dykeman E, Sankey OF, Lin N-T, Tsen S-WD, Kiang JG. Raman scattering studies of the low frequency vibrational modes of bacteriophage M13 in water. Nanotecnology 17:5474-5479, 2006.
85. Tsen KT, Kiang JG, Ferry DK, and Morkoc H. Subpicosecond time-resolved Raman studies of field-induced transient transport in an -based p-i-n semiconductor nanostructure. App Physics Lett, 89: 262101 (3 pages), 2006.
86. Tsen KT, Kiang JG, and Ferry DK. Subpicosecond transient Raman scattering studies of field-induced electron transport in an -based p-i-n nanostructure: Direct observation of the effects of electron momentum randomization. J Phys: Condens Matter 18:L585-L592, 2006.
87. Kiang JG, Peckham RM, Duke LE, Chaudry IH, Tsokos GC. Androstenediol inhibits trauma-hemorrhage-induced increase in caspase-3 by downregulating inducible nitric oxide synthase pathway. J App Physiol 102: 933-941, 2007.
88. Tsen KT, Dykeman E, Sankey OF, Tsen S-WD, Lin N-T, Kiang JG. Probing the low frequency vibrational modes of viruses with Raman scattering -- bacteriophage M13 in water. J Biomed Optics. 12: 024009 (6 pages), 2007.
89. Tsen KT, Kiang JG, Ferry DK, Morkoc H. Subpicosecond time-resolved Raman studies of LO phonons in GaN. Proc of SPIE 6473: 64730Q-1 – 64730Q-12, 2007.
90. Tsen KT, Kiang JG, Ferry DK, Morkoc H. Studies of longitudinal optical phonons in GaN by sybpicosecond time-resolved Raman Spectroscopy. Proc of SPIE 6471: 64710X-1 – 64710X-10, 2007.
91. Kiang JG, Bowman DP, Lu X, Li Y, Wu BW, Loh HH, Tsen KT, Tsokos GC. Geldanmaycin treatment inhibits hemorrhage-induced increases in caspase-3 activity: Role of inducible nitric oxide synthase. J App Physiol 103: 1045-1055, 2007.
92. Tsen KT, Kiang JG, Ferry DK, Lu H, Scheff WJ, Lin HW, Gwo S. Direct measurements of the lifetimes of longitudinal optical phonon modes and their dynamics in InN. App Physics Lett 90: 152107 (3 pages), 2007.
93. Tsen KT, Kiang JG, Ferry DK, Lu H, Scheff WJ, Lin HW, Gwo S. Subpicosecond time-resolved Raman studies of electron-longitudinal optical phonon interactions in InN. App Physics Lett 90: 172108 (3 pages), 2007.
94. Tsen KT, Kiang JG, Ferry DK, Lu H, Schaff WJ, Lin HW, Gwo S. Electron-density dependence of longitudinal-optical phonon lifetime in InN studied by subpicosecond time-resolved Raman spectroscopy. J Phy Condens Matter 19: 236219 (8 pages), 2007.
95. Tsen KT, TsenS-W D, Chang C-L, Hung C-F, Wu T-C, Kiang JG. Inactivation of viruses by coherent excitations with low power visible femtosecond laser. Virology J 4:50 (6 pages), 2007.
96. Tsen KT, TsenS-W D, Chang C-L, Hung C-F, Wu T-C, Kiang JG. Inactivation of viruses with a very low power visible femtosecond laser. J Physics: Condens Matter 19:322102 (9 pages), 2007.
97. Tsen KT, TsenS-W D, Chang C-L, Hung C-F, Wu T-C, Kiang JG. Inactivation of viruses by laser-driven coherent excitations via impulsive stimulated Raman scattering process. J Biomed Optics 12:064030 (6 pages), 2007.
98. Tsen KT, TsenS-W D, Sankey OF, Kiang JG. Selective inactivation of microorganisms by near-IR femosecond laser pulses. J Phy Condens Matter 19: 472201 (7 pages), 2007.
99. Kiang JG, Krishnan S, Lu X, Li Y. Inhibition of inducible nitric oxide synthase protects human T cells from hypoxia-induced injury. Mol Pharmacol 73:738-747, 2008.
100. Tsen KT, Tsen SWD, Hung CF, Wu TC, Kiang JG. Selective inactivation of human immunodeficiency virus with subpicosecond near-infrared laser pulses. J Phys Condens matter 20:25220 (4 pages), 2008.
