Beef quality traits of heifer in comparison with steer, bull and cow at various feeding environments.

The present review has been focused largely on the sex type differences in beef quality among heifers, cows, steers and bulls in various feeding environments. Genetic groups, feeding systems and gender are the major factors that change carcass characteristics and fatty acid profiles of cattle. Studies identified that heifer beef has super characteristics in eating quality and a better healthy composition in fatty acids than steer, cow and bull. Diet influences the variation of fatty acid profile; particularly the level of polyunsaturated fatty acids (PUFA) interacts with breed and sex. Animals finished in pasture systems were reported to show better ratios of PUFA/ saturated fatty acids and n-6/n-3. Carcasses of roughage-fed beef are lighter and have less marbling and lower quality grades but have higher cutability than carcasses of grain-fed bulls. Heifers and cows are reported to deposit more fat than steers and bulls. Among males, lower production of testosterone by steers favors more fat thickness compared with bulls. Marbling greatly varies among cattle belonging to different sexes, and particularly, females have genetic makeup that efficiently controls deposition. The current review identified that heifers can be a premium beef brand, while steer beef currently take a large part of market share across the world.

Upregulation of Mer receptor tyrosine kinase signaling attenuated lipopolysaccharide-induced lung inflammation.

Mer receptor tyrosine kinase (Mer) signaling plays a central role in the intrinsic inhibition of the inflammatory response to Toll-like receptor activation. Previously, we found that lung Mer protein expression decreased after lipopolysaccharide (LPS) treatment due to enhanced Mer cleavage. The purpose of the present study was to examine whether pharmacologically restored membrane-bound Mer expression upregulates the Mer signaling pathways and suppresses lung inflammatory responses. Pretreatment with the ADAM17 (a disintegrin and metalloproteinase-17) inhibitor TAPI-0 (tumor necrosis factor alpha protease inhibitor-0) reduced LPS-induced production of soluble Mer protein in bronchoalveolar lavage (BAL) fluid, restored membrane-bound Mer expression, and increased Mer activation in alveolar macrophages and lungs after LPS treatment. TAPI-0 also enhanced Mer downstream signaling, including phosphorylation of protein kinase b, focal adhesion kinase, and signal transducer and activator of transcription 1. As expected from enhanced Mer signaling, TAPI-0 also augmented suppressor of cytokine signaling-1 and -3 mRNA and protein levels and inhibited nuclear factor κB activation at 4 and 24 hours after LPS treatment. TAPI-0 suppressed LPS-induced inflammatory cell accumulation, total protein level elevation in BAL fluid, and production of inflammatory mediators, including tumor necrosis factor-α, interleukin-1ß, and macrophage inflammatory protein-2. Additionally, the effects of TAPI-0 on the activation of Mer signaling and the production of inflammatory responses could be reversed by cotreatment with specific Mer-neutralizing antibody. Restored Mer protein expression by treatment with TAPI-0 efficiently prevents the inflammatory cascade during acute lung injury.

Inhibiting Mer receptor tyrosine kinase suppresses STAT1, SOCS1/3, and NF-κB activation and enhances inflammatory responses in lipopolysaccharide-induced acute lung injury.

Mer signaling participates in a novel inhibitory pathway in TLR activation. The purpose of the present study was to examine the role of Mer signaling in the down-regulation of TLR4 activation-driven immune responses in mice, i.t.-treated with LPS, using the specific Mer-blocking antibody. At 4 h and 24 h after LPS treatment, expression of Mer protein in alveolar macrophages and lung tissue decreased, sMer in BALF increased significantly, and Mer activation increased. Pretreatment with anti-Mer antibody did not influence the protein levels of Mer and sMer levels. Anti-Mer antibody significantly reduced LPS-induced Mer activation, phosphorylation of Akt and FAK, STAT1 activation, and expression of SOCS1 and -3. Anti-Mer antibody enhanced LPS-induced inflammatory responses, including activation of the NF-κB pathway; the production of TNF-α, IL-1ß, and MIP-2 and MMP-9 activity; and accumulation of inflammatory cells and the total protein levels in BALF. These results indicate that Mer plays as an intrinsic feedback inhibitor of the TLR4- and inflammatory mediator-driven immune responses during acute lung injury.

Acute generalized exanthematous pustulosis caused by diltiazem.

Acute generalized exanthematous pustulosis is clinically characterized by fever, pruritus and an acute pustular eruption. It can be described as having an abrupt onset and then spontaneous resolution occurs shortly after the start of symptoms, and there is usually only a single episode. Most cases have been triggered by the ingestion of drugs. Diltiazem hydrochloride is a calcium channel blocker that is commonly used for treating hypertension and angina. This drug was found to be the responsible agent in our current patient. There have been 9 such case reports in the English medical literature, yet this is the first such report in the Korean medical literature. We present the case of a 51-year-old male who experienced an acute generalized exanthematous pustulosis due to diltiazem hydrochloride and we review the relevant literature.

Hint for association of single nucleotide polymorphisms and haplotype in SPINK5 gene with atopic dermatitis in Koreans.

