Emotions of high arousal, such as fear or joy, are associated with an increase in amplitude, F0, F0 range, F0 variability, jitter, shimmer and speech rate, as well as with fewer and shorter interruptions (inter-vocalization interval). By contrast, emotions of low arousal, such as boredom, induce a low F0, narrow F0 range and low speech rate (Scherer, 1986; Murray

& Arnott, 1993; Bachorowski & Owren, 1995; Banse & Scherer, 1996; Zei Pollermann & Archinard, 2002; Juslin & Scherer, 2005; Li et al., 2007). A recent study showed that source-related parameters linked to phonatory effort (tension), perturbation and voicing frequency allowed good classification of five emotions (relief, joy, panic/fear, hot anger U0126 cost and sadness), but did not allow good differentiation of emotional valence (Patel et al., 2011). Filter-related cues (energy distribution, formant frequencies) have been more rarely considered in studies of emotions (Juslin & Scherer, 2005). However, it seems that spectrum parameters, particularly the energy distribution in the spectrum, F3 and F4, contrary to source-related parameters, differ between emotions of similar arousal but different valence (Banse & Scherer, 1996; Laukkanen selleck chemicals et al., 1997; Zei Pollermann & Archinard, 2002; Waaramaa, Alku & Laukkanen, 2006; Waaramaa et al., 2010). Emotion perception studies showed that an increase in F3 is judged as more positive (Waaramaa et al., 2006, 2010). Valence could also

be reflected in other voice quality- and amplitude-related parameters, with positive emotions being characterized by steeper spectral slopes, narrower frequency ranges, less noisy signals (spectral noise), lower amplitude levels and earlier positions of the maximum peak frequency than negative ones (Hammerschmidt & Jürgens, 2007; Goudbeek & Scherer, 2010). Furthermore, the energy is lower in frequency in positive compared with negative emotions in a large portion of the spectrum (Zei Pollermann & Archinard, 2002; Goudbeek & Scherer, 2010). There are several difficulties associated with the study of affective prosody

in humans. First, voice parameters do not only result from the physiological state of the speaker, but also from socio-cultural and linguistic conventions, and more generally from voluntary control of emotion expression. Therefore, psychological, social 上海皓元 interactional and cultural determinants of voice production may counteract each other, and act as confounding factors in the study of affective prosody (Scherer, Ladd & Silverman, 1984; Scheiner & Fisher, 2011). Second, interferences can exist between linguistic and paralinguistic domains (i.e. between vocal emotion expression and semantic or syntactic cues). In particular, the investigation of the role of formants in emotional communication is rendered difficult by their linguistic importance. They have been suggested to be crucial for communicating emotional valence, but this hypothesis is difficult to test in humans (Laukkanen et al., 1997; Waaramaa et al., 2010).

For example, in a benign lesion that resembles cancer, even if glands are associated with intestinal metaplasia and inflammation, at a fixed distance, the cells are aligned at a tangent to the NBI afferent light, so whitish lines are clearly visible and the mucosal pattern

is retained. On the other hand, if for example the cancer glands are differentiated gastric cancer, distortion of the duct structure means few cells are aligned at a tangent to the NBI incoming rays, resulting in insufficient scattering of light to delineate the whitish lines, so the mucosal structural pattern is lost or unclear. Naturally, unlike a magnifying endoscopic examination, the vascular structure cannot be discerned, but it is of great significance that diagnostic ability is improved by observing the mucosal structure alone. With WLI

until now, diagnosis is based on the size and color of the lesion, and the characteristics of the lesion surface, LBH589 concentration surrounding mucosa, and gastric rugae, making the experience of the endoscopist important and causing great variability in the findings. Furthermore, the diagnostic process involved the following histological and qualitative process: (i) close examination of the entire stomach; (ii) recognition (detection) of the presence of a lesion; and (iii) taking a biopsy of the lesion. A similar diagnostic process occurs with transnasal endoscopy. However, histological examination of the biopsy specimen often produces a benign diagnosis, so many biopsies are actually unnecessary. AZD2281 In recent years, the efficacy of secondary preventative antiplatelet therapy, in particular low-dose aspirin, has been confirmed for a wide range of arteriosclerotic diseases, from myocardial infarction to stroke, by meta-analyses such as that conducted by the Antithrombotic Trialists’ Collaboration,[11] and prescriptions for antiplatelet agents

