[Patients' preferences for health-related use of Internet]. / Betegpreferenciák az egészségügyi célú internethasználatban.

INTRODUCTION: More sophisticated implementation of the Internet in healthcare improves medical services innumerably. To better understand the patients' preferences for health-related use of Internet is warranted. AIM: Our aim was to determine the patients' health-related Internet use. METHOD: Patients attending our private clinic between October 2016 and April 2017 were surveyed. RESULTS: 208 questionnaires have been evaluated. Most patients use Internet daily, primarily on mobiles. The majority have already searched for health-related information online, 19% do regularly. 53% are satisfied with online contents and open to websites recommended by physicians. 32% of patients have already communicated with doctors online and 93% are satisfied doing so. 8% of patients use health-related smartphone applications regularly, 6% use other Internet-based health-monitoring devices. 60% of patients have already chosen a physician based on web information, while 17% do regularly. 82% of respondents have not yet shared health-related information on the Internet. CONCLUSIONS: The Internet is widely used by patients seeking information about their health, yet they are dissatisfied with the quality. Many patients are open to recommendations offered by physicians regarding sources of online information. Online communication between physician and patient might increase patient satisfaction. There is no breakthrough in the use of health-related websites, mobile apps or devices in Hungary. The demand for such service could be considered moderate. Additionally, online patient forums are not specifically popular. The medical society in Hungary should accept that physician selection by patients depends more increasingly upon information made available online. Orv Hetil. 2018; 159(51): 2175-2182.

Severe neck infections that require wide external drainage: clinical analysis of 17 consecutive cases.

Infections in the neck layers and spaces are potentially life-threatening diseases causing further complications, like mediastinitis, airway obstruction, or sepsis. Despite of the need for a conservative approach, they still regularly require surgical intervention. Records of 17 patients with severe neck infections that were treated by wide external incision and open wound management were retrospectively analyzed. The aim of the study was to clinically characterize these most serious neck infections. The most common presenting symptoms were neck pain and tense neck mass (94-94%) regularly with fever (65%), always accompanied by a marked elevation of C reactive protein level (average 192 uG/l). These findings were constant and very similar among both the deep neck infection and necrotizing fasciitis cases. More than half of the patients (53%) had at least one systemic co-morbidity. The parapharyngeal space was most commonly affected (83%), but extended disease involving more than two major neck regions was found in 13 cases (76%). Dental (29%) was the most common primary infection, followed by peritonsillar abscess (23%), Microbiological results showed a wide variety of corresponding bacteria. Mediastinitis was developed in three cases (18%), and airway obstruction requiring tracheostomy in two cases (12%). All the patients survived. Severe neck infections are a heterogenous group of diseases regarding to the primary site of infection, microbiology, localisation and host reaction. However, rapidly developed, painful, tense neck mass with a highly elevated CRP level should always alert for an extended or phlegmonous process in the layers or spaces of the neck.

Homocysteine metabolism in peripheral blood mononuclear cells: evidence for cystathionine beta-synthase activity in resting state.

Activated peripheral blood mononuclear cells (PBMC) release homocysteine and possess cystathionine ß-synthase (CBS) activity; however, it was thought that there is no CBS in resting state. Previously, we found that nickel decreased intracellular homocysteine concentration in un-stimulated (e.g. resting) PBMC, suggesting that resting PBMC might also have active homocysteine metabolism. Here, we demonstrated that un-stimulated PBMC synthesize (incorporate L-[methyl-14C]methionine to DNA, lipids and proteins), release (increase extracellular homocysteine), and metabolize homocysteine. Intracellular homocysteine concentration varied with incubation time, depending on extracellular concentrations of methionine, homocysteine, and glutathione. Methionine synthase activity was constant and independent of thiol concentrations. In Western blot, CBS protein was clearly identified in freshly isolated PBMC. CBS protein level and activity increased with incubation time, upon stimulation, and similar to intracellular homocysteine, depending on intra- and extracellular homocysteine and glutathione concentrations. According to our knowledge, this is the first evidence that certifies homocysteine metabolism and regulatory role of CBS activity to keep balanced intracellular homocysteine level in resting PBMC. Homocysteine, released by PBMC, in turn can modulate its functions contributing to the development of hyperhomocysteinemia-induced diseases.

Internet-based health communication opportunities (blogs, podcasts, video channels) and the social media / Internetalapú egészségkommunikációs lehetoségek (blogok, podcastok, videócsatornák) és a közösségi média.

