脑膜瘤生物学特性的研究——流式细胞计对脑膜瘤DNA含量的分析及其生物学行为的相关研究

为了定量测试脑膜瘤WHO分级法的价值,作者应用倍体分类、增殖指数和S期细胞比率三项参数进行分析,发现这三项指标与WHO分级密切相关。脑膜瘤异形细胞、坏死、核分裂及脑浸润的出现与肿瘤WHO分级增加和肿瘤复发密切相关。这些结果特别对肿瘤的异质性和测量技术差异问题给予小心评价。     

Histopathological changes of gastric mucosa following oral administration of fumonisin B1 in mice

Fumonisin B1 is a common secondary metabolite produced by Fusarium moniliforme that occurs in corn and corn-based foods. This mycotoxin is toxic to many species of laboratory and domestic animals and is known to induce a variety of diseases such as hepatic cancer and renal and hepatic dysfunction. The structure of fumonisin B1 (FB1) resembles sphingolipids so it can inhibit synthesis of ceramide, an enzyme in the sphingolipid biosynthetic pathway. This inhibition leads to the disruption of sphingolipid metabolism and increased levels of sphinganine and sphingosine (sphingoid bases) in the serum of treated animals. It is believed that the toxicity effect of fumonisin B1 is the result of these sphingoid bases. In the present research, mice were treated with FB1 to determine its pathological effects on gastric gland and gastric mucosa in the treated mice. For this purpose, the mice were randomly assigned into two groups, namely, control (n?=?14) and treatment (n?=?15). The treatment group was fed with prepared food containing FB1 (150 mg/kg) for a period of 4 months. One day after the last treatment, all animals in both groups were euthanized and their stomach were sampled and prepared for microscopic analysis. Histopathological analysis revealed a significant decrease in parietal cell number and a significant increase in the number of inflammatory cells in gastric mucosa. Also, atrophy of gastric glands was observed. The study confirmed that FB1 poisoning can have toxicopathological effects such as gastric gland atrophy and gastritis on mice gastric tissue.     

Serum carbohydrate antigen 125 levels in nonischemic dilated cardiomyopathy: a useful biomarker for prognosis and functional mitral regurgitation

The authors investigated the prognostic relevance of serum carbohydrate antigen 125 (CA125) levels in nonischemic dilated cardiomyopathy (NICMP) and assessed whether increased levels relate to the degree of functional mitral regurgitation (FMR). Seventy-seven patients with NICMP were enrolled and followed-up for 10 ± 2 months in this prospective study. Receiver-operating characteristic analysis established a cutoff CA125 value of 25 U/mL for predicting mortality. Patients were divided into two groups according to their CA125 levels (CA125 <25 U/mL [n=58] and CA125 ≥ 25 U/mL [n=19]). Patients with high CA125 values had statistically worse functional status, higher B-type natriuretic peptide (BNP) levels, higher left ventricular volumes, lower ejection fraction, higher E/Em ratio, higher pulmonary artery systolic pressure, and more severe FMR. On the multivariate analysis, serum CA125 (P=.002) and severe FMR (P=.04) were identified as the independent predictors of mortality. Serum CA125 levels also correlated with BNP levels and FMR severity (P<.001). Serum CA125 is a powerful prognostic biomarker that is associated with the severity of heart failure, serum BNP levels and several echocardiographic parameters including left ventricular volumes, systolic and diastolic functions, pulmonary artery pressure, and the degree of FMR. Serum CA125 was also shown as an independent predictor of mortality during 10 ± 2 months of follow-up.     

Effect of blood donation-mediated volume reduction on regional right ventricular deformation in healthy subjects

Strain (S) and strain rate (SR) are known to be altered in diseases associated with right ventricular (RV) pressure/volume overload and RV myocardial dysfunction; however determinants of S/SR are incompletely understood. The aim of this study was to examine the effect of blood donation-mediated volume reduction on regional RV deformation in healthy young adults. Study population was composed of 61 consecutive healthy subjects who were volunteers for blood donation. All underwent standard echocardiography and two-dimensional S and SR imaging by speckle tracking before and after 450 mL blood donation. We found no change in RV lateral wall SR in all three segments. However, the S in the apical and mid segments of the RV lateral wall immediately decreased after blood donation [?26.2 ± 3.3 vs. ?23.2 ± 3.3 % (p < 0.0001) and ?28.2 ± 3.4 vs. ?27.1 ± 3.2 % (p = 0.009), respectively], whereas no change was observed in the basal segment. Moreover, changes in systolic S on the apical segment of the RV lateral wall before and after blood donation were significantly correlated with the changes in the RV size [end-diastolic area index, r = ? 0.369 (p = 0.003) and end-systolic area index, r = ? 0.319 (p = 0.012)] and changes in the stroke volume index [r = ? 0.436 (p < 0.001)]. Blood donation-mediated volume reduction in healthy subjects caused a regional difference in RV longitudinal deformation with the lower mid and apical S that was related to parameters of volume load severity. However, RV systolic SR was found to be resistant to the effects of volume depletion.     

