Colitis cystica profunda: MRI appearance

Colitis cystica profunda (CCP) is an uncommon benign condition characterized by mucin-filled cysts located in the submucosa, frequently associated with the solitary ulcer and rectal prolapse syndromes. The diagnosis of this entity is important as it can mimic rectal cancer and therefore may result in unnecessary surgical resection. Endoscopic examination and barium enema findings are suggestive but not specific, neither are superficial biopsy findings. Transrectal ultrasound is helpful in the diagnosis by imaging the layers of the rectal wall. The authors report a 16-year-old male with a rectal lesion mimicking malignant mass on endoscopic examination. The lesion was defined as CCP, based on MR imaging findings which disclosed multiple noninfiltrating submucosal cysts, confirmed by histopathological examination. To our knowledge, this is the first case of CCP in the radiology literature describing MRI findings.     

Chronic heavy ethanol consumption is associated with decreased platelet aggregation in rats

Although moderate alcohol consumption seems to be protective against atherosclerosis, coronary artery disease rate increases with its higher doses. Platelet aggregation is an important process which contributes to the atherosclerosis. The aim of this study was to determine whether heavy ethanol consumption stimulates or inhibits platelet aggregation. Fourteen adult male Wistar rats were used. Ethanol (7.2%, v/v) in a modified liquid diet was given to eight rats for 21 days, which mimicked characteristics similar to human chronic alcoholism. Six rats constituted the control group. Adenosine diphophate (ADP) and collagen-induced platelet aggregation was measured in whole blood. We found reduced ADP-induced mean maximal aggregation in the alcoholic rat group compared to the control group at dose of 5 microM (p < 0.005). We also found decreased platelet aggregation responses to collagen in the alcoholic group (p < 0.006 for 2 microg/ml collagen, and p < 0.05 for 5 microg/ml collagen). In conclusion, chronic heavy ethanol consumption results in the decreased platelet aggregation in a rat model of alcoholism. Therefore, increased mortality from coronary artery disease in chronic alcoholism may be explained by other factors such as dietary imbalances and coexisting conditions, which include hypertension and depression.     

Intraleucocyte platelet-activating factor levels in desmopressin-treated patients with haemophilia A and von Willebrand disease

Despite the intensive clinical use of 1-deamino-8-D-arginine vasopressin (desmopressin; DDAVP) for 20 years, its mechanism of action is still not completely explained. It has been proposed that DDAVP stimulates release of a 'second messenger' which in turn stimulates release of von Willebrand factor (vWF) from endothelial cells. Platelet-activating factor (PAF) and interleukin (IL)-6 were individually proposed to be mediators for haemostatic action. The aim of this study was to investigate cellular-based PAF levels in patients with haemophilia A (HA) and von Willebrand disease (vWD) before and after DDAVP treatment and also to look for any probable relationship between the haemostatic response of DDAVP and cellular PAF activities. In total, 20 patients (11 HA and nine vWD) were enrolled in the study. DDAVP was given subcutaneously as a single dose (0.3 microg kg(-1)). Ten patients responded to DDAVP and were defined as the 'able group' (four mild HA, six type 1 vWD). The remaining 10 patients did not respond to DDAVP and were defined as the 'unable group' (seven severe HA, three type 3 vWD). Released (extracellular) and intracellular (intraleucocyte) PAF levels under the stimulation of specific agents (A23187 and Zymosan) were measured by high-performance liquid chromatography and radioimmunoassay. Extracellular and intracellular PAF activities were not detected without stimulation in healthy children whereas significantly higher PAF levels were found in the patients (extracellular: 37.5 +/- 34.4 ng per 10(7) cells; intracellular: 24.8 +/- 23.5 ng per 10(7) cells; P=0.0001). Intracellular PAF levels obtained from in vitro unstimulated cells were significantly higher in DDAVP-responsive (able) patients in comparison to DDAVP-unresponsive (unable) patients (52.1 +/- 18.5 vs. 28.9 +/- 8.0 ng per 10(7)cells). After in vitro stimulation by A23187, intracellular PAF activities were significantly higher in patients than in controls (209.3 +/- 26.1 vs. 172 +/- 18.1 ng per 10(7) cells). Intracellular PAF levels obtained from in vitro stimulated cells by A23187 were also significantly higher in the 'able' patients in comparison to the 'unable' patients (277 +/- 43.5 vs. 225 +/- 30 ng per 10(7)cells). In conclusion, cellular PAF activities are significantly higher in patients with HA and vWD. We also suggest that PAF, especially intracellular PAF mediates intracellular signalling and may be one of the important mediators for the haemostatic response of DDAVP.     

