Should Screening for Colorectal Neoplasm Be Recommended in Patients at High Risk for Coronary Heart Disease: A Cross-Sectional Study

Colorectal neoplasm (CRN) and coronary heart disease (CHD) share common risk factors. We aimed to assess the risk for CRN in patients who are at high risk for developing CHD determined by measurements, which are independent from the risk factors for CRN.This study was conducted on individuals who underwent total colonoscopic examination and were without history of CHD. Two-hundred thirty-five subjects (82 with CRN and 153 with normal colonoscopic findings) participated in the study. Colorectal carcinoma (CRC) was defined as the presence of adenocarcinoma. We measured carotid intima media thickness (CIMT), flow-mediated dilation (FMD), and calculated Framingham risk score (FRS) for all participants. An increased CIMT (≥1.0 mm), a decreased FMD (<10%), and a high FRS (>20%) were defined as high risks for developing CHD. The risk and the prevalence of CRN were analyzed in relation to the risk for developing CHD.The ratio of the patients with overall-CRN and CRC was significantly higher in individuals who are at high risk for developing CHD compared with individuals who are at low risk for developing CHD by each 3 risk estimation method (P < 0.05 for all). An increased CIMT, a decreased FMD, and a high FRS score were significantly associated with the high risk for the presence of CRC (odds ratio [OR]: 6.018, OR: 3.699, and OR: 4.120, respectively). An increased CIMT, a decreased FMD, and an intermediate FRS were significantly associated with the risk for the presence of overall-CRN (OR: 3.607, OR: 1.866 and OR: 2.889, respectively).The risk for CRN increases as the risk for developing CHD increases. It can be suggested that screening for CRN can be recommended for individuals who are at high risk for developing CHD.     

The effect of in ovo ethanol exposure on retina and optic nerve in a chick embryo model system

Ocular anomalies seen in children with fetal alcohol syndrome (FAS) suggest that ocular structures are sensitive to alcohol exposure during their development. This study was designed to investigate the effect of in ovo ethanol (EtOH) exposure on retinal development and myelinization of optic nerve fibers at an ultra structural level in a chick embryo model system. Prior to incubation, fertilized chicken eggs were injected once with 100 microl of either 0.9% NaCl (vehicle control), or EtOH solutions at different doses (10, 30, or 50%, v:v in 0.9% NaCl) into their air sacs and incubated at 37.5 degrees C and saturation humidity. On day 20 embryos were analyzed in terms of their viability and growth and the optic cups including the optic nerves were dissected out. Specimens were processed for electron microscopy (EM). Results showed that, EtOH significantly decreased the viability of chick embryos (P < 0.045), and caused significant prenatal growth retardation (P < 0.004) in a dose-dependant manner. Light microscopy of semi thin sections revealed that prenatal exposure to EtOH resulted in both retinal degeneration and optic nerve hypoplasia (P < 0.001) in a dose-dependant manner. EM revealed that a dose-dependant decrease in the number of myelinated nerve fibers was profound in groups exposed to EtOH (P < 0.001). Furthermore, the myelin coats observed were thinner than those seen in control embryos. In groups exposed to EtOH myelin sheets were unorganized and contained vacuolar structures in between them. The tissue in between the cells and optic nerve fibers, on the other hand, lost its intact appearance with vacuolar and vesicular structures in between them. In addition, the optic nerve fibers contained granular accumulations in EtOH exposed groups. A dose dependent degeneration was also observed in retinas of EtOH exposed groups. The effect of EtOH was profound in pigment epithelium (PE), inner plexiform layer (IPL), and ganglion cell layer (GC). Mitochondrial deficiencies, and alterations in melanin granule number and distribution dominated the defects seen in PE. On the other hand, EM findings of all the affected layers were suggestive of induced cell death in EtOH exposed groups. Thus, this study suggests retinal development with the emphasis on melanin pigmentation in PE and optic nerve myelinization as potential targets of prenatal EtOH exposure and discusses potential mechanisms of EtOH action on these tissues.     

What Are the Clinical Implications of Nodular Gastritis? Clues from Histopathology

There is no widely accepted histopathological definition for nodular gastritis. In this study we aim to uncover the pathologic entity responsible for the nodular appearance and to find clues about the clinical implications of nodular gastritis. Antral biopsy specimens of 160 patients with nodular gastritis and 133 patients without nodular gastritis were examined by an experienced pathologist for dysplasia, foveolar hyperplasia, inflammatory activity, intraepithelial lymphocytosis, intestinal metaplasia, and lymphoid follicle/aggregate formation, and comparative analysis was performed between the two groups of patients. The presence of intraepithelial lymphocytosis was more frequent in patients with nodular gastritis (P < 0.05). There was no difference between the two groups regarding the other pathological features such as presence of dysplasia, inflammatory activity, intestinal metaplasia, lymphoid hyperplasia, and Helicobacter pylori (H. pylori) infection. Increase of intraepithelial lymphocytes may contribute to formation of macroscopical nodules in this peculiar type of gastritis. Nodular gastritis would not indicate a new therapeutic approach in addition to the current measures for Helicobacter pylori infection.     

