The reason we decided to compare a 22G FNA needle from

one industry with a 22G FNB device from another industry was that the preferred vendor for our institution did not manufacture an FNB device. GDC-0980 datasheet Therefore, the choice of products for this clinical trial had nothing to do with consultancy agreements or industry-specific bias. It was born out of necessity. In our study, we reported a diagnostic accuracy of 100% versus 89.3% for the FNA and FNB cohorts, respectively.1 Two other recent trials, one from the United States2 and the other from Canada,3 have evaluated the 22G ProCore needle. In the United States study that compared the 22G EchoTip ProCore with the 22G EchoTip FNA needle (as suggested by the author), a definite diagnosis was achieved in the first, second, and third passes in 45%, 72%, and 79% of ProCore procedures compared with 45%, 62%, and 62% of EchoTip FNA procedures (P = NS), respectively. A definite diagnosis using cell-block was achieved in 83% of cases. In the Canadian study of 44 patients with solid mass lesions, both 19G and 22G ProCore needles were used, and the diagnostic accuracy was 71%, with a technical failure rate of 13.6%. The findings of these 2 studies Daporinad purchase appear far more inferior to ours! There are no specific recommendations on how many times a lesion can be “jabbed”

during a single FNA pass. In our opinion, it is 12 to 16. We do not use suction for our FNA procedures. The manufacturer’s recommendation for ProCore, at the time the study was conducted, was 3 or 4 jabs, with use of suction. We followed those recommendations. We also believe that jabbing a lesion with a reverse-bevel needle 12 to 16 times can cause more bleeding, reduce cellularity, and diminish the yield further. This was clearly evident by the diminishing diagnostic yield with incremental FNB passes in our study. Irrespective of our opinion, other investigators2 and 3 had similar outcomes. No matter how hard one tries or what that compulsion might be, it is not possible to make a diagnosis happen on the third pass, as the author suggests: Oxymatrine The endosonographer

only performs, but it is the cytopathologist who renders diagnosis. Multiple endosonographers were involved in this trial, and the pathologist was blinded to the type of accessory being used. At the University of Alabama at Birmingham, a diagnosis by cell block is a last resort! A preliminary diagnosis is established in 98% of cases during the procedure. 4 Our cytopathology team has published more than 100 peer-reviewed articles related to EUS and are leaders in the field. EUS-FNA is multidisciplinary, and it is true that these excellent results cannot be reproduced in the real world. In our study, we did not establish a diagnosis by cell block in any patient in whom onsite diagnosis was inconclusive. One ought to remember that this was a small number (10.7%).

, 1964) and discovered in other fish, such as gobies, and invertebrates including octopuses, crabs, shellfishes, flat worms and ribbon worms ( Noguchi et al., 2006; Miyazawa buy Target Selective Inhibitor Library and Noguchi, 2001). TTX is produced primarily by marine bacteria, and it appears that it finds its way into pufferfish through the food chain ( Noguchi et al., 1986, Noguchi

et al., 1987 and Noguchi et al., 2006; Yasumoto et al., 1986; Narita et al., 1987; Simidu et al., 1987; Noguchi and Arakawa, 2008). Tissue-specific distribution of the toxin in TTX-bearing pufferfish, mainly the genus Takifugu, has been widely investigated from the view point of food hygiene ( Tani, 1945; Kanoh, 1988; Fuchi et al., 1991; Khora et al., 1991), revealing that while TTX is commonly distributed in the liver and ovaries, the localization in other tissues is species-specific ( Noguchi et al., 2006; Noguchi and Arakawa, 2008). For example, while TTX was detected only in the intestine besides the liver and ovaries in Takifugu rubripes, it was found to be concentrated in the skin and intestine and marginally present in the testes and skeletal muscle in Takifugu niphobles ( Noguchi et al., 2006; Noguchi and Arakawa, 2008). Previously, we demonstrated that tissue-specific distribution and the amount of TTX in the mature pufferfish T. niphobles were sex-dependent; female gonads and male liver showed the highest concentrations of the toxin followed by male skin ( Itoi et al., 2012). Species, sex, and

