Morphologic alteration in the muscles of patients with hypokalemic periodic paralysis or myopathy

1990 ◽  
Vol 48 (3) ◽  
pp. 222-223
Author(s):  
T. Shimizu ◽  
Y. Muranaka ◽  
I. Ohta ◽  
N. Honda
Keyword(s):  
Clinical Manifestations ◽  
Quadriceps Muscle ◽  
Honeycomb Structure ◽  
Periodic Paralysis ◽  
Ultrastructural Changes ◽  
Hypokalemic Periodic Paralysis ◽  
Electron Microscopic ◽  
Tubular Aggregates ◽  
Hypokalemic Myopathy ◽  
Transmission Electron

There have been many reports on ultrastructural alterations in muscles of hypokalemic periodic paralysis (hpp) and hypokalemic myopathy(hm). It is stressed in those reports that tubular structures such as tubular aggregates are usually to be found in hpp as a characteristic feature, but not in hm. We analyzed the histological differences between hpp and hm, comparing their clinical manifestations and morphologic changes in muscles. Materials analyzed were biopsied muscles from 18 patients which showed muscular symptoms due to hypokalemia. The muscle specimens were obtained by means of biopsy from quadriceps muscle and fixed with 2% glutaraldehyde (pH 7.4) and analyzed by ordinary method and modified Golgimethod. The ultrathin section were examined in JEOL 200CX transmission electron microscopy.Electron microscopic examinations disclosed dilated t-system and terminal cistern of sarcoplasmic reticulum (SR)(Fig 1), and an unique structure like “sixad” was occasionally observed in some specimens (Fig 2). Tubular aggregates (Fig 3) and honeycomb structure (Fig 4) were also common characteristic structures in all cases. These ultrastructural changes were common in both the hypokalemic periodic paralysis and the hypokalemic myopathy, regardless of the time of biopsy or the duration of hypokalemia suffered.

scholarly journals Nephrotic tunnels in glomerular basement membrane as revealed by a new electron microscopic method.

1994 ◽  
Vol 4 (12) ◽  
pp. 1965-1973
Author(s):  
Z Ota ◽  
K Shikata ◽  
K Ota
Keyword(s):  
Nephrotic Syndrome ◽  
Basement Membrane ◽  
Glomerular Basement Membrane ◽  
Three Dimensional ◽  
Minimal Change Nephrotic Syndrome ◽  
Renal Tissue ◽  
Honeycomb Structure ◽  
Ultrastructural Changes ◽  
Electron Microscopic ◽  
Transmission Electron

To clarify the ultrastructure in situ of the normal human glomerular basement membrane and ultrastructural changes of the glomerular basement membrane in patients with nephrotic syndrome, specimens of normal renal tissue and specimens from patients with membranous nephropathy, lupus nephritis, minimal change nephrotic syndrome, diabetic nephropathy, and Alport's syndrome were obtained. Specimens were examined by transmission electron microscopy by the newly devised "tissue negative staining method." Normal glomerular basement membrane showed a three-dimensional lattice-like meshwork of fibrils measuring 1.9 +/- 0.4 nm in diameter that formed numerous uniform, round, oval, or polygonal pores 2.5 +/- 0.4 nm in short diameter and 2.8 +/- 0.5 nm in long dimension. The nephrotic glomerular basement membrane revealed varying degrees of ultrastructural defects, the most prominent being tunnels and cavities. Tortuous tunnels measuring approximately 15 to 50 nm in diameter penetrated the entire glomerular basement membrane. Cavities of various shapes measuring 15 to 200 nm in diameter were diffusely scattered in the glomerular basement membrane and occasionally aggregated to form a honeycomb structure that occupied the whole thickness of the glomerular basement membrane. These defects appeared to be the pathway for protein leakage.

scholarly journals Hypokalemic Periodic Paralysis as the First Manifestation of Thyrotropin-Secreting Pituitary Adenoma

2019 ◽  
Vol 2019 ◽  
pp. 1-4
Author(s):  
Chatchon Kaewkrasaesin ◽  
Patinut Buranasupkajorn ◽  
Paisith Piriyawat ◽  
Sarat Sunthornyothin ◽  
Thiti Snabboon
Keyword(s):  
Pituitary Adenoma ◽  
Clinical Manifestations ◽  
Periodic Paralysis ◽  
Neurological Manifestation ◽  
Hypokalemic Periodic Paralysis ◽  
Thyrotoxic Periodic Paralysis ◽  
Pituitary Microadenoma ◽  
Clinical Syndromes

Thyrotoxic periodic paralysis is an unusual neurological manifestation of thyrotoxicosis, and even rarer when it occurs in thyrotropin-secreting pituitary adenoma, only 6 cases having been previously reported. We describe a case of pituitary microadenoma with clinical syndromes of thyrotoxicosis complicated with hypokalemic periodic paralysis. Clinical manifestations and proposed management are discussed.

