Our results should be considered in the light of four this website aspects of Lycaon biology: (1) larger packs are more able to defend kills against hyaenas (Carbone, du Toit & Gordon, 1997); (2) larger packs require more food, with larger prey rather than an increased number of kills providing a more economical option; (3) kudu, which form the most significant part of Lycaon diet (Rasmussen et al., 2008), are nocturnal to crepuscular and thus are more available in this time window, and indeed in Rasmussen et al. 2008, it is also demonstrated that larger packs select larger prey commensurate with pack

size; consequently with packs also commanding territories that are parapatric in time (Rasmussen, 1997), intraspecific competition is deemed an unlikely cause for this finding; (4) due to low light conditions, flight distances are smaller, and therefore, due to the extreme cost of chasing (Rasmussen et al., 2008), this time window is energetically more profitable. These points

selleck products apply equally to both the Hwange population and the Nyamandlovu one, between which we could detect no difference in the hunting conditions. So as pack sizes in the Nyamandlovu study were smaller, one would have expected less moonlight activity, not more. The only observable difference between the two areas lay in the extent of anthropogenic disturbance, so we conclude that this explains the contrasting behaviour of the two Lycaon populations. We now turn to the potential costs of sub-optimization and masking behaviours. medchemexpress Firstly, increased

foraging time associated with moonlit hunts, which due to the hypercursorial nature of this species, will represent appreciable energetic cost (Rasmussen et al., 2008). Furthermore, with light being a limiting factor, the costs of this suboptimal strategy is likely to reduce hunting success and cause even longer hunting hours than the model predicts. Secondly, a twofold increase in the probability of hyaena encounters will significantly increase kleptoparasitic cost (Carbone et al., 1997). While it may be hard to quantify the ‘cost’ of the behavioural adaptations, either due to social deficit incurred by spreading out when resting up (rather than sleeping in physical contact or close proximity as they usually do) perhaps resulting in reduced pack cohesion, or the lowered security for the pups, it is likely that such costs exist. Equally, rich literature on human shift workers demonstrates that diametric utilization of the diel cycle entails severe costs in health and performance (Van Reeth, 1998), so similar costs could affect the dogs. The accumulated impacts of these factors on the Nyamandlovu population may be reflected in the pack sizes AY and AYP being significantly less by 0.8 and 3.4, respectively. Nonetheless, in the short term at least, it appears that the tactic has some success insofar as the population persisted and produced dispersers.

01) and caused the lowest levels compared with othergroups (P < 0.01 Conclusion: The activation of hepatocyte growth factor promotes the apoptosis of hepatic stellate cell via downregulating Rho pathway. Key Word(s): 1.

HGF; 2. HGFA; 3. HSC; 4. RhoA; Presenting Author: ZHOU YUAN Additional Authors: GUO SHI-MING Corresponding Author: GUO SHI-MING Affiliations: Department of Gastroenterology, XinQiao Hospital Objective: The epidemiology of drug-induced liver injury (DILI) in China has rarely been studied before. The aim of the present study was to determine the etiology of DILI in a Chinese population by reporting a systematic Selleck Proteasome inhibitor analysis of Chinese literature published from1994 to 2011. Methods: A comprehensive database search of the Chinese literature was performed to obtain all of the relevant studies. The data, including the drug names and the patients’ sex, age, clinical classification and prognosis, were collected and analyzed Results: In this research, we found approximately 279 studies, including 24112patients.