tissue Selleck MG 132 specific differences in the distribution and concentration of TTX render unclear the exact function of the toxin in pufferfish, although it has been suggested that Ruxolitinib TTX may function as a chemical defense against predators ( Fuhrman, 1986; Kodama et al., 1985) and as pheromone during spawning ( Matsumura, 1995). In this study, we conducted predation experiments, measurement, and immunohistochemical analysis to elucidate the effect of TTX as a chemical defense in pufferfish larvae. Adult T. rubripes females captured from Ise Bay ( Supplementary

data, Fig. S1) and adult males from Enshu-Nada Sea ( Supplementary data, Fig. S1) were artificially bred, and the larvae subsequently grown in an aquaculture pond at Department of Sea-Farming, Aichi Fish Farming Institute. Fertilized T. rubripes eggs from wild specimens were also purchased from Marinetech (Aichi, Japan), and were hatched and grown in the aquarium at Department of Marine Science and Resources, Nihon University. Fertilized eggs of T. niphobles were collected from the coastal waters off Enoshima Island (35°17′N, 139°28′E) in the summer months (May–July) of 2009–2013, and the larvae subsequently grown in an aquarium at Department of Marine Science and Resources, Nihon University. Predation behavior was observed using T. rubripes larvae of 0–4 days post-hatch (dph) as the prey and several predator species in small aquaria and beakers. Juveniles of Japanese flounder Paralichthys olivaceus and sea bass Lateolabrax sp.

As a final remark,

the accurate and precise MALDI-FTICR mass measurements will allow a reliable match between the MS/MS-data obtained using other MS techniques such as LC-ESI-MS/MS and the peptides observed in the MALDI-FTICR spectra. The past decade, MS-based profiling studies have been carried out to determine disease-specific serum peptidome signatures in a “case–control” setting. Due to the relatively high biological variability of the serum peptidome (and proteome) a large number of samples are required for statistical Ferroptosis inhibitor clinical trial evaluation. Thus, high-throughput analytical methodologies have been adopted in combination with MS, pioneered by SELDI-TOF platforms. In the same period, high-throughput robotic platforms with

more flexible and user-defined sample preparation protocols were combined with MALDI-TOF read-out. Both low-resolution TOF-profiles with a wide m/z-range and high-resolution profiles with smaller m/z-windows were reported for proteins and peptides, respectively [7], [30] and [31]. However, single- or even multi-step protein fractionations still yield highly complex samples and the low resolving powers in linear mode SELDI- or MALDI-TOF profiles do not allow accurate quantification of the profiled species. Peptides up to m/z-values of 4500 can click here be routinely analyzed with isotopic resolution using TOF-analysers in reflectron mode, but at the cost of restricting the analyzed m/z-range and thus excluding proteins from the evaluation. Moreover, reflectron mode profiles still contain a significant number of overlapping Chorioepithelioma peptides, as we previously demonstrated in ultrahigh resolution MALDI-FTICR profiles [20]. In this study the ultrahigh resolving power provided by a 15 T MALDI-FTICR system was exploited in terms of discriminative power of case–control peptidome profiles

and identification of observed species. This is the first profiling study that reports on the application of such ultrahigh resolution profiles exemplified by a clinical cohort of serum samples from healthy individuals and PC patients. Aiming for cancer-specific peptide and protein signatures, these serum samples were first fractionated on a fully automated SPE-platform based on functionalized MBs and then profiled using a 15 T MALDI-FTICR mass spectrometer. In total, 487 peptides or small proteins (i.e. 196 and 291 in LM and HM spectra, respectively) were measured with isotopic resolution in the m/z-range 1–9 kDa and quantified with high accuracy and precision. The ultrahigh resolving power allowed the correct quantification of peptides or proteins that previously were observed to suffer from overlapping isotopic distributions in lower resolution profiles (see Fig. 2). Note that the total number of detectable peptides was higher, i.e. several peptides were detected only in few particular samples, probably due to a higher expression of a particular protein or an elevated protease activity.

