Assessment of pollution of the Boca de Camichin Estuary in Nayarit (Mexico) and its influence on oxidative stress in Crassostrea corteziensis oysters.

Boca de Camichin Estuary is one of the main producers of Crassostrea corteziensis oysters in Mexico, but the presence of pollutants can affect oyster production. Molluscs produce reactive oxygen species (ROS) in response to changes in the environment and pollution. These ROS induce oxidative damage in biomolecules. The main objective of this study was to evaluate pollution in the estuary and the subsequent oxidative stress in C. corteziensis oysters during the 2010 production cycle. For this aim, we performed monthly samplings in the oyster farms from January to May. We took water samples to quantify polycyclic aromatic hydrocarbon (PAH) and metal content; also, we evaluated oxidative damage (lipoperoxidation, lipidic hydroperoxides, protein oxidation) and enzyme activity (CAT, SOD, GPx, GST and AChE) in oyster gills. The results show the presence of Cu, Fe, Mn, naphthalene, benz[a]anthracene, pyrene, benz[a]pyrene and benzo[k]fluoranthene. On the other hand, AChE activity was not inhibited, which suggests that organophosphorus pollutants or carbamates were absent. Regarding oxidative stress, oysters from the estuary had oxidative damage in lipids, not proteins, and altered antioxidant enzyme activity, when compared to control organisms. Interestingly, we did not observe any correlation between the pollutants and the oxidative stress parameters evaluated in this study. Thus, we cannot rule out that a synergistic effect between the environmental variables and the pollutants is causing the oxidative stress in these oysters.

Evaluation of pollution in Camichin estuary (Mexico): pro-oxidant and antioxidant response in oyster (Crassostrea corteziensis).

The physiological system of molluscs, particularly pro-oxidant and antioxidant mechanisms, could be altered by pollutants and induce disturbance on health status and productive parameters of aquatic organisms, such as oyster. Therefore, the aim of this study was to evaluate the chemical contamination in water (total metals and polycyclic aromatic hydrocarbons) and oxidative stress parameters in oysters (Crassostrea corteziensis) in Camichin estuary, located in Mexican Tropical Pacific. The results obtained showed the presence of arsenic, lead and zinc, as well as naphthalene, pyrene and benzo[a]pyrene in concentrations relatively higher than criteria established by local and international guidelines. Regarding the biomarkers of oxidative stress response (H2O2 and O2 concentration, catalase activity, lipid peroxidation, and hydroperoxide concentration), differences between oyster from estuary and control group were significant. These results indicate that these pollutants could be related with oxidative stress detected in oyster.

Rational optimization of a transcription factor activation domain inhibitor.

Transcription factors are among the most attractive therapeutic targets but are considered largely 'undruggable' in part due to the intrinsically disordered nature of their activation domains. Here we show that the aromatic character of the activation domain of the androgen receptor, a therapeutic target for castration-resistant prostate cancer, is key for its activity as transcription factor, allowing it to translocate to the nucleus and partition into transcriptional condensates upon activation by androgens. On the basis of our understanding of the interactions stabilizing such condensates and of the structure that the domain adopts upon condensation, we optimized the structure of a small-molecule inhibitor previously identified by phenotypic screening. The optimized compounds had more affinity for their target, inhibited androgen-receptor-dependent transcriptional programs, and had an antitumorigenic effect in models of castration-resistant prostate cancer in cells and in vivo. These results suggest that it is possible to rationally optimize, and potentially even to design, small molecules that target the activation domains of oncogenic transcription factors.

Residual gammaH2AX foci as an indication of lethal DNA lesions.

