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This study aims to determine the species and evaluate the genetic diversity of the pathogenic and nonpathogenic Rhizoctonia spp. and anastomosis groups (AG) from wheat plants and rhizosphere soils in Turkey. Rhizoctonia species were isolated from plants and rhizosphere soils in wheat fields in 5 provinces in the Central Anatolian Region of Türkiye. As a result of the isolations, a total of 88 multinucleate (MN) and binucleate (BN) Rhizoctonia isolates were obtained. Identifications of the isolates were determined by rDNA-ITS sequence analyses. The identified isolates belonged to MN Waitea circinata var. zeae, W. circinata var. oryzae, W. circinata var. circinata, MN Rhizoctonia solani AG 2-1, AG 2-2, AG 3, AG 4-HGII, AG 4-HGIII, AG 5, AG 8, AG 11 and BN AG A, AG DI, AG E, AG G, AG H, AG I, AG I-like and AG K. The most isolated group was W. circinata var. circinata. In the pathogenicity studies, the most virulent group was determined as R. solani AG 4. Among the binucleate isolates, groups other than R. cerealis AG DI were not found to be pathogenic. Neighbor-joining phylogenetic trees of isolates were constructed from rDNA-ITS sequences. As a result of this study, the regional distribution of MN and BN Rhizoctonia AG isolates in important wheat production areas in the Central Anatolia Region, Türkiye was determined. In addition, this study is the first comprehensive study in which the genetic diversity of Rhizoctonia AGs isolates obtained from wheat and rhizosphere soils in the region was evaluated with a molecular approach. [ABSTRACT FROM AUTHOR]

Background/Aim: Pancreatic cancer represents the most lethal abdominal malignancy, the only chance for achieving an improvement in terms of survival being represented by radical surgery. Although it has been considered that venous invasion represents a contraindication for resection, recently it has been demonstrated that in regards to overall survival after radical resection, it is similar to the one reported after standard pancreatoduodenectomy. Case Report: A 53-year-old patient with no significant medical past was diagnosed with a borderline resectable pancreatic adenocarcinoma invading the superior mesenteric vein. The patient was submitted to pancreatoduodenectomy en bloc with superior mesenteric vein resection; the two jejunal veins were further anastomosed to the remnant portal vein. The postoperative outcome was favorable; the patient was discharged in the 10th postoperative day. Conclusion: Although technically more demanding, pancreatoduodenectomy en bloc with superior mesenteric vein resection and jejunal portal anastomosis is feasible and might offer a chance for long-term survival in borderline pancreatic head carcinoma invading the superior mesenteric vein [ABSTRACT FROM AUTHOR]

Context Prostatic artery embolization (PAE) has been established as a safe and effective treatment option for symptomatic benign prostatic hyperplasia (BPH). Thorough knowledge of detailed prostatic artery (PA) anatomy is essential. Aims The aim of this study was to provide a pictorial review of PA anatomy and prevalence of related anatomical variants, in addition to other anatomical and radiation dose considerations. Settings and Design Case series and review of literature. Materials and Methods We performed PAE for 210 patients from November 2015 to November 2020 under local anesthesia only. Anatomy, procedure duration, fluoroscopy time, radiation dose, technical success, and complications were analyzed. Statistical Analysis Used Descriptive statistics were analyzed using Microsoft Excel software. Results A total of 210 patients (420 sides) were analyzed. Double arterial supply on the same side was noted in 12 patients (5.7%). In 10 patients (4.7%), only a unilateral PA was identified. In two patients (0.9%), no PA could be identified. Frequencies of PA origins were calculated. Penile, rectal, and vesical anastomoses were identified with 79 (18.8%), 54 (12.9%), and 41 (9.8%) of PAs, respectively. Median skin radiation dose, procedure time, and fluoroscopy time were 505 mGy, 73 and 38 minutes, respectively. Complications occurred in nine patients (4.3%), none of them was major. Conclusions Knowledge of PA anatomy is essential when treating BPH by PAE for optimum results. There is no enough evidence to support routine use of preoperative computed tomography angiography and intraoperative cone-beam computed tomography as means of improving safety or efficacy. [ABSTRACT FROM AUTHOR]

Total proctocolectomy with ileal pouch-anal anastomosis is the surgical procedure of choice for patients with medicallyrefractory ulcerative colitis or ulcerative colitis with associated dysplasia. Although most patients after ileal pouch-anal anastomosis experience good functional outcomes, a number of complications may develop. Of the long-term complications, pouchitis is most common. Although most respond to antibiotic treatment, some patients develop chronic pouchitis, leading to substantial morbidity and occasionally pouch failure. In patients with pouchitis who are not responsive to conventional antimicrobial therapy, secondary causes of chronic pouchitis need to be considered, including Crohn's disease of the pouch. In recent years, more literature has become available regarding the medical management of chronic pouchitis andCrohn'sdisease of thepouch, including theuse of newerbiologic agents. Wehereinprovide a concise reviewon inflammatory complications involving the ileal pouch, including a focused approach to diagnosis andmedicalmanagement. [ABSTRACT FROM AUTHOR]

The article presents the discussion on patient with a history of coronary artery bypass grafting with in particular anastomosis of the right internal mammary artery (RIMA).

Background: The presence of extraintestinal manifestations may be associated with the development of pouchitis in patients with ulcerative colitis after ileal pouch–anal anastomosis. The aim of this study was to assess this correlation. Methods: A systematic literature search was performed using MEDLINE and the Cochrane Library. Studies published in English up to 22 May 2017 investigating the association between extraintestinal manifestations and development of pouchitis in adults with ulcerative colitis were included. Case reports were excluded. The association of extraintestinal manifestations with the development of overall and chronic pouchitis was investigated using a random‐effects model. Results: Of 1010 citations identified, 22 observational studies comprising 5128 patients were selected for analysis. The presence of extraintestinal manifestations was significantly associated with both chronic pouchitis (odds ratio 2·28, 95 per cent c.i. 1·57 to 3·32; P = 0·001) and overall pouchitis (odds ratio 1·96, 1·49 to 2·57; P < 0·001). Conclusion: The presence of extraintestinal manifestations is associated with development of pouchitis after ileal pouch–anal anastomosis. [ABSTRACT FROM AUTHOR]

