[Current therapeutic approach to diabetic macular edema refractory to laser coagulation]. / Abordarea terapeutica moderna a edemului macular diabetic rezistent la laserterapie.

The paper presents the evolution of a diabetic patient with CSME resistant to laser treatment. The intravitreal injection of Triamcinolone Acetonid represented a very efficient therapeutic solution the visual accuity improving for a period of 7-9 months.

Clinical Study on Abfraction Lesions in Occlusal Dysfunction.

The abfraction theory states that under the action of the occlusal forces non-axially transmitted, the flexion of the tooth occurs in the cervical area, which initially leads to the appearance of cracks in the enamel and dentin, followed by the destruction of the dental structure. These lesions allow bacterial plaque retention, lead to dental hypersensitivity and can affect the vitality of the dental pulp. Thus, the study included 102 participants, of both sexes, 54% representing the male gender (55 subjects) and 46% the female gender (47 subjects), aged between 20 and 80, from the urban area 76% (77 subjects) and rural 24% (25 subjects), who came to the Dental Medicine office, between August 2018 and August 2019, representing 57.3%, of the total number of patients treated during the aforementioned period. They have been described the acid and abrasive processes involved in the generation of these lesions,and special attention was paid to the role of mechanical stress occurring at the occlusal level, due to the transmission of forces outside the dental axis.

Identifying the Etiological Factors Involved in the Occurrence of Non-Carious Lesions.

The study group comprised a total of 21 subjects (10 women and 11 men) from the urban area aged 20 to 72 who presented themselves to treatment at the Dental Office during July-December 2018. The purpose of the study was to identify the etiological factors responsible for the occurrence of non-carious lesions in the patients involved in the study. The study group of 21 patients (10 women and 11 men) from the urban area, aged 20 to 72 years, were clinically examined and dental impressions were obtained in order to ascertain the study patterns. Subjects diagnosed with non-carious lesions filled a questionnaire based on which the risk factors that led to these changes were identified. The study models were used to assess the degree of cervical tooth damage, according to SMITH-KNIGHT index. The main etiological factors found to be responsible for the occurrence of non-carious lesions in the studied group were the excessive consumption of acidic and carbonated beverages (71.42%), the presence of gastro-esophageal reflux disease (14.28%), incorrect technique of brushing (28.57%), vicious habits-nail biting (14.28%), daily consumption of sunflower seeds (9.52%), use of toothpicks as auxiliary hygiene (19.04%) and night teeth grinding (4,76%).

Hypermethylation of the nel-like 1 gene is a common and early event and is associated with poor prognosis in early-stage esophageal adenocarcinoma.

The nel-like1 (NELL1) gene maps to chromosome 11p15, which frequently undergoes loss of heterozygosity in esophageal adenocarcinoma (EAC). NELL1 promoter hypermethylation was examined by real-time methylation-specific polymerase chain reaction in 259 human esophageal tissues. Hypermethylation of this promoter showed highly discriminative receiver-operator characteristic curve profiles, clearly distinguishing esophageal squamous cell carcinoma (ESCC) and EAC from normal esophagus (NE) (P<0.001). NELL1 normalized methylation values were significantly higher in Barrett's metaplasia (BE), dysplastic Barrett's (D) and EAC than in NE (P<0.0000001). NELL1 hypermethylation frequency was zero in NE but increased early during neoplastic progression, to 41.7% in BE from patients with Barrett's alone, 52.5% in D and 47.8% in EAC. There was a significant correlation between NELL1 hypermethylation and BE segment length. Three (11.5%) of 26 ESCCs exhibited NELL1 hypermethylation. Survival correlated inversely with NELL1 hypermethylation in patients with stages I-II (P=0.0264) but not in stages III-IV (P=0.68) EAC. Treatment of KYSE220 ESCC and BIC EAC cells with 5-aza-2'-deoxycytidine reduced NELL1 methylation and increased NELL1 mRNA expression. NELL1 mRNA levels in EACs with an unmethylated NELL1 promoter were significantly higher than those in EACs with a methylated promoter (P=0.02). Promoter hypermethylation of NELL1 is a common, tissue-specific event in human EAC, occurs early during Barrett's-associated esophageal neoplastic progression, and is a potential biomarker of poor prognosis in early-stage EAC.

Transcriptional profiling suggests that Barrett's metaplasia is an early intermediate stage in esophageal adenocarcinogenesis.

