Detection of pathological changes in the architectonics of polycrystalline blood films using laser-induced polarization interferometry

2021 ◽  
Author(s):  
D Kvasnyuk ◽  
L Trifonyuk ◽  
A. Strashkevich ◽  
N Kozan ◽  
Vladimir Ushenko ◽  
...  
Keyword(s):  
Induced Polarization ◽  
Pathological Changes ◽  
Polarization Interferometry

Reversal of cardiomyopathy resulting from prenatal exposure to ethanol

1984 ◽  
Vol 42 ◽  
pp. 716-717
Author(s):  
C. Uphoff ◽  
C. Nyquist-Battie
Keyword(s):  
Prenatal Exposure ◽  
Heart Development ◽  
Membrane Integrity ◽  
Ethanol Exposure ◽  
Prenatal Ethanol Exposure ◽  
Pathological Changes ◽  
Prenatally Exposed ◽  
Inner Mitochondrial Membrane ◽  
Fetal Alcohol ◽  
Newborn Mice

Fetal Alcohol Syndrone (FAS) is a syndrome with characteristic abnormalities resulting from prenatal exposure to ethanol. In many children with FAS syndrome gross pathological changes in the heart are seen with septal defects the most prevalent abnormality recorded. Few studies in animal models have been performed on the effects of ethanol on heart development. In our laboratory, it has been observed that prenatal ethanol exposure of Swiss albino mice results in abnormal cardiac muscle ultrastructure when mice were examined at birth and compared to pairfed and normal controls. Fig. 1 is an example of the changes that are seen in the ethanol-exposed animals. These changes include enlarged mitochondria with loss of inner mitochondrial membrane integrity and loss of myofibrils. Morphometric analysis substantiated the presence of these alterations from normal cardiac ultrastructure. The present work was undertaken to determine if the pathological changes seen in the newborn mice prenatally exposed to ethanol could be reversed with age and abstinence.

REPRODUCTIVE PERFORMANCE OF HAMSTERS WITH POLYACRYLAMIDE IMPLANTS CONTAINING ETHINYLOESTRADIOL

1972 ◽  
Vol 70 (2) ◽  
pp. 385-395 ◽  
Author(s):  
B. K. Davis ◽  
I. Noske ◽  
M. C. Chang
Keyword(s):  
Reproductive Performance ◽  
Mature Female ◽  
Pregnancy Rates ◽  
List Type ◽  
Pathological Changes ◽  
Apparent Effect ◽  
Tissue Sections ◽  
Main Target

ABSTRACT Mature female hamsters bearing subcutaneous polyacrylamide (PAA) implants, with ethinyloestradiol (EO), for at least 10 days prior to mating revealed: 0.5 and 2.5 mg EO in 7% PAA significantly disturb the timing of oestrus and mating, but have no apparent effect on rate of pregnancy, ovulation and implantation. 2.5 mg EO in 20 and 40% PAA conspicuously reduces the likelihood of pregnancy, although the occurrence of oestrus and mating are affected only slightly. Fertility in these hamsters was virtually restored, judging from pregnancy rates, when they were remated 11 days, or more, following removal of their implants (37 days after implantation), but significantly more foetuses were resorbed in these litters. From tissue sections of skin and muscle at the implant site, ovary, uterus, pituitary, adrenals and liver, PAA implants, without EO, cause no overt pathological changes in the bearer. Effects characteristic of oestrogen are present when these implants contain EO, and these include a conspicuous thickening of the epidermis and dermis; haemorrhagic lesions were also noted in the maternal placenta of animals with EO implants. There is an association between reproductive performance and the rate of EO release by an implant. A 7% PAA implant with 2.5 mg EO can release most of it within 2 days, and principally influences events (oestrus and mating) that precede the main target (pregnancy) of a 20% PAA implant, which releases the steroid over the longer interval of 7 days.

Cognitive dysfunctions associated with white matter damage due to cardiovascular burden – determinants and interpretations

2014 ◽  
Vol 45 (3) ◽  
pp. 334-345 ◽  
Author(s):  
Paweł Krukow
Keyword(s):  
Cerebral Cortex ◽  
White Matter ◽  
Cardiovascular Diseases ◽  
Cognitive Disorder ◽  
Theoretical Background ◽  
Dynamic Aspect ◽  
Pathological Changes ◽  
White Matter Damage ◽  
Neuropsychological Disorders ◽  
Considerable Research

AbstractAlthough considerable research has been devoted to cognitive functions deteriorating due to diseases of cardiovascular system, rather less attention has been paid to their theoretical background. Progressive vascular disorders as hypertension, atherosclerosis and carotid artery stenosis generate most of all pathological changes in the white matter, that cause specific cognitive disorder: disconnection syndromes, and disturbances in the dynamic aspect of information processing. These features made neuropsychological disorders secondary to cardiovascular diseases different than the effects of cerebral cortex damage, which may be interpreted modularly.