Összefoglaló. Az elmúlt években mind laikus, mind szakmai oldalról az internet vált az elso számú egészségügyi információforrássá, amit a COVID-19-pandémia tovább fokozott. Az online térben számos, különbözo jellegu platform áll rendelkezésre egészségkommunikációs célokra, melyek markánsan különböznek egymástól az átadható információ mennyiségében és minoségében, a létrehozásukhoz szükséges anyagi vagy idobeli ráfordításban, továbbá az ott létrehozott tartalom fogyasztási lehetoségeiben. Összefoglaló közleményünkben rendszerezve mutatjuk be a szöveg-, a hang-, illetve a videóalapú online egészségügyi edukációs formák elonyeit és hátrányait. Külön foglalkozunk a közösségi média (social media) egészségügyi vonatkozásaival, a benne rejlo lehetoségekkel, kiemelve a pandémia kapcsán felmerült problémákat. Az egyes platformok egészségüggyel kapcsolatos történelmének feldolgozása mellett gyakorlati oldalról mutatjuk be azok hasznosíthatóságát, elosegítve ezzel az online térbe terelt kollégák munkáját. Orv Hetil. 2022; 163(4): 132-139. Summary. In recent years, the internet has become the leading source of health-related information for both professionals and laymen, and this process has been further speeded up by the Covid-19 pandemic. There are many different platforms available for health communication purposes online, that vary greatly in the quantity and quality of transferable information; the time or financial input, which are necessary to create them; and the possibilities of the utilization of the created content. In our review, we present systematically the advantages and disadvantages of the text-, audio-, and video-based online health-related education platforms. We specify the health-related aspects of social media and its potential usability, focusing on the problems allied to the pandemic. We present the practical use of the different platforms from a healthcare perspective through the review of their respective histories, thus providing guidance to the colleagues working online. Orv Hetil. 2022; 163(4): 132-139.

Hydrogen sulfide inhibits the calcification and osteoblastic differentiation of vascular smooth muscle cells.

Osteoblastic differentiation of vascular smooth muscle cells (VSMCs) is involved in the pathogenesis of vascular calcification. Hydrogen sulfide (H(2)S) is a gas endogenously produced by cystathionine γ-lyase in VSMC. Here we determined whether H(2)S plays a role in phosphate-induced osteoblastic transformation and mineralization of VSMC. Hydrogen sulfide was found to inhibit calcium deposition in the extracellular matrix and to suppress the induction of the genes involved in osteoblastic transformation of VSMC: alkaline phosphatase, osteocalcin, and Cbfa1. Moreover, phosphate uptake and phosphate-triggered upregulation of the sodium-dependent phosphate cotransporter (Pit-1) were also prevented by H(2)S. Reduction of endogenous production of H(2)S by inhibition of cystathionine γ-lyase activity resulted in increased osteoblastic transformation and mineralization. Low plasma levels of H(2)S, associated with decreased cystathionine γ-lyase enzyme activity, were found in patients with chronic kidney disease receiving hemodialysis. Thus, H(2)S is a potent inhibitor of phosphate-induced calcification and osteoblastic differentiation of VSMC. This mechanism might contribute to accelerated vascular calcification in chronic kidney disease.

Red cells, hemoglobin, heme, iron, and atherogenesis.

OBJECTIVE: We investigated whether red cell infiltration of atheromatous lesions promotes the later stages of atherosclerosis. METHODS AND RESULTS: We find that oxidation of ferro (FeII) hemoglobin in ruptured advanced lesions occurs generating ferri (FeIII) hemoglobin and via more extensive oxidation ferrylhemoglobin (FeIII/FeIV=O). The protein oxidation marker dityrosine accumulates in complicated lesions, accompanied by the formation of cross-linked hemoglobin, a hallmark of ferrylhemoglobin. Exposure of normal red cells to lipids derived from atheromatous lesions causes hemolysis and oxidation of liberated hemoglobin. In the interactions between hemoglobin and atheroma lipids, hemoglobin and heme promote further lipid oxidation and subsequently endothelial reactions such as upregulation of heme oxygenase-1 and cytotoxicity to endothelium. Oxidative scission of heme leads to release of iron and a feed-forward process of iron-driven plaque lipid oxidation. The inhibition of heme release from globin by haptoglobin and sequestration of heme by hemopexin suppress hemoglobin-mediated oxidation of lipids of atheromatous lesions and attenuate endothelial cytotoxicity. CONCLUSIONS: The interior of advanced atheromatous lesions is a prooxidant environment in which erythrocytes lyse, hemoglobin is oxidized to ferri- and ferrylhemoglobin, and released heme and iron promote further oxidation of lipids. These events amplify the endothelial cell cytotoxicity of plaque components.

