1-fold increase in Δ5-desaturase (Δ5DS) and Fer-1 9.2-fold rise in Δ6-desaturase (Δ6DS) expression. Treatment with UDCA-LPE resulted in a striking down-regulation of both genes to baseline levels with the most pronounced effect on Δ6DS (Fig. 7B). Along this line, fatty acid elongase 5 (ELOVL5), which uses a broad array of C16-22 as substrates, was up-regulated almost six-fold in HFD mice and was decreased to levels of control mice by UDCA-LPE (Fig. 7B). SCD1 expression and protein levels, although not

increased in HFD mice, were reduced accordingly after UDCA-LPE administration (Fig. 7B, Supporting Fig. 4). Finally, analysis of diacylglycerol acyltransferase (DGAT) 1 and 2 revealed a drop in DGAT1 expression upon the HFD, which was reversed significantly by UDCA-LPE. Expression of DGAT2 showed a similar tendency with a slight decrease in learn more HFD mice and a moderate increase upon UDCA-LPE administration, but without reaching significance (Fig. 7C). Because currently available therapeutic approaches to NAFLD show rather limited effectiveness, novel treatment strategies are needed. We report here that UDCA-LPE, a synthetic bile acid–phospholipid conjugate, exerted potent hepatoprotective functions in two different dietary mouse models of NAFLD. Improvement in HFD and MCD diet-induced elevation of aminotransferases was further accompanied by considerable reduction in hepatic lipid overloading.

Moreover, the conjugate showed distinct anti-inflammatory properties, with the ability to down-regulate essential proinflammatory genes and to reduce levels of cytotoxic lipid intermediates such as LPC. Administration of UDCA-LPE further resulted in an inhibition of up-regulated genes crucial to de novo lipogenesis and fatty acid desaturation. Thus, UDCA-LPE has highly favorable characteristics for the treatment of

NAFLD. Proinflammatory cytokines and chemokines are crucial factors in the pathogenesis of NAFLD, perpetuating apoptosis and inflammation during disease progression. Chemokines like MCP1 were found to be up-regulated in the early phase of murine NAFLD23 and were also reported to be elevated in the plasma of NAFLD patients, exhibiting an association with disease severity24 Moreover, MCP1 was capable of inducing steatosis in cultured hepatocytes,25 Dimethyl sulfoxide and murine knockout of its receptor CCR2 as well as pharmacological antagonism of CCR2 efficiently lowered hepatic steatosis in mice fed an HFD, even indicating a direct role for MCP1 during lipogenesis26 Gut-derived endotoxins such as LPS have been implicated in the triggering of Kupffer cell activation with subsequent liberation of cytokines like TNF-α,13, 14 known to be critically involved in hepatocellular apoptosis. Recent data further revealed that steatotic primary hepatocytes derived from NAFLD livers are more sensitive to TNF-α–mediated apoptotic cell death than nonsteatotic control cells.

Primary outcome was inpatient mortality. Patient and hospital care variables were analyzed by multivariate, binary logit modeling to identify independent predictors of inpatient mortality. Results: 781,700 adult cirrhotics were admitted to hospitals participating in HCUP from 2002–2010. The number steadily increased by 38% from 72,164 in 2002 to 99,261 in 2010. Inpatient mortality decreased from 8.7% in 2002 to 5.0% in 2010 (p<0.05) while overall

non-cirrhotic inpatient mortality remained constant. However, LY294002 purchase age of cirrhotics increased with 51–60 year-olds having the greatest growth (27% to 37%). Mean Elixhauser Comorbidity Index steadily increased from 2.5 in 2002 to 3.4 in 201 0. The percentage of cirrhotics with decompensation remained steady at 18–20%. Factors independently associated with inpatient death included septicemia (OR 8.7, 8.4–9.1), hepatorenal syndrome (OR 6.3, 95% CI: 6.0–6.7), increased age (61–70 years old, OR 1.9, 1.8–2.0), liver cancer (OR 1.9, 1.8–2.1), and decompensated cirrhosis check details (OR 1.9, 1.8–1.9).

With each year the independent odds of inpatient death declined compared to 2002 (2003: OR 0.93, 0.88–0.99; 2010: OR 0.40, 0.37–0.44). Paracentesis/thora-centesis within 24 hrs was associated with a lower mortality (OR 0.78, 0.74–0.82), while esophagogastroduodenoscopy (EGD) within 24 hrs showed a trend (OR 0.96, 0.91–1.0). Hospital type (teaching/non-teaching; urban/non-urban) was not associated with survival. Summary: Inpatient mortality for cirrhotic patients in the US has steadily fallen by 43% between 2002 and 2010, despite increasing Thymidylate synthase age, comorbidities and stable rates of hepatic decompensation. Sepsis and hepatorenal syndrome are strongly associated with inpatient mortality, but early paracentesis/thoracentesis and EGD are associated with survival. Conclusions: Improved inpatient survival for cirrhotics in the US may be related to better care, including early diagnostic and therapeutic interventions. Disclosures: Monica Schmidt – Grant/Research

Support: Merck & Co.; Patent Held/Filed: HCCplex; Stock Shareholder: PleX Diagnostics Alfred S. Barritt – Grant/Research Support: Salix Pharmaceuticals; Speaking and Teaching: Abbott Molecular The following people have nothing to disclose: Eric S. Orman, Paul H. Hayashi Background: Acetaminophen (APAP), a heavily used over the counter (OTC) and prescribed(Rx) medication; is the leading cause of acute liver failure in the U.S. Prior studies have shown unintentional misuse as well as patient misunderstanding of the risks of concomitant use of APAP products and maximum daily doses. Objective: To evaluate variable labeling and counseling strategies to communicate proper use of APAP-containing products.

