Изменения систолической и диастолической фунции правого желудочка у больных ХОБЛ и хроническим легочным сердцем под влиянием длительного лечения престариумом

Catedra Boli Interne nr. 6, USMF „Nicolae Testemiţanu”The results of the complex examination of 40 patients with chronic obstruction pulmonary diseases complicated with chronic pulmonary heart showed up the activation of renin-angiotensin-aldosterone system (rising of renin and angiotensin converting enzyme activity, aldosterone plasmatic concentration). The rising of renin activity and aldosterone concentration correlate with the level of pulmonary hypertension, hypoxemia, structural and functional changes of right and left ventricle. The process of heart remodeling is characterized by increasing of anterior wall thickness and dimensions of right ventricle and right auricle, signs of diastolic (impaired or pseudonormal relaxation) and systolic dysfunction of right ventricle. The administration of inhibitor of angiotensin converting enzyme prestarium in compensated chronic pulmonary heart leads to depression of average pressure in the pulmonary artery, improvement of right ventricle and left ventricle diastolic function, and a tendency to decrease the thickness anterior wall of right ventricle, systolic and diastolic dimensions of both ventricles, dimensions of right auricle. По результатам комплексного обследования 40 больных ХОБЛ, осложненной ХЛС, выявлена активация РААС в виде увеличения активности ренина, АПФ и концентрации альдостерона в плазме крови. Повышение активности ренина и концентрации альдостерона взaимосвязано с уровнем ЛГ, гипоксемии, структурно-функциональными изменениями ПЖ и ЛЖ. Процесс ремоделирования сердца у больных ХОБЛ и ХЛС характеризуется увеличением толщины передней стенки и размеров полости ПЖ и ПП, признакaми диастолической дисфункции по типу замедленной релаксации или псевдонормального типа и нарушения систолической функции ПЖ. Назначение ингибитора АПФ престариума при компенсированном ХЛС через год от начала лечения приводит к уменьшению СрДЛА, улучшению диастолической функции ПЖ и ЛЖ, наблюдается тенденция к уменьшению толщины передней стенки ПЖ, систолического и диастолического размеров обоих желудочков, а также размеров ПП

Reversible hiatal hernias and the pathological migration of suprahiatal esogastric junction

