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OBJECTIVE: Cervical smear cytology, which is a gynecological cervical cancer screening test, can provide information about the presence of pathogenic microorganisms or the inflammation they cause. Among them, Ureaplasma urealyticum (Uu), which is a subspecies of Mycoplasma was held responsible for high-grade cervical intraepithelial lesions and malignancy due to long-lasting complicated vulvovaginitis clinic. We aimed at investigating the role of Uu in the inflammatory process of the cervix and to describe the cytological features that enable it to be recognized microscopically in cervical smear test. PATIENTS AND METHODS: Cervical smear and mycoplasma culture data of 123 women with complicated vulvovaginitis findings were evaluated. According to the Uu culture results, women were divided into two groups: the Uu-positive (n=59) and the Uu-negative group (n=64). The groups were compared in terms of cervical smear results, macroscopic view of the cervix, and secondary cytological evaluation results. RESULTS: The presence of inflammatory signs (83.1%) in the Uu-positive group was observed to be 83.1%, whereas 67.2% in the Uu-negative group, and the difference between the two groups was found to be significant (p=0.04). Besides, the difference in aggregated polymorphonuclear leukocytes (PMNL) between Uu-positive group (59.3%) and Uu-negative group (40.6%) was statistically significant (p=0.04). Similarly, nuclear atypia of epithelial cells in the Uu-positive group (33.9%) was observed to be higher than in the Uu-negative group (17.2%) (p=0.03). CONCLUSIONS: Uu causes inflammation of the cervix and cervical intraepithelial lesions. Aggregated PMNL observed in cervical smear cytology may be one of the findings that will give clues for Uu. [ABSTRACT FROM AUTHOR]

Byline: Mehmet. Aydin, C. Gundogdu, F. Akcay, N. Gursan BACKGROUND: Meningitis, termed as foreign material collection in the subarachnoid space, leads to various meningeal, cerebral and spinal cord pathologies. Meningitis [...]

Primary carcinoma of the fallopian tube is a rare gynecologic malignancy. Chronic tubal inflammation is associated with primary carcinoma of the fallopian tube. There are only a few reports on primary carcinoma of the fallopian tube coexisting with tuberculous salpingitis. We are reporting a patient with both the primary carcinoma of the fallopian tube and tuberculous salpingitis, which were detected in bilateral fallopian tubes. The histologic type was serous adenocarcinoma. The patient was treated with total abdominal hysterectomy, bilateral salpingo-oophorectomy, infracolic omentectomy, and bilateral pelvic lymphadenectomy followed by chemotherapy consisting of paclitaxel and cisplatin. She has been alive without evidence of disease for 18 months. [ABSTRACT FROM AUTHOR]

Abstract Background Though retrograde neuronal death and vascular insufficiency have been well established in plegics following intracerebral hemorrhage, the effects of plegia on arterial nervorums of peripheral nerves have not been reported. In this study, the histopathological effects of the intracerebral hemorrhage on the dorsal root ganglions and sciatic nerves via affecting the arterial nervorums were investigated. Methods This study was conducted on 13 male hybrid rabbits. Three animals were taken as control group and did not undergo surgery. The remaining 10 subjects were anesthetized and were injected with 0.50 ml of autologous blood into their right sensory-motor region. All rabbits were followed-up for two months and then sacrificed. Endothelial cell numbers and volume values were estimated a three dimensionally created standardized arterial nervorums model of lumbar 3. Neuron numbers of dorsal root ganglions, and axon numbers in the lumbar 3 nerve root and volume values of arterial nervorums were examined histopathologically. The results were analyzed by using a Mann-Whitney-U test. Results Left hemiplegia developed in 8 animals. On the hemiplegic side, degenerative vascular changes and volume reduction in the arterial nervorums of the sciatic nerves, neuronal injury in the dorsal root ganglions, and axonal injury in the lumbar 3 were detected. Statistical analyses showed a significant correlation between the normal or nonplegic sides and plegic sides in terms of the neurodegeneration in the dorsal root ganglions (p < 0.005), axonal degeneration in the lumbar 3 nerve roots (p < 0.005), endothelial cell degeneration in the arterial nervorums (p < 0.001), and volume reduction in the arterial nervorums (p < 0.001). Conclusion Intracerebral hemorrhage resulted in neurodegeneration in the dorsal root ganglion and axonolysis in the sciatic nerves, endothelial injury, and volume reduction of the arterial nervorums in the sciatic nerves. The interruption of the neural network connection in the walls of the arterial nervorums in the sciatic nerves may be responsible for circulation disorders of the arterial nervorums, and arterial nervorums degeneration could result in sciatic nerves injury.

