About

Kenneth Kim is an instructor of clinical physical therapy in the USC Division of Biokinesiology and Physical Therapy. He practices at USC Physical Therapy—University Park Campus, a faculty practice of the division, and specializes in treating all types of orthopedic and sports injuries. Dr. Kim is a Board-Certified Orthopedic Clinical Specialist and a member of the Orthopedic Section and Sports Section of the American Physical Therapy Association. He has been serving as a full-time instructor of clinical physical therapy at USC since 2013. In addition to his teaching role, he is a member of the USC Doctor of Physical Therapy Program’s admissions committee and serves as a course instructor and director for foundational courses focusing on therapeutic exercise during the first year of the DPT curriculum. Dr. Kim also volunteers as a faculty instructor for extracurricular groups that review didactic materials and apply them through live patient case examinations. He is actively involved in mentoring and teaching in post-professional education and continuing education courses, including serving as a primary mentor for USC orthopedic and sports residencies. Furthermore, he instructs in the Division’s Orthopedic Spine Seminar Series, which aims to enhance proficiency in physical therapy examination, evaluation, and intervention of musculoskeletal conditions, integrating concepts of manual therapy, movement science, and pain science.

Research topics

• Immunology
• Biology
• Intensive care medicine
• Pharmacology
• Biotechnology
• Medicine
• Internal medicine
• Chemistry
• Anesthesia

Selected publications

• “Betaone” barley water extract suppresses ovariectomy-induced osteoporosis in vivo and RANKL-induced osteoclast differentiation in vitro

  PLoS ONE · 2025-02-21 · 1 citations

  articleOpen accessCorresponding

  Betaone is a variety of barley developed by the Korea Rural Development Administration. This study investigated the anti-osteoporosis effects of Betaone barley water extract (B1W) on ovariectomy (OVX)-induced bone loss in mice. To elucidate its mechanism, the effect of B1W on osteoclasts was assessed by measuring the protein expression of nuclear factor-activated T cells c1 (NFATc1), the expression of genes involved in osteoclast differentiation, and bone pit assays. B1W (300 mg/kg/day) significantly increased bone mineral density and bone volume fraction, but decreased trabecular separation compared to the OVX group. B1W also showed a trend towards decreasing serum C-telopeptide of collagen type 1 levels in OVX mice. Additionally, B1W reduced the expression of NFATc1 and downregulated the mRNA expression levels of various marker genes such as c-Fos, tartrate-resistant acid phosphatase (TRAP), cathepsin K (CTSK), dendritic cell-specific transmembrane protein (DC-STAMP), and osteoclast-associated Ig-like receptor (OSCAR). B1W reduced the osteoclast activity in the receptor activator of nuclear factor-κB ligand (RANKL)-treated osteoclasts by inhibiting the mitogen-activated protein kinase (MAPK) pathway. Based on the results, B1W can be considered a useful candidate for a therapeutic agent for treating conditions of bone loss and could also be used as an ingredient in health supplements.

  PublisherDOI

• A Study on the Meaning of Masks in the Ballet Pulcinella

  Korean Journal of Sports Science · 2025-08-31

  article1st authorCorresponding
  PublisherDOI

• Are nanophotonic intermediate mirrors really effective in enhancing the efficiency of perovskite tandem solar cells?

  Nanophotonics · 2025-04-01 · 6 citations

  articleOpen access1st authorCorresponding

  An intermediate mirror has been proposed to enhance multijunction solar cell efficiency by selectively reflecting the light beyond higher energy bandgap of top cell, while simultaneously transmitting the rest of lower-energy light. Therefore, it reduces the higher-energy absorption spectral tail of the bottom cell (thermalization loss) and increase the absorption in the top cell. However, its effectiveness has only been theoretically validated in simplified tandem with basic components such as an antireflection coating (ARC) and top/bottom absorbers. In contrast, experimentally optimized tandem cells, such as perovskite (PVK)/silicon (Si) two-terminal configurations, include additional stacked electrodes, ultrathinned intermediate electrode, and random textures to maximize efficiency. Herein, we revisited the role of the intermediate mirror in these advanced tandem cells. Our results show that the incorporation of ideal intermediate mirror (IIM) does not improve efficiency both in textured and flat tandem cells, with its theoretical upper limit of efficiency being similar to or even lower than that of experimentally optimized cells.

