Interactions between Social Hierarchy and Some Udder Morphometric Traits upon Colostrum and Milk Physicochemical Characteristics in Crossbred Dairy Goats

The possible relationship between udder morphometric variables (UMVs), chemical quality (CHQ) of both colostrum (CA), and milk (MK), as affected by goat’s social rank (SR) (i.e., low-LSR, or high-HSR), was assessed. In late June, goats (Alpine–Saanen–Nubian x Criollo; n = 38; 25◦ N) were estrus-synchronized and subjected to a fixed-time artificial insemination protocol. Thereafter, in October, while a behavioral study was performed in confirmed-pregnant goats to define the SR classes (n = 15), live weight (LW), body condition (BCS), and serum glucose (GLUC) were registered on the last day of the behavioral study. The expected kidding date was 25 November. Both the UMVs (i.e., seven dates) and the CHQ (i.e., either one for CA and three times for MK) were collected across time (T). The UMVs involved udder perimeter (UDPER, cm), udder diameter (UDDIA, cm), left-teat (LTPER, cm) and right-teat perimeter (RTPER, cm), left-teat (LTLT, cm) and right-teat length (RTLT, cm), left-teat diameter (LTDIA, cm) and right-teat diameter (RTDIA, cm), and medium suspensory ligament (MSL, cm). The registered CHQ variables for both CA and MK were fat (FAT), protein (PRO), lactose (LAC), nonfat solids (NFS), freezing point (FP), and total solids (TS). The possible effect of SR, T, and the SR × T interaction upon the described response variables was tested. While LW favored the HSR goats (54.6 vs. 48.2 ± 1.7 kg; p 0.05) between SR. An SR × T interaction affected (p FAT, > PRO, and > NFS) during early lactation. Therefore, both social rank (i.e., HSR goats), as well as the temporal transition stage from the last third of pregnancy to the first phase of lactation (i.e., time), operated as important modulators upon both udder architecture and milk quality in crossbred dairy goats under a dry-semiarid production system

Anti-IgE IgG autoantibodies isolated from therapeutic normal IgG intravenous immunoglobulin induce basophil activation

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Chronic Proliferative Dermatitis in Sharpin Null Mice: Development of an Autoinflammatory Disease in the Absence of B and T Lymphocytes and IL4/IL13 Signaling.

SHARPIN is a key regulator of NFKB and integrin signaling. Mice lacking Sharpin develop a phenotype known as chronic proliferative dermatitis (CPDM), typified by progressive epidermal hyperplasia, apoptosis of keratinocytes, cutaneous and systemic eosinophilic inflammation, and hypoplasia of secondary lymphoid organs. Rag1−/− mice, which lack mature B and T cells, were crossed with Sharpin−/− mice to examine the role of lymphocytes in CDPM. Although inflammation in the lungs, liver, and joints was reduced in these double mutant mice, dermatitis was not reduced in the absence of functional lymphocytes, suggesting that lymphocytes are not primary drivers of the inflammation in the skin. Type 2 cytokine expression is increased in CPDM. In an attempt to reduce this aspect of the phenotype, Il4ra−/− mice, unresponsive to both IL4 and IL13, were crossed with Sharpin−/− mice. Double homozygous Sharpin−/−, Il4ra−/−mice developed an exacerbated granulocytic dermatitis, acute system inflammation, as well as hepatic necrosis and mineralization. High expression of CHI3L4, normally seen in CPDM skin, was abolished in Sharpin−/−, Il4ra−/− double mutant mice indicating the crucial role of IL4 and IL13 in the expression of this protein. Cutaneous eosinophilia persisted in Sharpin−/−, Il4ra−/−mice, although expression of Il5 mRNA was reduced and the expression of Ccl11 and Ccl24was completely abolished. TSLP and IL33 were both increased in the skin of Sharpin−/− mice and this was maintained in Sharpin−/−, Il4ra−/− mice suggesting a role for TSLP and IL33 in the eosinophilic dermatitis in SHARPIN-deficient mice. These studies indicate that cutaneous inflammation in SHARPIN-deficient mice is autoinflammatory in nature developing independently of B and T lymphocytes, while the systemic inflammation seen in CPDM has a strong lymphocyte-dependent component. Both the cutaneous and systemic inflammation is enhanced by loss of IL4 and IL13 signaling indicating that these cytokines normally play an anti-inflammatory role in SHARPIN-deficient mice