Objectives: Ectopic breast cancer may present anywhere in the milk line, from the axilla to the groin which is extremely rare in the inguinal region. Despite morphologic differences, ectopic breast tissue presents characteristics related to orthotopic breast tissue in terms of function and pathologic degeneration. The case report describes the treatment of a unique ectopic breast carcinoma which was located in the inguinal region with a common femoral vein invasion., Methods: We present a unique case of an ectopic breast carcinoma presenting in an unusual anatomic location along the milk line. The study was approved by the local Ethics Committee (protocol no: 12.01.2023-2023/02) Informed consent was obtained from the patient., Results: The patient is surgically treated and supplemented with neoadjuvant chemotherapy,radiotherapy and endocrine therapy. Histopathological examination revealed the diagnosis of invasive ductal carcinoma. The right common femoral vein was reconstructed with bovine pericardial patch after totally removal of the mass., Conclusions: This report alerts the reader to be cognizant of the unusual location of an ectopic breast cancer which was detected in the inguinal region with a common femoral vein invasion and discusses the treatment, suggesting novel therapeutic advice that could bring considerable clinical advantages. A multidisciplinary approach should be warranted in such cases to confirm a complete remission.

Estrogens play a pivotal role in the development and proliferation of hormone-dependent breast cancer. Apart from free estrogens, which can directly activate the estrogen receptor (ER) of tumor cells, sulfo-conjugated steroids, which maintain high plasma concentrations even after menopause, first have to be imported into tumor cells by carrier-mediated uptake and then can be cleaved by the steroid sulfatase to finally activate ERs and cell proliferation. In the present study, expression of the sodium-dependent organic anion transporter SOAT was analyzed in breast cancer and its role for hormone-dependent proliferation of T47D breast cancer cells was elucidated. The SOAT protein was localized to the ductal epithelium of the mammary gland by immunohistochemistry. SOAT showed high expression in different pathologies of the breast with a clear ductal localization, including ductal hyperplasia, intraductal papilloma, and intraductal carcinoma. In a larger breast cancer cDNA array, SOAT mRNA expression was high in almost all adenocarcinoma specimen, but expression did not correlate with either the ER, progesterone receptor, or human epidermal growth factor receptor 2 status. Furthermore, SOAT expression did not correlate with tumor stage or grade, indicating widespread SOAT expression in breast cancer. To analyze the role of SOAT for breast cancer cell proliferation, T47D cells were stably transfected with SOAT and incubated under increasing concentrations of estrone-3-sulfate (E 1 S) and estradiol at physiologically relevant concentrations. Cell proliferation was significantly increased by 10 -9 M estradiol as well as by E 1 S with EC 50 of 2.2 nM. In contrast, T47D control cells showed 10-fold lower sensitivity to E 1 S stimulation with EC 50 of 21.7 nM. The E 1 S-stimulated proliferation of SOAT-T47D cells was blocked by the SOAT inhibitor 4-sulfooxymethylpyrene., In Conclusion: The present study clearly demonstrates expression of SOAT in breast cancer tissue with ductal localization. SOAT inhibition can block the E 1 S-stimulated proliferation of T47D breast cancer cells, demonstrating that SOAT is an interesting novel drug target from the group of E 1 S uptake carriers for anti-proliferative breast cancer therapy.

Objective: We assessed whether ultrasonography (US) can be used in combination with cone beam computed tomography (CBCT) to image intraosseous jaw lesions., Material and Methods: Using CBCT and US, we evaluated 123 lytic intraosseous jaw lesions diagnosed in 121 patients with guidance from the CBCT findings. The lesions were classified into two groups based on histopathological evaluation: (1) cysts and (2) tumors and tumor-like lesions. US and histopathological findings on the lesions of the two groups and their relationships with each other were also assessed. Results are reported as means ± standard errors, and p < 0.001 was accepted as indicating statistical significance., Result: In total, 123 lesions were evaluated; 74 (60.2%) were cysts and 49 (39.8%) were tumors or tumor-like lesions. The CBCT and US findings were compatible as far as dimensional measurements of the lesions in the three planes (p < 0.001). The US and histopathological findings on the content of the lesions correlated (p < 0.001)., Conclusion: CBCT provides useful information for diagnosing intraosseous jaw lesions. Because it offers no valid Hounsfield unit (HU) value, it does not differentiate between solid and cystic masses. Thus, US can be used with CBCT to image intraosseous jaw lesions caused by buccal cortical thinning or perforation., Clinical Relevance: US provides useful information about intraosseous jaw lesions and can be used with CBCT to image such lesions caused by buccal cortical thinning or perforation. Clinicians can take this information into consideration when evaluating intraosseous jaw pathology.

