scholarly journals Memoirs: Changes in Chondriosomes Occurring in Pathological Conditions

1913 ◽  
Vol s2-58 (231) ◽  
pp. 553-566
Author(s):  
J. O. WAKELIN BARRATT

(1) The mitochondria of hepatic cells in pigmeuted degeneration of the liver assume a brownish-black colour and form the pigment-granules characteristic of this condition. (2) In severe hæmoglobinæmia the chondriosomes of the cells of the convoluted tubules are more readily demonstrable than in the normal condition, their staining capacity being increased. In this condition the mitochondrial elements reach an abnormally large size and are observed to take part in the elimination of hæmoglobin. (3) In pathological conditions in which rapid cell proliferation is occurring, the chondriosomes of the prickle layer of the epidermis appear of large size and stain with unusual facility, details of their structure being readily observable. In this respect they contrast with normal epidermal chondriosomes, which stain imperfectly.

2014 ◽  
Vol 11 (4) ◽  
pp. 1503-1509
Author(s):  
Baghdad Science Journal

Objective: In this study ,the effects of silver nanoparticles (Ag NPs)were investigated on the liver and kidney tissues. Methodology: The produced nanoparticles have an average particle size of about 30 nm. Eighteen male albino rats were used by dividing them into three groups, each group comprise 6 rats. First group(control group) given food and water like other groups by liberty. Second group was tail injected by (AgNPs) at dose of (0.4 mg/kg. body weight/day). Third group was injected by (AgNPs) at dose of (0.6 mg/kg. body weight/day) for 15 days. All animals were sacrified at the end of experiment. The liver and kidney tissues specimens were fixed in 10% formalin and histological preparations were carried out then stained with H&E. Pathological changes in liver and kidney tissues were showed. Results: Histopathological studies revealed the harmful effect of the silver nanoparticles uses on the liver and kidney rats, second group that treated with Ag NPs (0.4 mg/kg.body.weight/day), kidney sections showed enlargement of collecting tubules, increase in interstitial tissue medulla, necrosis and enlargement in proximal and distal convoluted tubules. Liver showed enlargement of the central vein and degeneration of hepatic cells. Third group that treated with Ag NPs (0.6 mg/kg. body weight/day); kidney sections showed hyperplasia of the interstitial connective tissue of renal medulla with hemorrhages, renal cortex showed, degenerative changes and necrosis of proximal and distal convoluted tubules. Liver section showed congestion and necrosis of hepatic cells. Conclusion: Silver nanoparticles cause damage in liver and kidney tissues. Recommendation: Further study is needed for the effect of Ag NPs on the other tissues.


2015 ◽  
Vol 5 ◽  
pp. S3 ◽  
Author(s):  
Parul Gupta ◽  
Satendra Kumar ◽  
Pushpendra Sahu ◽  
Senthil Venugopal

1955 ◽  
Vol 1 (2) ◽  
pp. 111-118 ◽  
Author(s):  
Edward W. Dempsey ◽  
George B. Wislocki

After chronic administration of a dilute solution of silver nitrate in drinking water to rats, mice, and guinea pigs, granular deposits of metallic silver were detected in electron micrographs of the kidney, liver, thyroid, and pancreas. The silver deposits were in the form of extremely dense, angular particles with sharp outlines. They varied from aggregates a few microns in diameter down to granules at the limit of resolution of the electron microscope. The principal sites of deposition were (1) basement membranes, especially those of the renal glomeruli, proximal convoluted tubules, and various glands, and those associated with vascular endothelium, and (2) the cytoplasm of fixed and free macrophages. Both in Kupffer cells lining hepatic sinusoids and in the wandering macrophages of other tissues, the silver was segregated in discrete vacuoles. In addition, granular deposits were observed in occasional vesicular structures in the proximal convoluted tubules of the kidney, the hepatic cells, and the pancreatic acinar cell. These structures, in favorable preparations, contained an outer double layered membrane and internal folds similar to those of mitochondria, from which they appear to have been derived. The significance of these findings in heavy metal poisoning and in cellular physiology is briefly discussed.


2016 ◽  
Vol 44 (05) ◽  
pp. 997-1008 ◽  
Author(s):  
Feifei Ma ◽  
Lijuan Hu ◽  
Ming Yu ◽  
Feng Wang

Hypoxia-inducible factor-1 (HIF-1) is an [Formula: see text] dimeric transcription factor. Because HIF-1[Formula: see text] is instable with oxygen, HIF-1 is scarce in normal mammalian cells. However, HIF-1[Formula: see text] is expressed in pathological conditions such as cancer and obesity. Inhibiting HIF-1[Formula: see text] may be of therapeutic value for these pathologies. Here, we investigated whether emodin, derived from the herb of Rheum palmatum L, which is also known as Chinese rhubarb, and is native to China, regulates HIF-1[Formula: see text] expression. Male C57BL/6 mice without or with diet-induced obesity were treated with emodin for two weeks, while control mice were treated with vehicle. HIF-1[Formula: see text] expression was determined by Western blot. We found that emodin inhibited obesity-induced HIF-1[Formula: see text] expression in liver and skeletal muscle but did not regulate HIF-1[Formula: see text] expression in the kidneys or in intra-abdominal fat. In vitro, emodin inhibited HIF-1[Formula: see text] expression in human HepG2 hepatic cells and Y1 adrenocortical cells. Further, we investigated the mechanisms of HIF-1[Formula: see text] expression in emodin-treated HepG2 cells. First, we found that HIF-1[Formula: see text] had normal stability in the presence of emodin. Thus, emodin did not decrease HIF-1[Formula: see text] by stimulating its degradation. Importantly, emodin decreased the activity of the signaling pathways that led to HIF-1[Formula: see text] biosynthesis. Interestingly, emodin increased HIF-1[Formula: see text] mRNA in HepG2 cells. This may be a result of feedback in response to the emodin-induced decrease in the protein of HIF-1[Formula: see text]. In conclusion, emodin decreases hepatic HIF-1[Formula: see text] by inhibiting its biosynthesis.


