Donald R. Mattison – författare

The cause of many of the adverse reproductive outcomes and developmental diseases among offspring is not well understood. Most of the epidemiologic and experimental animal research has focused on the relationship between maternal exposures including medications, tobacco smoke, alcohol, infections, and occupation and the occurrence of spontaneous abortion, low birth weight, and birth defects. The potential role of paternal exposures has not been investigated as extensively despite long-standing animal research that demonstrates the induction of mutations in the male germ cell after exposure to certain agents and subsequent reproductive failure or early pregnancy loss. Given this relative lack of interest, acquisition of epidemiologic data and the development of a definitive model or mechanism for potential male-mediated effects has been hindered. However, recent laboratory and epidemiologic investigations have suggested that paternal exposures may be more important than previously suspected. This topic has been termed by some as "male-mediated developmental toxicity. " This is meant to refer to the effects of exposures and other factors relating to the male parent that result in toxicity to the conceptus and abnormal development. The developmental endpoints of interest can include fetal loss, congenital abnormalities, growth retardation, cancer, and neurobehavioral effects. These effects may operate through a variety of mechanisms including gene mutation, chromosomal aberrations, seminal fluid transfer of toxicants and epigenetic events.

Each year in the United States approximately 440,000 babies are born premature. These infants are at greater risk of death, and are more likely to suffer lifelong medical complications than full-term infants. Clinicians and researchers have made vast improvements in treating preterm birth; however, little success has been attained in understanding and preventing preterm birth. Understanding the complexity of interactions underlying preterm birth will be needed if further gains in outcomes are expected.

The Institute of Medicine''s Roundtable on Environmental Health Sciences, Research, and Medicine sponsored a workshop to understand the biological mechanism of normal labor and delivery, and how environmental influences, as broadly defined, can interact with the processes of normal pregnancy to result in preterm birth. This report is a summary of the main themes presented by the speakers and participants.

Each year in the United States approximately 440,000 babies are born premature. These infants are at greater risk of death, and are more likely to suffer lifelong medical complications than full-term infants. Clinicians and researchers have made vast improvements in treating preterm birth; however, little success has been attained in understanding and preventing preterm birth. Understanding the complexity of interactions underlying preterm birth will be needed if further gains in outcomes are expected.

The Institute of Medicine''s Roundtable on Environmental Health Sciences, Research, and Medicine sponsored a workshop to understand the biological mechanism of normal labor and delivery, and how environmental influences, as broadly defined, can interact with the processes of normal pregnancy to result in preterm birth. This report is a summary of the main themes presented by the speakers and participants.

The U.S. Food and Drug Administration (FDA) has approved dozens of hormone therapy products for men and women, including estrogen, progesterone, testosterone, and related compounds. These products have been reviewed for safety and efficacy and are indicated for treatment of symptoms resulting from hormonal changes associated with menopause or other endocrine-based disorders. In recent decades, an increasing number of health care providers and patients have turned to custom-formulated, or compounded, drug preparations as an alternative to FDA-approved drug products for hormone-related health concerns. These compounded hormone preparations are often marketed as "bioidentical" or "natural" and are commonly referred to as compounded bioidentical hormone therapy (cBHT).

In light of the fast-growing popularity of cBHT preparations, the clinical utility of these compounded preparations is a substantial public health concern for various stakeholders, including medical practitioners, patients, health advocacy organizations, and federal and state public health agencies. This report examines the clinical utility and uses of cBHT drug preparations and reviews the available evidence that would support marketing claims of the safety and effectiveness of cBHT preparations. It also assesses whether the available evidence suggests that these preparations have clinical utility and safety profiles warranting their clinical use and identifies patient populations that might benefit from cBHT preparations in lieu of FDA-approved BHT.

Building from the perspective of reproductive and developmental biology, Computational Methods for Reproductive and Developmental Toxicology provides a timely and comprehensive overview of approaches in reproductive and developmental toxicology.The book, which is part of the QSAR in Environmental and Health Sciences series, is divided into three broad sections. The first provides a review of methods and approaches to meet the need for safety assessments in product development and regulatory approaches for environmental chemicals. The next one reviews the biological processes and endpoints involved in reproduction and development. The final and largest section summarizes protocols for evaluating biological processes and endpoints within reproduction and development. It also discusses informatics resources and computational methods. The book takes a cross-disciplinary approach bringing together developmental, reproductive and systems biology, chemistry, toxicology, pharmacology, biostatistics, information sciences, bioinformatics, and computational approaches. This valuable resource provides those in the field with the necessary knowledge to evaluate both classic and recent approaches to characterize toxicity.