A 2-year-old, spayed female, Korean domestic short-hair cat was presented with depression and vomiting. The patient had history of weight loss lasting seven months. Physical examination revealed icterus in the pinna, oral mucosa, and sclera. Based on ultrasonography and computed tomography, tentative diagnosis was extrahepatic biliary tract obstruction with acquired portosystemic shunt (PSS). Tumor or inflammation of hepatobiliary system was suspected as the cause of obstruction of the common bile duct. But it could not be determined without biopsy. The severely dilated cystic duct was considered to cause portal hypertension and secondary multiple PSS. The patient expired without histopathologic examination. [ABSTRACT FROM AUTHOR]

Background/Aims: Gastric varices (GVs) are a major cause of upper gastrointestinal bleeding in patients with liver cirrhosis. The current treatments of choice are balloon-occluded retrograde transvenous obliteration (BRTO) and the placement of a transjugular intrahepatic portosystemic shunt (TIPS). We aimed to compare the efficacy and outcomes of these two methods for the management of GV bleeding. Methods: This retrospective study included consecutive patients who received BRTO (n=157) or TIPS (n=19) to control GV bleeding from January 2005 to December 2014 at a single tertiary hospital in Korea. The overall survival (OS), immediate bleeding control rate, rebleeding rate and complication rate were compared between patients in the BRTO and TIPS groups. Results: Patients in the BRTO group showed higher immediate bleeding control rates (p=0.059, odds ratio [OR]=4.72) and lower cumulative rebleeding rates (logrank p=0.060) than those in the TIPS group, although the difference failed to reach statistical significance. There were no significant differences in the rates of complications, including pleural effusion, aggravation of esophageal varices, portal hypertensive gastropathy, and portosystemic encephalopathy, although the rate of the progression of ascites was significantly higher in the BRTO group (p=0.02, OR=7.93). After adjusting for several confounding factors using a multivariate Cox analysis, the BRTO group had a significantly longer OS (adjusted hazard ratio [aHR]=0.44, p=0.01) and a longer rebleeding-free survival (aHR=0.34, p=0.001) than the TIPS group. Conclusions: BRTO provides better bleeding control, rebleeding-free survival, and OS than TIPS for patients with GV bleeding. [ABSTRACT FROM AUTHOR]

Congenital portosystemic shunts (CPSS) are rare vascular malformations that create an abnormal connection between portal and systemic veins resulting in complete or partial diversion of the portal flow away from the liver to the systemic venous system. Different anatomic types exist and several classifications have been proposed. They can be associated with other malformations especially cardiac and heterotaxia. The main complications include hepatic encephalopathy, liver tumors, portopulmonary hypertension, and pulmonary arteriovenous shunts. Diagnosis relies on imaging, and prenatal diagnosis is possible. Spontaneous closure of the CPSS is possible in some anatomic forms during the first year of life. When the CPSS remains patent, radiologic or surgical closure of the CPSS may prevent, resolve, or stabilize complications. Interventional radiology plays a key role for both the preoperative evaluation with occlusion test to assess the exact anatomy and to measure portal pressure after occlusion of the CPSS. Endovascular closure is the first option for treatment when possible. [ABSTRACT FROM AUTHOR]

Aim: Congenital portosystemic shunts (CPSS) are rare, congenital malformations that are increasingly often discovered during the fetal period, and for which, the manifestations and evolution are poorly understood. The objective of this review is to describe the phenotype and evolution of forms diagnosed in the antenatal period.Materials and Methods: We performed a systematic review of the literature cited in Pubmed between 1982 and 2016 for CPSS cases diagnosed during the fetal period.Results: We identified 123 cases. The median age at diagnosis was 25 GA (14-38 weeks GA). Eighty patients had 128 associated congenital anomalies. The congenital abnormalities most frequently associated with antenatal diagnosis of CPSS were congenital cardiac disease (30 cases), intrauterine growth restriction (21 cases), vascular anomalies (14 cases), and trisomy 21 (7 cases). Seventy-five complications were reported in the literature. The most frequent were antenatal hemodynamic abnormalities (27 cases), neonatal cholestasis (11 cases), and hyperammonemia (10 cases). Twenty-nine patients had no complications. The choice of treatment was conservative in 29/56 cases, interventional radiology in 15 cases and surgery in 15 cases (three of the latter after failure of embolization).Conclusion: From this review, we propose an algorithm for the perinatal management of this congenital abnormality. [ABSTRACT FROM AUTHOR]

Background:Variability in functional outcome after ileal-pouch anal anastomosis (IPAA) is to a large extent unexplained. The aim of this study was to perform multiple physiological and biochemical tests including an endoscopic examination with histology on IPAA patients with well and poorly functioning pouches to determine factors, or combinations thereof, contributing to functional outcome. Methods:All patients with ulcerative colitis undergoing restorative proctocolectomy between 2000 and 2013 (N = 108) were interviewed using a pouch functioning score. The best and worst functioning quartiles were invited to undergo examination with a barostat measuring pouch volume at preset variable distension pressures, and a pouch endoscopy. Results:Forty five of 58 eligible patients agreed to participate. The most significant physiological parameter differing between the well and poorly functioning pouches was pouch volume at first sensation, urge and discomfort (pvalue <.001). Urge volumes were 213 (CI 171–256) ml for poorly and 352 (CI 305–401) ml for well functioning pouches. Pouchitis episodes were negatively correlated to function. The poorly functioning patients had a higher prevalence of histological signs of inflammation and hand-sewn anastomosis, and a longer remaining rectal cuff, however, nonsignificant. The pouch pressure at sensation thresholds did not differ between the groups. Conclusions:Pouch volume is the most dominant predictor of pouch function in this study. The present comprehensive study of a multitude of different factors that possibly could be contributing to functional outcome, failed to shed much further light on the functional variability among pouch patients. The pouch physiology remains to a large extent unexplained. [ABSTRACT FROM PUBLISHER]