have increased rapidly. The proportion of patients undergoing endoscopic MCE examinations on antiplatelet therapy has also risen. Until recently, it was routine to suspend antiplatelet therapy for some time prior to an endoscopy, but it has been reported that the risk of a cardiac event increases 3.14 times when patients with coronary artery disease discontinue aspirin therapy.[12] In July 2012, the Japan Gastroenterological Endoscopy Society[13] published new guidelines regarding antiplatelet therapy, and it is now possible to perform biopsies without ceasing aspirin. However, there is a possibility of bleeding after the biopsy, so this is limited to cases where malignancy is strongly suspected. Accordingly, the use of nonmagnified close examination with NBI in screening endoscopies, as conducted in this study, is expected to become more important in the future. We anticipate that the diagnostic capability of ultrathin transnasal endoscopy in screening endoscopies will continue to improve in the future.

For example, in a benign lesion that resembles cancer, even if glands are associated with intestinal metaplasia and inflammation, at a fixed distance, the cells are aligned at a tangent to the NBI afferent light, so whitish lines are clearly visible and the mucosal pattern

is retained. On the other hand, if for example the cancer glands are differentiated gastric cancer, distortion of the duct structure means few cells are aligned at a tangent to the NBI incoming rays, resulting in insufficient scattering of light to delineate the whitish lines, so the mucosal structural pattern is lost or unclear. Naturally, unlike a magnifying endoscopic examination, the vascular structure cannot be discerned, but it is of great significance that diagnostic ability is improved by observing the mucosal structure alone. With WLI

until now, diagnosis is based on the size and color of the lesion, and the characteristics of the lesion surface, selleck surrounding mucosa, and gastric rugae, making the experience of the endoscopist important and causing great variability in the findings. Furthermore, the diagnostic process involved the following histological and qualitative process: (i) close examination of the entire stomach; (ii) recognition (detection) of the presence of a lesion; and (iii) taking a biopsy of the lesion. A similar diagnostic process occurs with transnasal endoscopy. However, histological examination of the biopsy specimen often produces a benign diagnosis, so many biopsies are actually unnecessary. Sirolimus concentration In recent years, the efficacy of secondary preventative antiplatelet therapy, in particular low-dose aspirin, has been confirmed for a wide range of arteriosclerotic diseases, from myocardial infarction to stroke, by meta-analyses such as that conducted by the Antithrombotic Trialists’ Collaboration,[11] and prescriptions for antiplatelet agents

have increased rapidly. The proportion of patients undergoing endoscopic 上海皓元 examinations on antiplatelet therapy has also risen. Until recently, it was routine to suspend antiplatelet therapy for some time prior to an endoscopy, but it has been reported that the risk of a cardiac event increases 3.14 times when patients with coronary artery disease discontinue aspirin therapy.[12] In July 2012, the Japan Gastroenterological Endoscopy Society[13] published new guidelines regarding antiplatelet therapy, and it is now possible to perform biopsies without ceasing aspirin. However, there is a possibility of bleeding after the biopsy, so this is limited to cases where malignancy is strongly suspected. Accordingly, the use of nonmagnified close examination with NBI in screening endoscopies, as conducted in this study, is expected to become more important in the future. We anticipate that the diagnostic capability of ultrathin transnasal endoscopy in screening endoscopies will continue to improve in the future.

Louis, MO) to 1–15 μmol/L. HCC cell viability was determined at 72 hours after addition of 1–15 μmol/L sorafenib or DMSO by WST-8 assay using cell count reagent sulforaphane (Nacalai Tesque, Kyoto, Japan) as previously described.20 The small interfering RNA (siRNA) method was used

to knockdown ADAM9 as previously described.20 At 24 hours after transfection, the cells were analyzed for specific depletion of the messenger RNA (mRNA) of ADAM9 by real-time reverse transcription polymerase chain reaction (RT-PCR) according to the manufacturer’s instructions (Applied Biosystems, Foster City, HSP inhibitor CA). The following siRNAs were used: ADAM9, 5′-UGUCCAAACACAUUAAUCCCGCCUG-3′; scramble control, 5′-UGUCGCACAAACACUUAACUCCCUG-3′. HCC cells were cultured with tumor necrosis factor-α protease inhibitor-I (TAPI-I, 50 μmol/L; Calbiochem, San Diego, CA) or sorafenib (1 μmol/mL) for 24 hours and the supernatants were harvested. The supernatants of cultured HCC cells were harvested at 24 hours after transfection with siRNA. The levels of soluble MICA were determined by DuoSet MICA enzyme-linked immunosorbent assay (ELISA) kit (R&D Systems, Minneapolis, MN). For the detection selleck chemical of membrane-bound MICA, cells were incubated with anti-MICA antibody (Ab) (Santa Cruz Biotechnology, Santa Cruz, CA) and stained with phycoerythrin-goat anti-mouse

