The peanut wild relative Arachis stenosperma accession V10309 was identified as resistant to a number of pests and diseases, including LLS and rust. Aiming to better understand the mechanisms of resistance of A. stenosperma to C. personatum and P. arachidis, determine initial key steps

of the plant–pathogen interaction and to contribute for studies on genes involved Selumetinib concentration in this interaction, ultrastructural analysis was performed on leaves of A. stenosperma V10309 (wild, resistant) and A. hypogaea cv. IAC-Tatu (cultivated, susceptible) inoculated with C. personatum or P. arachidis. For both fungal species, adhesion, germination of spores and hyphal proliferation occurred in both species but was more limited and later in A. stenosperma than in A. hypogaea, and no successful penetration was observed in the former. These data suggest that in A. stenosperma, infection is hampered at the stage of penetration. This is the first morphological description of the first hours of the interaction of plant pathogenic fungi

and the resistant wild species A. stenosperma. “
“Sporadic incidences of Citrus tristeza virus (CTV) in western Crete resulting from the introduction of a mild strain (Spanish isolate T385) have been reported previously. Further analysis within this region has MK-8669 identified an emerging second CTV strain with minimal genetic divergence, sharing 99% nucleotide identity with the severe stem-pitting isolate Taiwan-Pum/SP/T1. Other severe isolates from the Mediterranean region appear in the same phylogenetic cluster, indicating movement or new introductions and the need for targeted control actions and improved phytosanitary measures in this area. “
“Rice black-streaked dwarf virus (RBSDV) is transmitted naturally to important crops such as rice, maize, barley and wheat in a persistent manner by the planthoppers, Laodelphax striatellus, Unkanodes sapporona and Unkanodes albifascia. Insect vector transmission

Flavopiridol (Alvocidib) tests are the basis for identifying viral incidence, evaluating the resistance of varieties and selecting resistance sources for rice and maize breeding. A simple, rapid and reliable method is described by which virus-free small brown planthoppers (L. striatellus) acquired RBSDV from frozen infected rice leaves and transmitted it to healthy rice and maize plants. After feeding on frozen infected rice leaves, the planthoppers were tested by RT-PCR for the presence of virus after 10, 15, and 22 days, respectively. The percentages of RBSDV-containing insects were 0, 25 and 71.43% of L. striatellus fed on frozen infected rice leaves compared to 0, 28.25 and 71.43% of L. striatellus fed on fresh infected rice leaves, respectively. In transmission tests, three of eight rice seedlings (37.

5 cells which were then infected with JFH1. Overexpression of FOXO3 increased FHRE-reporter activity at least 10-fold. JFH1 further stimulated FHRE-luciferase reporter activity of all constructs except S574A (Fig. 4A). In addition, HCV caused nuclear translocation

of the WT, S294A, and S425A mutants but not the S574A mutant as assessed by either fractionation and western blotting (Fig. 4B, densitometry analysis in Fig. S4C) or immunofluorescence (Fig. 4C). We further examined the effect of HCV on FOXO3 mutants by cIEF (Fig. 4D). As seen previously, HCV caused an acidic shift of the dominant nuclear FOXO3 peak from pI 6.0 to pI 5.7 (Fig. 4E) and this was blocked by JNK inhibitor (Fig. S4E). The S425A substitution had no effect on this shift, but the S574A mutation completely abolished the formation of the acidic buy CAL-101 shift species (Fig. 4D). The effect of HCV on the S294 mutant was more complex and infection resulted in loss of the single dominant species and its replacement with multiple more acidic forms. To confirm that S574 is phosphorylated by JNK, we overexpressed a constitutively active

form of JNK1 selleckchem in cells transfected with either WT or S574A FOXO3. Figure 4E shows that, like HCV, JNK1 stimulates FHRE-luciferase activity of WT, but not S574A FOXO3. Figure 4F shows that JNK1 also generated a novel FOXO3 peak with identical pI to that produced by HCV. Finally, we used liquid chromatography, mass spectroscopy (LC-MS) to analyze FOXO3 from cells infected with HCV. A peptide-ion corresponding to the residues 570-606 was observed with phosphorylation on S574 (Fig. S5). These results demonstrate that S574 is a previously

