Epidermoid cyst of the cecum of an elderly man with no previous history of surgery: a case report and review of literature

BACKGROUND: Pure, benign epidermoid cysts of the abdominal viscera are rare. There have been only four reports of epidermoid cysts of the cecum in the literature, two following appendectomies and attributed to the surgical procedure, and two in female patients, raising the possibility of dermoid cysts related to the ovaries. PATIENTS AND METHODS: We report the first case of epidermoid cyst of the cecum in an elderly man with no previous history of trauma or surgery, detected by computed tomography as an incidental finding of extraluminal cystic cecal mass. It was treated by partial colectomy. Pathologically the cyst was roughly spherical, extending from and expanding the serosal surface of the cecum with no communication through the muscularis wall. Histologically the inner lining of the cyst was composed of benign, mature, keratinized, stratified squamous epithelium with a well formed granular layer. No calcification, hair, teeth, or bone elements was detected. RESULTS: The interesting finding in our case is the unusual anatomical location and the age and sex of the patient. The patient had no history of any abdominal surgical procedures. The most likely explanation for the presence and development of an epidermoid cyst in this location is the result of an aberrant ectodermal implantation during embryogenesis. CONCLUSION: Awareness of the possibility of the presence of epidermoid cysts in this area with distinctive radiological findings consistent with a well circumscribed benign cyst should be considered in the differential diagnosis of cysts within the abdomen.     

Retrograde movement of tRNAs from the cytoplasm to the nucleus in Saccharomyces cerevisiae

In eukaryotes, tRNAs transcribed in the nucleus function in cytoplasmic protein synthesis. The Ran-GTP-binding exportin, Los1p/Xpo-t, and additional pathway(s) mediate tRNA transport to the cytoplasm. Although tRNA movement was thought to be unidirectional, recent reports that yeast precursor tRNA splicing occurs in the cytoplasm, whereas fully spliced tRNAs can reside in the nucleus, require that either the precursor tRNA splicing machinery or mature tRNAs move from the cytoplasm to the nucleus. Our data argue against the first possibility and strongly support the second. Combining heterokaryon analysis with fluorescence in situ hybridization, we show that a foreign tRNA encoded by one nucleus can move from the cytoplasm to a second nucleus that does not encode the tRNA. We also discovered nuclear accumulation of endogenous cytoplasmic tRNAs in haploid yeast cells in response to nutritional deprivation. Nuclear accumulation of cytoplasmic tRNA requires Ran and the Mtr10/Kap111 member of the importin-beta family. Retrograde tRNA nuclear import may provide a novel mechanism to regulate gene expression in eukaryotes.     

Role of protein synthesis in the protection conferred by ozone-oxidative-preconditioning in hepatic ischaemia/reperfusion

The liver is damaged by sustained ischaemia during liver transplantation, and the reperfusion after ischaemia results in further functional impairment. Ozone oxidative preconditioning (OzoneOP) protected the liver against ischaemia/reperfusion (I/R) injury through different mechanisms. The aim of this study was to investigate the influence of the inhibition of protein synthesis on the protective actions conferred by OzoneOP in hepatic I/R. Rats were treated with cycloheximide (CHX) in order to promote protein synthesis inhibition after OzoneOP treatment. Plasma transaminases, malondialdehyde and 4-hydroxyalkenals and morphological characteristics were measured as an index of hepatocellular damage; Cu/Zn-superoxide dismutase (SOD), Mn-SOD, catalase, total hydroperoxides and glutathione levels as markers of endogenous antioxidant system. OzoneOP increased Mn-SOD isoform and ameliorated mitochondrial damage. CHX abrogated the protection conferred by OzonoOP and decreased Mn-SOD activity. Cellular redox balance disappeared when CHX was introduced. Protein synthesis is involved in the protective mechanisms mediated by OzoneOP. Ozone treatment preserved mitochondrial functions and cellular redox balance.     

Dietary fatty acids modulate chronic colitis, colitis-associated colon neoplasia and COX-2 expression in IL-10 knockout mice

OBJECTIVE: The effects of different dietary oils on the development of colitis-associated colon cancer have not been studied. The present study examined the effect of different dietary oils on the severity of chronic colitis, development of colitis-associated premalignant changes, and colonic expression of cyclooxygenase-2 (COX-2) in interleukin-10 knockout (IL-10-/-) mice. METHODS: IL-10-/- mice were fed chow supplemented with corn oil (CO; control, n=28), olive oil (OO; n=29), or fish oil (FO; n=35) for 12 wk and their colons were studied for colitis score, premalignant changes, and COX-2 expression. RESULTS: The average colitis score was higher in the FO than in the CO group. Similarly, the incidence of severe colitis (score>or=3) was significantly higher in the FO than in the CO and OO groups (50% versus 7.7% and 3.7%, respectively, P<0.05). Dysplasia was more frequent in the FO and less frequent in the OO than in the CO group (47% and 4% versus 15%, respectively, P<0.05). Conversely, aberrant crypt foci and crypt index were significantly higher in the FO than in the CO group. Colitis score, aberrant crypt foci, and crypt index did not differ between the OO and CO groups. COX-2 immunostaining was significantly lower in the OO than in CO group (P<0.05) but not different between the FO and CO groups. CONCLUSIONS: In IL-10-/- mice, fish oil exacerbates chronic colitis and colitis-associated premalignant changes. Conversely, olive oil inhibits COX-2 immunostaining and decreases the risk of neoplasia associated with chronic colitis.     