immunoglobulin (Ig) (Beckman Coulter, Fullerton, CA) as a secondary reagent and then subjected to flow cytometric analysis using a FACScan flow cytometer (Becton Dickinson, San Jose, CA). Total RNA was isolated using the RNeasy Mini Kit (Qiagen K.K., Tokyo, Japan), and was reverse transcribed using SuperScript III First-Strand Synthesis System (Invitrogen, Carlsbad, CA). The mRNA levels were evaluated using ABI-Prism 7900 Sequence Detection System (Applied Biosystems). Ready-to-use assays (Applied Biosystems)

were used for the quantification of ADAM9 (Hs00177638_m1), and β-actin (Hs99999903_m1) mRNAs according to the manufacturer’s instructions. β-Actin mRNA from each sample was quantified as an endogenous control of internal RNA. Peptides of 20 amino acid residues either partially overlapping each other, covering the α3 domain to the C-terminal end of MICA were synthesized by Sigma. Each peptide substrate (30 μM) was incubated with 50 nM of recombinant ADAM9 in a buffer containing 10 mM HEPES (pH 7.2) and 0.0015% Brij (Sigma). After digestion, the samples were passed over a C18 media (ZipTipC18; Millipore, Billerica, MA), eluted with acetonitrile, and analyzed by matrix-assisted laser desorption/ionization–time of flight/mass spectrometry (MALDI-TOF/MS) to determine the masses of the products and thereby the cleavage site recognized by ADAM9. An expression vector of MICA, pcDNA-MICA, was constructed by using specific complementary DNA (cDNA) from the human hepatoma-derived cell line, Huh-7, as described.

The existence of PHA was related to the more rapid growth velocity and higher coagulase activity compared ATCC 29213 to ATCC 25923. Conclusion: PHA can be reliably achieved in a Bama minipig by injecting the mixture of S. aureus ATCC 29213 and venous blood clot into liver parenchyma. Abscess-formation stage should be observed after the 21st day of the operation. http://www.selleckchem.com/products/ch5424802.html The pathogenesis for ATCC 29213 PHA in Bama minipig might be related to its growth velocity and high coagulase activity.

The animal model of human PHA might be a better tool than previously reported ones for investigating new therapeutic modalities and its possible pathogenesis. Key Word(s): 1. hepatic abscess; 2. S. aureus; 3. minipig; 4. model; Presenting Author: GUOHUI JIAO Additional Authors: BANGMAO WANG, ZONGSHUN LV, WEILI FANG, YULONG YANG, JIE ZHANG, RUI LIN, WEI ZHAO Corresponding Author: BANGMAO WANG Affiliations: Department selleck screening library of Gastroenterology, Tianjin Medical

University General Hospital Objective: Hepatic-associated immunoglobulin-A nephropathy (IgAN) being clinically silent with majority of patients presents with microscopic hematuria, proteinurea, and mild renal impairment. In the auto-immune conditions, high levels of polyclonal free light chains could also be discovered. As a reflection of B cell activation, it can give insight into the activity of the adaptive immune system. Methods: We report a case of hepatic-associated IgAN in a female as a cotton-making factory worker with cryptogenic liver cirrhosis, portal hypertension, nephrotic syndrome and high-level of light chain in circulation without definite evidence of organ deposition. Results: A middle-aged

woman with idiopathic portal hypertension, nephrotic syndrome and hemorrhagic ascites was presented. Pathohistological examinations showed “Banti’s liver”, and diffuse proliferative glomerulonephritis. Laboratory investigations showed normal ALT and AST level, extremely low albumin 17 g/L (35–50 g/L), elevated IgA level and serum creatinine, serum anti-nuclear antibody was Carnitine palmitoyltransferase II positive at 1:100. Serum lambda-type light chain was positive countinously. The urine examination showed proteinuria. Following initiation of treatment to reduce portal pressure, a gradual decrease of proteinuria and serum creatinine to normal range was noted. However, the ascites returned to yellow-appearance without significant reduction. Impaired hepatic clearance of circulating IgA immune complexes and subsequent deposition in renal glomeruli has been considered principally in the pathogenesis of liver cirrhosis associated IgAN. In our case, light chain abnormality could also be found simultaneously which is rare among the previous reports. Free light chains are proteins produced by B lymphocytes during the process of antibody synthesis. Thus, more evidence is needed to be investigated in such cases in respect of further adaptive-immune regulation therapy strategy.