Mixtures of Uncaria and Tabebuia extracts are potentially chemopreventive in CBA/Ca mice: a long-term experiment.

A long-term experimental animal model was developed by our research group for the evaluation of potential chemopreventive effects. The inhibitory effects of agents on carcinogen (7,12-dimethylbenz[a]anthracene (DMBA) induced molecular epidemiological biomarkers, in this case the expression of key onco/suppressor genes were investigated. The expression pattern of c-myc, Ha-ras, Bcl-2, K-ras protooncogene and p53 tumour suppressor gene were studied to elucidate early carcinogenic and potential chemopreventive effects. The consumption of so-called Claw of Dragon tea (CoD™ tea) containing the bark of Uncaria guianensis, Cat's Claw (Uncaria sp. U. tomentosa) and Palmer trumpet-tree (Tabebuia sp. T. avellanedae) was able to decrease the DMBA-induced onco/suppressor gene overexpression in a short-term animal experiment. In a following study CBA/Ca mice were treated with 20 mg/kg bw DMBA intraperitoneally (i.p.) and the expression patterns of onco/suppressor genes were examined at several time intervals. According to the examined gene expression patterns in this long-term experiment the chemopreventive effect of CoD™ tea consumption could be confirmed.

Mal de débarquement syndrome ­ "sickness of disembarkment" / [Mal de débarquement szindróma - "partraszállási betegség"]

Mal de débarquement syndrome is an uncommon vestibular disorder characterized by a constant sensation of swaying or motion after one disembarks from a vehicle such as a ship or plane, however, spontaneous onset also appears. These symptoms temporarily subside when the patient is subjected again to passive motion like driving a car. Chronic fatigue, anxiety, and depression are frequently associated with primary symptoms. The diagnosis is challenging, and often made by the patients themselves. The underlying pathophysiology and definitive therapy are unknown. Exposure to optokinetic stimulations and transcranial magnetic stimulations open therapeutic perspectives. We report a case series of 5 patients who presented with constant rocking, bobbing sensation that had been ongoing for several months. We found normal inner-ear function, non-related abnormalities and normal brain imaging. By presenting our patients' histories, we discuss the different diagnostic issues that help to diagnose this condition. We aimed to report the most recent findings on aetiology and treatment methods and to share our experiences with different therapeutic attempts. Mal de débarquement syndrome is a diagnosis of exclusion and often unrecognized. A thorough clinical history, negative or non-specific clinical findings with a high degree of suspicion are needed for recognizing this disorder. Increasing awareness can lead to early diagnosis and prevent multiple physician visits and unnecessary diagnostic testing. Frequent diagnostic failure has a negative impact on the quality of life, associated with anxiety and depression. Orv Hetil. 2020; 161(20): 846-851.

Associations of adiponectin with paraoxonase 1 and sE-selectin in hemodialyzed patients.

BACKGROUND/AIMS: In hemodialyzed (HD) patients, adiponectin and sE-selectin levels are elevated, while antioxidant paraoxonase 1 activity (PON1) is decreased. We determined if the hyperadiponectinemia in HD patients has a protective effect on the decrease in PON1 and elevation in sE-selectin in kidney failure. METHODS AND DESIGN: Predialysis serum adiponectin, PON1 and sE-selectin as well as other metabolic variables were measured in 70 HD patients. RESULTS: Adiponectin had (1) no association with PON1 or sE-selectin, (2) a positive association with dialysis efficiency and HDL-C, and (3) an inverse association with BMI, waist circumference, HOMA IR, triglyceride, hsCRP, fibrinogen, and albumin. Moreover, albumin, BMI, and HOMA-IR were independent negative predictors of adiponectin. CONCLUSIONS: In kidney failure, in contrast to normal renal function, higher adiponectin levels had no correlation with PON1 activity or the sE-selectin level. However, adiponectin has an association with dialysis efficiency and, similar to individuals with preserved kidney function, traits of metabolic syndrome. In addition to BMI and HOMA-IR, the serum albumin concentration is also one of the independent negative predictors of the serum adiponectin level. Collectively, these findings may add details to the understanding of the role that adiponectin plays in chronic renal disease related to 'reverse epidemiology'.

