/filters:quality(90)/prod01/production-cdn-pxl/media/umassdartmouth/profiles/engineering/Lamya-Karim.jpg?text=945+WebP)
Lamya Karim, PhD
Associate Professor
Bioengineering
Contact
508-999-8560
poevmqDyqewwh2ihy
Textiles 214
Education
| 2011 | Rensselaer Polytechnic Institute |
| Stony Brook University | BE |
Teaching
- Biomechanics
- Mechanobiology
- Biomedical Devices
Teaching
Programs
Programs
- Bioengineering BS, BS/MS
- Biomedical Engineering
- Biomedical Engineering and Biotechnology MS, PhD
- Engineering and Applied Science PhD
Teaching
Online and Continuing Education Courses
Construction and functional principles of medical devices. An array of medical devices and implants will be reverse engineered to reveal their basic design, construction and operating principle. The final project will be to develop your own design for a device or implant.
Register for this course.
Discussion of the laws and regulations applied to medical products development, manufacturing, testing, marketing, and post-marketing surveillance. This course provides an overview of regulatory affairs related to biomedical devices and a foundation to understand the differences in regulations between countries with a focus on the US FDA requirements. This course also teaches risk management about medical products.
Register for this course.
Research
Research awards
- $ 2,577 awarded by Montana State University for AGE Assessment for Germ Free Study
Research
Research interests
- Biomechanics
- Mechanobiology
- Orthopedics
- Skeletal aging & osteoporosis
- Skeletal aging & osteoporosis
Skeletal fragility in patients with type 2 diabetes is a growing public health issue. The prevalence of diabetes is increasing rapidly, and diabetics have three times greater fracture risk compared to non-diabetics. The causes of diabetic skeletal fragility are not well established, which makes it difficult for clinicians to make decisions regarding fracture prevention in this population. Numerous micro-scale changes may contribute to skeletal health issues in these patients. For instance, changes in bone matrix composition due to accumulation of non-enzymatic chemical crosslinks can lead to poor bone quality and in turn deteriorate bone’s mechanical integrity. These crosslinks can also lead to an increase in the formation of micro-scale damage within bone. Further, some patients have altered bone microarchitecture that could contribute to their increased fracture risk, and these microarchitectural changes may result from altered bone cell behavior. Thus, we aim to investigate the biomolecular and cellular mechanisms of skeletal fragility in diabetes and other major clinical conditions. The ultimate goal of our research is to help improve diagnostic methods for fracture risk assessment and clinical management of patients at risk for fracture.