29 Although STAT3 is a survival signal for hepatocytes, selective deletion of STAT3 in hepatocytes did not induce apoptosis and mortality. This may be due to maintained STAT3 activation in myeloid cells that limits inflammatory responses such as TNF-α and IFN-γ production. Deletion of STAT3 in both myeloid cells and hepatocytes in STAT3Hep−/−Mye−/− mice resulted High Content Screening in high levels of serum TNF-α and IFN-γ and hepatic STAT1 activation, which resulted in massive apoptosis of hepatocytes and high mortality. It has been recently proposed that STAT3 inhibitors may be used in the treatment of hepatocellular carcinoma (HCC).30 The present findings advocate caution

with such an approach, because global inhibition of STAT3 may result in a strong innate inflammatory

response and liver failure, especially in the remnant liver of patients with HCC following liver resection. Indeed, liver failure after resection was often seen in patients with HCC with elevated inflammatory responses due to sepsis.31 Additionally, elevated STAT1 expression and activation in the liver were found in patients with chronic liver disease,32 which may impair liver regeneration. Thus, a strategy to increase STAT3/STAT1 ratio in both hepatocytes and leukocytes may have a beneficial effect in preventing liver failure in patients Sirolimus cost with HCC who have elevated inflammatory responses after liver resection. Additional Supporting Information may be found in the online version of this article. “
“Aim:  Cucurbitacin B (CuB) is an active component isolated from various plants used as folk medicine in Asian countries and has shown diverse antitumor activities. There is, however, no documented effect of CuB on the migration and invasion of human hepatoma

cells yet. The purpose of this study was to assess the effect of CuB on the migration and invasion of hepatoma cells and to explore the possible mechanism. Methods:  Human hepatoma cell lines HepG2 and BEL-7402 were used for the study. Effects of CuB on cancer cell migration and invasion were evaluated in vitro with wound healing and transwell assays. The effect of CuB on the expression of matrix metalloproteinase (MMP)-9, mitogen-activated MCE公司 protein kinases (MAPKs), Akt, nuclear factor-κB (NF-κB), c-Fos and c-Jun was investigated with gelatin zymography and/or western blotting. Results:  Cucurbitacin B has significantly suppressed 12-O-tetradecanoylphorbol 13-acetate (TPA)-induced cell invasion and migration in a concentration-dependent manner, which was accompanied with suppression of TPA-induced MMP-9 expression through inactivation of phosphorylation of extracellular signal-regulated kinase (ERK) 1/2, p38 and Akt. In the nucleus, it has also strongly suppressed TPA-stimulated expression of NF-κB, c-Jun and c-Fos.

1). At the least, a revised staging of cirrhosis should start with its main classification of compensated SCH772984 and decompensated cirrhosis. Compensated cirrhosis in turn would comprise two substages: without varices (stage 1) or with varices (stage 2). However, staging of compensated cirrhosis could be further refined as (1) no portal hypertension (HVPG <6 mmHg); (2) portal hypertension that is not clinically significant (HVPG between 6 and 10 mmHg); and (3) clinically significant portal hypertension (HVPG > 10 mmHg or presence of collaterals). Substaging of decompensated cirrhosis is not as well-defined but would likely be classified according to both the degree of portal

hypertension and the degree of liver/circulatory dysfunction (with recurrent variceal hemorrhage, refractory ascites, and hepatorenal syndrome representing more severe stages) (Fig. 1). It remains possible that additional technologies apart from HVPG will emerge that can further discriminate the pathological and selleck chemicals functional state of the liver. Such information could be vital to optimize the timing

and nature of antifibrotic therapies, or the need for liver transplantation. Thus far, liver stiffness measurement (LSM) obtained by transient elastography is the most promising noninvasive approach for monitoring fibrosis progression associated with worsening portal hypertension. LSM has an excellent correlation with HVPG values below

a threshold of 10–12 mmHg.29, 30 Although these findings need to be further substantiated in larger independent studies, they suggest that LSM may be useful in the detection of clinically significant portal hypertension and, thereby, in further subclassifying compensated cirrhosis. On the other hand, LSM may not be accurate in decompensated cirrhosis where, in addition to intrahepatic vascular resistance, there are complex hemodynamic changes.31 Nonetheless, it will be important to evaluate, in longitudinal studies, whether single LSM values or dynamic medchemexpress changes over time are predictive of initial or further decompensation, or the response to pharmacological therapy.32, 33 We encourage the practicing community, pathologists, and investigators to move beyond the simple characterization of cirrhosis as a single stage and instead begin thinking of cirrhosis as a series of critical steps that, if left unchecked, culminate in hepatic decompensation. A new framework for classifying cirrhosis will require integration of both current and emerging knowledge about liver structure and function. From one stage, there should emerge many. “
“Recent evidences indicate that hepatic steatosis suppresses autophagic proteolysis. The present study evaluated the correlation between autophagic function and cathepsin expression in the liver from patients with non-alcoholic fatty liver disease (NAFLD).