Early modification of c-myc, Ha-ras and p53 expressions by chemical carcinogens (DMBA, MNU).

7,12-Dimethylbenz[a]anthracene (DMBA) and N-methyl-N-nitrosourea (MNU) are important environmental carcinogens. Their different biological effects were examined in CBA/Ca H-2(K) haplotype inbred mice on the gene expression of c-myc, Ha-ras and p53 through a 24 hour period. Elevated expression of c-myc and Ha-ras genes was found in the spleen, lung, thymus and lymph nodes 6 and 12 hours after DMBA treatment and in the lung and thymus 3 hours after MNU treatment. In the liver, DMBA induced strong onco/suppressor gene expression as early as 6 hours after the treatment, but MNU increased the p53 gene expression 12 hours after the treatment. The gene expression patterns reflected the different mechanism of the direct acting MNU and metabolically activated DMBA. This phenomenon provides evidence as to the usefulness of detection of onco/supressor key gene expression as early molecular epidemiological biomarkers of carcinogenesis and carcinogenic exposure in animal model, useful in human cancer prevention practice as well.

Effects of tocopherols and 2,2'-carboxyethyl hydroxychromans on phorbol-ester-stimulated neutrophils.

Tocopherol vitamers [e.g., alpha-, gamma- and delta-tocopherol (alpha-TOC, gamma-TOC and delta-TOC, respectively)] and their water-soluble 2,2'-carboxyethyl hydroxychroman metabolites (e.g., alpha-, gamma- and delta-CEHC) all possess antioxidant properties. As a consequence, and similarly to other natural antioxidants, vitamin E compounds may be useful in preventing inflammatory and oxidative-stress-mediated diseases. In this study, we investigated the concentration-dependent effect of tocopherols and water-soluble metabolites on a key event in oxidative stress, for example, the oxidative burst in neutrophils. It was found that not only alpha-TOC but also gamma-TOC and delta-TOC as well as alpha-, gamma- and delta-CEHC at physiological concentrations inhibit superoxide anion (O2(*-)) production in phorbol-ester-stimulated neutrophils. This effect was mediated by the inhibition of the translocation and activation of protein kinase C (PKC) enzyme, which is the key event in the phorbol-ester signaling. Importantly, CEHCs were stronger inhibitors of PKC as compared with the vitamer precursors, and the gamma forms of both tocopherol and CEHC showed the highest inhibitory activities. Tocopherols, but not CEHCs, directly inhibit the fully activated nicotine-adenine-dinucleotide phosphate (NADPH) oxidase. However, none of the test compounds was able to directly scavenge O2(*-) when tested in a cell-free system. In conclusion, vitamin E compounds can control the neutrophil oxidative burst through the negative modulation of PKC-related signaling and NADPH oxidase activity. As an original finding, we observed that CEHC metabolites might contribute to regulate PKC activity in these cells. These results may have important implications in the anti-inflammatory and antioxidant role of vitamin E compounds.

GSTM, GSTT and p53 polymorphisms as modifiers of clinical outcome in colorectal cancer.

BACKGROUND: Cancer of the colorectal region is the second most frequent cause of death among malignant diseases. The influence of two allelic polymorphisms of GSTM1 and GSTT1, and that of p53 gene codon 72 on colon cancer was investigated. PATIENTS AND METHODS: Intraoperatively removed tissue samples were processed from colorectal cancer patients. Cancer-free human samples were used as matched controls. Samples were digested with proteinase-K. DNA solution was used for PCR amplification. RESULTS: No significant difference was found between tumor patients and controls in the investigated polymorphisms. A significant association was found in Dukes' B stage patients between the GSTM1 and p53 gene variants and survival. In patients with GSTM1 null genotype and p53 Arg/Pro heterozygotes or Pro/Pro homozygotes the chance of survival is significantly lower than in the case of GSTM1+ and p53 Arg/Arg variants (p=0.009 and p=0.008, respectively). CONCLUSION: The significance of the investigated polymorphisms in prognosis is dependent on the tumor stage. These parameters might be used in certain cases as prognostic biomarkers in clinical diagnostics and in the planning of individual therapy.

Early modification of c-myc, Ha-ras and p53 expressions by N-methyl-N-nitrosourea.