A Scanning and Transmission Electron Microscopic Study of Rotavirus-Induced Intestinal Lesions in Neonatal Gnotobiotic Dogs

1986 ◽  
Vol 23 (4) ◽  
pp. 443-453 ◽  
Author(s):  
C. A. Johnson ◽  
T. G. Snider ◽  
W. G. Henk ◽  
R. W. Fulton
Keyword(s):  
Epithelial Cells ◽  
Ultrastructural Changes ◽  
Post Inoculation ◽  
Electron Microscopic ◽  
Intestinal Villi ◽  
Villus Atrophy ◽  
Intestinal Lesions ◽  
Transmission Electron ◽  
Transmission Electron Microscopic ◽  
Subsequent Propagation

Neonatal gnotobiotic dogs orally inoculated with canine rotavirus had ultrastructural changes limited to the jejunal and ileal regions of the small intestine. Early scanning electron microscopic findings consisted of swollen villus epithelial cells, denuded foci on intestinal villi, and slight to moderate villus atrophy. Later changes were slight villus atrophy with no denuded intestinal villi. Transmission electron microscopic changes in villus epithelial cells from 12 to 48 hours post-inoculation included: rotavirus particles associated with intracytoplasmic vacuoles near the terminal web and apical tubules; viral particles in dilated cisternae of rough endoplasmic reticulum; and moderate numbers of necrotic cells having no microvilli, swollen mitochondria, membrane-bound lipid-like material in the cytoplasm, clumped chromatin around the periphery of the nucleus, and disruption of the cytoplasmic membrane. In jejunum and ileum at 72 to 154 hours post-inoculation, there were fewer necrotic villus epithelial cells and fewer virus particles. In addition, the ultrastructural morphology of the majority of the villus epithelial cells was similar to crypt epithelium. These studies showed that rotavirus infected the villus epithelial cells with subsequent propagation of the rotavirus and destruction of villus epithelial cells.

scholarly journals Ultrastructural changes of the placenta in cases of preeclampsia

2021 ◽  
Vol 3 (2) ◽  
pp. 047-060
Author(s):  
Abdelghany Hassan Abdelghany ◽  
Ahmed Abdelghany Hassan ◽  
Sarah Abdelghany Hassan ◽  
Rania Mohamed Fawzy
Keyword(s):  
Microscopic Study ◽  
Thick Layer ◽  
Glycogen Storage ◽  
Caesarian Section ◽  
Ultrastructural Changes ◽  
Electron Microscopic ◽  
Transmission Electron ◽  
Placental Blood ◽  
Placental Blood Flow ◽  
Fibrinoid Degeneration

The placenta plays vital roles during fetal development and growth. The ultrastructure of the placenta together with remodeling of the uterine spiral arteries are very important to maintain the utero-placental blood flow. Preeclampsia (PE) is a multifactorial disorder with abnormal placentation affecting the mother and fetus. The aim of this study was to study the ultrastructural abnormalities of the placenta in cases of PE. The placentas of 10 PE women and 10 controls were studied. Women of PE group were delivered by caesarian section while seven control women were delivered vaginally, and three by caesarian section. Placental samples were studied both morphologically and histologically by light and transmission electron microscopy. Light microscopic study of control placentas showed numerous microvilli, few syncytial knots, thin-walled blood vessels. PE placentas showed reduced number of microvilli with numerous syncytial knots, thick-walled vessels, edematous spaces, fibrotic areas and fibrinoid degeneration. Electron microscopic study of the control placentas showed a thick layer of syncytiotrophoblast (Sy), numerous microvilli and a thin layer of cytotrophoblast (Cy). PE placenta showed hypertrophy of Cy with atrophy of Sy and scarce microvilli. The trophoblast showed edematous vacuoles and glycogen storage areas. The villous core had congested capillaries, edematous spaces, glycogen storage areas and widespread areas of fibrosis. All the changes in PE placentas were attributed to hypoxia and oxidative stress and reduced utero-placental flow due to abnormal remodeling of the uterine spiral arteries that was aggravated by the thick placental barrier and the presence of edema, fibrosis and glycogen storage areas.

