[9] HSCs could function as antigen presenting cells, as they have the ability to process protein antigens and present peptides to CD4+ and CD8+ T cells.[13]

Moreover, HSCs have been shown to express retinoic acid early inducible-1 (RAE1), cluster of differentiation 1d (CD1d), and major histocompatibility complex (MHC) I and II, and directly interact with immune cells, such as T cells,[13] NKT cells,[14] natural killer (NK) cells[10] (Table 2). HSCs also express several pattern recognition receptors, such as Toll-like receptors (TLRs)[12, 30, 31] and retinoic acid-inducible gene I (RIG-I),[8] indicating INK 128 ic50 that HSCs possess innate immunity against pathogen infection. The host innate immune system recognizes pathogens and responds to their stimuli mainly through TLRs. TLRs are key sensors of host innate immunity to pathogens. Several TLR members play a critical role in recognition of viral nucleic acids.[32] TLR-3 has a crucial role in virus-mediated innate immune responses,[33-35] as it recognizes dsRNA[36] that either constitutes the genome of one class of viruses or is generated during the life cycle of many viruses, including HCV.[33-35, 37] Sensing through TLR-3 activates interferon (IFN) signaling pathway and induces the production of type I IFNs (IFN-α/β). IFN-α/β has been recognized as the first

line of the TLR-3 activation-mediated antiviral response.[38] In addition, TLR-3 signaling also induces type III IFN expression.[39-41] Therefore, the activation of TLR-3 Selleckchem AZD1208 by its ligand poly I : C in viral target Ribose-5-phosphate isomerase cells could inhibit virus infections, including HCV.[37] A very recent study[12] demonstrated that HSCs express functional TLR-3, activation of which induced production of IFN-β, and inhibited HCV replicon replication.[12] Our recent study[15] showed that TLR-3 signaling of HSCs could induce type III IFN expression, which contributed

to HSCs-mediated HCV inhibition in hepatocytes. In addition to TLR-3, HSCs also express TLR-2,[29] TLR-4[30] and TLR-9.[31] HSCs express the stable levels of TLR-2 that respond to HCV core protein, inducing fibrogenic actions.[29] A recent study also showed that HCV core protein induces fibrogenic actions of HSCs via TLR-2 signaling pathway.[29] TLR-4 activation by lipopolysaccharides (LPS) in HSCs enhances TGF-β signaling and hepatic fibrosis.[30] HSCs express TLR-9 that are involved in liver fibrosis, as evidenced by TLR-9-deficient mice being resistant to liver fibrosis.[31] RIG-I is now well known as an important mediator of antiviral immunity. RIG-I can detect viral genomic RNA during negative-strand RNA virus infection[42] and trigger a type I IFN-mediated immune response that protects the host against viral infection.[43] RIG-I can recognize HCV genome, inducing innate immune response to restrict HCV replication in hepatocytes.

22 Lai et al.17 reported an increased risk of hepatocellular carcinoma in type selleck products 2 diabetic patients within the Keelung Community in northern Taiwan, but they did not further analyze the relationship between diabetes and biliary tract neoplasm. The aim of this study was to estimate the hazard rates and relative risks of malignant neoplasms of the liver and biliary tract in diabetic population according to sex and various age stratifications using a nationally representative diabetic cohort selected from National Health Insurance (NHI). BMI, body mass index; BNHI, Bureau of National Health Insurance; CI, confidence interval; HR, hazard ratio; ICD-9, International