These therapies most often include fluconazole for candida, acyclovir for HSV and ganciclovir or foscarnet for CMV. Other rare infections include mycobacteria, other bacteria, actinomycosis and other virial, fungal and protozoal infections. “
“Aberrant expression of the chemokine CXC chemokine ligand (CXCL)10 has been linked to the severity of hepatitis C virus (HCV)-induced

liver injury, but the underlying molecular mechanisms remain check details unclear. In this study, we describe a yet-unknown proapoptotic effect of CXCL10 in hepatocytes, which is not mediated through its cognate chemokine receptor, but the lipopolysaccharide receptor Toll-like receptor 4 (TLR4). To this end, we investigated the link of CXCL10 expression selleck compound with apoptosis in HCV-infected patients and in murine liver injury models. Mice were treated with CXCL10 or neutralizing antibody to systematically analyze effects on hepatocellular apoptosis in vivo. Direct proapoptotic functions of CXCL10 on different liver cell types were evaluated in detail in vitro. The results showed that CXCL10 expression was positively correlated with liver cell apoptosis in humans and mice. Neutralization of CXCL10

ameliorated concanavalin A–induced tissue injury in vivo, which was strongly associated with reduced liver cell apoptosis. In vitro, CXCL10 mediated the apoptosis of hepatocytes involving TLR4, but not CXC chemokine receptor 3 signaling. Specifically, CXCL10 induced long-term protein kinase B and Jun N-terminal kinase activation, leading to hepatocyte apoptosis by caspase-8, caspase-3, and p21-activated kinase

2 cleavage. Accordingly, systemic application of CXCL10 led to TLR4-induced liver cell apoptosis in vivo. Conclusion: The results identify CXCL10 and its noncognate receptor, TLR4, as a proapoptotic signaling cascade during liver injury. Antagonism of the CXCL10/TLR4 pathway might be a therapeutic option in liver diseases associated with increased Vorinostat datasheet apoptosis. (HEPATOLOGY 2013) Acute hepatitis, cirrhosis, and hepatocellular carcinoma are associated with acute or chronic loss of hepatocellular integrity, which leads to increased mortality in many affected patients.1 Despite different causes of liver cell injury, a major mechanism leading to hepatic dysfunction is hepatocyte apoptosis.2 Thus, a better understanding of programmed cell death within the liver appears important to develop new therapeutic options for many different disease entities. However, the molecular mediators controlling hepatocyte apoptosis have not been fully deciphered in vivo and in vitro. In recent years, the contribution of chemokines to acute and chronic liver diseases has been reported in patients and in animal models.3 Chemokines are a class of small (8-12-kDa) chemotactic cytokines orchestrating the influx of immune cells into sites of inflammation, but also directly affect the biology of resident cells.

Losartan-M6PHSA did not affect metalloproteinase type 2 and 9 activity and did not cause apoptosis of activated HSCs. Conclusion: Short-term treatment with HSC-targeted losartan markedly Z-VAD-FMK in vitro reduces advanced liver fibrosis. This approach may provide a novel means to treat chronic liver diseases. (HEPATOLOGY 2010.) Hepatic fibrosis is the consequence of most types of chronic liver diseases.1 There are no effective therapies to treat liver fibrosis

in patients in which the causative agent cannot be removed.2 In experimentally-induced liver fibrosis, several agents reduce progression of the disease.3 Inhibitors of the renin-angiotensin system (RAS) are probably the most promising drugs. There is extensive evidence indicating that the RAS regulates liver fibrogenesis.4 AP24534 RAS components are overexpressed in livers with fibrosis and angiotensin II induces inflammatory and fibrogenic effects in vivo and in activated hepatic stellate cells through AT1 receptors (HSC).5, 6 The

blockade of AT1 receptors reduces the accumulation of activated HSCs and attenuates liver fibrosis in rats7 and AT1 receptor–deficient mice exhibit attenuated response to hepatic inflammation and fibrosis.8 However, the efficacy of AT1 receptor blockers to reverse established fibrosis is unknown. We propose an innovative approach to deliver drugs to activated HSCs, increasing the concentration in the liver at the sites of active fibrogenesis. Moreover, drug delivery can be useful to avoid systemic undesirable effects such as renal dysfunction. The drug delivery system