Notably, all major aa replacements in the HVR1 in persistence subjects were centripetal (i.e., substitutions that change toward the 1a worldwide consensus sequence); in contrast, every clearance subject examined had centrifugal replacements (Fig. 4). Variations in IL28B are associated with outcome of HCV infection,12-14 but the mechanistic links between the protective genotype and spontaneous outcome remain unknown. Prospective monthly follow-up of HCV-uninfected subjects who became acutely infected revealed (1) a strong correlation between IL28B genotype

and initial HCV-RNA level during primary acute HCV infection (P = 0.00005), with the favorable IL28B genotype (rs12979860-C homozygosity) correlated with higher initial viremia level, and (2) a strong positive correlation between initial HCV-RNA

level and spontaneous clearance (P = 0.00099). Selleck NVP-BEZ235 These findings are both counterintuitive and consistent with findings in other studies. In this study, spontaneous resolution was more strongly predicted by initial HCV-RNA http://www.selleckchem.com/products/R788(Fostamatinib-disodium).html level than by IL28B genotype, with the former association reaching statistical significance, even in this relatively small cohort. The association of protective IL28B genotype with high initial viremia resonates with recent findings from chronic infection that the protective IL28B genotype is associated with higher (i.e., untreated) HCV-RNA levels12 and lower intrahepatic IFN-stimulating gene (ISG) levels.39 Previous work demonstrated that lower baseline ISG expression predicts response to treatment.40, 41 It is apparent that IL28B genotype predisposes toward a phenotype that is associated with clinical outcome, and that the association between phenotype and outcome is likely to be stronger than for genotype 上海皓元医药股份有限公司 because other factors are likely to contribute.15 Taken together, the

current and previous work suggest that the protective IL28B genotype is one factor that predisposes to high initial HCV-RNA during acute infection and low baseline ISG during chronic infection and that these represent measurable phenotypes in vivo that strongly predict the outcomes of interest (i.e., spontaneous resolution and treatment response, respectively). Our group recently assessed cytokine and chemokine levels in this cohort as potential markers of such a phenotype, but found no correlation between early levels of those factors and outcome or IL28B genotype.42 These data may appear to differ somewhat from previous findings showing that higher HCV-RNA level is correlated with persistence of acute infection.19, 20 Most studies investigating acute HCV infection have used either clinical symptoms (i.e., jaundice as well as other nonspecific symptoms) or first clinical presentation/visit to identify acute infection.

4 An ultrasonographic study of patients with T2DM showed a 69% prevalence of NAFLD.21 In another study, 127 of 204 diabetic patients displayed fatty infiltration on ultrasound, and 87% of the patients with fatty infiltration who consented to biopsy had histologic confirmation of NAFLD.22 High serum triglyceride levels and low serum HDL levels

are very common in patients with NAFLD. The prevalence of NAFLD in individuals with dyslipidemia attending lipid clinics was estimated to be 50%.23 Age, gender and ethnicity are also associated with a differential prevalence for NAFLD.4 A number of studies have shown that the prevalence of NAFLD increases with age.24-28 The likelihood of disease progression to advanced fibrosis or mortality increases in older patients with NAFLD.29-31 Many recent studies have reported Ipatasertib molecular weight that male gender is a risk factor for fatty liver disease.4