Methylnitrosourea (MNU) is a well-known pluripotent direct-acting carcinogen. Formation of MNU following incubation of various meats with additional nitrite under in vitro acidic conditions is possible. It is possible that many species, including humans, are exposed to carcinogenic MNU, generated in their alimentary tract. Previously, an animal model was developed by our research group to investigate the expression of three genes c-myc, Ha-ras and p53 as early molecular epidemiological biomarkers of carcinogenic exposure or carcinogenesis caused by DMBA (dimethylbenz[alpha]anthracene). The aim of this study was to investigate the early effect of MNU on the gene expression levels. MNU is a direct-acting carcinogen which spontaneously and rapidly degrades, so any effect on the gene expression is observed in 24 hours. Our results show the maximum effect in vivo on the gene expression at 12 hours after the MNU treatment; on the other hand, 24 hours after the treatment, the elevated gene expressions decreased in target organs (bone marrow, lung, lymph nodes). Our results correspond to "long-term" experiments of the carcinogenic effect of MNU in different target organs. Our findings suggest that MNU has an impact on the expression of c-myc, Ha-ras and p53 genes in 12 hours, especially in bone marrow. Overexpression of these genes occurs as an early biological effect of exposure to chemical carcinogens. According to our results, the high expression of these genes could indicate MNU exposure and these genes could take part in MNU-induced tumorigenesis.

Relationship between serum nickel and homocysteine concentration in hemodialysis patients.

Severe hyperhomocysteinemia (HHC) is associated with atherosclerosis. In hemodialysis (HD) patients, one of the main causes of death is cardiovascular disease. In animals, trace elements such as cobalt, copper, iron, and nickel ameliorated vitamin B(12) deficiency-induced HHC. However, correlations between plasma total homocysteine (tHcy) and trace elements in HD patients have not been investigated. Therefore, tHcy, folate, vitamin B(12), trace elements (cobalt, copper, iron, and nickel), and some laboratory parameters such as serum total protein, albumin, transferrin, ferritin, C-reactive protein (CRP), and interleukin-6 concentrations were determined in 122 hemodialysis patients. When patients were divided into groups according to their tHcy, we found no significant differences in concentrations of cobalt, copper, and total protein, while nickel was higher, and folate, vitamin B(12), and iron were lower in patients with lower than higher tHcy. In univariate regression analysis, tHcy negatively correlated with concentrations of folate (r = -0.302, p < 0.006), vitamin B(12) (r = -0.347, p < 0.0001), nickel (r = -0.289, p < 0.006), and CRP (r = -0.230, p < 0.02) and positively with serum albumin (r = 0.316, p < 0.0004) and hemoglobin (r = 0.329, p < 0.0001) values. No relationship between tHcy and serum concentrations of cobalt, copper, iron, or other laboratory parameters was found in HD patients. The effect of cobalt and nickel on homocysteine production was assessed in human peripheral mononuclear cells (PBMCs). Nickel but not cobalt at concentrations found in HD patients significantly inhibited homocysteine, cysteine, and S-adenosylhomocysteine production in human PBMCs. These results suggest that nickel might also be involved in the regulation of the methionine-folate cycle in humans, as was demonstrated in animal experiments.

[Omega-3 polyunsaturated fatty acids in the prevention of atherosclerosis]. / Az omega-3 többszörösen telítetlen zsírsavak az atherosclerosis megelôzésében.

Cardioprotective action of omega-3 polyunsaturated fatty acids such as eicosapentaenoic and docosahexaenoic acid in fish and alpha-linolenic acid in plants was demonstrated in primary and secondary clinical trials. Fish oil therapy causes a marked decrease in serum triacylglycerol and very low density lipoprotein levels and increases moderately high density lipoprotein levels without any adverse effects. Omega-3 fatty acids decrease slightly, but significantly blood pressure, enhance endothelial function, they have anti-aggregator, anti-thrombotic and anti-inflammatory effects as well. These beneficial effects are in connection with modification of gene transcription levels of some key molecules such as nuclear factor-kappaB and sterol element binding receptor protein-1c, which regulate for example expression of adhesion molecules or several receptors involved in triglyceride synthesis (hepatocyte X receptor, hepatocyte nuclear factor 4alpha, farnesol X receptor, and peroxisome proliferator-activated receptors). On the basis of these observations, the supplementation of the diet with omega-3 fatty acids (fish, fish oil, linseed, and linseed oil or canola oil) is advisable in primary and secondary prevention.

Heme, heme oxygenase, and ferritin: how the vascular endothelium survives (and dies) in an iron-rich environment.