The portacaval shunting (PCS) prevents portal hypertension and recurrent bleeding of esophageal varices. On the other hand, it can induce chronic hyperammonemia and is considered to be the best model of mild hepatic encephalopathy (HE). Pathogenic mechanisms of HE and dysfunction of the brain in hyperammonemia are not fully elucidated, but it was originally suggested that the pathogenetic defect causes destruction of antioxidant defense which leads to an increase in the production of reactive oxygen species (ROS) and the occurrence of oxidative stress. In order to gain insight into the pathogenic mechanisms of HE in the brain tissue, we investigated the effects of PCS in rats on free radicals production and activity levels of antioxidant and prooxidant enzymes in mitochondria isolated from different brain areas. We found that O 2 ·− production, activities of Mn-superoxide dismutase (Mn-SOD), glutathione peroxidase (GPx), glutathione reductase (GR), glutathione transferase (GT), nitric oxide synthase (NOS), and levels of carbonylated proteins differed between the four brain regions both in the amount and response to PCS. In PCS rats, Mn-SOD activity in the cerebellum was significantly decreased, and remained unchanged in the neocortex, hippocampus and striatum compared with that in sham-operated animals. Among the four brain regions in control rats, the levels of the carbonyl groups in mitochondrial proteins were maximal in the cerebellum. 4 weeks after PCS, the content of carbonylated proteins were higher only in mitochondria of this brain region. Under control conditions, O 2 ·− production by submitochondrial particles in the cerebellum was significantly higher than in other brain regions, but was significantly increased in each brain region from PCS animals. Indeed, the production of O 2 ·− by submitochondrial particles correlated with mitochondrial ammonia levels in the four brain regions of control and PCS-animals. These findings are the first to suggest that in vivo levels of ammonia in the brain directly affect the rate of mitochondrial O 2 ·− production. [ABSTRACT FROM AUTHOR]

Purpose: Sphincter-preserving operations performed with bladder-preserving surgery and a cystourethral anastomosis (CUA) do not require a urinary stoma, but leakage from the CUA may develop. The aim of this study was to evaluate the efficacy of performing an additional flap operation. Methods: The subjects were 39 patients who underwent bladder-preserving surgery for advanced rectal cancer involving the prostate, between 2001 and 2015.32 of whom had a CUA and one of whom had a neobladder. Five of these 32 patients underwent an ileal flap operation, 2 underwent an omental flap operation, and 3 underwent an operation using both flaps. Results: Leakage developed in 3 (30%) of the 10 patients who underwent additional flap operations, but in 14 (60.9%) of the 23 patients who did not undergo a flap operation. The mean periods of catheterization for the patients who suffered leakage were 31 weeks (8-108 weeks) in those without a flap and 16 weeks (8-20 weeks) in those with a flap. Four (33.3%) of the 12 patients with leakage after surgery without a flap had a period of urinary catheterization >30 weeks, and 2 (16.7%) had leakage of CTCAE grade 3. There were no cases of leakage after flap surgery. Conclusion: An additional flap operation may decrease the risk of leakage from a CUA. [ABSTRACT FROM AUTHOR]

Purpose: The present work examines α-synuclein expression in the nigrostriatal system of a rat chronic hepatic encephalopathy model induced by portacaval anastomosis (PCA). There is evidence that dopaminergic dysfunction in disease conditions is strongly associated with such expression. Possible relationships among dopaminergic neurons, astroglial cells and α-synuclein expression were sought. Methods: Brain tissue samples from rats at 1 and 6 months post-PCA, and controls, were analysed immunohistochemically using antibodies against tyrosine hydroxylase (TH), α-synuclein, glial fibrillary acidic protein (GFAP) and ubiquitin (Ub). Results: In the control rats, TH immunoreactivity was detected in the neuronal cell bodies and processes in the substantia nigra pars compacta (SNc). A dense TH-positive network of neurons was also seen in the striatum. In the PCA-exposed rats, however, a reduction in TH-positive neurons was seen at both 1 and 6 months in the SNc, as well as a reduction in TH-positive fibres in the striatum. This was coincident with the appearance of α-synuclein-immunoreactive neurons in the SNc; some of the TH-positive neurons also showed α-synuclein immunoreactivity. In addition, α-synuclein accumulation was seen in the SNc and striatum at both 1 and 6 months post-PCA, whereas α-synuclein was only mildly expressed in the nigrostriatal pathway of the controls. Astrogliosis was also seen following PCA, as revealed by increased GFAP expression from 1 month to 6 months post-PCA in both the SN and striatum. The astroglial activation level in the SN paralleled the reduced neuronal expression of TH throughout PCA exposure. Conclusion: α-synuclein accumulation following PCA may induce dopaminergic dysfunction via the downregulation of TH, as well as astroglial activation. [ABSTRACT FROM AUTHOR]

Ammonia is neurotoxic, and chronic hyperammonemia is thought to be a major contributing factor to hepatic encephalopathy in patients with liver disease. Portacaval shunting of rats is used as an animal model to study the detrimental metabolic effects of elevated ammonia levels on body tissues, particularly brain and testes that are deleteriously targeted by high blood ammonia. In normal adult rats, the initial uptake of label (expressed as relative concentration) in these organs was relatively low following a bolus intravenous injection of [N]ammonia compared with lungs, kidneys, liver, and some other organs. The objective of the present study was to determine the distribution of label following intravenous administration of [N]ammonia among 14 organs in portacaval-shunted rats at 12 weeks after shunt construction. At an early time point (12 s) following administration of [N]ammonia the relative concentration of label was highest in lung with lower, but still appreciable relative concentrations in kidney and heart. Clearance of N from blood and kidney tended to be slower in portacaval-shunted rats versus normal rats during the 2-10 min interval after the injection. At later times post injection, brain and testes tended to have higher-than-normal N levels, whereas many other tissues had similar levels in both groups. Thus, reduced removal of ammonia from circulating blood by the liver diverts more ammonia to extrahepatic tissues, including brain and testes, and alters the nitrogen homeostasis in these tissues. These results emphasize the importance of treatment paradigms designed to reduce blood ammonia levels in patients with liver disease. [ABSTRACT FROM AUTHOR]

