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Mycoplasma pneumonia of swine (MPS) is caused by Mycoplasma hyopneumoniae (M.hp) and is a common chronic respiratory disease of pigs. Recently, a genetically selected variant of the Landrace pig (Miyagino L2) has a lower incidence of pulmonary MPS lesions. We investigated the pathological and immunological characteristics of MPS resistance in these pigs (n = 24) by comparing with the normal landrace pig (control: n = 24). The pathological MPS lung lesion score in MPS-selected landrace pigs was significantly lower than in the control. The gene expression of interleukin (IL)-12p40, which acts as a chemoattractant and a component of the bioactive cytokines IL-12 and IL-23, was significantly higher at the hilar lymph nodes, lung, and spleen in MPS-selected landrace pigs than in control landrace pigs, and these were negatively correlated with the macroscopic MPS lung lesion score. In summary, we demonstrate that resistance against MPS in Miyagino L2 pigs is associated with IL-12p40 up-regulation, in comparison with normal landrace pigs without the MPS vaccine. In addition, a comparative study of macroscopic MPS lung lesions and IL-12p40 gene expression in lung and hilar lymph nodes may lead to beneficial selection traits for the genetic selection for MPS resistance in pigs., (© 2020 Japanese Society of Animal Science.)

Objectives: Recent advances in endoscopic technology have allowed its application to middle ear surgery. An antifog agent is necessary for endoscopy because moisture and blood may obscure visibility. Ultrastop is one of the most commonly used antifog agents. The current study examined the ototoxic effect of topical application of Ultrastop in the guinea pig ear., Study Design: A preliminary experimental animal study., Setting: University hospital., Subjects and Methods: Eighteen male Hartley guinea pigs (weight, 480-620 g) were divided into 3 groups to be treated with Ultrastop, gentamicin (50 mg/mL, positive control), or saline solution (negative control). After auditory brainstem responses were measured, topical solutions of 0.2 mL were applied through a small hole made at the tympanic bulla. Posttreatment auditory brainstem responses were obtained 14 days after the treatment. The extent of middle ear damage was investigated and scored., Results: The saline-treated group showed no deterioration in auditory brainstem response threshold. The Ultrastop-treated and gentamicin-treated groups showed severe deterioration in auditory brainstem response threshold. Middle ear examination revealed extensive changes in the Ultrastop-treated group and medium changes in the gentamicin-treated group., Conclusion: Ultrastop applied topically to the guinea pig middle ear caused significant middle ear inflammation and hearing impairment., (© American Academy of Otolaryngology-Head and Neck Surgery Foundation 2014.)

Background: Curcumin, the yellow pigment in turmeric, has been shown to prevent tumor progression in a variety of tissues in rodents. The authors investigated the effect of curcumin on human carcinoma cell lines to determine whether constitutive interleukin-8 (IL-8) production of tumor cells was correlated with nuclear factor kappaB (NF-kappaB) activation and cell growth activity., Methods: A human pancreatic carcinoma cell line, SUIT-2, was incubated with various concentrations of curcumin for 2 hours. Biologic features, including IL-8 production, DNA binding activity, transactivation of NF-kappaB, cell growth activity, cell viability, and the expression of IL-8 receptors (CXCR1 and CXCR2) were analyzed., Results: The constitutive production of IL-8 was inhibited by curcumin at concentrations of 10-100 microM in a dose dependent manner. NF-kappaB activity was reduced significantly by curcumin treatment. Pretreatment with curcumin inhibited the growth rate of carcinoma cells significantly. Such cell growth inhibition by curcumin was not recovered by exogenous recombinant IL-8. The investigation of expression in IL-8 receptors, CXCR1 and CXCR2, revealed that the expression of both receptors was enhanced remarkably by curcumin. Exogenous IL-8 could not recover this enhancement of IL-8 receptors. These results suggest that curcumin inhibits IL-8-induced receptor internalization., Conclusions: The authors concluded that curcumin contributed not only to the inhibition of IL-8 production but also to signal transduction through IL-8 receptors. These data suggest that curcumin reduces numerous IL-8 bioactivities that contribute to tumor growth and carcinoma cell viability. From this point of view, curcumin is a potent anticancer agent that inhibits the production of proinflammatory cytokines, including IL-8, by tumor cells., (Copyright 2002 American Cancer Society.)

The effects of cilostamide, a cyclic nucleotide phosphodiesterase 3 (PDE3) selective inhibitor, on vascular intimal hyperplasia were evaluated using a single-balloon injury model and a double-injury model in which the rat common carotid artery was subjected to a second injury at a site injured 14 days previously. In the double-injury model, the second balloon injury caused more severe intimal hyperplasia (intima/media (IM) ratio, 1.88+/-0.10) than in the single-injury model (1.09+/-0.08). Histopathological study revealed that vascular smooth muscle cells (VSMC) were the predominant cell-type in the affected neointimal area. Oral administration of cilostamide for 2 weeks after the second injury suppressed intimal hyperplasia in the double-injury model (30 mg kg(-1) bid, 83% inhibition in terms of the IM ratio, P<0.05; 100 mg kg(-1) bid, 69% inhibition, P<0.05). Similar effects were also observed in the single-injury model with oral administration of cilostamide for 2 weeks (100 mg kg(-1) bid, 36% inhibition, P<0.01). Cilostamide inhibited DNA synthesis of cultured VSMC stimulated by foetal calf serum or different kinds of growth factors, but did not affect their migration stimulated by platelet-derived growth factor (PDGF)-BB. Cilostamide significantly increased the cyclic AMP concentration of VSMC dose-dependently. These results indicate that cilostamide suppresses intimal hyperplasia both in the single- and double-injury models of rat, presumably by inhibiting proliferation rather than migration of VSMC. It is suggested that PDE3 inhibitors might find application in preventing intimal hyperplasia following angioplasty such as percutaneous transluminal coronary angioplasty (PTCA) or stent.