Statistical Classification of Diseases and Related Health Problems, 9th edition; NHI, National Health Insurance; PIN, personal identification number. Taiwan’s NHI program is a universal health program that was introduced in March 1995. By the end of 1996, approximately 96% of the total Taiwanese population had enrolled in the NHI program,23 and the state-run Bureau of National Health Insurance (BNHI) had contracted with 97% of hospitals as well as 90% of clinics all over the island.24 The BNHI accumulates all administrative and claims

data for Taiwan, and the National Health Research Institute cooperates with the BNHI to establish an NHI research database. For the precision selleck kinase inhibitor of the claim data, the BNHI performs expert reviews on a random sample of every 50-100 ambulatory and inpatient claims in each hospital and clinic quarterly, and false reports of diagnosis yield a severe penalty from the BNHI.25 With ethical approval from the National Health Research Institute, we used data for the ambulatory care claims, all inpatient claims, and updated registry for beneficiaries from 1997 to 2006 for this study. All NHI datasets can be interlinked with each individual personal identification number (PIN). Diabetic ambulatory crotamiton care claims record patients with diabetes-related diagnoses with International Statistical Classification of Diseases and

Related Health Problems, 9th edition (ICD-9) code 250 or A-code A181. An individual was classified as a diabetic patient if she or he had an initial diabetes-related diagnosis at any time in 2000 and then experienced one or more additional diagnoses within the subsequent 12 months. The first and last outpatient visits within 1 year must be >30 days apart to avoid accidental inclusion of miscoded patients.26 To detect newly diagnosed malignant neoplasm cases, we excluded those patients admitted to the hospitals for any kinds of malignant neoplasm (ICD-9: 140-208) during 1997-1999 from our diabetic group. In Taiwan, BNHI issues major illness/injury certificates to all patients who suffer from malignant neoplasm, and these patients are exempt from copayment to the NHI if they are admitted for the illness associated with the related malignancy.

In addition, Jansen and colleagues have examined human articular tissue explants exposed to blood in tissue culture, and have demonstrated that coculture with the anti-inflammatory cytokine IL-10 was correlated with reduced production of IL-1β and TNF-α

from synovium, and with protection of cartilage [33]. Although it is buy Dabrafenib unlikely that therapy to oppose inflammatory cytokines is a strategy that would be necessary for most individuals, such therapy may be appropriate in the future should tools or markers be developed to identify individuals who are particularly at risk for early joint deterioration. Haemostasis is often the first defensive response following tissue injury. It not only stops the loss of blood but also results in the production of a variety of mediators that can influence subsequent defences, including inflammation, immunity and tissue repair. When all goes well, the body can defend itself against further injury and restore tissue structure and function. However, wound healing can be delayed or defective for many reasons. Ageing, diabetes and vascular disease are well-recognized causes of impaired wound healing in the general population. Drugs, such as corticosteroids and cancer

chemotherapy can delay healing as well. While the literature is rather limited, there is also evidence that GSK1120212 conditions that impair haemostasis also impair wound healing. There are good theoretical reasons to support this theory. However, there is a limited amount of experimental data, and essentially no human data. Studies in

rabbits showed that healing after tooth extraction is delayed in anticoagulated animals [34]. However, closure of an excisional cutaneous wound is not delayed in mice lacking fibrinogen [35] or the thrombin-activatable fibrinolysis inhibitor (TAFI) [36]. The healed wounds in mice with defective fibrin clot formation or stability Thymidine kinase do, however, display histological abnormalities. The dermal defect is not always filled as it should be, but rather squamous epithelium tends to migrate down into the defect, leaving a cystic space or sinus tract. Thus, formation of an adequate fibrin clot provides a framework for appropriate formation of granulation tissue to fill a tissue defect. Our group has used a mouse model of haemophilia B (HB, coagulation factor IX knockout) to study healing of cutaneous punch biopsy wounds [22]. We found that healing is impaired as these mice only generate very low levels of thrombin at the site of injury. They do form a normal haemostatic platelet plug and deposit small amounts of fibrin around the periphery of the wound. However, the platelet plug is not adequately stabilized by a fibrin meshwork, which leads to delayed bleeding in the 12–24 h after wounding.

