Wyniki wyszukiwania

1

Involvement of serum anti-retinal antibodies in the pathophysiology of diabetic retinopathy: a pilot study

100%

Weglarz M., Romanowska-Dixon B., Wilanska J., Sanak M., Karska-Basta I.

Journal of Physiology and Pharmacology

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2020

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tom 71

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nr 5

2

Decreased immunoreactivity of von Willebrand factor may reflect persistent nature of the endothelial dysfunction in non-ischemic heart failure

100%

Reichman-Warmusz E., Brzozowska-Zasada M., Wojciechowska C., Dudek D., Warmusz O., Wojnicz R.

Folia Histochemica et Cytobiologica

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2021

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tom 59

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nr 2

3

Pathophysiology of portal hypertension

100%

Cichoz-Lach H., Celinski K., Slomka M., Kasztelan-Szczerbinska B.

Journal of Physiology and Pharmacology. Supplement

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2008

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tom 59

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nr 2

In last years significant progress in recognizing mechanisms of portal hypertension pathophysiology was done. However, some unclear topics in this disease still exist. Portal hypertension is primarily caused by the increase in resistance to portal outflow and secondly by an increase in splanchnic blood flow. Portal hypertension is associated with changes in the intrahepatic, systemic, and portosystemic collateral circulation. Alterations in vasoreactivity (vasodilation and vasoconstriction) play a central role in the pathophysiology of portal hypertension by contributing to increased intrahepatic resistance, hyperdynamic circulation, and expansion of the collateral circulation. Among vasoactive substances which are activated in portal hypertension nitric oxide (NO) is considered as the most important vasodilator. Endothelin-1 and cyclooxygenase-derived prostaglandins are the main vasoconstrictor factors. The imbalance between the hyperresponsiveness and overproduction of vasoconstrictors and the hyporesponsiveness and impaired production of vasodilators are the mechanisms responsible of the increased vascular tone in the sinusoidal area of the liver. New concepts in the pathophysiology of portal hypertension find the significant role of hepatic stellate cells activated by endothelial factors which cause vascular remodeling as an adaptive response of the portal vessels wall. The most frequent causes of portal hypertension include portal vein thrombosis, storage diseases of the liver, hepatic cirrhosis (independent of etiology), hepatic veins thrombosis and schistosomiasis. Understanding the pathophysiology of portal hypertension could be of great utility in preventing and curing the complications of portal hypertension, such as esophageal varices, hepatic encephalopathy, ascites.

4

New insights into physiology and pathophysiology by resistance-volume recordings

86%

Ulmer W. T., Schafer T.

Journal of Physiology and Pharmacology. Supplement

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2004

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tom 55

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nr 3

149-153

This work deals with the assessment of airway resistance in the course of a single breath. The study showed the presence of an early increase in the resistance at the beginning of expiration, which intensifies during expiration and ends up with a sharp decline during expiring the last remaining volume of ca 350 ml. The dynamic changes in airway resistance over a breath depend on the disharmonic interplay between diaphragm function and bronchial wall tonus. Thus, airway resistance is not constant during breathing, as could be misleadingly judged from the total resistance averaged over a breath. The study underscores the importance of recording the resistance-volume curves alongside the standard flow-volume curves to be able to discern the peculiarities of airway resistance changes during a single breath. Knowing changes in the instantaneous airway resistance characteristic for a given lung pathology could appreciably improve the diagnostic and therapeutic powers.

5

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Pathophysiology of ischemic reperfusion injury and the molecular targets involved in amelioration of brain injury by herbal medicine

86%

Badamasi I. M.

Journal of Pre-Clinical and Clinical Research

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2021

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tom 15

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nr 2

6

Edward Stanislaw Czarnecki 1892-1970

86%

Mietkiewski E.

Acta Physiologica Polonica

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1987

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tom 38

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nr 3

7

Placental prostate-specific antigen content in preeclampsia

86%

Can M., Acikgoz S., Guven B., Bayar U. O.