101. Atkins JL, Hammamiech R, Jett M, Gorbounov NV, Asher LV, Kiang JG. α-Defensin-4 and asymmetric dimethyl arginine (ADMA) increase in mesenteric lymph after hemorrhage in anesthetized rats. Shock 30: 411-146, 2008.
102. Tsen KT, Tsen S-W D, Chang C-L, Hung C-F, Wu T-C, Ramakrishna K, Mossman K, Kiang JG. Inactivation of viruses with a femtosecond laser via impulsive stimulated Raman scattering. In: Optical Interactions with Tissue and Cells XIX (edited by Steven L. Jacques, William P. Roach, Robert J. Thomas), Proc. of SPIE 6854: 68540N1-6854N10, 2008.
103. Tsen KT, Kiang JG, Ferry DK, Lu H, Scheff WJ, Lin HW, Gwo S. Dynamics of LO phonons in InN studied by subpicosecond time-resolved Raman spectroscopy. In: Ultrafast Phenomena in Semiconductors and Nanostructure Materials XII (edited by J.J. Song, K.T. Tsen, M. Betz and A. Elezzabi), Proc. of SPIE Vol. 6892: 689206 (12 pages), 2008.
104. Kiang JG, Kiang SC, Bowman PD. 17-DMAG inhibits hemorrhage-induced injury in small intestine and lung by inactivating caspase-3. International Proceedings of International Shock Congress K628C0171:23-27, 2008.
105. Tsen KT, Tsen SWD, Hung CF, Wu TC, Kibler K, Jacob B, Kiang JG. Selective inactivation of human immunodeficiency virus with an ultrashort pulsed laser. Proc. of SPIE 7175: 717510-1 – 717510-8, 2009.
106. Kiang JG, Smith JA, and Agravante NG. Geldanamycin analog 17-DMAG inhibits iNOS and caspases in gamma irradiated human T cells. Radiat Res 172: 321-330, 2009.
107. Gorbunov NV, Kiang JG. Up-regulation of Autophagy in the Small Intestine Paneth Cell in Response to Total-Body γ-Irradiation. J Pathol 219: 242-252, 2009.
108. Jiao W, Kiang JG, Cary L, Elliott TB, Pellmar TC, Ledney GD. COX-2 inhibitors are contraindicated for therapy of combined injury. Radiat Res 172: 686-697, 2009.
109. Tsen KT, Tsen S-WD, Fu Q, Lindsay SM, Kibler K, Jacobs B, Wu TC, Karanam B, Jagu S, Roden RBS, Hung C-F, Sankey OF, Ramakrishna B, Kiang JG. Photonic approach to the selective inactivation of viruses with a near-infrared subpicosecond fiber laser. J Biomed Opt 14: 064042 (10 pages), 2009.
110. Kiang JG, Jiao W, Cary L, Mog SR, Elliott TB, Pellmar TC, Ledney GD. Wound trauma increases radiation-induced mortality by increasing iNOS, cytokine concentrations, and bacterial infections. Radiate Res 173: 319-332, 2010.
111. Kiang JG, Garrison BR, Gorbunov NV. Radiation combined injury: DNA damage, apoptosis, and autophagy. Adapt Med 2: 1-10, 2010. doi: 10.4247/AM.2010.ABA004.
112. Daly MJ, Gaidamakova EK, Matrosova VY, Kiang JG, Fukumoto R, Wehr NB, Viteri G, Berlett BS, Levine RL. Small molecule proteome-shield in Deinococcus radiodurans. PLoS One 5(9): e12570 (15 pages), 2010.
113. Gorbunov NV and Kiang JG. Activation of IL-1β pathway and augmentation of Paneth cell α-defensin-4 in small intestine following total-body γ-irradiation. Intl J Immunopathol Pharmacol 23: 1111-1123, 2010.
114. Kiang JG, Smith JA, Agravante NG, Gorbunov NV. Geldanamycin analog 17-DMAG has radioprotective activity in mice. Radiat Res, in review.
115. Fukumoto R, Kiang JG. Geldanamycin analog 17-DMAG limits apoptosis in human peripheral blood cells by inhibition of p53 activation and its interaction with heat shock protein 90 kDa after ionizing radiation. Radiat Res 176: 333-345, 2011.
