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1

Analysis of Expression of Acetylcholine and Acetylcholinesterase in the Urinary Bladder in Vesicoureteral Reflux in Children

100%

Apoznański W.

Polish Journal of Surgery

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2007

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vol. 79

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issue 5

375-384

EN

Numerous disorders of the lower urinary tract observed in children, such as dysfunctional voiding, infections or vesicoureteral reflux, may be caused by defective synchronization between the central nervous system and the activity of the lower urinary tract. The analysis of acetylcholine and acetylcholinesterase's activity - the mediator and inhibitor of neurotransmission in the parasympathetic nervous system - can provide a lot of information concerning the extent to which the anomalies have developed and the possibility of pharmacological correction of the aforementioned lower urinary tract pathology.The aim of the study was to determine the role of the parasympathetic nervous system in the pathological creation of vesicoureteral reflux.Material and methods. This study was conducted between the years 2000 and 2004 in the Clinic of Pediatric Surgery and Urology of Wrocław Medical University. Thirty children who underwent surgical correction of vesicoureteral reflux underwent full-thickness biopsy of the bladder wall during the procedure. In each case, the biopsy was taken from the top of the bladder incision used to perform uretrocy-stoneostomy; those children formed group "0". Nineteen children with neurogenic dysfunction of the lower urinary tract who had bladder-augmenting surgery also underwent biopsy from the top of the bladder incision; those children formed group "N". Results of the bladder wall's tests of 6 children who have undergone surgery to open the bladder for a different reason than vesicoureteral reflux were also analyzed (control group - K). The biopsies of the bladder wall were put on ice and immediately sent to the Immunohistochemy Laboratory of the Pathological Anatomy Institute of the Medical University in Wrocław. These samples underwent a reaction with monoclonal antybodies against acetylcholine and acetylcholinesterase to determine acetylcholine and acetylcholinesterase activity. Because of considerable difficulty in objective determination of the intensity of the colour reaction, an arbitrary division into three structural areas of the bladder was introduced:- epithelium- blood vessel endothelium- muscle layerIn order to interpret the results of the tests, a statistical analysis was performed.Results. Statistical analysis of the results shows a strong correlation between the occurrence of bladder instability and ACH stimulation in the bladder wall's muscle layer, both in children with vesicoureteral reflux and with neurogenic dysfunction of the lower urinary tract. A similar reaction occurs with ACHE and bladder instability. Degrees of this correlation suggest a strong cause-and-effect relationship between parasympathetic activity and the bladder instability phenomenon. One could ask at this point if it is caused by too much ACH or not enough ACHE activity. The performed analyses indicate that both processes are present.Conclusion. One of the preconditions of vesicoureteral reflux occurrence is excessive stimulation of the parasympathetic nervous system in bladder wall epithelium.

2

Cardiac Rehabilitation in Heart Failure. Part I, Mechanism

100%

Kujawska A., Husejko J., Marszałek A., Szczęśniak Ż., Topka W., Gajos M., Androsiuk-Perkowska J., Perkowski R., Natalia S., Kujawski S., Kędziora-Kornatowska K.

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EN

Diagnosis and treatment issues among heart failure (HF) patients are becoming one of the most important points in public health of developed countries, largely due to the aging of population and the fact that HF affects mainly the elderly. In this review we would like to focus on pathophysiology of exercise intolerance in patients with heart failure and potential benefits of cardiac rehabilitation (CR). Analysis of articles in the EBSCO database using keywords: heart failure, cardiac rehabilitation, exercise training, pathophysiology. HF can be described as a composite syndrome which results from structural or functional impairment of ventricular filling or blood ejection. Patients have variety of symptoms which usually are nonspecific. The most frequently occurring symptoms of HF are dyspnea and fatigue, which may restrict exercise capacity, and fluid retention. There are many possible pathophysiological factors involved in the development of exercise intolerance. Based on the available literature pathological changes in central hemodynamic function, pulmonary system, skeletal muscles, endothelial function and neurohumoral system can be distinguished. They play a crucial role in the pathogenesis of HF symptoms and represent a potential curative object. HF patients are characterized by diminished functional performance. Exercise training has many potential profits in patients with heart failure, including an increase in peak oxygen uptake, improvement in central hemodynamics, peripheral vascular and skeletal muscle function and has become part of evidence-based clinical therapy in these patients.