Acta Biochimica Polonica

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2012

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tom 59

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nr 3

Preeclampsia is a multisystem disorder that can manifest clinically with hypertension and proteinuria. Previous studies reported the presence of placental PSA in normal pregnancy but no study has been done in preeclampsia. The aim of this study was to investigate PSA content in preeclampsia. Preeclampsia was diagnosed according to the American College of Obstetricians and Gynecologists criteria. Placentas were obtained from 33 preeclamptic and 34 normotensive women. Placenta samples were homogenized and the supernatants were immediately analyzed. The tissue PSA content was measured by Immulite 2000 PSA assay. The data were analyzed with Student's t-test and Pearson correlation test. There was a significant difference in placental PSA content between preeclamptic and normotensive women. Placental content of PSA was higher in the preeclamptic group with intrauterine growth restriction (IUGR) than in the preeclamptic and normotensive pregnant without IUGR groups. No significant difference was found in this respect between preeclamptic and normotensive women without IUGR. In conclusion, we found that placental PSA content is elevated in preeclampsia and negatively correlated with infant birth weight. Further studies will be necessary to define the roles of PSA more precisely and to examine its effects on the pathophysiology of preeclampsia.

8

The pathophysiology of intracerebral haemorrhage

86%

Karwacki Z., Kowianski P., Witkowska M., Karwacka M., Dziewiatkowski J., Morys J.

Folia Morphologica

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2006

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tom 65

|

nr 4

295-300

Spontaneous intracerebral haemorrhage carries a high mortality rate and treatment of the disease raises more questions then answers. Mass effect, ischaemia and toxicity of blood components are responsible for brain tissue damage. Initially occurring disturbances of cerebral blood flow have a temporary character and do not play a key role in the pathology of intracerebral haematoma. Oedema formatting in the 24–48 hours after intracerebral bleeding is the result of multidirectional processes. The pathological mechanism that underlines it is the function of activation of systemic complement and cascade of coagulation. In the light of these findings, further clinical and experimental investigations should be focused on these factors.

9

Cardiac chemoreflex sensitivity in critically ill patients

86%

Schueller P. O., Steiner S., Hennersdorf M. G., Strauer B. E.

Journal of Physiology and Pharmacology. Supplement

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2008

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tom 59

|

nr 6

623-627

10

Cardiac rehabilitation in heart failure. Part I. Mechanism

86%

Kujawska A., Husejko J., Marszalek A., Szczesniak Z., Topka W., Gajos M., Androsiuk-Perkowska J., Perkowski R., Skierkowska N., Kujawski S., Kedziora-Kornatowska K.

Central European Journal of Sport Sciences and Medicine

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2018

|

tom 21

|

nr 1

11

The pathogenesis and pathophysiology of acute pancreatitis

86%

Steer M. L.

Journal of Physiology and Pharmacology. Supplement

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1998

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tom 49

|

nr 2

12

The role of phospholipases A2 in the pathophysiology of acute pancreatitis. A review

86%

Hietaranta A. J., Kemppainen E. A., Gronroos J. M., Nevalainen T. J.

Journal of Physiology and Pharmacology. Supplement

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1998

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tom 49

|

nr 2

13

Silver-binding nucleolar organizer regions [AgNORs] in the normal epithelium of different parts of the digestive tract in rats

86%

Zaczek M., Maciejowski J., Gil K., Szot W., Chlap Z.

Folia Histochemica et Cytobiologica

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1994

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tom 32

|

nr 2

14

Impact of fetal-maternal tolerance in hematopoietic stem cell transplantation

86%

Teshima T., Matsuoka K., Ichinohe T.

Archivum Immunologiae et Therapiae Experimentalis

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2006

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tom 54

|

nr 3

15

4-OH-TEMPO prevents the morphological alteration of rat thymocytes primed to apoptosis by oxidative stress inducer ButOOH

86%

Kossowska E., Zauszkiewicz A., Kubasik-Juraniec J., Tukaj C., Spodnik J. H., Hallman A., Klimek J., Syta E., Figarski A., Wakabayashi T., Wozniak M.

Folia Morphologica

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2004

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tom 63

|

nr 3

Thymocytes exposed to the pro-oxidant tert–butyl-hydroperoxide (ButOOH) display a number of dramatic changes in morphology similar to those observed in the case of dexamethasone-treated cells. Both reagents induce nuclear chromatin peripheral aggregation below the nuclear membrane. Some nuclei themselves break up producing two or more fragments. ButOOH-treated cells are morphologically characterised by cell shrinkage, extensive surface blebbing and, finally, fragmentation into membrane–bound apoptotic bodies composed of cytoplasm and tightly packed with or without nuclear fragments. An increased level of lipid hydroxyperoxides was detected after exposure of thymocytes to ButOOH. Both oxidative stress markers and morphological damage to cells were prevented by the antioxidant 4-OH-TEMPO.