BACKGROUND: Evidence suggests that tumor cells exposed to some DNA damaging agents are more likely to die if they retain microscopically visible gammaH2AX foci that are known to mark sites of double-strand breaks. This appears to be true even after exposure to the alkylating agent MNNG that does not cause direct double-strand breaks but does produce gammaH2AX foci when damaged DNA undergoes replication. METHODS: To examine this predictive ability further, SiHa human cervical carcinoma cells were exposed to 8 DNA damaging drugs (camptothecin, cisplatin, doxorubicin, etoposide, hydrogen peroxide, MNNG, temozolomide, and tirapazamine) and the fraction of cells that retained gammaH2AX foci 24 hours after a 30 or 60 min treatment was compared with the fraction of cells that lost clonogenicity. To determine if cells with residual repair foci are the cells that die, SiHa cervical cancer cells were stably transfected with a RAD51-GFP construct and live cell analysis was used to follow the fate of irradiated cells with RAD51-GFP foci. RESULTS: For all drugs regardless of their mechanism of interaction with DNA, close to a 1:1 correlation was observed between clonogenic surviving fraction and the fraction of cells that retained gammaH2AX foci 24 hours after treatment. Initial studies established that the fraction of cells that retained RAD51 foci after irradiation was similar to the fraction of cells that retained gammaH2AX foci and subsequently lost clonogenicity. Tracking individual irradiated live cells confirmed that SiHa cells with RAD51-GFP foci 24 hours after irradiation were more likely to die. CONCLUSION: Retention of DNA damage-induced gammaH2AX foci appears to be indicative of lethal DNA damage so that it may be possible to predict tumor cell killing by a wide variety of DNA damaging agents simply by scoring the fraction of cells that retain gammaH2AX foci.

gammaH2AX expression in tumors exposed to cisplatin and fractionated irradiation.

PURPOSE: Is retention of gammaH2AX foci useful as a biomarker for predicting the response of xenograft tumors to cisplatin with X-ray? Is a similar approach feasible using biopsies from patients with cervical cancer? EXPERIMENTAL DESIGN: Mice bearing SiHa, WiDr, or HCT116 xenograft tumors were exposed to cisplatin and/or three daily doses of 2 Gy. Tumors were excised 24 h after treatment and single cells were analyzed for clonogenic fraction and retention of gammaH2AX foci. Tumor biopsies were examined using 47 paraffin-embedded sections from untreated tumors and 24 sections from 8 patients undergoing radiochemotherapy for advanced cancer of the cervix. RESULTS: Residual gammaH2AX measured 24 h after cisplatin injection accurately predicted surviving fraction in SiHa and WiDr xenografts. When a clinically equivalent protocol using cisplatin and fractionated irradiation was employed, the fraction of xenograft cells lacking gammaH2AX ranked survival accurately but underestimated tumor cell kill. Residual gammaH2AX foci were detected in clinical samples; on average, only 25% of tumor nuclei exhibited one or more gammaH2AX foci before treatment and 74% after the start of treatment. CONCLUSION: gammaH2AX can provide useful information on the response of human tumors to the combination of cisplatin and radiation, but prediction becomes less accurate as more time elapses between treatment and tumor biopsy. Use of residual gammaH2AX as a biomarker for response is feasible when cell survival exceeds approximately 20%, but heterogeneity in endogenous and treatment-induced gammaH2AX must be considered.

Explanation for excessive DNA single-strand breaks and endogenous repair foci in pluripotent mouse embryonic stem cells.

Pluripotent mouse embryonic stem cells (mES cells) exhibit approximately 100 large gammaH2AX repair foci in the absence of measurable numbers of DNA double-strand breaks. Many of these cells also show excessive numbers of DNA single-strand breaks (>10,000 per cell) when analyzed using the alkaline comet assay. To understand the reasons for these unexpected observations, various methods for detecting DNA strand breaks were applied to wild-type mES cells and to mES cells lacking H2AX, ATM, or DNA-PKcs. H2AX phosphorylation and expression of other repair complexes were measured using flow and image analysis of antibody-stained cells. Results indicate that high numbers of endogenous gammaH2AX foci and single-strand breaks in pluripotent mES cells do not require ATM or DNA-PK kinase activity and appear to be associated with global chromatin decondensation rather than pre-existing DNA damage. This will limit applications of gammaH2AX foci analysis in mES cells to relatively high levels of initial or residual DNA damage. Excessive numbers of single-strand breaks in the alkaline comet assay can be explained by the vulnerability of replicating chromatin in mES cells to osmotic shock. This suggests that caution is needed in interpreting results with the alkaline comet assay when applied to certain cell types or after treatment with agents that make chromatin vulnerable to osmotic changes. Differentiation of mES cells caused a reduction in histone acetylation, gammaH2AX foci intensity, and DNA single-strand breakage, providing a link between chromatin structural organization, excessive gammaH2AX foci, and sensitivity of replicating mES cell chromatin to osmotic shock.