3

Early concepts on the mechanism of peritonitis with special regard to the experimental work of Karol Klecki

75%

Gryglewski R. W., Gryglewski R. W.

Folia Medica Cracoviensia

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2021

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vol. 61

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issue 2

4

Extraesophageal manifestations of gastroesophageal reflux disease – pathophysiology, diagnosis and management

75%

Dobrzyński P., Ziuzia L.

Polski Przegląd Otorynolaryngologiczny

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2016

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vol. 5(2)

26-45

EN

Gastroesophageal reflux disease (GERD) is defined as a condition in which the reflux of stomach contents causes troublesome symptoms and/or complications. This common disease may also present with atypical, extraesophageal symptoms. Laryngopharyngeal reflux (LPR) is the reflux of gastric contents into the throat and larynx, which causes symptoms such as globus, throat clearing, hoarseness and chronic cough. GERD and LPR may be related to many dis-eases, including laryngitis, asthma, COPD, chronic rhinosinusitis, otitis media, dental erosions, and even laryngeal cancer or life-threatening events. The diagnosis of LPR is based on clinical symptoms (measured by RSI), laryngoscop-ic signs (evaluated in RFS), an empiric trial of proton pomp inhibitor (PPI) therapy, 24-hour pH monitoring, impedance monitoring, esophageal manometry and endoscopic examination. The most common management is double-dose PPI therapy for at least six months. When this treatment is ineffective, the surgery should be considered. However, di-agnosis and treatment of LPR is still controversial. Further studies are necessary to establish an optimal algorithm for the management of LPR.

5

The pathophysiology of Lennox-Gastaut syndrome – a review of clinico-electrophysiological studies

75%

Yagi K.

Journal of Epileptology

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2015

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vol. 23

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issue 1

7-23

EN

Introduction. Lennox-Gastaut syndrome (LGS) is a type of therapy-resistant epileptic syndrome. Since the establishment of our Epilepsy Center in 1975 we have performed many studies to assess the clinical symptoms, seizure manifestations, sleep and long-term follow-up of the clinical course and changes on electroencephalographs (EEGs) in patients with LGS. Aim. To review the updated pathophysiology of LGS based on our own clinico-electrophysiological data referring to recent advances in brain research. Methods. All of our previously published and unpublished data were reviewed in order to investigate the pathophysiology of LGS and using PubMed database for relevant literature. Results and Discussion. While LGS usually occurs in infancy, it has become apparent that there is a form of late-onset LGS (L-LGS) that may occur at age eight or older. L-LGS often occurs when there is a history of encephalitis/encephalopathy or status epilepticus. The long-term progression of LGS includes mainly tonic seizures that persist and are the basis of LGS. In approximately 30% of cases, the basic symptoms of LGS remain 10 years or longer after long-term progression, while the rest lose their characteristics, although the condition is residual in 60% of cases and remission occurs in fewer than 10%. Among the characteristic seizures associated with LGS, atypical absence seizures occur in response to a diverse range of EEG features; wherein, while they are mostly short, they are accompanied by a state of enervation along with a tendency for it to be unclear when the seizure has ended. Drop attacks can in fact be categorized into those in which the subject falls over due to hypertonia in the muscles used to maintain body posture and those in which the subject falls over due to loss of tension in the posture-retaining muscles. Tonic seizures range from those manifesting in the form of extremely mild axial muscle tonicity, open eyes and respiratory changes, accompanied by high voltage, fast rhythm (averaging 14 ± 0.4 Hz), or tonicity from axorhyzomelic muscles to the peripheral muscles, accompanying global tonic seizures, and EEG features showing low voltage fast activity (averaging 22 ± 0.6 Hz) from desynchronization. A total of 1191 clinical seizures were recorded upon overnight polysomnography and videotape, and seizure symptoms and their ictal EEGs were analyzed. In LGS, seizure activity increases during slow wave sleep, inhibiting progression into the further sleep stages but falls significantly during rapid eye movement (REM) sleep. Conclusions. From the research into seizure symptoms, clinical progression, sleep and seizures during sleep, it was believed that in LGS epileptic native lesions occur due to mesencephalic reticular formation, in the thalamic reticular system and, as a result of recent of brain physiology research, it is considered that LGS is an epileptic reticulo-thalamo-cortical system disorder. This has been supported by EEG-fMRI findings (Siniatchikin et al., 2011). Further research is therefore necessary to elucidate the role of the reticular formation in controlling the thalamo-cortical networks in humans.

