Aim: To present on video our current most used technique of robot-assisted resection of renal tumour (RR). Material: We performed 274 RRs between June 2020 and November 2024. Our technique is based on a modification of conventional laparoscopic renal resection, of which we performed 599 between August 2004 and May 2020. RRs currently account for over one third of the surgical procedures for kidney cancer at our institution. Laparoscopic (rarely robotic assisted) nephrectomy is almost as frequent. Open resection accounts for about 17% and open nephrectomy for slightly less. Open resections are mainly indicated for more complex tumours, for tumors with significant \"toxic\" fat capsule, and when combined with other procedures, mostly for intestinal malignancies. RR is routinely performed by two console surgeons, occasionally by two additional ones. Operation technique: General anaesthesia. Optional urinary catheter inserted. Lateral position 60-70°. Upper limbs extended in front, close together. Operative field prepared for eventual lumbotomy. Transperitoneal approach. The capnoperitoneum is created with a Veres needle, CO2 pressure 12 mmHg. Assist port 12 mm slightly lateral to the umbilicus. Four 8-mm robotic ports are inserted pararectally under visual control. Four-arm daVinci Xi robotic system is inserted. Ports craniocaudally: 1. ProGrasp, 2. bipolar grasper (bipolar forceps Maryland or more often fenestrated) or monopolar curved scissors (Hot shears) according to the operated side and the dominant hand of the operator, 3. camera 30°, 4. the second of the mentioned instruments from port 2. The scissors are alternated with a needle driver, usually the Large SutureCut needle driver. In the Toldt line, the peritoneum is opened, the colon is retracted medially, and the Gerota fascia is opened medially from the kidney. The necessary part of the kidney is dissected from the fat capsule for good access to the tumour. The tumour is verified sonographically with a drop-in probe inserted through the assistant port. Scissors can be used to mark the line of resection on the kidney. The ureter is verified and the hilar vessels are released. The artery(s) or necessary branch is bypassed with tubing and clamped with the SCANLAN® robotic endo-bulldog. Only in central tumours is the vein also clamped. Knowledge of the topographic anatomy of the vessels from two-phase CT angiography is very helpful at this stage. The effectiveness of ischemia is verified by Doppler; exceptionally (especially in selective clamping of the artery branches) by NIR imaging with FireFly® with administration of indocyanine green - Verdye® 1.25-2.5 mg. The tumour is resected with cold scissors with a rim of healthy tissue. Suturing of the base is performed with an absorbable self-anchoring barbed suture (V-Loc® 90, size 3-0, 1/2 needle 26 mm). The edges of the kidney are mattress sutured with another suture, tightened with Absolok® AP300 absorbable clips (polydioxanone PDS, size ML) - \"sliding clips\" technique. The second layer of the parenchyma is sewn with simple continuation stitches, mostly without continuous anchoring. For more superficial tumours, a straight suture of the parenchyma is

• MeSH
• Laparoscopy MeSH
• Humans MeSH
• Kidney Neoplasms * surgery   MeSH
• Nephrectomy MeSH
• Robotic Surgical Procedures methods   MeSH
• Check Tag
• Humans MeSH

Kidney dysfunction often leads to neurological impairment, yet the complex kidney-brain relationship remains elusive. We employed spatial and bulk metabolomics to investigate a mouse model of rapid kidney failure induced by mouse double minute 2 (Mdm2) conditional deletion in the kidney tubules to interrogate kidney and brain metabolism. Pathway enrichment analysis of a focused plasma metabolomics panel pinpointed tryptophan metabolism as the most altered pathway with kidney failure. Spatial metabolomics showed toxic tryptophan metabolites in the kidneys and brains, revealing a connection between advanced kidney disease and accelerated kynurenine degradation. In particular, the excitotoxic metabolite quinolinic acid was localized in ependymal cells in the setting of kidney failure. These findings were associated with brain inflammation and cell death. Separate mouse models of ischemia-induced acute kidney injury and adenine-induced chronic kidney disease also exhibited systemic inflammation and accumulating toxic tryptophan metabolites. Patients with advanced chronic kidney disease (stage 3b-4 and stage 5) similarly demonstrated elevated plasma kynurenine metabolites, and quinolinic acid was uniquely correlated with fatigue and reduced quality of life. Overall, our study identifies the kynurenine pathway as a bridge between kidney decline, systemic inflammation, and brain toxicity, offering potential avenues for diagnosis and treatment of neurological issues in kidney disease.

