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Head and neck cancer (HNC) is the sixth most common malignancy worldwide. Although current modalities offer a wide variety of therapy choices, head and neck carcinoma has poor prognosis due to its diagnosis at later stages and development of resistance to current therapeutic tools. In the current study, we aimed at exploring the roles of miR-200c-3p during head and neck carcinogenesis and acquisition of taxol resistance. We analyzed miR-200c-3p levels in HNC clinical samples and cell lines using quantitative real-time polymerase chain reaction and evaluated the effects of differential miR-200c-3p expression on cancer-related cellular phenotypes using in-vitro tools. We identified and characterized a direct target of miR-200c-3p using in-silico tools, luciferase and various in-vitro assays. We investigated potential involvement of miR-200c-3p/SSFA2 axis in taxol resistance in-vitro. We found miR-200c-3p expression as significantly downregulated in both HNC tissues and cells compared to corresponding controls. Ectopic miR-200c-3p expression in HNC cells significantly inhibited cancer-related phenotypes such as viability, clonogenicity, migration, and invasion. We, then, identified SSFA2 as a direct target of miR-200c-3p and demonstrated that overexpression of SSFA2 induced malignant phenotypes in HNC cells. Furthermore, we found reduced miR-200c-3p expression in parallel with overexpression of SSFA2 in taxol resistant HNC cells compared to parental sensitive cells. Both involved in intracellular cytoskeleton remodeling, we found that SSFA2 works collaboratively with IP3R1 to modulate resistance to taxol in HNC cells. When considered collectively, our results showed that miR-200c-3p acts as a tumor suppressor microRNA and targets SSFA2/IP3R1 axis to sensitize HNC cells to taxol., Competing Interests: Declaration of competing interest Fatma SANLI, Arzu Tatar, and Betul Gundogdu declare that they have no conflict of interests. Omer Faruk Karatas holds stocks in EcoTech Biotechnology. The terms of this arrangement have been reviewed and approved by Erzurum Technical University in accordance with its policy on objectivity in research., (Copyright © 2024 Elsevier B.V. All rights reserved.)

Head and neck squamous cell carcinoma (HNSCC) is one of the most aggressive neoplasms, which requires more effective prevention and treatment modalities. Previous studies found that protein O-fucosyltransferase 1 (POFUT1) upregulation promotes carcinogenesis, although the potential roles, underlying molecular mechanisms, and biological implications of POFUT1 in HNSCC were not investigated. In this study, in silico analyses referred POFUT1 as a potential oncogene in HNSCC. Further analysis of tumor and normal tissue samples as well as HNSCC cells with quantitative real-time polymerase chain reaction, Western blot analysis, and immunohistochemistry showed significant overexpression of POFUT1 in HNSCC clinical tumor tissue specimens and cell lines compared to corresponding controls. In vitro investigations revealed that overexpression of POFUT1 promoted phenotypes associated with cancer aggressiveness and its knockdown in HNSCC cells suppressed those phenotypes. Further xenograft experiments demonstrated that POFUT1 is an oncogene in vivo for HNSCC. Immunohistochemical analysis with human clinical samples and cancer cell-dorsal root ganglion ex-vivo coculture model showed that deregulation of POFUT1 is involved in the perineural invasion of HNSCC cells. These results suggest POFUT1 expression as a potential prognostic marker for patients with head and neck cancer and highlight its potential as a target for HNSCC therapy, although more molecular clues are needed to better define the functions of POFUT1 related to HNSCC carcinogenesis., (© 2023 International Federation of Cell Biology.)

Head and neck squamous cell carcinoma (HNSCC) is the sixth most common malignant cancer type worldwide. Although the therapeutic modalities currently used for patients with HNSCC improved in recent decades, HNSCC prognosis is still poor. Therefore, it is an urgent necessity to understand the pathogenesis of HNSCC, to develop novel and effective treatment strategies, and to characterize and identify the oncogenes that are responsible for an aggressive HNSCC phenotype. In this study, we aimed to better understand the roles of miR-1825 in the pathogenesis of HNSCC. We examined the impacts of miR-1825 deregulation on the cancer-associated phenotypes using in vitro tests evaluating cell viability, clonogenicity, cell migration, invasion, apoptosis, and stem cell characteristics. In addition, we investigated the effects of miR-1825 overexpression on the tumor formation capacity of head and neck cancer cells in vivo using nude mice. We searched for potential targets of miR-1825 using microarray analysis and luciferase assay. We found that miR-1825 expression is upregulated in head and neck cells and clinical tumor samples in comparison to corresponding controls, where it potentially acts as an oncogene. We, then, showed that ectopic miR-1825 overexpression promotes cellular phenotypes related to head and neck cancer progression in vitro and has a stimulating potential on cancer formation in vivo. We also identified FREM1 as a direct target of miR-1825 and demonstrated its reduced expression in HNSCC samples using immunohistochemistry analysis. Collectively, we suggest that the miR-1825/FREM1 axis serves as an important mediator of HNSCC development, where miR-1825 acts as an oncogene., (© 2023 The Authors. Journal of Cellular Biochemistry published by Wiley Periodicals LLC.)

Background: Acrylamide causes hepatotoxicity with the effect of oxidative stress and inflammatory processes. Carvacrol is a monoterpenic phenol with antioxidant and anti-inflammatory properties. Aims: To determine the effects of carvacrol on oxidative liver injury induced by acrylamide administration in rats. Methods: Rats were divided into three groups of six animals each: healthy group acrylamide group (ACR), and acrylamide + carvacrol group (TACR). First, carvacrol (50 mg/kg) was administered intraperitoneally to the CACR group. One hour later, acrylamide (20 mg/kg) was given orally to the ACR and CACR groups. This procedure was performed for 30 days, after which the animals were sacrificed. The malondialdehyde (MDA) and total glutathione (tGSH) levels, total oxidant (TOS) and total antioxidant status (TAS), tumor necrosis factor-alpha (TNF-α), interleukin-1beta (IL-1β), and nuclear factor kappa b (NF-κB) were measured in the excised liver tissues. Alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels were determined in blood serum samples. Liver tissues were also examined histopathologically. Results: In the ACR group, malondialdehyde, TOS, ALT, AST levels, and NF-κB, IL-1β, and TNF-α levels were found to be high, and tGSH and total antioxidant status levels were low. In addition, diffuse degenerative changes and necrosis in hepatocytes, and moderate inflammation in the portal region were detected in the liver tissues of the ACR group. While carvacrol prevented the biochemical changes induced by acrylamide, it also alleviated the damage in the histological structure. Conclusion: Carvacrol may be used for liver damage caused by acrylamide., Competing Interests: The authors declare that the research was conducted in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest., (Copyright © 2023 Cerrah, Ozcicek, Gundogdu, Cicek, Coban, Suleyman, Altuner, Bulut and Suleyman.)