unrecognized site that is necessary for HCV to cause the JNK-dependent alteration in protein pI, nuclear localization, and transcriptional activity. Arginine methylation has been shown to regulate the stability and nuclear localization of FOXO1[17] and since ethanol is known to alter cellular methylation potential,[18] we examined whether changes in methylation could be responsible for ethanol effects on FOXO3. We addressed this question using cIEF of immunoprecipitated FOXO3. Figure 5A shows that cytosolic FOXO3 from untreated cells was 5-Fluoracil methylated but the novel ethanol induced cytosolic species at pI 5.66 was not. Functional consequences of FOXO3 methylation defects were tested using the methyl donor, betaine.[19] Addition of betaine completely prevented the HCV/ethanol-induced inhibition of FHRE reporter activity (Fig. 5B) and decrease in FOXO3 target gene mRNA expression (Fig. 5C). Betaine also restored HCV-induced nuclear translocation of FOXO3 in the presence of ethanol and prevented the decrease in steady-state levels of SOD2 protein (Fig. 5D). Figure 5E demonstrates that betaine also restored both of the HCV-induced nuclear species of FOXO3 (pI 5.85 and 6.62) that are decreased or eliminated by the HCV/ethanol combination.

23-26 Thus, we used TNF-α selleck kinase inhibitor to mimic natural immunomediated apoptosis and found that the JFH-1/S2–replicating cells have lower susceptibility to the apoptosis induced by these cytokines. In JFH-1/S2–transfected cells, TNF-α–induced apoptosis detected by TUNEL assay was substantially lower than that of JFH-1/wt–transfected cells (Fig. 4). We confirmed it by staining with anticleaved PARP. In complete agreement with the results produced by way of TUNEL assay, the number of anticleaved PARP stained cells among JFH-1/S2–infected cells was significantly lower than that among JFH-1/wt–infected cells (Fig. 5). In our previous study,

we reported that HCV-specific immune responses with T cell proliferation and interferon-γ production were maintained until the disappearance of viremia in the patient serum–infected chimpanzee.11 This finding indicates that continuous selection pressure in the infected chimpanzee might have contributed to the emergence of a clone with an ability to escape the cytokine-induced apoptosis. We are not sure whether this phenotype of JFH-1/S2 is due to its lower replication VX-770 efficiency and thus lower production of HCV proteins. The accumulation of viral proteins might predispose cells to the apoptosis induced by TNF-α. To answer this question, it will be necessary

to investigate the genomic regions of JFH-1/S2 and cellular host factors responsible for the ability of this strain to escape the apoptosis. Fenbendazole By way of mapping analysis for JFH-1/S2, we could determine responsible regions;

NS5B was for lower replication efficiency (Supporting Fig. 1B), and P7 and NS2 were for enhanced viral particle assembly (Supporting Table 2). For the evasion of apoptosis, we could not specify the responsible region, because both chimeric constructs, JFH-1/S2-wt and JFH-1/wt-S2, showed less susceptibility to cytokine-induced apoptosis to a certain extent. These data indicate that both structural and nonstructural regions might have contributed to the acquisition of this phenotype. Previously, a potent antiapoptotic effect of the HCV NS5A protein was described.27 NS5A interacts with Bin1, which is a nucleocytoplasmic c-Myc–interacting protein with tumor suppressor and apoptotic properties, thus inhibiting Bin1-associated apoptosis. Because JFH-1/S2 contains several mutations in the NS5A region (Supporting Table 1), one or more mutations in this protein may be associated with antiapoptotic effects. In conclusion, we demonstrated that the JHF-1/S2 strain acquired phenotypes of lower replication, higher virus production, and less susceptibility to cytokine-induced apoptosis. These phenotypes were associated with mutations that emerged 23 weeks after infection in a chimpanzee, and might have contributed to long-term infection in vivo. Such control of viral functions by specific mutations may be a key viral strategy to establish persistent infection. We are grateful to Francis V. Chisari for providing the Huh-7.5.

[130] Ultimately, the effects of these amino acids may turn out to have more important effects on promotion of maintenance of lean body mass than a direct effect on HE. 30. Daily energy intakes should be 35-40 kcal/kg ideal body weight (GRADE I, A, 1). 31. Daily protein intake should be 1.2-1.5

g/kg/day (GRADE I, A, 1). 32. Small meals or liquid nutritional supplements evenly distributed throughout the day and a late-night snack should be offered (GRADE I, A, 1). 33. Oral BCAA supplementation may allow recommended nitrogen intake to be achieved and maintained in patients intolerant of dietary protein (GRADE II-2, B, 2). Liver transplantation remains the only treatment option for HE that does not improve on any other treatment, but is not without its risks. The management of these buy Palbociclib potential transplant candidates as practiced in the United States has been published elsewhere,[131, 132] and European guidelines are under way. Hepatic encephalopathy by itself is not considered an indication for LT unless associated with poor liver function.