Scopul lucrării. In diverse conditii fiziologice și patologice jonctiunea esofago-gastrică (JEG) poate migra suprahiatal. Diapazonul deplasării reversibile a JEG suprahiatal este diferit. Din acest punct de vedere se deosebesc 3 situații anatomo-fiziologice: (1) migrație fiziologică reversibilă a JEG suprahiatal, (2) migrație excesivă (patologică) a JEG suprahiatal și (3) hernii hiatale reversibile. Diferențierea acestor situații nu este bine clarificată. Scopul studiului a fost evaluarea endoscopică a ratei patologiei cauzal-asociate ca criteriu de diferențiere a situațiilor sus-numite, în funcție de diapazonul și tipul migratiei JEG suprahiatal. Materiale și metode. Au fost analizate endoscopic (proendoscopie si în retroflexia endoscopului din stomac) 470 cazuri de migrație a JEG prin orificiul hiatal în mediastinul posterior (suprahiatal). Investigatiile au fost efectuate de un singur endoscopist. S-a folosit complexul endoscopic Olympus Exera III GIF HQ190. Metodologia măsurărilor endoscopice și criteriile de determinare pentru patologia asociată au fost unice pentru toți pacienții. Patologie causal- asociată s-a considerat esofagita de reflux, sechelele cicatriceale posterozive și postulceroase postreflux, esofagul columnar metaplaziat cu metaplazie gastrica și esofagul Barrett. Rata patologiei asociate a fost calculată conform criteriului „absent-prezent” pentru fiecare pacient indiferent de numărul patologiilor asociate și tipul lor. Diferenta ratei patologiei asociate migratiei suprahiatale JEG a fost calculată pentru grupurile delimitate cu înălțimea migrației 0.5 cm, 1.0 cm, 1.5 cm, 2.0 cm, 2.5 cm și 3.0 cm. Rezultate. Migratia reversibilă a JEG suprahiatal sub 0.5 cm a fost cauzal-asociată patologic în 2,94%. Corespunzător înălțimii migratiei JEG suprahiatal, rata patologiei asociate a alcătuit: pentrudiapazonul 0.5÷0,9 cm – 8.54%, pentru diapazonul 1,0÷1,4 cm – 9,20 %, pentru diapazonul 1,5÷1,9 cm – 10.45%, pentru diapazonul 2.0÷2,4 cm – 93.62%, pentru diapazonul 2.5÷2.9 cm – 84.5%, pentru migrația ≥3.0 cm – 87,5%. Asfel, s-au apreciat două puncte semnificative: migrația sub 0.5 cm a fost asociată cauzal-patologic cu o rată practic nulă (zero) a patologiei de reflux și distanța de migratie de 20 mm a fost apreciată ca punctul cu care face cea mai înaltă diferență de asociere causal-patologică a diapazoanelor adiacente. Concluzii. Astfel, sub aspect endoscopic, (1) migrația reversibilă a JEG suprahiatal până la 0.5 cm poate fi considerată migrație fiziologică. (2) migrație reversibilă excesivă (patologică) a JEG suprahiatal poate fi considerată deplasarea JEG pe un diapason ≥0.5 cm ÷ ˂2.0cm, (3) hernie hiatală glisantă reversibilă poate fi considerată deplasarea reversibilă a JEG suprahiatal cu 20 mm si mai mult.Aim of study. In various physiological and pathological conditions, the gastroesophageal junction (GEJ) can migrate suprahiatal. The range of reversible displacement of the suprahiatal GEJ is different. From this point of view, there are 3 anatomical-physiological situations: (1) reversible physiological migration of suprahiatal GEJ, (2) excessive (pathological) migration of suprahiatal GEJ and (3) reversible hiatal hernias. The differentiation of these situations is not well clarified. The objective of the present study was the endoscopic evaluation of the rate of causal-associated pathology as a criterion for differentiating the above situations, depending on the diapason and the type of suprahiatal GEJ migration. Materials and methods. 470 cases of migration of GEJ through the hiatal orifice into the posterior mediastinum (suprahiatal) were analyzed endoscopically (proendoscopy and retroflexion of the stomach endoscope). The investigations were performed by an endoscopist. The Olympus Exera III GIF HQ190 endoscopic complex was used. The methodology of endoscopic measurements and the determination criteria for the associated pathology were unique for all patients. Causal-associated pathology was considered erosive reflux esophagitis, post-erosive and post-reflux scarring sequelae, esophageal columnar metaplasia with gastric metaplasia and Barretts esophagus. The rate of associated pathology was calculated according to the ”absent-present” criterion for each patient regardless of the number of associated pathologies and their type. The difference in the rate of pathology associated with suprahiatal GEJ migration was calculated for the groups delimited with the migration height of 0.5 cm, 1.0 cm, 1.5 cm, 2.0 cm, 2.5 cm and 3.0 cm. Results. Reversible migration of suprahiatal GEJ below 0.5 cm was pathologically-associated in 2.94%. Corresponding to the height of the suprahiatal GEJ migration, the rate of the associated pathology was: for the 0.5 ÷ 0.9 cm range - 8.54%, for the 1.0 ÷ 1.4 cm range - 9.20%, for the 1.5 ÷ 1.9 cm range - 10.45%, for the 2.0 ÷ 2.4 cm range - 93.62%, for the 2.5 ÷ 2.9 cm range - 84.5%, for the migration ≥3.0 cm - 87.5%. Thus, two significant points were assessed: the migration below 0.5 cm was causally- pathologically associated with an insignificant rate (2.94%) of reflux pathology and the migration distance of 20 mm was assessed as the point with which it makes the highest difference (10.43% and 93,42%) in causal-pathological association of adjacent tuning forks. Conclusions. Thus, from an endoscopic point of view, (1) reversible migration of suprahiatal GEJ up to 0.5 cm can be considered a physiological migration. (2) excessive (pathological) reversible migration of the suprahiatal EGJ can be considered the displacement of the GEJ on a tuning fork ≥0.5 cm ÷ ˂2.0cm, (3) reversible sliding hiatal hernia can be considered the reversible displacement of the suprahiatal GEJ by 20 mm and more

Влияние озонотерапии на показатели гуморального и клеточного иммунитета у больных с дуоденальной язвой