In this process, Esrrb forms a complex with Oct4 and Sox2, and synergistically upregulates the expression of pluripotency genes in MEFs. Remarkably, with the help of other Yamanaka factors (Klf4/Sox2/c-Myc), another orphan nuclear receptor, Nr5a2, was able to substitute for Oct4 in iPSC generation [38]. In addition, Nr5a2 could greatly enhance iPSC reprogramming in conjunction with activation of another nuclear receptor, RARa/g [39]. The finding that the RARa agonist (CD437) and RARg agonist (AM580) dramatically increased reprogramming efficiency further supports the notion that nuclear receptors play important roles in regulating

somatic cell reprogramming. Many studies demonstrated that small-molecule epigenetic modifiers could significantly influence reprogramming process and even substitute for certain reprogramming LY2109761 ic50 transcription factors (Figure 2). BIX01294, an inhibitor of G9a histone methyltransferase (HMTase),

was shown to enable reprogramming of neural precursor cells or fibroblasts transduced with only two TFs, Oct4 and Klf4 [6]. Besides well-known HDAC inhibitors (e.g. VPA, NaB) that have been demonstrated to facilitate reprogramming in various contexts [40 and 41], Parnate, an inhibitor of histone demethylase LSD1, was shown to enhance iPSC reprogramming as well [9]. Interestingly, the well-known antioxidant compound vitamin C was recently shown to enhance reprogramming by modulating the activity of the histone demethylases Jhdm1a/1b [42]. These findings highlight the dynamic changes of histone selleck products modifications in reprogramming. Recent mechanistic studies of iPSC reprogramming further illustrated how epigenetic changes are orchestrated in the early and late stages of reprogramming. Koche et al. showed that activated chromatin marks (e.g. H3K4 methylation) were targeted to promoters of pluripotency and developmentally regulated genes (e.g. Fgf4 and Lin28) before transcriptional

activation during the early phase of iPSC reprogramming [ 43]. It was also reported that two epigenetic factors, Parp1 and Tet2, were recruited to pluripotency loci (e.g. Nanog and Esrrb) and established early epigenetic marks by converting 5-methylcytosine (5mC) into 5-hydroxymethylcytosine (5hmC) during reprogramming [ 44]. Interestingly, it was reported that along with Klf4, Sox2, and c-Myc, another Thiamet G Tet family protein Tet1 could enable somatic cell reprogramming in the absence of the key transcription factor Oct4 or nuclear receptors Esrrb and Nr5a2 [ 45], highlighting the important role of DNA demethylation (through hydroxymethylation) in reprogramming. Furthermore, other specific histone modifications were identified to occur in reprogramming. For example, inhibition of the H3K79 histone methyltransferase DOT1L (e.g. by a small molecule inhibitor) and the H3K9 methyltransferase Setdb1 (e.g. by RNAi) was shown to enhance iPSC generation [ 46 and 47].

CLS identifies IBD from controls and CLS >15 appears to have some value in predicting patients who will require TE. Figure options Download full-size image Download high-quality image (154 K) Download as PowerPoint slide “
“Early-onset Crohn’s disease (CD) accounts for 25% of cases but is distinct from adult-onset CD by a more severe disease activity index, increased

Autophagy inhibitor immunosuppressant requirement, and more extensive intestinal involvement. The pathogenic link between chronic inflammatory diseases and angiogenesis prompted investigations into its role in inflammatory bowel disease. We hypothesize that VEGF driven angiogenesis plays a significant role in Crohn’s disease inflammation. Pediatric patients (n=13), ages 12 to 16, at our institution having undergone resection involving the terminal ileum for CD were compared to controls (n=5) with non-inflammatory indications for

resection. Additionally, from each Crohn’s pathology specimen, inflamed and non-inflamed ileum were obtained for comparison. Samples were evaluated for inflammation using the Crohn’s Histology Index of Severity (range 0-13) and for microvessel density by quantitative endothelial cell immunohistochemistry using CD31. Corresponding tissues were assessed for VEGF-A mRNA and protein expression by RT-PCR and Western blot respectively. Results expressed as mean±SEM were analyzed for significance (P≤0.05) by ANOVA and Student’s t-test. Inflammation scores were significantly increased (Fig 1) between inflamed CD and controls (5.8±0.7 vs 0.62±0.38, P<0.001), Selleckchem MAPK inhibitor and between paired inflamed and non-inflamed ileum (5.8±0.7 vs 1.2±0.6, P< 0.001). Increased microvessel density was observed in both inflamed and non-inflamed CD groups compared to controls (inflamed 24,955±3,202μm2, non-inflamed 18,719±2,050μm2, control 9,032±1,474μm2), with statistical significance (P=0.008) only present between