However, cases do occur where HE severely compromises the patient’s quality of life and cannot be improved despite maximal medical therapy and who may be LT candidates despite otherwise good liver status. Large PSSs may cause neurological disturbances and persistent HKI-272 manufacturer HE, even after LT. Therefore, shunts should be identified and embolization considered before or during transplantation.[133] Also, during the transplant workup, severe hyponatremia should be corrected slowly. Hepatic encephalopathy Methisazone should improve after transplant, whereas neurodegenerative disorders will worsen. Therefore, it is important to distinguish HE from other causes of mental impairment, such as Alzheimer’s disease and small-vessel cerebrovascular disease. Magnetic resonance imaging and spectroscopy

of the brain should be conducted, and the patient should be evaluated by an expert in neuropsychology and neuro-degenerative diseases.[134] The patient, caregivers, and health professionals should be aware that transplantation may induce brain function impairment and that not all manifestations of HE are fully reversible by transplantation.[135] One difficult and not uncommon problem is the development of a confusional syndrome in the postoperative period. The search of the cause is often difficult, and the problem may have multiple origins. Patients with alcoholic liver disease (ALD) and those with recurrent HE before transplantation are at higher risk. Toxic effects of immunosuppressant drugs are a frequent cause, usually associated with tremor and elevated levels in blood. Other adverse cerebral effects of drugs may be difficult to diagnose. Confusion associated with fever requires a diligent, systematic search for bacterial or viral causes (e.g., cytomegalovirus).

“
“For this study, we have examined the literature and the morphological diversity, as well as analyzed the nuclear SSU rDNA sequences of two very common and cosmopolitan species formerly known as Euglena deses Ehrenb. and Euglena intermedia (G. A. Klebs) F. Schmitz. Our studies have shown that there is evidence for distinguishing only one species (E. deses). Here, we define new diagnostic features for E. deses, namely, periplast ornamentation (the presence of small papillae—discovered for the first time in this species) and the lateral location of the anterior Rapamycin canal opening, from which the flagellum emerges. We also designate the epitype

and emend the diagnosis for E. deses. “
“The diazotrophic unicellular cyanobacterium Cyanothece sp. ATCC 51142 demonstrates circadian patterns in nitrogenase activity, H2 production and glycogen storage when grown under nitrogen-fixing, 12:12 light:dark (L:D) conditions. In this study, we grew Cyanothece sp. ATCC 51142, and another strain in this genus, Cyanothece sp. PCC 7822, under long-day (16:8 L:D) and short-day (8:16 L:D) nitrogen-fixing conditions to determine if they continued to display circadian rhythms. Both strains demonstrated similar circadian patterns for all three metabolic parameters when grown under long-day conditions. However, the strains responded differently to short-day selleck inhibitor growth conditions.

Cyanothece sp. ATCC 51142 retained reasonable circadian patterns under 8:16 L:D conditions, whereas Cyanothece sp. PCC 7822 had quite damped patterns without a clear circadian pattern. In particular, glycogen storage changed heptaminol very little throughout the day and we ascribe this to the difference in the type

of glycogen granules in Cyanothece sp. PCC 7822 which has small β-granules, compared to the large, starch-like granules in Cyanothece sp. ATCC 51142. The results suggested that both mechanistic and regulatory processes play a role in establishing the basis for these metabolic oscillations. “
“Brown algae of the order Laminariales, commonly referred to as kelps, are the largest and most productive primary producers in the coastal inshore environment. The genus Ecklonia (Lessoniaceae, Phaeophyceae) consists of seven species with four species in the Northern Hemisphere and three in the Southern Hemisphere. It was recently transferred to the family Lessoniaceae based on phylogenetic analyses of nuclear and chloroplastic markers, though the type of the genus was not included and its relationship to allied genera Eckloniopsis and Eisenia remained unresolved. The present study is the first to produce a phylogeny focussed on the genus Ecklonia. It included sequences from nuclear, mitochondrial and chloroplastic DNA, for most of the distribution range of the three current Southern Hemisphere species (E. radiata, E.