The aim of this study is to investigate the effect of metyrosine on ischemia-reperfusion (I/R) induced ovarian injury in rats in terms of biochemistry and histopathology. Rats were divided into: ovarian I/R (OIR), ovarian I/R+50 mg/kg metyrosine (OIRM) and sham (SG) operations. OIRM group received 50 mg/kg metyrosine one hour before the application of the anesthetic agent, OIR and SG group rats received equal amount of distilled water to be used as a solvent orally through cannula. Following the application of the anesthetic agent, ovaries of OIRM and OIR group rats were subjected to ischemia and reperfusion, each of which took two hours. This biochemical experiment findings revealed high levels of malondialdehyde (MDA) and cyclo-oxygenase-2 (COX-2) and low levels of total glutathione (tGSH), superoxide dismutase (SOD) and cyclo-oxygenase-1 (COX-1) in the ovarian tissue of OIR group, with significant histopathological injury. In metyrosine group, MDA and COX-2 levels were lower than the OIR group whereas tGSH, SOD and COX-1 levels were higher, with slighter histopathological injury. Our experimental findings indicate that metyrosine inhibits oxidative and pro-inflammatory damage associated with ovarian I/R in rats. These findings suggest that metyrosine could be useful in the treatment of ovarian injury associated with I/R.

Objectives: Diets and nutritional habits are critical during carcinogenic processes, where a diet poor in fruits and vegetables and rich in meat and other foods of animal origin facilitates carcinogenesis. In this study, we aimed at investigating the possible involvement of vitamin D deficiency (VDD) and high cholesterol (HC) together in oral squamous cell carcinoma (OSCC) through modulating glycolysis., Subjects and Methods: We compared total cholesterol, LDL, HDL, triglycerides, LDH, and vitamin D levels of OSCC patients and control individuals. We used GEO datasets for gene set enrichment and 4-nitroquinoline-1-oxide induced in vivo oral carcinogenesis models to investigate contribution of VDD and HC during carcinogenesis via possible modulation of glycolysis., Results: We found that VDD and HC co-exist in OSCC patients, and deregulation of cholesterol and vitamin D levels results in enrichment of genes related to glycolysis. We, then, demonstrated that VDD and HC on their own and together facilitated the formation of larger tumors in 4NQO-induced in vivo cancer models, which are suppressed by glycolysis inhibition., Conclusion: We reported collaborative contribution of HC and VDD during oral carcinogenesis, which is mainly carried out via altering energy metabolism in tumor cells., (© 2022 Wiley Periodicals LLC.)

Background: Cyclophosphamide is a drug used in various types of cancer. It can cause oxidative and inflammatory ovarian damage and infertility. Thiamine pyrophosphate (TPP) to be investigated for its effect on cyclophosphamide-induced ovarian damage and reproductive dysfunction in the present study is the active metabolite of thiamine. It has been shown that TPP protects organs and tissues from oxidative stress and proinflammatory cytokine damage., Objectives: To investigate the effect of TPP against the ovarian damage and reproductive dysfunction caused by cyclophosphamide in rats., Material and Methods: Albino Wistar type female rats were divided into healthy control (HG), cyclophosphamide (CYC) and TPP + cyclophosphamide (TPPC) groups (for each group, n = 12). Thiamine pyrophosphate at a dose of 25 mg/kg was injected intraperitoneally (ip.) in the TPPC group, and 0.9% NaCI solution was injected ip. in the CYC and HG groups. One hour after the injection, 75 mg/kg of cyclophosphamide was administered ip. in the TPPC and CYC groups. This procedure was repeated once a day for 30 days. At the end of this period, 6 rats from each group were euthanized with a high dose of anesthetic (50 mg/kg of sodium thiopental). Biochemical and histopathological examinations were performed on the extracted ovarian tissue. The remaining animals were kept in the laboratory with mature male rats for 2 months for reproduction., Results: Thiamine pyrophosphate significantly decreased the cyclophosphamide-induced increase in the levels of the oxidant parameter malondialdehyde (MDA), proinflammatory nuclear factor kappa B (NF-κB), tumor necrosis factor alpha (TNF-α), and interleukin 1 beta (IL-1β). In addition, TPP decreased the severe histopathological damage associated with cyclophosphamide in the ovarian tissue and prevented infertility., Conclusions: Our experimental results have suggested that TPP could be beneficial in the treatment of cyclophosphamide-induced ovarian injury and infertility.

Purpose: Development of chemoresistance is one of the major obstacles to the treatment of head and neck squamous cell carcinoma (HNSCC). The PI3K/Akt pathway, involved in drug resistance, has been found to be overactivated in > 90% of HNSCCs. Aberrant activation of the FGF receptors (FGFRs) has been reported to cause overactivation of the PI3K/Akt pathway and to be associated with the maintenance of stem cell features, which is controlled via SOX2 expression. In this study, we aimed at investigating the potential of using AZD4547, an orally bioavailable FGFR inhibitor, to overcome taxol-resistance by targeting the FGFR/Akt/SOX2 axis in HNSCC., Methods: We initially evaluated FGFR2 and SOX2 expression using in silico tools. We analyzed the FGFR/Akt/SOX2 axis in normal/tumor tissue pairs and in recombinant FGF2 treated HNSCC cells. Next, we explored the effects of AZD4547 alone and in combination with taxol on the proliferation, migration and colony forming capacities of parental/taxol-resistant cells using in vitro models., Results: We found that the p-FGFR, p-AKT, p-GSK-3β and SOX2 expression levels were higher in tumor tissues than in its corresponding normal tissues, and that AZD4547 effectively suppressed the expression of FGFR and its downstream targets in recombinant FGF2 treated HNSCC cells. We also found that AZD4547 diminished the viability, migration and colony forming capacity of HNSCC cells, and that co-treatment with taxol potentiated the impact of taxol on these cells. Finally, we found that AZD4547 inhibited the overexpressed FGFR/Akt/SOX2 axis and profoundly suppressed cancer-related phenotypes in taxol-resistant HNSCC cells., Conclusion: From our data we conclude that AZD4547 may increase the impact of taxol during HNSCC treatment. We suggest AZD4547 as a therapeutic agent to overcome taxol-resistance., (© 2021. Springer Nature Switzerland AG.)