Mouse but not human embryonic stem cells are deficient in rejoining of ionizing radiation-induced DNA double-strand breaks.

Mouse embryonic stem (mES) cells will give rise to all of the cells of the adult mouse, but they failed to rejoin half of the DNA double-strand breaks (dsb) produced by high doses of ionizing radiation. A deficiency in DNA-PK(cs) appears to be responsible since mES cells expressed <10% of the level of mouse embryo fibroblasts (MEFs) although Ku70/80 protein levels were higher than MEFs. However, the low level of DNA-PK(cs) found in wild-type cells appeared sufficient to allow rejoining of dsb after doses <20Gy even in G1 phase cells. Inhibition of DNA-PK(cs) with wortmannin and NU7026 still sensitized mES cells to radiation confirming the importance of the residual DNA-PK(cs) at low doses. In contrast to wild-type cells, mES cells lacking H2AX, a histone protein involved in the DNA damage response, were radiosensitive but they rejoined double-strand breaks more rapidly. Consistent with more rapid dsb rejoining, H2AX(-/-) mES cells also expressed 6 times more DNA-PK(cs) than wild-type mES cells. Similar results were obtained for ATM(-/-) mES cells. Differentiation of mES cells led to an increase in DNA-PK(cs), an increase in dsb rejoining rate, and a decrease in Ku70/80. Unlike mouse ES, human ES cells were proficient in rejoining of dsb and expressed high levels of DNA-PK(cs). These results confirm the importance of homologous recombination in the accurate repair of double-strand breaks in mES cells, they help explain the chromosome abnormalities associated with deficiencies in H2AX and ATM, and they add to the growing list of differences in the way rodent and human cells deal with DNA damage.

Electrophysiological and morphological heterogeneity of slow firing neurons in medial septal/diagonal band complex as revealed by cluster analysis.

Slow firing septal neurons modulate hippocampal and neocortical functions. Electrophysiologically, it is unclear whether slow firing neurons belong to a homogeneous neuronal population. To address this issue, whole-cell patch recordings and neuronal reconstructions were performed on rat brain slices containing the medial septum/diagonal band complex (MS/DB). Slow firing neurons were identified by their low firing rate at threshold (<5 Hz) and lack of time-dependent inward rectification (Ih). Unsupervised cluster analysis was used to investigate whether slow firing neurons could be further classified into different subtypes. The parameters used for the cluster analysis included latency for first spike, slow after-hyperpolarizing potential, maximal frequency and action potential (AP) decay slope. Neurons were grouped into three major subtypes. The majority of neurons (55%) were grouped as cluster I. Cluster II (17% of neurons) exhibited longer latency for generation of the first action potential (246.5+/-20.1 ms). Cluster III (28% of neurons) exhibited higher maximal firing frequency (25.3+/-1.7 Hz) when compared with cluster I (12.3+/-0.9 Hz) and cluster II (11.8+/-1.1 Hz) neurons. Additionally, cluster III neurons exhibited faster action potentials at suprathreshold. Interestingly, cluster II neurons were frequently located in the medial septum whereas neurons in cluster I and III appeared scattered throughout all MS/DB regions. Sholl's analysis revealed a more complex dendritic arborization in cluster III neurons. Cluster I and II neurons exhibited characteristics of "true" slow firing neurons whereas cluster III neurons exhibited higher frequency firing patterns. Several neurons were labeled with a cholinergic marker, Cy3-conjugated 192 IgG (p75NTR), and cholinergic neurons were found to be distributed among the three clusters. Our findings indicate that slow firing medial septal neurons are heterogeneous and that soma location is an important determinant of their electrophysiological properties. Thus, slow firing neurons from different septal regions have distinct functional properties, most likely related to their diverse connectivity.