To investigate the relationship between Barrett's esophagus (BE) and esophageal adenocarcinoma (EAC), we determined gene expression profiles of discrete pathological stages of esophageal neoplasia using a sequence-verified human cDNA microarray. Fifty one RNAs, comprising 24 normal esophagi (NE), 18 BEs, and nine EACs were hybridized to cDNA microarrays. Five statistical analyses were used for the data analysis. Genes showing significantly different expression levels among the three sample groups were identified. Genes were grouped into functional categories based on the Gene Ontology Consortium. Surprisingly, the expression pattern of BE was significantly more similar to EAC than to NE, notwithstanding the known histopathologic differences between BE and EAC. The pattern of NE was clearly distinct from that of EAC. Thirty-six genes were the most differentially modulated, according to these microarray data, in BE-associated neoplastic progression. Twelve genes were significantly differentially expressed in cancer-associated BE's plus EAC (as a single combined tissue group) vs noncancer-associated BE's. These genes represent potential biomarkers to diagnose EAC at its early stages. Our results demonstrate that molecular events at the transcriptional level in BE are remarkably similar to BE's-associated adenocarcinoma of the esophagus. This finding alarmingly implies that BE is biologically closer to cancer than to normal esophagus, and that the cancer risk of BE is perhaps higher than we had imagined. These findings suggest that changes modulated at the molecular biologic level supervene earlier than histologic changes, and that BE is an early intermediate stage in the process of EAC.

SABRE hyperpolarisation of vitamin B3 as a function of pH.

In this work we describe how the signal enhancements obtained through the SABRE process in methanol-d4 solution are significantly affected by pH. Nicotinic acid (vitamin B3, NA) is used as the agent, and changing pH is shown to modify the level of polarisation transfer by over an order of magnitude, with significant improvements being seen in terms of the signal amplitude and relaxation rate at high pH values. These observations reveal that manipulating pH to improve SABRE enhancements levels may improve the potential of this method to quantify low concentrations of analytes in mixtures. 1H NMR spectroscopy results link this change to the form of the SABRE catalyst, which changes with pH, resulting in dramatic changes in the magnitude of the ligand exchange rates. The presented data also uses the fact that the chemical shifts of the nicotinic acids NMR resonances are affected by pH to establish that hyperpolarised 1H-based pH mapping with SABRE is possible. Moreover, the strong polarisation transfer field dependence shown in the amplitudes of the associated higher order longitudinal terms offers significant opportunities for the rapid detection of hyperpolarised NA in H2O itself without solvent suppression. 1H and 13C MRI images of hyperpolarised vitamin B3 in a series of test phantoms are presented that show pH dependent intensity and contrast. This study therefore establishes that when the pH sensitivity of NA is combined with the increase in signal gain provided for by SABRE hyperpolarisation, a versatile pH probe results.

Global gene expression profiling in Barrett's esophagus and esophageal cancer: a comparative analysis using cDNA microarrays.

In order to identify and contrast global gene expression profiles defining the premalignant syndrome, Barrett's esophagus, as well as frank esophageal cancer, we utilized cDNA microarray technology in conjunction with bioinformatics tools. We hybridized microarrays, each containing 8000 cDNA clones, to RNAs extracted from 13 esophageal surgical or endoscopic biopsy specimens (seven Barrett's metaplasias and six esophageal carcinomas). Hierarchical cluster analysis was performed on these results and displayed using a color-coded graphic representation (Treeview). The esophageal samples clustered naturally into two principal groups, each possessing unique global gene expression profiles. After retrieving histologic reports for these tissues, we found that one main cluster contained all seven Barrett's samples, while the remaining principal cluster comprised the six esophageal cancers. The cancers also clustered according to histopathological subtype. Thus, squamous cell carcinomas (SCCAs) constituted one group, adenocarcinomas (ADCAs) clustered separately, and one signet-ring carcinoma was in its own cluster, distinct from the ADCA cluster. We conclude that cDNA microarrays and bioinformatics show promise in the classification of esophageal malignant and premalignant diseases, and that these methods can be applied to small biopsy samples.

[Trauma from light induced by the operating microscope in the rat retina]. / Fototraumatisme induse de microscopul operator pe retina de sobolan.

The study proposes to analyze the lesions show to the retina level of the rat exposes to light of an operate microscope Zeiss Op Mi 220 (without filters). The conditions of the experiment was created such as the photochemical effect of the radiation to predominate more than thermic effect. Rat's retinae was visualized through photonic and electronic microscopy. The images show that the maximal lesions are situated to the level of the retinal pigment epithelium and of photoreceptors cells. The histological aspects presume the action of the free radicals in the production of the lesions.

Prognosis of colorectal cancer: clinical, pathological and therapeutic correlation.

INTRODUCTION: Significant progress in the knowledge of carcinogenesis and natural history of colorectal carcinoma (CRC), especially in polyp-cancer sequention and time for transition, are important prerequisites for a new approach to diagnosis. Surgical resection is the mainstay therapy for colorectal cancer, and pathologic assessment of the resected specimen provides data for assessment of outcome and rationale for adjuvant therapy. A pathology report includes TNM stage, tumor type, histologic grade, status of resection margins, and vascular invasion. AIM: The purpose of this paper was to highlight the pathological features and their correlations with postoperative evolution and prognosis of this cancer. PATIENTS AND METHODS: Data was collected using the database system of the Emergency County Hospital of Craiova, Romania. A total of 302 patients from January 2003 to December 2005 were included. RESULTS: The average survival for the entire group was 44.35 ± 28.94 months, and the D'Agostino-Pearson test for batch distribution showed abnormal distribution with two peaks, separated by a group of five patients who survived between 37 and 8 months. Fifty-one (38.05%) patients presented a median survival of 73.54 ± 10.47 months. CONCLUSIONS: Factors that contribute to a favorable prognosis in CRC are vegetant gross tumors and papillary microscopic forms, G1 and G2 degree of differentiation and disease diagnosed in stages I and II.

