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Skin in the diapered area is continuously threatened by exposure to changes in pH levels, overhydration, mechanical friction, and fecal enzymes, making diaper rash a common occurrence among babies. Up to one third of infants may exhibit clinical symptoms of diaper rash at any time, and more than half of babies between the ages of 4 and 15 months develop diaper rash at least once in a 2-month period. Despite misperceptions that disposable diapers are related to an increase in diaper rash, the incidence of diaper dermatitis is on the decline, largely due to significant improvements in disposable diaper construction and materials. Modern-day disposable diapers are specifically designed to limit exposure to irritants in the diaper area, reduce overhydration, inhibit skin barrier compromise, and help maintain normal skin pH levels and have been thoroughly evaluated for safety and skin compatibility.

Disposable diapers are primarily composed of polymers, such as cellulose, polypropylene, polyester, and polyethylene, which are biologically inert and not bioavailable. They are used in clothes, fabrics, personal hygiene products, and other materials that are commonly in contact with the skin. Each component used throughout the production process must undergo rigorous safety evaluations and assessments and are proven to be well tolerated and safe for their intended uses. No materials are incorporated into a diaper until their safety is confirmed through robust assessments, and additional factors are integrated into the process to compensate for the uncertainty associated with extrapolating toxicity data. After a thorough assessment of the materials and final product, extensive skin compatibility evaluations are conducted as appropriate. This rigorous safety process provides reassurance that consumers can rely on the safety of these diapers.

The developing nervous system is particularly vulnerable to vitamin A deficiency. Retinoid has been proposed to be a posteriorizing factor during hindbrain development, although direct evidence in the mammalian embryo is lacking. In the present study, pregnant vitamin A-deficient (VAD) rats were fed purified diets containing varying levels of all-trans-retinoic acid (atRA; 0, 0.5, 1.5, 6, 12, 25, 50, 125, or 250 microg/g diet) or were supplemented with retinol. Hindbrain development was studied from embryonic day 10 to 12.5 ( approximately 6 to 40 somites). Normal morphogenesis was observed in all embryos from groups fed 250 microg atRA/g diet or retinol. The most caudal region of the hindbrain was the most sensitive to retinoid insufficiency, as evidenced by a loss of the hypoglossal nerve (cranial nerve XII) in embryos from the 125 microg atRA/g diet group. Further reduction of atRA to 50 microg/g diet led to the loss of cranial nerves IX, X, XI, and XII and associated sensory ganglia IX and X in all embryos as well as the loss of hindbrain segmentation caudal to the rhombomere (r) 3/4 border in a subset of embryos. Dysmorphic orthotopic otic vesicles or immature otic-like vesicles in both orthotopic and caudally ectopic locations were also observed. As the level of atRA was reduced, a loss of caudal hindbrain segmentation was observed in all embryos and the incidence of otic vesicle abnormalities increased. Perturbations in hindbrain segmentation, cranial nerve formation, and otic vesicle development were associated with abnormal patterning of the posterior hindbrain. Embryos from VAD dams fed between 0.5 and 50 microg atRA/g diet exhibited Hoxb-1 protein expression along the entire neural tube caudal to the r3/r4 border at a time when it should be restricted to r4. Krox-20 protein expression was expanded in r3 but absent or reduced in presumptive r5. Hoxd-4 mRNA expression was absent in the posterior hindbrain, and the rostral limit of Hoxb-5 protein expression in the neural tube was anteriorized, suggesting that the most posterior hindbrain region (r7/r8) had been deleted and/or improperly patterned. Thus, when limiting amounts of atRA are provided to VAD dams, the caudal portion of the hindbrain is shortened and possesses r4/r5-like characteristics, with this region finally exhibiting r4-like gene expression when retinoid is restricted even more severely. Thus, regions of the anterior hindbrain (i.e., r3 and r4) appear to be greatly expanded, whereas the posterior hindbrain (r5-r8) is reduced or absent. This work shows that retinoid plays a critical role in patterning, segmentation, and neurogenesis of the caudal hindbrain and serves as an essential posteriorizing signal for this region of the central nervous system in the mammal.

Background Normal embryonic development and survival in utero is dependent on an adequate supply of vitamin A. Embryos from vitamin A-deficient (VAD) pregnant rats fed an inadequate amount of all-trans retinoic acid (atRA; 12 μg per g of diet or ∼230 μg per rat per day) exhibit severe developmental abnormalities of the anterior cardinal vein and hindbrain by embryonic day (E) 12.5 and die shortly thereafter. Methods In the present study, we sought to determine whether supplementation of VAD-RA supported (12 μg per g of diet) pregnant rats with retinol (ROL) at the late-gastrula (presomite or rat E9.5) or early somite stages (E10.5), or provision of higher levels of atRA throughout this period could prevent abnormalities in the developing cardiovascular and nervous systems. Results A newly described defect in the sinuatrial venus valve along with enlarged anterior cardinal veins and nervous system abnormalities and the later death of embryos are prevented by supplementing pregnant animals with ROL on the morning of E9.5. If ROL supplementation is delayed by 1 day (E10.5), most embryos are abnormal and die by E18.5. Supplementation of VAD rats with atRA (250 μg per g of diet) between E8.5 and E10.5 also prevents the cardiovascular and nervous system abnormalities and a significant number of these embryos survive to parturition. Thus, high levels of atRA can obviate the need for ROL between E9.5 and E10.5. Conclusions These results support an essential role for retinoid signaling between the late gastrula and early somite stages in the rat embryo for normal morphogenesis of the primitive heart tube and the posterior hindbrain. Further, these results suggest that embryonic death occurring at midgestation in the VAD rat may be linked to the abnormal development of one or both of these embryonic structures. Teratology 62:374–384, 2000. © 2000 Wiley-Liss, Inc.