Clinical studies, including twin studies, support the concept that the risk of atopic dermatitis (AD) may be mediated through skin-specific genes, rather than simply through systemic immune or atopy risk genes. The SPINK5 gene is expressed on epithelial surfaces and may provide protection against other allergenic serine proteases. Mutations in the SPINK5 gene result in Netherton syndrome, a disorder characterised by AD, ichthyosis, and elevated serum IgE levels. We genotyped 21 single nucleotide polymorphisms (SNPs) from the SPINK5 gene for 1090 case-control samples (631 patients with AD and 459 normal controls) and analysed the SNPs and haplotypes in this gene and also searched for gene-gene interactions between SPINK5 and the DEFB1 gene that we previously reported. Six SNPs [rs17718511 (P = 0.026), rs17860502 (P = 0.024), KN0001820 (P = 0.045), rs60978485 (P = 0.007), rs17718737 (P = 0.02), and rs1422985 (P = 0.038)] and the haplotype TAA (rs60978485, rs6892205, rs2303064; P = 0.023) in the SPINK5 gene showed significant different allelic or genotypic distributions between the AD group and the control group. We also found that four SNPs [rs17718511 (P = 0.033), rs17860502 (P = 0.031), rs60978485 (P = 0.005), rs17718737 (P = 0.023)] and the haplotype TAA (P = 0.02) in the SPINK5 gene showed associations with the susceptibility of the allergic type of AD (ADe). In addition to this finding, we speculate that the SNPs from DEFB1 and SPINK5 affect the individual susceptibility to development of ADe in an additive manner. This study provides evidence for a significant interaction between allergens and the SPINK5 gene that may contribute to ADe susceptibility.

A case of morpheaform sarcoidosis.

Sarcoidosis is an idiopathic multisystem disease with various cutaneous presentations, and it is characterized by the presence of non-caseating granulomas in the affected organs. The specific manifestations are papules, plaques, nodules, ulcers and scar. We report here on a variant of sarcoidosis on a 71-year-old woman who showed an indurated plaque on the forearm. Her lesion's appearance was clinically similar to that of a morphea and the appearance of the lesion was unlike the commonly observed manifestations of sarcoidosis.

Pseudoxanthoma elasticum-like papillary dermal elastolysis developed in early middle age.

Pseudoxanthoma elasticum-like papillary dermal elastolysis is a rare acquired elastolytic disorder characterized by papules that resemble pseudoxanthoma elasticum, and it typically affects elderly women. Histopathological examination shows atrophic epidermis and band-like loss of elastic tissue in the papillary dermis. The pathogenesis is assumed to be related to intrinsic aging because it affects elderly people and shows the loss of elastic tissue. We report a case of pseudoxanthoma elasticum-like papillary dermal elastolysis in early middle age presenting typical clinical and histopathological findings. The patient was a 41-year-old woman who had had her lesions for 10 years. We propose that younger patients, hitherto unknown, can be affected by this disorder and suggest that mechanisms other than intrinsic aging are involved in its pathogenesis.

Inducible nitric-oxide synthase is an important contributor to prolonged protective effects of ischemic preconditioning in the mouse kidney.

Ischemic preconditioning renders the mouse kidney resistant to subsequent ischemia. Understanding the mechanisms responsible for ischemic preconditioning is important for formulating therapeutic strategies aimed at mimicking protective mechanisms. We report that the resistance afforded by 30 min of bilateral kidney ischemia persists for 12 weeks after preconditioning. The protection is reflected by improved postischemic renal function, reduced leukocyte infiltration, reduced postischemic disruption of the actin cytoskeleton, and reduced postischemic expression of kidney injury molecule-1 (Kim-1). The protection is observed in both BALB/c and C57BL/6J strains of mice. Thirty minutes of prior ischemia increases the expression of inducible nitric-oxide synthase (iNOS) and endothelial NOS (eNOS) and the expression of heat shock protein (HSP)-25 and is associated with increased interstitial expression of alpha-smooth muscle actin (alpha-SMA), an indication of long term postischemic sequelae. Treatment with Nomega-nitro-l-arginine (l-NNA), an inhibitor of NO synthesis, increases kidney susceptibility to ischemia. Gene deletion of iNOS increases kidney susceptibility to ischemia, whereas gene deletion of eNOS has no effect. Pharmacological inhibition of NOS by l-NNA or l-N6-(1-iminoethyl) lysine (l-NIL, a specific inhibitor of iNOS) mitigates the kidney protection afforded by 30 min of ischemic preconditioning. Fifteen minutes of prior ischemic preconditioning, which does not result in the disruption of the actin cytoskeleton, impairment of renal function, increased interstitial alpha-SMA, or increased iNOS or eNOS expression, but does increase HSP-25 expression, partially protects the kidney from ischemia on day 8 via a mechanism that is not abolished by l-NIL treatment. Thus, iNOS is responsible for a significant component of the long term protection afforded the kidney by ischemic preconditioning, which results in persistent renal interstitial disease, but does not explain the preconditioning seen with shorter periods of ischemia.