Iron-derived reactive oxygen species are involved in the pathogenesis of numerous vascular disorders. One abundant source of redox active iron is heme, which is inherently dangerous when it escapes from its physiologic sites. Here, we present a review of the nature of heme-mediated cytotoxicity and of the strategies by which endothelium manages to protect itself from this clear and present danger. Of all sites in the body, the endothelium may be at greatest risk of exposure to heme. Heme greatly potentiates endothelial cell killing mediated by leukocytes and other sources of reactive oxygen. Heme also promotes the conversion of low-density lipoprotein to cytotoxic oxidized products. Hemoglobin in plasma, when oxidized, transfers heme to endothelium and lipoprotein, thereby enhancing susceptibility to oxidant-mediated injury. As a defense against such stress, endothelial cells upregulate heme oxygenase-1 and ferritin. Heme oxygenase opens the porphyrin ring, producing biliverdin, carbon monoxide, and a most dangerous product-redox active iron. The latter can be effectively controlled by ferritin via sequestration and ferroxidase activity. These homeostatic adjustments have been shown to be effective in the protection of endothelium against the damaging effects of heme and oxidants; lack of adaptation in an iron-rich environment led to extensive endothelial damage in humans.

Relationship of endogenous hyperleptinemia to serum paraoxonase 1, cholesteryl ester transfer protein, and lecithin cholesterol acyltransferase in obese individuals.

Altered activities of high-density lipoprotein (HDL)-associated antioxidant enzyme paraoxonase 1 (PON1) and lipid transfer proteins, for example, cholesteryl ester transfer protein (CETP) and lecithin cholesterol acyltransferase (LCAT), participating in lipoprotein remodeling seem to play important roles in obesity-related accelerated atherosclerosis. Inverse associations of PON1 with obesity and serum leptin levels have been demonstrated. However, the relationship of leptin with CETP and LCAT in humans is less clear. Our aims were to investigate whether the elevated leptin level is (a) an independent predictor of low PON1 and (b) associated with alterations of CETP and LCAT activities. Seventy-four white subjects forming 3 age- and sex-matched groups were included into the study (groups 1 and 2: nondiabetic obese patients, n = 25 with body mass index [BMI] 28-39.9 kg/m2 and n = 25 with BMI >or=40 kg/m2, respectively; and group 3: 24 healthy, normal-weight control subjects). Paraoxonase 1 correlated inversely with BMI (r = -0.39, P < .01), waist circumferences (r = -0.42, P < .001), and leptin concentrations (r = -0.38, P < .001). However, in a multiple regression model, neither these variables nor others, for example, age, sex, blood pressure, insulin resistance (in homeostasis model assessment of insulin resistance [HOMA-IR]), HDL cholesterol, low-density lipoprotein cholesterol, or lipid peroxidation (measured as thiobarbituric acid reactive substances), proved to be independent predictors of PON1. Lecithin cholesterol acyltransferase correlated negatively with BMI (r = -0.40, P < .01), waist circumferences (r = -0.42, P < .001), and leptin levels (r = -0.40, P < .01). During multiple regression analyses, BMI was an independent predictor of LCAT after adjustments for age, sex, HOMA-IR, and HDL cholesterol. However, this was replaced by leptin and HOMA-IR when leptin was also included into the model. The CETP activities correlated with HOMA-IR (r = 0.33, P < .01), thiobarbituric acid reactive substances (r = 0.45, P < .001), and leptin (r = 0.36, P < .01) levels in univariate but not in multivariate models. Elevated leptin level is an independent predictor of low LCAT, but not PON1, activity. In a population with a wide range of BMI, LCAT correlates inversely with obesity and CETP directly with insulin resistance.

Association between allelic polymorphisms of metabolizing enzymes (CYP 1A1, CYP 1A2, CYP 2E1, mEH) and occurrence of colorectal cancer in Hungary.