Statistic analysis was performed using SPSS version 17.0. Results: Among 278 subjects included in this study, age group was 40–49 years old (36,7%), with female dominated whole subjects 202 (72,7%). Most of them

were in middle to low educational Alpelisib order level 116 (41,7%). As many as 50,7% subjects had normal body mass index. We had 11 subjects with positive result of I-FOBT with its prevalence 4%. Conclusion: Prevalence of positive result of I-FOBT was 4%. Further study was needed to be performed to estimate diagnostic study of I-FOBT in Indonesia. Key Word(s): 1. Colorectal Cancer; 2. I-FOBT; 3. Screening; Presenting Author: MURDANI ABDULLAH Additional Authors: DADANG MAKMUN, ARIFAHRIAL SYAM, AHMAD FAUZI, KAKA RENALDI, MARCELLUS SIMADIBRATA Corresponding Author: MURDANI ABDULLAH Affiliations: Department of Internal Medicine, Faculty of Medicine, University of Indonesia-dr. Cipto Mangunkusumo Hospital, Jl. Diponegoro no. 71, Jakarta Pusat, Indonesia; Department of Internal Medicine, Faculty of Medicine, University of Indonesia-dr. Cipto Mangunkusumo Hospital, Jl. Diponegoro no. 71, Jakarta Pusat, Indonesia; Department of Internal Medicine, Faculty of Medicine, University of Indonesia-dr. Cipto Mangunkusumo

Hospital, Jl. Diponegoro no. 71, Jakarta Pusat, Indonesia; Department of Internal Medicine, Faculty of Medicine, University of Indonesia-dr. Cipto Mangunkusumo Hospital, Jl. Diponegoro no. 71, Jakarta Pusat, Indonesia; Department of Internal Medicine, find more Faculty of Medicine, University of Indonesia-dr. Cipto Mangunkusumo Hospital, Jl. Diponegoro no. 71, Jakarta Pusat, Indonesia; Department of Internal Medicine, Faculty of Medicine, University of Indonesia-dr. Cipto Mangunkusumo Hospital, Jl. Diponegoro no. 71, Jakarta Pusat, Indonesia Objective: To determine the prevalence of gastroesophageal reflux disease (GERD) among urban population in Depok Indonesia

and any association with predictive risk Plasmin factors and socioepidemiological factors status. Methods: Design of this study was cross-sectional. Subjects were recruited by stratified random cluster sampling in asymptomatic populations residing in about 5 district health center in Depok, West Java, Indonesia. The study was conducted during 2012. Case report forms and GERD-Q is used to determine patient demographics and prevalence of GERD in the study subjects. Data analysis was performed using SPSS version 17.0. Results: A total of 278 subjects were recruited in this study. Highest age group is 40–49 years about 102 people (36.7%), and is dominated by women as many as 202 (72.7%). Most of them had elementary-junior high school that is 116 people (41.7%). A total of 50.7% of respondents had a body mass index (BMI) is normal. In this research found that 26 people (9.4%) were included in the criteria for GERD. Statistical analysis found significant association between education level, economic level, asthma status, and delayed gastric emptying (p < 0,05) with GERD.

Statistic analysis was performed using SPSS version 17.0. Results: Among 278 subjects included in this study, age group was 40–49 years old (36,7%), with female dominated whole subjects 202 (72,7%). Most of them

were in middle to low educational Selleck GSK1120212 level 116 (41,7%). As many as 50,7% subjects had normal body mass index. We had 11 subjects with positive result of I-FOBT with its prevalence 4%. Conclusion: Prevalence of positive result of I-FOBT was 4%. Further study was needed to be performed to estimate diagnostic study of I-FOBT in Indonesia. Key Word(s): 1. Colorectal Cancer; 2. I-FOBT; 3. Screening; Presenting Author: MURDANI ABDULLAH Additional Authors: DADANG MAKMUN, ARIFAHRIAL SYAM, AHMAD FAUZI, KAKA RENALDI, MARCELLUS SIMADIBRATA Corresponding Author: MURDANI ABDULLAH Affiliations: Department of Internal Medicine, Faculty of Medicine, University of Indonesia-dr. Cipto Mangunkusumo Hospital, Jl. Diponegoro no. 71, Jakarta Pusat, Indonesia; Department of Internal Medicine, Faculty of Medicine, University of Indonesia-dr. Cipto Mangunkusumo Hospital, Jl. Diponegoro no. 71, Jakarta Pusat, Indonesia; Department of Internal Medicine, Faculty of Medicine, University of Indonesia-dr. Cipto Mangunkusumo