6

Znaczenie receptora estrogenów oddziałującego z białkami G w fizjologii i patofizjologii

63%

Cygankiewicz A., Jacenik D.

Folia Medica Lodziensia

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2015

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vol. 42

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issue 2

145-168

EN

Estrogens, without doubt, play a pivotal role in the regulation of both physiological and pathological processes. A plethora of intercellular signaling pathways are regulated by estrogens on both genomic, and non–genomic pathways via canonical ERα and ERβ receptors. Studies published in recent years showed that not all biological effects of estrogens can be attributed to the classical model of estrogen signaling. Aside canonical ERα and ERβ receptors a G–protein coupled estrogen receptor plays its role in estrogen mediated regulation of various tissues and organs. Ubiquitous presence of G–protein coupled estrogen receptor in different tissues, as well as observed de–regulation of its expression in multiple pathologies suggest an important role of this receptor in functioning of cells, tissues and organisms. Activation/deactivation of GPER estrogen receptor takes place during the metabolism of carbohydrates, lipids and immunological response, it is involved in a number of events from reproductive, cardiovascular, neurological and skeletal systems.

PL

Estrogeny, bez wątpienia, odgrywają istotną rolę w regulacji procesów fizjologicznych i patofizjologicznych. Za pośrednictwem kanonicznych recepto– rów estrogenów ERα i ERβ hormony te modulują wiele ścieżek sygnałowych w komórce zarówno na drodze genomowej, jak i niegenomowej. Wyniki badań ostatnich lat ujawniają, że nie wszystkie biologiczne efekty estrogenów wynikają z ich klasycznego modelu działania. Obok kanonicznych receptorów ERα i ERβ w estrogenozależnej regulacji funkcjonowania wielu tkanek i narządów pośred– niczy receptor estrogenów oddziałujący z białkami G. Powszechne występowa– nie receptora estrogenów oddziałującego z białkami G w różnych tkankach, jak i obserwowana deregulacja jego ekspresji w określonych patologiach pozwala domniemywać o istotnej roli tego receptora w funkcjonowaniu komórek, tkanek i organizmów. Aktywacja/dezaktywacja receptora estrogenów GPER ma miejsce podczas metabolizmu węglowodanów i lipidów czy odpowiedzi immunologicznej, zaangażowana jest w wiele zdarzeń ze strony układu rozrodczego, sercowo– naczyniowego, nerwowego oraz kostnego.

7

Zaburzenia kaskady transformujących czynnikow wzrostu typu β w wybranych patologiach człowieka

63%

Zakrzewski P.

Folia Medica Lodziensia

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2012

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vol. 39

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issue 2

265-292

EN

A transforming growth factor β type (TGFβ) cascade is a multifactorial signalling pathway, which controls the plethora of cellular processes responsible for human organism homeostasis. The importance of alterations of TGFβ-induced signalling remains unknown. Up till now, impaired TGFβ signalling has been observed in pathologies of the musculoskeletal, cardiovascular and reproductive systems. Abnormalities in the TGFβ pathway can be either genetically determined or appear as spontaneous disorders which emerged during embryonic development. Understanding the role of the TGFβ pathway in the aetiology of various diseases appears to be necessary as it may serve in developing new strategies for therapeutic or diagnostic methods.

PL

Kaskada sygnalizacyjna transformujących czynników wzrostu typu β (TGFβ) stanowi indukowany przez wiele cytokin szlak przekazywania sygnału w komórce, pod kontrolą którego znajduje się szereg procesów komórkowych odpowiedzialnych za prawidłowe funkcjonowanie ludzkiego organizmu. Znaczenie zaburzeń sygnalizacji indukowanej czynnikami TGFβ pozostaje nadal nie do końca poznane. Niemniej jednak już na obecnym etapie badań stwierdzić można ich bezsprzeczny udział w patologiach układu kostno-mięśniowego, układu krwionośnego czy układu rozrodczego.

