Larve chironomus plumosus (diptera, insecta) izvor esencijalnih masnih kiselina za ishranu šaranske mlađi

U cilju ispitivanja koliko su larve Chironomus plumosus-a pogodne za ishranu gajenih slatkovodnih riba, pre svega šarana, ižvršena je analiza hemijskog i masnokiselinskog sastava larvi koje su prikupljene na kraju tromesečnog perioda gajenja šaranske mlađi u dva eksperimentalna ribnjačka bazena u Centru za ribarstvo i primenjenu hidrobiologiju Poljoprivrednog fakulteta Univerziteta u Beogradu. Udeo sirovih proteina u larvama Chironomus plumosus-a iznosio je 6,61 u jezeru L1 odnosno 6,18% u jezeru L2, što predstavlja vrednost adekvatnu za rast svih slatkovodnih vrsta riba. Sadržaj lipida bio je 0,49 odnosno 0,73%, što je energetski povoljno za sve ribe koje žive u toplim vodama. Prirodnu hranu (larve Chironomus plumosus) karakteriše i visok sadržaj vode: 88,95 u L1 i 89,62% u L2, a što ih čini pogodnom za ishranu šaranske malađi. Lipidnu frakciju larvi Chironomidae u jezeru L1 je činilo 45.36% zasićenih i 53.96 nezasićenih masnih kiselina. U lipidnoj frakciji larvi Chironomidae iz jezera L2 nađeno je 53.47% zasićenih i 46.42% nezasićenih masnih kiselina. Od polinezasićenih (esencijalnih) masnih kiselina nađenih u hironomidama u jezeru L1, najveći deo je pripadao ω-6 linolnoj kiselini (21,37%), zatim ω-3 linolenskoj (3,21%) i eikozopentanskoj ω-3 kiselini (1,27%). Sadržaj linolne kiseline u larvama Chironomidae iz jezera L2 je bio niži i iznosio je 9,78%, eikozopentanska ω-3 kiselina je zastupljena sa 0,45%, a sadržaj linoleinske kiseline je bio viši i iznosio 7,78%. Nedostatak PUFA sa 22 C atoma je verovatno povezan sa slabom enzimatskom sposobnošću larvi Chironomidae za sintezu ovih kiselna iz njihovih prekursora PUFA sa 18 C atoma. Izmerena količina ω-3 i ω-6 masnih kiselina u larvama Chironomus plumosus je iznosila 0,21 u L1, a u jezeru L2 0,81, zadovoljava nutritivne zahteve šarana

Dental Treatment for Special Needs Patients Under General Anaesthesia: A 14-year Experience from South Bosnia and Herzegovina

We conducted a retrospective analysis of records of special needs patients (SNPs) who received dental treatment under orotracheal-intubation general anaesthesia (OIGA) at Caritas Centre St. Family in Mostar, Bosnia and Herzegovina during the 14-year period from January 2005 to December 2018. Of the 7,085 SNPs who received dental treatment, 1,220 (17.2%) received dental treatment under OIGA: 829 (67.9%) males and 391 (32.1%) females. The patients’ mean age was 18.3±10.9 years (747 paediatric and 473 adult patients). Mental retardation and psychiatric problems were the most common medical conditions (81.22%). The most common indication for dental treatment under OIGA was behaviour management (87.21%), and 81% of the patients had an urgent need for treatment. Many of the patients had restorative treatment (3,833) and tooth extractions (3,681). From 2011 onwards, the number of tooth extractions decreased significantly. Annual trends revealed a rapid increase of patients every year. The mean dental treatment duration was 95.3±12.1 min; the mean time under OIGA was 98±8.5 min. No serious adverse effects occurred. There was increase of annual trend of SNP in OIGA. The number of extractions decreased while the number of preventive and restorative dental treatments increased