Neurocalcin (NC) is a recently described calcium-binding protein isolated and characterized from bovine brain. NC belongs to the neural calcium-sensor proteins defined by the photoreceptor cell-specific protein recoverin that have been proposed to be involved in the regulation of calcium-dependent phosphorylation in signal transduction pathways. We analyzed the distribution and morphology of the NC-immunoreactive (IR) neurons in the rat dorsal hippocampus and the coexistence of NC with GABA and different neurochemical markers which label perisomatic inhibitory cells [parvalbumin (PV) and cholecystokinin (CCK)], mid-proximal dendritic inhibitory cells [calbindin D28k (CB)], distal dendritic inhibitory cells [somatostatin (SOM) and neuropeptide Y (NPY)], and interneurons specialized to innervate other interneurons [calretinin (CR) and vasoactive intestinal polypeptide (VIP)]. NC-IR cells were present in all layers of the dentate gyrus and hippocampal fields. In the dentate gyrus, NC-IR cells were concentrated in the granule cell layer, especially in the hilar border, whereas in the CA fields they were most frequently found in the stratum radiatum. NC-IR cells were morphologically heterogeneous and exhibited distinctive features of non-principal cells. In the dentate gyrus, pyramidal-like, multipolar and fusiform (horizontal and vertical) cells were found. In the CA3 region most NC-IR cells were multipolar, but vertical and horizontal fusiform cells also appeared. In the CA1 region, where NC-IR cells showed most frequently vertically arranged dendrites, multipolar, bitufted and fusiform (vertical and horizontal) cells could be distinguished. All the NC-IR cells were found to be GABA-IR in all hippocampal layers and regions, and they represented about 19% of the GABA-positive cells. NC/CB, NC/CR and NC/VIP double-labeled cells were found in all hippocampal regions, and represented 29%, 24% and 18% of the NC-IR cells, respectively. NC and CCK did not coexist in the dentate gyrus; however, 9% of the NC-IR cells in the CA fields also contained CCK. No coexistence of NC with PV, SOM or NPY was found in any hippocampal region. We conclude that NC is exclusively expressed by interneurons in the rat hippocampus. NC-IR cells are a morphologically and neurochemically heterogeneous subset of GABAergic non-principal cells, which, on the basis of the known termination pattern of the colocalizing markers, are also functionally heterogeneous and are mainly involved in feed-forward dendritic inhibition in the commissural-associational and Schaffer collateral termination zones (CB containing cells), in innervation of other interneurons (CR- and VIP-containing cells), and in perisomatic inhibition (CCK-containing cells). NC is never present in perisomatic inhibitory PV-containing cells, or in feed-back distal dendritic inhibitory SOM/NPY-containing cells.

Hepatocellular carcinoma (HCC) associated with cirrhosis and HCC developing in a noncirrhotic liver may have differing pathogeneses. To study this possibility, 425 autopsied cases of HCC were investigated. Of these, 45 livers were not cirrhotic, 50 were highly cirrhotic (liver weight less than 99 g), and the remaining 331 were cirrhotic but not so highly. The average age was significantly older in the highly cirrhotic group, suggesting a longer premalignant period of chronic liver disease. The liver weight in the noncirrhotic group was about 3.5 times that in the highly cirrhotic group. Hepatitis B surface antigen was positive in serum in only 9.3% and in liver tissue in 10% in the noncirrhotic cases, the positivity rate being much lower compared with other groups (P less than 0.005--0.01), yet antibody to HB core was positive in 90%. The antibody titers were low, however, indicating that these noncirrhotic patients had in the past had HB virus (HBV) infection with no residual chronic B hepatitis. Analysis of the grades of anaplasia of cancer tissue demonstrated an inverse correlation between the degree of fibrosis and grade of anaplasia, i.e., the more advanced the fibrosis, the less anaplastic the cancer. These data suggest that HCC arising in highly cirrhotic liver and in noncirrhotic livers have different pathogenetic backgrounds, and that HBV infection, even though transient, has a certain role in hepatocarcinogenesis. The generally held conjecture that HCC in a noncirrhotic liver is caused by nonviral carcinogens and HCC arising on the ground of cirrhosis is due to HBV seems untenable in such a simple concept.

1 The potentiating effect of a low concentration of various vascular contractile agonists on the response of rabbit aortic strips to acetylcholine was examined. 2 A marked parallel displacement to the left (potentiation; not additive effect) of the dose-response curve for acetylcholine was observed when 5-hydroxytryptamine (5-HT), noradrenaline, histamine, angiotensin II or KCl were added at a concentration that caused only slight contraction (0.2 to 0.3 g) in the strips. This leftward displacement (potentiation) of the dose-response curve by these agonists was reversed to the control response curve by the respective blocking agents for each agonist, although the blocking agents themselves did not shift the acetylcholine dose-response curve to the right. Atropine produced a rightward displacement of the dose-response curve for acetylcholine. 3 The addition of an extremely low concentration of 5-HT or KCl which did not cause contraction, also produced a potentiation. 4 The order of potency of the agonists in potentiating the acetylcholine-induced contraction was KCl > 5-HT greater than or equal to histamine greater than or equal to angiotensin II > noradrenaline. 5 The contractile response of aortic strips to carbamylcholine was also potentiated by these agonists. 6 The results suggest that the potentiation by these agonists was not mediated through muscarinic receptors but through the respective receptors for each agonist.