A Kalman filter-based approach to reduce the effects of geometric errors and the measurement noise in the inverse ECG problem

In this article, we aimed to reduce the effects of geometric errors and measurement noise on the inverse problem of Electrocardiography (ECG) solutions. We used the Kalman filter to solve the inverse problem in terms of epicardial potential distributions. The geometric errors were introduced into the problem via wrong determination of the size and location of the heart in simulations. An error model, which is called the enhanced error model (EEM), was modified to be used in inverse problem of ECG to compensate for the geometric errors. In this model, the geometric errors are modeled as additive Gaussian noise and their noise variance is added to the measurement noise variance. The Kalman filter method includes a process noise component, whose variance should also be estimated along with the measurement noise. To estimate these two noise variances, two different algorithms were used: (1) an algorithm based on residuals, (2) expectation maximization algorithm. The results showed that it is important to use the correct noise variances to obtain accurate results. The geometric errors, if ignored in the inverse solution procedure, yielded incorrect epicardial potential distributions. However, even with a noise model as simple as the EEM, the solutions could be significantly improved.     

Cell cycle markers have different expression and localization patterns in neuron-like PC12 cells and primary hippocampal neurons

Recent studies have indicated that bone marrow stromal cells (BMSCs) have significant tropism towards glioma which makes them play an important role in carrying genes/drugs to inhibit the growth of glioma as cell vehicles. But BMSCs may differentiate into neural cells under entocranial environment and few researches support the idea that neurally differentiated bone marrow stromal cells (N-D-BMSCs) still hold the capacity of migrating to the tumor sites. The aim of our study was to investigate the tropism of N-D-BMSCs towards C6 glioma. In vitro migration assay was employed by transwell co-culture system and Student's t-test analysis indicated that N-D-BMSCs had the significant tropism towards C6 glioma-conditioned medium (GCM) (P < 0.01). Furthermore, the vascular endothelial growth factor (VEGF) bioactivity of the C6 GCM was neutralized by the anti-rat VEGF antibody and our data suggested that the VEGF from C6 GCM hold chemoattraction for N-D-BMSCs and some other cytokines from the C6 GCM may be responsible for the chemoattraction for N-D-BMSCs. In vivo migration assay was carried out with cells transplantation and one way ANOVA analysis indicated that the tropism of N-D-BMSCs towards C6 glioma sites presented time variation (P-value = 2.9E−20). Moreover, multiple comparisons for the time variables with the Student's t-test and the results suggested that the migration capacity of N-D-BMSCs towards C6 glioma sites reach the peak on the 7th day after transplantation. These results demonstrate that N-D-BMSCs as well as BMSCs have significant tropism towards C6 glioma.     

Hereditary neuropathies

PURPOSE OF REVIEW: The purpose of this review is to help neurologists understand new concepts in hereditary neuropathies, from the clinician's point of view, in the molecular era after the burst of information regarding peripheral nerve biology. RECENT FINDINGS: Recent studies have focused on understanding the pathomechanisms involved in hereditary neuropathies. In the past year identification of new genes has slowed down since scientists have concentrated more on the function of genes causing Charcot-Marie-Tooth disease and Schwann cell-axon interactions to reveal the molecular cell biology of the disease. Animal models for the most common subtypes of human Charcot-Marie-Tooth disease are now available. SUMMARY: Rapid advances in the molecular genetics and cell biology of hereditary neuropathies have highlighted the great genetic complexity of Charcot-Marie-Tooth disease. The evolution from a simple clinical classification to a complex molecular one has not facilitated our understanding of the disease. Moreover, the new molecular classification is not simple to use as different mutations of the same gene produce a range of phenotypes. The clinicians have to look for specific clinical and electrophysiological clues to direct the patient to appropriate genetic testing.     