In the original version of this article, '123 lytic intraosseous jaw lesions diagnosed in 112 patients' was incorrectly presented as '123 lytic intraosseous jaw lesions diagnosed in 121 patients' and 'an average age of 31.7 ± 15.4 (range, 6-72)' was incorrectly presented as 'average age of 15.4 ± 31.7 (range, 6-72)'.

Aim: To investigate the relationship between neuron density of the superior cervical sympathetic ganglia and pupil diameter in subarachnoid hemorrhage., Material and Methods: This study was conducted on 22 rabbits; 5 for the baseline control group, 5 for the SHAM group and 12 for the study group. Pupil diameters were measured via sunlight and ocular tomography on day 1 as the control values. Pupil diameters were re-measured after injecting 0.5 cc saline to the SHAM group, and autologous arterial blood into the cisterna magna of the study group. After 3 weeks, the brain, superior cervical sympathetic ganglia and ciliary ganglia were extracted with peripheral tissues bilaterally and examined histopathologically. Pupil diameters were compared with neuron densities of the sympathetic ganglia and ciliary ganglia which were examined using stereological methods., Results: Baseline values were; normal pupil diameter 7.180±620 ?m and mean neuron density of the superior cervical sympathetic ganglia 6.321±510/mm3, degenerated neuron density of ciliary ganglia was 5±2/mm3 after histopathological examination in the control group. These values were measured as 6.850±578 ?m, 5.950±340/mm3 and 123±39/mm3 in the SHAM group and 9.910±840 ?m, 7.950±764/mm3 and 650±98/mm3 in the study group. A linear relationship was determined between neuron density of the superior cervical sympathetic ganglia and pupil diameters (p < 0.005). Degenerated ciliary ganglia neuron density had an inverse effect on pupil diameters in all groups (p < 0.0001)., Conclusion: Highly degenerated neuron density of the ciliary ganglion is not responsible for pupil dilatation owing to parasympathetic pupilloconstrictor palsy, but high neuron density of the pupillodilatatory superior cervical sympathetic ganglia should be considered an important factor for pupil dilatation.

Contrast media (CM) is known to have nephrotoxic adverse effects. Epigallocatechin-3-gallate (EGCG) is the most abundant and active catechin in green tea, and has strong antioxidant and anti-inflammatory properties. This study investigated whether EGCG can reduce contrast-induced nephrotoxicity (CIN), alone or with glycerol (GLY)-induced renal damage, and to understand its mechanisms of protection against toxicity, using models of GLY and CIN in rats. The rats were separated into eight groups (n = 6 in each), as follows: Healthy, GLY, CM, GLY + CM, CM + EGCG 50 mg/kg (po), GLY + CM + EGCG 50 mg/kg (po), CM + EGCG 100 mg/kg (po), and GLY + CM + EGCG 100 mg/kg (po). Both doses of EGCG protected against CM-induced renal dysfunction, as measured by serum creatinine and blood urea nitrogen (BUN). In addition, EGCG treatment markedly improved CIN-induced oxidative stress, and resulted in a significant down-regulatory effect on tumor necrosis factor (TNF)-α and nuclear factor (NF)-κB mRNA expression. Moreover, histopathological analysis showed that EGCG also attenuated CM-induced kidney damage. Considering the potential clinical use of CM and the numerous health benefits of EGCG, this study showed the protective role of multi-dose EGCG treatment on CIN and GLY-aggravated CIN through different mechanisms.

Objective: Recent evidence suggests that oxidative stress is involved in the pathophysiology of many human diseases. It has been demonstrated that oxidative stress is associated with intrauterine growth restriction (IUGR), and the depletion of placental antioxidant systems has been suggested as a key factor in this disease. Our aims were to explore the possible role of antioxidant paraoxonase-2 (PON2) and paraoxonase-3 (PON3) in the pathophysiology of unexplained IUGR., Methods: We have studied the expression of mRNA for PON2, PON3 in placental tissues by using RT-qPCR. Two groups, consisting of normal (n = 18) and unexplained IUGR pregnancies (n = 20) were compared., Results: Our results demonstrated that there were no significant differences in the mRNA expressions of PON2, PON3 between the two groups (p = 0.28, p = 0.90, respectively). PON2 and PON3 were down-regulated in IUGR. Antenatal steroid therapy had no effect on the expression mRNA in placentae of unexplained IUGR pregnancies compared to non-treated group., Conclusions: These results suggest that PON2, PON3 mRNA levels were not changed significantly in placentae of IUGR when compared to normal pregnant women.