8

Aktualne poglądy na patogenezę i leczenie zespołu zmęczenia w stwardnieniu rozsianym

63%

Brola W., Fudala M.

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2011

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vol. 11

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issue 1

23-28

EN

Fatigue, defined as subjective lack of energy to start and continue any activity without any connections with depression and muscular weakness, is one of the most common and troublesome symptoms of multiple sclerosis (MS). It concerns almost all patients, and in approximately half of them it is a major symptom. It may occur in cases of patients with little neurological symptoms and significantly affect the quality of life. In spite of intensive researches in last years pathophysiology of fatigue syndrome has not been enough recognized. The role of various mechanisms has been suggested: local prefrontal cortex and basal ganglia atrophy, changes in activity of B lymphocytes, disturbances of glutaminergic transmission caused by proinflammatory cytokines (TNF-α, IL-1β and IL-6), hypothalamic-pituitary-adrenal axis dysfunction, disturbances of astroglia metabolism with dehydroepiandrosteron (DHEA) decreased level and decreased levels of neurotransmitters noradrenaline and serotonin as well. The diagnosis of fatigue syndrome is based on anamnesis,physical examination, screening laboratory tests and evaluation by means of scales, for example Fatigue Severity Scale (FSS), Modified Fatigue Impact Scale (MFIS). The necessary condition is to exclude depression or additional organic conditions (anaemia, cardiovascular disorders, kidney diseases or hypothyroidism). Treatment of fatigue is not sufficiently effective. Pharmacological treatment leads to slight improvement although recent clinical trials with modafinil and fampridine have given promising results. Beneficial influence of physical exercises, cryotherapy and magnetotherapy has been observed. What may help in therapy is emotional support, cognitive-behavioural therapy and psychotherapy as well as avoidance of factors which may increase fatigue such as fever, anxiety, depression, pain, sleep disturbances, and also some drugs like opiates and benzodiazepines.

PL

Zmęczenie, definiowane jako subiektywne odczucie braku energii do rozpoczynania i podtrzymywania dowolnej aktywności pozostające bez związku z depresją lub osłabieniem siły mięśniowej, jest jednym z najczęstszych i zwykle najbardziej uciążliwych objawów stwardnienia rozsianego (SR). Dotyczy prawie wszystkich chorych, natomiast u ponad połowy jest objawem dominującym. Może występować u chorych ze stosunkowo niewielkimi objawami neurologicznymi i w znacznym stopniu wpływać na jakość życia. Mimo intensywnych badań w ostatnich latach patofizjologia zespołu zmęczenia nie jest w pełni poznana. Za występowanie zmęczenia w SR odpowiedzialne mogą być różne mechanizmy: lokalny zanik kory przedczołowej i jąder podstawy, zmiana aktywności limfocytów B, zaburzenia transmisji glutaminergicznej przez cytokiny prozapalne (TNF-α, IL-1β i IL-6), nieprawidłowe funkcjonowanie osi podwzgórze – przysadka – nadnercza, zaburzenia metabolizmu astrogleju i spadek produkcji dehydroepiandrosteronu (DHEA) oraz obniżenie poziomu neuroprzekaźników noradrenaliny i serotoniny. Rozpoznanie zespołu zmęczenia opiera się na wywiadzie, badaniu fizykalnym, przesiewowych badaniach laboratoryjnych i skalach oceniających zmęczenie, np. Skali Ciężkości Zmęczenia (FSS) i Skali Oddziaływania Zmęczenia (MFIS). Warunkiem koniecznym jest wykluczenie depresji oraz dodatkowych przyczyn organicznych (niedokrwistości, chorób serca, nerek czy niedoczynności tarczycy). Leczenie zmęczenia jest mało skuteczne. Farmakoterapia daje niewielką poprawę, chociaż ostatnie próby z zastosowaniem modafinilu i famprydyny przyniosły obiecujące rezultaty. Zaobserwowano korzystny wpływ ćwiczeń fizycznych, krioterapii i magnetostymulacji. Pomocne są też wsparcie emocjonalne chorego, terapia poznawczo-behawioralna i psychoterapia oraz unikanie czynników mogących nasilać zmęczenie, takich jak gorączka, lęk, depresja, ból, zaburzenia snu, czy niektórych leków, np. opiatów, benzodiazepin.