Increased serum hepcidin levels during treatment with deferasirox in iron-overloaded patients with myelodysplastic syndrome

Hepcidin is a major regulator of iron metabolism. We evaluated changes in serum hepcidin during 3 months of therapy with the iron-chelator deferasirox in patients with low-risk myelodysplastic syndrome and iron overload. Serum hepcidin was found to be high in these patients, correlated with their iron and oxidative status, and further increased by treatment with deferasirox. These findings support the concept that the hepcidin level represents a balance between the stimulating effect of iron overload and the inhibitory effects of erythropoietic activity and oxidative stress. These preliminary findings favour the rationale for iron chelation therapy in such patients.     

Summary of current consensus on the effect of smoking on implant therapy

Implant therapy has become a very predictable treatment option in the general population; however, there are certain factors that increase the risk of implant failure. The 2008 National Health Interview Survey estimates that 24.8 million men and 21.1 million women are smokers. The literature regarding cigarette smoking and dental implants currently suggests that advising the patient to stop smoking completely is best, but if this approach is not tenable, then the patient should be warned of the increased risk of implant failure and postoperative complications.     

The Saudi Project for Assessment of Coronary Events (SPACE) registry: Design and results of a phase I pilot study

OBJECTIVE:

The delay between the availability of clinical evidence and its application to the care of patients with acute coronary syndrome (ACS) in the Kingdom of Saudi Arabia remains undefined. The Saudi Project for Assessment of Coronary Events (SPACE) registry provides a comprehensive view of the current diagnostic and treatment strategies for patients with ACS; thus, the registry may be used to identify opportunities to improve the care of these patients.

METHODS:

Eight hospitals in different regions of Saudi Arabia were involved in the pilot phase of the registry, from December 2005 to July 2006. The study patients included individuals with ST segment elevation myocardial infarction (STEMI), non-STEMI and unstable angina.

RESULTS:

A total of 435 patients (77% men and 80% Saudis) with a mean age of 57.1 years were enrolled. Medical history included previously diagnosed ischemic heart disease (32%), percutaneous coronary intervention (12%), diabetes mellitus (53%), hypertension (48%), current smoking (39%), hyperlipidemia (31%) and family history of premature coronary artery disease (11%). The median door-to-needle time for fibrinolytic therapy received by patients with STEMIs was 90 min. Inhospital medications included acetylsalicylic acid (98%), clopidogrel (73%), angiotensin-converting enzyme inhibitors (74%), beta-blockers (73%), statins (88%), unfractionated heparin (80%), low-molecular weight heparin (22%) and glycoprotein IIb/IIIa inhibitors (9%). The inhospital mortality rate was 5%.

CONCLUSION:

The first nationwide registry of patients with ACS in the Kingdom of Saudi Arabia is presented. In contrast to registries from developed countries, our cohort is characterized by a younger age at presentation and a much higher prevalence of diabetes mellitus. Most patients with STEMIs did not receive fibrinolytic therapy within the time recommended in the American College of Cardiology/American Heart Association guidelines. The results of the present pilot study show potential targets for improvement in care.     

Combined thirty-day exposure to thioacetamide and choline-deprivation alters serum antioxidant status and crucial brain enzyme activities in adult rats

Choline (Ch) is an essential nutrient that seems to be involved in a wide variety of metabolic reactions and functions that affect the nervous system, while thioacetamide (TAA) is a well-known hepatotoxic agent. The induction of prolonged Ch-deprivation (CD) in rats receiving TAA (through the drinking water) provides an experimental model of mild progressive hepatotoxicity that could simulate commonly-presented cases in clinical practice. In this respect, the aim of this study was to investigate the effects of a 30-day dietary CD and/or TAA administration (300 mg/L of drinking water) on the serum total antioxidant status (TAS) and the activities of brain acetylcholinesterase (AChE), Na⁺,K⁺-ATPase and Mg²⁺-ATPase of adult rats. Twenty male Wistar rats were divided into four groups: A (control), B (CD), C (TAA), D (CD+TAA). Dietary CD was provoked through the administration of Ch-deficient diet. Rats were sacrificed by decapitation at the end of the 30-day experimental period and whole brain enzymes were determined spectrophotometrically. Serum TAS was found significantly lowered by CD (−11% vs Control, p < 0.01) and CD+TAA administration (−19% vs Control, p < 0.001), but was not significantly altered due to TAA administration. The rat brain AChE activity was found significantly increased by TAA administration (+11% vs Control, p < 0.01), as well as by CD+TAA administration (+14% vs Control, p < 0.01). However, AChE was not found to be significantly altered by the 30-day dietary CD. On the other hand, CD caused a significant increase in brain Na⁺,K⁺-ATPase activity (+16% vs Control, p < 0.05) and had no significant effect on Mg²⁺-ATPase. Exposure to TAA had no significant effect on Na⁺,K⁺-ATPase, but inhibited Mg²⁺-ATPase (−20% vs Control, p < 0.05). When administered to CD rats, TAA caused a significant decrease in Na⁺,K⁺-ATPase activity (−41% vs Control, p < 0.001), but Mg²⁺-ATPase activity was maintained into control levels. Our data revealed that an adult-onset 30-day dietary-induced CD had no effect on AChE activity. Treatment with TAA not only reversed the stimulatory effect of CD on adult rat brain Na⁺,K⁺-ATPase, but caused a dramatic decrease in its activity (−41%). Previous studies have linked this inhibition with metabolic phenomena related to TAA-induced fulminant hepatic failure and encephalopathy. Our data suggest that CD (at least under the examined 30-day period) is an unfavorable background for the effect of TAA-induced hepatic damage on Na⁺,K⁺-ATPase activity (an enzyme involved in neuronal excitability, metabolic energy production and neurotransmission).