Aim: Cerebral vasospasm after subarachnoid hemorrhage (SAH) may lead to a devastating neurological outcome by inducing cerebral ischemia. However the role of external carotid artery (ECA) vasospasm has been rarely reported in the literature. The aim of this study was to elucidate the effect of ECA vasospasm on cerebral ischemia related neurodegeneration in the cerebral cortex after SAH., Material and Methods: This study was performed on 23 rabbits, divided into three groups: control (n=5), sham (n=5), and SAH (n=13). Experimental SAH was performed by injecting 0.75 mL auricular arterial homologous blood into the cisterna magna. After three weeks, the animals were decapitated and the common carotid arteries with their external and internal branches and the brains were examined histopathologically. Vasospasm indexes (VSI) of ECAs and internal carotid arteries (ICAs) and degenerated glial cell numbers of temporal cortices (n/mm3) were estimated stereologically and the results were compared statistically., Results: Temporal cortex glial cell density was estimated as 136.950±9.257/mm3 in normal rabbits, 131.324±7.987/mm3 in sham, 112.320±6.112/mm3 in light, and 97.543±5.432/mm3 in severe ECA vasospasm. The mean VSI values of ECA of all groups were 1.95±0.21, 2.15±0.29, 2.95±0.65 and 3.12±0.276, respectively. Statistical differences between the VSI values of ECA and degenerated neuron densities in temporal cortices were significant (p < 0.005)., Conclusion: ECA vasospasm was observed to have a more important predictive role on the serious cerebral ischemia and neuronal degeneration after SAH. The mechanism may be related to ischemia of the parasympathetic ganglia of the lower cranial nerves and dorsal root ganglion.

Background: The blood supply of the lower spinal cord is heavily dependent on the artery of Adamkiewicz. The goal of this study was to elucidate the effects of lumbar subarachnoid hemorrhage (SAH) on the lumbar 4 dorsal root ganglion (L4DRG) cells secondary to Adamkiewicz artery (AKA) vasospasm., Materials and Methods: This study was conducted on 20 rabbits, which were randomly divided into three groups: Spinal SAH ( n = 8), serum saline (SS) (SS; n = 6) and control ( n = 6) groups. Experimental spinal SAH was performed. After 20 days, volume values of AKA and neuron density of L4DRG were analyzed., Results: The mean alive neuron density of the L4DRG was 15420 ± 1240/mm 3 and degenerated neuron density was 1045 ± 260/mm 3 in the control group. Whereas, the density of living and degenerated neurons density were 12930 ± 1060/mm 3 and 1365 ± 480/mm 3 in serum saline (SS), 9845 ± 1028/mm 3 and 4560 ± 1340/mm 3 in the SAH group. The mean volume of imaginary AKAs was estimated as 1,250 ± 0,310 mm 3 in the control group and 1,030 ± 0,240 mm 3 in the SF group and 0,910 ± 0,170 mm 3 in SAH group. Volume reduction of the AKAs and neuron density L4DRG were significantly different between the SAH and other two groups ( P < 0.05)., Conclusion: Decreased volume of the lumen of the artery of Adamkiewicz was observed in animals with SAH compared with controls. Increased degeneration the L4 dorsal root ganglion in animals with SAH was also noted. Our findings will aid in the planning of future experimental studies and determining the clinical relevance on such studies., Competing Interests: There are no conflicts of interest.

Background: Hydrocephalus is a serious complication of subarachnoid hemorrhage (SAH). Obstruction of the cerebral aqueduct may cause hydrocephalus after SAH. Although various etiologic theories have been put forward, choroidal artery vasospasm-related ependymal desquamation and subependymal basal membrane rupture as mechanisms of aqueductal stenosis have not been suggested in the literature., Methods: This study was conducted on 26 hybrid rabbits. Five rabbits were placed in a control group, 5 were placed in a sham group, and the remaining rabbits (n = 16) were placed in the SAH group. In the first 2 weeks, 5 animals in the SAH group died. The other 21 animals were decapitated after the 4-week follow-up period. Choroidal artery changes resulting from vasospasm, aqueduct volume, ependymal cell density, and Evans index values of brain ventricles were obtained and compared statistically., Results: Mean aqueduct volume was 1.137 mm(3) ± 0.096, normal ependymal cell density was 4560/mm(2) ± 745, and Evans index was 0.32 ± 0.05 in control animals (n = 5); these values were 1.247 mm(3) ± 0.112, 3568/mm(2) ± 612, and 0.34 ± 0.15 in sham animals (n = 5); 1.676 mm(3) ± 0.123, 2923/mm(2) ± 591, and 0.43 ± 0.09 in animals without aqueductal stenosis (n = 5); and 0.650 mm(3) ± 0.011, 1234/mm(2) ± 498, and 0.60 ± 0.18 in animals with severe aqueductal stenosis (n = 6). The choroidal vasospasm index values were 1.160 ± 0.040 in the control group, 1.150 ± 0.175 in the sham group, 1.760 ± 0.125 in the nonstenotic group, and 2.262 ± 0.160 in the stenotic group. Aqueduct volumes, ependymal cell densities, Evans index, and choroidal artery vasospasm index values were statistically significantly different between groups (P < 0.05)., Conclusions: Ependymal cell desquamation and subependymal basal membrane destruction related to choroidal artery vasospasm may lead to aqueductal stenosis and hydrocephalus after SAH., (Copyright © 2016 Elsevier Inc. All rights reserved.)