Objectives: This study investigated the efficacy and complications of albendazole use after surgery in patients with pulmonary hydatid cysts., Methods: One hundred fifty-three consecutive patients who met the study criteria out of 215 patients who received prophylaxis with albendazole after surgery for isolated pulmonary hydatid cysts in our clinic between January 2011 and December 2020 were analysed retrospectively., Results: Eighty-six out of 153 (56.2%) of cases were male and 67 (43.8%) were female. The average age was 24.6 ± 17.4 (between 3 and 71 years), 76 of them (49.7%) were 18 years old and younger, while 77 (50.3%) were adults. All cases were approached transthoracically and a total of 170 operations were performed on the 153 cases. Fever, weakness and dizziness were reported in only one patient who was given albendazole treatment. A partial increase in liver enzymes was observed in 16 cases (10.5%) after albendazole treatment. Mild leukopoenia and neutropenia were observed in only one of the cases. In 1 case, a second operation was performed 30 months later due to recurrence. Albendazole treatment was not required to be discontinued in any of the cases. Mortality was not observed in any of the cases. Factors such as mean age, cyst size and hospitalization period did not have a statistically significant effect on any changes in liver enzymes tests following albendazole therapy (P > 0.05)., Conclusions: Albendazole treatment can safely be used for postoperative prophylaxis in patients with pulmonary hydatid cysts in a controlled manner without causing serious complications., Subj Collection: 152., (© The Author(s) 2021. Published by Oxford University Press on behalf of the European Association for Cardio-Thoracic Surgery.)

Purpose: Reactive oxygen species (ROS), interleukin-1β (IL-1β) and tumor necrosis factor-α (TNF-α) have been shown in the pathogenesis of acrylamide neurotoxicity. Hippophae rhamnoides L. extract (HRE) has a cytoprotective effect by stabilizing the production of ROS, IL-1β and TNF-α. The objective of the article was to investigate the effect of HRE on acrylamide-induced brain damage in rats biochemically and histopathologically., Methods: To the HRE+acrylamide only (ACR) group (n=6) of the animals, HRE was administered orally at a dose of 50 mg / kg into the stomach by gavage. The same volume of solvent (olive oil) was administered orally to the ACR (n=6) and healthy (HG) (n=6) groups. One hour after HRE administration, acrylamide was given orally at a dose of 20 mg/kg to HRE+ACR and ACR groups in the same way. This procedure was repeated once a day for 30 days. At the end of this period, brain tissues extracted from animals killed with 50 mg/kg thiopental anesthesia were examined biochemically and histopathologically., Results: It has been shown that HRE prevents the increase of malondialdehyde (MDA), myeloperoxidase (MPO), IL-1β and TNF-α with acrylamide and the decrease of total glutathione (tGSH) and glutathione reductase (GSHRd) levels in brain tissue., Conclusions: HRE may be useful in the treatment of acrylamide-induced neurotoxicity.

Objective: In this study, we aimed to compare the results of patients who underwent surgery by thoracotomy and Video-assisted thoracoscopic surgery (VATS) in mediastinal neurogenic tumors., Materials and Methods: Twenty-six consecutive cases (12 males and 14 females; mean age 39.4 ± 22.3 years; range 1-72 years) who were histopathologically diagnosed as having mediastinal neurogenic tumors between January 2000 and August 2020 were included in a single-center, retrospective study., Results: There were 5 (19.2%) children and 21 (80.8%) adults. Lesions in all cases were located in the posterior mediastinum. Schwannoma was detected histopathologically in 18 cases (69.2%), and all of these cases were adult patients. Resection was performed by thoracotomy in 14 cases (7 right and 7 left) and 12 cases by thoracoscopy (7 right and 5 left). The mean tumor size was 7.4 ± 1.9 cm (range 5-12 cm) in the thoracotomy group and 4.3 ± 1.9 cm (range 2-7 cm) in the VATS group (P = .001). Mean operative time was 101.7 ± 27.8 min (range 70-150 min) in the thoracotomy group and 77.9 ± 24.3 min (range 60-150 min) in the VATS group (P = .014). Mean postoperative hospital stay was 7.4 ± 4.0 days (range 3-20 days) in the thoracotomy group and 4.7 ± 1.7 days (range 2-7 days) in the VATS group (P = .040)., Conclusion: Most of the mediastinal neurogenic tumors are benign and surgical resection is required in their treatment. With increasing experience, resection can be performed thoracoscopically in most cases.

Aziz Sancar, Nobel Prize winning Turkish scientist, made several discoveries which had a major impact on molecular sciences, particularly disciplines that focus on carcinogenesis and cancer treatment, including molecular pathology. Cloning the photolyase gene, which was the initial step of his work on DNA repair mechanisms, discovery of the "Maxicell" method, explanation of the mechanism of nucleotide excision repair and transcription-coupled repair, discovery of "molecular matchmakers", and mapping human excision repair genes at single nucleotide resolution constitute his major research topics. Moreover, Sancar discovered the cryptochromes, the clock genes in humans, in 1998, and this discovery led to substantial progress in the understanding of the circadian clock and the introduction of the concept of "chrono-chemoterapy" for more effective therapy in cancer patients. This review focuses on Aziz Sancar's scientific studies and their reflections on molecular pathology of neoplastic diseases. While providing a new perspective for researchers working in the field of pathology and molecular pathology, this review is also an evidence of how basic sciences and clinical sciences complete each other.

Background: Multinucleated giant cell (MGC) present in a variety of non-neoplastic and neoplastic lesions of the thyroid on cytology samples. We aimed to investigate whether certain MGC features that can help us in routine cytopathology practice., Method: One hundred and thirty seven cases thyroid fine-needle aspiration material, which was diagnosed as indeterminate or malignant according to the Bethesda categorization, were reviewed. All cytomorphological features of the MGCs were documented. These features correlated with Bethesda categories and the final diagnosis of the subsequent surgical specimen., Results: The presence of the MGCs was identified in 42% of the samples (58 cases-total 236 MGCs). Eighty eight of them (37%) had dense cytoplasm, 148 of them had foamy cytoplasm. The mean number of dense and foamy MGC per case was higher in the malignant category (3.2 for dense MGC and 6 for foamy MGC per case). All dense MGCs were found to be in patients with papillary thyroid carcinoma (PTC). Remarkably, follicular patterned lesions had less often dense MGC compared to papillary patterned lesions (16.6% and 46.8% respectively). We detected a nuclear irregularity in 49 dense MGC (55%), groove-like features in 24 dense MGC (27.2%), and presence of some material/cell in 8 dense MGC (9%)., Conclusion: The presence of dense MGC is an important finding for guiding accurate Bethesda categorization, especially in indeterminate and malignant categories. Besides, the presence of some material or cell in MGCs cytoplasm can be an important indicator for the prognosis of the PTC cases., (© 2020 Wiley Periodicals LLC.)

