Effect of environmental factors on coastal fisheries

Factors which threaten sustainable commercial fisheries are considered in this paper. Oil and grease, suspended solids, overfishing impact on fishes and fisheries. Whereas overfishing declines adult fish values; the duo of oil and suspended solids clog and disable gills of affected fishes and deplete insolation. And barnacles foul boats

The development of atherosclerosis in a patient with diabetes mellitus

Scientific supervisors: Zhuravka N. V., assistant; Shop I. V., PhD, associate professorАктуальні питання сучасної медицини: Тези доповідей XVІ Міжнародної наукової конференції студентів, молодих вчених та фахівців 28-29 березня 2019 р. – Х.: ХНУ імені В. Н. Каразіна, 2019. – C. 336-337

Aquaporin-4 and brain edema.

Aquaporin-4 (AQP4) is a water-channel protein expressed strongly in the brain, predominantly in astrocyte foot processes at the borders between the brain parenchyma and major fluid compartments, including cerebrospinal fluid (CSF) and blood. This distribution suggests that AQP4 controls water fluxes into and out of the brain parenchyma. Experiments using AQP4-null mice provide strong evidence for AQP4 involvement in cerebral water balance. AQP4-null mice are protected from cellular (cytotoxic) brain edema produced by water intoxication, brain ischemia, or meningitis. However, AQP4 deletion aggravates vasogenic (fluid leak) brain edema produced by tumor, cortical freeze, intraparenchymal fluid infusion, or brain abscess. In cytotoxic edema, AQP4 deletion slows the rate of water entry into brain, whereas in vasogenic edema, AQP4 deletion reduces the rate of water outflow from brain parenchyma. AQP4 deletion also worsens obstructive hydrocephalus. Recently, AQP4 was also found to play a major role in processes unrelated to brain edema, including astrocyte migration and neuronal excitability. These findings suggest that modulation of AQP4 expression or function may be beneficial in several cerebral disorders, including hyponatremic brain edema, hydrocephalus, stroke, tumor, infection, epilepsy, and traumatic brain injury

MRI Visualization of Whole Brain Macro- and Microvascular Remodeling in a Rat Model of Ischemic Stroke: A Pilot Study

Using superparamagnetic iron oxide nanoparticles (SPION) as a single contrast agent, we investigated dual contrast cerebrovascular magnetic resonance imaging (MRI) for simultaneously monitoring macro- and microvasculature and their association with ischemic edema status (via apparent diffusion coefficient [ADC]) in transient middle cerebral artery occlusion (tMCAO) rat models. High-resolution T1-contrast based ultra-short echo time MR angiography (UTE-MRA) visualized size remodeling of pial arteries and veins whose mutual association with cortical ischemic edema status is rarely reported. ??R2?????R2*-MRI-derived vessel size index (VSI) and density indices (Q and MVD) mapped morphological changes of microvessels occurring in subcortical ischemic edema lesions. In cortical ischemic edema lesions, significantly dilated pial veins (p???=???0.0051) and thinned pial arteries (p???=???0.0096) of ipsilateral brains compared to those of contralateral brains were observed from UTE-MRAs. In subcortical regions, ischemic edema lesions had a significantly decreased Q and MVD values (p???<???0.001), as well as increased VSI values (p???<???0.001) than normal subcortical tissues in contralateral brains. This pilot study suggests that MR-based morphological vessel changes, including but not limited to venous blood vessels, are directly related to corresponding tissue edema status in ischemic stroke rat models

Determination of intestine length to standard length ratio of some fishes from Ikpoba River and Ovia River, Nigeria with a review of culture of Parachanna obscura (Pisces:Channidae)

The gut length to standard length ratios of twelve fish species from the Ovia and Ikpoba Rivers were calculated to work out their feeding level in the food chain. The mean ratio of five species Brycinus macrolepidotus Smith, 0.9 Parachanna obscura (Gunther), 1.0, Papyrocranus afer. Gunthel; 0.35, and Xenomystus nigri Gunther 0.75, classify them as carnivores. Four species Synodontis eupterus Boulenger; 4.4 S.schall (Bloch and Schneider) 4.8, Tilapia mariae Boulenger, 3.5, and T. tilli (Gervais), 4.7, are herbivores. Three intermediate ratio species B. longipinnis (Gunther), 1.3,Chrysichthys furcatus (Gunther) 1.6, and Clenopoma kingsleyae Gunther, 1.8, are omnivores. The body depth of seven of the species was measured and expressed as percentage of the standard length to ascertain the accommodative capacity of the fish for the gut. In addition a review of culture of snake head fish Parachanna obscura is presented

Cystathionine beta synthase deficiency and brain edema associated with methionine excess under betaine supplementation: Four new cases and a review of the evidence.