inflamed CD selleck chemical and control subjects (Fig 2). Expression of tissue VEGF-A mRNA was upregulated in CD (CD 8.5±2.51 vs control 2.32±0.58, P=0.034), and was associated with an increased trend in VEGF-A protein levels (VEGF/GAPDH, CD 3.96 vs control 2.20, P=0.53). Angiogenesis is associated with pediatric Crohn’s disease as observed by increased microvessel density that correlates with greater inflammation in resected ileal specimens. At the molecular level, we demonstrate elevated VEGF transcription and protein levels, which implicates a VEGF pathway for angiogenesis associated inflammation in early-onset Crohn’s disease. Further investigations regarding mechanism of angiogenesis, its relationship to inflammation, and effectiveness of anti-angiogenic therapies are warranted. Fig 1.  Inflammation score (range 0-13) of inflamed pediatric Crohn’s disease ileum increased compared to both non-inflammed Crohn’s diseae and control. Results expressed as mean ± SEM (*P <0.001).

, 2003, 1998; Makkar and Becker, 1999). In addition, species with low levels of phorbol esters do not cause toxicity when they are heated ( Makkar et al., 1998a and Makkar et al., 1998b). The similarity of the clinical signs and the pathology

of poisoning by J. ribifolia with the experimental poisoning by other species of Jatropha ( Oliveira et al., 2008; Ferreira et al., 2011), suggests that the active principle in J. ribifolia is also phorbol esters. selleck chemicals Phorbol esters are carcinogenic and cause gastrointestinal irritation, diarrhea, hyperplasic reactions of the skin, reduced milk yield, and a negative effect on muscle development leading to decreased meat production ( Bourin et al., 1982; Horiuchi et al., 1987; Gandhi et al., 1995). Inflammatory activity is attributed to the synthesis and release of chemical pro-inflammatory mediators ( Weinstein et al., 1979; Goel et al., 2007). The semiarid region of Brazil is characterized by a warm climate with a mean temperature of 26 °C and a mean precipitation of 500–800 mm annually. The rains are irregular, and in some years, rainfall is insignificant or low. The rainy season is short,

from January/February to April/May. The relative humidity is low, ranging from 60% to 75%, and the vegetation, named caatinga, is an exclusive Brazilian biome, occupying almost 11% of the country. The caatinga vegetation is characterized by bushes with twisted branches and deep roots, cacti and bromeliads and is typical of selleck screening library what is found in arid conditions (xerophytic). The Jatropha species J. mutabilis,

Cytidine deaminase J. ribifolia, and J. mollissima are found in the caatinga ( Oliveira, 2011); however, intoxication by these species has not been reported, and most of the farmers state that these three species are not palatable and that they are not consumed by the animals, even when forage is in short supply. It is possible that the outbreaks reported here resulted from some of the goats ingesting J. ribifolia as a result of the severe shortage of forage during the dry season and that, later, social facilitation influenced other animals to eat the plant. Another factor contributing to the poisoning could be the continued degradation of the caatinga vegetation because of excessive grazing ( Oliveira, 2011), resulting in the predominance of more drought-resistant and less palatable Jatropha species. However, the goats did not consume J. mutabilis or J. mollissima, which were found in the same paddock as J. ribifolia. The reason why goats ingested J. ribifolia but not the other species is unknown, but J. ribifolia is closer to the ground and more available than J. mutabilis and J. mollissima, which are taller species. All three Jatropha species are very resistant to drought, and they continue to sprout during the dry period. One way to control the poisoning is to remove affected animals from the paddocks allowing them to recover.

Web-based interventions can be very attractive because they are convenient, easily accessible, and can maintain anonymity and privacy [33]. Grant support for the three described studies: for the IBS study: Dutch Digestive Foundation; for the Diabetes type 2 study: OAUC and The Research

Council of Norway (RCN); for the chronic widespread pain study: The DAPT nmr Research Council of Norway Grant no: 182014/V50. These funding sources had no involvement in the conduct of the research, preparation of the article, study design, collection, analysis and interpretation of data, writing of the report; and decision to submit the paper for publication. No potential conflicts of interest relevant to this article were reported. All authors read and approved the final manuscript. The last author initiated the paper and drafted the first submission, the first author revised the initial draft together with the co-authors. Each Dasatinib author was funded by her own institute. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the article. “
“Health organizations are increasingly present online through websites that provide health information to consumers [1]. These websites represent an effort by health organizations to respond to the increasing number of consumers

who look for health Janus kinase (JAK) information on the internet, by offering quality information [2]. In the area of spinal cord injury (SCI), key organizations have promoted online endeavors that provide valuable information [3]. For example, the International Spinal Cord Society launched elearnSCI.org, which, although specifically targeted to health professionals, can be accessed by consumers. The Canadian