Objective  The aim of our study was to evaluate the effect of two different doses of lycopene, an antioxidant, on experimentally induced ovarian ischemia/reperfusion (IR) injury in rat model. Materials and Methods  Twenty-four female rats were randomly divided into four groups: sham operation (group 1), 3-hour ischemia, 3-hour reperfusion (IR) (group 2), and IR + 100 mg/kg lycopene (PO) (group 3), IR + 200 mg/kg of lycopene (group 4). The rats' superoxide dismutase (SOD), myeloperoxidase (MPO) activities, malondialdehyde (MDA), and glutathione (GSH) levels were calculated. Ovarian tissue damage was assessed using a histopathological scoring system. Results  Serum parameter levels and histological scores showed that treatment with lycopene may be conservative approach to prevent IR injury after the ovarian detorsion procedure.The improvement with lycopene was higher at 200 mg than at 100 mg. The MPO and MDA values were significantly lower in groups 3 and 4 as compared with group 2 ( p < 0.05), whereas the MPO and MDA values were lower in group 4 as compared with group 3.The SOD and GSH values were significantly higher in groups 3 and 4 as compared with group 2 ( p < 0.05), whereas the SOD and GSH values were higher in group 4 as compared with group 3.Tissue damage scores were elevated in the IR group compared with the sham group, but the treatment with different lycopene doses after reperfusion improved the histopathological tissue damage scores. Conclusion  The results showed that lycopene treatment reduced ovarian IR damage. Antioxidant activity was found to increase in a dose-dependent manner. Lycopene treatment may be conservative approach for ovarian torsion patients after the detorsion procedure to prevent IR damage., Competing Interests: Author ContributionEthics Committee ApprovalConflict of Interest P. T. Y. contributed to data collection/management and protocol/project development. H. U. contributed to manuscript writing/editing and data analysis. B. G. contributed to data analysis. E. P. contributed to protocol/project development. S. A. contributed to protocol/project development. Y E. T. contributed to data collection/management. Z. H. contributed to data analysis and protocol/project development. Ethics committee approval was received for this study from the ethics committee of Ataturk University. Animals were treated in accordance with the Guide for the Care and Use of Laboratory Animals (8th Edition, National Academies Press). No conflict of interest was declared by the authors.

Background and Objective: Metformin (MET) has been used as an antidiabetic agent for type II diabetes. At the same time, recent researches have shown that the clinical improvement of MET is useful for nerve damage. In this study, we investigated the analgesic effect of MET in paclitaxel (PAC)-induced neuropathic pain., Materials and Methods: Forty-two adult, female rats, Wistar strain weighing 220 ± 10 g were randomly divided into 5 experimental groups. PAC was intraperitoneally (IP) administered (2.0 mg/kg) for 4 groups every other day (0, 2, 4, and 6 days). By the 30 th day, MET (100, 200, and 400 mg/kg) was administered to 4 groups. Before and after treatment, basal pain threshold values were measured with Randall-Selitto analgesiometer test. At the end of experiment, pathological values were measured in selected regions including brain (motor cortex, M1), spinal cord (L4-L5), sciatic nerve, and muscle., Results: According to our results, PAC-induced neuropathic pain reached to highest level at 14 th day. Four hundred milligram/kilogram concentration of MET remarkably decreased PAC-induced neuropathic pain. On the other hand, pathologic features have shown that PAC had significant pathological change in the brain and spinal cord while in the peripheral nerves and muscles had not shown any pathological change., Conclusion: The pathological results of the current study for the first time demonstrated that MET beside of its antidiabetic effects reversed neuropathic pain induced by PAC. Consequently, this research can be promising for cancer patients that suffering from neuropathic pain induced by anticancer drugs., Competing Interests: None

Purpose: Cancer is the leading cause of death in economically developed countries and the second leading cause of death in developing countries. The relationship between genetic polymorphisms and cancer risk has been extensively researched. In the present study, we evaluated the association between polymorphisms in two DNA repair genes, ERCC2 Lys751Gln (rs13181) and XRCC2 Arg188His (rs3218536) and the risk of colorectal, stomach, HCC, prostate and lung cancer., Methods: This study was planned by the Medical Biology Unit and Department of Internal Medicine, Pathology and Surgical Medicine Sciences of Ataturk University. A total of 40 colon cancer, 40 gastric cancer, 40 hepatocellular carcinoma (HCC), 40 prostate cancer, and 40 lung cancer patients and 40 healthy individuals over 18 years of age were enrolled in the study (Controls). All patients and healthy subjects underwent ERCC2 Lys751Gln rs13181 and XRCC2 Arg188His rs3218536 genotyping. After collection of 10 ml venous blood from the patients, DNA was isolated and single nucleotide polymorphism (SNP) analysis was performed using Roche 480 Real-Time PCR device. Results were analyzed using SPSS version 23.0 software., Results: There were statistically significant differences in ERCC2 Lys751Gln rs13181 polymorphism variants GG colon and GT in the colon control and GG,TTprostate cancer groups when compared with the control group.. GG variant of XRCC2 Arg188 rs3218536 was higher in the gastric patient group. AG variant of XRCC2 Arg188 rs3218536 was higher in gastric control group Conclusion: The results of the present study demonstrate that ERC22 Lys751Gln polymorphisms may be associated with the development of colon and prostate cancers in the Turkish population. This was a small-scale study, and the results should be corroborated with further research including larger groups of patients with each cancer type and more healthy controls.

Background: Although posttraumatic mesenteric artery ischemia is attributed to various etiologies, sacral parasympathetic network/mesenteric artery relations have not been studied so far. The primary objective of this study is to elucidate whether there is a relationship between Onuf's nucleus ischemia and mesenteric artery vasospasm following subarachnoid hemorrhage (SAH)., Methods: This study was conducted on 22 rabbits. The animals were grouped as follows: 5 of animals control, 5 SHAM which saline was given, and 12 animals study group that was homologous blood injected into the spinal subarachnoid space at the Lı level. Neurodegeneration in Onuf's nucleus, axonal degeneration of S2 roots, and mesenteric arteries vasospasm indexes (VSI; Wall surface/Lumen surface), brachias of mesentery arteries in various tissues and ischemic mucosal changes of intestines of all animals were determined histopathologically. Important degenerative changes were detected in axons in S2 roots and Onuf's nucleus in severe mesenteric artery vasospasm observed., Results: The mean degenerated neuron density of Onuf's nucleus (n/mm 3 ), degenerated axon density in S2 roots (n/mm 2 ), and VSI values of mesenteric arteries of control, SHAM, and study groups were estimated as 5.00 ± 1.58, 4.00 ± 1.58, 1.76 ± 0.13; 18.29 ± 4.31, 11.00 ± 2.24, 2.23 ± 0.20; and 135.21 ± 30.75, 117.33 ± 22.11, 2.81 ± 0.44, respectively. Statistical analyses between the VSI values, mucosal ischemic changes degenerated neurons in Onuf's nucleus, and axons in S2 levels were meaningful (p < 0.005)., Conclusion: We interestingly noticed that Onuf's nucleus-S2 roots complex degeneration plays an important role in mesenteric artery vasospasm and the development of intestinal ischemic mucosal changes following SAH which has not been extensively mentioned in the literature., (Copyright © 2019. Published by Elsevier Taiwan LLC.)