Pruritus is a common symptom in chronic liver diseases, which may also alter thermal sensitivity. The underlying mechanisms remain unclear and treatments are not satisfactory. Portal-systemic shunting has been proposed to alter thermal sensitivity in cirrhotics. Inflammation-induced enhanced activity of the Transient Receptor Potential Vanilloid 1 (TRPV1) may contribute to pruritus and thermal hyperalgesia. Sildenafil reduces neuroinflammation in portacaval shunt (PCS) rats. The aims were to assess whether: (1) PCS rats show enhanced scratching or thermal sensitivity; (2) TRPV1 activity is enhanced in PCS rats; (3) treatment with sildenafil reduces TRPV1 activation, scratching and thermal hyperalgesia. Rats were treated with sildenafil beginning 3 weeks after surgery. The number of scratches performed were counted. Thermal hyperalgesia was analyzed using the Hargreaves' Plantar Test. TRPV1 activation by measuring the increase in Ca induced by capsaicin in dorsal root ganglia neurons. PCS rats show enhanced scratching behavior, reaching 66 ± 5 scratches/h (p < 0.01) at 21 days after surgery, while controls show 37 ± 2 scratches/h. PCS rats show thermal hyperalgesia. Paw withdrawal latency was reduced (p < 0.05) to 10 ± 1 s compared to controls (21 ± 2 s). Capsaicin-induced calcium increase was higher in dorsal root ganglia cultures from PCS rats, indicating TRPV1functional increase. PCS rats show enhanced scratching behavior and thermal sensitivity and are a good model to study these alterations in chronic liver diseases. Enhanced sensitivity and activity of TRPV1 channel underlies these alterations. Treatment with sildenafil reduces TRPV1 channel sensitivity and activity and normalizes scratching behavior and thermal sensitivity. [ABSTRACT FROM AUTHOR]

Inflammation contributes to cognitive impairment in patients with hepatic encephalopathy (HE). However, the process by which peripheral inflammation results in cognitive impairment remains unclear. In animal models, neuroinflammation and altered neurotransmission mediate cognitive impairment. Taking into account these data, we hypothesized that in rats with HE: (1) peripheral inflammation is a main contributor to neuroinflammation; (2) neuroinflammation in hippocampus impairs spatial learning by altering AMPA and/or NMDA receptors membrane expression; (3) reducing peripheral inflammation with infliximab (anti-TNF-a) would improve spatial learning; (4) this would be associated with reduced neuroinflammation and normalization of the membrane expression of glutamate receptors. The aims of this work were to assess these hypotheses. We analyzed in rats with portacaval shunt (PCS) and control rats, treated or not with infliximab: (a) peripheral inflammation by measuring prostaglandin E2, IL10, IL-17, and IL-6; (b) neuroinflammation in hippocampus by analyzing microglial activation and the content of TNF-a and IL-1b; (c) AMPA and NMDA receptors membrane expression in hippocampus; and (d) spatial learning in the Radial and Morris water mazes. We assessed the effects of treatment with infliximab on peripheral inflammation, on neuroinflammation and AMPA and NMDA receptors membrane expression in hippocampus and on spatial learning and memory. PCS rats show increased serum prostaglandin E2, IL-17, and IL-6 and reduced IL-10 levels, indicating increased peripheral inflammation. PCS rats also show microglial activation and increased nuclear NF-kB and expression of TNF-a and IL-1b in hippocampus. This was associated with altered AMPA and NMDA receptors membrane expression in hippocampus and impaired spatial learning and memory in the radial and Morris water maze. Treatment with infliximab reduces peripheral inflammation in PCS rats, normalizing prostaglandin E2, IL-17, IL-6, and IL-10 levels in serum. Infliximab also prevents neuroinflammation, reduces microglial activation, translocates NF-kB into nucleoli and normalizes TNF-a and IL-1b content in hippocampus. This was associated with normalization of AMPA receptors membrane expression in hippocampus and of spatial learning and memory. The results suggest that peripheral inflammation contributes to spatial learning impairment in PCS rats. Treatment with anti-TNF-a could be a new therapeutic approach to improve cognitive function in patients with HE. [ABSTRACT FROM AUTHOR]

A temporary portocaval shunt ( TPCS) associated with retrohepatic vena cava preservation prevents the edema caused by splanchnic congestion during liver transplantation ( LT), especially for non-cirrhotic cases. We herein report a modified TPCS technique using the recanalized umbilical vein and an end-to-side recanalized umbilico-caval anastomosis for use during pediatric living donor liver transplantation ( LDLT). This work evaluated a group of pediatric patients who underwent LDLT between 2001 and 2014 with the conventional TPCS (n=16) vs the recanalized umbilico-caval shunt (the crossed fingers method, n=10). The crossed fingers method was performed by suturing an end-to-side anastomosis of the patent or recanalized umbilical vein to the vena cava using a continuous monofilament suture like 'crossing the fingers,' that is, placing the left portal vein across the portal vein trunk next to it. The preoperative, surgical, and postoperative characteristics were similar in both groups except for the significantly shorter portal vein clamping time for the crossed fingers method. This method can allow the portal circulation to be totally decompressed before and after implanting the graft and while maintaining the hemodynamic stability throughout all stages of pediatric LDLT. [ABSTRACT FROM AUTHOR]

Background: Peripheral inflammation contributes to the neurological alterations in hepatic encephalopathy (HE). Neuroinflammation and altered GABAergic neurotransmission mediate cognitive and motor alterations in rats with HE. It remains unclear (a) if neuroinflammation and neurological impairment in HE are a consequence of peripheral inflammation and (b) how neuroinflammation impairs GABAergic neurotransmission. The aims were to assess in rats with HE whether reducing peripheral inflammation with anti-TNF-α (1) prevents cognitive impairment and motor in-coordination, (2) normalizes neuroinflammation and extracellular GABA in the cerebellum and also (3) advances the understanding of mechanisms linking neuroinflammation and increased extracellular GABA.Methods: Rats with HE due to portacaval shunt (PCS) were treated with infliximab. Astrocytes and microglia activation and TNF-α and IL-1β were analyzed by immunohistochemistry. Membrane expression of the GABA transporters GAT-3 and GAT-1 was analyzed by cross-linking with BS3. Extracellular GABA was analyzed by microdialysis. Motor coordination was tested using the beam walking and learning ability using the Y maze task.Results: PCS rats show peripheral inflammation, activated astrocytes, and microglia and increased levels of TNF-α and IL-1β. Membrane expression of GAT-3 and extracellular GABA are increased, leading to impaired motor coordination and learning ability. Infliximab reduces peripheral inflammation, microglia, and astrocyte activation and neuroinflammation and normalizes GABAergic neurotransmission, motor coordination, and learning ability.Conclusions: Neuroinflammation is associated with altered GABAergic neurotransmission and increased GAT-3 membrane expression and extracellular GABA (a); peripheral inflammation is a main contributor to the impairment of motor coordination and of the ability to learn the Y maze task in PCS rats (b); and reducing peripheral inflammation using safe procedures could be a new therapeutic approach to improve cognitive and motor function in patients with HE [ABSTRACT FROM AUTHOR]