Objective: The Adamkiewicz artery (AKA) supplies pudendal nerve roots and conus medullaris. The aim of this study was to elucidate if there is any relationship between neurodegenerative changes of the Onuf nucleus (ON)-pudendal nerve ganglia complex secondary to vasospasm of the AKA after spinal subarachnoid hemorrhage (SAH)., Methods: This study was conducted on 22 rabbits, which were randomly divided into 3 groups: control (n = 5), sham (n = 5), and spinal SAH (n = 12). Experimental spinal SAH was induced at the L2 level. After 2 weeks, the ON-pudendal nerve ganglia complex and AKA were examined histopathologically. Bladder volume values were estimated, and results were analyzed statistically., Results: Two animals died within the first week of experiment. Histopathologically, severe vasospasm of the AKA and neuronal degeneration and neuronal apoptosis were observed in the ON-pudendal nerve ganglia complex in 5 animals of the SAH group. The mean volume of the imaginary AKA, mean bladder volumes, and degenerated neuron densities of ON and pudendal nerve ganglia were estimated. We found that vasospasm of the AKA led to numerous neuron degenerations in ON and pudendal ganglia and consequently urinary retention (P < 0.005)., Conclusions: ON-pudendal nerve ganglia complex degeneration secondary to vasospasm of the AKA may be a cause of urinary retention after spinal SAH., (Copyright © 2016 Elsevier Inc. All rights reserved.)

Objective: To study the potential nephroprotective role of agomelatine in rat renal tissue in cases of contrast-induced nephrotoxicity (CIN). The drug's action on the antioxidant system and proinflammatory cytokines, superoxide dismutase (SOD) activity, levels of glutathione (GSH) and malondialdehyde (MDA) and the gene expression of interleukin-6 (IL-6), tumour necrosis factor (TNF)-α and nuclear factor kappa B (NF-κB) was measured. Tubular necrosis and hyaline and haemorrhagic casts were also histopathologically evaluated., Methods: The institutional ethics and local animal care committees approved the study. Eight groups of six rats were put on the following drug regimens: Group 1: healthy controls, Group 2: GLY (glycerol), Group 3: CM (contrast media--iohexol 10 ml kg(-1)), Group 4: GLY+CM, Group 5: CM+AGO20 (agomelatine 20 mg kg(-1)), Group 6: GLY+CM+AGO20, Group 7: CM+AGO40 (agomelatine 40 mg kg(-1)) and Group 8: GLY+CM+AGO40. The groups were evaluated by one-way analysis of variance and Duncan's multiple comparison test., Results: Agomelatine administration significantly improved the serum levels of blood urea nitrogen (BUN) and creatinine, SOD activity, GSH and MDA. The use of agomelatine had substantial downregulatory consequences on TNF-α, NF-κB and IL-6 messenger RNA levels. Mild-to-severe hyaline and haemorrhagic casts and tubular necrosis were observed in all groups, except in the healthy group. The histopathological scores were better in the agomelatine treatment groups., Conclusion: Agomelatine has nephroprotective effects against CIN in rats. This effect can be attributed to its properties of reducing oxidative stress and inhibiting the secretion of proinflammatory cytokines (NF-κB, TNF-α and IL-6)., Advances in Knowledge: CIN is one of the most important adverse effects of radiological procedures. Renal failure, diabetes, malignancy, old age and non-steroidal anti-inflammatory drug use pose the risk of CIN in patients. Several clinical studies have investigated ways to avoid CIN. Theophylline/aminophylline, statins, ascorbic acid and iloprost have been suggested for this purpose. Agomelatine is one of the melatonin ligands and is used for affective disorders and has antioxidant features. In this study, we hypothesized that agomelatine could have nephroprotective, antioxidant and anti-inflammatory effects against CIN in rats.