There were 265 reports the sex of 21789 patients, 11787 males and 10002 females. The therapeutics included (but not limited Vadimezan research buy to) tuberculostatics, CAMs (complementary and alternative medicines), antibiotics, NSAIDs (Non-Steroidal Antiinflammatory Drugs), anti-neoplastics, central nervous system agents, antithyroid drugs, and immunomodulators. Of all these drugs, tuberculostatics and CAMs were the most common etiologies of DILI in China. Conclusion: DILI in China has a different etiology than in Europe and America. NSAIDs, which are the most common causes of DILI in Western populations, are

uncommon in China. Consequently, government, physicians and patients should pay more attention to potential CAMs use in DILI. Key Word(s): 1. Etiology; 2. liver injury; 3. tuberculostatics; 4. Drug-induced; Presenting Author: ENQIANG LINGHU Corresponding Author: ENQIANG LINGHU Affiliations: MCE公司 Department of Gastroenterology and Hepatology, the Chinese PLA General Hospital Objective: Endoscopic variceal ligation and sclerotherapy are the main treatment for esophageal varices, but not for varices with diameter less than 3 mm. The aim of this study is to assess the clinical usefulness of argon plasma coagulation (APC) inthe treatment of esophageal varices. Methods: Seven patients with esophageal varices treated withAPC were investigated retrospectively in our hospital since 2007. According to LDRf classification and Child- Pugh score, the esophageal varices and liver function were recorded respectively. After APC, the recurrent period of varices was calculated, and the recurrent bleeding plus other related complications were analyzed. Results: view of the obtained clinical materials, all the seven patients were recorded as LeD0.3Rf0 and Child A. The recurrent periods were from 4to 17 months.

However, within the ICU group an inverse correlation between CYP7A1 protein and the serum levels of total BAs was observed. (ρ = −0.347, P = 0.0001). In contrast, mRNA expression of CYP8B1, an enzyme involved in the synthesis of CA, was increased by 240% (P < 0.0001). In ICU patients, mRNA expression of the basolateral uptake transporters NTCP, OATP2, and OATP8 was down-regulated compared with controls (Fig. 3), but NTCP immunohistochemical staining did not differ between

groups (Table 3). OATP2/8 staining had a clear intensity learn more gradient from centrolobular to periportal regions in control patients. In 11/34 ICU patients a more uniform and extended staining with gradient fading was observed (Table 3). In contrast, mRNA levels of MRP3 and MRP4, the basolateral efflux transporters, were strongly up-regulated. Immunohistochemistry confirmed a marked up-regulation of MRP3 staining in ICU patients compared with control subjects (P < 0.0001) (Table 3). Moreover, whereas controls only exhibited basolateral MRP3 Daporinad concentration staining in the centrolobular zone of the liver lobule, ICU patients showed a strong

panlobular honeycomb staining pattern (Fig. 4). For MRP3, mRNA and protein levels were in agreement (ρ = 0.432, P = 0.004). Moreover, MRP3 expression correlated positively with the degree of bilirubinostasis both at the mRNA level (ρ = 0.529, P = 0.0003) and protein level (ρ = 0.591, P < 0.0001). There was also a strong correlation between the MRP3 protein levels and biochemical markers of cholestatic liver dysfunction, i.e., the serum levels of total bilirubin (ρ = 0.625, P = 0.0003), GGT (ρ = 0.519, P = 0.005),

ALP (ρ = 0.551, P = 0.002), G-CA (ρ = 0.494, P = 0.0008), and G-CDCA (ρ = 0.484, P = 0.001). Due to technical limitations, we were not able to stain for MRP4. mRNA expression of the canalicular efflux pumps BSEP, MRP2, MDR1, and MDR3 was significantly higher in ICU patients compared with control patients (Fig. 3). In contrast to the increased mRNA expression, protein expression of BSEP was down-regulated (Table 3). The normal regular BSEP immunohistochemical staining pattern became irregular and discontinuity was observed in cholestatic zones. Severely cholestatic areas had no discernable immunostaining. In concert with the mRNA expression, MRP2 immunostaining was up-regulated in ICU patients MCE in comparison with controls (P = 0.02) and correlated well with the degree of bilirubinostasis (ρ = 0.512, P = 0.0004), ductular reaction (ρ = 0.433, P = 0.003), and the serum levels of total bilirubin (ρ = 0.502, P = 0.003). MDR1 and MDR3 staining was also up-regulated. At the canalicular domain of the hepatocytes, a fine linear MDR3 pattern, seen in control subjects, evolved towards a strong double strand pattern of staining around multiple dilated canaliculi in ICU patients (Fig. 4). This is indicative of a very strong up-regulation of MDR3 protein.