The possible existence of the same pattern of porto-caval connection in dogs having a single congenital portosystemic shunt (CPSS) and in dogs having multiple acquired portosystemic shunt (MAPSS) secondary to portal hypertension (PH) was evaluated. Retrospective evaluation of all CT examinations of patients having portosystemic shunt (PSS) was performed in a 4-year time period. All anomalous porto-caval connections were assessed for anatomical pattern and compared with published veterinary literature. Records of 25 dogs were reviewed. 16 dogs had a single CPSS (CPSS group), and 9 dogs had multiple acquired PSS secondary to PH (APSS group). The splenophrenic shunt pattern was found in 3 dogs of the CPSS group as a single congenital anomaly without PH and in 2 dogs of the APSS group associated with MAPSS and ascites due to different hepatic diseases causing PH. These findings corroborate two hypotheses: 1) Splenophrenic PSS should be considered as a classical CPSS but if this is not sufficient to alleviate a PH developed after birth because of eventual hepatic or portal diseases, in this case ascites and acquired portal collaterals may develop. In this case, MAPSS and CPSS may coexist. 2) The pattern of splenophrenic PSS, classically described among CPSS, may develop as acquired portal collateral in dogs with PH and it should also be included in the category of APSS. These preliminary findings may be helpful in reconsidering the classical haemodynamics of porto-caval diseases, enrich the classification of APSS in dogs and refine the imaging evaluation of patients with PH. Keywords: Computed tomography, Dog, Portal hypertension, Portosystemic shunt. [ABSTRACT FROM AUTHOR]

Objective: Esophageal variceal bleeding is the most dangerous complication in patients with liver cirrhosis, and it is accompanied by high mortality. Their treatment can be complex, and requires a multidisciplinary approach. This review examines current approaches to the management of patients with liver cirrhosis who have acute esophageal variceal bleeding. Methods: PubMed, Google Scholar, and Cochrane Systematic Reviews were searched for articles published between 1987 and 2015. Relevant articles were identified using the following terms: ‘esophageal variceal bleeding’, ‘portal hypertension’ and ‘complications of liver cirrhosis’. The reference lists of articles identified were also searched for other relevant publications. Inclusion criteria were restricted to the management of patients with liver cirrhosis who have acute esophageal variceal bleeding. Results: It is currently recommended to combine vasoactive drugs (preferable somatostatin or terlipressin) and endoscopic therapies (endoscopic band ligation as first choice, sclerotherapy if endoscopic band ligation not feasible) for the initial treatment of acute variceal bleeding. Antibiotic prophylaxis must be regarded as an integral part of the treatment. The use of a Sengstaken–Blakemore tube is appropriate only in cases of refractory bleeding if the above methods cannot be used. An alternative to balloon tamponade may be the installation of self-expandable metal stents. The transjugular intrahepatic portosystemic shunt is an extremely useful technique for the treatment of acute bleeding from esophageal varices. Although most current clinical guidelines classify it as second-line therapy, the Baveno VI workshop recommends early transjugular intrahepatic portosystemic shunt with expanded polytetrafluoroethylene-covered stents within 72 h (ideally <24 h) in patients with esophageal variceal bleeding at high risk of treatment failure (e.g. Child–Turcotte–Pugh class C < 14 points or Child–Turcotte–Pugh class B with active bleeding) after initial pharmacological and endoscopic therapy. Urgent surgical intervention is rarely performed and can be considered only in case of failure of conservative and/or endoscopic therapy and being unable to use a transjugular intrahepatic portosystemic shunt. Among surgical operations described in the literature are a variety of portocaval anastomosis and azygoportal disconnection procedures. Conclusions: To improve the results of treatment for patients with liver cirrhosis who develop acute esophageal variceal bleeding, it is important to stratify patients into risk groups, which will allow one to tailor therapeutic approaches to the expected results. [ABSTRACT FROM PUBLISHER]

The mechanism of the nearly universal decreased muscle strength in cirrhosis is not known. We evaluated whether hyperammonemia in cirrhosis causes contractile dysfunction independent of reduced skeletal muscle mass. Maximum grip strength and muscle fatigue response were determined in cirrhotic patients and controls. Blood and muscle ammonia con- centrations and grip strength normalized to lean body mass were measured in the portacaval anastomosis (PCA) and sham-operated pair-fed control rats (n = 5 each). Ex vivo contractile studies in the soleus muscle from a separate group of Sprague-Dawley rats (n = 7) were performed. Skeletal muscle force of contraction, rate of force development, and rate of relaxation were measured. Muscles were also subjected to a series of pulse trains at a range of stimulation frequencies from 20 to 110 Hz. Cirrhotic patients had lower maximum grip strength and greater muscle fatigue than control subjects. PCA rats had a 52.7 ± 13% lower normalized grip strength compared with control rats, and grip strength correlated with the blood and muscle ammonia concentrations (r2 = 0.82). In ex vivo muscle preparations following a single pulse, the maximal force, rate of force development, and rate of relaxation were 12.1 ± 3.5 g vs. 6.2 ± 2.1 g; 398.2 ± 100.4 g/s vs. 163.8 ± 97.4 g/s; -101.2 ± 22.2 g/s vs. -33.6 ± 22.3 g/s in ammonia-treated compared with control muscle preparation, respectively (P < 0.001 for all comparisons). Tetanic force, rate of force development, and rate .of relaxation were depressed across a range of stimulation from 20 to 110 Hz. These data provide the first direct evidence that hyperammonemia impairs skeletal muscle strength and increased muscle fatigue and identifies a potential therapeutic target in cirrhotic patients. [ABSTRACT FROM AUTHOR]

Portal hyperperfusion is detrimental to small-for-size livers (SFSLs) in liver transplantation. Surgical techniques modulating portal inflow provide the most effective approach to protect the SFSL. In this report, we describe a technique creating an allograft portacaval shunt that effectively attenuates portal inflow without a requirement of extensive surgical dissection in the recipient during the transplantation. [ABSTRACT FROM AUTHOR]

A case study is presented of a 38-year-old men presented with hepatocellular carcinoma. Ultrasound and computed tomography of abdomen and pelvis showed low-density lesion within the right lobe, along with portacaval shunt and absence of right or left portal veins; and paitent suffered ongoing liver regeneration and absence of encephalopathy during his hospital stay.