Septal GABAergic neurons are selectively vulnerable to pilocarpine-induced status epilepticus and chronic spontaneous seizures.

The septal region of the basal forebrain plays a critical role modulating hippocampal excitability and functional states. Septal circuits may also play a role in controlling abnormal hippocampal hyperexcitability in epilepsy. Both lateral and medial septal neurons are targets of hippocampal axons. Since the hippocampus is an important epileptogenic area in temporal lobe epilepsy, we hypothesize that excessive excitatory output will promote sustained neurodegeneration of septal region neurons. Pilocarpine-induced status epilepticus (SE) was chosen as a model to generate chronic epileptic animals. To determine whether septal neuronal populations are affected by hippocampal seizures, immunohistochemical assays were performed in brain sections obtained from age-matched control, latent period (7 days post-SE) and chronically epileptic (more than one month post-SE survival) rats. An anti-NeuN (neuronal nuclei) antibody was used to study total neuronal numbers. Anti-ChAT (choline acetyltransferase), anti-GAD (glutamic acid decarboxylase) isoenzymes (65 and 67), and anti-glutamate antibodies were used to reveal cholinergic, GABAergic and glutamatergic neurons, respectively. Our results revealed a significant atrophy of medial and lateral septal areas in all chronically epileptic rats. Overall neuronal density in the septum (medial and lateral septum), assessed by NeuN immunoreactivity, was significantly reduced by approximately 40% in chronically epileptic rats. The lessening of neuronal numbers in both regions was mainly due to the loss of GABAergic neurons (80-97% reduction in medial and lateral septum). In contrast, populations of cholinergic and glutamatergic neurons were spared. Overall, these data indicate that septal GABAergic neurons are selectively vulnerable to hippocampal hyperexcitability, and suggest that the processing of information in septohippocampal networks may be altered in chronic epilepsy.

Effect of Chlorpyrifos on the Hematology and Phagocytic Activity of Nile Tilapia Cells (Oreochromis niloticus).

Chlorpyrifos is an organophosphorous insecticide widely used in agriculture and domestic activities. However, little is known about the effect of this pesticide on the immune system of fish and other alterations of its physiological system. The aims of the present study were the evaluation of the LC(50) (lethal concentration(50)) and the potential toxicity of this substance on Nile tilapia (Oreochromis nilotucus), as well as its effect on some hematological values and phagocytic functions of this fish. Results obtained showed that chlorpyrifos does not have any effect on the following parameters: number of red blood cells, hemoglobin, hematocrit, mean corpuscular volume (MCV), mean corpuscular hemoglobin (MCH), and mean corpuscular hemoglobin concentration (MCHC). However, the phagocytic index and the percentage of phagocytic active cells were significantly affected, which could indicate that phagocytic parameters from Nile tilapia are more sensitive than hematological ones to assess the effect of acute intoxication with chlorpyrifos.

[Clinical management of terrorist bomb explosions]. / Atención a las víctimas por ataque terrorista con explosivos.

At 07:39 on 11 March 2004 terrorist bomb explosions ocurred in 4 trains in Madrid killing 177 people instantly and 14 more later in the hospital. This report describes the organization, clinical management and patterns of injuries in casualties who were taken to our chil-patients were taken to the Gregorio Marañon hospital and 12 to the children's one. The mean age was 16 years (14-21), Two of them were critically ill and needed intensive care (ITP 5). Tympanic perforations occurred in 81% victims with moderate to severe trauma, shrapnel wounds in 36% and eye lesions in 27%. Among critically ill patients blast lung injury, cranial and abdominal trauma were the most important lesions. Training in AITP courses and hospital logistics were essential in clinical management of these casualties.

Angioscopic findings during coronary angioplasty of coronary occlusions.

