ABSTRACT
We assessed the efficacy and tolerability of the augmentation of antidepressants (ATDs) with atypical antipsychotics (AAPs) to treat patients with major depressive disorder. A retrograde study to identify relevant patient data included databases of PubMed, EMBASE, Cochrane Central Register of Controlled Trials, and Database of Abstracts of Reviews of Effects. Data from 17 trials, involving 3807 participants, were identified. The remission rate (RR) and overall response rate (ORR) of adjunctive treatment with AAPs were significantly higher than placebo treatment: RR=1.90 (95%CI=1.61-2.23, z=7.74, P<0.00001) and ORR=1.68 (95%CI=1.45-1.94, z=7.07, P<0.00001). We found that the short-term (4 weeks) treatment [ORR=1.70 (95%CI=0.98-2.95, Z=1.89, P=0.06)] was significantly different from the long-term (6-12 weeks) treatment [ORR=1.68 (95%CI=1.45-1.94, z=7.07, P<0.00001)]. No significant difference in ORR was observed between groups with or without sedative drugs. The discontinuation rate due to adverse effects was higher for adjunctive treatment with AAPs: ORR=3.32 (95%CI=2.35-4.70, z=6.78, P<0.00001). These results demonstrate that the augmentation of ATDs with AAPs (olanzapine, quetiapine, aripiprazole, and risperidone) was more effective than a placebo in improving response and remission rates, although associated with a higher discontinuation rate due to adverse effects.
Subject(s)
Adolescent , Adult , Aged , Humans , Middle Aged , Young Adult , Antidepressive Agents/administration & dosage , Antipsychotic Agents/administration & dosage , Antipsychotic Agents/adverse effects , Depressive Disorder, Major/drug therapy , Antidepressive Agents/adverse effects , Benzodiazepines/administration & dosage , Benzodiazepines/adverse effects , Chemotherapy, Adjuvant , Double-Blind Method , Drug Synergism , Dibenzothiazepines/administration & dosage , Dibenzothiazepines/adverse effects , Piperazines/administration & dosage , Piperazines/adverse effects , Quinolones/administration & dosage , Quinolones/adverse effects , Randomized Controlled Trials as Topic , Remission Induction , Risperidone/administration & dosage , Risperidone/adverse effects , Treatment OutcomeABSTRACT
<p><b>INTRODUCTION</b>The device closure of atrial septal defects has evolved over the years. In the early days of transcatheter occlusion, balloon sizing was used to choose an appropriate sized device. We postulate that balloon sizing does not value-add to the procedure and is unnecessary.</p><p><b>MATERIALS AND METHODS</b>Patients who had balloon sizing, with (Group 1, n = 38) or without (Group 2, n = 21) atrial septal defect closure, were compared to another group (Group 3, n = 64) who had atrial septal defect closure without balloon sizing. Although the atrial septal defect size (mm) in those without balloon sizing (Group 3) compared to patients who had balloon sizing (Group 1) (18.3 +/- 5.4 vs 14.8 +/- 5.8; P = 0.021) was larger, the Amplatzer septal occluder size chosen (mm) (21.6 +/- 6.3 vs 21.2 +/- 8.1; P = 0.693) was similar.</p><p><b>RESULTS</b>We analysed the degree of absolute sizing, defined as [(Balloon or Amplatzer occluder size) - (transoesophageal echocardiography size)], versus relative sizing, which is defined as [(Balloon or Amplatzer occluder size)--(transoesophageal echocardiography size) / (Balloon or Amplatzer occluder size)]. It was evident that there was greater absolute and relative over-sizing (6.3 +/- 4.4 mm vs 4.2 +/- 2.1 mm; P = 0.009 and 28.3 +/- 15.4% vs 20.0 +/- 7.0%; P = 0.001, respectively) in patients with balloon sizing (Group 1) compared to those who did not (Group 3). Even a greater degree of absolute (5.1 +/- 3.9 mm vs 9.5 +/- 4.7 mm; P <0.001) and relative over-sizing (24.8 +/- 15.6% vs 33.0 +/- 13.6%; P = 0.001) was observed in patients who had balloon sizing but there was no closure (Group 2) compared to those who had balloon sizing and closure of their defects (Group 1).</p><p><b>CONCLUSION</b>Our results showed that balloon sizing tended to over-size the atrial septal defect. This may have an important bearing in selecting a larger device than necessary, or even precluding transcatheter closure of the larger atrial septal defects. It is also associated with increased procedural, fluoroscopy time and cost. We suggest that balloon sizing may no longer be necessary in the protocol of device closure of an atrial septal defect.</p>