1,2 In recent years, several studies have uncovered a significant proportion of patients with reflux esophagitis but with no symptoms. In the well conducted, population-based, Kalixanda study from Sweden, for example, up to 36.8% of patients with erosive esophagitis had no symptoms.3 ZD1839 price Other studies from the Asian Pacific region have shown a prevalence of asymptomatic reflux esophagitis ranging from 26.4% to 35.0% (Table 1).3–7 In this issue of the Journal of Gastroenterology and Hepatology, Cho and colleagues from Korea, in a survey of over 5000 patients undergoing health-screening gastroscopy, found that 145 of 320 (45.3%) patients with erosive esophagitis

were asymptomatic.7 This is indeed a large proportion of patients who have “silent GERD”. In another endoscopy-based study, Ho et al. found that 33.9% of 186 patients with erosive esophagitis had no typical symptoms of heartburn

and acid regurgitation. Instead these patients had predominant complaints of “wind” and abdominal distension.8 Clearly, the problem could be one of interpretation of symptoms. It has long been known that many Asian patients do not exactly understand the meaning of heartburn and acid BAY 57-1293 cost regurgitation9 and there is a large overlap between reflux and dyspeptic symptoms.10 Furthermore, non-cardiac chest pains, for example, have often been considered in the Asia–Pacific region to be a manifestation of GERD and many patients with non-cardiac chest pains have been shown to have underlying Vorinostat GERD.10 This notwithstanding, silent GERD is now a well-recognized entity. Fass and Dickman11 have defined silent GERD as the presence of esophageal mucosal injury that is typical of GERD (erosions, peptic ulceration and Barrett’s esophagus) during upper gastrointestinal endoscopy in individuals who lack typical or atypical extra-esophageal manifestations of GERD. The ramifications of such a “disease” are huge. The list of reflux-related diseases caused by silent disease include: refractory asthma, persistent laryngopharyngitis, poor sleep, dental caries, Barrett’s esophagus

and, particularly in children, unexplained asthma and recurrent pneumonia.11 Of practical concern is the screening for Barrett’s esophagus. Currently, only patients with symptomatic GERD are screened for Barrett’s esophagus. How do you screen for a disease without symptoms? The whole adult population would require evaluation and this is clearly a monumental if not impossible task. Although Barrett’s esophagus and Barrett’s associated adenocarcinoma are still uncommon in the Asia–Pacific region, this may change with the rapid emergence of GERD in the region.9 What factors determine or predict silent reflux disease? In this study, Cho et al.7 identified older age and male sex as predictive factors. Nozu and Komiyama5 and Wang et al.6 also identified male sex as a predictive factor for silent esophagitis.

As shown in Fig. 1A, β2SP overexpression decreased the expression of several proteins responsible for cell cycle regulation including phosphorylated Rb (pRb). Comparing protein expression from identical preparations,

the most dramatic reduction in expression was for CDK4 (33% of control), suggesting that CDK4 is a downstream effector in cell cycle regulation mediated by β2SP signaling. Then we further compared the expression levels of CDK4, cyclin D1, pRb, and Rb upon transfection of β2SP in HepG2 and SNU475 cells in three independent experiments. The most remarkable reductions of CDK4 were shown in HepG2 (39%) and SNU475 (31%) cells (Fig. 1B). However, it was not clear that the change in CDK4 due to the loss of β2SP was sufficient to disrupt the cell cycle. Thus, we tested whether the increase in Rb phosphorylation OSI906 was due to the down-regulation of β2SP or activation of CDK4. We inhibited β2SP expression in SNU-475 cells by the infection of a lentivirus containing shRNA against β2SP and then analyzed Rb phosphorylation. β2SP expression was decreased by 44% after lentiviral infection and Rb phosphorylation

was increased by 55%, whereas ICG-001 cell line the levels of Rb were unchanged (Fig. 1C). To determine whether CDK4 is responsible for Rb phosphorylation due to the down-regulation of β2SP, we inhibited CDK4 expression by siRNA in SNU-475 cells infected with β2SP shRNA. CDK4 siRNA in the presence of β2SP shRNA restored Rb phosphorylation to basal levels (Fig. 1C). These results suggest that CDK4 is a key regulator of Rb phosphorylation affected by β2SP expression. We then determined whether the induction of CDK4 expression due to the down-regulation of β2SP accelerates cell cycle progression. SNU-475