OBJECTIVES: This study sought to elucidate angioscopic findings in totally occluded vessels before and after intervention. BACKGROUND: Coronary angioscopy allows direct visualization of the lumen surface of the coronary arteries; however, the utility of coronary angioscopy during coronary angioplasty of vessels with a total occlusion is unknown. METHODS: Twenty-one consecutive patients (mean [+/- SD] 58 +/- 9 years, range 39 to 77; 3 women, 18 men) undergoing dilation of an occluded vessel were studied with coronary angioscopy. Occlusions were classified as functional in 8 patients (Thrombolysis in Myocardial Infarction [TIMI] flow grade 1) and anatomic in 13 (TIMI flow grade 0). Once the guide wire had crossed the occlusion, coronary angioscopy was attempted before and after angioplasty. RESULTS: In all patients, coronary angioscopy before dilation visualized protruding material occluding the coronary lumen where the guide wire was wedged. The occlusion consisted of red thrombus in 19 patients (90%) (2 with isolated occlusive thrombus, 17 with thrombus associated with atherosclerotic plaque) and protruding yellow plaque in 2 patients (10%). However, on angiography only 7 occlusions (33%) had data consistent with thrombus (p < 0.01 vs. coronary angioscopy). Successful dilation was obtained in 20 patients. After dilation, coronary angioscopy was repeated in 18 patients, revealing residual thrombus with plaque in 16 (89%) and a residual yellow plaque in 2. In addition, coronary angioscopy revealed coronary dissections in 13 patients (72%); however, angiography revealed dissections only in 10 patients (55%) and residual thrombus in 2 (10%) (p < 0.001). In one patient, coronary angioscopy visualized silent distal embolization of a red thrombus not previously recognized on angiography. CONCLUSIONS: Before intervention, coronary angioscopy provides unique insights into the pathologic substrate of occluded coronary vessels. An occlusive plaque with thrombus is the most common underlying substrate in these lesions. After successful dilation, angiographically silent mural thrombus is seen in most patients. This information could be used to assist in the selection of candidates and type of coronary interventions and could also prove to be of prognostic value in patients with occluded vessels.

Determinants of coronary compliance in patients with coronary artery disease: an intravascular ultrasound study.

OBJECTIVES: The aim of this study was to elucidate determinants of coronary compliance in patients with coronary artery disease. BACKGROUND: Intravascular ultrasound potentially enables in vivo evaluation of coronary artery compliance. METHODS: Twenty-seven patients (mean age [+/- SD] 57 +/- 11 years, three women) undergoing coronary angioplasty were studied with intravascular ultrasound imaging. A mechanical intravascular ultrasound system (4.8F, 20 MHz) was used. A total of 58 different coronary segments (proximal to the target angiographic lesion) were studied. Of these, 35 were located in the left anterior descending, 9 in the left main, 8 in the left circumflex and 6 in the right coronary arteries. During intravascular ultrasound imaging, 22 segments (38%) appeared normal, but 36 (62%) had plaque (24 fibrotic, 3 lipidic and 9 calcified). Systolic-diastolic changes in area (delta A) and pressure (delta P) with respect to vessel area (A) were used to study normalized compliance (Normalized compliance = [delta A/A]/delta P [mm Hg-1 x 10(3)]). RESULTS: Lumen area and plaque area were 12.6 +/- 5.7 and 3 +/- 3 min2, respectively. Plaque was concentric (more than two quadrants) at 10 sites, but the remaining 26 plaques were eccentric. Compliance was inversely related to age (r = -0.34, p < 0.05) but was not related to other clinical variables. Compliance was greater in the left main coronary artery (3.9 +/- 2.1 vs. 1.8 +/- 1.2 mm Hg-1, p < 0.05) and in coronary segments with normal findings on ultrasound imaging (2.9 +/- 1.9 vs. 1.6 +/- 1.1 mm Hg-1, p < 0.01). Moreover, at diseased coronary segments compliance was lower in calcified plaques than in other types of plaques (1.2 +/- 0.7 vs. 2.3 +/- 1.6 mm Hg-1, p < 0.01) but was similar in concentric and eccentric plaques (1.6 +/- 1.5 vs. 1.6 +/- 0.9 mm Hg-1). Plaque area (r = -0.38, p < 0.01) was inversely correlated with compliance. On multivariate analysis, only age and plaque area were independently related to compliance. CONCLUSIONS: Intravascular ultrasound may be used to evaluate compliance in patients with coronary artery disease. Compliance is reduced with increasing age and is mainly determined by the arterial site and by the presence, size and characteristics of plaque on intravascular ultrasound imaging.