However, within the ICU group an inverse correlation between CYP7A1 protein and the serum levels of total BAs was observed. (ρ = −0.347, P = 0.0001). In contrast, mRNA expression of CYP8B1, an enzyme involved in the synthesis of CA, was increased by 240% (P < 0.0001). In ICU patients, mRNA expression of the basolateral uptake transporters NTCP, OATP2, and OATP8 was down-regulated compared with controls (Fig. 3), but NTCP immunohistochemical staining did not differ between

groups (Table 3). OATP2/8 staining had a clear intensity Midostaurin order gradient from centrolobular to periportal regions in control patients. In 11/34 ICU patients a more uniform and extended staining with gradient fading was observed (Table 3). In contrast, mRNA levels of MRP3 and MRP4, the basolateral efflux transporters, were strongly up-regulated. Immunohistochemistry confirmed a marked up-regulation of MRP3 staining in ICU patients compared with control subjects (P < 0.0001) (Table 3). Moreover, whereas controls only exhibited basolateral MRP3 MS 275 staining in the centrolobular zone of the liver lobule, ICU patients showed a strong

panlobular honeycomb staining pattern (Fig. 4). For MRP3, mRNA and protein levels were in agreement (ρ = 0.432, P = 0.004). Moreover, MRP3 expression correlated positively with the degree of bilirubinostasis both at the mRNA level (ρ = 0.529, P = 0.0003) and protein level (ρ = 0.591, P < 0.0001). There was also a strong correlation between the MRP3 protein levels and biochemical markers of cholestatic liver dysfunction, i.e., the serum levels of total bilirubin (ρ = 0.625, P = 0.0003), GGT (ρ = 0.519, P = 0.005),

ALP (ρ = 0.551, P = 0.002), G-CA (ρ = 0.494, P = 0.0008), and G-CDCA (ρ = 0.484, P = 0.001). Due to technical limitations, we were not able to stain for MRP4. mRNA expression of the canalicular efflux pumps BSEP, MRP2, MDR1, and MDR3 was significantly higher in ICU patients compared with control patients (Fig. 3). In contrast to the increased mRNA expression, protein expression of BSEP was down-regulated (Table 3). The normal regular BSEP immunohistochemical staining pattern became irregular and discontinuity was observed in cholestatic zones. Severely cholestatic areas had no discernable immunostaining. In concert with the mRNA expression, MRP2 immunostaining was up-regulated in ICU patients MCE in comparison with controls (P = 0.02) and correlated well with the degree of bilirubinostasis (ρ = 0.512, P = 0.0004), ductular reaction (ρ = 0.433, P = 0.003), and the serum levels of total bilirubin (ρ = 0.502, P = 0.003). MDR1 and MDR3 staining was also up-regulated. At the canalicular domain of the hepatocytes, a fine linear MDR3 pattern, seen in control subjects, evolved towards a strong double strand pattern of staining around multiple dilated canaliculi in ICU patients (Fig. 4). This is indicative of a very strong up-regulation of MDR3 protein.