“
“For this study, we have examined the literature and the morphological diversity, as well as analyzed the nuclear SSU rDNA sequences of two very common and cosmopolitan species formerly known as Euglena deses Ehrenb. and Euglena intermedia (G. A. Klebs) F. Schmitz. Our studies have shown that there is evidence for distinguishing only one species (E. deses). Here, we define new diagnostic features for E. deses, namely, periplast ornamentation (the presence of small papillae—discovered for the first time in this species) and the lateral location of the anterior buy LEE011 canal opening, from which the flagellum emerges. We also designate the epitype

and emend the diagnosis for E. deses. “
“The diazotrophic unicellular cyanobacterium Cyanothece sp. ATCC 51142 demonstrates circadian patterns in nitrogenase activity, H2 production and glycogen storage when grown under nitrogen-fixing, 12:12 light:dark (L:D) conditions. In this study, we grew Cyanothece sp. ATCC 51142, and another strain in this genus, Cyanothece sp. PCC 7822, under long-day (16:8 L:D) and short-day (8:16 L:D) nitrogen-fixing conditions to determine if they continued to display circadian rhythms. Both strains demonstrated similar circadian patterns for all three metabolic parameters when grown under long-day conditions. However, the strains responded differently to short-day www.selleckchem.com/products/CAL-101.html growth conditions.

Cyanothece sp. ATCC 51142 retained reasonable circadian patterns under 8:16 L:D conditions, whereas Cyanothece sp. PCC 7822 had quite damped patterns without a clear circadian pattern. In particular, glycogen storage changed selleck screening library very little throughout the day and we ascribe this to the difference in the type

of glycogen granules in Cyanothece sp. PCC 7822 which has small β-granules, compared to the large, starch-like granules in Cyanothece sp. ATCC 51142. The results suggested that both mechanistic and regulatory processes play a role in establishing the basis for these metabolic oscillations. “
“Brown algae of the order Laminariales, commonly referred to as kelps, are the largest and most productive primary producers in the coastal inshore environment. The genus Ecklonia (Lessoniaceae, Phaeophyceae) consists of seven species with four species in the Northern Hemisphere and three in the Southern Hemisphere. It was recently transferred to the family Lessoniaceae based on phylogenetic analyses of nuclear and chloroplastic markers, though the type of the genus was not included and its relationship to allied genera Eckloniopsis and Eisenia remained unresolved. The present study is the first to produce a phylogeny focussed on the genus Ecklonia. It included sequences from nuclear, mitochondrial and chloroplastic DNA, for most of the distribution range of the three current Southern Hemisphere species (E. radiata, E.

4D). These results indicate that

C/EBPβ blocks TNFα-induced apoptosis by the inhibition of caspase activation. Our findings suggested that the loss of C/EBPβ would result in an increase in hepatocyte sensitivity to TNFα. Selleck Silmitasertib To investigate this possibility, primary hepatocytes were isolated from littermate control wild-type mice and c/ebpβ knockout mice, placed in culture, and examined for their sensitivity to TNFα-induced death. TNFα treatment alone was not sufficient to induce death in either wild-type or C/EBPβ null hepatocytes (data not shown). When the hepatocytes were sensitized to TNFα by infection with Ad5IκB, however, cell death at 10 and 24 hours in the knockout cells was two-fold greater than in wild-type cells (Fig. 5A). Knockout cells had greater levels of the cleaved active forms of caspase 3 and caspase 7 that resulted in increased

caspase activity as indicated by cleavage of the caspase substrate poly(ADP-ribose) polymerase (Fig. 5B). We have therefore been able to demonstrate with both overexpression and loss-of-function approaches that C/EBPβ mediates hepatocyte resistance to TNFα cytotoxicity. http://www.selleckchem.com/products/chir-99021-ct99021-hcl.html The in vivo function of C/EBPβ in LPS-induced liver injury was determined. The ability of C/EBPβ to block TNFα-dependent liver injury in vivo was examined by comparing the degree of liver injury in wild-type and c/ebpβ−/− mice after the administration of a usually nontoxic dose of LPS. Wild-type mice had normal ALT levels after