CASE REPORT A 2-year-old entire female Golden Retriever and 1-year-old entire male Newfoundland mixed-breed dog were diagnosed with a right division and a central division intrahepatic portosystemic shunt, respectively. The anomalous vessel was ligated in the first dog and attenuated with a cellophane band in the second. Portal hypertension was controlled in both dogs by creating a portocaval venograft, with an ameroid constrictor placed around the venografts to cause gradual attenuation. Both dogs improved clinically following surgery. Postoperative abdominal ultrasonography confirmed intrahepatic portosystemic shunt ligation and gradual attenuation of the portocaval venograft in the first dog but a thrombus was identified within the caudal vena cava 4 weeks after surgery. Postoperative abdominal ultrasonography 6 days after surgery of the second dog demonstrated a thrombus in the central branch of the portal vein; serial ultrasound showed progressive attenuation of the intrahepatic portosystemic shunt and venograft. Treatment of the thrombi included administration of clopidogrel, aspirin and dalteparin. The thrombus was <50% of its first documented size 15 weeks postoperatively in the first dog and was absent 5 weeks after surgery in the second dog. CONCLUSIONS Controlling portal hypertension using a portocaval venograft with simultaneous occlusion or attenuation of an intrahepatic shunt showed encouraging results [ABSTRACT FROM AUTHOR]

Purpose: Intestinal anastomosis is a fundamental procedure in general surgery and required to restore intestinal continuity following resection. The aim of this study was to evaluate whether a gentamicin-coated polyvinylidene fluoride (PVDF) suture material has beneficial effect on anastomotic healing. Methods: Ninety Sprague-Dawley rats were divided into three groups: a PVDF-suture group, a gentamicin-coated PVDF (GPVDF)-suture group and a control group using Maxon® (polyglycolid- co-trimethylene carbonate). For each animal, a colonic anastomosis was performed. Ten animals from each group were sacrificed on postoperative days 3, 5, and 14. Measurements of anastomotic bursting pressure were performed on days 3 and 5. At each time, collagen type I/III ratio, MMP 2 and MMP-9 expression and the proliferation index (Ki67) were analyzed. Results: In total, 90 animals underwent surgery without postoperative complications. Bursting strength in the GPVDF group was significantly elevated on day 5. Immunohistochemistry showed significant increase of the collagen type I/III ratio for PVDF and GPVDF on days 3 and 5. MMP2 was significantly increased for PVDF on days 3 and 5 and for GPVDF on day 5. The analysis of MMP9 revealed significant increase compared to control on day 3 and 5 (GPVDF) as well as on day 5 (PVDF). Staining for Ki67 revealed a significant elevation on postoperative day 3 for the PVDF and the GPVDF group. Conclusions: The present data shows the feasibility of PVDF as suture material for colonic anastomosis and confirms the ability of gentamicin to increase the stability of colonic anastomosis when used as coating material. [ABSTRACT FROM AUTHOR]

Background Although a temporary portocaval shunt (TPCS) improves hemodynamic stability during liver transplantation, the role of TPCS is controversial. We assessed the effects of TPCS in patients undergoing living-donor liver transplantation (LDLT) with a difficult total hepatectomy. Methods We analyzed outcomes by means of retrospective review of 116 LDLTs performed in our institution from May 2011 to October 2013; among these, 33 recipients received TPCS (group I) and 83 did not (group II). We performed TPCS in a high-risk group, such as those with severe perihepatic adhesions, severe retrohepatic adhesions to the vena cava, or massive bleeding during total hepatectomy. Patient demographics and intraoperative and postoperative variables were reviewed. Results No significant differences were observed in the perioperative variables except intraoperative blood loss. The transfusion requirement and operative time in group I were similar to those in group II despite the higher blood loss and more complicated cases. Hemodynamic status and the vasopressor requirement during the operation were similar between the 2 groups. We also compared 2 subgroups to evaluate the effects of TPCS more precisely in the high-risk patients: subgroup A (Model for End-Stage Liver Disease score [MELD], >20) and subgroup B (MELD, ≤20). The intraoperative requirements for platelet concentrate and epinephrine during the early reperfusion phase in subgroup A were significantly lower than those in subgroup A without TPCS. Conclusions TPCS was a safe and useful procedure to improve hemodynamic status and postoperative LDLT outcomes in high-risk and select patients. [ABSTRACT FROM AUTHOR]

Worm transplantation studies show that physiological and reproductive status of the worm is influenced by the microenvironment of the host and critical for vaccine design. Worm migration studies in rats with 75Se-methionine labeled cercariae demonstrated that resistance to reinfection (R/R) requires a host immune response resulting in worm death. In permissive hosts, inflammation due to anti eggs immunity leads to host death, whereas in non-permissive hosts this is not the case due to reduced egg burdens. Eggs-induced pathology and inflammatory debris resulting from immune attack on worms are important for vaccine design. Protective immune responses are perhaps induced when naïve hosts are vaccinated with either schistosome-derived molecules or attenuated cercariae as suggested by the induction of protective anti-parasite antibodies and monoclonals. However, these immunological strategies rarely produce 85-90% R/R as is achievable by portal-caval shunting. Alternatively, induction of anti-schistosoma immunity may induce portacaval shunting, seems highly unlikely although not yet tested. Differential screening with sera from twice-infected rats, protective (F2x) from Fisher vs. non-protective (W2x) from Wistar-Furth rats, was used to identify candidate vaccine antigens. [ABSTRACT FROM AUTHOR]

We report a case of gastric cancer in a patient with non-cirrhotic hyperammonemia secondary to a spontaneous portacaval shunt. The patient, a 69-year-old male, had more than 40 years of abdominal discomfort. On gastroscopy, 2.0 × 1.5-cm irregular uplift ulcers were seen on the lesser curvature of the stomach, and tissue biopsy revealed poorly differentiated adenocarcinoma. His hyperammonemia was found on celiac angiography to be due to the formation of a spontaneous portacaval shunt. Imaging revealed no evidence of cirrhosis or portal hypertension. The patient ultimately underwent a distal gastrectomy and gastroduodenal anastomosis; the spontaneous portacaval shunt was left untreated. Postoperatively, there were no short-term complications such as anastomotic leakage, stricture, or bleeding, and the patient's blood ammonia level decreased to within the normal range. Radical gastrectomy without splenectomy or closure of the abnormal shunt was feasible for the treatment of gastric cancer in a patient with non-cirrhotic hyperammonemia. [ABSTRACT FROM AUTHOR]