• MeSH
• Acute Kidney Injury metabolism   chemically induced   pathology   MeSH
• Renal Insufficiency, Chronic metabolism   pathology   complications   MeSH
• Kynurenine * metabolism   MeSH
• Quinolinic Acid * toxicity   metabolism   blood   MeSH
• Kidney metabolism   pathology   MeSH
• Humans MeSH
• Metabolomics MeSH
• Disease Models, Animal MeSH
• Brain * metabolism   pathology   MeSH
• Mice MeSH
• Tryptophan * metabolism   MeSH
• Animals MeSH
• Check Tag
• Humans MeSH
• Male MeSH
• Mice MeSH
• Female MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH

An excessive increase in reactive oxygen species (ROS) levels is one of the main causes of mitochondrial dysfunction. However, when ROS levels are maintained in balance with antioxidant mechanisms, ROS fulfill the role of signaling molecules and modulate various physiological processes. Recent advances in mitochondrial bioenergetics research have revealed a significant interplay between mitochondrial peroxiredoxins (PRDXs) and monoamine oxidase-A (MAO-A) in regulating ROS levels. Both proteins are associated with hydrogen peroxide (H2O2), MAO-A as a producer and PRDXs as the primary antioxidant scavengers of H2O2. This review focuses on the currently available knowledge on the function of these proteins and their interaction, highlighting their importance in regulating oxidative damage, apoptosis, and metabolic adaptation in the heart. PRDXs not only scavenge excess H2O2, but also act as regulatory proteins, play an active role in redox signaling, and maintain mitochondrial membrane integrity. Overexpression of MAO-A is associated with increased oxidative damage, leading to mitochondrial dysfunction and subsequent progression of cardiovascular diseases (CVD), including ischemia/reperfusion injury and heart failure. Considering the central role of oxidative damage in the pathogenesis of many CVD, targeting PRDXs activation and MAO-A inhibition may offer new therapeutic strategies aimed at improving cardiac function under conditions of pathological load related to oxidative damage. Keywords: Mitochondria, Peroxiredoxin, Monoamine oxidase-A, Reactive oxygen species, Cardioprotective signaling.

• MeSH
• Humans MeSH
• Monoamine Oxidase * metabolism   MeSH
• Oxidative Stress MeSH
• Peroxiredoxins * metabolism   MeSH
• Reactive Oxygen Species * metabolism   MeSH
• Signal Transduction * MeSH
• Mitochondria, Heart metabolism   enzymology   MeSH
• Animals MeSH
• Check Tag
• Humans MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH
• Review MeSH

Arteriální hypertenze patří k ovlivnitelným rizikovým faktorům aterosklerózy a její časná léčebná intervence významně snižuje kardiovaskulární morbiditu a mortalitu. Léčbu se snažíme přizpůsobit konkrétnímu pacientovi na míru dle tíže hypertenze a jeho kardiovaskulárnímu i metabolickému rizikovému profilu. Trendem současné terapie je využívání fixních kombinací, neboť nám umožní rychlejší dosažení cílových hodnot krevního tlaku s menším množstvím nežádoucích účinků a zejména zlepšení adherence k léčbě. Kombinace beta-blokátoru (bisoprololu) a inhibitoru ACE (perindoprilu) má komplementární účinky na sympatický nervový systém a osu renin-angiotensin-aldosteronovou. Kombinace těchto léků účinně snižuje krevní tlak i tepovou frekvenci, což zlepšuje kardiovaskulární prognózu vybraných nemocných. Článek je věnován indikacím těchto léků u pacientů jak v léčbě nekomplikované hypertenze, tak v sekundární prevenci u pacientů s ischemickou chorobou srdeční. Důraz je kladen zejména na postavení beta-blokátorů.

Arterial hypertension is one of the controllable risk factors for atherosclerosis, and early medical intervention significantly reduces cardiovascular morbidity and mortality. The treatment should be tailored to the given patient according to the severity of hypertension and cardiovascular and metabolic risk profile. The trend in current therapy is to use fixed combinations to achieve blood pressure target values more rapidly with fewer side effects and to improve adherence to treatment. The combination of a beta blocker (bisoprolol) and an ACE inhibitor (perindopril) has complementary effects on the sympathetic nervous system and the renin-angiotensin-aldosterone axis. The combination of these drugs effectively lowers blood pressure and heart rate, which improves the cardiovascular prognosis of selected patients. The article deals with the indications of these drugs both in the treatment of uncomplicated hypertension and in secondary prevention in patients with coronary artery disease. Particular emphasis is placed on the role of beta blockers.