We analyzed 803 HBeAg-positive patients treated with PEG-IFN in three global studies with available HBsAg measurements. A stopping-rule based on absence of a decline from baseline was compared to a prediction-rule that uses HBsAg levels of <1,500 IU/mL and >20,000 IU/mL to identify patients with high and low probabilities of response. Patients with Fostamatinib mw an HBsAg level <1,500 IU/mL at week 12 achieved response (HBeAg loss with HBV DNA <2,000 IU/mL at 6 months

posttreatment) in 45%. At week 12, patients without a decline in HBsAg achieved a response in 14%, compared to only 6% of patients with HBsAg >20,000 IU/mL, but performance varied across HBV genotype. In patients treated with PEG-IFN monotherapy (n = 465), response rates were low in patients with Selleckchem CH5424802 genotypes A or D if there was no decline of HBsAg by week 12 (negative predictive value [NPV]: 97%-100%), and in patients with genotypes B or C if HBsAg at week 12 was >20,000 IU/mL (NPV: 92%-98%). At week 24, nearly all patients with HBsAg >20,000 IU/mL failed to achieve a response,

irrespective of HBV genotype (NPV for response and HBsAg loss 99% and 100%). Conclusion: HBsAg is a strong predictor of response to PEG-IFN in HBeAg-positive CHB. HBV genotype-specific stopping-rules may be considered at week 12, but treatment discontinuation is indicated in all patients with HBsAg >20,000 IU/mL at week 24, irrespective of HBV genotype. (Hepatology 2013;53:872–880) Chronic hepatitis B (CHB) affects over 350 million people and is one of the leading causes of cirrhosis and hepatocellular carcinoma.[1] Antiviral treatment with peginterferon-alfa (PEG-IFN)

may result in suppression of HBV DNA, hepatitis B e antigen (HBeAg) loss, and medchemexpress hepatitis B surface antigen (HBsAg) clearance.[2-5] Response to PEG-IFN therapy is durable, and patients with a sustained response have a reduced risk of developing hepatocellular carcinoma.[6-8] However, clinical application of PEG-IFN is compromised by the limited response rates and the occurrence of side effects.[3-5] Careful selection of patients with the highest probabilities of response to PEG-IFN therapy is therefore essential. Several studies have shown that response rates are higher in patients with HBV genotypes A or B versus C or D,[3, 5, 9] and in patients with higher levels of alanine aminotransferase (ALT)[5, 9] and lower levels of HBV DNA.[9] Recent studies also suggest that host factors such as IL28B genotype, as well as viral characteristics such as absence of precore and/or core promoter mutants also influence response probabilities.[10, 11] Nevertheless, prediction models incorporating these variables have only limited discriminatory capabilities.

We analyzed 803 HBeAg-positive patients treated with PEG-IFN in three global studies with available HBsAg measurements. A stopping-rule based on absence of a decline from baseline was compared to a prediction-rule that uses HBsAg levels of <1,500 IU/mL and >20,000 IU/mL to identify patients with high and low probabilities of response. Patients with LDK378 molecular weight an HBsAg level <1,500 IU/mL at week 12 achieved response (HBeAg loss with HBV DNA <2,000 IU/mL at 6 months

posttreatment) in 45%. At week 12, patients without a decline in HBsAg achieved a response in 14%, compared to only 6% of patients with HBsAg >20,000 IU/mL, but performance varied across HBV genotype. In patients treated with PEG-IFN monotherapy (n = 465), response rates were low in patients with Sirolimus molecular weight genotypes A or D if there was no decline of HBsAg by week 12 (negative predictive value [NPV]: 97%-100%), and in patients with genotypes B or C if HBsAg at week 12 was >20,000 IU/mL (NPV: 92%-98%). At week 24, nearly all patients with HBsAg >20,000 IU/mL failed to achieve a response,

irrespective of HBV genotype (NPV for response and HBsAg loss 99% and 100%). Conclusion: HBsAg is a strong predictor of response to PEG-IFN in HBeAg-positive CHB. HBV genotype-specific stopping-rules may be considered at week 12, but treatment discontinuation is indicated in all patients with HBsAg >20,000 IU/mL at week 24, irrespective of HBV genotype. (Hepatology 2013;53:872–880) Chronic hepatitis B (CHB) affects over 350 million people and is one of the leading causes of cirrhosis and hepatocellular carcinoma.[1] Antiviral treatment with peginterferon-alfa (PEG-IFN)

