The ability to control the alignment and organization of cell populations has great potential for tissue engineering and regenerative medicine. A variety of approaches such as nano/microtopographical patterning, mechanical loading, and nanocomposite synthesis have been developed to engineer scaffolds able to control cellular properties and behaviors. In this work, a patterned liquid crystal polymer network (LCN) film is synthesized by using a nematic liquid crystal template in which the molecular orientations are predesigned by photopatterning technique. Various configurations of polymer networks such as linear and circular patterns are created. When neural tumor cells are plated onto the templated LCN films, the cell alignment, migration, and proliferation are directed in both linear and curvilinear fashions following the pattern of the aligned polymer chains. A complex LCN pattern with zigzag geometry is also fabricated and found to be capable of controlling cell alignment and collective cellular organization. The demonstrated control of cell dynamics and organization by LCN films with various molecular alignments opens new opportunities to design scaffolds to control cultured cell organization in a manner resembling that found in tissues and to develop novel advanced materials for nerve repair, tissue engineering, and regenerative medicine applications.
Induction of lactation was attempted in 12 heifers and 12 cows with estradiol benzoate (.011 mg/kg body weight per day) subcutaneous for 10 days or that plus progesterone (.1 mg + .25 mg/kg body weight per day) for 7 days. Milking commenced on day 20 for those treated with the mixture and on day 11 for the others. Lactations were induced (minimum of 4.5 kg of milk/day) in five of six heifers and two of six cows by the mixture and in six of six heifers and three of six cows for estradiol benzoate. Milk production was 44% of herdmates in the 16 induced lactations. Cows on the single treatment had lower production than the other three groups. Ovarian status, cycling, cystic, or static, was affected adversely in 5 of 16 animals induced successfully. Two of the 16, both heifers, carried calves to term following induction. The transition to normal composition of milk was slower for single than double treatment. Lactose increased slowly to normal over the 1st wk of milking while protein decreased slowly. Estrogen and progesterone in milk of induced cows were approximately twice as concentrated as in normal postparturient cows, probably because milk production was halved.
Albino mice were used to test the effect of simultaneous pregnancy on lactation in successive lactations. Weights of litters were used to estimate lactational performance by standardizing litters at eight pups on day 1 postpartum and weighing pups immediately after a normal nursing period on days 10, 14 and 20 of lactation. Eight dams were used in each of two treatments:lactating-nonpregnant and lactating-pregnant. Dams were sibling pairs for each treatment to reduce variation. Dams that were simultaneously pregnant and lactating had heavier litters on day 20 of the first lactation and on days 14 and 20 of the second lactation as compared to their lactating-nonpregnant siblings. The results imply that pregnancy provides a stimulus to concurrent and sucessive lactation in the mouse. This may be due to the effect of placental hormones on delaying mammary involution or on maintaining high milk synthesis past day 10 of lactation.
To determine the cutaneous effects of in utero and lactational exposure to the AHR ligand 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), pregnant C57BL/6J mice were exposed by gavage to a vehicle or 5 μg TCDD/kg body weight at embryonic day 12 and epidermal barrier formation and function were studied in their offspring from postnatal day 1 (P1) through adulthood. TCDD-exposed pups were born with acanthosis. This effect was AHR-dependent and subsided by P6 with no evidence of subsequent inflammatory dermatitis. The challenge of adult mice with MC903 showed similar inflammatory responses in control and treated animals, indicating no long-term immunosuppression to this chemical. Chloracne-like sebaceous gland hypoplasia and cyst formation were observed in TCDD-exposed P21 mice, with concomitant microbiome dysbiosis. These effects were reversed by P35. CYP1A1 and CYP1B1 expression in the skin was increased in the exposed mice until P21, then declined. Both CYP proteins co-localized with LRIG1-expressing progenitor cells at the infundibulum. CYP1B1 protein also co-localized with a second stem cell niche in the isthmus. These results indicate that this exposure to TCDD causes a chloracne-like effect without inflammation. Transient activation of the AhR, due to the shorter half-life of TCDD in mice, likely contributes to the reversibility of these effects.
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