116. Kiang JG, Agravante NG, Smith JT, Bowman PD. 17-DMAG increases Bcl-2 and inhibits hemorrhage-induced increases in iNOS activation, caspase-3 activity and TNF-a. Cell & Bioscience 1: 21 (10 pages), 2011.
117. Tsen KT, Tsen SWD, Fu Q, Lindsay SM, Li Z, Yan H, Cope S, Vaiana S, Kiang JG. Studies of inactivation of encephalomyocaditis virus, M13 bacteriophage and Salmomella typhimurium by using a visible femtosecond laser irradiation: insight into the possible inactivation mechanisms. J Biomed Optics 16: 078003 (11 pages), 2011.
118. Whitnall MH, Cary LH, Moroni M, Ngudiankama BF, Landauer MR, Singh VK, Ghosh SP, Kulkarni S, Miller AC, Kiang JG, Srinivasan V, Xiao M. United States Armed Forces Radiobiology Research Institute countermeasures program and related policy questions. Proceedings,Hiroshima University, 2012.
119. Kiang JG, Garrison BR, Burns TM, Zhai M, Dews IC, Ney PH, Fukumoto R, Cary LH, Elliott TB, Ledney GD. Wound trauma alters ionizing radiation dose assessment. Cell Bioscience 2: 20 (12 pages), 2012.
120. Tsen S-W D, Wu TC, Kiang JG, Tsen KT. Prospects for a novel ultrashort pulsed laser technology for pathogen inactivation. J Biomed Sci 19: 62 (11 pages), 2012.
121. Kiang JG. Overview of biological effects of irradiation combined injury. NATO-HFM-223-P5:1-18, 2012.
122. Fukumoto R, Cary LH, Gorbunov NV, Elliott TB, Kiang JG. Ciprofloxacin modulates cytokine profiles, accelerates bone marrow recovery and mitigates ileum injury after radiation combined with wound trauma. PLoS One 8: e58389 (11 pages), 2013. doi: 10.1371/journal.pone.0058389. PMID: 23520506
123. Gorbunov NV, Garrison BR, McDaniel DP, Zhai M, Liao1 P-J, Nurmemet N, Kiang JG. Adaptive redox response of mesenchymal stromal cells to stimulation with lipopolysaccharide inflammagen: mechanisms of remodeling of tissue barriers in sepsis. Oxid Med Cell Longev 2013: 186795 (16 pages), 2013. doi: 10.1155/2013/186795. PMID: 23710283
124. Lu X, Nurmemet D, Bolduc DL, Elliott TB, Kiang JG. Radioprotective effects of oral 17-DMAG in mice: Bone marrow and small intestine. Cell Bioscience 3: 36 (16 pages), 2013. doi: 10.1186/2045-3701-3-36. PMID: 24499553
125. Kiang JG, Ledney GD. Skin injuries reduce survival and modulate corticosterone, C-reactive protein, complement component 3, IgM, and prostaglandin E2 after whole-body reactor-produced mixed field (n + γ-photons) irradiation. Oxid Med Cell Longev, 2013: 821541 (10 pages), 2013. doi: 10.1155/2013/821541. PMID: 24175013
126. Kiang JG, Garrison BR, Smith JT, Fukumoto R. Ciprofloxacin as a potential radio-sensitizer to tumor cells and a radioprotectant for normal cells: Differential effects on -H2AX formation, p53 phosphorylation, Bcl-2 production, and cell death. Cell Mol Biochem 393: 133-143, 2014. doi: 10.1007/s11010-014-2053-z. PMID: 24802382
127. Kiang JG, Fukumoto R. Ciprofloxacin increases survival after ionizing irradiation combined injury: gamma-H2AX formation, cytokine/chemokine, and red blood cells. Health Physics 106: 720-726, 2014. doi: 10.1097/HP.0000000000000108. PMID: 24776905
128. Fukumoto R, Burns TM, Kiang JG. Ciprofloxacin Enhances Stress Erythropoiesis in Spleen and Increases Survival after Whole-Body Irradiation Combined with Skin-Wound Trauma, PLoS One 9(2): e90448, 2014. doi: 10.1371/journal.pone.0090448. PMID: 24587369
129. Kiang JG, Zhai M, Liao P-J, Bolduc DL, Elliott TB, Gorbunov NV. Pegylated G-CSF inhibits blood cell depletion, increases platelets, blocks splenomegaly, and improves survival after whole-body ionizing irradiation but not after irradiation combined with burn. Oxid Med Cell Longev 2014: 481392 (10 pages), 2014. doi: 10.1155/2014/481392. PMID: 24738019