CBS deficient individuals undergoing betaine supplementation without sufficient dietary methionine restriction can develop severe hypermethioninemia and brain edema. Brain edema has also been observed in individuals with severe hypermethioninemia without concomitant betaine supplementation. We systematically evaluated reports from 11 published and 4 unpublished patients with CBS deficiency and from additional four cases of encephalopathy in association with elevated methionine. We conclude that, while betaine supplementation does greatly exacerbate methionine accumulation, the primary agent causing brain edema is methionine rather than betaine. Clinical signs of increased intracranial pressure have not been seen in patients with plasma methionine levels below 559 μmol/L but occurred in one patient whose levels did not knowingly exceed 972 μmol/L at the time of manifestation. While levels below 500 μmol/L can be deemed safe it appears that brain edema can develop with plasma methionine levels close to 1000 μmol/L. Patients with CBS deficiency on betaine supplementation need to be regularly monitored for concordance with their dietary plan and for plasma methionine concentrations. Recurrent methionine levels above 500 μmol/L should alert clinicians to check for clinical signs and symptoms of brain edema and review dietary methionine intake. Levels approaching 1000 μmol/L do increase the risk of complications and levels exceeding 1000 μmol/L, despite best dietetic efforts, should be acutely addressed by reducing the prescribed betaine dose

Assessment of pulmonary edema: principles and practice

Pulmonary edema increasingly is recognized as a perioperative complication affecting outcome. Several risk factors have been identified, including those of cardiogenic origin, such as heart failure or excessive fluid administration, and those related to increased pulmonary capillary permeability secondary to inflammatory mediators. Effective treatment requires prompt diagnosis and early intervention. Consequently, over the past 2 centuries a concentrated effort to develop clinical tools to rapidly diagnose pulmonary edema and track response to treatment has occurred. The ideal properties of such a tool would include high sensitivity and specificity, easy availability, and the ability to diagnose early accumulation of lung water before the development of the full clinical presentation. In addition, clinicians highly value the ability to precisely quantify extravascular lung water accumulation and differentiate hydrostatic from high permeability etiologies of pulmonary edema. In this review, advances in understanding the physiology of extravascular lung water accumulation in health and in disease and the various mechanisms that protect against the development of pulmonary edema under physiologic conditions are discussed. In addition, the various bedside modalities available to diagnose early accumulation of extravascular lung water and pulmonary edema, including chest auscultation, chest roentgenography, lung ultrasonography, and transpulmonary thermodilution, are examined. Furthermore, advantages and limitations of these methods for the operating room and intensive care unit that are critical for proper modality selection in each individual case are explored

Physical exercise and cardiac death due to pneumonia in male teenagers [Iznenadna smrt zbog upalće pluća za vrijeme tjelovježbe u trojice mladića]

From 1998 to 2008 we noticed 3 cardiac deaths in male teenagers aged 18-19 during or after physical exercise. The first was working at the site recreatively, the second was engaged in soccer recreatively and the third was professional soccer player. One felt general tiredness and was exhausted of a heavily physical effort, the other after physical exercise became septic and the third was without symptoms. One died suddenly during physical exercise at the field and two died in the hospital. At the forensic autopsy the first had bilateral bacterial pneumonia, possible high-altitude non-cardiogenic pulmonary edema and cerebral edema. The second had bilateral bacterial pneumonia, adult respiratory distress syndrome, disseminated intravascular coagulation, suprarenal bleeding, cerebral edema, hypoplastic right coronary artery and myocardial fibrosis. The third had bilateral bacterial pneumonia, fibrinous pericarditis, cerebral contusion with edema, thickenning of the left ventricle 20 mm and hypoplastic ascending aorta. In Croatia the death rate among athletes reached 0.15/ 100,000, in athletes suffered of acute pneumonia 0.28/ 100,000, in others who practice exercise recreatively 0.57/ 100,000 (p = 0.0068), in all males who practice exercise recreatively 0.75/ 100,000 (p = 0.0014). Physical exercise is contraindicated in acute respiratory tract infections. Every such case has to be treated by physician. When to start with physical training after bacterial pneumonia depends on disappearing of clinical and X-ray signs of pneumonia, normalization of erythrocite sedimentation rate and of white cell count