16

Extent of metallothionein expression in correlation with expression of Ki-67 antigen in soft tissue fibrosarcomas in dogs

86%

Nowak M., Madej J. A., Dziegiel P.

Bulletin of the Veterinary Institute in Puławy

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2007

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tom 51

|

nr 1

This study is aimed at a immunocytochemical demonstration of metallothionein and Ki-67 expression, and to define the correlation between the markers in spontaneous fibrosarcomas in dogs. Material for the study was sampled during operative procedures from 27 dogs of various breeds, aging 5 to 16 years. The neoplastic tumours were histopathologically verified and immunohistochemical reactions were conducted to detect MT and Ki-67. Microphotographs of the preparations were subjected to computer-assisted image analysis. In light of the numerous established studies for a high prognostic value of Ki-67, for this reason we have identified in our studies a weak correlation between the expressions of MT and Ki-67 (r = 0.15), which allows us to conclude that the presence of metallothioneins in the cells of soft tissue fibrosarcomas in dogs does not manifest an unequivocal relationship with augmented proliferative potential of tumour cells, as it was demonstrated in similar tumours in humans.

17

Food allergy and the oral immunotherapy approach

72%

Cabrera C. M., Urra J. M.

Archivum Immunologiae et Therapiae Experimentalis

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2015

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tom 63

|

nr 1

18

Magnesium in pathophysiology and therapy of affective disorders

72%

Poleszak E., Nowak G.

Journal of Elementology

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2006

|

tom 11

|

nr 3

p.389-397,fig.,ref.

Magnesium possesses activity in a broad range of biochemical processes in living organisms. This review focus on the role of magnesium in pathophysiological and therapeutical mechanisms of affective disorders. Magnesium as an antagonist of the N-methyl-D- -aspartate (NMDA)/glutamate receptor complex, is active in the antidepressant screen test, forced swim test in rodents. Clinical studies, although providing very limited amount of data, suggest possible efficacy of magnesium in mania (bipolar affective disorders). Magnesium deficiency induced depression-like behavior in animals, and such an effect in humans is also suggested. All the available data indicate the importance of magnesium homeostasis in pathophysiology and therapy of affective disorders.

19

Pathophysiology and clinical characteristics of pain in most common locations in cancer patients

72%

Leppert W., Zajaczkowska R., Wordliczek J., Dobrogowski J., Woron J., Krzakowski M.

Journal of Physiology and Pharmacology

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2016

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tom 67

|

nr 6

20

Pathophysiological mechanism of cardiac arrhytmias as a key for optimal nonpharmacological treatment

72%

Kozluk E.

Journal of Physiology and Pharmacology. Supplement

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2006

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tom 57

|

nr 11

69-77

Pathological automatism and triggered activity had focal origin. Thus, the treatment has to be aimed at ablation of the arrhythmogenic region. Some arrythmogenic places can be precisely characterized by analysis of ECG patterns. Among them are foci located close to the pulmonary veins, sinus node, ventricular outflow tracts or mitroaortic commissura. Classical ablation of these loci is highly successful. In other types of focal arrhythmias electroanatomical systems make possible to create 3D map, with activation sequence allowing for identification of the place where the arrhythmia could be eliminated. In reentrant mechanism of the arrhythmia the impulse circulates around the loop via the cardiac muscle. In case of the atrioventricular nodal reentrant tachycardia, atrial flutter or bundle branch ventricular tachycardia the loop can be easily outlined. Ablation can be performed using the anatomical method without induction of the tachycardia. In patients with the ventricular tachycardia with multiple forms or hemodynamically unstable it is possible to perform electranatomical map with visualization of the scar and the border zones. In this case the proarrhythmic region in the borderline zone is the aim of linear ablation without induction of tachycardias. In the chaotic tachycardias (atrial or ventricular fibrillation), the arrythmogenic substrate is too much dispersed to destroy them. Therefore, the ablation is aimed at the trigger which is initiating the arrhythmia (for instance the pathological Purkinje fibers). The excitability of the substrate may be also modified by pacemakers (ventricular or atrial resynchronization). In the life-threatening arrhythmias implantable cardioverter-defibrillator is necessary.

Ograniczanie wyników

Involvement of serum anti-retinal antibodies in the pathophysiology of diabetic retinopathy: a pilot study