Paraplegic Association Ontario in partnership with the Toronto Rehabilitation Institute launched SpinalCordConnections.ca. As part of the Victorian Spinal Cord Injury Program, SpinalHub.com.au was launched by a partnership of several Australian organizations. In the German landscape, the Manfred Sauer Foundation launched Der-Querschnitt.de. In producing these websites, health organizations invest significant resources to provide health information in the traditional one-way (professional-to-consumer) model of communication: health information is created by groups of experts in the field as a resource to educate the community [4]. These educational endeavors are important. They foster the growth of health literacy that is at the core of self-management of health conditions [5] and [6]. However, as shown in the past few years, one-way communication as a channel for influencing health behavior has limitations [4] and [7].

6). Quantification revealed that this difference was statistically significant (Fig. 7). In recent years, research on flavonoids is increasing. The interest in these compounds is due to the evidence of various pharmacological properties and their presence in many human foods (Muzitano et al., 2008 and Dajas et al., 2003). Furthermore, epidemiological studies have evaluated the correlation between reduced rates of cardiovascular disease and cytoprotection in neurological disorders in populations with diets rich in flavonoids (Bastianetto Smad signaling and Quirion, 2002, Esposito et al., 2002 and Procházková

et al., 2011). In fact, recent studies with flavonoids in models of brain ischemia, most of them with the flavonoid widely found in plant products, quercetin, have shown significant neuroprotection and promotion of functional outcome (Lee et al., 2011 and Rivera Silmitasertib order et al., 2008). A flavonoid with molecular structure similar to quercetin and putative neuroprotective action is rutin. Few previous studies with models of global brain ischemia have been conducted, showing protective effect of rutin when administrated in pre-ischemic stage (Abd-El-Fattah et al., 2010, Gupta et al., 2003 and Pu et al., 2007) or after

ischemia induction (Gupta et al., 2003). Regarding focal ischemia, a recent study evaluated rutin administration during 21 days before the induction of ischemia by middle cerebral artery occlusion (MCAO), revealing protective action (Khan et al., 2009). Here, we studied the therapeutic potential of rutin when administrated after induction of focal thermocoagulatory ischemic lesion in sensorimotor cortex, a model previously used by our research group to investigate therapeutic approaches

(Giraldi-Guimarães et al., 2009). Administration of rutin from the beginning of ischemic process, by daily i.p. injections during the first five post-ischemic days, promoted sensorimotor recovery of impaired forelimb. Moreover, although no reduction of lesion volume was found, rutin reduced neurodegeneration in lesion periphery. Thus, the results indicate that rutin also has significant neuroprotective effect when administrated after the occurrence Nutlin-3 mw of a focal cortical ischemia, suggesting that this flavonoid might be used to treat ischemic damage in the acute phase of stroke. We observed more sensorimotor recovery with the dose of 50 mg/kg than with 100 mg/kg. We are not able to explain this result, but previous reports about treatment of focal brain ischemia with quercetin, a structurally related flavonoid, have also shown better effects with lower than with higher doses (Pandey et al., 2011 and Rivera et al., 2004). After post-mortem observation of the peritoneal cavity of our animals, we observed that those treated with 100 mg/kg had clusters of insoluble rutin, which was not observed in those treated with 50 mg/kg (data not shown).

The compounds showed low toxicity effects on normal and higher cytotoxic on tumor cells, a very desired advantage in new lead anticancer chemicals to overwhelmed adverse effects due to therapeutic narrow window, pharmacological multiple resistance and morphological and physiological similarities between transformed and normal cells. The authors have declared that there is no conflict of interest. We are grateful to the Brazilian agencies Conselho Nacional de Desenvolvimento Científico e Tecnológico (CNPq), Fundação de Amparo à