Catedra Medicină internă nr. 6, USMF “Nicolae Testemiţanu”, Universitatea „Lucian Blaga”, Sibiu, România, Spitalul Clinic al Ministerului Sănătăţii, Chişinău, Conferinţa Ştiinţifico-Practică „Medicina modernă, actualităţi şi perspective”, consacrată aniversării de 40 de ani ai Spitalului Clinic al Ministerului Sănătăţii, 27-28 mai, 2010, Chişinău, Republica MoldovaThe study included 180 patients with chronic duodenal ulcer H. pylori associated in exacerbation. The patients underwent: physical examination, laboratory diagnosis fibrogastroscopy and laboratory exams for H. pylori. Under the influence of ozonotherapy both cellular and humoral components of the immune status were stimulated. Sometimes the effects of ozonotherapy occured 6 weeks after the treatment. It was established that the inclusion of ozonotherapy with the standard treatment contributed to the increase of H. pylori eradication. В исследование были включены 180 больных хронической язвой двенадцатиперстной кишки в стадии обострения и положительной H. pylori. Изучено влияние озонотерапии на клеточные и гуморальные звенья иммунитета. При исследовании иммунного статуса наблюдалась активация T- и B-клеточного ответа. Эффективность озонотерапии наблюдалась через 6 недель после окончания лечения. Было установлено, что включение озонотерапии в базисное лечение способствовало увеличению эрадикации H. pylori

Cyclin D1 and mammary carcinoma: new insights from transgenic mouse models

Cyclin D1 is one of the most commonly overexpressed oncogenes in breast cancer, with 45–50% of primary ductal carcinomas overexpressing this oncoprotein. Targeted deletion of the gene encoding cyclin D1 demonstrates an essential role in normal mammary gland development while transgenic studies provide evidence that cyclin D1 is a weak oncogene in mammary epithelium. In a recent exciting development, Yu et al. demonstrate that cyclin D1-deficient mice are resistant to mammary carcinomas induced by c-neu and v-Ha-ras, but not those induced by c-myc or Wnt-1. These findings define a pivotal role for cyclin D1 in a subset of mammary cancers in mice and imply a functional role for cyclin D1 overexpression in human breast cancer

Cyclin A is a prognostic indicator in early stage breast cancer with and without tamoxifen treatment

Overexpression of G1-S regulators cyclin D1 or cyclin A is frequently observed in breast cancer and is also to result in ligand-independent activation of oestrogen receptor in vitro. This might therefore, provide a mechanism for failure of tamoxifen treatment. We examined by immunohistochemical staining the effect of deregulation of these, and other cell cycle regulators on tamoxifen treatment in a group of 394 patients with early stage breast cancer. In univariate analysis, expression of cyclin A, Neu, Ki-67 index, and lack of OR expression were significantly associated with worse prognosis. When adjusted by the clinical model (for lymph node status, age, performance status, T-classification, grade, prior surgery, oestrogen receptor status and tamoxifen use), only overexpression of cyclin A and Neu were significantly associated with worse prognosis with hazard ratios of, respectively, 1.709 (P=0.0195) and 1.884 (P=0.0151). Overexpression of cyclin A was found in 86 out of the 201 OR-positive cases treated with tamoxifen, and was the only independent marker associated with worse prognosis (hazard ratio 2.024, P=0.0462). In conclusion, cyclin A is an independent predictor of recurrence of early stage breast cancer and is as such a marker for response in patients treated with tamoxifen

Genomic deletion and promoter methylation status of Hypermethylated in Cancer 1 (HIC1) in mantle cell lymphoma

Mantle cell lymphomas (MCL), characterized by the t(11;14)(q13;q32), frequently carry secondary genetic alterations such as deletions in chromosome 17p involving the TP53 locus. Given that the association between TP53-deletions and concurrent mutations of the remaining allele is weak and based on our recent report that the Hypermethylated in Cancer 1 (HIC1) gene, that is located telomeric to the TP53 gene, may be targeted by deletions in 17p in diffuse large B-cell lymphoma (DLBCL), we investigated whether HIC1 inactivations might also occur in MCL. Monoallelic deletions of the TP53 locus were detected in 18 out of 59 MCL (31%), while overexpression of p53 protein occurred in only 8 out of 18 of these MCL (44%). In TP53-deleted MCL, the HIC1 gene locus was co-deleted in 11 out of 18 cases (61%). However, neither TP53 nor HIC1 deletions did affect survival of MCL patients. In most analyzed cases, no hypermethylation of the HIC1 exon 1A promoter was observed (17 out of 20, 85%). However, in MCL cell lines without HIC1-hypermethylation, the mRNA expression levels of HIC1 were nevertheless significantly reduced, when compared to reactive lymph node specimens, pointing to the occurrence of mechanisms other than epigenetic or genetic events for the inactivation of HIC1 in this entity