Background: The relationship between superior cervical ganglia (SCG) ischemia due to bilateral common carotid artery ligation (BCCAL) and basilar artery (BA) reconfiguration was investigated., Methods: Twenty-three rabbits were randomly divided into 3 groups: group III rabbits underwent BCCAL (n = 13), group II rabbits were sham-operated controls (n = 5), and group I rabbits did not undergo surgery (n = 5). Degenerated neuron densities (DND) within the SCG were correlated with the BA vasodilatation index (VDI)., Results: Mean live and DND in SCG of group I rabbits were 11.235 ± 982/μm 3 and 11 ± 3/μm 3 , respectively, with a mean heart rate of 294 ± 21 beats/min. Mean SCG DND and heart rates were 213 ± 42/μm 3 and 242 ± 17 beats/min for the sham group (group II) rabbits and 1743 ± 285/μm 3 and 199 ± 19 beats/min for the study group (group III) rabbits, respectively. The BA VDI values in the sham group (group II) (1.32 ± 0.10) and the study group (group III) (0.976 ± 0.112) significantly differed from those in the control group (group I) (1.65 ± 0.12; P < 0.005) versus the sham group (group II) (P < 0.0001) versus the BCCAL applied group (group III) and between group II and group III (P < 0.005)., Conclusions: A meaningful and paradoxic correlation was detected between the BA VDI values and degenerated neuron density of SCG after BCCAL. Although a low degenerated neuron density within SCG may provoke excessive sympathetic activity and prevent excessive BA dilatation with steno-occlusive carotid artery diseases, a high degenerated neuron density may cause dangerous vasodilatation of BA., (Copyright © 2019 Elsevier Inc. All rights reserved.)

Stroke remains among the leading causes of disability and death worldwide. Fibrinolytic therapy is associated with poor patency and functional outcomes. Recently, multiple randomized trials have been published that have consolidated the role of endovascular therapy for ischemic stroke due to large vessel occlusion in the anterior cerebral circulation. This manuscript reviews the current understanding of the endovascular management of acute stroke including technical aspects and current evidence base., (Copyright © 2018. Published by Elsevier Inc.)

Sepsis is a life-threatening organ dysfunction condition response resulting in acute lung injury. Urotensin II (UII), an endogenous vasoactive peptide, is widely distributed in pulmonary, cardiovascular, central nervous, renal and metabolic systems, and especially in inflammatory regions. This study aimed to investigate whether urotensin II (UII) and UII receptor (UTR) antagonists play a role in the inflammatory response to sepsis-induced lung damage and they are possible therapeutic targets. In the study, 78 male Balb-c mice were used. A cecal ligation and puncture (CLP)-induced polymicrobial sepsis model was applied, and the effects of human urotensin II (agonist) and urantide and palosuran (antagonists) were investigated on lung tissues. Glutathione and malondialdehyde levels and SOD activity of lung tissues were investigated in addition to TNF-α, IL-1β, IL-6, NF-κB, and UTR mRNA levels. Also, lung sections were histopathologically evaluated. Urantide and palosuran, UII receptor antagonists, decreased proinflammatory cytokines such as TNF-α, IL-1β, IL-6, NF-κB, and also decreased oxidative stress parameters in lung tissue, which are markers of damage. UTR mRNA expression was increased in septic lungs, and both antagonists significantly decreased the elevated receptor level. Also, histopathological examination showed beneficial effects of both agonists on lung tissue. The results of this study help to understand the inflammatory and therapeutic contribution of the UII/UTR system on sepsis-induced lung damage. We can suggest that UTR receptor antagonists may be evaluated as a potential drug which reduces sepsis-induced lung damage in the future.

Objectives: To evaluate the safety and efficacy of percutaneous device closure of patent foramen ovale (PFO) for secondary prevention of ischemic stroke BACKGROUND: Stroke remains the leading cause of serious long-term disability in the United States. The effectiveness of a percutaneous PFO closure in the prevention of recurrent cryptogenic strokes has not been established., Methods: We performed a literature search using PubMed, EMBASE, Cochrane Central Register of Controlled Trials, Google Scholar, and Internet-based sources from January 2003 to September 2017. Randomized controlled trails (RCTs) comparing percutaneous PFO closure to medical therapy alone., Results: Five RCTs (CLOSURE I, PC Trial, REDUCE, RESPECT, and CLOSE) with 1,829 patients in the device group and 1,611 patients in the medical group met inclusion criteria. The cumulative incidence of recurrent stroke was 2.02% in the PFO closure arm and 4.4% in the medical therapy group (RR 0.42, 95%CI 0.20, 0.91; P = 0.03). There was no difference in the incidence of death [0.7% vs. 0.9%; RR 0.76 (95% CI 0.35, 1.64), P = 0.49] or adverse events during the follow-up period [24.6% vs. 23.7% (RR 1.03; 95% CI 0.91, 1.16), P = 0.65] between the closure and medical therapy groups. Incidence of atrial fibrillation was significantly higher in closure group compared to medical therapy [4% vs. 0.6% (RR 4.73; 95% CI 2.09, 10.70), P = 0.0002]. The comparative effectiveness of PFO closure (compared to medical therapy) was significantly more pronounced in those younger than 45 years, males, larger shunts and disc design platforms (P < 0.05)., Conclusions: Based on the results of this analysis of randomized trial data, percutaneous PFO closure appears to be a safe and effective therapeutic option for the secondary prevention of ischemic stroke in patients with PFO and cryptogenic stroke., (© 2018 Wiley Periodicals, Inc.)

Aim: The present study was designed to evaluate the effects of irinotecan hydrochloride (IRI)- or metformin hydrochloride (MET)-loaded poly-lactic-co-glycolic acid (PLGA) nanoparticles (NPs) for the treatment of glioblastoma multiforme using in vitro neuron and U-87 MG glioblastoma cell cultures and in vivo animal model., Methods: The cytotoxic and neurotoxic effects of pure drugs, blank NPs and MET- and IRI-loaded PLGA NPs were investigated in vitro (using methylthiazolyldiphenyl-tetrazolium bromide assay) and in vivo (using Cavalieri's principle for estimation of cancer volume)., Results: 1 and 2 mM doses of MET and MET-loaded PLGA NPs, respectively, significantly reduced the volume of extracted cancer., Conclusion: Consequently, MET- and IRI-loaded PLGA NPs may be a promising approach for the treatment of glioblastoma multiforme.