Hospital, Jl. Diponegoro no. 71, Jakarta Pusat, Indonesia; Department of Internal Medicine, Faculty of Medicine, University of Indonesia-dr. Cipto Mangunkusumo Hospital, Jl. Diponegoro no. 71, Jakarta Pusat, Indonesia; Department of Internal Medicine, Ixazomib price Faculty of Medicine, University of Indonesia-dr. Cipto Mangunkusumo Hospital, Jl. Diponegoro no. 71, Jakarta Pusat, Indonesia; Department of Internal Medicine, Faculty of Medicine, University of Indonesia-dr. Cipto Mangunkusumo Hospital, Jl. Diponegoro no. 71, Jakarta Pusat, Indonesia Objective: To determine the prevalence of gastroesophageal reflux disease (GERD) among urban population in Depok Indonesia

and any association with predictive risk selleck factors and socioepidemiological factors status. Methods: Design of this study was cross-sectional. Subjects were recruited by stratified random cluster sampling in asymptomatic populations residing in about 5 district health center in Depok, West Java, Indonesia. The study was conducted during 2012. Case report forms and GERD-Q is used to determine patient demographics and prevalence of GERD in the study subjects. Data analysis was performed using SPSS version 17.0. Results: A total of 278 subjects were recruited in this study. Highest age group is 40–49 years about 102 people (36.7%), and is dominated by women as many as 202 (72.7%). Most of them had elementary-junior high school that is 116 people (41.7%). A total of 50.7% of respondents had a body mass index (BMI) is normal. In this research found that 26 people (9.4%) were included in the criteria for GERD. Statistical analysis found significant association between education level, economic level, asthma status, and delayed gastric emptying (p < 0,05) with GERD.

Marine algae have a highly important role in sustaining nearshore marine ecosystems and are considered a significant component of marine bioinvasions. Here, we examined the patterns of respiration and light-use efficiency across macroalgal assemblages with different

levels of species richness and evenness. Additionally, we compared our results between native and invaded macroalgal assemblages, using the invasive brown macroalga Sargassum muticum (Yendo) Fensholt as a model species. Results showed that the presence selleck screening library of the invader increased the rates of respiration and production, most likely as a result of the high biomass of the invader. This effect disappeared when S. muticum lost most of its biomass after senescence. Moreover, predictability–diversity relationships of macroalgal assemblages varied between native

and invaded assemblages. Hence, the introduction of high-impact invasive species may trigger major changes in ecosystem functioning. The impact of S. muticum may be related to its greater biomass in the invaded assemblages, although species interactions and seasonality influenced the magnitude of the impact. Natural diversity is being modified worldwide by changes learn more such as species loss and biological invasions of NIS (Vitousek et al. 1997, Sala et al. 2000). Understanding the consequences of such changes on ecosystem functioning has become a key topic of next ecological research (e.g., Worm et al. 2006, Byrnes et al. 2007, Airoldi and Bulleri 2011). The argument that biodiversity loss could lead to a reduction in global ecosystem functioning (i.e., interactions between biotic assemblages or with their abiotic environment) emerged as an issue in the early 1990s (e.g., Ehrlich and Wilson 1991, Naeem et al. 1994). Conversely, in some systems local species richness has increased significantly due to recent establishment of NIS, although the long-term consequences of these introductions are still debated (Sax and Gaines 2003). The