• MeSH
• Adrenergic beta-Antagonists pharmacology   therapeutic use   MeSH
• Drug Combinations MeSH
• Hypertension * drug therapy   MeSH
• Angiotensin-Converting Enzyme Inhibitors pharmacology   therapeutic use   MeSH
• Myocardial Ischemia prevention & control   MeSH
• Comorbidity MeSH
• Humans MeSH
• Check Tag
• Humans MeSH
• Publication type
• Review MeSH

askulitidy velkých tepen (LVV, large vessel vasculitis) postihují aortu a velké, z ní odstupující tepny. Řadíme sem především V2 nemoci, a sice obrovskobuněčnou arteritidu (GCA, Giant cell arteritis) a Takayasu arteriitis (TAK). Obě nemoci jsou vzácné, také proto jejich časná diagnostika často selhává. GCA (dříve nazývaná Hortonovou temporální arteritis) je idiopatické zánětlivé onemocnění probíhající zejména ve stěně medie a adventicie. Pojí se často i s extravaskulárním zánětem, nejčas - těji ve formě polymyalgia revmatica. V současné době je zřejmé, že tato arteriitida zahrnuje širokou škálu fenotypového vyjádření: rozlišujeme GCA velkých cév (LV-GCA) a kraniální formu GCA (C-GCA). Takayasu arteritis je charakteristická postižením tepen odstupujících z aorty, zejména subklaviálních, kde granulomatózní zánět vede ke vzniku stenóz až uzávěrů. Postižena je nejen medie a adventicie, ale i intima. Diagnostika se opírá o zobrazovací metody, zejména PET/CT (s průkazem zvýšené metabolické tepen aktivity ve stěnách tepen), k přesnému zobrazení tepen slouží CT nebo MR angiografie. Iniciálním vyšetřením je duplexní ultrasonografie. Laboratorním vyšetřením zjišťujeme známky zánětu (zvýšení CRP a sedimentace erytrocytů), chybí specifický marker pro monitoraci aktivity nemoci. Výsledky léčby u LVV jsou obecně lepší než u většiny systémových zánětlivých onemocnění a stavů s postižením cév malého kalibru. LVV však není benigním onemocněním. V dlouhodobém horizontu je nutno vést nemocné do remise léčbou založenou na imunosupresi, včetně nových biologických přípravků, a následně sledovat a léčit potenciální vznik ischemie různých cílových orgánů. I tak jsou relapsy časté a chronické vaskulární komplikace jsou zdrojem významné morbidity.

Large vessel vasculitis (LVV) affects the aorta and the large arteries branching from it. There are 2 diseases in particular, namely Giant cell arteritis (GCA) and Takayasu arteritis (TAK). Both diseases are rare, which is why early diagnosis often fails. GCA (formerly called Horton's temporal arteritis) is an idiopathic inflammatory disease taking place mainly in the wall of the media and adventitia. It is often associated with extravascular inflammation, most commonly in the form of polymyalgia rheumatica. It is now clear that this arteritis includes a wide range of phenotypic expression: a distinction is made between large vessel GCA (LV-GCA) and the cranial form of GCA (C-GCA). Takayasu arteritis is characterized by involvement of the arteries arising from the aorta, especially the subclavian arteries, where granulomatous inflammation leads to stenosis and occlusion. Not only the media and adventitia are affected, but also the intima. Diagnostics is based on imaging methods, especially PET/CT (with evidence of increased metabolic activity in the arterial walls), CT or MR angiography is used for accurate imaging of the arteries. The initial examination is duplex ultrasonography. Laboratory examination is used to detect signs of inflammation (elevated CRP and erythrocyte sedimentation rate); there is no specific marker to monitor disease activity. Treatment outcomes in LVV are generally better than in most systemic inflammatory diseases and conditions with small vessel involvement. However, LVV is not a benign disease. In the long term, it is necessary to guide patients into remission with immunosuppression-based therapies, including novel biologic agents, and then monitor and treat potential ischemia of various target organs. Even so, relapses are common and chronic vascular complications are a source of significant morbidity.