treatment with low-dose LPS, but ALT Phosphatidylinositol diacylglycerol-lyase levels were increased in knockout mice (Fig. 6A). Reflective of the predominantly apoptotic nature of TNFα-induced hepatocyte death, a much greater increase occurred in the numbers of terminal deoxynucleotidyl transferase–mediated dUTP nick-end labeling (TUNEL)-positive cells in LPS-treated c/ebpβ−/− mice compared with littermate controls (Fig. 6B). The steady-state numbers of TUNEL-positive cells in the liver were increased eight-fold at 6 hours and four-fold at 24 hours in null mice compared with control mice. To ensure that injury from LPS represented toxicity from TNFα, C/EBPβ null mice were examined for sensitivity to injury from TNFα. An injection of TNFα led to liver injury in knockout but not wild-type mice as demonstrated by increased serum ALT levels (Fig. 6C) and numbers of apoptotic cells (Fig. 6D) at 6 hours. C/EBPβ therefore mediates hepatocyte resistance to TNFα toxicity in vivo as well as in vitro. In the absence of NF-κB signaling, TNFα-induced JNK activation is converted from a transient to prolonged response that triggers cell death in part through altered protein degradation of antiapoptotic proteins. To examine whether the proapoptotic effects of JNK during TNFα-dependent injury in vivo are mediated via degradation of C/EBPβ, we investigated the effect of loss of jnk2 on C/EBPβ induction after GalN/LPS treatment.

6 was followed by several other

case reports and small series,7-12 suggesting that the centrilobular variant represents an early, severe or acute presentation of AIH, which may either evolve into the classical portal-based hepatitis or remain centrilobular.11, 12 In the largest series to date, 20 of 114 (18%) of liver biopsies from classical AIH patients (none with ALF) had predominantly centrilobular necroinflammation, four of whom had exclusive centrilobular disease.11 Patients with the centrilobular variant more often presented as an acute hepatitis, had higher hepatic activity indices, and had less fibrosis than did the classical portal-based variants; centrilobular hemorrhage resembling hepatic venous outflow obstruction (MHN4 in the present work) has also been noted.12 Although these reports described Selleckchem GSK2126458 patients with acute AIH without ALF, a few subsequent cases of ALF considered likely autoimmune feature central perivenulitis as the histological hallmark of severe, immune-mediated liver injury.8, 9 The individual histological features of autoimmunity are not entirely specific www.selleckchem.com/products/dabrafenib-gsk2118436.html to AI-ALF. Although the 16 liver specimens from patients with

“defined” etiology exhibited fewer features of autoimmunity, those from all five patients with HBV-ALF and two of nine from APAP-ALF were characterized by at least some autoimmune features. Several explanations are plausible, including more than one etiology, misdiagnosis, similar immunopathogenesis, or evolution from an early metabolite-mediated necrosis to a lymphocyte-plasma cell mediated injury following exposure of autoantigens. A similar immunopathogenesis between AI-ALF and HBV-induced ALF seems likely, as overwhelming viral infections are known to activate B lymphocytes to differentiate into plasma cells secreting immunoglobulin M (IgM) and IgG against the hepatitis B core antigen.23, 24 Moreover, despite the classical description of APAP-induced hepatotoxicity as bland centrilobular necrosis, the innate immune system also participates in liver injury.25 It should be emphasized that the aim of the current study was to identify

AI-ALF among subjects with indeterminate etiology, and no single test, including liver histology, is capable of cinching the diagnosis; AI-ALF remains a diagnosis IKBKE based on exclusion of viral and drug etiologies first, but also requires histological and serological evaluation. Although liver biopsies are not performed routinely in ALF due to bleeding risk, our observations suggest that the information provided by histology may be worth the risk in indeterminate cases. It remains unclear whether the centrilobular variant of AIH represents the same or a different disease as the classical portal-based variant. Perivenulitis and centrilobular necrosis are also features of atypical liver allograft rejection, which appears to be distinct from classical, portal-based rejection in that it resists immunosuppression and may presage chronic rejection.

172, -0.453-0.110) (SMD in spine BMD: -0.169, -0.476-0.138). selleck chemical Sensitivity analyses showed consistent results. Publication bias was detected in the analysis of bone fractures and osteoporosis. Conclusion: Current publications

indicate significant association between bone fractures and ALD, independent of osteoporosis or BMD. Due to the qualitative and quantitative heterogeneity among studies, further research using homogeneous populations and control of confounding risk factors for fractures are needed to elucidate the mechanism of bone fractures in ALD. Association between alcoholic liver disease and bone fractures. The size of each square is proportional to the study’s weight. Diamond is the summary estimate from the pooled studies with 95% CI. CI: confidence interval. (Random effect