Genetic Drivers of Kidney Defects in the DiGeorge Syndrome

Background The DiGeorge syndrome, the most common of the microdeletion syndromes, affects multiple organs, including the heart, the nervous system, and the kidney. It is caused by deletions on chromosome 22q11.2; the genetic driver of the kidney defects is unknown. Methods We conducted a genomewide search for structural variants in two cohorts: 2080 patients with congenital kidney and urinary tract anomalies and 22,094 controls. We performed exome and targeted resequencing in samples obtained from 586 additional patients with congenital kidney anomalies. We also carried out functional studies using zebrafish and mice. Results We identified heterozygous deletions of 22q11.2 in 1.1% of the patients with congenital kidney anomalies and in 0.01% of population controls (odds ratio, 81.5; P=4.5×10(-14)). We localized the main drivers of renal disease in the DiGeorge syndrome to a 370-kb region containing nine genes. In zebrafish embryos, an induced loss of function in snap29, aifm3, and crkl resulted in renal defects; the loss of crkl alone was sufficient to induce defects. Five of 586 patients with congenital urinary anomalies had newly identified, heterozygous protein-altering variants, including a premature termination codon, in CRKL. The inactivation of Crkl in the mouse model induced developmental defects similar to those observed in patients with congenital urinary anomalies. Conclusions We identified a recurrent 370-kb deletion at the 22q11.2 locus as a driver of kidney defects in the DiGeorge syndrome and in sporadic congenital kidney and urinary tract anomalies. Of the nine genes at this locus, SNAP29, AIFM3, and CRKL appear to be critical to the phenotype, with haploinsufficiency of CRKL emerging as the main genetic driver. (Funded by the National Institutes of Health and others.)

Cerebral Vasoreactivity Evaluated by Transcranial Color Doppler and Breath-Holding Test in Patients after SARS-CoV-2 Infection

From the beginning of the SARS-CoV-2 virus pandemic, it was clear that the virus is highly neurotrophic. Neurological manifestations can range from nonspecific symptoms such as dizziness, headaches and olfactory disturbances to severe forms of neurological dysfunction. Some neurological complication can occur even after mild forms of respiratory disease. This study’s aims were to assess cerebrovascular reactivity in patients with nonspecific neurological symptoms after SARS-CoV-2 infection. A total of 25 patients, aged 33–62 years, who had nonspecific neurological symptoms after SARS-CoV-2 infection, as well as 25 healthy participants in the control group, were assessed for cerebrovascular reactivity according to transcranial color Doppler (TCCD) which we combined with a breath-holding test (BHT). In subjects after SARS-CoV-2 infection, there were statistically significantly lower flow velocities through the middle cerebral artery at rest period, lower maximum velocities at the end of the breath-holding period and lower breath holding index (BHI) in relation to the control group. Changes in cerebral artery flow rate velocities indicate poor cerebral vasoreactivity in the group after SARS-CoV-2 infection in regard to the control group and suggest vascular endothelial damage by the SARS-CoV-2 virus

Isoflurane post-conditioning stimulates the proliferative phase of myocardial recovery in an ischemia-reperfusion model of heart injury in rats

Summary. The application of isoflurane in a postconditioning manner, during early reperfusion following a period of coronary occlusion, has numerous beneficial effects on the ischemic myocardium, including reduction of infarct size. It does so by stimulating a sequence of well studied anti-apoptotic pro-survival mechanisms in a similar manner to various ‘ischemic’ pre-/postconditioning approaches which achieve their cardio protective effects in both laboratory and clinical situations. Proliferation of newly formed blood vessels, resulting in formation of highly vascularized granulation tissue, is an essential stage of infarct healing. It can be evaluated by detecting various angiogenic factors, including vascular endothelial growth factor (VEGF) and platelet endothelial cell adhesion molecule-1 (PECAM-1/CD31) or by quantification of expression of vascular smooth muscle progenitors, such as Nestin. Expression of these three markers was used to evaluate the effect of early isoflurane post-conditioning in ischemia-reperfusion type cardiac injury. A large reduction in infarct size (59.3% of control), and marked increase of expression of VEGF (43.4%), PECAM1/CD31 (136%) and Nestin (77.9%) was found in experimental animals when compared to control animals that did not receive isoflurane treatment. Hence, based on our results, we can emphasize two morphologically detectable benefits of isoflurane post-conditioning: a marked reduction in infarct size and much better organization/vascularization of necrotic tissue

