1. Chang, H.M., Lin, H.C., Cheng, H.L., Liao, C.K., Tseng, T.J., Renn, T.Y., Lan, C.T. and Chen, L.Y.* (2021) Melatonin successfully rescues the hippocampal molecular machinery and enhances anti-oxidative activity following early-life sleep deprivation injury. Antioxidants 10: 774.
2. Renn, T.Y., Yang, C.P., Wu, U.I., Chen, L.Y., Mai, F.D., Tikhonova, M.A., Amstislavskaya, T.G., Liao, W.C., Lin, C.T., Liu, Y.C.* and Chang, H.M.* (2022) Water composed of reduced hydrogen bonds activated by localized surface plasmon resonance effectively enhances anti-viral and anti-oxidative activities of melatonin. Chemical Engineering Journal 427: 131626.
3. Chen, Y.T., Chen, L.Y., Renn, T.Y., Cheng, M.S., Wang, C.T., Klimenkov, I.V., Sudakov, N.P., Liao, W.C., Chen, Y.J. and Chang, H.M.* (2022) Olfactory stimulation successfully improves swallowing function of aged rats through activating orbitofronto-medullary networks and enhancing DHPR-RyR-mediated neuromuscular activities. Journals of Gerontology – Biological Sciences 77: 235-242.
4. Liao, W.C., Yao, R.A., Chen, L.Y., Renn, T.Y., Klimenkov, I.V., Sudakov, N.P., Mai, F.D., Chen, Y.T.* and Chang, H.M.* (2022) Olfactory stimulation successfully modulates the neurochemical, biochemical, and behavioral phenotypes of the visceral pain. Molecules 27: 7659.
5. Ishida, E., Furusho, H., Renn, T.Y., Shiba, F., Chang, H.M., Oue, H., Terayama, R., Ago, Y., Tsuga, K. and Miyauchi, M.* (2023) Mouse maternal odontogenic infection with Porphyromonas gingivalis induces cognitive decline in offspring. Frontiers in Pediatrics 11: 1203894.
6. Wen, C.C., Lin, J.C.Y., Salamanca, E., Teng, N.C., Lin, Y.J., Wu, Y.F.*, Chang, H.M.* and Chang, W.J.* (2025) Full-length 16S rRNA sequencing reveals microbial characteristics in supragingival plaque of periodontitis patients. Journal of Dental Sciences 20: 1739-1748.
7. Chang, H.M., Lin, H.C., Renn, T.Y., Liu, Y.C., Yen, K.J., Liao, C.K., Tikhonova, M.A., Amstislavskaya, T.G., Singh, S.K. and Chen, L.Y.* (2026) Manifold hepatoprotective actions of -lipoic acid on metabolic function through redox regulation, inflammatory modulation, and anti-apoptosis after chronic sleep-deprived injury. Frontiers in Nutrition 12: 1679494.
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| Developmental origins of health and disease (DOHaD) is a well-established framework proposing that environmental factors during early-life, such as chronic sleep deprivation (CSD), can permanently influence individual’s long-term health and vulnerability to chronic diseases. However, the transgenerational impact of parental early-life sleep history on the offspring remains poorly understood. Moreover, whether parental CSD would exert sex-specific, divergent programming effects on offspring health still remains largely unknown. This study aims to delineate the transgenerational consequences of maternal and paternal CSD on musculoskeletal, neuro-cognitive, and metabolic development of the offspring. Weaning male and female rats were subjected to three weeks of CSD (PPD 21-42 days). Following recovery, rats were mated, and their offspring were evaluated at adulthood. Multidisciplinary approaches including spectrometric, ultrastructural, biochemical, immunohistochemical, bioenergetic, and behavioral methodologies were used to detect the calcium intensity, protein expression, cellular bioenergetics, oxidative stress level, osteo-microarchitecture, and cognitive/metabolic function of the hippocampus, liver, and femoral bone, respectively. Maternal CSD significantly compromised offspring neuro-cognitive and metabolic function, evidenced by reduced hippocampal calcium and pCREB expression, exhibit anxiolytic-like behavior in elevated plus-maze test, increased hepatic stress protein, impaired serum metabolic profiles, alongside elevated hippocampal and hepatic malondialdehyde level and decreased bio-energetic markers (cytochrome oxidase, Na+/K+ ATPase). Conversely, paternal CSD specifically resulted in reduced bone mineral density and disrupted trabecular microarchitecture of the femoral bone. These findings demonstrate a sex-specific dichotomy in developmental programming of the offspring. Maternal CSD programs “software” deficits in neuro-cognitive and metabolic function, while paternal CSD impairs “hardware” musculoskeletal integrity. |