  PublisherOA PDFDOI

• Real-Time Autophagic Flux Measurements in Live Cells Using a Novel Fluorescent Marker DAPRed

  BIO-PROTOCOL · 2024-01-01

  articleOpen access

  Autophagy is a conserved homeostatic mechanism involved in cellular homeostasis and many disease processes. Although it was first described in yeast cells undergoing starvation, we have learned over the years that autophagy gets activated in many stress conditions and during development and aging in mammalian cells. Understanding the fundamental mechanisms underlying autophagy effects can bring us closer to better insights into the pathogenesis of many disease conditions (e.g., cardiac muscle necrosis, Alzheimer's disease, and chronic lung injury). Due to the complex and dynamic nature of the autophagic processes, many different techniques (e.g., western blotting, fluorescent labeling, and genetic modifications of key autophagy proteins) have been developed to delineate autophagy effects. Although these methods are valid, they are not well suited for the assessment of time-dependent autophagy kinetics. Here, we describe a novel approach: the use of DAPRed for autophagic flux measurement via live cell imaging, utilizing A549 cells, that can visualize and quantify autophagic flux in real time in single live cells. This approach is relatively straightforward in comparison to other experimental procedures and should be applicable to any in vitro cell/tissue models. Key features • Allows real-time qualitative imaging of autophagic flux at single-cell level. • Primary cells and cell lines can also be utilized with this technique. • Use of confocal microscopy allows visualization of autophagy without disturbing cellular functions.

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• Effects of nanoparticles on sensitivity to injury and role of autophagy in alveolar epithelial cells

  Physiology · 2024-05-01

  article

  Autophagy, a housekeeping mechanism, is crucial in the maintenance of normal cellular function. Although the involvement of autophagic processes is recognized in numerous diseases, it is unknown how cellular homeostasis might be affected by alterations in available autophagic activity and/or autophagic capacity. In this study, we measured autophagic flux and cellular damage in primary cultured monolayers of rat alveolar epithelial cells (AEC) exposed separately and sequentially to two different autophagy inducers. Rat AEC monolayers were exposed apically for 24 hrs to (1) polystyrene nanoparticles (PNP, 20 nm, carboxylated, near-infrared dye-labeled), (2) tunicamycin (TN, a disruptor of protein synthesis and inducer of the unfolded protein response, at 1-15 μg/mL), or (3) TN (1-15 μg/mL) after 12 hrs of PNP pre-incubation. Release of the cytoplasmic enzyme lactate dehydrogenase (LDH) was used as an indicator of cellular damage and quantified by an LDH assay from Dojindo (Rockville, MD). Autophagic flux was assessed by live cell imaging using confocal microscopy and 0.1 μM DAPRed (Dojindo; Rockville, MD) in the presence (for 1 hr) and absence of 40 μM chloroquine. Serial z sections were collected over the entire cell volume of live single cells to detect DAPRed (autophagosome) fluorescence. PNP were taken up into AEC, where their cytosolic presence induced a gradually increased autophagic flux, reaching a steady state at ~10-24 hrs. When AEC were exposed to TN alone for 24 hrs, autophagy was also activated. Cellular damage in the presence of TN, determined by increased LDH release, revealed dose-dependent injury with LD 50 of 8.12 μg/mL over 24 hr TN exposure. When AEC were pre-exposed to PNP for 12 hrs and subsequently exposed to TN, increased LDH release was seen with LD 50 of 3.95 μg/mL. In summary, the intracellular presence of PNP taken up from apical fluid of rat AEC monolayers activated autophagy. When cellular protein synthesis was disrupted with TN alone, autophagy was also activated. Furthermore, TN induced dose-dependent cellular damage in AEC. However, after pre-exposure to PNP, TN induced greater cellular damage observed as increased LDH release. These results suggest that autophagic capacity is limited and that pre-induction of autophagy by inhaled PNP makes AEC more susceptible to secondary injury by TN. These findings are consistent with the hypothesis that environmental stressors (e.g., ambient air nanoparticles) exert their harmful effects, at least in part, by reducing available autophagic activity/capacity, thereby causing nanoparticle-exposed AEC to be more susceptible to secondary injury. Funding: NIH; WRMPPF. This is the full abstract presented at the American Physiology Summit 2024 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

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• Foreign DNA injection through coleoptile leads to fixation of novel traits in rice