applied in this study uses mannose 6-phosphate modified human serum albumin (M6PHSA), a carrier that delivers drugs to activated HSCs.9 M6PHSA binds to the mannose-6-phosphate/insulin growth factor type II receptor (M6P/IGII-R), a surface exposed receptor that is de novo expressed in activated HSCs during liver fibrogenesis.10 Prior studies demonstrated rapid and efficient accumulation of drug-M6PHSA conjugates Methisazone in the fibrotic liver.11, 12 To conjugate losartan to M6PHSA, we employed a novel type of platinum linker called ULS (Universal Linkage System), which can bind losartan via a coordinative bond at one of the aromatic nitrogen atoms in the tetrazole group.13–15 Application of this coordinative linker technology has several important advantages, for instance straightforward coupling of drugs, adequate stability of conjugates, and slow-release of the active pharmacon within target cells.11 In the present study, we administered losartan-M6PHSA for a short period of time to rats with advanced fibrosis. We demonstrate that losartan-M6PHSA accumulates exclusively in the fibrotic liver at the sites of activated HSCs. Importantly, treatment with losartan-M6PHSA, but not free losartan given orally, reduced both hepatic inflammation and fibrosis.

All of them tolerated highly selective TACE Saracatinib well, as the residual volume of the normal liver was maintained at least more than 40% the total volume of the liver in each case. In this study 11 patients underwent one-session TACE, and one patient received a second TACE due to unsatisfactory shrinkage of the tumor. Plain CT was performed to evaluate the lipiodol deposition of the lesions in all patients 7-10 days after

each TACE. Conventional serum chemical tests including liver biochemical tests, complete blood cell counts, prothrombin time, and AFP were detected before ablation. In addition, chest radiography, abdominal ultrasonography, and electrocardiogram (ECG) were assessed before HIFU ablation. Enhanced CT or MRI was applied to evaluate the information of each tumor including its size, location, number, and enhancement before treatment and periodically after HIFU ablation. The device used for the HIFU procedure was a Model-JC200 HIFU system (Chongqing Haifu (HIFU) Tech, Chongqing, China). It consisted of US therapy transducers with a US generator, a real-time diagnostic US device, a six-direction

movement system, computer units for automated control, a treatment bed, and a degassed BVD-523 water circulation unit. A 12-cm diameter PZT-4 piezo-ceramic transducer was employed to produce therapeutic US energy. The frequency of the transducers was 0.8 MHz, with various focal lengths ranging from 135 to 155 mm. A US imaging device (Esaote DU3, Genova, Italy) was used as a real-time imaging guidance in the HIFU system, with a 2.5-3.5 MHz probe. This diagnostic probe was situated in the center of the HIFU transducer, and the integrated transducer was then placed in the bag filled with degassed water. HIFU procedure was performed 2-3 weeks after TACE. All patients received general anesthesia for HIFU treatment,

which prevented patient discomfort and mobilization. After suitable anesthesia was achieved, the patient was positioned either prone or on his or her right side, so that the fantofarone skin overlaying the targeted lesion would be easily put in contact with the degassed water. With movement of the integrated transducer, the targeted liver tumor was clearly identified on US imaging, and the targeted volume was divided into parallel slices of 5-mm separation. The operator outlined the margin of the treated region in each of the slices, including the tumor and at least 1 cm of normal tissue surrounding the tumor. The range of the target of the each slice was automatically recorded by the computer in three orthogonal directions. After a detailed planning session was finished, a linear scanning track of HIFU exposure was selected as an ablative scheme. Using provisional therapeutic parameters based on the depth and vascular supply of the target region, the tumor on each slice was completely ablated from the deep to shallow regions, and this process was repeated slice by slice to achieve entire tumor treatment.

30,31 In subjects with persistent heartburn despite PPI treatment,

RAD001 doses of up to 20 mg trice daily have been used.31 In addition to its effect on TLESR rate, baclofen appears to be also effective in attenuating pain-associated responses using an experimental rodent model.32 This effect, which appears to be mediated by central mechanisms, could be also used in treating refractory GERD patients, where esophageal hypersensitivity is the leading underlying mechanism. Because the drug crosses the blood–brain barrier, a variety of central nervous system (CNS)-related side-effects have been reported. They primarily include somnolence, confusion, dizziness, lightheadedness, drowsiness, weakness, and trembling. The side-effects are likely an important limiting factor in the routine usage of baclofen in clinical practice.