Paleobiology ◽  
2006 ◽  
Vol 32 (4) ◽  
pp. 666-675 ◽  
Author(s):  
Zbyněk Roček ◽  
Ronald Böttcher ◽  
Richard Wassersug

We describe three giant palaeobatrachid fossil tadpoles of the genusPalaeobatrachus(Nieuwkoop-Faber [NF] stages 60–64) from the Miocene of Randecker Maar, Germany. The largest was 150 mm at the beginning of metamorphosis (stage 60), whereas the smallest was 100 mm and approaching the end of metamorphosis (stage 64). In contrast, normal palaeobatrachid tadpoles and their pipid relatives, both extinct and extant, rarely exceed 60 mm in length. We review here both ecological and pathological conditions that are conducive to the development of gigantism in tadpoles. Tadpoles that lack a thyroid gland become exceptionally large and arrest development at early hindlimb stages (NF stages 53–56). However, the advanced metamorphic stages of the giantPalaeobatrachustadpoles indicate that they were able to metamorphose, and thus were not athyroid. Environmental factors—pond size and permanence, predators, duration of the growing season—may all contribute to tadpole gigantism in certain extant anuran species. We identify suites of ecological features that distinguish extant anurans with large tadpoles from high-latitude and high-altitude permanent lakes in temperate regions (e.g., certainRanaandTelmatobius) from tropical species, such asPseudis paradoxa, whose tadpoles normally achieve large size in temporary seasonal ponds. The paleoecology of Randecker Maar suggests thatPalaeobatrachustadpoles lived in a permanent semitropical lake, but one with few predators.


2012 ◽  
Vol 122 (12) ◽  
pp. 555-573 ◽  
Author(s):  
Shaobin Wang ◽  
Ping Song ◽  
Ming-Hui Zou

AMPK (AMP-activated protein kinase) is one of the key players in maintaining intracellular homoeostasis. AMPK is well known as an energy sensor and can be activated by increased intracellular AMP levels. Generally, the activation of AMPK turns on catabolic pathways that generate ATP, while inhibiting cell proliferation and biosynthetic processes that consume ATP. In recent years, intensive investigations on the regulation and the function of AMPK indicates that AMPK not only functions as an intracellular energy sensor and regulator, but is also a general stress sensor that is important in maintaining intracellular homoeostasis during many kinds of stress challenges. In the present paper, we will review recent literature showing that AMPK functions far beyond its proposed energy sensor and regulator function. AMPK regulates ROS (reactive oxygen species)/redox balance, autophagy, cell proliferation, cell apoptosis, cellular polarity, mitochondrial function and genotoxic response, either directly or indirectly via numerous downstream pathways under physiological and pathological conditions.


2019 ◽  
Vol 6 (2) ◽  
pp. 73-79 ◽  
Author(s):  
T. N Savchenko ◽  
I. A Dergacheva ◽  
Lyudmila A. Ozolinya

According to last research, receptors for vitamin D are found in many organs and tissues. Vitamin D deficiency leads to the development of pathological conditions in children and adults. The non-classical effects of vitamin D are important in modulating congenital and acquired immunity, regulating cell proliferation, in the progress of diabetes, the pathology of the cardiovascular system, and autoimmune diseases. The inverse correlation between the level of 25(OH)D3 and the incidence of cancer has been determined. Vitamin D affects the course of pregnancy, and the decidual and placental tissues synthesize 1.25(OH)2D. Vitamin deficiency is found in pregnant women with preeclampsia and gestational diabetes. Timely diagnosis and adequate correction of the level of vitamin D in the blood reduces the risk of developing diseases.


2019 ◽  
Vol 49 (11) ◽  
pp. 1341-1352 ◽  
Author(s):  
Parul Gupta ◽  
Teja Naveen Sata ◽  
Naushad Ahamad ◽  
Rakibul Islam ◽  
Ajay K. Yadav ◽  
...  

1976 ◽  
Vol 108 (8) ◽  
pp. 859-864 ◽  
Author(s):  
F. T. Bird

AbstractThe last larval stadium of the spruce budworm, Choristoneura fumiferana (Clemens), is extended, if infection by an entomopoxvirus is in an advanced stage at the normal time of pupation. The larvae attain an abnormally large size. Part of this increase in size is caused by a proliferation and subsequent infection and swelling of fat body cells.


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