Suggested method for closed treatment of fractures of the carpal scaphoid: hypothesis supported by dissection and clinical practice.

The anatomy and kinetics of the carpus with special reference to the fractured scaphoid are described. Clinical, radiological and post-mortem studies of the wrist show that the scaphoid can be immobilized and compressed in its long axis, with the wrist held in full supination, mid-dorsiflexion and full ulnar deviation. Immobilization of the upper limb in this position for four weeks has achieved union of those fractures of the scaphoid which are often problematical, i.e. the displaced fracture, fractures of the proximal pole, and those exhibiting delay in union of many months. The method of manipulation and immobilization in a plaster of Paris cast is described, and some clinical examples are presented. The indications for the complications of the method of treatment are discussed and briefly compared with other methods of treatment.     

Phylogenetic, ontogenetic, and pathological aspects of the urine-concentrating mechanism

The urine-concentrating mechanism is one of the most fundamental functions of avian and mammalian kidneys. This particular function of the kidneys developed as a system to accumulate NaCl in birds and as a system to accumulate NaCl and urea in mammals. Based on phylogenetic evidence, the mammalian urine-concentrating mechanism may have evolved as a modification of the renal medulla's NaCl accumulating system that is observed in birds. This qualitative conversion of the urine-concentrating mechanism in the mammalian inner medulla of the kidneys may occur during the neonatal period. Human kidneys have several suboptimal features caused by the neonatal conversion of the urine-concentrating mechanism. The urine-concentrating mechanism is composed of various functional molecules, including water channels, solute transporters, and vasopressin receptors. Abnormalities in water channels aquaporin (AQP)1 and AQP2, as well as in the vasopressin receptor V2R, are known to cause nephrogenic diabetes insipidus. An analysis of the pathological mechanism involved in nephrogenic diabetes insipidus suggests that molecular chaperones may improve the intracellular trafficking of AQP2 and V2R, and, in the near future, such chaperones may become a new clinical tool for treating nephrogenic diabetes insipidus.     

Sensitive and Noninvasive Detection of Aberrant SFRP2 and MGMT-B Methylation in Iranian Patients with Colon Polyps

Background: The pathogenesis of sporadic colorectal cancer (CRC) is influenced by the patient genetic background and environmental factors. Based on prior understanding, these are classified in two major pathways of genetic instability. Microsatellite instability (MSI) and CPG island methylator phenotype (CIMP) are categorized as features of the hypermethylated prototype, and chromosomal instability (CIN) is known to be indicative of the non-hypermethylated category. Secreted frizzled related protein 2 (SFRP2), APC1A in WNT signaling pathway and the DNA repair gene, O6-methylguanine-DNA methyltransferase (MGMT), are frequently hypermethylated in colorectal cancer. Detection of methylated DNA as a biomarker by easy and inexpensive methods might improve the quality of life of patients with CRC via early detection of cancer or a precancerous condition. Aim: To evaluate the rate of SFRP2 and MGMT hypermethylation in both polyp tissue and serum of patients in south Iran as compared with matched control normal population corresponding samples. Materials and Methods: Methylation-specific PCR was used to detect hypermethylation in DNA extracted from 48 polypoid tissue samples and 25 healthy individuals. Results: Of total polyp samples, 89.5% had at least one promoter gene hypermethylation. The most frequent methylated locus was SFRP2 followed by MGMT-B (81.2 and 66.6 percent respectively). Serologic detection of hypermethylation was 95% sensitive as compared with polyp tissue. No hypermethylation was detected in normal tissue and serum and its detection in patients with polyps, especially of serrated type, was specific. Conclusions: Serologic investigation for detection of MGMT-B, SFRP2 hypermethylation could facilitate prioritization of high risk patients for colonoscopic polyp detection and excision.