spread of NIS has been considered one of the strongest anthropogenic impacts on natural ecosystems by changing abiotic factors, community structure, and ecosystem properties (Mack et al. 2000, Byers 2002, Ruesink et al. 2006). Life history features of invaders may be key factors in determining the fate and the impact of invasions. For instance, invasion by canopy-forming macroalgae (e.g., Sargassum muticum, Undaria pinnatifida) may influence the structure of understory assemblages by modifying levels of light, sedimentation (Airoldi 2003) or water movement (Eckman et al. 1989). Introduced species often exhibit novel features compared to native species and may have disproportionately high impacts on native ecosystem functioning (Ruesink et al. 2006).

Duewell P, Hajime K, Rayner KJ et al. NLRP3 inflammasomes are required for atherogenesis and activated by cholesterol crystals. Nature 2010; 464: 1357–1361 C LEUNG,1,2 CB HERATH,1,2 J ZHIYUAN,1,2 T LEONG,2 JM FORBES,1,3 PW ANGUS1,2 1The University of Melbourne, Victoria, 2Liver Unit, Austin Hospital, Heidelberg, Victoria, 3Mater Medical Research Institute, South Brisbane,

Queensland Introduction: Advanced glycation end-products (AGEs) content is high in western diets and may contribute to tissue injury via RAGE (receptor for AGEs). Here, we determined if manipulation Autophagy activator of dietary AGE intake affects NAFLD progression and whether these effects are mediated via RAGE. Methods: Male C57B6 mice were fed a high fat, high fructose, high cholesterol (HFHC) diet for 33 weeks and compared with animals on normal chow. A third group were given a HFHC diet that was high in AGEs through baking. Another group was given a HFHC diet that was marinated in vinegar to prevent the formation of AGEs. In a second experiment, RAGE KO animals were fed a HFHC diet or a high AGE HFHC diet and compared with WT controls. Hepatic biochemistry, histology, picro-sirius red morphometry and hepatic mRNA were determined.

We also determined the effects of AGEs on primary Kupffer cells (KCs). Results: The long term HFHC diet model generated significant steatohepatitis and fibrosis. Hepatic 4-hydroxynonenal content (a marker of chronic oxidative stress) and hepatocyte ballooning (a marker of cellular injury) were significantly increased with a HFHC diet and CH5424802 chemical structure further increased with a high AGE HFHC diet and abrogated by vinegar marination. Similarly, the high AGE HFHC diet significantly increased picrosirius red staining, α-smooth muscle actin and collagen type 1A gene expression compared with HFHC alone and this was reduced by vinegar marination. The increased oxidative stress, hepatocyte ballooning and fibrosis associated with a high AGE HFHC diet was significantly reduced in corresponding high AGE HFHC RAGE KO animals. We found KCs express RAGE and take

up AGEs. AGEs increase ROS generation and proliferation (as measured by BrDU uptake) in these cells. Similar results were achieved with primary Thalidomide hepatic stellate cells (HSCs). Conclusions: In the HFHC model of NAFLD, manipulation of dietary AGEs modulates liver injury, inflammation, and liver fibrosis via a RAGE dependent pathway. Our cell work suggests that these proinflammatory and profibrotic effects are mediated via direct effects on KCs and HSCs via RAGE. This suggests that pharmacological and dietary strategies targeting the AGE/RAGE pathway could slow the progression of NAFLD. Our results also have important implications for diabetes associated NAFLD, a condition in which endogenous AGE production and RAGE expression is increased.