Context: Somato-sensitive innervation of bowels are maintained by lower segments of spinal cord and the blood supply of the lower spinal cord is heavily dependent on Adamkiewicz artery. Although bowel problems are sometimes seen in subarachnoid hemorrhage neither Adamkiewicz artery spasm nor spinal cord ischemia has not been elucidated as a cause of bowel dilatation so far., Aims: The goal of this study was to study the effects Adamkiewicz artery (AKA) vasospasm in lumbar subarachnoid hemorrhage (SAH) on bowel dilatation severity., Settings and Design: An experimental rabbit study., Materials and Methods: The study was conducted on 25 rabbits, which were randomly divided into three groups: Spinal SAH (N = 13), serum saline (SS) (SS; N = 7) and control (N = 5) groups. Experimental spinal SAH was performed. After 21 days, volume values of descending parts of large bowels and degenerated neuron density of L5DRG were analyzed., Statistical Analysis Used: Statistical analysis was performed using the PASW Statistics 18.0 for Windows (SPSS Inc., Chicago, Illinois). Two-tailed t-test and Mann-Whitney U-tests were used. The statistical significance was set at P < 0.05., Results: The mean volume of imaginary descending colons was estimated as 93 ± 12 cm(3) in the control group and 121 ± 26 cm(3) in the SS group and 176 ± 49 cm(3) in SAH group. Volume augmentations of the descending colons and degenerated neuron density L5DRG were significantly different between the SAH and other two groups (P < 0.05)., Conclusion: An inverse relationship between the living neuronal density of the L5DRG and the volume of imaginary descending colon values was occurred. Our findings will aid in the planning of future experimental studies and determining the clinical relevance on such studies.

Background: Hepatitis B virus infection is one of the major world health problems. Epigallocatechin-3 gallate is the major component of the polyphenolic fraction of green tea and it has an anti-viral, anti-mutagenic, anti- tumorigenic, anti-angiogenic, anti-proliferative, and/or pro-apoptotic effects on mammalian cells. In this study, our aim was to investigate the inhibition of HBV replication by epigallocatechin-3 gallate in the Hep3B2.1-7 hepatocellular carcinoma cell line., Materials and Methods: HBV-replicating Hep3B2.1-7 cells were used to investigate the preventive effects of epigallocatechin-3 gallate on HBV DNA replication. The expression levels of HBsAg and HBeAg were determined using ELISA. Quantitative real-time-PCR was applied for the determination of the expression level of HBV DNA., Results: Cytotoxicity of epigallocathechin-3-gallate was not observed in the hepatic carcinoma cell line when the dose was lower than 100 μM. The ELISA method demonstrated that epigallocatechin-3 gallate have strong effects on HBsAg and HBeAg levels. Also it was detected by real-time PCR that epigallocatechin-3 gallate could prevent HBV DNA replication., Conclusions: The obtained data pointed out that although the exact mechanism of HBV DNA replication and related diseases remains unclear, epigallocatechin-3 gallate has a potential as an effective anti-HBV agent with low toxicity.

Aim: Pulmonary arteries are mainly innervated by sympathetic vasoconstrictor and parasympathetic vasodilatory fibers. We examined whether there is a relationship between the neuron densities of hilar parasympathetic ganglia and pulmonary vasospasm in subarachnoid hemorrhage (SAH)., Material and Methods: Twenty-four rabbits were divided into two groups: control (n=8) and SAH (n=16). The animals were observed for 20 days following experimental SAH. The number of hilar parasympathetic ganglia and their neuron densities were determined. Proportion of pulmonary artery ring surface to lumen surface values was accepted as vasospasm index (VSI). Neuron densities of the hilar ganglia and VSI values were compared statistically., Results: Animals in the SAH group experienced either mild (n=6) or severe (n=10) pulmonary artery vasospasm. In the control group, the mean VSI of pulmonary arteries was 0.777±0.048 and the hilar ganglion neuron density was estimated as 12.100±2.010/mm < sup > 3 < /sup > . In SAH animals with mild vasospasm, VSI=1.148±0.090 and neuron density was estimated as 10.110±1.430/mm < sup > 3 < /sup > ; in animals with severe vasospasm, VSI=1.500±0.120 and neuron density was estimated as 7.340±990/mm < sup > 3 < /sup > ., Conclusion: There was an inverse correlation between quantity and neuron density of hilar ganglia and vasospasm index value. The low numbers and low density of hilar parasympathetic ganglia may be responsible for the more severe artery vasospasm in SAH.

Scaffold-based bone defect reconstructions still face many challenges due to their inadequate osteoinductive and osteoconductive properties. Various biocompatible and biodegradable scaffolds, combined with proper cell type and biochemical signal molecules, have attracted significant interest in hard tissue engineering approaches. In the present study, we have evaluated the effects of boron incorporation into poly-(lactide-co-glycolide-acid) (PLGA) scaffolds, with or without rat adipose-derived stem cells (rADSCs), on bone healing in vitro and in vivo. The results revealed that boron containing scaffolds increased in vitro proliferation, attachment and calcium mineralization of rADSCs. In addition, boron containing scaffold application resulted in increased bone regeneration by enhancing osteocalcin, VEGF and collagen type I protein levels in a femur defect model. Bone mineralization density (BMD) and computed tomography (CT) analysis proved that boron incorporated scaffold administration increased the healing rate of bone defects. Transplanting stem cells into boron containing scaffolds was found to further improve bone-related outcomes compared to control groups. Additional studies are highly warranted for the investigation of the mechanical properties of these scaffolds in order to address their potential use in clinics. The study proposes that boron serves as a promising innovative approach in manufacturing scaffold systems for functional bone tissue engineering., (Copyright © 2014 Elsevier B.V. All rights reserved.)