Building from the perspective of reproductive and developmental biology, Computational Methods for Reproductive and Developmental Toxicology provides a timely and comprehensive overview of approaches in reproductive and developmental toxicology.The book, which is part of the QSAR in Environmental and Health Sciences series, is divided into three br

Building from the perspective of reproductive and developmental biology, Computational Methods for Reproductive and Developmental Toxicology provides a timely and comprehensive overview of approaches in reproductive and developmental toxicology.The book, which is part of the QSAR in Environmental and Health Sciences series, is divided into three broad sections. The first provides a review of methods and approaches to meet the need for safety assessments in product development and regulatory approaches for environmental chemicals. The next one reviews the biological processes and endpoints involved in reproduction and development. The final and largest section summarizes protocols for evaluating biological processes and endpoints within reproduction and development. It also discusses informatics resources and computational methods. The book takes a cross-disciplinary approach bringing together developmental, reproductive and systems biology, chemistry, toxicology, pharmacology, biostatistics, information sciences, bioinformatics, and computational approaches. This valuable resource provides those in the field with the necessary knowledge to evaluate both classic and recent approaches to characterize toxicity.

Building from the perspective of reproductive and developmental biology, Computational Methods for Reproductive and Developmental Toxicology provides a timely and comprehensive overview of approaches in reproductive and developmental toxicology.The book, which is part of the QSAR in Environmental and Health Sciences series, is divided into three br

The cause of many of the adverse reproductive outcomes and developmental diseases among offspring is not well understood. Most of the epidemiologic and experimental animal research has focused on the relationship between maternal exposures including medications, tobacco smoke, alcohol, infections, and occupation and the occurrence of spontaneous abortion, low birth weight, and birth defects. The potential role of paternal exposures has not been investigated as extensively despite long-standing animal research that demonstrates the induction of mutations in the male germ cell after exposure to certain agents and subsequent reproductive failure or early pregnancy loss. Given this relative lack of interest, acquisition of epidemiologic data and the development of a definitive model or mechanism for potential male-mediated effects has been hindered. However, recent laboratory and epidemiologic investigations have suggested that paternal exposures may be more important than previously suspected. This topic has been termed by some as "male-mediated developmental toxicity. " This is meant to refer to the effects of exposures and other factors relating to the male parent that result in toxicity to the conceptus and abnormal development. The developmental endpoints of interest can include fetal loss, congenital abnormalities, growth retardation, cancer, and neurobehavioral effects. These effects may operate through a variety of mechanisms including gene mutation, chromosomal aberrations, seminal fluid transfer of toxicants and epigenetic events.

The cause of many of the adverse reproductive outcomes and developmental diseases among offspring is not well understood. Most of the epidemiologic and experimental animal research has focused on the relationship between maternal exposures including medications, tobacco smoke, alcohol, infections, and occupation and the occurrence of spontaneous abortion, low birth weight, and birth defects. The potential role of paternal exposures has not been investigated as extensively despite long-standing animal research that demonstrates the induction of mutations in the male germ cell after exposure to certain agents and subsequent reproductive failure or early pregnancy loss. Given this relative lack of interest, acquisition of epidemiologic data and the development of a definitive model or mechanism for potential male-mediated effects has been hindered. However, recent laboratory and epidemiologic investigations have suggested that paternal exposures may be more important than previously suspected. This topic has been termed by some as "male-mediated developmental toxicity. " This is meant to refer to the effects of exposures and other factors relating to the male parent that result in toxicity to the conceptus and abnormal development. The developmental endpoints of interest can include fetal loss, congenital abnormalities, growth retardation, cancer, and neurobehavioral effects. These effects may operate through a variety of mechanisms including gene mutation, chromosomal aberrations, seminal fluid transfer of toxicants and epigenetic events.

Each year in the United States approximately 440,000 babies are born premature. These infants are at greater risk of death, and are more likely to suffer lifelong medical complications than full-term infants. Clinicians and researchers have made vast improvements in treating preterm birth; however, little success has been attained in understanding and preventing preterm birth. Understanding the complexity of interactions underlying preterm birth will be needed if further gains in outcomes are expected. The Institute of Medicinea (TM)s Roundtable on Environmental Health Sciences, Research, and Medicine sponsored a workshop to understand the biological mechanism of normal labor and delivery, and how environmental influences, as broadly defined, can interact with the processes of normal pregnancy to result in preterm birth. This report is a summary of the main themes presented by the speakers and participants.