Glycophenotype of prostatic carcinomas

The factors that affect the progression of prostatic carcinoma are poorly understood, but it is known that carbohydrate antigens on the tumour cell surface play a role in the transforming and metastatic processes. The present report aimed to perform a comparative, lectin-histochemical study of benign and carcinomatous prostates, using a battery of 15 lectins, in combination with monoclonal antibodies against Lewis antigens, and a semi quantitative study, to investigate the changes in glycosylation patterns that occur in prostatic carcinoma. Blocks from 27 necropsy cases of prostatic carcinoma were sectioned and stained with H&E, 15 biotinylated lectins chosen to probe for a wide range of oligosaccharide sequences within several categories of glycoprotein glycans, using a lectin-biotin avidin–peroxidase method, and monoclonal antibodies against Lewis^a, sialyl Lewis^a and sialyl Lewis^x antigens. The glycophenotype of prostatic carcinoma differed from that of the noncancerous prostate in revealing more intense staining with the following lectins (AAA, UEA-1, DBA, WFA, VVA, HPA, BSA-1_B4, MPA, ECA, AHA and CTA), while the binding patterns of (GNA and NPA) were almost similar in both prostatic carcinoma and the noncancerous prostate. Lewis antigens are found to be expressed in prostatic carcinomas but not in the noncancerous prostate. The observations of this study suggest that the gylcophenotype of transformed prostatic cells was modified. It showed a moderate increase in, and changing patterns of, fucosylation and galactosylation, increased branching of side chains and sharp rise in 2 deoxy, 2 acetamido galactosylation and masking process by sialylation, especially by α2–3 and α2–6 linkages. O-glycans seems to play an important role in the glycosylation patterns found in prostate carcinoma cells.     

The GSTP1 Ile105Val polymorphism is not associated with susceptibility to colorectal cancer

The glutathione S transferase (GST) family is a major part of cellular defense mechanisms against endogenous and exogenous substances, many of which have carcinogenic potential. Alteration in the expression level or structure of the glutathione-S-transferase (GST) enzymes may lead to inadequate detoxification of potential carcinogens and consequently contribute to cancer development. A member of the glutathione-S-transferase (GST) family, GSTP1, is an attractive candidate for involvement in susceptibility to carcinogen-associated colorectal cancer. An A>G transition in exon 5 resulting in an Ile105Val amino acid substitution has been identified which alters catalytic efficiency. The present study investigated the possible impact of Ile105Val GSTP1 polymorphism on susceptibility to colorectal cancer. in Jordan We examined 90 tissue samples previously diagnosed with colorectal carcinoma, and 56 non-cancerous colon tissues. DNA was extracted from paraffin embedded tissues and the status of the GSTP1 polymorphism was determined using a polymerase chain reaction restriction fragment length polymorphism (RFLP) method. No statistically significant differences were found between colorectal cancer cases and controls for the GSTP1 Ile/Ile, Ile/Val and Val/Val genotypes. The glutathione S-transferase polymorphism was not associated with risk in colorectal cancer cases in Jordan stratified by age, sex, site, grade or tumor stage. In conclusion, the GSTP1 Ile105Val polymorphism is unlikely to affect the risk of colorectal cancer.     

Transmission of bone strain in the craniofacial bones of edentulous human skulls upon dental implant loading

STATEMENT OF PROBLEM: Little is known about how craniofacial bones that are distant from dental implants are loaded. Whether bone experiences different strain when implants of different diameters are loaded is unknown. PURPOSE: This study was designed to (1) characterize bone strain both adjacent to and distant from dental implants and (2) compare bone strain in response to the same loads on small-diameter and large-diameter implants. MATERIAL AND METHODS: On 4 edentulous, dry adult human skulls, the buccopalatal midpoint of the edentulous occlusal surface was marked unilaterally in the maxillary first molar area with a round bur. A hole for implant placement was prepared, and 2 self-tapping titanium implants (3.75 x 7 mm and 4 x 7 mm) were placed in the same location and at the same orientation, one after the other. A 4-mm-long titanium abutment was connected to the implant. Each implant was loaded 10 degrees lateral to its longitudinal axis, simulating a lateral occlusal force in 3 of the skulls. In skull 2, loading was along the longitudinal axis of the implant and simulated a vertical occlusal force. The magnitude of the ramp forces was 0 to 100 N. Uniaxial strain gages and/or 3-element strain rosettes were implanted in the supramolar cortical bone, the supraincisor cortical bone, the zygomaticomaxillary suture, and the zygomaticotemporal suture. All strain gages/rosettes were excited with 500 mV DC, and the output signals were recorded with a strain conditioner. Tensile strain was expressed as positive values and compressive strain as negative values. Student t tests were used to test for normal distribution of bone strain within each skull; Wilcoxon tests were applied for skewed distribution between small- and large-diameter implants and between 50-N and 100-N loads (P相似文献   

Effect of waterpipe tobacco smoking on airway inflammation in murine model of asthma

Objective: There has been an increase in the popularity of waterpipe tobacco smoking (WTS) worldwide, especially in the younger population, including asthma patients. In this study, we investigated the effects of waterpipe smoking on airway inflammation, cytokine levels and oxidative stress markers in an antigen-driven murine model of asthma.

Materials and methods: Balb/c mice were divided into four groups; (1) control (received fresh air, ovalbumin sensitization and saline challenge), (2) WTS (received WTS, ovalbumin sensitization and saline challenge), (3) Ova S/C (received fresh air, ovalbumin sensitization and ovalbumin challenge) and (4) simultaneous WTS and Ova S/C (received WTS, ovalbumin sensitization and ovalbumin challenge). Airway inflammatory cells were evaluated in the broncho-alveolar lavage fluid. Cytokines [interleukin (IL)-13, 10 and 18] and oxidative stress markers [superoxide dismutase (SOD), catalase and glutathione peroxidase (GPx)] were evaluated in the lung homogenates.

Results: Chronic exposure to WTS significantly increased the number of airway inflammatory cells in mice, specifically: eosinophils, neutrophils, macrophages and lymphocytes. The level of IL-13 in the lungs was increased and the level of IL-10 was reduced (p?Chronic WTS potentiated the increase in inflammatory cells induced by Ova S/C (p?p?Conclusions: Chronic WTS exposure induced airway inflammation in control mice and enhanced airway inflammation in murine model of asthma.