For example, in a study of 26,527 subjects undergoing medical checkups, the prevalence of NAFLD was 31% in men and 16% in women.32 Compared to non-Hispanic whites, Hispanic individuals have significantly higher and non-Hispanic blacks have significantly lower prevalence of NAFLD.15, 33-35 Selleckchem MK-8669 The prevalence of NAFLD in American-Indian and Alaskan-Native populations appears lower, ranging from 0.6% to 2.2%, although the lack of histologic definition makes it likely that is an underestimate.36, 37 There are data to suggest that hypothyroidism, hypopituitarism, hypogonadism, sleep apnea, and polycystic ovary syndrome independent of obesity are important risk factors for the presence of NAFLD (Table 4).3 The evolution of hepatic histologic changes in patients with NAFL and NASH has been investigated by several studies, but these generally included smaller number of patients and had relatively modest duration of follow-up.4, 7 Nonetheless, it is generally agreed that patients with simple steatosis

have very MCE slow, if any, histological progression, while patients with NASH can exhibit histological progression to cirrhotic-stage disease.4, 7 The long term outcomes of patients with NAFLD and NASH have been reported in several studies.31, 38-45 Their detailed discussion is beyond the scope of this guideline, but their findings can be summarized as follows; (a) patients with NAFLD have increased overall mortality compared to matched control populations, (b) the most common cause of death in patients with NAFLD, NAFL and NASH is cardiovascular disease, and (c) patients with NASH (but not NAFL) have an increased liver-related mortality rate. Another piece of indirect evidence that supports the progressive nature of NASH is in the features of cryptogenic cirrhosis which is closely related to NAFLD.

4 An ultrasonographic study of patients with T2DM showed a 69% prevalence of NAFLD.21 In another study, 127 of 204 diabetic patients displayed fatty infiltration on ultrasound, and 87% of the patients with fatty infiltration who consented to biopsy had histologic confirmation of NAFLD.22 High serum triglyceride levels and low serum HDL levels

are very common in patients with NAFLD. The prevalence of NAFLD in individuals with dyslipidemia attending lipid clinics was estimated to be 50%.23 Age, gender and ethnicity are also associated with a differential prevalence for NAFLD.4 A number of studies have shown that the prevalence of NAFLD increases with age.24-28 The likelihood of disease progression to advanced fibrosis or mortality increases in older patients with NAFLD.29-31 Many recent studies have reported Epacadostat concentration that male gender is a risk factor for fatty liver disease.4

For example, in a study of 26,527 subjects undergoing medical checkups, the prevalence of NAFLD was 31% in men and 16% in women.32 Compared to non-Hispanic whites, Hispanic individuals have significantly higher and non-Hispanic blacks have significantly lower prevalence of NAFLD.15, 33-35 Protein Tyrosine Kinase inhibitor The prevalence of NAFLD in American-Indian and Alaskan-Native populations appears lower, ranging from 0.6% to 2.2%, although the lack of histologic definition makes it likely that is an underestimate.36, 37 There are data to suggest that hypothyroidism, hypopituitarism, hypogonadism, sleep apnea, and polycystic ovary syndrome independent of obesity are important risk factors for the presence of NAFLD (Table 4).3 The evolution of hepatic histologic changes in patients with NAFL and NASH has been investigated by several studies, but these generally included smaller number of patients and had relatively modest duration of follow-up.4, 7 Nonetheless, it is generally agreed that patients with simple steatosis

have very MCE公司 slow, if any, histological progression, while patients with NASH can exhibit histological progression to cirrhotic-stage disease.4, 7 The long term outcomes of patients with NAFLD and NASH have been reported in several studies.31, 38-45 Their detailed discussion is beyond the scope of this guideline, but their findings can be summarized as follows; (a) patients with NAFLD have increased overall mortality compared to matched control populations, (b) the most common cause of death in patients with NAFLD, NAFL and NASH is cardiovascular disease, and (c) patients with NASH (but not NAFL) have an increased liver-related mortality rate. Another piece of indirect evidence that supports the progressive nature of NASH is in the features of cryptogenic cirrhosis which is closely related to NAFLD.

The MP preparations were characterized by way of fluorescence-activated cell sorting (FACS) with an LSR2 sorter (Becton Dickinson, San Jose, CA) and cytometric data was analyzed with FlowJo 8.8.6 software (Tree Star, Inc., Ashland, Oregon). MP particles were gated on forward and sidescatter acquired from runs including 500 standard beads (Becton Dickinson, San Jose, CA). The number of CD3 (CD11a, CD14, CD147) and AnnexinV (eBioscience, San Diego, CA; GeneTex Inc., Irvine, CA for CD147) double-positive events were calculated relative to the number of beads added to the samples. To avoid unspecific antibody binding, Fc receptors on MPs and target cells were blocked with AG-014699 order FcR Blocking Reagent

(Miltenyi Biotec). Antibody solutions were centrifuged prior to FACS to avoid artifacts due to aggregation. Human peripheral blood was collected in citrate-containing tubes (BD Vacutainer, Buff. Na. Citrate [9NC]; BD, Franklin Lakes, NJ) from patients and healthy controls (protocol approved by the Beth Israel Deaconess Medical Center, approval no. 2004-P-000318).