Portacaval shunting is a model for hepatic encephalopathy that causes chronic hyperammonemia, disruption of metabolic, signaling, and neurotransmitter systems, and progressive morphological changes. Exposure of cultured cells to ammonia raises intralysosomal pH and inhibits proteolysis, and the present study tested the hypothesis that proteolytic capacity is diminished in portacaval-shunted rats. Proteins were labeled in vivo with tracer doses of diisopropylfluorophosphate (DFP) and clearance of label was assayed. This approach labeled proteins independent of protein synthesis, which is reported to be altered in shunted rats, and avoided complications arising from re-utilization of labeled amino acids that causes underestimation of degradation rate. Characterization of DFP labeling showed that protein labeling was fast, about 50 % of the label was released during a 24 h interval, labeling by DFP metabolites was negligible, inhibition of brain acetylcholinesterase was not detectable, and labeling by [H]- and [C]DFP was equivalent. To assay degradative capacity, proteins were first labeled with [H]DFP, followed by labeling with [C]DFP that was given 24 or 72 h later. The H/C ratio in each animal was used as a relative measure of removal of H-labeled proteins. H/C ratios were generally significantly higher in portacaval-shunted rats than in controls, consistent with reduced proteolytic capacity. Assays of amino acid incorporation into brain protein generally replicated literature reports, supporting the conclusion that protein synthesis unlikely to be markedly inhibited and amino acid recycling influences calculated protein synthesis rates in shunted rats. Therapeutic strategies to reduce ammonia level would help normalize lysosomal functions and protein and lipid turnover. [ABSTRACT FROM AUTHOR]

Neuroinflammation plays a main role in neurological deficits in rats with minimal hepatic encephalopathy (MHE) due to portacaval shunt (PCS). Treating PCS rats with SB239063, an inhibitor of MAP-kinase-p38, reduces microglial activation and brain inflammatory markers and restores cognitive and motor function. The translocator protein-(18-kDa) (TSPO) is considered a biomarker of neuroinflammation. TSPO is increased in brain of PCS rats and of cirrhotic patients that died in hepatic coma. Rats with MHE show strong microglial activation in cerebellum and milder in other areas when assessed by MHC-II immunohistochemistry. This work aims were assessing: 1) whether binding of TSPO ligands is selectively increased in cerebellum in PCS rats; 2) whether treatment with SB239063 reduces binding of TSPO ligands in PCS rats; 3) which cell type (microglia, astrocytes) increases TSPO expression. Quantitative autoradiography was used to assess TSPO-selective H-(R)-PK11195 binding to different brain areas. TSPO expression increased differentially in PCS rats, reaching mild expression in striatum or thalamus and very high levels in cerebellum. TSPO was expressed in astrocytes and microglia. Treatment with SB239063 did not reduces [H]-PK11195 binding in PCS rats. SB239063 reduces microglial activation and levels of inflammatory markers, but not binding of TSPO ligands. This indicates that SB239063-induced neuroinflammation reduction in PCS rats is not mediated by effects on TSPO. Also, enhanced TSPO expression is not always associated with cognitive or motor deficits. If enhanced TSPO expression plays a role in mechanisms leading to neurological alterations in MHE, SB239063 would interfere these mechanisms at a later step. [ABSTRACT FROM AUTHOR]

Background & Aims The pathogenesis of hepatic encephalopathy ( HE) is multifactorial and often associated with the development of brain oedema. In addition to ammonia playing a central role, systemic oxidative stress is believed to aggravate the neuropsychological effects of ammonia in patients with chronic liver disease ( CLD). The aim of this study was to (i) induce systemic oxidative stress in hyperammonaemic portacaval anastomosed ( PCA) rats by inhibiting the antioxidant glutathione using Dimethyl maleate ( DEM) and (ii) investigate whether a synergistic relationship between ammonia and oxidative stress contributes to the pathogenesis of brain oedema in CLD. Methods Four-week PCA and sham-operated rats received DEM (0.4-4 mg/kg/day) for the last 10 days before sacrifice when oxidative stress markers [reactive oxygen species ( ROS) and malondialdehyde ( MDA)] were assessed in blood and frontal cortex. Brain water content was measured using a specific gravimetric technique. Results Dimethyl maleate induced an increase in ROS and MDA in the blood, but not in the brain, of the PCA rats, compared with non-treated PCA rats. This was accompanied with an increase in brain water content ( PCA+ DEM: 78.45 ± 0.13% vs. PCA: 77.38 ± 0.11%, P < 0.001). Higher doses of DEM induced systemic oxidative stress in sham-operated controls, but brain oedema did not develop. Conclusions Dimethyl maleate provoked systemic, not central, oxidative stress in PCA rats, resulting in the development of brain oedema. Independently, hyperammonaemia and systemic oxidative stress do not precipitate brain oedema; therefore, our findings sustain that a synergistic effect between hyperammonaemia and systemic oxidative stress is responsible for the development of brain oedema in HE. [ABSTRACT FROM AUTHOR]

Portal vein branching anomaly occurs due to aberration of normal anastomotic patterns and involution of vitelline veins during development of portal vein. Anatomical knowledge of portal vein and its branching pattern is important for hepatobiliary surgeon and gastrointestinal intervention radiologist. We are reporting a case of absence of portal vein bifurcation showing single main intrahepatic portal vein with gradual decreasing caliber distally, in a young female patient on contrastenhanced computed tomography study of abdomen. Few cases of absence of portal bifurcation have been reported in literature so far. [ABSTRACT FROM AUTHOR]

Purpose: To observe a case of congenital extrahepatic portosystemic shunt and discuss it from the embryological and clinical viewpoints. Methods: An 85-year-old female cadaver was employed for a dissection course at Aichi Medical University in 2009. Results: There was no evidence of liver cirrhosis macroscopically or microscopically. A portosystemic shunt was observed that involved communication between the inferior mesenteric vein, inferior vena cava (IVC), and left ovarian vein by a single Y-shaped shunt vessel. Conclusions: To the best of our knowledge, this is the first reported case of the above-mentioned three veins being connected by a single Y-shaped shunt vessel. Considering the other venous diameters, the shunt appeared to flow into the splenic vein and IVC. It cannot be denied that this shunt may have led to hepatic encephalopathy, although the shunt effect may have been minimal. Embryological development of IVC appears to occur close to the plexus of anastomosing vitelline veins, forming the portal vein. [ABSTRACT FROM AUTHOR]