Involvement of pro-apoptotic and anti-apoptotic factors in the early development of the human pituitary gland

The spatial and temporal pattern of appearance of pro-apoptotic caspase-3 and p53 proteins, and anti-apoptotic bcl-2 protein was investigated in the developing pituitary gland of 6 human embryos 5-8- weeks old, using morphological and immunohistochemical techniques. Their dynamic appearance was analyzed in the Rathke's pouch (future adenohypophysis), mesenchyme, and in the developing neurohypophysis. In the 5th and 6th week, caspase-3 positive cells appeared in the Rathke's pouch (5%) and stalk (11%), in the mesenchyme, but not in the neurohypophysis. In the 6th and 7th week, apoptotic cells were more numerous in the caudal part of the Rathke's pouch due to its separation from the oral epithelium. Pro-apoptotic p53 protein was detected in all parts of the pituitary gland throughout the investigated period. Nuclear condensations characterized cells positive to caspase-3 and p53 proteins. Apoptotic cells displayed condensations of nuclear chromatin on an ultrastructural level as well. While caspase-3 dependent pathway of cell death participated in morphogenesis of the adenohypophysis and associated connective tissue, p53-mediated apoptosis most likely participates in morphogenesis of all parts of the gland, including neurohypophysis. The anti-apoptotic bcl-2 protein was also detected in all parts of the developing gland. With advancing development, the positivity to bcl-2 protein increased in the cells of the adenohypophysis, while it decreased in the neurohypophysis. Bcl-2 protein probably prevented cell death in all parts of the gland and enhanced cell differentiation. The described pattern of appearance of the investigated pro-apoptotic and antiapoptotic factors might be important for normal morphogenesis and function of the pituitary gland

The role of prostaglandin E2 in acute acetaminophen hepatotoxicity in mice

Prostaglandin E2 (PGE2), which is synthesized by many cell types, has a cytoprotective effect in the gastrointestinal tract and in several other tissues and cells. On the other hand, overdose or chronic use of a high dose of acetaminophen (Paracetamol, APAP) is a major cause of acute liver failure in the western world. These observations prompted us to investigate whether PGE2 plays a role in host defence to toxic effect of APAP. (CBAT6T6xC57Bl/6)F1 hybrid mice of both sexes were intoxicated with a single lethal or high sublethal dose of APAP, which was administered to animals by oral gavage. Stabile analogue of PGE2, 16,16-dimethyl PGE2 (dmPGE2), or inhibitor of its production, CAY10526, were given intraperitoneally (i.p.) 30 minutes before or 2 hours after APAP administration. The toxicity of APAP was determined by observing the survival of mice during 48 hours, by measuring concentration of alanine-aminotransferase (ALT) in plasma 20-22 hours after APAP administration and by liver histology. The results have shown that PGE2 exhibits a strong hepatoprotective effect when it is given to mice either before or after APAP, while CAY10526 demonstrated mainly the opposite effect. Immunohistochemical or immunofluorescent examinations in the liver tissue generally support these findings, suggesting that PGE2 inhibited APAP-induced activation of nuclear factor kappa B (NF-κB). Similarly, PGE2 down regulated the activity of inducible nitric oxide synthase (iNOS), which was up regulated by APAP. Thus, by these and perhaps by other mechanisms, PGE2 contributes to the defence of the organism to noxious effects of xenobiotics on the liver

The effect of glucagon and cyclic adenosine monophosphate on acute liver damage induced by acetaminophen