MPs were isolated by way of differential centrifugation, and S100-MPs were characterized by way of FACS using staining for Annexin find more V, CD3, CD4, CD8, CD14, CD15, CD41, and CD25 (eBioscience) as detailed above. Levels of T cell MPs were correlated with liver histology as detailed in the Supporting Materials and Methods. HSCs (200 × 103/well) were seeded into six-well culture plates

and serum-starved for 24 hours, followed by incubation with 1 × 103 or 50 × 103 S10-MPs or S100-MPs for 24 hours, and RNA extraction using TRIzol reagent (Invitrogen, Carlsbad, CA). ST (0.04 μM/mL) or plain medium served as controls. One microgram of RNA was reverse-transcribed using random primers and Superscript RNase H-reverse transcriptase (Invitrogen). Primers and probes are listed in Supporting Table 2. Relative transcript levels were quantified on a LightCycler 1.5 (Roche, Mannheim, Germany) using the TaqMan methodology. MP membranes were labeled with the PKH26 lipid dye (Sigma-Aldrich, St. Louis, MO). Labeled S10-MPs and S100-MPs were coincubated with LX-2 cells for 0-1, 30, and 60 minutes, washed extensively, and fixed with 2% paraformaldehyde for 15 minutes at room Sitaxentan temperature. HSCs (200 × 103/well) were seeded into six-well cell culture plates (BD Labware, Franklin Lakes, NJ) for 12 hours, serum-starved for 24 hours, followed by incubation with 100 × 103 S100-MPs for 1 minute up to 24 hours. Cells were then washed with phosphate-buffered saline and collected using trypsin/ethylene diamine tetraacetic acid (Cellgrow, Manassas, VA), and single-cell suspensions stained with anti–CD3-APC were followed by FACS analysis. Tumor necrosis factor α (TNFα) (PeproTech) was added to HSC cultures, and ICAM-1 expression assessed after 2, 4, and 24 hours by FACS using anti–ICAM-1 PE (eBioscience, San Diego, CA).

(HEPATOLOGY 2011;) The AP-1 transcription factor complex is composed of

Jun (c-jun, JunB, JunD) and Fra proteins (c-fos, fosB, fra-1, fra-2), and regulates physiological processes such as stress responses, apoptosis, inflammation, and cancer development.1 Genetic overexpression or deletion of single components of AP-1, however, has revealed the specific involvement of the individual AP-1 members selleck chemicals in various disease processes. Fra-1tg mice develop osteosclerosis and have a reduced lifespan, most likely due to progressive destruction of the bone marrow.2 Apart from its effects on bone metabolism, there are several data about the role of Fra-1 in tumor and metastasis development. Overexpression of fra-1 has been reported in several transformed human cell lines3 and possible target genes were also detected.4 Further, there are some data about DNA binding activity of the AP-1 complex in various types of human tumor such hepatocellular carcinoma (HCC), gastric carcinoma, and breast carcinoma.5, 6 A particular involvement of fra-1 in hepatocellular and biliary disorders is not yet known. Cholangiopathies are a frequent cause of impaired liver function and may progress to liver cirrhosis.7 Several disorders with different etiology,

such as primary biliary cirrhosis (PBC), drug-induced cholangiopathy, and graft versus host disease (GVHD) primarily affect the small bile ducts. In contrast, primary sclerosing cholangitis (PSC) mainly involves the large intra- and extrahepatic bile selleck chemical ducts. The pathogenesis of liver