Duewell P, Hajime K, Rayner KJ et al. NLRP3 inflammasomes are required for atherogenesis and activated by cholesterol crystals. Nature 2010; 464: 1357–1361 C LEUNG,1,2 CB HERATH,1,2 J ZHIYUAN,1,2 T LEONG,2 JM FORBES,1,3 PW ANGUS1,2 1The University of Melbourne, Victoria, 2Liver Unit, Austin Hospital, Heidelberg, Victoria, 3Mater Medical Research Institute, South Brisbane,

Queensland Introduction: Advanced glycation end-products (AGEs) content is high in western diets and may contribute to tissue injury via RAGE (receptor for AGEs). Here, we determined if manipulation selleck chemical of dietary AGE intake affects NAFLD progression and whether these effects are mediated via RAGE. Methods: Male C57B6 mice were fed a high fat, high fructose, high cholesterol (HFHC) diet for 33 weeks and compared with animals on normal chow. A third group were given a HFHC diet that was high in AGEs through baking. Another group was given a HFHC diet that was marinated in vinegar to prevent the formation of AGEs. In a second experiment, RAGE KO animals were fed a HFHC diet or a high AGE HFHC diet and compared with WT controls. Hepatic biochemistry, histology, picro-sirius red morphometry and hepatic mRNA were determined.

We also determined the effects of AGEs on primary Kupffer cells (KCs). Results: The long term HFHC diet model generated significant steatohepatitis and fibrosis. Hepatic 4-hydroxynonenal content (a marker of chronic oxidative stress) and hepatocyte ballooning (a marker of cellular injury) were significantly increased with a HFHC diet and see more further increased with a high AGE HFHC diet and abrogated by vinegar marination. Similarly, the high AGE HFHC diet significantly increased picrosirius red staining, α-smooth muscle actin and collagen type 1A gene expression compared with HFHC alone and this was reduced by vinegar marination. The increased oxidative stress, hepatocyte ballooning and fibrosis associated with a high AGE HFHC diet was significantly reduced in corresponding high AGE HFHC RAGE KO animals. We found KCs express RAGE and take

up AGEs. AGEs increase ROS generation and proliferation (as measured by BrDU uptake) in these cells. Similar results were achieved with primary Fossariinae hepatic stellate cells (HSCs). Conclusions: In the HFHC model of NAFLD, manipulation of dietary AGEs modulates liver injury, inflammation, and liver fibrosis via a RAGE dependent pathway. Our cell work suggests that these proinflammatory and profibrotic effects are mediated via direct effects on KCs and HSCs via RAGE. This suggests that pharmacological and dietary strategies targeting the AGE/RAGE pathway could slow the progression of NAFLD. Our results also have important implications for diabetes associated NAFLD, a condition in which endogenous AGE production and RAGE expression is increased.

Duewell P, Hajime K, Rayner KJ et al. NLRP3 inflammasomes are required for atherogenesis and activated by cholesterol crystals. Nature 2010; 464: 1357–1361 C LEUNG,1,2 CB HERATH,1,2 J ZHIYUAN,1,2 T LEONG,2 JM FORBES,1,3 PW ANGUS1,2 1The University of Melbourne, Victoria, 2Liver Unit, Austin Hospital, Heidelberg, Victoria, 3Mater Medical Research Institute, South Brisbane,

Queensland Introduction: Advanced glycation end-products (AGEs) content is high in western diets and may contribute to tissue injury via RAGE (receptor for AGEs). Here, we determined if manipulation PLX-4720 cost of dietary AGE intake affects NAFLD progression and whether these effects are mediated via RAGE. Methods: Male C57B6 mice were fed a high fat, high fructose, high cholesterol (HFHC) diet for 33 weeks and compared with animals on normal chow. A third group were given a HFHC diet that was high in AGEs through baking. Another group was given a HFHC diet that was marinated in vinegar to prevent the formation of AGEs. In a second experiment, RAGE KO animals were fed a HFHC diet or a high AGE HFHC diet and compared with WT controls. Hepatic biochemistry, histology, picro-sirius red morphometry and hepatic mRNA were determined.