130. Kiang JG, Zhai M, Liao P-J, Elliott TB, Gorbunov NV. Ghrelin therapy improves survival after whole-body ionizing irradiation combined with wound or burn: Amelioration of leukocytopenia, thrombopenia, splenomegaly, and bone marrow injury. Oxid Med Cell Longev 2014: 215858, 2014. doi: 10.1155/2014/215858. PMID: 25374650
131. Gorbunov NV, Elliott TB, McDaniel DP, Zhai M, Liao P-J, Kiang JG. Mitophagy and mitochondrial remodeling in mouse mesenchymal stromal cells following a challenge with Staphylococcus epidermidis. J Cell Mol Med 19:1133-1150, 2015. doi: 10.1111/jcmm.12518. PMID: 25721260
132. Kiang JG, Gorbunov NV. Bone marrow mesenchymal stem cells increases survival after ionizing irradiation combined with wound trauma: Characterization and therapy. J Cell Sci Ther 5:190 (8 pages), 2014. doi: 10.4172/2157-7013.1000190
133. Elliott TB, Bolduc DL, Ledney GD, Kiang JG, Fatanmi OO, Wise S, Romaine PLP, Newman VL, Singh VK. Combined immunomodulator and antimicrobial therapy eliminates polymicrobial sepsis and modulates cytokine production in mice exposed to radiation and combined injury. Int J Radiat Biol 91(9):690-702, 2015. doi: 10.3109/09553002.2015.1054526. PMID: 25994812
134. Swift JM, Smith JT, Kiang JG. Ciprofloxacin therapy mitigates ATP loss after irradiation combined with wound trauma: Preservation of pyruvate dehydrogenase and inhibition of pyruvate dehydrogenase kinase 1. Radiat Res 183: 684-692, 2015. PMID: 26010714
135. Swift JM, Smith JT, Kiang JG. Hemorrhage Trauma Increases Radiation-Induced Trabecular
Bone Loss and Marrow Cell Depletion in Mice. Radiat Res 183: 578-583, 2015. doi: 10.1667/RR13960.1 PMID: 25897554
136. Swift JM, Swift SN, Smith JT, Kiang JG, Allen MR. Skin wound trauma, following high-dose radiation exposure, amplifies and prolongs skeletal tissue loss. Bone 81: 487-494, 2015. doi: 10.1016/j.bone.2015.08.022 PMID: 26335157
137. Islam A, Bolduc DL, Zhai M, Kiang JG, Swift JM. Daily Captopril Dosing Increases Survival after Whole-Body Ionizing Irradiation but Decreases Survival after in combination with Combined Burn Trauma in Mice. Radiat Res 184:273-279, 2015. doi: 10.1667/RR14113.1. PMID: 26305295
138. Kiang JG, Smith JT, Anderson MN, Swift JM, Gupta P, Balakathiresan N, Maheshwari RK. Hemorrhage exacerbates radiation effects on survival, leukocytopenia, thrombopenia, erythropenia, bone marrow cell depletion and hematopoiesis, and inflammation-associated microRNAs expression in kidney. PLoS ONE 10:e0139271, 2015. doi: 10.1371/journal.pone.0139271. PMID: 26422254
139. Klionsky DJ…Kiang JG…Zughaler SM. Guidelines for the use and interpretation of assays for monitoring autophagy (3rd edition). Autophagy 12: 1-222, 2016. PMID: 26799652
140. Kiang JG. Adult mesenchymal stem cells and radiation injury. Health Phys 111:198-203, 2016. doi: 10.1097/HP.0000000000000459. PMID: 27356065
141. Gupta P, Gayen M, Smith JT, Matrosova VY, Gaidamakova EK, Daly MJ, Kiang JG, Maheshwari RK. MDP: A Deinococcus Mn2+-Decapeptide Complex Protects Mice from Ionizing Radiation. PLoS One 11: e0160575, 2016. doi: 10.1371/journal.pone.0160575. PMID: 27500529
142. Kiang JG. Exacerbation of mild hypoxia on acute radiation syndrome and subsequent mortality. Adaptive Med 9(1): 28-33, 2017. doi: 10.4247/AM.2017.ABG170