may result in suppression of HBV DNA, hepatitis B e antigen (HBeAg) loss, and 上海皓元医药股份有限公司 hepatitis B surface antigen (HBsAg) clearance.[2-5] Response to PEG-IFN therapy is durable, and patients with a sustained response have a reduced risk of developing hepatocellular carcinoma.[6-8] However, clinical application of PEG-IFN is compromised by the limited response rates and the occurrence of side effects.[3-5] Careful selection of patients with the highest probabilities of response to PEG-IFN therapy is therefore essential. Several studies have shown that response rates are higher in patients with HBV genotypes A or B versus C or D,[3, 5, 9] and in patients with higher levels of alanine aminotransferase (ALT)[5, 9] and lower levels of HBV DNA.[9] Recent studies also suggest that host factors such as IL28B genotype, as well as viral characteristics such as absence of precore and/or core promoter mutants also influence response probabilities.[10, 11] Nevertheless, prediction models incorporating these variables have only limited discriminatory capabilities.

We analyzed 803 HBeAg-positive patients treated with PEG-IFN in three global studies with available HBsAg measurements. A stopping-rule based on absence of a decline from baseline was compared to a prediction-rule that uses HBsAg levels of <1,500 IU/mL and >20,000 IU/mL to identify patients with high and low probabilities of response. Patients with selleck screening library an HBsAg level <1,500 IU/mL at week 12 achieved response (HBeAg loss with HBV DNA <2,000 IU/mL at 6 months

posttreatment) in 45%. At week 12, patients without a decline in HBsAg achieved a response in 14%, compared to only 6% of patients with HBsAg >20,000 IU/mL, but performance varied across HBV genotype. In patients treated with PEG-IFN monotherapy (n = 465), response rates were low in patients with Selleckchem Ruxolitinib genotypes A or D if there was no decline of HBsAg by week 12 (negative predictive value [NPV]: 97%-100%), and in patients with genotypes B or C if HBsAg at week 12 was >20,000 IU/mL (NPV: 92%-98%). At week 24, nearly all patients with HBsAg >20,000 IU/mL failed to achieve a response,

irrespective of HBV genotype (NPV for response and HBsAg loss 99% and 100%). Conclusion: HBsAg is a strong predictor of response to PEG-IFN in HBeAg-positive CHB. HBV genotype-specific stopping-rules may be considered at week 12, but treatment discontinuation is indicated in all patients with HBsAg >20,000 IU/mL at week 24, irrespective of HBV genotype. (Hepatology 2013;53:872–880) Chronic hepatitis B (CHB) affects over 350 million people and is one of the leading causes of cirrhosis and hepatocellular carcinoma.[1] Antiviral treatment with peginterferon-alfa (PEG-IFN)

may result in suppression of HBV DNA, hepatitis B e antigen (HBeAg) loss, and medchemexpress hepatitis B surface antigen (HBsAg) clearance.[2-5] Response to PEG-IFN therapy is durable, and patients with a sustained response have a reduced risk of developing hepatocellular carcinoma.[6-8] However, clinical application of PEG-IFN is compromised by the limited response rates and the occurrence of side effects.[3-5] Careful selection of patients with the highest probabilities of response to PEG-IFN therapy is therefore essential. Several studies have shown that response rates are higher in patients with HBV genotypes A or B versus C or D,[3, 5, 9] and in patients with higher levels of alanine aminotransferase (ALT)[5, 9] and lower levels of HBV DNA.[9] Recent studies also suggest that host factors such as IL28B genotype, as well as viral characteristics such as absence of precore and/or core promoter mutants also influence response probabilities.[10, 11] Nevertheless, prediction models incorporating these variables have only limited discriminatory capabilities.