Fate of stent-related side branches after coronary intervention in patients with in-stent restenosis.

OBJECTIVES: We sought to assess the fate of stent (ST)-related side branches (SB) after coronary intervention in patients with in-ST restenosis. BACKGROUND: In-ST restenosis constitutes a therapeutic challenge. Although the fate of lesion-related SB after conventional angioplasty or initial coronary stenting is well established, the outcome of ST-related SB in patients with in-ST restenosis undergoing repeat intervention is unknown. METHODS: One hundred consecutive patients (age 61 +/- 11 years, 22 women) undergoing repeat intervention for in-ST restenosis (101 ST) were prospectively studied. Two hundred and twenty-six SB spanned by the ST were identified. The SB size, type, ostium involvement, location within the ST and take-off angle were evaluated. The SB TIMI (Thrombolysis in Myocardial Infarction trial) flow grade was studied in detail before, during, immediately after the procedure, and at late angiography. RESULTS: Occlusion (TIMI flow grade = 0) was produced in 24 (10%) SB, whereas some degree of flow deterioration (> or = 1 TIMI flow grade) was observed in 57 SB (25%). The SB occlusion was associated with non-Q wave myocardial infarction in two patients (both had large and diseased SB). Side-branch occlusion at the time of initial stenting (RR [relative risk] 11.1, 95% CI [confidence interval] 3.5-35.5, p < 0.001), diabetes (RR 3.5, 95% CI 1.1-10.5, p = 0.02), SB ostium involvement (RR 5.0, 95% CI 1.4-17.2, p = 0.004), baseline SB TIMI flow grade <3 (RR 5.5, 95% CI 1.7-18.1, p = 0.005), and restenosis length (RR 1.05 95% CI 1.01-1.11, p = 0.03) were identified as independent predictors of SB occlusion. Late angiography in 19 initially occluded SB revealed that 17 (89%) were patent again. The long-term clinical event-free survival (81% vs. 82% at two years) in patients with and without initial SB occlusion was similar. CONCLUSIONS: Occlusion or flow deterioration of SB spanned by the ST is relatively common during repeat intervention for in-ST restenosis. Several factors (mainly anatomic features) are useful predictors of this event. However, most SB occlusions are clinically silent and frequently reappear at follow-up.

Clinical and angiographic implications of coronary stenting in thrombus-containing lesions.

OBJECTIVES: This study sought to determine the results of coronary stenting in thrombus-laden lesions. BACKGROUND: The angiographic evidence of intracoronary thrombus has classically been considered a formal contraindication to stent implantation. However, with increasing use of stenting, the indications for this technique have widened to include treatment of patients who have an acute coronary syndrome or lesions with adverse anatomic features. METHODS: We studied 86 consecutive patients (mean age +/- SD 61 +/- 11 years, 14 women) undergoing coronary stenting of a thrombus-containing lesion; the procedure was performed electively in 39% and after angioplasty failure in 61%. Sixty-four patients (75%) were treated for unstable angina, and 19 (22%) underwent the procedure during an acute myocardial infarction. A specific protocol that included clinical and late angiographic follow-up was used. RESULTS: Angiographic success was obtained in 83 patients (96%). Five patients (6%) died during the hospital stay despite angiographic success; four of these had cardiogenic shock, and one (1%) had subacute stent thrombosis. Non-Q wave myocardial infarction developed in five additional patients (6%), and four of these five had data consistent with distal embolization. Of the 78 patients discharged with angiographic success, 67 (86%) were event-free and clinically improved at last follow-up visit (12 +/- 11 months). During the follow-up period, eight patients required repeat angioplasty, one patient required heart transplantation, and two patients died. Quantitative angiography demonstrated excellent angiographic results after stenting (minimal lumen diameter 0.31 +/- 0.4 vs. 2.77 +/- 0.6 mm). Late angiographic follow-up (5.5 +/- 1 months) was obtained in 50 patients with 54 lesions (93% of eligible), revealing a minimal lumen diameter of 2.0 +/- 1 mm and restenosis (lumen narrowing > 50%) in 18 lesions (33%). CONCLUSIONS: Coronary stenting constitutes an effective therapeutic strategy for patients with thrombus-containing lesions, either after failure of initial angioplasty or electively as the primary procedure. Coronary stenting in this adverse anatomic setting results in a high degree of angiographic success, a low incidence of subacute thrombosis and an acceptable restenosis rate.