143. Kiang JG, Zhai M, Liao P.-J., Ho C, Gorbunov NV, Elliott TB. Thrombopoietin receptor agonist mitigate hematopoietic acute radiation syndrome and improves survival after whole-body ionizing irradiation followed by wound trauma. Mediators of Inflammation 2017:7582079, 2017. doi: 10.1155/2017/7582079 PMID: 28408792
144. Kiang JG, Zhai M, Bolduc DL, Smith JT, Anderson MN, Ho C, Lin B, Jiang S. Combined therapy of pegylated-G-CSF and Alx4100TPO improves survival and mitigate acute radiation syndrome after whole-body ionizing irradiation alone and followed by wound trauma. Radiat Res 188:476-490, 2017. doi: 10.1667/RR14647.1 PMID: 28850300
145. Kiang JG, Smith JT, Anderson MN, Elliott TB, Gupta P, Balakathiresan N, Maheshwari RK, Knollmann-Ritschel B. Hemorrhage enhances cytokine, complement component 3, and caspase-3, and regulates microRNAs associated with intestinal damage after whole-body gamma-irradiation in combined injury. PLoS ONE 12(9):e0184393, 2017. doi: 10.1371/journal.pone.0184393.PMID: 28934227
146. Gorbunov NV, Kiang JG. Ghrelin therapy decreases incidents of intracranial hemorrhage in mice after whole-body ionizing irradiation combined with burn trauma. Int J Mol Sci 18(8). pii: E1693, 2017. doi: 10.3390/ijms18081693. PMID: 28771181
147. Kiang JG, Smith JT, Hegge SR, Ossetrova N. Circulating cytokine/chemokine concentrations respond to ionizing radiation doses but not radiation dose rates: granulocyte-colony stimulating factor and interleukin-18. Radiat Res, in press, 2018.
148. Kiang JG, Anderson MN, Smith JT. Ghrelin therapy sustains granulocyte colony-stimulating factor and keratinocyte factor to mitigate hematopoietic syndrome and spleen after whole-body ionizing irradiation combined with wound. Cell Biosci 8:27, 2018. doi: 10.1186/s13578-018-0225-3.
149. Li X, Cui W, Hull L, Smith JT, Kiang JG, Xiao M. Effects of low-moderate doses of γ-radiation on mouse hematopoietic and immune system. Radiat Res, in review, 2018.

E-Book (1)
1. Gorbunov NV, Kiang JG. Autophagy-mediated innate defense mechanism in crypt cells responding to impairment of small intestine barrier after total-body gamma-photon irradiation. Cell Biology Research Progress, Nova Science Publishers, INC. Hauppauge, NY. ISBN: 978-1-62417-374-5 http://www.novapublishers.com, 2012.

Book chapters (10)
1. Yan X, Lu PY, and Kiang JG. Qigong: basic science studies in Biology. In: Healing, Intention, and Energy medicine Science, Research Methods and Clinical Implications. (Eds. WB Jonas and C Crawford) Churchill Livingstone, London, UK pp. 103-119, 2003.
2. Kiang JG and McClain DE. Heat stress. In: Combat Medicine Basic and Clinical Research in Military, Trauma, and Emergency Medicine (Eds. GC Tsokos and JL Atkins), Humana Press, New Jersey, pp. 83-101, 2003.
3. Kiang JG. Human bioenergy effects at the cellular and molecular level. In: Life and Mind In Search of Physical Basis (ed. S. Savva), Trafford Publishing, Victoria BC, Canada, pp. 117-137, 2007.
4. Tsen KT, Tsen SWD, Dykeman EC, Sankey OF, Kiang JG. Inactivation of viruses with femtosecond laser pulses. In: Contemporary Trends in Bacteriophage research (Ed: Horace T. Adams), Nova Science Publishers, NY, ISBN: 978-1-60692-181-4, pp. 151-177, 2009.
5. Kumar KS, Kiang JG, Whitnall MH, Hauer-Jensen M. Perspectives in radiological and nuclear countermeasures. In: Textbook of Military Medicine, pages 239-266, 2012.
6. Gorbunov NV, Kiang JG. Autophagy-mediated innate defense mechanism in crypt cells responding to impairment of small intestine barrier after total-body gamma-photon irradiation. In: Autophagy: Principles, Regulation and Roles in Disease (ed: Gorbunov NV), Nova Science Pulbishers, INC. Hauppauge, NY. 2012.