Biochemical, histopathological, and transmission electron microscopic ultrastructural changes in mice after exposure to silver nanoparticles

2015 ◽  
Vol 31 (8) ◽  
pp. 945-956 ◽  
Author(s):  
Mohammad Azam Ansari ◽  
Haris M. Khan ◽  
Aijaz A. Khan ◽  
Mohammad A. Alzohairy ◽  
Mohammad Waseem ◽  
...  
Keyword(s):  
Silver Nanoparticles ◽  
Ultrastructural Changes ◽  
Electron Microscopic ◽  
Transmission Electron ◽  
Transmission Electron Microscopic

scholarly journals Autophagy is affected in patients with hypokalemic periodic paralysis: an involvement in vacuolar myopathy?

2021 ◽  
Vol 9 (1) ◽  
Author(s):  
Thomas O. Krag ◽  
Sonja Holm-Yildiz ◽  
Nanna Witting ◽  
John Vissing
Keyword(s):  
Electron Microscopy ◽  
Transmission Electron Microscopy ◽  
Gene Transcription ◽  
Systemic Effect ◽  
Periodic Paralysis ◽  
Muscle Fibres ◽  
Hypokalemic Periodic Paralysis ◽  
Vacuolar Myopathy ◽  
Autophagy Gene ◽  
Transmission Electron

AbstractHypokalemic periodic paralysis is an autosomal dominant, rare disorder caused by variants in the genes for voltage-gated calcium channel CaV1.1 (CACNA1S) and NaV1.4 (SCN4A). Patients with hypokalemic periodic paralysis may suffer from periodic paralysis alone, periodic paralysis co-existing with permanent weakness or permanent weakness alone. Hypokalemic periodic paralysis has been known to be associated with vacuolar myopathy for decades, and that vacuoles are a universal feature regardless of phenotype. Hence, we wanted to investigate the nature and cause of the vacuoles. Fourteen patients with the p.R528H variation in the CACNA1S gene was included in the study. Histology, immunohistochemistry and transmission electron microscopy was used to assess general histopathology, ultrastructure and pattern of expression of proteins related to muscle fibres and autophagy. Western blotting and real-time PCR was used to determine the expression levels of proteins and mRNA of the proteins investigated in immunohistochemistry. Histology and transmission electron microscopy revealed heterogenous vacuoles containing glycogen, fibrils and autophagosomes. Immunohistochemistry demonstrated autophagosomes and endosomes arrested at the pre-lysosome fusion stage. Expression analysis showed a significant decrease in levels of proteins an mRNA involved in autophagy in patients, suggesting a systemic effect. However, activation level of the master regulator of autophagy gene transcription, TFEB, did not differ between patients and controls, suggesting competing control over autophagy gene transcription by nutritional status and calcium concentration, both controlling TFEB activity. The findings suggest that patients with hypokalemic periodic paralysis have disrupted autophagic processing that contribute to the vacuoles seen in these patients.

scholarly journals AUTOIMMUNE OOPHORITIS AND THEIR CORRECTION BY GLUCOCORTICOIDS

2013 ◽  
Vol 12 (3) ◽  
pp. 76-81
Author(s):  
T. V. Tupitsyna ◽  
S. V. Logvinov ◽  
O. A. Tikhonovskaya ◽  
M. L. Dmitrieva
Keyword(s):  
Electron Microscopy ◽  
Osmium Tetroxide ◽  
Comparison Group ◽  
Ultrastructural Changes ◽  
Electron Microscopic ◽  
Antral Follicles ◽  
Transmission Electron ◽  
Group 12 ◽  
Pathologic Processes ◽  
Autoimmune Oophoritis