9

Patofizjologia zespołów cieśni

63%

Hupało M.

Aktualności Neurologiczne

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2006

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vol. 6

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issue 4

242-245

EN

The paper reviews the pathophysiology of both acute and chronic peripheral nerve entrapments. Factors influencing susceptibility of the nerve fibers to such an injury were presented. Pathophysiological mechanisms influencing extent of the injury of the nerve were looked at, taking into consideration cases of double crush syndrome. Moreover, pathological changes occurring in the instances of short-lasting acute compression of the nerve were described, namely metabolic conduction block and segmental, local perinodal demyelinization with partial or complete conduction block. Furthermore, microscopic and ultrastructural changes found in chronically compressed nerves were presented in detail, explaining the mechanisms of demyelinization injury in the early phase of entrapment neuropathy and demyelinization-axonal injury in the advanced stage of the disease. This paper reviews two best known grading systems of peripheral nerve injuries, i.e. Seddon’s and Sunderland’s classifications which assess the functional condition of the nerve and ongoing histological changes. These classifications were explained along with neurophysiological data in order to facilitate understanding of neurography and EMG tests results as the guide for therapy and prognosis.

PL

W pracy przedstawiono mechanizmy uszkodzenia nerwów obwodowych na skutek ucisku. W pierwszym rzędzie zwrócono uwagę na czynniki determinujące podatność nerwów na ten rodzaj urazu, starając się przy tym wyjaśnić, od czego zależy rozległość uszkodzenia kompresyjnego nerwu, uwzględniając m.in. zespół podwójnego zmiażdżenia (double crush syndrome). Ponadto w pracy omówiono zmiany patofizjologiczne w nerwach obwodowych, rozwijające się na skutek nagłego, krótkotrwałego ucisku, tj. metaboliczny blok przewodzenia i odcinkową, miejscową, przywęzłową demielinizację z częściowym lub całkowitym blokiem przewodzenia. Oprócz tego bardzo szczegółowo przedstawiono zmiany mikroskopowe i ultrastrukturalne zachodzące w nerwach narażonych na długotrwały ucisk, wyjaśniając mechanizmy uszkodzenia demielinizacyjnego w początkowej fazie zespołów cieśni oraz uszkodzenia demielinizacyjno-aksonalnego w bardzo zaawansowanym stadium tejże choroby. W pracy przedstawiono także dwie najbardziej znane klasyfikacje uszkodzeń nerwów obwodowych, tj. wg Seddona oraz wg Sunderlanda, pozwalające ocenić stan funkcjonalny nerwu i zmiany histologiczne w nim zachodzące. Klasyfikacje te wzbogacono o informacje i komentarze neurofizjologiczne, ułatwiające interpretację wyników badań przewodnictwa i EMG, będące przy tym źródłem wskazówek terapeutycznych i rokowniczych.

Refine search results

Analysis of Expression of Acetylcholine and Acetylcholinesterase in the Urinary Bladder in Vesicoureteral Reflux in Children

Cardiac Rehabilitation in Heart Failure. Part I, Mechanism

Early concepts on the mechanism of peritonitis with special regard to the experimental work of Karol Klecki

Extraesophageal manifestations of gastroesophageal reflux disease – pathophysiology, diagnosis and management

The pathophysiology of Lennox-Gastaut syndrome – a review of clinico-electrophysiological studies

Znaczenie receptora estrogenów oddziałującego z białkami G w fizjologii i patofizjologii

Zaburzenia kaskady transformujących czynnikow wzrostu typu β w wybranych patologiach człowieka

Aktualne poglądy na patogenezę i leczenie zespołu zmęczenia w stwardnieniu rozsianym

Patofizjologia zespołów cieśni