fibrosis in these disorders is yet unclear but may see more involve parenchymal cells such as hepatic stellate cells (HSCs) and cholangiocytes as well as natural killer (NK) cells. Cholangiocytes are key players in the hepatic response to biliary injury.8 Cholangiocytes respond to various types of injury with proliferation and stimulation of HSC.7 Thus, a common histological finding in the earlier phases of cholangiopathy is proliferation of the small bile ducts. This is often accompanied by an inflammatory infiltrate in the portal tracts. Although the etiology of cholangiopathy varies, the pathogenic processes may share similarities. Inflammation and bile duct proliferation is ultimately followed by a loss of bile ducts and, in the case of chronic cholestatic diseases, by a fibrotic response.9 The exact mechanisms how cholangiocyte injury triggers liver fibrosis are unclear. Several rodent models for cholangiopathy including bile duct-ligation and xenobiotic-administration or spontaneous models have been described.9 Inducible rodent models are indeed helpful for studying the pathways during cholangiopathy development but they cannot reproduce the exact disease course. Spontaneous rodent models are rare. One of the well studied ones is the Mdr2 knockout mouse. The Mdr2 knockout mouse lacks bile phospholipids leading to disruption of bile ducts and, moreover, leakage of bile acids to the portal tract.

The N mice on the AIN-93M diet exhibited significantly increased hepatic iron contents (p < 0.05) and hepatic triglycerides (p < 0.05) compared with N mice fed the control diet. Splenic iron contents in N mice were significantly lower than those in J mice, even if control diets. The serum hep-cidin-25 to hepatic iron ratio was significantly higher in J mice compared with N mice on the AIN-93M diet. There were no differences in iron levels or fatty accumulation between J mice on the AIM-93M or control diet. The antioxidant status assessed by the ratio of BAP to dROM (p < 0.05) and microarray analysis revealed inhibition of p oxidation and mitochondrial complex IV. CPT1/2 expression levels

in mitochondria were significantly lower in N mice fed AIN-93M than in J mice fed AIN-93M. Finally, complex

IV function was significantly decreased AZD1152-HQPA ic50 in N mice fed AIN-93M. In particular, the expression of the complex IV subunit (COX 7a2), which is thought to decrease due to the upregulation of methylation by aging and oxidative stress, was altered in N mice fed AIN-93M. Conclusions: The inhibition of COX 7a2 in mitochondrial complex IV might induce hepatic oxidative stress, fat accumulation, and iron metabolic disorder. Disclosures: The following people have nothing to disclose: Masaaki Korenaga, Mihoko Tsuji, Miyuki Kondo, Erina Kumagai, Misuzu Ueyama, Keiko Korenaga, Kazumoto Murata, Tatsuya Kanto, Naohiko Masaki, Masashi Mizokami Background and Aims:

Nonalcoholic fatty liver disease (NAFLD) is highly selleck chemicals llc correlated to obesity and commonly found in developed countries. NAFLD is defined as excessive lipid accumulation in the liver, i.e., hepatosteatosis, characterized by elevated plasma levels of TG and LDL cholesterol, reduced HDL cholesterol and high blood pressure, and fasting hyper-glycemia. Targeting the liver can be challenging as most of the drugs available usually have significant side effects. As the main cells concerned with liver inflammation overexpressed CD98 during NAFLD, we aim here to investigate how a reduction/knock down of CD98 expression via CD98 siRNA loaded into nanoparticles Cyclic nucleotide phosphodiesterase (NPs) can ameliorate the overall liver inflammation. Methods: NPs were made by double emulsion/solvent evaporation technique. To insure lysosomal escape and thus biological efficiency of the siRNA, we pre-complexed NPs with a small positive polymer called polyethylenimine (PEI). In vitro experiment have been performed on mice macrophages (MP) and human hepatic (HH) cells. Age and gender matched wild type (WT) mice were used for in vivo experiments to induce fatty liver by providing to mice 70% fat diet for 8 weeks. Mice were exposed to fat diet food for 8 weeks and received NPs loaded with CD98siRNA by intravenous injections twice a week. Control mice received scrambled siRNA loaded NPs along with fat diet.

Our recent work suggested that clopidogrel significantly induced apoptosis in human gastric epithelial cells (GES-1) through p38 MAPK activation, ultimately disrupting gastric mucosal barrier. However, the detailed mechanism of action is still Torin 1 research buy unknown. Methods: In this study, human gene expression microarray and gene ontology analysis were used to evaluate impact of clopidogrel on gene expression in GES-1 cells; real-time

