The anatomical variations of the portal vein and the hepatic artery ramifications were analysed on liver corrosion casts in 20 dogs as a possible aid in the surgical management of the organ. The portal vein ramified similarly in all dogs. It divided into the smaller right portal branch from which vessels for the caudate process and both right lobes arose and the substantial left portal branch, which supplied the remaining liver portions and in 12 cases also the dorsal part of the right lateral lobe. Right lateral, right medial and left branches are the major arteries originating from the hepatic artery; however, their origin and course varied among individual animals. In 10 livers, the right lateral and the left branches originated from the hepatic artery, while the right medial branch arose from the left branch and usually supplied the right medial lobe solely. In nine livers, the right medial branch arose directly from the hepatic artery and supplied quadrate lobe and gallbladder as well, while in one liver the common artery, which subsequently divided into lobar branches, branched away from the hepatic artery. An additional branch for the caudate process, originating directly from the hepatic artery, was observed in 10 livers. Certain liver portions received the arterial blood from two major branches, which was particularly characteristic for the right medial lobe (six livers) and caudate process (10 livers). The course of the major arterial branches was also variable, although they proceeded in close anatomical relationship with the portal vein branches. The left arterial branch accompanied the left portal branch on its dorsal aspect (15 cases) or crossed it from the caudal aspect (five cases). The right lateral branch crossed the initial parts of the left and right portal branches either from cranial (12 cases) or caudal aspects (eight cases), while the right medial branch always crossed the left portal branch from its caudal aspect.

Exposure to widespread lipophilic and bioaccumulative polychlorinated biphenyls (PCBs) induces diverse biochemical and toxicological responses in various organs, including the bone. The aim of this study was to evaluate the changes in growth rate, geometry, serum, and bone biochemical parameters and biomechanics of juvenile rat femur induced by lactational exposure to nonplanar PCB-155 and planar PCB-169 individually and in combination. Fifteen lactating Wistar rats were divided into four groups (PCB-169, PCB-155, PCB-155+169, and control), and PCBs were administered intraperitoneally at different time points after delivery. Femurs from 22-day-old offspring were analyzed by microCT, three-point bending test and inductively coupled plasma-mass spectrometry (ICP-MS) to obtain data on bone geometry, biomechanics and mineral composition. The serum levels of calcium, phosphate and alkaline phosphatase were also determined. Lactational exposure to planar PCB-169 resulted in shorter and thinner femurs, reduced endosteal and periosteal perimeters, smaller total cross-sectional and medullary areas, and lowered serum bone marker levels and calcium levels in the bone, while femur mechanical properties were not significantly altered. The changes observed in the combination exposure (PCB-155+169) group were similar to those observed in the PCB-169 group but were less pronounced. In summary, our results demonstrate that alterations in lactationally exposed offspring were primarily induced by planar PCB-169. The milder outcome in the combined group suggested that the PCB-169-mediated toxic effects on the bone might be reduced by a nonplanar PCB-155 congener. © 2016 Wiley Periodicals, Inc. Environ Toxicol 32: 1135-1146, 2017.

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This study examined the frequency, morphological and immunohistochemical characteristics of the giant fibres in the longissimus muscle of local Krsko polje pigs with different Ryr1 genotypes. Giant fibres were round-shaped and had significantly increased cross-sectional area compared with normal muscle fibres. Only fast-twitch glycolytic fibres were affected, usually showing enhanced succinate dehydrogenase activity. On the ultrastructural level, the dilation of the sarcoplasmic reticulum, swelling of mitochondria and destruction of myofilaments was observed. The incidence of giant fibres was the highest in Ryr1 dimutant pigs (Ryr1 nn), which also exhibited lower muscle pH1 than heterozygous (Ryr1 Nn) or pigs with the wild Ryr1 gene (Ryr1 NN). However, the giant fibres were also present in pigs free of Ryr1 gene mutation. Our results suggest that the giant fibre syndrome depends mostly upon the rate and intensity of early post-mortem glycolysis, which results in acidity of muscle tissue. We suppose that the giant fibre formation is a result of excessive intracellular lactate accumulation in some fast-twitch glycolytic fibres. This process could also explain the ultrastructural alterations and the consequent changes in the oxidative enzymes and myofibrillar ATPase staining pattern observed in our and some previous studies.