• MeSH
• Arteritis * diagnosis   classification   physiopathology   therapy   MeSH
• Adrenal Cortex Hormones administration & dosage   MeSH
• Antibodies, Monoclonal, Humanized administration & dosage   MeSH
• Cardiovascular Agents administration & dosage   MeSH
• Humans MeSH
• Giant Cell Arteritis diagnosis   drug therapy   pathology   MeSH
• Takayasu Arteritis surgery   diagnosis   drug therapy   pathology   MeSH
• Check Tag
• Humans MeSH
• Publication type
• Review MeSH

Diabetic foot attack je akutní manifestací syndromu diabetické nohy, která vyžaduje rychlou diagnózu a časně zahájenou komplexní terapii založenou na multidisciplinární spolupráci s cílem zachránit postiženou končetinu či nemocného. Termín attack má právě evokovat nutnost rychlé reakce po vzoru heart attack. Pacienti s diabetem a akutní manifestací syndromu diabetické nohy jsou ohroženi v případě neadekvátních opatření vysokou amputací dolní končetiny, která je spojena s vysokou celkovou morbiditou a mortalitou. Komplexní terapie zahrnuje systémovou antibiotickou terapii, opakovaný chirurgický débridement ulcerace, revaskularizaci v případě prokázané ischémie dolní končetiny a individualizovanou formu odlehčení končetiny. Bez zajištění následné ambulantní podiatrické dispenzarizace významně narůstá riziko recidivy.

Diabetic foot attack is an acute manifestation of diabetic foot syndrome that requires rapid diagnosis and early initiation of complex therapy based on multidisciplinary team cooperation to save the affected limb. The term "attack" evokes the need for a rapid reaction as for "heart attack". Patients with diabetes mellitus and acute manifestations of diabetic foot syndrome have high risk for amputation of the lower limb, which is associated with higher morbidity and mortality. Complex therapy includes systemic antibiotic therapy, surgical debridement of ulceration, revascularization in the case of proven lower limb ischemia and an individualized offloading. Without the subsequent outpatient podiatric follow-up, the risk of recurrence increases significantly.

• MeSH
• Acute Disease MeSH
• Anti-Bacterial Agents therapeutic use   MeSH
• Diabetic Foot * diagnosis   complications   therapy   MeSH
• Humans MeSH
• Arthropathy, Neurogenic * diagnosis   complications   therapy   MeSH
• Check Tag
• Humans MeSH
• Publication type
• Review MeSH

• MeSH
• Biochemistry MeSH
• Metabolic Diseases MeSH
• Pathology MeSH

• Conspectus
• Patologie. Klinická medicína
• Učební osnovy. Vyučovací předměty. Učebnice
• NML Fields
• biochemie
• patologie
• NML Publication type
• učebnice vysokých škol

Abdominální katastrofa je závažný klinický stav, který obvykle vzniká jako komplikace při léčbě nitrobřišních netraumatických onemocnění anebo při poranění břicha. Kniha je odborným pojednáním, které vychází z dlouholetých zkušeností autorského kolektivu. Provází čtenáře všemi etapami léčby pacientů a pozornost věnuje jednotlivým úskalím léčby.

• Keywords
• Anesteziologie, resuscitace, emergency,
• MeSH
• Abdomen pathology   MeSH
• Comprehensive Health Care MeSH
• Digestive System Diseases therapy   MeSH
• Nutrition Therapy MeSH
• Critical Care MeSH
• Emergency Treatment MeSH
• Catastrophic Illness therapy   MeSH

• NML Fields
• gastroenterologie
• anesteziologie a intenzivní lékařství
• urgentní lékařství