Vitamin A is required for reproduction and normal embryonic development. We have determined that all- trans- retinoic acid (atRA) can support development of the mammalian embryo to parturition in vitamin A-deficient (VAD) rats. At embryonic day (E) 0.5, VAD dams were fed purified diets containing either 12 μg of atRA per g of diet (230 μg per rat per day) or 250 μg of atRA per g of diet (4.5 mg per rat per day) or were fed the purified diet supplemented with a source of retinol (100 units of retinyl palmitate per day). An additional group was fed both 250 μg of atRA per g of diet in combination with retinyl palmitate. Embryonic survival to E12.5 was similar for all groups. However, embryonic development in the group fed 12 μg of atRA per g of diet was grossly abnormal. The most notable defects were in the region of the hindbrain, which included a loss of posterior cranial nerves (IX, X, XI, and XII) and postotic pharyngeal arches as well as the presence of ectopic otic vesicles and a swollen anterior cardinal vein. All embryonic abnormalities at E12.5 were prevented by feeding pharmacological amounts of atRA (250 μg/g diet) or by supplementation with retinyl palmitate. Embryos from VAD dams receiving 12 μg of atRA per g of diet were resorbed by E18.5, whereas those in the group fed 250 μg of atRA per g of diet survived to parturition but died shortly thereafter. Equivalent results were obtained by using commercial grade atRA or atRA that had been purified to eliminate any potential contamination by neutral retinoids, such as retinol. Thus, 250 μg of atRA per g of diet fed to VAD dams (≈4.5 mg per rat per day) can prevent the death of embryos at midgestation and prevents the early embryonic abnormalities that arise when VAD dams are fed insufficient amounts of atRA.

4,5 ABSTRACT. We used published accounts to describe the known statewide distribution of the lone star tick, Amblyomma americanum, in New Jersey and field surveys to characterize the geographical range of A. americanum and selected A. americanum-transmitted pathogens in Monmouth County, the hypothesized northern limit of the species distribution. Ticks were collected using standardized methods from 50 widely dispersed public access areas within 18 municipalities to produce estimates of relative abundance among sites. Collected A. americanum adults were stored at 280uC until processed for DNA extraction. Individual ticks were subjected to polymerase chain reaction analyses to detect the presence of Ehrlichia chaffeensis, E. ewingii, Rickettsia amblyommii, and Borrelia lonestari. The range of A. americanum was generally limited to the southern half of New Jersey. Within Monmouth County, we collected A. americanum from 9 of 18 municipalities (50%) and 24 (48%) of the surveyed properties. We found at least 1 pathogen at 17 (70.8%) sites located within 6 of 9 municipalities, while all 4 target pathogens were detected in 5 of those 6 (83.3%) municipalities. The geographical distribution of A. americanum and its associated pathogens appeared to be restricted to the southern portion of the county. Possible factors governing the distribution are discussed.

Vitamin A plays an essential role in vertebrate embryogenesis. In the present study, pregnant vitamin A-deficient (VAD) rats were maintained during early pregnancy on the short half-life vitamin A metabolite, all- trans retinoic acid (atRA), in an amount sufficient to support normal development to E10.5, with a higher level of atRA (250 μg atRA/g diet) provided from embryonic day (E) 8.5–10.5 to prevent mid-gestational resorption. When limiting amounts of atRA (1.5 or 12 μg/g diet) were provided after E10.5, a highly reproducible and penetrant state of late fetal vitamin A deficiency (late VAD) was induced in the organs of developing fetuses. In addition, late VAD fetuses displayed both anteriorization of cervical regions and novel posteriorization events at the thoracic and sacral levels of the skeleton, and showed sternal and pelvic malformations not previously observed in early VAD or genetic models. The expression of several Hox genes ( Hoxd3 and Hoxb4 ) was altered in late VAD embryos, with a reduction in Hoxd3 noted as early as 1 day after instituting deficiency. All late VAD-induced malformations were prevented by the addition of retinol starting at E10.5, whereas provision of a high level of atRA throughout pregnancy improved but could not completely rescue the development of all organ systems. This work defines a nutritional model in which vitamin A deficiency can be induced during fetal development, and reveals new functions for the vitamin in the development of the axial and appendicular skeleton.