Pesquisa de Minas Gerais (FAPEMIG) and Fundação de Amparo à Pesquisa LDK378 ic50 do Estado do Piauí (FAPEPI) for financial support. “
“There is currently much debate as to whether vitamin A and associated retinoid derivatives are beneficial or harmful

to the gastrointestinal (GI) tract, a situation primarily driven by clinical case reports claiming a putative causal relationship between retinoid treatment with 13-cis-retinoic acid (13-cis-RA, isotretinoin) and the occurrence of ulcerative colitis (UC) and Crohn’s disease (CD), i.e. two forms of chronic inflammatory bowel disease (IBD) (Crockett et al., 2010 and Reddy et al., 2006). Contrary to this, key basic research data do, in fact, support anti-inflammatory effects of retinoids on the GI tract (Bai Z-VAD-FMK ic50 et al., 2009 and Iwata and Yokota, 2011). Nevertheless, the case for retinoids being beneficial or harmful to the GI tract has only infrequently been based on robust scientific evidence and, thus far, it has not been possible to confirm or refute a causative relationship (Crockett et al., 2009). Ideally, further prospective or well-designed retrospective pharmacoepidemiological studies are needed to definitively establish causality. Understanding of the pathophysiology of IBD has markedly increased recently with a number of pre-disposing genetic risk factors identified for CD and (to Rho a lesser extent) UC, along with a number of environmental triggers considered as potential key mediators of disease development (Rogler, 2011). Although

more risk factors are expected to follow (Barrett et al., 2008, Latella et al., 2010 and Nguyen et al., 2006), the role of many these in the pathophysiology of CD, for example, is unclear (Mathew, 2008) and, nevertheless, account for only a fraction of observed CD incidence (Torkamani et al., 2008). Key environmental triggers include dietary factors, food additives or drugs (Cosnes, 2010, Hou et al., 2011a, Hou et al., 2011b, Järnerot et al., 1983, Katschinski et al., 1988, Martini and Brandes, 1976, Silkoff et al., 1980 and Thornton et al., 1979), and cigarette smoking (Avidan et al., 2005, Cosnes et al., 2001, Cosnes et al., 1996 and Kane et al., 2005) while psychological factors may influence disease course (Cámara et al., 2010, Danese et al., 2004 and Levenstein, 2002).

On admission transbulbar sonography revealed reduced ONSD of 4.1 mm on the right and 4.3 mm on the left side. After failure of medical treatment three consecutive targeted epidural blood patches were performed and a gradual extension of the ONSD was observed in both optic nerves [right 5.2 mm, left 5.3 mm]. In this article we documented changes of ONSD that were in line with BMN 673 manufacturer initial clinical improvement and secondary worsening under

conservative treatment and final improvement after occlusion of the cervical CSF leakage. Many studies on normal values found a relatively wide interindividual range of ONSD measurements [7], [9] and [12]. Thus, as described previously absolute measurements of

ICP will not be possible by transbulbar sonography [2]. Furthermore, with a false-negative rate of approximate 10%, ONSD values should only be interpreted in conjunction with clinical data and neuroimaging results. Killer et al. found a decreased CSF circulation along the optic nerve in patients with IIH that seems to be a consequence of the complex trabecular architecture of the subarachnoid space of the optic nerve [23]. They proposed a compartment syndrome of the optic nerve sheath in sustained ICP elevation, as in IIH. In addition, Hayreh described varying degrees of communication between the intracranial subarachnoid space and the optic nerve sheath in different individuals [1]. This variety of the optic nerve sheath compliance and CSF fluid dynamics may limit the sonographic ONSD assessment in its value, especially for follow-up examinations, but on the PI3K inhibitor other hand, Phosphatidylinositol diacylglycerol-lyase may possibly allow to identify individual patients with continuing optic nerve compression albeit therapeutic lumbar puncture. Thus, studying long-term changes of the ONSD in different neurological disorders may be an interesting issue of future investigations. With respect to the high variation of normal ONSD values published it is urgently

necessary to determine consistent sonographic data in larger multicenter studies. In summary, as a noninvasive and cost-effective bedside method transbulbar B-mode sonography is a promising technique for clinical neurologists. It may serve as an additional tool in neurocritical care medicine for detection of raised ICP. The method is of particular interest in situations when invasive ICP monitoring is contraindicated or when the expertise for invasive monitor placement is not immediately available. Furthermore, it aids in the diagnostic work-up and in the follow-up of patients with IIH and in conditions of decreased ICP. “
“Sudden retinal blindness is a common complication of temporal arteritis (TA) due to ischemic optic neuropathy (ION) caused by vasculitic occlusion of the central retinal artery (CRA), the posterior ciliary artery (PCA) and other orbital arteries [1].