Coronary stenting for acute coronary dissection after coronary angioplasty: implications of residual dissection.

OBJECTIVES: The aim of this study was to assess the implications of residual coronary dissections after stenting. BACKGROUND: Coronary stenting is currently used in selected patients with coronary dissection after angioplasty. However, in some patients the total length of the dissection may not be completely covered with the device. METHODS: Forty-two consecutive patients (mean [+/- SD] age 58 +/- 11 years; 39 men, 3 women) undergoing stenting for a major coronary dissection after angioplasty were studied. RESULTS: Thirty (67%) coronary dissections were small (< or = 15 mm), and 29 (64%) were occlusive (Thrombolysis in Myocardial Infarction [TIMI] flow grade < or = 2). In 3 patients, coronary stenting was unable to open large occlusive dissections, but a good angiographic result was obtained in 39 patients (93%). After stenting, 22 of these patients (56%) had no visible residual dissections, and 13 (33%) had small and 4 (10%) had large residual dissections. These residual dissections were stable and did not compromise coronary flow. In a repeat angiogram (24 h later) the stent was patent in all 39 patients. However, two patients experienced a subacute stent occlusion. Of the remaining 37 patients, 36 (97%) had a late angiogram after stenting. Quantitative angiography revealed a reduction in minimal lumen diameter at the stent site (2.6 +/- 0.4 vs. 2 +/- 0.7 mm, p < 0.05) and a trend toward improvement in vessel diameter at the site of the previous residual dissection (1.7 +/- 0.6 vs. 1.9 +/- 0.5 mm, p < 0.1). The angiographic image of residual dissection disappeared in all patients. These factors provided a rather smooth angiographic appearance at follow-up. The four patients with large residual dissections after stenting did not have restenosis and were asymptomatic at last visit. CONCLUSIONS: Coronary stenting is effective in the management of acute coronary dissections after angioplasty. In this setting, small residual dissections are frequently seen but have a good outcome and disappear at follow-up. Large residual dissections may have a good outcome if coronary flow is not impaired and no residual stenosis is visualized.

Propensity and mechanisms of restenosis in different coronary stent designs: complementary value of the analysis of the luminal gain-loss relationship.

OBJECTIVES: This study sought to investigate the influence of stent design on the long-term angiographic outcome. BACKGROUND: The proportional relationship between vessel injury and late luminal loss in percutaneous revascularization should be best appreciated in coronary stenting, where recoil and shrinkage are theoretically minimal. It is unclear whether all stent designs can counterbalance this reactive loss by achieving a large initial luminal gain (bigger is better). METHODS: In 523 lesions successfully stented, the long-term angiographic results of slotted-tube (n = 331), coil (n = 85), multicellular (n = 70) and self-expandable mesh (n = 37) stent designs were compared using the angiographic gain-loss relationship (GLR). RESULTS: Restenosis rate was 10% for multicellular, 20% for slotted-tube, 46% for coil and 49% for self-expandable designs (p = 0.001). At a difference with other designs, no significant GLR was found in coil stents, suggesting additional mechanisms of luminal loss (i.e., plaque protrusion, stent compression) to neointimal proliferation. Significant differences in late loss between stents were found within each quartile of luminal gain, suggesting a specific role of design in luminal loss. Multivariate analysis identified use of coil and self-expandable stents, vessel size, minimal luminal diameter preintervention, luminal gain and stent length as variables with independent predictive value for several indices of angiographic long-term outcome. CONCLUSIONS: The analysis of GLR: 1) demonstrates that stent design influences late luminal loss; 2) challenges the applicability of the widely accepted "bigger is better" approach to all stent designs; and 3) appears as a valuable tool in assessing long-term stent performance.