The purpose of this study was to investigate the effect of etoricoxib on oxidative injury induced with ischemia-reperfusion (I/R) in rat kidney tissue in terms of biochemistry and immunohistochemistry. Male Albino Wistar rats were divided into renal I/R (RIR), 50 mg/kg etoricoxib+RIR (ETO-50), 100 mg/kg etoricoxib+RIR (ETO-100) and sham operation (SG) groups. Animals in the ETO-50 and ETO-100 groups were given etoricoxib by the oral route at dosages of 50 and 100 mg/kg, respectively. The RIR and SG groups were given distilled water as solvent. One hour after drug administration, 1h of ischemia and 3h of reperfusion were applied to the left kidneys of all rats (apart from SG) under 25 mg/kg thiopental sodium anesthesia. At the end of that time, kidneys were extracted and biochemical and immunohistochemical analyses were performed. Etoricoxib reduced, in a dose-dependent manner, levels of MDA, MPO and COX-2 that normally rise with I/R in rat kidney tissues. Etorixicob did not alter COX-1 activity at 50 and 100 mg/kg doses, but significantly prevented loss of tGSH in tissues with I/R. In addition, Bcl-2' gene expression inhibited with I/R was prevented in renal tubular and glomerular cells. Furthermore, etoricoxib significantly decreased the caspase-3 gene expression which increased with I/R. Etoricoxib significantly prevented I/R injury in a dose-dependent manner. The results of this study show that etoricoxib treatment could decrease kidney injury during IR., (Copyright © 2014 Elsevier B.V. All rights reserved.)

Background: The choroid plexuses (CPs) are brain structures located in the brain ventricles, involved in the production and reabsorption of cerebrospinal fluid (CSF) components, cerebral immune surveillance, and various endocrine-enzymatic activities and acts as a CSF-blood barrier. This study investigated to determine if there is a link between ischemic CP injury and meningo-cerebral inflammation processes., Material and Methods: This study was conducted on 18 rabbits. Four rabbits were used as the baseline group to examine the normal structures. Fourteen of the rabbits were used as the study group by injecting 1.00cc of homologous blood into their cisterna magna. The animals were followed by daily monitoring for ten days and then slaughtered. Apoptotic degeneration of the CP cells was determined and statistical analyses were carried out using normal and apoptotic CP cell numbers. Data analyses were comprised of Mann-Whitney U tests. Differences were considered to be significant if p < 0.005., Results: Five animals belonging to the study group died between the 5th and 8th days. Unconsciousness, neck stiffness, convulsion, fever, apnea, cardiac arrhythmia, and breathing disturbances were observed in all of the animals who subsequently died. Intraventricular blood leakage was detected in all the dead and three surviving animals. Choroidal artery spasm, choroidal ependymal cell injury, choroidal cell apoptosis, pia-arachnoid thickening, meningocortical adhesions and blood cell density in the subarachnoid spaces were more severe in the more CP degenerated animals than those of the others. There were significant differences between the apoptotic CP cell density and blood cell density in the subarachnoid spaces (p < 0.005)., Conclusions: Subarachnoid hemorrhage (SAH) extending to brain ventricles causes ischemic degeneration of the CP by way of triggered choroidal artery vasospasm. It should be emphasized that the prevention of CP function may be an important part of the protection of the brain in SAH.