Subject(s)
Adolescent , Adult , Aged , Child , Child, Preschool , Female , Humans , Male , Middle Aged , Young Adult , Cardiac Catheterization , Methods , Echocardiography, Transesophageal , Heart Septal Defects, Atrial , Diagnostic Imaging , Pathology , General Surgery , Septal Occluder DeviceABSTRACT
To investigate genome size evolution, it is usually informative to compare closely related species that vary dramatically in genome size. A whole genome duplication (polyploidy) that occurred in rice (Oryza sativa) about 70 million years ago has been well documented based on current genome sequencing. The presence of three distinct duplicate blocks from the polyploidy, of which one duplicated segment in a block is intact (no sequencing gap) and less than half the length of its syntenic duplicate segment, provided an excellent opportunity for elucidating the causes of their size variation during the post-polyploid time. The results indicated that incongruent patterns (shrunken, balanced and inflated) of chromosomal size evolution occurred in the three duplicate blocks, spanning over 30 Mb among chromosomes 2, 3, 6, 7, and 10, with an average of 20.3% for each. DNA sequences of chromosomes 2 and 3 appeared to had become as short as about half of their initial sequence lengths, chromosomes 6 and 7 had remained basically balanced, and chromosome 10 had become dramatically enlarged (approximately 70%). The size difference between duplicate segments of rice was mainly caused by variations in non-repetitive DNA loss. Amplification of long terminal repeat retrotransposons also played an important role. Moreover, a relationship seems to exist between the chromosomal size differences and the nonhomologous combination in corresponding regions in the rice genome. These findings help shed light on the evolutionary mechanism of genomic sequence variation after polyploidy and genome size evolution.
Subject(s)
Chromosomes, Plant/genetics , Evolution, Molecular , Genome, Plant/genetics , Oryza/genetics , Terminal Repeat Sequences/genetics , Gene Duplication , Genes, Plant , Base Sequence , Repetitive Sequences, Nucleic AcidABSTRACT
CONTEXT: Survivin is an inhibitor of apoptosis that is selectively over-expressed in common human cancers, but not in normal tissues, and that correlates with aggressive disease and unfavorable outcomes. AIMS: To identify the role of survivin in bladder carcinogenesis and the correlation between survivin protein expression and the occurrence of spontaneous apoptosis, proliferative activity of cancer cells. SETTINGS AND DESIGN: Retrospective analysis. METHODS AND MATERIAL: Bladder transitional cell cancer (BTCC) tissue samples for 128 patients were investigated, with normal bladder tissues serving as controls. From these tumor samples, 42 (32.8%) were grade I, 59 (46.1%) were grade II, and 27 (21.1%) were grade III; 72 (56.2%) were superficial, 56 (43.8%) were invasive. The survivin protein level was quantified by Western blot analysis. The apoptotic index (AI) using in situ labeling apoptotic DNA fragment kit and the Ki-67 labeling index (Ki-67LI) with an anti-Ki-67 monoclonal antibody were analyzed in these tumors, respectively. STATISTICAL ANALYSIS USED: Differences in the S/beta ratio between tumor grade and stage were evaluated by using unpaired t-test and F-test. The relationships between the S/beta ratios and AIs, Ki-67LIs of tumors were evaluated by Pearson correlation coefficient. RESULTS: High survivin levels were detected by Western blot analysis in tumor tissue extracts. None of the expression of survivin protein was found in normal bladder tissues. Survivin levels were significantly different from different clinical stages and pathological grades of the tumors (P > 0.05, respectively). Spearman rank correlation test revealed a positively correlation between survivin protein level and the proliferative activity (P < 0.001) and failed to find significant correlation between AI and survivin protein level (P > 0.05). CONCLUSIONS: Survivin protein expression played an important role in the malignant progression of BTCC.