Recent investigations suggest that glucagon might have a potentially important hepatoprotective activity. We investigated the effect of glucagon in a model of acetaminophen-induced liver injury. CBA male mice were injected intraperitoneally with a lethal (300 mg/kg) or sublethal (150 mg/kg) dose of acetaminophen. The liver injury was assessed by observing the survival of mice, by liver histology and by measuring the concentration of alanine-aminotransferase (ALT). Inducible nitric oxide synthase (iNOS) and nuclear factor kappa B (NF-κB) protein expressions were determined immunohistochemically. Hepatic levels of reduced glutathione (GSH) and cyclic adenosine monophosphate (cAMP) were also measured. Results show that glucagon, dose and time dependently, protects against acetaminophen-induced hepatotoxicity. This protection was achieved with a dose of 0.5 mg/kg of glucagon given intraperitoneally 15 min before or 1 h after acetaminophen. Treatment of animals with acetaminophen elevated ALT and nitrite/nitrate concentration in the plasma, enhanced iNOS and NF-κB expression and reduced GSH and cAMP concentration in the liver. Animals treated with glucagon had higher hepatic cAMP level, lower ALT and nitrite/nitrate concentration in plasma and lower expression of iNOS in liver cells than animals in control group, whereas there was no difference in the expression of NF-κB. Glucagon did not prevent the loss of GSH content caused by acetaminophen. Our investigation indicates that glucagon has a moderately protective effect against acetaminophen-induced liver injury, which is, at least partially, mediated through the downregulation of iNOS and through the increase in hepatic cAMP content, but it is not mediated through the modulation of NF-κB activity

Factors That Determine Completion Rates of Biomedical Students in a PhD Programme

Purpose: The purpose of this retrospective study is to identify potential predictors of academic success or failure in Doctor of Philosophy (PhD) programmes in the field of biomedicine. Based on these, the policies and structure of academic programmes granting PhD degrees in biomedicine might be improved. Literature review (State of the art): At the present moment, most European and all of the EU doctoral education systems in biomedicine are regulated by the Salzburg principles of the Bologna process. Almost all the programmes formally comply with regulations, but the degree to which rules are applied varies greatly. The European Research Council (ERC) and various stakeholders’ associations, such as the Organisation for PhD Education in Biomedicine and Health Sciences in the European System (ORPHEUS), have recognised this and in their policies, they recommend regular evaluation of PhD programme structures. One such evaluation that was conducted at our institution motivated us to search for quantifiable factors that can help the process of PhD programme structural reform. Since the literature is scarce on this matter, we decided to conduct analysis of our own data and thus study the relationships between recommended EU policies and real-world data. Methods: Biology of Neoplasms is a PhD programme founded under Bologna process rules. It enrols students with Doctor of Medicine (MD), Doctor of Dental Medicine (DMD) or similar degrees in the biomedical field. A large portion of enrolled PhD students work full time in medical practices. A retrospective analysis was conducted on students who enrolled between 2006 and 2017. In order to quantify academic success, outcome measures of graduation (completion) rate, time to graduation, average impact factor of published papers comprising a PhD thesis and the ratio of the latter two were formed. Age, sex, employment institution, mentor experience and tuition subsidy were considered as potential predictors. Results: A total of 124 students were enrolled in the study—38% male. Out of the total, 21 (16.94%) students discontinued the study programme and 22 students graduated (17.7%). The average impact factor (IF) of published papers was 2.66 ± 1.51. Mentor experience (Odds ratio (OR) = 6.7) and student employment in academia (OR = 11.7) were significant predictors of successful graduation. Stricter criteria for graduation had no effect on graduation in newly enrolled students. Likewise, sex, tuition subsidy and age did not affect graduation rates. Surprisingly, time to graduation was not affected by any of the considered predictors. On the other hand, students that were mentored by experienced mentors and employed in academia outperformed their peers in terms of impact factors of publications related to their thesis. Conclusion: Characteristics such as gender, age at enrolment and even tuition paid by the institution do not have a significant impact on completion rate. Experienced mentors and employment in academic institutions seem to be the factors that predict a successful completion of a PhD programme. Furthermore, our results give a quantifiable support to the ORPHEUS and ERC recommendations and policies. These conclusions can be easily applied to any PhD programme formed under the tenets of the Bologna process