model) Disclosures: The following people have nothing to disclose: Chang Seok Bang, Hyo Sun Kim, Sang Hyun Park, Eun Jin Kim, Ki Tae Suk, Dong Joon Kim Somatostatin analogues (SA) reduce liver volumes (LVs) in patients with polycystic liver disease (PLD). However, these patients show a considerable variability in treatment responses, making it difficult to predict response to SA therapy. Our aim was to Napabucasin ic50 identify specific patient, disease or treatment characteristics that predict response in PLD during SA therapy. We pooled the individual patient data of 4 trials (NCT00771888,NCT00426153, NCT01157858, NCT01354405) of long-acting SAs (120 mg lanreotide or 40 mg octreotide) for 6 or 12 months in PLD that included liver volume as the primary outcome. We performed uni- and multivariate linear regression analysis with 9 preselected patient, disease and drug variables to identify independent predictors of response, defined as percent change in LV. Secondary outcome was percent

change in kidney volume in the ADPKD subgroup. All analyses were Non-specific serine/threonine protein kinase adjusted for baseline LV and center effect (random). We included 153 PLD patients (86% female, mean age 50 years, median LV 4974 ml, 69% ADPKD) from 3 international centers, all treated with octreotide (n=70) or lanreotide (n=83). Mean reduction in LV was 4.2% (range −31.7% to +9.7%). Uni- and multivariate linear regression revealed that elevated baseline alkaline phosphatase (ALP) was associated with increased response during SA therapy (−2.7%, 95% CI −5.1% to −0.2%, p = 0.037), independently of baseline LV. Duration of therapy (6 vs 12 months), SA type and eGFR did not affect response. Elevated ALP remained associated with LV response (−3.2%, 95% CI −6.0 to −0.3%, p=0.029) in ADPKD patients (n=100), but did not predict response in kidney volumes (0.1%, 95% CI −3.1 to 3.3%, p = 0.97). Elevated ALP is associated with response in polycystic liver disease during SA therapy, and could possibly serve as a prognostic marker in this disease.

172, -0.453-0.110) (SMD in spine BMD: -0.169, -0.476-0.138). selleck compound Sensitivity analyses showed consistent results. Publication bias was detected in the analysis of bone fractures and osteoporosis. Conclusion: Current publications

indicate significant association between bone fractures and ALD, independent of osteoporosis or BMD. Due to the qualitative and quantitative heterogeneity among studies, further research using homogeneous populations and control of confounding risk factors for fractures are needed to elucidate the mechanism of bone fractures in ALD. Association between alcoholic liver disease and bone fractures. The size of each square is proportional to the study’s weight. Diamond is the summary estimate from the pooled studies with 95% CI. CI: confidence interval. (Random effect

model) Disclosures: The following people have nothing to disclose: Chang Seok Bang, Hyo Sun Kim, Sang Hyun Park, Eun Jin Kim, Ki Tae Suk, Dong Joon Kim Somatostatin analogues (SA) reduce liver volumes (LVs) in patients with polycystic liver disease (PLD). However, these patients show a considerable variability in treatment responses, making it difficult to predict response to SA therapy. Our aim was to learn more identify specific patient, disease or treatment characteristics that predict response in PLD during SA therapy. We pooled the individual patient data of 4 trials (NCT00771888,NCT00426153, NCT01157858, NCT01354405) of long-acting SAs (120 mg lanreotide or 40 mg octreotide) for 6 or 12 months in PLD that included liver volume as the primary outcome. We performed uni- and multivariate linear regression analysis with 9 preselected patient, disease and drug variables to identify independent predictors of response, defined as percent change in LV. Secondary outcome was percent

change in kidney volume in the ADPKD subgroup. All analyses were Epothilone B (EPO906, Patupilone) adjusted for baseline LV and center effect (random). We included 153 PLD patients (86% female, mean age 50 years, median LV 4974 ml, 69% ADPKD) from 3 international centers, all treated with octreotide (n=70) or lanreotide (n=83). Mean reduction in LV was 4.2% (range −31.7% to +9.7%). Uni- and multivariate linear regression revealed that elevated baseline alkaline phosphatase (ALP) was associated with increased response during SA therapy (−2.7%, 95% CI −5.1% to −0.2%, p = 0.037), independently of baseline LV. Duration of therapy (6 vs 12 months), SA type and eGFR did not affect response. Elevated ALP remained associated with LV response (−3.2%, 95% CI −6.0 to −0.3%, p=0.029) in ADPKD patients (n=100), but did not predict response in kidney volumes (0.1%, 95% CI −3.1 to 3.3%, p = 0.97). Elevated ALP is associated with response in polycystic liver disease during SA therapy, and could possibly serve as a prognostic marker in this disease.