Objective: Alveolar echinococcosis (AE) is a rare life-threatening parasitic infection. Computed tomography perfusion (CTP) imaging has the potential to provide both quantitative and qualitative information about the tissue perfusion characteristics. The purpose of this study was the examination of the characteristic features and feasibility of CTP in AE liver lesions., Material and Methods: CTP scanning was performed in 25 patients who had a total of 35 lesions identified as AE of the liver. Blood flow (BF), blood volume (BV), portal venous perfusion (PVP), arterial liver perfusion (ALP), and hepatic perfusion indexes (HPI) were computed for background liver parenchyma and each AE lesion., Results: Significant differences were detected between perfusion values of the AE lesions and background liver tissue. The BV, BF, ALP, and PVP values for all components of the AE liver lesions were significantly lower than the normal liver parenchyma (p<0.01)., Conclusions: We suggest that perfusion imaging can be used in AE of the liver. Thus, the quantitative knowledge of perfusion parameters are obtained via CT perfusion imaging., Competing Interests: Conflict of Interest: No conflict of interest was declared by the authors.

Aim: Neurogenic pulmonary edema (NPE) is the most serious complication of subarachnoid hemorrhage (SAH). As vagal nerves have vital roles in lung functions, vagal ischemia may have a causative role in the pathogenesis of NPE. We examined whether there was a relationship between vagal complex ischemia and lung immune complexes occupying the lymph node infarct in SAH., Material and Methods: Thirty-two rabbits were divided into three groups: Control (n=5), SHAM (n=5) and SAH group (n=22). SAH was created by autologous blood injection into the cisterna magna and followed-up for 3 weeks. Vasospasm index (VSI) was defined as the ratio of the lung lymph node arteries (LLNA) wall section (wall ring) surface to the lumen surface. Degenerated axon numbers of vagal nerves, neuron densities of the nodose ganglion (NG) and VSIs of LLNA were compared for all groups., Results: The mean degenerated vagal nerve axon density, neuron density of NG, and VSI of LLNA were 26±8/mm < sup > 2 < /sup > , 30±5/mm < sup > 3 < /sup > , and 0.777±0.048 in the control group; 1300±100/mm2, 720±90/mm < sup > 3 < /sup > , and 1.148±0.090 in the animals with slight vasospasm (n=12); and 7300±530/mm < sup > 2 < /sup > , 5610±810/mm3, and 1.500±0.120 in the animals with severe vasospasm (n=10), respectively., Conclusion: Degenerated vagal axon and NG neuron density may be a causative factor in the development of LLNA vasospasm induced lymph node infarct in SAH. Lung lymph node infarct may be an important factor in the prognosis of NPE.

Context: Sudden death from subarachnoid hemorrhage (SAH) is not uncommon., Aims: The goal of this study is to elucidate the effect of the cervical spinal roots and the related dorsal root ganglions (DRGs) on cardiorespiratory arrest following SAH., Settings and Design: This was an experimental study conducted on rabbits., Materials and Methods: This study was conducted on 22 rabbits which were randomly divided into three groups: control ( n = 5), physiologic serum saline (SS; n = 6), SAH groups ( n = 11). Experimental SAH was performed. Seven of 11 rabbits with SAH died within the first 2 weeks. After 20 days, other animals were sacrificed. The anterior spinal arteries, arteriae nervorum of cervical nerve roots (C6-C8), DRGs, and lungs were histopathologically examined and estimated stereologically., Statistical Analysis Used: Statistical analysis was performed using the PASW Statistics 18.0 for Windows (SPSS Inc., Chicago, Illinois, USA). Intergroup differences were assessed using a one-way ANOVA. The statistical significance was set at P < 0.05., Results: In the SAH group, histopathologically, severe anterior spinal artery (ASA) and arteriae nervorum vasospasm, axonal and neuronal degeneration, and neuronal apoptosis were observed. Vasospasm of ASA did not occur in the SS and control groups. There was a statistically significant increase in the degenerated neuron density in the SAH group as compared to the control and SS groups ( P < 0.05). Cardiorespiratory disturbances, arrest, and lung edema more commonly developed in animals in the SAH group., Conclusion: We noticed interestingly that C6-C8 DRG degenerations were secondary to the vasospasm of ASA, following SAH. Cardiorespiratory disturbances or arrest can be explained with these mechanisms., Competing Interests: There are no conflicts of interest.

Background: Photophobia is defined as a painful psychosomatic discomfort triggered by intense light flow through the pupils to the brain, but the exact mechanism through which photophobia is induced by subarachnoid hemorrhage (SAH) is not well understood. In this study, we aimed to investigate whether there was any relationship between the mydriasis induced by the degeneration of the ciliary ganglion (CG) and photophobia in instances of SAH., Materials and Methods: Five of a total of 25 rabbits were used as the intact control group; five were used in the sham-operated control group; and the remaining 15 were used as the SAH group, which was created by injecting autologous blood into their cisterna magna. All animals were examined daily for 20days to evaluate their level of photophobia, after which their brains, CGs and superior cervical ganglia (SCGs) were extracted bilaterally. The densities of normal and degenerated neurons in these ganglia were examined by stereological methods., Results: In SAH animals with a high photophobia score, the mean pupil diameter and density of degenerated neurons density in the CG were greater than in cases with a low photophobia score (p<0.05). Further analysis revealed that the increase in the density of degenerated neurons in the CG following SAH resulted in the paralysis of the parasympathetic pathway of the pupillary muscles and mydriasis, which facilitates the excessive transfer of light to the brain and photophobia., Conclusion: Our findings indicate that SAH results in a high density of degenerated neurons in the CG, which induces mydriasis and is an important factor in the onset of photophobia. This phenomenon is likely due to more light energy being transferred through mydriatic pupils to the brain, resulting in vasospasm of the supplying arteries., (Copyright © 2016 Elsevier Ireland Ltd. All rights reserved.)

Background: Cardiac arrest is a major life-threatening complication of subarachnoid hemorrhage (SAH). Although medullary cardiocirculatuar center injury and central sympathetic overactivity have been suspected of initiating coronary artery spasm-induced cardiac arrest, we aimed to elucidate the effects of vagal ischemia at the brainstem on coronary vasospasm and sudden death in SAH., Methods: Twenty-six rabbits were randomly divided into 3 groups. Control (n = 5); SHAM (n = 8), and SAH group (n = 13). Experimental SAH was applied by injecting homologous blood into the cisterna magna, and the SHAM group was injected with isotonic saline solution also in the cisterna magna., Twenty-one days after the injection, histopathologic changes of the neuron density of nodose ganglia, the vasospasm index values of the coronary arteries, and the electrocardiographic events were analyzed., Results: Increased vasospasm index of the coronary arteries and degenerated neuron density of nodose ganglion were significantly different between animals with SAH, control, and SHAM groups (P < 0.005). If neurons of the nodose ganglia are lesioned due to ischemic insult during SAH, the heart rhythm regulation by vagus afferent reflexes is disturbed., Conclusions: We found that there is causal relationship between nodose ganglion degeneration and coronary vasospasm. Our finding could be the reason that many cardiac events occur in patients with SAH. Vagal pathway paralysis induced by indirect sympathetic overactivity may trigger coronary vasospasm and heart rhythm disturbances. Our findings will aid in the planning of future experimental studies and in determining the clinical relevance of such studies., (Copyright © 2016 Elsevier Inc. All rights reserved.)

