To investigate the effects of acute cold stress (ACS) on chicken heart after cold stimulation, female broilers were raised in either normal (C) or gradually decreasing temperatures (CS I and CS II) for 34 days followed by a 24 h ACS at 7°C. Cardiac tissues were collected from the pre-ACS and ACS time points to analyze the histopathological changes, antioxidant status and the expression of heat shock proteins, inflammatory factors and immune-related cytokines. The CS II heart tissues showed shrunken cell membranes and nuclei, disordered or ruptured myocardial fibers, higher MDA content and upregulation in HSP27, HSP40, HSP70, NF-κB, COX-2, PTGEs, iNOS, TNF-α and IL-4 mRNAs, and in protein levels of HSP40, NF-κB and iNOS and reduction in CAT, GSH-px and SOD activity, as well as HSP90 and IFN-γ levels compared to the control tissues before ACS. In contrast, the HSPs were significantly increased, and the inflammatory and immune related factors were unaltered prior to the ACS in the CS I compared to the C group. Following ACS, MDA content was significantly increased and antioxidant activity was significantly decreased in the CS I and CS II groups compared to the C group. The levels of HSP27, HSP70, HSP90, inflammatory factors and IL-4 were significantly reduced and that of IFN-γ was significantly increased in CS I broiler hearts; the reverse trends were seen in CS II relative to CS I. Compared to the pre-ACS levels, that of HSP27, HSP40, HSP60, inflammatory factors and IL-4 were increased and IFN-γ was decreased in the C and CS II groups after ACS. Therefore, cold stimulation at drastically lower temperatures induced cardiac damage, which was further aggravated by ACS. In contrast, cold stimulation at only 3°C lower than normal temperature improved the adaptability of the broilers to ACS.

Background: S100A7 is a secreted protein and its overexpression has been previously associated with carcinogenesis of certain cancers. This study was undertaken to investigate the possibility that overexpression of S100A7 protein might be detected in the sera of patients with lung cancer. Methods: RNA and protein levels of S100A7 were examined in 60 pairs of frozen lung cancer tissues by RT-PCR and western blot. The specific expression of this protein and its cellular distribution were investigated in 145 paraffin embedded lung cancer samples, six benign lung disease and 21 normal lung tissues by immunohistochemistry. The S100A7 protein level was further analysed in serum from 112 patients with lung cancer, 20 with benign lung diseases and 31 healthy individuals by ELISA. Results: Specific expression of both S100A7 mRNA and protein was found in squamous cell carcinomas, adenosquamous carcinomas and large cell lung carcinomas, whereas neither was detected in adenocarcinomas or paired non-cancerous lung tissues. Further immunohistochemical analysis identified positive staining of S100A7 only in squamous cell carcinomas and large cell lung carcinomas, but not in other subtypes of lung cancer and normal lung tissues. Weak expression was also found in the inflammatory cells of benign lung diseases. Our most important finding is that elevated S100A7 protein could be detected in the sera of patients with squamous cell carcinomas. Conclusion: S100A7 was only expressed in squamous cell carcinomas and large cell lung carcinomas and an increase in the level of S100A7 protein in serum may serve as a potential marker for lung cancer diagnosis.

Acclimation can alleviate the damage caused by adverse environmental factors. To investigate the effects of cold stimulation on immunity in tracheal of broilers, 360 one-day-old chicks were raised at normal temperatures during 1-7 days. From 8 day, G1 (control) continued to be raised at normal temperatures, whereas G2 and G3 (treatment groups) were cold-stimulated at 3°C and 12°C below the temperature of G1, respectively. At 42 day, all the groups were subjected to a 24-hr acute cold stress, designated as S1, S2, and S3. Tracheal tissues were collected to detect gene levels of immunoglobulins, antimicrobial peptides, Hsps, and cytokines, and oxidative stressrelated indicators at 14 day, 42 day, and 43 day, and protein levels of Hsps and proinflammatory cytokines as well as morphology changes at 42 day and 43 day. The results showed that, compared with 42G1, tracheal structure of 42G2 was basically intact, and gene levels of immunoglobulins and antimicrobial peptides increased (p < 0.05), whereas tracheal structure of 42G3 was destroyed, with decreased levels of immunoglobulins (p < 0.05), and increased levels of Hsps and proinflammatory cytokines (p < 0.05). At 43 day, tracheal damage was visible and gene levels of immunoglobulins and antimicrobial peptides decreased in S1 (p < 0.05). Tracheal structure was relatively intact and gene levels of antimicrobial peptides increased in S2 (p < 0.05). Compared with S1 and S3, immune-related gene levels in S2 were higher, and Hsps and proinflammatory cytokines levels were lower. The results demonstrate that cold stimulation of lower 3°C from 8 to 42 day led to cold acclimation, which improved immunity of tracheal mucosa and resistance to cold stress in broilers.

Mastitis is characterized by an inflammation of the mammary gland of dairy animals and humans; this condition is one of the major causes of economic losses in dairy industries. Selenium (Se), a biological trace element, modulates the functions of many regulatory proteins in signal transduction and provides advantages for animals with inflammatory diseases, including mastitis. The current study aimed to assess the protective effects and the active mechanism of Na(2)SeO(3) against lipopolysaccharide (LPS)-induced inflammation in mouse mammary epithelial cells (MMECs). Our results showed that LPS-induced expressions of cyclooxygenase-2 and tumor necrosis factor-α significantly decreased after Se was supplemented to Se-deficient MMECs. Na(2)SeO(3) also suppressed LPS-induced nuclear factor-κB activation, inhibitory kappa B degradation, and ERK, JNK, and P38 phosphorylation in a dose-dependent manner. These results suggested that Se functions as an anti-inflammatory agent in mastitis.