PCR and Western blot analysis were applied to determine all related genes. The MTT massay and Annexin V/Propidium Iodide Double Staining were used to test the viability and apoptosis of the cells. Results: The gene microarray analysis identified 79 genes that were differentially expressed (P < 0.05 and fold-change >3) when cells were treated with or without clopidogrel. Gene ontology analysis revealed that response to stress and cell apoptosis dysfunction were ranked as top 10 cellular events being

affected, and that the major components of endoplasmic reticulum stress-mediated apoptosis pathway – CHOP and TRIB3 – were up-regulated in a concentration- and time-dependent manner when treated with clopidogrel. Pathway analysis LEE011 revealed that phosphorylation of MAPKs was activated, but that only SB-203580 (a p38-specific MAPK inhibitor) attenuated apoptosis of GES-1 cells and over-expression of

CHOP, which Adenosine triphosphate of both were induced by clopidogrel. Conclusion: It is concluded that increased endoplasmic reticulum stress response is involved in clopidogrel-induced gastric mucosal injury through activation of the p38/MAPK signaling pathway. Key Word(s): 1. Clopidogrel; 2. ER stress; 3. Gastric injury; 4. p38/MAPK; Presenting Author: AKIHIRO MATSUMI Additional Authors: ATSUSHI IMAGAWA, HIROYUKI TERASAWA, KEIKO TAKEUCHI, HITOMI ENDO, HIROYUKI SAKAE, YASUNARI YOSHIDA, HISAE YASUHARA, HIDEKI JINNNO, EISUKE KAJI, HIDENORI HATA, AKIO MORIYA, MORIHITO NAKATSU, MASAHARU ANDO Corresponding Author: AKIHIRO MATSUMI, ATSUSHI IMAGAWA, HIROYUKI TERASAWA, KEIKO TAKEUCHI, HITOMI ENDO, HIROYUKI SAKAE, YASUNARI YOSHIDA, HISAE YASUHARA, HIDEKI JINNNO, EISUKE KAJI, AKIO MORIYA, MORIHITO NAKATSU, MASAHARU ANDO Affiliations: Mitoyo General Hospital Objective: Whether continuous administration of antiplatelet agents during gastric ESD is significantly efficacious in treating post-ESD bleeding remains a controversial issue. In addition, ESD treatment during continuous aspirin administration has been accepted in Japan because a new guideline for endoscopic procedures under antithrombotic therapy was established in 2012.

The bottom line in this discussion is that CAM BTK screening is out there, and both patients and their doctors know it. Unless and until conventional medicine can offer complete, affordable, and well-tolerated cures, our patients

will look outside of traditional medicine for help. We don’t need to embrace every alternative medical system to serve our patients, but there exists a wide variety of modalities which, whether we incorporate them into our practices or not, need to be on our radar, and with which we need more than a passing familiarity. Moreover, we need to provide some guidance to our patients in these areas if we are truly to be their advocate in health care. There is no well-organized, generally accepted, comprehensive review of CAM. Most reviews only address those modalities for which there is Western-style validation. And while this is useful, it does not help us to understand those treatments that are in wide use without

that validation. Most studies break CAM down into four general categories plus the inevitable “other” category. By various names, these groups are shown in Table 1. In general, the Western, evidence-based literature is stronger for these groups (although still pretty scant), and there have been excellent recent reviews.[4] For this reason, I will not go through the evidence base here. In the not-so-distant past, other modalities, such as physical therapy might have been included, but are now regarded as traditional. In addition to the above, there are complete medical systems with often unique diagnostic as well as treatment components. The most widely this website used of these are Ayurveda, classical Chinese medicine, Ureohydrolase homeopathy, chiropractic, and naturopathy. Because these are medical systems rather than discrete interventions, studies are much harder to come by and in general, each has its own internal

logic. It is much more difficult to evaluate a system which is based on centuries of trial and error or of an oral tradition. For example, here is one explanation of the use of Chinese herbals in headache, abstracted from several website on the topic: Description of the headache: One-Sided Headache, Occipital headache, Headache behind the eyes, or Pain at the Vertex (top of the head) The Liver monitors the emotional environment. Negative emotions heat up the Liver, as does alcohol, and other substances of abuse. Because heat rises, along the Liver Channel it will affect the eyes and head. Heat may also involve the Gall Bladder Channel, affecting the side of the head. A one-sided or migraine headache is a Liver/Gall Bladder headache. In Classical Chinese Medicine, Tian Ma Gouteng Wan and Xiao Yao Wan (both of which AG was taking) are used to treat this kind of headache. Description of headache: Frontal headaches Hot, wet conditions in the head can create swelling that is not relieved by anti-inflammatory drugs.