Background: Increasing sinus pneumatization and the accompanying alveolar bone resorption complicate dental implant placement. This problem can be overcome today by raising the maxillary sinus floor with graft materials. Bisphosphonates are commonly used to accelerate the recovery of the graft materials and to prevent resorption., Objectives: The purpose of this study is to investigate whether systemic administration of a bisphosphonate (alendronate) would improve new bone formation and reduce fibrous tissue formation over a 6-week follow-up in rabbits treated with two different grafting materials for maxillary sinus floor augmentation., Materials and Methods: This experimental animal study was conducted at the Experimental Medical Application and Research Center at Erzurum/ Turkey. Twelve New Zealand rabbits, each weighing between 2.7 and 3.3 kg, were used. Twenty-four maxillary sinus floor elevation operations were performed, two on each animal (n = 24). Each elevation was repaired with either deproteinized bovine bone (xenograft) or autogenous bone graft obtained from the iliac crest. Both groups were divided into 2 subgroups: saline-treated and alendronate-treated. All groups underwent the same surgical procedures and evaluation, and were sacrificed at the 6th postoperative week. Sinuses augmented with deproteinized bovine bone (xenograft) and autogenous bone graft were examined histopathologically and histomorphometrically., Results: At 6 weeks, the bone area was significantly larger in the Xenograft-Alendronate group (33.0% ± 5.0%) than in the Xenograft-Saline group (20.8% ± 4.9%) and the bone area was significantly larger in the Autogenous-Alendronate group (43.3% ± 3.8%) than in the Autogenous-Saline group (37.5% ± 6.6%) (P = 0.001). The histomorphometric and histopathological results consistently showed that alendronate stimulated bone formation and reduced fibrous tissue formation in maxillary sinus augmentation grafts, especially in the deproteinized bovine bone group (xenograft)., Conclusions: Alendronate may be considered a therapeutic option for improving the bone formation process and reducing resorption in different bone grafting procedures. Further detailed studies should focus on dosage and time-dependent effects of alendronate on bone remodeling.

Objectives: This study sought to evaluate the safety and efficacy of stent retriever for the management of acute ischemic stroke., Background: Stroke is the third leading cause of death and the most common cause of disability in the United States. Early reperfusion has been associated with favorable outcomes. Stent retrievers are novel endovascular devices that provide vessel recanalization via thrombus retrieval mechanical thrombectomy., Methods: The authors performed a literature search using PubMed, EMBASE, and Cochrane Central Register of Controlled Trials from May 2005 to May 2015. Randomized controlled trails (RCTs) comparing endovascular therapy (ET) with the use of retrievable stents against standard therapy (ST) for the management of acute stroke were included., Results: Five RCTs (the MR CLEAN, ESCAPE, EXTEND-IA, SWIFT-PRIME, and REVASCAT studies) with 634 patients in the ET group and 653 patients in the ST group met inclusion criteria. The frequency of a low 90-day modified Rankin Score (0 to 2) in the intervention group was 42.6% compared with 26.1% in the control group (odds ratio: 2.43; 95% confidence interval [CI]: 1.9 to 3.09; p < 0.0001). The frequency of intracranial bleeding was 4.2% in the ET group compared with 4.3% in the ST group (risk ratio: 1.08; 95% CI: 0.64 to 1.82; p = 0.78). 90-day mortality was 15.1% in the ET group compared with 18.7% in the ST group (risk ratio: 0.81; 95% CI: 0.58 to 1.12; p = 0.19). There was no evidence of significant heterogeneity or publication bias for any of the endpoints., Conclusions: On the basis of the results of this meta-analysis of RCTs, ET with stent retrievers appears as a safe and effective therapeutic option for acute ischemic stroke due to large vessel occlusion., (Copyright © 2015 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.)

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.

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.

Alveolar echinococcosis (AE) is a chronic progressive infestation inducing a slowly progressing, life-threatening tumor-like growth in the liver. It may spread to other organs by regional extension or hematogenous or lymphatic metastasis. Herein, we report a fifteen-year-old patient diagnosed with AE of the liver and simultaneous lung and brain metastasis with a literature review.

Our objective was to compare and contrast clinical features of black and white patients seen in the UAMS ALS/Motor Neuron Disease (MND) clinic from January 2001 to December 2010. Death certificate information was reviewed to determine race of Arkansans who died of ALS/MND between 1999 and 2006. We used a retrospective chart review of patients with ALS/MND seen at least once in our clinic and reviewed state death certificate data. Results showed that from 1999 to 2006, 466 Arkansas deaths were attributed (immediate or contributory) to ALS/MND; 17 (3.6%) were black, four (0.9%) other, and 445 (95.5%) white. During this period, the proportion of black Arkansans was 17%. From 2001 to 2010, we saw 330 patients with ALS/MND: 30 (9.1%) black, six (1.8%) other, 294 (89.1%) white. Average onset age for whites was 58.1 + 12.4 years, for blacks 52.8 + 13.0 (p = 0.038). Gender, onset site, time from symptom onset to first clinic visit and initial vital capacity were similar between the groups. Initial ALSFRS-R was 37.5 + 7.2 for whites and 30.8 + 8.5 (p = 0.004) for blacks. A first or second degree relative with ALS/MND was reported by 8.1% of whites and by none of the black patients (p = 0.15). Riluzole, PEG and non-invasive ventilation use was similar between the groups. Median tracheostomy-free survival was 36 months for white and 40 months for black patients (p = 0.475). In conclusion, although blacks appear relatively spared from ALS/MND, they present at an earlier age and are functionally worse at their first visit. Investigating the genetic make-up of blacks with the disease may help identify genes that modify risk of developing ALS/MND.

Central pontine myelinolysis is a demyelinating disorder characterized by the loss of myelin in the center of the basis pontis usually caused by rapid correction of chronic hyponatremia. The clinical features vary depending on the extent of involvement. Demyelination can occur outside the pons as well and diagnosis can be challenging if both pontine and extrapontine areas are involved. We herein report a case of myelinolysis involving pons, lateral geniculate bodies, subependymal region, and spinal cord. To the best of our knowledge, this case represents the second case of spinal cord involvement in osmotic demyelination syndrome and the first case of involvement of thoracic region of spinal cord.