BACKGROUND: Genetic polymorphisms of metabolizing enzymes may affect the risk of cancer formation in humans. Since the diet can contain polycyclic aromatic hydrocarbons (PAHs) and heterocyclic amines (HAs), the relationship between polymorphisms of enzymes involved in PAH and HA metabolism and the occurrence of sporadic colorectal cancer was studied. PATIENTS AND METHODS: Five hundred colorectal cancer patients and 500 controls were genotyped for cytochrome P450 enzymes (CYP) 1A1 Ile/Val, CYP 1A2*1F, CYP 2E1 c1/c2, microsomal epoxy hydrolase (mEH) exon 3 Tyr113His and exon 4 His139Arg polymorphisms by allele-specific polymerase chain reaction (PCR) or PCR-restriction fragment length polymorphism (RFLP). RESULTS: The presence of CYP 1A1 Val, CYP 2E1 c2 and mEH exon 3 His alleles was statistically significantly associated with the occurrence of colorectal cancer (OR: 1.44 95% CI: 1.04-2.00; OR: 1.74 95% CI: 1.15-2.65; OR: 1.79 95% CI: 1.10-2.92, respectively). CONCLUSION: These findings suggest that allelic polymorphism of metabolizing enzymes play an important role in human colorectal carcinogenesis by affecting the metabolism of dietary carcinogens.

Morbidity and mortality trends in very-very low birth weight premature infants in light of recent changes in obstetric care.

OBJECTIVE: In this study, we describe trends in morbidity and mortality of preterm infants with less than 500mg birth weight in the changing landscape of obstetric and neonatal care. STUDY DESIGN: During a ten year study period between 2006 and 2016 we assessed outcome data for all neonates with less than 500mg birth weight born at our Neonatal Intensive Care Unit. We divided study subjects into two groups based on whether their birth date fell in the first half (2006-2010; n=39) versus the second half (2011-2015; n=27) of the study period comparing clinical outcomes in the two groups. We also assessed several clinical parameters for association with postnatal survival by comparing relative frequencies for each clinical parameter among surviving infants versus mortality cases. RESULTS: Survival rate for preterm neonates with less than 500mg birth weight born between 2006 and 2010 was 30.8%. This survival rate rose to 70.4% in the second half of the study period between 2011 and 2015 (p<0.05). Among surviving babies premature birth was found to be predominantly associated with maternal hypertension or intrauterine growth restriction while in those who died premature birth due to premature rupture of membranes and spontaneous preterm labor were significantly more common. All surviving infants with less than 500mg birth weight were born via cesarean section whereas among those who died cesarean section had been performed in only 80% and vaginal delivery in 20% representing a significant difference between the groups (p<0.05). The majority (90.3%) of surviving infants with less than 500mg birth weight had received surfactant therapy while the proportion of neonates receiving surfactant therapy among mortality cases was significantly lower (65.2%; p<0.05). DISCUSSION: Our findings suggest that among premature neonates with less than 500mg birth weight preterm delivery due to premature rupture of membranes and intrauterine infections represents the worse mortality risk. Steroid prophylaxis and measures to prevent and treat intrauterine infections with appropriate use of antibiotics can markedly improve survival in these cases. In premature neonates with less than 500mg birth weight survival is more favorable after cesarean section compared to vaginal delivery.

Target-organ damage in adolescent hypertension. Analysis of potential influencing factors, especially nitric oxide and endothelin-1.

BACKGROUND AND PURPOSE: To assess the role of the nitric oxide-endothelin imbalance in the development of target-organ damages (carotid intima-media thickness and left ventricular mass index) in adolescent hypertension. METHODS: 125 adolescents--67 hypertensive and 58 normotensive--underwent routine anthropology (height, weight) and blood pressure measurements, and laboratory (glucose, cholesterol and triglyceride levels) testing as well as sampling blood for determination of the plasma concentrations of nitric oxide (NOx) and endothelin-1 (ET-1), followed by measurement of the carotid intima-media thickness (IMT) and left ventricular mass index (LVMI). RESULTS: Plasma concentration of NOx was significantly lower (27.7+/-13.7 vs. 35.8+/-7.0 micromol/l, respectively, p<0.001) and ET-1 was higher (3.11+/-3.9 vs. 1.09+/-1.07 fmol/ml, respectively, p<0.001) in hypertensive adolescents than that of controls. NOx negatively, endothelin positively correlated with blood pressure values, especially with systolic BP. An inverse relationship has been found between NOx and ET-1 concentrations (r=-0.29, p<0.003). In this adolescent population body weight, systolic blood pressure and plasma ET-1 were the most important factors influencing IMT, whereas LVMI correlated with height and weight and systolic BP of the teenagers. CONCLUSIONS: NO/endothelin imbalance seems to play a role in the development of hypertension and target-organ damages in adolescence. Further studies are encouraged in order to clarify the pathophysiological role of NO/endothelin imbalance in adolescent hypertension.