Comparative effects of risedronate,atorvastatin, estrogen and SERMs on bone mass and strength in ovariectomized rats

Objective

The aim of this study was to investigate bone protective effects of risedronate, atorvastatin, raloxifene and clomiphene citrate in ovariectomized rats.

Methods

Our study was conducted on 63 rats at Experimental Research Center of Celal Bayar University. Six-month-old rats were divided into seven groups. There were five drug administered ovariectomized groups, one ovariectomized control group without drug administration and one non-ovariectomized control group without drug administration. Eight weeks postovariectomy, rats were treated with the bisphosphonate risedronate sodium, the statin atorvastatin, the estrogen 17β-estradiol and the selective estrogen receptor modulators (SERMs) raloxifene hydrochloride and clomiphene citrate by gavage daily for 8 weeks. At the end of the study, rats were killed under anesthesia. For densitometric evaluation, left femurs and tibiae were removed. Left femurs were also used to measure bone volume. Right femurs were used for three-point bending test.

Results

Compared to ovariectomized group, femur cortex volume increased significantly in non-ovariectomized group (p = 0.016). Compared to non-ovariectomized group, distal femoral metaphyseal and femur midshaft bone mineral density values were significantly lower in ovariectomized group (p = 0.047). In ovariectomy + atorvastatin group, whole femur and femur midshaft bone mineral density and three-point bending test maximal load values were significantly higher than ovariectomized group (p = 0.049, 0.05, and 0.018). When compared to the ovariectomized group, no significant difference was found with respect to femoral maximum load values in groups treated with risedronate, estrogen, raloxifene and clomiphene (p = 0.602, 0.602, 0.75, and 0.927). In ovariectomy + risedronate group, femur midshaft bone mineral density values were significantly higher than the values in ovariectomized group (p = 0.023). When compared to ovariectomized group, no significant difference was found with respect to femur midshaft bone mineral density values in groups treated with estrogen, raloxifene and clomiphene (p = 0.306, 0.808, and 0.095).

Conclusions

While risedronate sodium prevented the decrease in bone mineral density in ovariectomized rats, atorvastatin maintained mechanical characteristics of bone and also prevented the decrease in bone mineral density as risedronate sodium.     

Management of neuroendocrine carcinomas of the breast: A rare entity

Neuroendocrine (NE) carcinoma of the breast is extremely rare and constitutes less than 0.1% of all breast tumors. Only a few studies are currently available in the literature and a standard approach to treating this tumor has yet to be established. The aim of this study was to apply pathological treatment modalities in clinical practice and to select the most appropriate treatment accordingly. Six female patients were diagnosed with primary NE carcinoma of the breast. The patients underwent modified radical mastectomy with axillary dissection. Pathological specimens were stained with hematoxylin and eosin and an immunohistochemical panel of antibodies [neuron-specific enolase (NSE), chromogranin, synoptophysin, estrogen and progesterone receptor, c-erbB2 and Ki-67]. The results showed that tumor size ranged from 2 to 4.5?cm in diameter. Lymph node metastasis was detected in 4 (67%) patients. Estrogen and progesterone receptor expression was found in 5 (83%) patients. None of the patients expressed c-erbB2. Chromogranin was found to be positive in 5 (83%) patients. Synoptophysin expression was detected in 5 (83%) patients. NSE was stained in 4 (67%) patients. An intraductal component was found in 5 (83%) patients. Lymphovascular invasion was found in 5 (83%) patients. Adjuvant chemotherapy was administered to patients with a Ki-67 index of ≥10%. Radiotherapy was administered to 4?(67%)?patients, and 4?(67%) patients received hormonal therapy. The mean follow-up time was 31.1?months (range?12-52). All 6 patients survived, although following chemotherapy and tamoxifen, the disease progressed in 1?patient who received second-line hormonal therapy. In conclusion, NE carcinoma of the breast is a distinct entity. Management of this rare tumor may include surgery and radiotherapy depending on the size of the tumor and lymph node status. However, the exact role of chemotherapy and hormonal therapy has yet to be established. Adjuvant chemotherapy is recommended for patients with a Ki-67 index of ≥10%, and hormonal treatment appears to be feasible in patients who are positive for estrogen and/or progesterone receptor.