We also determined the effects of AGEs on primary Kupffer cells (KCs). Results: The long term HFHC diet model generated significant steatohepatitis and fibrosis. Hepatic 4-hydroxynonenal content (a marker of chronic oxidative stress) and hepatocyte ballooning (a marker of cellular injury) were significantly increased with a HFHC diet and GS-1101 nmr further increased with a high AGE HFHC diet and abrogated by vinegar marination. Similarly, the high AGE HFHC diet significantly increased picrosirius red staining, α-smooth muscle actin and collagen type 1A gene expression compared with HFHC alone and this was reduced by vinegar marination. The increased oxidative stress, hepatocyte ballooning and fibrosis associated with a high AGE HFHC diet was significantly reduced in corresponding high AGE HFHC RAGE KO animals. We found KCs express RAGE and take

up AGEs. AGEs increase ROS generation and proliferation (as measured by BrDU uptake) in these cells. Similar results were achieved with primary Thalidomide hepatic stellate cells (HSCs). Conclusions: In the HFHC model of NAFLD, manipulation of dietary AGEs modulates liver injury, inflammation, and liver fibrosis via a RAGE dependent pathway. Our cell work suggests that these proinflammatory and profibrotic effects are mediated via direct effects on KCs and HSCs via RAGE. This suggests that pharmacological and dietary strategies targeting the AGE/RAGE pathway could slow the progression of NAFLD. Our results also have important implications for diabetes associated NAFLD, a condition in which endogenous AGE production and RAGE expression is increased.

“
“(Headache 2010;50:1164-1174) Introduction.— Cluster headaches (CH) are primary headaches marked by repeated short-lasting attacks of severe, unilateral head pain and associated autonomic symptoms. Despite aggressive management with medications, oxygen therapy, nerve blocks, as well as various lesioning and neurostimulation therapies, a number of patients are incapacitated and suffering. The sphenopalatine ganglion (SPG) has been implicated in the pathophysiology of CH and has been a target for blocks, lesioning, and other surgical approaches. For this reason, it was selected as a target for an acute neurostimulation selleck products study. Methods.— Six patients with refractory chronic CH were treated with short-term (up to

1 hour) electrical stimulation of the SPG during an acute CH. Headaches were spontaneously present at the time of stimulation or were triggered with agents known to trigger clusters headache in each patient. A standard percutaneous infrazygomatic approach was used to place a needle at the ipsilateral SPG in the pterygopalatine fossa under fluoroscopic guidance. Electrical Palbociclib supplier stimulation was performed using a temporary stimulating electrode. Stimulation was performed at various settings during maximal headache intensity. Results.— Five patients had CH during the initial evaluation. Three returned 3 months later for a second evaluation. There were 18 acute and distinct CH attacks

with clinically maximal visual analog scale (VAS) intensity of 8 (out of 10) and above. SPG stimulation resulted in complete resolution of the headache in 11 attacks, partial resolution (>50% VAS reduction) in 3, and minimal to no relief in 4 attacks. Associated autonomic Rebamipide features

of CH were resolved in each responder. Pain relief was noted within several minutes of stimulation. Conclusion.— Sphenopalatine ganglion stimulation can be effective in relieving acute severe CH pain and associated autonomic features. Chronic long-term outcome studies are needed to determine the utility of SPG stimulation for management and prevention of CH. “
“Serotonin (5-hydroxytryptamine)1B/1D agonists are vasoconstrictors that can affect coronary and cerebral arteries. Retrosternal chest, arm, and jaw pain following triptan use is generally attributed to “triptan sensations” and dismissed as noncardiac. However, triptans narrow normal coronary arteries and occasionally trigger vasospasm. They are contraindicated in atherosclerotic vascular disease. Part 1 of this review examines the relationship of medications used in migraine with the likelihood of causing vasospasm or vasoconstriction, and the triggering of cardiac arrhythmias. We report an illustrative case of polymorphic ventricular tachyarrhythmia, electrocardiogram changes consistent with cardiac ischemia, and acquired corrected QT interval lengthening following oral sumatriptan in a 53-year-old migraineur without risk factors for coronary artery disease (CAD).