Associate Professor of Dermatology, Associate Professor of Orthopaedic Surgery, Johns Hopkins University School of Medicine
Dermatology
Dr. Lloyd S. Miller, MD
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Lloyd Miller works in the field of Dermatology. He attended State University of New York Downstate Medical Center College of Medicine. He received 2 awards: "CMS Meaningful Use Stage 1 Certification" and "Fellow (FAAD)". Lloyd Miller is also a published physician. He has 34 publication published. The most recent publication is: Nonredundant Roles of Interleukin-17A (IL-17A) and IL-22 in Murine Host Defense against Cutaneous and Hematogenous Infection Due to Methicillin-Resistant Staphylococcu... He accepts Medicare.
Publications
- Nonredundant Roles of Interleukin-17A (IL-17A) and IL-22 in Murine Host Defense against Cutaneous and Hematogenous Infection Due to Methicillin-Resistant Staphylococcu...
- Combination Prophylactic Therapy with Rifampin Increases Efficacy against an Experimental Staphylococcus epidermidis Subcutaneous Implant-Related Infection.
- Vancomycin plus Rifampin Combination Therapy has Enhanced Efficacy Against an Experimental Staphylococcus aureus Prosthetic Joint Infection.
- Staphylococcus aureus recognition by hematopoietic stem and progenitor Cells via TLR2/MyD88/PGE2 stimulates granulopoiesis in wounds.
- In Vivo Bioluminescence Imaging to Evaluate Systemic and Topical Antibiotics against Community-Acquired Methicillin-Resistant Staphylococcus aureus-Infected Skin Wound...
- Neutrophil-derived IL-1β Is Sufficient for Abscess Formation in Immunity against Staphylococcus aureus in Mice.
- Monitoring Bacterial Burden, Inflammation and Bone Damage Longitudinally Using Optical and μCT Imaging in an Orthopaedic Implant Infection in Mice.
- Cutting Edge: Nitrogen Bisphosphonate-Induced Inflammation Is Dependent upon Mast Cells and IL-1.
- Coordinate regulation of neutrophil homeostasis by liver X receptors in mice.
- Host-pathogen interactions between the Skin and Staphylococcus aureus.
- Innate and adaptive immune responses against Staphylococcus aureus Skin infections.
- Mouse model of chronic post-arthroplasty Infection: Noninvasive in vivo bioluminescence imaging to monitor bacterial burden for long-term study.
- Immunity against Staphylococcus aureus cutaneous Infections.
- A MyD88-dependent IFNγR-CCR2 signaling circuit is required for mobilization of monocytes and host defense against systemic bacterial challenge.
- Noninvasive in vivo imaging to evaluate immune responses and antimicrobial therapy against Staphylococcus aureus and USA300 MRSA Skin infections.
- Protective role of IL-1β against post-arthroplasty Staphylococcus aureus Infection.
- Neutrophil survival and c-kit(+)-progenitor proliferation in Staphylococcus aureus-infected Skin wounds promote resolution.
- Lucky number seven: RNase 7 can prevent Staphylococcus aureus Skin colonization.
- The role of the transcription factor CREB in immune function.
- IL-23 and IL-17A, but not IL-12 and IL-22, are required for optimal Skin host defense against Candida albicans.
- IL-17 is essential for host defense against cutaneous Staphylococcus aureus Infection in mice.
- A mouse model of post-arthroplasty Staphylococcus aureus joint Infection to evaluate in vivo the efficacy of antimicrobial implant coatings.
- A critical role for hemolysins and bacterial lipoproteins in Staphylococcus aureus-induced activation of the Nlrp3 inflammasome.
- Downstream signals for MyD88-mediated phagocytosis of Borrelia burgdorferi can be initiated by TRIF and are dependent on PI3K.
- Immunological mechanisms underlying the genetic predisposition to severe Staphylococcus aureus Infection in the mouse model.
- Dynamics of neutrophil infiltration during cutaneous wound healing and Infection using fluorescence imaging.
- Toll-like receptors in Skin.
- Inflammasome-mediated production of IL-1beta is required for neutrophil recruitment against Staphylococcus aureus in vivo.
- Human keratinocyte Toll-like receptors promote distinct immune responses.
- MyD88 mediates neutrophil recruitment initiated by IL-1R but not TLR2 activation in immunity against Staphylococcus aureus.
- TGF-alpha regulates TLR expression and function on epidermal keratinocytes.
- Induction of secreted human immunodeficiency virus type 1 (HIV-1) resistance factors in CD4-positive T lymphocytes by attenuated HIV-1 Infection.
- Toll-like receptors in the Skin.
Schools
SUNY Downstate Medical Center College Of Medicine
St Lukes Roosevelt Hospital Center
University Of California Los Angeles
Procedures Preformed
- Destruction of Benign Skin Lesion
Conditions Treated
- Actinic Keratosis
- Athlete's Foot
- Atopic Dermatitis (Eczema)
- Basal Cell Carcinoma
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Doctors Specialties
- Dermatology
Accepted Insurances
Awards
- CMS Meaningful Use Stage 1 Certification
- Fellow (FAAD)
Education
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UCLA Medical Center -
St Luke's-Roosevelt Hospital Center -
State University of New York Downstate Medical Center College of Medicine
Hospital
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Johns Hopkins Bayview Medical Center -
Johns Hopkins Hospital -
Ronald Reagan UCLA Medical Center -
Santa Monica-UCLA Medical Center and Orthopaedic Hospital
Drug Facts
| NPI NUMBER | 1952379513 | |
| NPPES Provider LastName | MILLER | |
| NPPES Provider FirstName | LLOYD | |
| NPPES Provider ZIPCode | 900953075 | |
| NPPES Provider State | CA | |
| Specialty Description | Dermatology | |
| Total Claim Count | 65.0 | |
| Distinct Opioid Count | 0.0 | |
| Opioid Claim Count | 0.0 | |
| Percent Opioid Claims | 0.0 |
Helpful Reviews
Medicare Facts
| National Provider Identifier [NPI] | 1952379513 |
| Last Name Of The Provider | MILLER |
| First Name Of The Provider | LLOYD |
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