Pneumocephalus: An unusual complication of lumbar arthrodesis. A clinical case and literature review.

UNLABELLED: Pneumocephalus is an uncommon but serious complication of spinal surgery and its management and pathophysiology is not widely recognized. The incidence of symptomatic tension pneumocephalus secondary to posterior spinal arthrodesis is unknown. CASE REPORT: The case is reported of a rare case of a 41 year old woman with diagnosis of L3-L4, L4-L5 disc disease and left disc herniation L4-L5. A posterior spinal arthrodesis L3-L5, L3-L4 and L4-L5 discectomies and release of the left L5 root, was performed without apparent complications. Twenty-four hours after surgery the patient developed generalized headache, neck stiffness, and dysarthria. MRI and CT scans revealed a huge pneumocephalus in the subarachnoid space, predominantly in the left frontal lobe without midline shift, which originated in the lumbar spinal canal. The patient was treated conservatively, with progressive neurological improvement after 72 hours, and clinical and radiological normalization after 7 days. DISCUSSION: Pneumocephalus is a rare but potentially serious complication of spine surgery related in most cases with inadvertent dural tear during the operation. Most collections are small, behave benign, and respond to conservative therapy. In the present case, an inadvertent dural tear, produced a pneumocephalus. A high degree of suspicion is needed to make the diagnosis, prompt treatment, as well as remedying the source of air to prevent unwanted morbidity and mortality.

Angioscopic characteristics of coronary narrowing in patients with recurrent myocardial ischemia after myocardial infarction.

Coronary angioscopy was used to elucidate the underlying substrate of the culprit lesion in 20 patients with postinfarction ischemia and in 19 patients with other types of unstable angina. Plaque characteristics were similar in both groups, but red thrombi and occlusive thrombi were more frequently seen in patients with postinfarction ischemia.

Percutaneous transluminal coronary angioplasty after non-Q-wave acute myocardial infarction.

The value of percutaneous transluminal coronary angioplasty (PTCA) for ischemia after a non-Q-wave acute myocardial infarction (AMI) was assessed prospectively in 33 consecutive patients. In 30 patients the indication for the procedure was post-AMI angina and 3 patients underwent PTCA for silent ischemia. A total of 43 lesions were attempted at 63 +/- 94 days after the non-Q-wave AMI. Primary PTCA success was obtained in 30 (91%) patients and no major complications occurred. Angiographic evaluation was performed either for symptoms or for protocol (7 +/- 1 months after PTCA) in 28 (93%) of the 30 patients with successful PTCA, but 2 patients (7%) who were asymptomatic refused the repeat angiogram. Twenty (71%) had no restenosis and 8 (29%) had restenosis. Of these, 5 patients with restenosis underwent a successful repeat PTCA (6 +/- 1 months after the initial procedure). At the last clinical follow-up (17 +/- 8 months), 2 of the 30 (7%) patients successfully dilated presented with stable angina despite medical treatment, whereas the rest (93%) remained asymptomatic. During the study period no patient died, had an AMI or required coronary artery bypass grafting. Thus, selected patients with ischemia after a non-Q-wave AMI, a "high-risk population," can be effectively treated with PTCA with an initial success rate and angiographic restenosis rate similar to that of the general PTCA population and appear to have sustained symptomatic benefit remaining free of subsequent cardiac events.