This may explain why the optimal hepatectomy for HCC has not yet been agreed upon, despite numerous studies based on postoperative survival. BECAUSE HCC SPREADS through the blood flowing away from the

tumor, it is reasonable to determine the safety margin of locoregional therapy (e.g. hepatectomy or ablation therapy) by directly demonstrating the TBF. In 2000, we first reported the case of a HCC patient who underwent hepatectomy, the safety margin of which was based on TBF.[43] Because the blood flow from the tumor can be examined LY294002 research buy by preoperative computed tomography (CT) under hepatic angiography (CTHA), the TBF drainage area (i.e. high-risk area for IM) is preoperatively demonstrated as the safety margin, namely, the distance between the edge of the tumor click here and the peripheral margin of the TBF drainage area (Fig. 1a,b). Hepatic dissection is performed, securing the safety margin, the adequacy of which is repeatedly

confirmed by intraoperative ultrasonography.[43] Using these procedures, the high-risk area of IM can be completely resected with a minimal but essential hepatectomy (Fig. 1c). However, patients with venous tumor invasion demonstrated preoperatively are not indicated for TBF-based hepatectomy because TBF is not correctly examined due to the interference by tumor thrombus. By comparing the CTHA images and the corresponding cut surface of the resected liver specimen, we could confirm that the safety margin was achieved (Fig. 1d). ACCORDING TO THE CTHA results, the TBF drainage area differs from tumor to tumor. Its shape is generally irregular and its width varies by site.[39] The TBF pattern is classified into three types: marginal, portal vein and hypovascular (Fig. 2). In the marginal type, the

TBF drainage area is limited to the peritumoral MCE公司 region, which corresponds to the description of “corona enhancement” reported by Ueda et al.[44] Partial hepatic resection was commonly performed in these patients.[39] Major hepatic resection was performed only in selected patients with large tumors. In contrast, the portal vein type represents the TBF drainage through the major portal branches, and the anatomical hepatectomy, including lobectomy or segmentectomy, was performed to dissect the whole TBF drainage area. Tumors of hypovascular type have poor TBF, which is difficult to detect by CTHA. The safety margin cannot be determined in this type of HCC; therefore, only limited, partial hepatectomy with a minimal surgical margin was performed in these patients. TUMOR RECURRENCE AFTER surgery is caused either by IM or by MC. Theoretically, IM can be divided into the following two types according to the mechanism of hematogenous spread of tumor. Tumor blood first flows in the TBF drainage area, by which IM may develop. This type of IM is localized in this area, and tentatively designated as “local IM” because it can be treated by local therapy.

This may explain why the optimal hepatectomy for HCC has not yet been agreed upon, despite numerous studies based on postoperative survival. BECAUSE HCC SPREADS through the blood flowing away from the

tumor, it is reasonable to determine the safety margin of locoregional therapy (e.g. hepatectomy or ablation therapy) by directly demonstrating the TBF. In 2000, we first reported the case of a HCC patient who underwent hepatectomy, the safety margin of which was based on TBF.[43] Because the blood flow from the tumor can be examined www.selleckchem.com/products/pf-06463922.html by preoperative computed tomography (CT) under hepatic angiography (CTHA), the TBF drainage area (i.e. high-risk area for IM) is preoperatively demonstrated as the safety margin, namely, the distance between the edge of the tumor LY2606368 ic50 and the peripheral margin of the TBF drainage area (Fig. 1a,b). Hepatic dissection is performed, securing the safety margin, the adequacy of which is repeatedly

confirmed by intraoperative ultrasonography.[43] Using these procedures, the high-risk area of IM can be completely resected with a minimal but essential hepatectomy (Fig. 1c). However, patients with venous tumor invasion demonstrated preoperatively are not indicated for TBF-based hepatectomy because TBF is not correctly examined due to the interference by tumor thrombus. By comparing the CTHA images and the corresponding cut surface of the resected liver specimen, we could confirm that the safety margin was achieved (Fig. 1d). ACCORDING TO THE CTHA results, the TBF drainage area differs from tumor to tumor. Its shape is generally irregular and its width varies by site.[39] The TBF pattern is classified into three types: marginal, portal vein and hypovascular (Fig. 2). In the marginal type, the