Study of molecular prognostic factors Bcl-2 and EGFR in rectal mucinous carcinomas.

Colorectal cancer is an important public health problem worldwide, being the fourth most common cancer in men and the third most common in women. Colorectal cancer incidence is higher in developing countries due to the prevalence of obesity associated with reduced physical activity. Rectal mucinous carcinomas, especially the "signet ring cell" type, have a worse prognosis compared with other varieties of colorectal carcinomas, being diagnosed in more advanced stage and more prone to lymph node and peritoneal metastases. Our study comprised 37 cases with rectal adenocarcinoma with mucinous component operated in the Surgical Clinics of the Emergency County Hospital of Craiova, between 2006 and 2010. The aim of this study was to evaluate some molecular prognostic factors for rectal mucinous carcinomas namely B-cell lymphoma 2 (Bcl-2) and epidermal growth factor receptor (EGFR), and their correlations with the main morpho-clinical parameters of these patients. Thus, we immunohistochemically assessed the degree of apoptosis of tumor cells in mucinous rectal carcinomas using the Bcl-2 marker, and tumor aggressiveness using the EGFR responsiveness. In our study, the percentage of Bcl-2+ cases was 43.24%, with no significant statistical correlation between the Bcl-2 expression and histopathological subtype of mucinous adenocarcinoma. The evaluation of tumor aggressiveness in terms of EGFR responsiveness showed a reduced expression in carcinomas correlated with the increase in quantity of the mucinous component. In addition, EGFR reactivity was increased in the tumor invasion front.

MicroRNA-192 and -215 are upregulated in human gastric cancer in vivo and suppress ALCAM expression in vitro.

The dismal outcome of gastric cancer patients highlights the need for diagnostic biomarkers and effective therapeutic targets, such as microRNAs. We sought to discover microRNAs involved in gastric cancer, and to elucidate their downstream target mechanisms. Both cultured gastric epithelial cells (HFE145 and NCI-N87) and primary human gastric tissues (31 non-neoplastic stomach (NS) and 25 gastric carcinomas (GC)) were studied. MicroRNA microarrays and quantitative RT-PCR were applied to discover and verify differentially expressed microRNAs. in vitro cell migration and invasion, cell proliferation, cell cycle and apoptosis assays were executed to elucidate biological effects of microRNA-192 and -215. Western blotting and luciferase assays were performed to confirm direct messenger RNA targeting by microRNA-192 and -215. MicroRNA microarray analyses revealed that 25 and 20 microRNAs were upregulated and downregulated in GC vs NS, respectively. Expression levels of both microRNA-192 and -215 were significantly higher in GC than in NS (P<0.05). Luciferase assays suggested that microRNA-215 inhibits activated leukocyte cell adhesion molecule (ALCAM) expression at the posttranscriptional level. In addition, expression levels of ALCAM were significantly lower in GC than in NS. Mimics and inhibitors, respectively, of microRNA-192 or -215 exerted no effect on cell cycle or apoptosis in the immortalized normal gastric cell line HFE145 or the gastric cancer cell line NCI-N87. However, mimics of microRNA-192 or -215 significantly increased growth rates in HFE145 cells, whereas inhibitors of microRNA-192 or -215 caused significant decreases in growth rates in NCI-N87 cells. ALCAM knockdown by an ALCAM-specific siRNA significantly increased cell growth in HFE145 cells. Both transfection of mimics of microRNA-192 or -215 and ALCAM knockdown by an ALCAM-specific siRNA significantly increased the migration of HFE145 cells. In conclusion, in gastric cancer, both microRNA-192 and -215 are overexpressed in vivo and exert cell growth and migration-promoting effects in vitro, thus representing potential microRNAs with a role in cancer in the human stomach.

The role of the renin-angiotensin system in arterial hypertension in hypercorticism.

The authors have studied on 25 cases of hypercorticism, one of the mechanisms of producing arterial hypertension, the renin-angiotensin system. The study showed that in only 20% of the cases plasma renin activity was high whereas in the remaining 80% other mechanisms were responsible for the hypertension. In the cases in which the plasma activity of renin was high, by studying the changes in the value of electrolytes we were able to derive some understanding of the mechanism of action of the RA2A system. Thus, the literature data show that sometimes the excess of glucocorticoids causes hypertension by activating directly the RA2A system and concomitently inhibiting the renin-kalikrein system (RKKS) and PgS; at other times, the excess of glucocorticoids is exerted on the same renin-angiotensin system, but via ACTH and ADH, the electrolytes values being those that demonstrate the borrowed mechanism.