7. Gorbunov NV, Garrison BR, Zhai M, McDaniel DP, Ledney GD, Elliott TB, Kiang JG. Autophagy-mediated defense response of mouse mesenchymal stromal cells (MSCs) to challenge with Escherichia coli. In: Protein Interaction / Book 1; ISBN 979-953-307-577-7. Eds.: Cai J and Wang H. InTech Open Access Publisher; www.intechweb.org. pp. 23-44, 2012.
8. Kiang JG, Fukumoto R, Gorbunov NV. Lipid peroxidation after ionizing irradiation leads to apoptosis and autophagy. In: Lipid Peroxidation; ISBN 980-953-307-143-0. Eds.: Angel Catala, InTech Open Access Publisher: www.intechweb.org, Rijeka, Croatia. pp.261-278, 2012.
9. Gorbunov NV, Elliott TB, McDaniel DP, Lund K, Liao PJ, Zhai M, Kiang JG. Up-regulation of autophagy defense mechanisms in mouse mesenchymal stromal cells in response to ionizing irradiation followed by bacterial challenge. In: Autophagy, ISBN 980-953-307-971-9. Ed: Yannick Bailly, InTech Open Access Publisher: www.intechweb.org, Rijeka, Croatia. pp. 331-350, 2013.
10. Kiang JG. Characterization and therapeutic uses of adult mesenchymal stem cells. In: Stem Cell Toxicity and Medicine (ed. S.C. Sahu). Wiley & Sons, West Sussex, pp. 288-301, 2016.

1983 Ph.D., Central Drug Research Institute (KU), India
1978 M.Sc., Kanpur University, India
1975 B.Sc., Magadh University, India

Mechanism of radiation injury and advanced development of radiation countermeasures
My laboratory focuses attention on the molecular basis of radiation injury which results in acute radiation syndromes (ARS), and the mechanism of action of potential radiation countermeasures. Our ultimate goal is to develop radiation countermeasures to protect military personnel, first responders and civilians from succumbing to ARS following radiation exposure whether it is accidental or as a result of deliberate attack. To achieve this goal we are currently investigating the mechanism of action of gamma-tocotrienol (GT3, an isomer of Vitamin E), Ex-RAD (a chlorobenzylsulphone derivative), toll-like receptor (TLR) ligands (CBLB502), and anti-ceramide antibody at the cellular level, by evaluating cell signaling pathways (cytokine expression, p53 pathway, TLR activation) including DNA damage and repair pathways.
In collaboration with corporate partners, my lab is developing several radiation countermeasures which are under advanced stages of development. CBLB502 and anti-cermide antibody appear to be promising. Ex-RAD has been shown to have both radioprotective and radiomitigative properties. Ex-RAD protects the hematopoietic system and is able to increase survival of irradiated mice by alleviating the severe radiation induced pancytopenia and restoring select bone marrow functions through the up-regulation of the PI3-kinase/AKT pathways and pathways involved with the DNA damage response and DNA repair. Ex-RAD studies have received significant funding from DMRDP (DoD) and BARDA (HHS).
My lab is also working to develop GT3, as a radiation countermeasure in collaboration with Prof. Martin Hauer-Jensen. It has shown great promise in rodent model, capable of mobilizing progenitors, and its radioprotective efficacy is mediated through G-CSF in murine model. Recently, we found that a single administration of GT3, without additional support (fluids, antibiotics, blood products, etc.), was just as effective as multiple administrations of G-CSF, the current gold standard of radiation countermeasures approved by US FDA, with full support. Based on the promising results of our pilot study using the large animal model, we have received funding from CDMRP (DoD) for the advanced development of GT3.
Additionally, we are working to develop a novel anti-ceramide antibody in collaboration with Prof. Richard Kolesnick of Sloan Kettering and Ceramide Theraprutics as a radiation countermeasure, capable of being administered prior to or after radiation exposure. Studies have indicated that this potential countermeasure inhibits ceramide-mediated endothelial apoptosis, which provides significant protection against radiation induced, potentially fatal, gastrointestinal syndrome. Additional studies have shown that a single chain variable fragment of the full length antibody molecule is effective in doses one tenth of the full length version. This project had been supported by DMRDP (DoD). Additional countermeasures being investigated are CBLB612, CBLB613, and myeloid progenitors in collaboration with various academic and corporate partners with support from various funding agencies such as BARDA, NIAID, JPC7, CDMRP, and DMRDP.