TBF drainage area is limited to the peritumoral 上海皓元 region, which corresponds to the description of “corona enhancement” reported by Ueda et al.[44] Partial hepatic resection was commonly performed in these patients.[39] Major hepatic resection was performed only in selected patients with large tumors. In contrast, the portal vein type represents the TBF drainage through the major portal branches, and the anatomical hepatectomy, including lobectomy or segmentectomy, was performed to dissect the whole TBF drainage area. Tumors of hypovascular type have poor TBF, which is difficult to detect by CTHA. The safety margin cannot be determined in this type of HCC; therefore, only limited, partial hepatectomy with a minimal surgical margin was performed in these patients. TUMOR RECURRENCE AFTER surgery is caused either by IM or by MC. Theoretically, IM can be divided into the following two types according to the mechanism of hematogenous spread of tumor. Tumor blood first flows in the TBF drainage area, by which IM may develop. This type of IM is localized in this area, and tentatively designated as “local IM” because it can be treated by local therapy.

The total costs of preventive headache therapy by type of treatment were then evaluated and compared over time. Results.— During the initial months of treatment, PPT with inexpensive mediations (<0.75 $/day) represents the least costly regimen and is comparable to MCBT in expense until 6 months. After 6 months, PPT is expected to become more costly, particularly when medication cost exceeds 0.75$ a day. When using an expensive medication (>3 $/day),

preventive drug treatment becomes more expensive than CBBT after the first year. Long-term, and within year 1, MCBT was found to be the least costly approach to migraine prevention. Conclusions.— Through year 1 of treatment, selleck inhibitor inexpensive prophylactic medications (such as generically available beta-blocker or tricyclic antidepressant medications) and behavioral interventions utilizing limited delivery formats (MCBT) are the least costly of the empirically validated interventions. This analysis suggests that, relative to pharmacologic options, limited format behavioral interventions are cost-competitive in the early phases of treatment and become

more cost-efficient as the years of treatment accrue. “
“Glutamate (Glu) and AZD5363 mouse glutamine (Gln) are strongly compartmentalized (in neurons for Glu and in astrocytes for Gln). The visual cortex is the brain region with a higher neuron/astrocyte ratio (the highest neuronal density and the relatively lowest density of astrocytes). Elevations in extracellular Glu or potassium above certain thresholds are likely candidates to be the final common steps in the multiple distinct processes that can lead to cortical spreading depression. Astrocytes play a key role in this phenomenon, by acting as a sink for extracellular Glu and potassium, as well as generally acting as a buffer for the ionic and neurochemical changes that initiate and propagate cortical spreading depression. The purpose of this study was to medchemexpress quantify Glu

and Gln to generate Glu/Gln ratios in women with migraine during the interictal state compared with healthy control women. Twenty-seven patients with migraine (8 with aura and 19 without aura) and 19 matched healthy controls were included in the study. We performed proton magnetic resonance spectroscopy in the anterior paracingulate cortex and occipital cortex (OC). Spectral analysis was performed by LCModel, allowing a separation of Glu and Gln using a 3T machine. The main result was a significantly higher Glu/Gln ratio in the OC of migraine patients compared with healthy control subjects (4.87 for migraineurs [standard deviation (SD) = 2.74] and 3.42 for controls [SD = 1.52], P = .042). We also observed higher Glu levels (6.98 for migraineurs [SD = 0.85] and 6.22 for controls [SD = 0.97], P = .007) and Glu/creatine + phosphocreatine ratio (1.18 for migraineurs [SD = 0.18] and 1.00 for controls [SD = 0.16], P = .001) in anterior paracingulate cortex in migraine patients but saw no differences in Glu/Gln ratio (2.79 for migraineurs [SD = 1.11] and 2.