  Plant Physiology Reports · 2024-12-14

  article
  PublisherDOI

• Kinetics of autophagic activity in nanoparticle-exposed lung adenocarcinoma (A549) cells

  Autophagy Reports · 2023-03-15 · 3 citations

  articleOpen access

  Autophagy, a homeostatic mechanism, is crucial in maintaining normal cellular function. Although dysregulation of autophagic processes is recognized in certain diseases, it is unknown how maintenance of cellular homeostasis might be affected by the kinetics of autophagic activity in response to various stimuli. In this study, we assessed those kinetics in lung adenocarcinoma (A549) cells in response to exposure to nanoparticles (NP) and/or Rapamycin. Since NP are known to induce autophagy, we wished to determine if this phenomenon could be a driver of the harmful effects seen in lung tissues exposed to air pollution. A549 cells were loaded with a fluorescent marker (DAPRed) that labels autophagosomes and autolysosomes. Autophagic activity was assessed based on the fluorescence intensity of DAPRed measured over the entire cell volume of live single cells using confocal laser scanning microscopy (CLSM). Autophagic activity over time was determined during exposure of A549 cells to single agents (50 nM Rapamycin; 80 μg/mL, 20 nm carboxylated polystyrene NP (PNP); or, 1 μg/mL ambient ultrafine particles (UFP) (<180 nm)), or double agents (Rapamycin + PNP or Rapamycin + UFP; concomitant and sequential), known to stimulate autophagy. Autophagic activity increased in all experimental modalities, including both single agent and double agent exposures, and reached a steady state in all cases ~2 times control from ~8 to 24 hrs, suggesting the presence of an upper limit to autophagic capacity. These results are consistent with the hypothesis that environmental stressors might exert their harmful effects, at least in part, by limiting available autophagic response to additional stimulation, thereby making nanoparticle-exposed cells more susceptible to secondary injury due to autophagic overload.

  PublisherDOI

• Preparation of temperature-pH dual-responsive hydrogel from hydroxyethyl starch for drug delivery

  Colloid & Polymer Science · 2023-03-07 · 6 citations

  articleSenior author
  PublisherDOI

• Kinetics of macroautophagy in lung adenocarcinoma (A549) cells exposed to nanoparticles

  Physiology · 2023-05-01

  article

  Macroautophagy is an intracellular process helping to maintain normal cellular function. Dysregulation of autophagy is recognized in certain diseases, but it is unknown how maintenance of cellular homeostasis might be affected by the kinetics of autophagy in response to various stimuli. In this study, we measured autophagy kinetics in A549 cells exposed to nanoparticles (NP) (including ambient ultrafine particles (UFP)) and/or Rapamycin. A549 cells were apically exposed (t=0-24hrs) in four experimental settings: (1) control exposure only to culture fluid; (2) exposure to polystyrene NP (PNP), UFP or Rapamycin; (3) concurrent exposure to PNP and Rapamycin or UFP and Rapamycin; and, (4) sequential (in both orders) exposure to a first agent (PNP, UFP or Rapamycin) at t=0-5hrs, followed by exposure to an additional agent (Rapamycin after PNP (or UFP) and PNP (or UFP) after Rapamycin) at t=5-24hrs. Autophagic activity was assessed using fluorescence intensity of DAPRed (a marker for autophagosomes and autolysosomes; 0.1 μM; Dojindo; Rockville, MD) or BacMam RFP-GFP-LC3B (Thermo Fisher; Waltham, MA) in the presence or absence of 40 μM chloroquine measured over the entire cell volume of live single cells using confocal laser scanning microscopy. Autophagic flux was calculated as the difference of observed fluorescence intensity of DAPRed or RFP-GFP-LC3B in the presence and absence of chloroquine. Autophagic flux increased in all experimental modalities, including both single agent and double agent exposures, and reached steady state in all cases ~2 times control from ~8 to 24 hrs, suggesting the presence of an upper limit to autophagic activity. Rapamycin exposure alone induced a rapid rise in autophagic flux, peaking at ~3hrs post exposure, followed by a lowered steady state autophagic flux for up to 24hrs. Exposure to PNP or UFP alone also increased autophagic flux, gradually reaching steady state at ~10-24hrs. During concurrent double exposure to Rapamycin and PNP or UFP at t=0, the steady state level of autophagic flux remained comparable to that observed with single exposures to Rapamycin, PNP or UFP for up to 24 hrs. Under sequential exposure conditions, the steady state level of autophagic flux did not exceed the steady state level observed in single or concurrent exposures. In summary, exposure to nanoparticles activates macroautophagy in a time-dependent manner in A549 cells. Autophagic activity demonstrated comparable steady state levels after exposure to single or dual stimuli, indicating an effective upper limit of autophagic flux in A549 cells under our experimental conditions. These findings suggest that environmental stressors might exert their harmful effects, at least in part, by limiting available autophagic capacity, thereby making NP-exposed cells more susceptible to secondary injury due to autophagic overload. Funding: NIH; WRMPPF This is the full abstract presented at the American Physiology Summit 2023 meeting and is only available in HTML format. There are no additional versions or additional content available for this abstract. Physiology was not involved in the peer review process.