Background: Cerebrospinal fluid (CSF) secretion may be increased in the early phases of subarachnoid hemorrhage (SAH), possibly via ischemic glossopharyngeal nerve discharges, and decreased due to glossopharyngeal nerve degeneration in the late phase of SAH; but this reflex pathway has not been definitively investigated. We studied the relationship between petrous ganglion of the glossopharyngeal nerve (GPN) and water vesicles of the choroid plexus (CP) in the early and late phases of SAH., Methods: This study was conducted on 30 rabbits, divided into four groups, with five rabbits in the control group (group I), five rabbits in the sham group (Group II), and 20 rabbits in the SAH group. In the SAH group, five of the animals were decapitated after 4 days of cisternal blood injections (Group III), and the other 15 animals were decapitated after 20 days of injections (Group IV). The Petrous Ganglia and CPs of lateral ventricles were removed and stained for stereological analysis., Results: The mean number of follicles per cubic millimeter was 5.3 ± 1.2 the in control group (Group I), 4.5 ± 0.9 in the sham group (Group II), 16.60 ± 3.77 the in early decapitated group (Group III), and 4.30 ± 0.84 in the late decapitated group (Group IV). The mean number of degenerated neuron density of petrous ganglions was 6 ± 2, 50 ± 6, 742 ± 96, and 2.420 ± 350 in the control (Group I), sham (Group II), early decapitated (Group III), and late decapitated group (Group IV), respectively. The mean number of water vesicles was statistically different after SAH between the early decapitated group (group III) and the late decapitated group (group IV) (P < 0.05)., Conclusions: We studied the relationship between petrous ganglion cells of the GPN and water vesicles of CP in the early and late phases of SAH, and found that CP vesicles are increased in the early phase of SAH due to irritation of GPN, and decreased in the late phase due to ischemic insult of the petrous ganglion and parasympathetic innervation of the CP.

The purpose of this study was to investigate the biochemical, histopathological and immunohistochemical effects of venous blood on ischemia/reperfusion-induced oxidative DNA damage and mutation in rabbit kidneys in comparison to melatonin treatment, which has a known protective effect against ischemia/reperfusion (IR) injury. The rabbits were divided into five groups: renal ischemia (RI), renal ischemia-reperfusion (RIR), renal ischemia-venous blood-reperfusion (RIVR), melatonin + renal ischemia-reperfusion (MRIR), and the healthy sham control group (HG). Melatonin (2.5 mg/kg delivered intraperitoneally) was administered one hour prior to ischemia. In the RIVR group, 1 ml of venous blood was administered 5 minutes before the reperfusion. The xanthine oxidase activity in the kidney tissue was determined as 53.50 ± 1.72, 31.00 ± 6.39, 45.66 ± 9.20, 28.66 ± 6.05 and 14.33 ± 1.28 U/g protein; the MDA levels were 6.32 ± 0.02, 19.50 ± 1.33, 7.00 ± 0.96, 7.50 ± 0.76 and 4.75 ± 0.34 mmol/g protein; and the GSH levels were 4.50 ± 1.08, 2.76 ± 0.13, 5.48 ± 0.22, 4.93 ± 0.55 and 6.98 ± 0.33 nmol/g protein in the RI, RIR, RIVR, MRIR and HG groups, respectively. Blood, blood urea nitrogen (BUN) and creatinine levels were classified as high only in the RIR group. The MRIR and RIVR groups, in which oxidative stress was best suppressed, had much milder histopathological and immunohistochemical findings compared to the RIR group. This study has revealed that it is useful to initiate reperfusion of the ischemic tissue with venous blood.

Background: Stenoocclusive carotid artery disease causes important histomorphologic changes in all craniocervical vasculatures, such as luminal enlargement, vascular wall thinning, elongation, convolutions, and aneurysm formation in the posterior circulation. Although increased pressure, retrograde blood flow, and biochemical factors are described in the pathogenesis of vascular remodelisation, the vasoregulatory role of the autonomic nervous system has not been investigated thus far. We investigated the relationship between the sympathetic nervous system and the severity of histomorphologic alterations of basilar arteries after bilateral common carotid artery ligation (BCCAL)., Material and Methods: This study was conducted on 21 rabbits. The rabbits were randomly divided into three groups: baseline group (n = 5), sympathectomy non-applied group (SHAM; n = 8), and sympathectomy applied group (n = 8) before bilateral common carotid artery ligation. Permanent ligation of the prebifurcations of the common carotid arteries was performed to replicate stenoocclusive caroid artery disease. Basilar artery volumes were measured after ligation. Volumes of the basilar arteries were estimated by stereologic methods and compared between groups., Results: Luminal enlargement, wall thinning, elongation, convolutions, and doligoectatic configurations were detected in the majority of basilar arteries. The mean basilar arterial volume was 4.27 ± 0.22 mm3 in the baseline group; 5.28 ± 0.67 mm(3) in the SHAM group, and 8.84 ± 0.78 mm3 in the study group. The severity of basilar enlargement was significantly higher in the study group compared with the SHAM (p < 0.005) and baseline groups (p < 0.001)., Conclusions: Sympathectomy causes basilar artery enlargment, which is beneficial for maintaining cerebral blood flow; however, it also causes wall thinning, elongation, convolution, and aneurysm formation, which may be hazardous in stenoocclusive carotid artery disease. Sympathectomy can prevent new vessel formation and hyperthyrophic changes at the posterior circulation. Neovascularisation is not detected adequately in sympathectomised animals.