Tularemia: potential role of cytopathology in differential diagnosis of cervical lymphadenitis: Multicenter experience in 53 cases and literature review

Tularemia is a zoonosis caused by Francisella tularensis. Tularemia outbreaks occurred in Central Anatolia during 2009 and 2011. We evaluated the clinical characteristics and cytomorphologies of fine needle aspirations (FNAs) from cervical lymph nodes in serologically confirmed tularemia cases. To our knowledge, this is the first large series concerning FNA morphology of Tularemia. FNA smears of 53 patients of the 290, diagnosed by microagglutination tests and PCR, were evaluated at three Pathology centers. FNAs were performed by cytopathologists or ear‐nose‐throat surgeons. Of all patients, 17 had also lymph node resections. FNAs showed the presence of suppuration and abscess. Rare epithelioid histiocytes and granulomas, seldom phagocytosed bacilli‐like microorganisms were observed. On histopathology; granulomas, necrosis, and suppurative inflammation extending extracapsular areas were seen. Tularemia is endemic in certain areas of the Northern Hemisphere. The benefit from cytopathology is limited and cytological suspicion should be confirmed by serology. However FNA cytology is helpful in differential diagnosis of tularemia and other diseases presented with suppurative, granulomatous cervical lymphadenitis. It is also useful in providing the material for PCR and culture in early phase when the serology is negative and the treatment is more effective.     

Is the level of C-reactive protein correlated with the extent of carotid atherosclerosis?

BACKGROUND: Increased intima-media thickness (IMT) of the common carotid arteries (CCA) and elevated levels of highly sensitive C-reactive protein (hsCRP) are both shown to be associated with the occurrence of stroke. We investigated whether elevated hsCRP level is a risk factor for the increased IMT of the CCA independent of other proven risk factors for the ischemic stroke and studied the interaction between hsCRP level and the extent of carotid atherosclerosis. METHODS AND RESULTS: We studied 104 patients aged between 30 to 92 years who were admitted to our neurology department with acute ischemic stroke. All patients underwent a clinical evaluation, laboratory investigations, and neuroultrasonographic examination. In 24 patients with normal ultrasonographic examination, mean hsCRP levels was 8.6 + 6.7 mg/L. Mean hsCRP level was 18.0 + 25.6 mg/L in patients having increased intima to media thickness (> 1.2 mm); 32.7 + 49.1 mg/L in patients who had atheromatous plaques without significant narrowing; and 23.9 + 27.3 mg/L in patients with internal carotid artery stenosis more than 50%. hsCRP levels and the extent of the atherosclerosis showed a significant relationship (p = 0.040). In multiple regression analyses, this relationship was found to be independent of other proven risk factors. The only variable that showed a significant relation with the level of hsCRP was the HDL level. A negative correlation was found between hsCRP and HDL levels. CONCLUSIONS: We conclude that elevated hsCRP level is an indirect risk factor for the ischemic stroke through its relation with the extent of the carotid atherosclerosis, and this relation is independent of other known risk factors.     

IL-1 beta depresses respiration and anoxic survival via a prostaglandin-dependent pathway in neonatal rats

IL-1 beta has been proposed to be an important mediator linking infection, apnea, and sudden infant death syndrome. We hypothesized that IL-1 beta acts in this capacity by depressing brainstem respiratory neurons via a prostaglandin-dependent pathway. For studying the effects of IL-1 beta on respiration as well as the mechanism underlying its actions, 7-d-old rats received an initial injection (i.p.) of NaCl or a cyclooxygenase inhibitor (indomethacin, 10 mg/kg) followed by a second injection (i.p.) at 30 min of NaCl, recombinant rat IL-1 beta (10 microg/kg), or lipopolysaccharide (LPS; 100 microg/kg). Respiration during normoxia and in response to anoxia (100% N2) was examined at 60 min after the second injection using flow and barometric plethysmography. Animals given IL-1 beta breathed more slowly and died more often after anoxia. LPS also reduced the rats' ability to autoresuscitate and survive an anoxic challenge. Indomethacin prevented the depressive effects during normoxia and the adverse effects on survival. For investigating drug-induced changes in central respiratory activity, IL- 1 beta (1.0 or 1.25 ng/mL) and prostaglandin E2 (5 or 20 microg/L) was applied to the brainstem-spinal cord preparation of 0- to 4-d-old rats. Whereas IL-1 beta exerted no effect on respiration measured at the C4 ventral root during a 60-min period, prostaglandin E2 reversibly inhibited respiratory activity. These findings suggest that IL-1 beta does not inhibit respiratory neurons directly but may depress breathing and hypoxic defense via a prostaglandin-mediated mechanism.