Arbaclofen placarbil (also known as XP19986) is a novel transported pro-drug of the pharmacologically active R-isomer of baclofen. The drug is currently in clinical development for the treatment of refractory GERD. Arbaclofen placarbil was designed to be efficiently http://www.selleckchem.com/products/avelestat-azd9668.html absorbed in the gastrointestinal tract and rapidly metabolized to release R-baclofen after absorption. Unlike baclofen, arbaclofen placarbil is well absorbed from the colon, allowing the drug to be delivered in a sustained release formulation that may allow less frequent dosing and thus reduced fluctuations in plasma exposure. This in turn may lead to potentially improved efficacy through a combination of greater duration of action, subject’s convenience, and better safety profile compared with baclofen.33,34 A recent study demonstrated that arbaclofen significantly reduced the total number of reflux episodes over 12 h in 44 patients with GERD.34 The most efficacious dose of arbaclofen (60 mg) significantly reduced acid reflux episodes by 35% and heartburn

episodes associated with reflux by 49%. Arbaclofen had a favorable 3-mercaptopyruvate sulfurtransferase tolerability and safety profile across the evaluated doses with no significant difference compared with placebo. Recently, the makers of arbaclofen placarbil halted further development due to lack of clinical efficacy in a phase 2B trial. Lesogaberan, a new GABAB agonist, with a better CNS safety profile was developed in order to overcome the side-effects of baclofen. The physiological effects of lesogaberan were evaluated in a small group of patients with persistent GERD-related symptoms despite PPI therapy.35 In this placebo-controlled, cross-over study, lesogaberan significantly decreased the rate of TLESRs, increased basal Lower Esophageal Sphincter (LES) pressure, decreased esophageal acid exposure and decreased the number of postprandial reflux episodes. Furthermore, a decrease in the proximal extent of gastroesophageal reflux events was also demonstrated. However, there was no difference in the number of reflux symptom episodes between the two arms of the study.

However, it would be more valuable if they could provide us with the threshold level of HBV DNA reduction at 12 weeks to achieve HBV undetectability in their cases. As a result, the authors in this article1 tested an approach which is absolutely not valid and nor practical at present. Currently, we believe that ETV monotherapy is not a good alternative as a rescue therapy

www.selleckchem.com/products/U0126.html for cases with LAM and or LAM/ADV resistance, whereas continued treatment resulted in virus suppression in a higher percentage of patients in the series of Shim and colleagues. ETV is obviously not a drug with a high genetic barrier to resistance in the setting of LAM refractoriness. In such situations, we have to admit the effectiveness of other alternative drugs, including tenofovir. Yucel Ustundag*, Omer Topalak†, * Zonguldak Karaelmas University School of Medicine, Department of Internal Medicine, Gastroenterology Clinics, Zonguldak, Turkey,

† Dokuz Eylül University School of Medicine, Department of Internal Medicine, Gastroenterology Clinics, Izmir, Turkey. buy Enzalutamide “
“A 50 year old male presented with nodular swellings on his lower limbs, buttocks, abdomen, chest and back for 15 days. He denied any history of abdominal pain or steatorrhea. He was a known hypertensive and a diabetic for three years. He had a history of chronic alcohol abuse (30 years). At presentation his vital signs were stable but he appeared pale. Multiple subcutaneous nodules of variable consistency were present in the lower limbs, abdomen and buttocks. The swellings on the buttock, back and upper chest wall were firm and

tender (Figure 1A and B). The findings of fine needle aspiration cytology and biopsy of the cutaneous lesions revealed lobular panniculitis with foci of fat necrosis. In the areas of necrosis ghost adipocytes were also seen (Figure 2A and B). His investigations revealed low haemoglobin (Hb-7.8 gm/dL) with peripheral blood smear showing macrocytes, microcytes and PRKACG hypersegmented neutrophils suggestive of combined deficiency anemia. His serum amylase was 2115 U/L and his lipase was 1870 U/L. Serum calcium was 7. 9 mg/dL. Serum triglyceride was 132 mg %. Contrast CT abdomen revealed changes of acute on chronic pancreatitis with evidence of a hypodense collection in the region of head, multiple calcifications and dilation of main pancreatic duct (Figure 3A and 3B). The patient was managed with conservatively and improved with resolution of pain and normalisation in levels of amylase. Panniculitis is inflammation in the adipose tissue which can result from numerous causes. Pancreatic panniculitis is a rare cause of panniculitis resulting from enzyme mediated saponification of fat. Some of the lesions may ulcerate and yield an oily secretion. Histopathology is characterised by a predominantly lobular panniculitis with foci of fat necrosis and an imflammatory infiltrate at periphery.