Background Portal vein arterialization ( PVA) has been used as a salvage inflow technique when hepatic artery ( HA) reconstruction is deemed impossible in liver transplantation ( LT) or hepatopancreatobiliary ( HPB) surgery. Outcomes and the management of possible complications have not been well described. Methods The present study analysed outcomes in 16 patients who underwent PVA during the period from February 2005 to January 2011 for HA thrombosis post- LT ( n = 7) or after liver resection ( n = 1), during curative resection for locally advanced HPB cancers (requiring HA interruption) ( n = 7) and for HA resection without reconstruction ( n = 1). In addition, a literature review was conducted. Results Nine patients were women. The median age of the patients was 58 years (range: 30-72 years). Recovery of intrahepatic arterial signals and PVA shunt patency were documented using Doppler ultrasound until the last follow-up (or until shunt thrombosis in some cases). Of five postoperative deaths, two occurred as a result of haemorrhagic shock, one as a result of liver ischaemia and one as a result of sepsis. The fifth patient died at home of unknown cause. Three patients (19%) had major bleeding related to portal hypertension ( PHT). Of these, two underwent re-exploration and one underwent successful shunt embolization to control the bleeding. Four patients (25%) had early shunt thrombosis, two of whom underwent a second PVA. After a median follow-up of 13 months (range: 1-60 months), 10 patients (63%) remained alive with normal liver function and one submitted to retransplantation. Conclusions Portal vein arterialization results in acceptable rates of survival in relation to spontaneous outcomes in patients with completely de-arterialized livers. The management of complications (especially PHT) after the procedure is challenging. Portal vein arterialization may represent a salvage option or a bridge to liver retransplantation and thus may make curative resection in locally advanced HPB cancers with vascular involvement feasible. [ABSTRACT FROM AUTHOR]

Aim Rats with portacaval shunt ( PCS) are useful experimental models of human hepatic encephalopathy in chronic liver dysfunction. We have previously shown that PCS modifies amine neurotransmitter systems in the CNS and increases voluntary alcohol intake by rats. Hepatocyte transplantation, used in acute liver failure, has recently also been applied to chronic liver diseases, which prompted us to investigate whether the altered brain amine system and the drinking behavior in long-term shunted rats could be normalized by hepatocyte transplants. Methods Hepatocytes, isolated from syngeneic donors by collagenase digestion, were injected (3 × 106 cells/rat) into the pancreatic tail region, 6 months after PCS. Hepatic function was evaluated by measuring urine urea and plasma L-histidine concentrations. A free choice test with two bottles (tap water and 10% ethyl alcohol) was performed for 3 days to assess the rats' preference for alcohol. The rats were euthanized 2 months posttransplantation. Brain histamine and 5-hydroxyindoleacetic acid (5- HIAA) levels were measured by radioenzymatic assay and by HPLC- EC, respectively, N- tele-methylhistamine by GC/ MS while MAOA and MAOB activities by isotopic procedures. Results Portacaval shunt rats with hepatocyte transplants gave more urea than before transplantation, with lower plasma L-His levels and higher body weight versus the PCS counterparts. Also, those rats consumed less alcohol. The CNS amines and 5- HIAA concentrations, as well as MAO-B activity, being abnormally high in untreated PCS rats, significantly reduced after PCS hepatocyte treatment. Conclusions The results support the therapeutic values of hepatocyte transplants in chronic liver diseases and the temporary character of PCS-exerted CNS dysfunctions. [ABSTRACT FROM AUTHOR]

Background/Aims: The relationship between portal hemodynamics and fundal varices has not been well documented. The purpose of this study was to understand the pathophysiology of fundal varices and to investigate bleeding risk factors related to the presence of spontaneous portosystemic shunts, and to examine the hepatic venous pressure gradient (HVPG) between fundal varices and other varices. Methods: In total, 85 patients with cirrhosis who underwent HVPG and gastroscopic examination between July 2009 and March 2011 were included in this study. The interrelationship between HVPG and the types of varices or the presence of spontaneous portosystemic shunts was studied. Results: There was no significant difference in the HVPG between fundal varices (n=12) and esophageal varices and gastroesophageal varices type 1 (GOV1) groups (n=73) (17.1±7.7 mm Hg vs 19.7±5.3 mm Hg). Additionally, there was no significant difference in the HVPG between varices with spontaneous portosystemic shunts (n=28) and varices without these shunts (n=57) (18.3±5.8 mm Hg vs 17.0±8.1 mm Hg). Spontaneous portosystemic shunts increased in fundal varices compared with esophageal varices and GOV1 (8/12 patients [66.7%] vs 20/73 patients [27.4%]; p=0.016). Conclusions: Fundal varices had a high prevalence of spontaneous portosystemic shunts compared with other varices. However, the portal pressure in fundal varices was not different from the pressure in esophageal varices and GOV1. [ABSTRACT FROM AUTHOR]

Abstract: The character of the changes in cell populations within the jejunal graft mucosa during the initial adaptation phase in the host body was investigated. 24 adult male Wistar rats underwent intestinal heterotopic allotransplantation. Aorto-aortal and porto-caval anastomoses were performed using the end-to-side microsurgery technique. Graft tissues were compared to the intestinal tissues of the recipients. This study demonstrates that: (1) Distinct injury to the graft mucosa 1h after transplantation was accompanied by significant reduction in numbers of epithelial secretory cell populations. The injury was more intense in the mesenteric portion. Six hours after transplantation the graft mucosa was covered by a continuous epithelium, but the number of goblet and Paneth cells was found to be less than 30% of that in the recipient epithelium. (2) In comparison with recipients, myeloperoxidase-positive cell numbers increased significantly in the graft mucosa 1h after transplantation. In the epithelial layer, denudation and destruction of villi was associated with a significant reduction in intraepithelial lymphocyte numbers. A significant decrease in mucosal mast cell numbers was detected 6h after transplantation. They attained only 10% of the number found in the recipients. (3) Time-dependent changes in the graft mucosa revealed that CD163-positive cells increased significantly in the graft mucosa during 6h after transplantation and reached the level found in the recipients. In contrast, the myeloperoxidase-positive cell population significantly decreased in the graft mucosa within the initial 6h. [Copyright &y& Elsevier]