Explore chapters and articles related to this topic
Recent In-Depth Insights of Nature-Based Anti-Worm Therapeutic Medications: Emerging Herbal Anthelmintics
Published in Debarshi Kar Mahapatra, Cristóbal Noé Aguilar, A. K. Haghi, Applied Pharmaceutical Practice and Nutraceuticals, 2021
Ankita Soni, Paras Kothari, Debarshi Kar Mahapatra
Helminths are foreign bodies, invasive, and antigenic and therefore stimulate the immune system. Adult Schistosomes mansoni cause infection in the blood vessels around the small intestine. These worms lay eggs in the vessels lumen and are trapped inside the liver which results in precipitation of hypersensitivity reaction by the antigens and thereby causing the formation of granuloma. The liver sinusoids become blocked which results in an impaired blood flow, leading to fibrosis of the liver. The immune-mediated changes can be clearly seen in skin, lungs, liver, and intestine. The severity of the indirect changes leads to chronic nature of infection. Another cause to infection is the soil-transmitted helminthiasis. Ascaris lumbricoides is the mostly responsible and accounts about 5–35% of all bowel obstructions. These worms are rarely noticed unless passed in stools.8
Liver Blood Flow
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
The small vessels of the portal vein and hepatic artery run parallel to each other in the substance of the liver, accompanied by bile canaliculi, forming the hepatic triad. The hepatic triad vessels (i.e. arteriole and venule) eventually form anastomoses to form the sinusoids. Thus, the sinusoids form a specialized capillary system that facilitates exchange with the hepatocytes. The mixed portal venous and hepatic arterial blood from the hepatic portal vein and the hepatic artery flow from the periphery to the central veins of the hepatic acinus.
Oedema, Haemorrhage and Thrombosis
Published in Jeremy R. Jass, Understanding Pathology, 2020
Right heart failure leads to congestion within the sinusoids of the liver and spleen. Sinusoids are lined by endothelial cells (like capillaries), but are separated by fenestrations (gaps) and lack a supporting basement membrane, a design that allows cells such as motile phagocytic cells to squeeze in and out of sinusoids with ease. The macroscopic appearance of a congested liver upon slicing has been likened to a section through a nutmeg. The dark fern-like tracery is the blood that has accumulated in the sinusoids and central vein of the microscopic liver lobules. The term ‘nutmeg liver’ dates back to the autopsy days of Karl Rokitansky.
Pathology of breast cancer metastasis and a view of metastasis to the brain
Published in International Journal of Neuroscience, 2023
Md Sakibuzzaman, Shahriar Mahmud, Tanzina Afroze, Sawsan Fathma, Ummul Barakat Zakia, Sabrina Afroz, Farzina Zafar, Maksuda Hossain, Amit Barua, Sabiha Akter, Hasanul Islam Chowdhury, Eram Ahsan, Shayet Hossain Eshan, Tasnuva Tarannum Fariza
Initial arrest of CTCs notably takes place in liver sinusoidal capillaries [91,92]. The fenestrated endothelium of the sinusoid facilitates the transmigration of the cells. The tumor cells then proliferate in the liver. During this process, several inflammatory factors (TNF-α and IL-6), as well as chemokines and their receptors (CXCR4, CCR2, and CCR5), play a crucial role in metastasis. Tumor cell interactions in the tumor microenvironment result in overexpression of various factors that activate transcription of target genes and signaling pathways to form metastasis [93]. Vermeulen et al. [94] showed that some cancer metastases to the liver exhibit three different histologic growth patterns: pushing, replacement, and desmoplastic. Breast cancer liver metastasis mainly follows the ‘replacement’ pattern. The replacement pattern occurs by adopting the stroma, without induction of hypoxia or angiogenesis. In consequence, there is minimal disturbance of the liver architecture.
Chebulagic acid attenuates HFD/streptozotocin induced impaired glucose metabolism and insulin resistance via up regulations of PPAR γ and GLUT 4 in type 2 diabetic rats
Published in Toxicology Mechanisms and Methods, 2022
Ganesh Vasu, Ramalingam Sundaram, Karuppiah Muthu
Figure 8 portrays hematoxylin and eosin staining of the liver of control and experimental rats. Pathologically, the liver of normal control rats showed no dilated blood sinusoids with red blood cells and congestion of the area around the central vein (Figure 8(A)). Section of hepatic tissues of diabetic rat showed dilated blood sinusoids with red blood cells and congestion of the area around the central vein. Hepatocytes were found to be swollen with fatty deposits. These features are the characteristic of a diabetic liver. There was the distortion of the lumen of the sinusoids. Inflammatory changes were observed in the region of the portal triad with the polymorph nuclear cells infiltrating the area of the portal triad. The features of necrosis were characteristically observed in the region around the portal triad. Collagen deposits were also observed in the region of the portal triad (Figure 8(B)). The liver of the diabetic rats treated with chebulagic acid and metformin did not reveal any infiltration of the portal triad. Blood sinusoids were normal and no congestion was observed in the region near the central vein and the portal triad. The microstructure resembled a normal liver (Figure 8(C,D)).
Modified check loss for efficient estimation via model selection in quantile regression
Published in Journal of Applied Statistics, 2021
Yoonsuh Jung, Steven N. MacEachern, Hang Joon Kim
For simulations, data from a sinusoid curve with period 1, along with several error distributions are generated. That is, iid from the standard uniform distribution, and iid from some error distribution. Error distributions considered are normal, t, gamma, and exponential distribution where the qth quantile is zero with standard deviation 0.2. The t-distributions, with 5 and 10 degrees of freedom, are scaled to have standard deviation 0.2. A fine grid search of the smoothing parameter is conducted to select the ‘best’ value by CV and CV.M. As in the previous section, the performance of the two validation functions is judged by the percentage reduction in MSE and excess MSE. To calculate the excess MSE, a base model is defined by the minimum MSE across the fine grid of smoothing parameter values, given a data set. The simulation consists of 1000 replicates with sample size 500, 1000 and 2000.