Background: Owing to the variability of histopathological features and biological behaviour in gastric carcinoma, a great number of categorisation methods such as classical histopathologic grading, Lauren classification, the TNM staging system and the newly presented Goseki grading method are used by pathologists and other scientists. In our study, we aimed to investigate whether Goseki grade and tumour location have an effects on survival of gastric cancer cases., Materials and Methods: Eighty-four patients with gastric adenocarcinoma were covered in the investigation. The importance of Goseki grading system and tumour location were analysed in addition to the TNM staging and other conventional prognostic parameters., Results: The median survival time in our patients was 35 months (minimum: 5, maximum: 116). According to our findings, there was no relation between survival and tumour size (p=0.192) or classical histological type (p=0.270). In contrast, the Goseki grade and tumour location significantly correlated with survival (p=0.007 and p<0.001, respectively). Additionally, tumours of the intestinal type had a longer median survival time (60.0 months) than diffuse tumours (24.0 months)., Conclusions: In addition to the TNM staging system, tumour location and the Goseki grading system may be used as significant prognostic parameters in patients with gastric cancer.

Background: Controversy persists regarding the management of patients with cryptogenic stroke and patent foramen ovale (PFO). We performed a meta-analysis of randomized controlled trials comparing PFO closure with medical therapy., Methods and Results: A prospective protocol was developed and registered using the following data sources: PubMed, Cochrane Register of Controlled Trials, conference proceedings, and Internet-based resources of clinical trials. Primary analyses were performed using the intention-to-treat method. Three randomized trials comparing percutaneous PFO closure vs. medical therapy for secondary prevention of embolic neurological events formed the data set. Baseline characteristics were similar. During long-term follow-up, the pooled incidence of the primary endpoint (composite of stroke, death, or fatal stroke) was 3.4% in the PFO closure arm and 4.8% in the medical therapy group [risk-reduction (RR) 0.7 (0.48-1.06); p=0.09]. The incidence of recurrent neurological events (secondary endpoint) was 1.7% for PFO closure and 2.7% for medical therapy [RR 0.66 (0.35-1.24), p=0.19]. There was no difference in terms of death or adverse events between the two groups., Conclusions: While this meta-analysis of randomized clinical trials demonstrated no statistical significance in comparison to medical therapy, there was a trend towards overall improvement in outcomes in the PFO closure group., (© 2013.)

Despite recent advancements in the treatment of coronary artery disease (CAD), it remains the commonest cause of death in the world. Although traditional risk factors partially account for the development of CAD, other novel risk factors have recently been implicated. Specifically, chronic inflammation has been postulated to play a role in the development and propagation of this disease. The purpose of this review is to examine the available evidence to determine if patients with chronic inflammatory muscle diseases have higher rates of cardiovascular disease.

Morvan syndrome is characterized by central, autonomic, and peripheral hyperactivity. Examples of central hyperactivity include confusion, memory problems, hallucinations, insomnia, and myoclonus; examples of autonomic hyperactivity include hyperhidrosis and fluctuations in blood pressure; examples of peripheral hyperreactivity include clinical or electrophysiological evidence of painful cramps, myokymia, and neuromyotonia. We present a typical case of Morvan syndrome and the first detailed review of the clinical and therapeutic literature of all 27 cases from the English language literature. Morvan syndrome is considered to be an autoimmune disorder and antibodies against voltage-gated potassium channels are found in most cases. Oral immunomodulatory therapy, intravenous immunoglobulin, and plasmapharesis may be entertained. Thymoma is found in approximately 50% of cases and thymectomy may be curative as in our particular case.

Prominent acral mutilating ulcers can be present in sensorimotor neuropathies. Although diabetes mellitus is the most common cause of neuropathic ulcers, these skin lesions may manifest in nondiabetic neuropathies. The dermatologic abnormalities may even precede the onset of typical neuropathic symptoms, leading to diagnostic confusion. Therefore, a broad differential diagnosis of neurological and systemic disorders should be considered when evaluating patients who have acral skin ulcerations. We report 3 cases of mutilating ulcers associated with nondiabetic neuropathies. The first case is a woman with multiple ulcerations on her forearm, hands, and toes. Her nerve biopsy revealed neuropathy with multiple congophilic deposits consistent with amyloid neuropathy. The second case is a woman with necrotic painless ulcer on her heel. Nerve biopsy in this patient revealed features suggestive of vasculitic neuropathy. The third case is a man with multiple ulcers on his extremities. A sural nerve biopsy in this patient was consistent with leprous neuropathy.

The objective of this study was to assess the short-term efficacy and safety of terbutaline, a beta2-adrenergic agonist, in patients with myasthenia gravis (MG) in a randomized, double-blind, placebo-controlled, crossover study. The primary endpoint for efficacy was a reduction of at least 3 points in the quantitative MG score (QMGS). Secondary endpoints included changes in the functional disability scale (FDS), forced vital capacity (FVC), grip strength, anti-acetylcholine receptor (AChR) antibody levels and decremental response. During the terbutaline phase, five of eight (63%) patients had an improvement in the QMGS of 3.0 or greater, while 3/8 (38%) patients had improvement in the FDS of one grade. No improvement was seen during the placebo period. Statistical analysis using Wilcoxon signed-rank test confirmed that terbutaline treatment resulted in a significant improvement in QMGS. There was no change in FVC, grip strength or anti-AChR antibody levels, but there was an improvement in the decremental response during terbutaline phase. Terbutaline was well-tolerated in all study subjects. We conclude that terbutaline may be an effective adjunct therapy in a subset of patients with myasthenia, although confirmation with larger trials will be required.

MRI is a promising tool that can be used as an adjunctive test during the evaluation of patients who have myopathy and can help raise the diagnostic yield of a planned biopsy. It also has promise as a clinical endpoint. This article discusses abnormalities visible on MRI of muscle and the use of MRI in patients who have myopathy.

Chronic inflammatory demyelinating polyneuropathy (CIDP) is a term applied to a spectrum of immune-mediated demyelinating neuropathies that are heterogeneous in clinical manifestations and probably in pathogenesis. Although histopathologic studies of CIDP have been complicated by a relapsing course of the inflammatory reaction and its predominance in proximal nerve segments, many clues point to involvement of both cellular and humoral immune factors in the pathogenesis. Uncertainties remain regarding the provoking antigen(s) and location of the initial T cell activation. Breakdown of blood nerve barrier by activated T cells and its cytokines is followed by a local intraneural immune response with recruitment of macrophages and secretion of toxic factors, which cause damage to the myelin and axons. Activated T cells may also induce B cells to produce antibodies against nerve/myelin antigens. This review summarizes our current knowledge of the immunopathogenesis and insight from animal models of CIDP.