EFFECT OF KAGOCEL PREPARATION ON THE GENERATIVE FUNCTION OF EXPERIMENTAL ANIMALS AT ITS ADMINISTRATION IN THE INFANTILE PERIOD OF THEIR DEVELOPMENT

2017 ◽  
pp. 42-49
Author(s):  
T. A. Borovskaya ◽  
M. E. Poluektova ◽  
A. V. Vychuzhanina ◽  
V. A. Mashanova ◽  
Yu. A. Shchemerova
Keyword(s):  
Toxic Effect ◽  
Reproductive System ◽  
Safety Profile ◽  
Therapeutic Dose ◽  
Antiviral Drug ◽  
Experimental Studies ◽  
Reproductive Age ◽  
Pathological Changes ◽  
Pediatric Practice ◽  
Experimental Animals

In experimental studies on rats (males, females) at their infantile stage starting from 10 days, a potential delayed toxic effect of the antiviral drug Kagocel on the reproductive system was studied. The drug was administered for 12 days in a therapeutic dose and at a dose 10-fold higher than the therapeutic one. Reproductive safety was estimated after animals reached the reproductive age (2.5 months). It was found out that the drug, when administered in both doses, does not decrease the fertility of animals, does not induce morphological and pathological changes in the sex glands, and does not have toxic effect on the offspring. Obtained data characterize Kagocel as a preparation with a wide reproductive safety profile and show that it can be used in pediatric practice for infants.

Testicular Injury Attenuated by Rapamycin Through Induction of Autophagy and Inhibition of Endoplasmic Reticulum Stress in Streptozotocin- Induced Diabetic Rats

2019 ◽  
Vol 19 (5) ◽  
pp. 665-675 ◽  
Author(s):  
Wenjiao Shi ◽  
Zhixin Guo ◽  
Ruixia Yuan
Keyword(s):  
Oxidative Stress ◽  
Endoplasmic Reticulum ◽  
Endoplasmic Reticulum Stress ◽  
Protective Effect ◽  
Er Stress ◽  
B Cell Lymphoma ◽  
Diabetic Rats ◽  
Pathological Changes ◽  
Rapamycin Treatment ◽  
Related Proteins

Background and Objective: This study investigated whether rapamycin has a protective effect on the testis of diabetic rats by regulating autophagy, endoplasmic reticulum stress, and oxidative stress. Methods: Thirty male Sprague-Dawley rats were randomly divided into three groups: control, diabetic, and diabetic treated with rapamycin, which received gavage of rapamycin (2mg.kg-1.d-1) after induction of diabetes. Diabetic rats were induced by intraperitoneal injection of streptozotocin (STZ, 65mg.Kg-1). All rats were sacrificed at the termination after 8 weeks of rapamycin treatment. The testicular pathological changes were determined by hematoxylin and eosin staining. The protein or mRNA expression of autophagy-related proteins (Beclin1, microtubule-associated protein light chain 3 (LC3), p62), ER stress marked proteins (CCAAT/enhancer-binding protein (C/EBP) homologous protein (CHOP), caspase-12), oxidative stress-related proteins (p22phox, nuclear factor erythroid2-related factor 2 (Nrf2)) and apoptosis-related proteins (Bax, B cell lymphoma-2 (Bcl-2)) were assayed by western blot or real-time fluorescence quantitative PCR. Results: There were significant pathological changes in the testes of diabetic rats. The expression of Beclin1, LC3, Nrf2, Bcl-2 were significantly decreased and p62, CHOP, caspase12, p22phox, and Bax were notably increased in the testis of diabetic rats (P <0.05). However, rapamycin treatment for 8 weeks significantly reversed the above changes in the testis of diabetic rats (P <0.05). Conclusion: Rapamycin appears to produce a protective effect on the testes of diabetic rats by inducing the expression of autophagy and inhibiting the expression of ER-stress, oxidative stress, and apoptosis.

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