  PublisherDOI

• Autophagic activity in response to nanoparticle exposure of A549 cells

  The FASEB Journal · 2022-05-01

  article

  We have shown previously that lung adenocarcinoma (A549) cells internalize polystyrene nanoparticles (PNP). Once intracellular, PNP stimulate autophagy in A549 cells and over time are delivered to lysosomes, with subsequent egress from the cells by lysosomal exocytosis. We also found evidence that A549 cell exposure to either PNP or ambient air pollution ultrafine particles (UFP) leads to lysosomal dysfunction. In the current study, we assessed if there is a potential limit to autophagic capacity in A549 cells. In the presence of chloroquine (40 μM, 1 hr), A549 cells were exposed to a fluorescent marker, DAPRed (Dojindo; Rockville, MD), that labels autophagosomes and autolysosomes. Autophagic activity was assessed based on the fluorescence intensity of DAPRed, which was measured in serial z sections over the entire cell volume in live, single cells using confocal laser scanning microscopy. Single exposure (50 nM Rapamycin as positive control, 80 μg/mL of 20 nm carboxylated PNP, or 1 μg/mL of UFP (&lt;180 nm, collected in Los Angeles)) and double exposure (Rapamycin + PNP or Rapamycin + UFP) models were utilized to determine the kinetics of autophagic activity over 24 hr. Data on autophagic activity were also obtained by measurement of fluorescence intensities using LC3‐GFP‐RFP in response to PNP/UFP exposures. LC3‐GFP‐RFP was transduced (700:1 virus particle per cell ratio; Thermo Fisher Scientific; Waltham, MA) into A549 cells and expression of LC3‐GFP‐RFP was assessed using confocal microscopy. We found that autophagic activity remained relatively constant in unexposed A549 cells (negative control) as opposed to a rapid increase (&gt;3 times negative control) with a peak at ~3‐5 hr post exposure in Rapamycin‐exposed cells. Both PNP and UFP exposure resulted in gradual elevations in autophagic activity, reaching a steady state (at ~2.5 times negative control) at ~8‐10 hr post exposure with no appreciable change from ~10 to 24 hr. Combining Rapamycin with PNP or UFP caused a rapid rise in autophagic activity (peaking &lt;5 hr post exposure); however, no difference in steady state autophagic capacity (~2.5 times negative control) was observed in comparison to either PNP or UFP exposure over 24 hr. Similar time courses of elevated autophagic activity were observed by increased fluorescence of LC3‐GFP‐RFP in response to 24 hr exposure to Rapamycin, PNP or UFP. In addition, higher expression of LC3‐RFP indicated higher levels of autophagosome fusion with autolysosomes (increased autophagic flux). These data suggest that environmental stressors might exert their harmful effects, at least in part, by limiting available autophagic capacity, thereby making nanoparticle‐exposed cells more susceptible to secondary injury.

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Recent grants

• NIH Grant R01HL038658

  NIH · $3.0M · 2006

Frequent coauthors

• Edward D. Crandall

  Rogers (United States)

  233 shared

• Zea Borok

  University of California, San Diego

  138 shared

• Arnold Sipos

  University of Southern California

  86 shared

• Vincent H.L. Lee

  67 shared

• Yong Ho Kim

  42 shared

• Young–Jin Son

  Sunchon National University

  33 shared

• Carsten Ehrhardt

  Trinity College Dublin

  32 shared

• Per Flodby

  Hastings Center

  30 shared

Labs

• Health Equity LabPI

Education

• Other, Physical Therapy

  University of Southern California

• Other, Physical Therapy

  University of Southern California