BACKGROUND: Short and rare episodes of atrial fibrillation (AF) are commonly detected using implanted devices (device-detected AF) in patients with prior stroke or transient ischemic attack (TIA). The effectiveness and safety of oral anticoagulation in patients with prior stroke or TIA and device-detected AF but with no ECG-documented AF is unclear. METHODS AND RESULTS: This prespecified analysis of the NOAH-AFNET 6 (Non-Vitamin K Antagonist Oral Anticoagulants in Patients With Atrial High Rate Episodes) trial with post hoc elements assessed the effect of oral anticoagulation in patients with device-detected AF with and without a prior stroke or TIA in the randomized, double-blind, double-dummy NOAH-AFNET 6 trial. Outcomes were stroke, systemic embolism, and cardiovascular death (primary outcome) and major bleeding and death (safety outcome). A prior stroke or TIA was found in 253 patients with device-detected AF randomized in the NOAH-AFNET 6 (mean age, 78 years; 36.4% women). There was no treatment interaction with prior stroke or TIA for any of the primary and secondary time-to-event outcomes. In patients with a prior stroke or TIA, 14 out of 122 patients experienced a primary outcome event with anticoagulation (5.7% per patient-year). Without anticoagulation, there were 16 out of 131 patients with an event (6.3% per patient-year). The rate of stroke was lower than expected (anticoagulation: 4 out of 122 [1.6% per patient-year]; no anticoagulation: 6 out of 131 [2.3% per patient-year]). Numerically, there were more major bleeding events with anticoagulation in patients with prior stroke or TIA (8 out of 122 patients) than without anticoagulation (2 out of 131 patients). CONCLUSIONS: Anticoagulation appears to have ambiguous effects in patients with device-detected AF and a prior stroke or TIA in this hypothesis-generating analysis of the NOAH-AFNET 6 in the absence of ECG-documented AF, partially due to a low rate of stroke without anticoagulation.

• MeSH
• Anticoagulants * administration & dosage   adverse effects   therapeutic use   MeSH
• Administration, Oral MeSH
• Time Factors MeSH
• Stroke * prevention & control   etiology   MeSH
• Double-Blind Method MeSH
• Atrial Fibrillation * drug therapy   complications   diagnosis   MeSH
• Pacemaker, Artificial MeSH
• Hemorrhage chemically induced   MeSH
• Humans MeSH
• Aged, 80 and over MeSH
• Aged MeSH
• Ischemic Attack, Transient * prevention & control   etiology   MeSH
• Treatment Outcome MeSH
• Check Tag
• Humans MeSH
• Male MeSH
• Aged, 80 and over MeSH
• Aged MeSH
• Female MeSH
• Publication type
• Journal Article MeSH
• Multicenter Study MeSH
• Randomized Controlled Trial MeSH

Neonatal hypoxic-ischemic (HI) brain insult is a major cause of neonatal mortality and morbidity. To assess the underlying pathological mechanisms, we mapped the spatiotemporal changes in polyamine, amino acid, and neurotransmitter levels, following HI insult (by the Rice-Vannucci method) in the brains of seven-day-old rat pups. Matrix-assisted laser desorption/ionization mass spectrometry imaging of chemically modified small-molecule metabolites by 4-(anthracen-9-yl)-2-fluoro-1-methylpyridin-1-ium iodide revealed critical HI-related metabolomic changes of 22 metabolites in 14 rat brain subregions, much earlier than light microscopy detected signs of neuronal damage. For the first time, we demonstrated excessive polyamine oxidation and accumulation of 3-aminopropanal in HI neonatal brains, which was later accompanied by neuronal apoptosis enhanced by increases in glycine and norepinephrine in critically affected brain regions. Specifically, putrescine, cadaverine, and 3-aminopropanal increased significantly as early as 12 h postinsult, mainly in motor and somatosensory cortex, hippocampus, and midbrain, followed by an increase in norepinephrine 24 h postinsult, which was predominant in the caudate putamen, the region most vulnerable to HI. The decrease of γ-aminobutyric acid (GABA) and the continuous dysregulation of the GABAergic system together with low taurine levels up to 36 h sustained progressive neurodegenerative cellular processes. The molecular alterations presented here at the subregional rat brain level provided unprecedented insight into early metabolomic changes in HI-insulted neonatal brains, which may further aid in the identification of novel therapeutic targets for the treatment of neonatal HI encephalopathy.

• MeSH
• Rats MeSH
• Metabolomics MeSH
• Brain * metabolism   MeSH
• Hypoxia-Ischemia, Brain * metabolism   pathology   MeSH
• Neurons metabolism   MeSH
• Neurotransmitter Agents * metabolism   MeSH
• Animals, Newborn * MeSH
• Polyamines * metabolism   MeSH
• Rats, Sprague-Dawley MeSH
• Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization methods   MeSH
• Animals MeSH
• Check Tag
• Rats MeSH
• Animals MeSH
• Publication type
• Journal Article MeSH