Autoimmune oophoritis (AO) is characterized by damage of generative and endocrine elements of the ovaries and leads to the formation of secondary insufficiency of the gonads. A question about the use of glucocorticoids (GC) for the correction of AO remains debatable.Objective: to study the electron-microscopic changes of structural-tissue cells in autoimmune ovariano ophoritis and after its correction by glucocorticoids in the experiment.The material. The experiment was performed on outbred white Mature rats-female. The main group of animals (12 rats) were simulated AO by intra-peritoneal introduction of antigens of ovarian. At 5th day prednisolone was injected to rats («Nycomed», Austria) in the dose of 3 mg/kg of body weight intramuscularly 14-day course. A comparison group (12 rats) were the animals with the model AO no course Ledger therapy. Controlintact rats (6 animals). Taking of the material was carried out by the 20th and the 60th day.Methods. The study of the ultrastructure ovaries were performed using transmission electron microscopy. The material was fixed 2.5% glutaraldehyde, postfixed in 2% solution of osmium tetroxide, dehydrated in ethyl alcohols rising concentration and placed in a mixture of resins Epon-Araldite. Sections were prepared on Ultrotom III (LKB, Sweden). To view the drugs used an electron microscope JEM-7A (Japan). Results. On the 20th day of the pilot AO there are significant ultrastructural changes of vessels, concerning mainly endothelial layer. Degenerative and destructive changes affected endocrinocytes in the composition of the libraries and granular, овоциты majority of antral follicles. The 60-day pathologic processes involved and preantral follicles in the medulla develop perivascular fibrosis-sclerotic changes. Holding GC therapy on the 5th day AO reduces ultrastructural breach the walls of blood vessels, limits migration of immune cells in the home defeat on the 20th day. By the 60th day in the conditions of the restored the blood tissue transport is the formation of full-fledged generative elements, confirmed by the results of electron microscopy study.Conclusion. The obtained experimental data are demonstrated the therapeutic efficacy of the GC-therapy in the early stages of AO.

Correlative light and transmission electron microscopy of tubular aggregates in skeletal muscle

1992 ◽  
Vol 50 (1) ◽  
pp. 660-661
Author(s):  
Thomas G. Manfredi ◽  
Wenjing Ding ◽  
Roderick Bronson
Keyword(s):  
Electron Microscopy ◽  
Skeletal Muscle ◽  
Transmission Electron Microscopy ◽  
Animal Models ◽  
Muscle Pain ◽  
Periodic Paralysis ◽  
Human Muscle ◽  
Tubular Aggregates ◽  
Transmission Electron ◽  
Gender Specific

Tubular aggregates (TAs) have been identified with a number of myopathies in humans. Periodic paralysis and muscle pain are frequently associated with TAs. Very little is known about the functional and anatomical significance of TAs in myopathic and aging human muscle. Recently, animal models for TAs have been identified which suggested that TAs are gender specific. However, recent studies suggest a need for more controls.

scholarly journals Prevention of AMI Induced Ventricular Remodeling: Inhibitory Effects of Heart-Protecting Musk Pill on IL-6 and TNF-Alpha

2017 ◽  
Vol 2017 ◽  
pp. 1-7 ◽  
Author(s):  
Wei Cen ◽  
Zhiliang Chen ◽  
Ning Gu ◽  
Ralph Hoppe
Keyword(s):  
Inflammatory Cytokines ◽  
Ventricular Remodeling ◽  
Ultrastructural Changes ◽  
Coronary Artery Ligation ◽  
Sprague Dawley ◽  
Electron Microscopic ◽  
Artery Ligation ◽  
Necrosis Factor Alpha ◽  
Transmission Electron ◽  
Factor Alpha

Heart-Protecting Musk Pill (HMP) is a Traditional Chinese Medicine (TCM) that has been used for the prevention and treatment of coronary heart disease in clinic. The current study investigated the effect of HMP on the concentrations of interleukin-6 (IL-6) and tumor necrosis factor-alpha (TNF-α) and observed the relationship between level changes of inflammatory cytokines and ventricular remodeling in rats with acute myocardial infarction (AMI). Animal models of AMI were made by coronary artery ligation in Sprague-Dawley (SD) rats. AMI rats showed increased levels of IL-6 and TNF-α. Treatment with HMP decreases IL-6 and TNF-αconcentrations in rats with AMI. Histopathological and transmission electron microscopic findings were also essentially in agreement with biochemical findings. The results of our study revealed that inflammatory cytokines IL-6 and TNF-αinduce cardiac remodeling in rats after AMI; HMP improves cardiac function and ameliorates ventricular remodeling by downregulating the expression of IL-6 and TNF-αand further suppressing the ultrastructural changes of myocardial cells.

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