cells were infected with the β2SP shRNA lentivirus followed by treatment with a CDK4 inhibitor, and then analyzed cell cycle phases by fluorescence-activated cell sorting (FACS) with propidium iodide (PI) staining. The number of cells in G1 phase was significantly decreased from 46% to 35% upon the knockdown of β2SP (Fig. 2A,B). Additional treatment with CDK inhibitor (200 nM) in β2SP short hairpin RNA (shRNA)-treated cells returned 43% of the cells to old G1. However, we did not detect the additional accumulation of cells in G1 phase in control lentiviral-treated cells exposed to the same CDK4 inhibitor. Taken together, these data demonstrate that dysregulation of the cell cycle resulting from the disruption of β2SP expression is mediated by CDK4 activation and Rb phosphorylation. We further investigated the mechanism by which β2SP modulates CDK4 by examining interactions between these proteins. Recent reports indicate that CDK4 phosphorylates Smad3 to inhibit its transcriptional activity and antiproliferative functions.7 Thus, we sought to determine whether CDK4 phosphorylates β2SP as it does Smad3.

In contrast, specific regions across the HBx gene and precore that encode non structural regulatory or signaling elements, generally displayed higher viral diversity within HBsAg loss subjects compared to buy CH5424802 controls. These distinct patterns may reflect different mechanisms

by which coding regions for structural or nonstructural elements respond to adaptive pressure resulting in the common endpoint of HBsAg loss. Disclosures: Kathryn M. Kitrinos – Employment: Gilead Sciences, Gilead Sciences; Stock Shareholder: Gilead Sciences, Gilead Sciences Paul N. Hengen – Employment: Gilead Sciences Raul E. Aguilar Schall – Employment: Gilead Sciences, Inc. Phillip Dinh – Employment: Gilead Sciences Hendrik W. Reesink – Consulting: Abbott, Gilead, Astex, Merck, Roche, Janssen Cilag, GlaxoSmithKline, Tibotec/JJ, PRA-International; Grant/Research Support: Vertex, Boehringer Ingelheim, Anadys, Phenomix, Chugai, Japan Tobacco, Santaris, SGS, Idenix, BMS Fabien Zoulim – Advisory Committees or Review Panels: Gilead; Consulting: Roche; Grant/Research Support: Gilead, Scynexis, Roche; Speaking and Teaching:

Novartis, Roche, Janssen, Bristol Myers Squibb, Gilead Prista Charuworn – Employment: Gilead Sciences; Stock Shareholder: Gilead Sciences Background: During treatment with highly potent nucleo(s)tide analogues serum HBV DNA levels become suppressed to undetectable levels during the first treatment year in most patients and HBV genome analysis becomes infeasible. However, HBV RNA remains detectable in serum in many patients with undetectable HBV DNA. We have investigated Y-27632 the evolution of HBV variants by sequence analysis of serum HBV RNA in patients with HBV resistance mutations who were achieving undetectable HBV DNA levels during consecutive treatment with tenofovir (TDF). Methods: Nineteen patients who received monotherapy with TDF 245 mg/day for a mean of 40±14 (range, 21-76) months after prior treatment failure to lamivu-dine (n=4), adefovir (n=1) or both (n=14) were retrospectively analyzed. Sixteen patients were male, 16 HBeAg positive, the mean HBV DNA was 6.3±1.5 (3.8-9.6)

log 10 copies/mL and HBV genotypes A, B, D and E were present in 3,2, 13 and 1 patient, respectively. From serum samples stored at -20°C representing the start of TDF treatment GPX6 and consecutive time points HBV DNA was amplified by a real time PCR targeting the HBV core region and HBV RNA after reverse transcription by a real time PCR targeting the x gene with HBV RNA specific RACE primers (minimal detectable quantity was 100 and 500 copies/mL, respectively). The rt region and the overlapping s gene of HBV were sequenced in all samples with HBV DNA or HBV RNA levels > 1000 copies/mL (n=103). Results: During TDF treatment HBV DNA decreased to levels < 1000 and < 100 copies/mL after a mean duration of 13±8 (3-32) and 34±14 (3-76) months, respectively.

In the nervous system, areas of concentration include the periaqueductal gray matter, rostral ventral medulla (RVM), locus ceruleus, and dorsal horn regions of the spinal cord. Side effects of opioids are numerous and presumably related to systems that contain these receptors (Table 1). Supraspinal effects include euphoria, sedation, sleep disturbance, see more respiratory depression, cough suppression, pupillary constriction, truncal

rigidity, nausea and vomiting, and temperature dysregulation (hyperthermia or hypothermia). They can also lower seizure threshold by some as yet unknown mechanism. Peripheral effects include bradycardia (although meperidine causes tachycardia), hypotension, constipation and gastroparesis, renal function depression, and pruritus.[3] There is also ample evidence that there is an effect by many opioids on the endocrine and immune systems.[4, 5] Interestingly, unlike the analgesic and euphoric properties, some of these effects do not seem to abate with continued use, including gastrointestinal dysfunction, miosis, and, to some extent, respiratory depression.[3] In the United States, recreational use of opioids was not common until the Civil War years (1861-1865) and became even more widespread when heroin was synthesized in 1874 and marketed as a tonic for many symptoms

including pain. Intravenous heroin use blossomed after World War II, which became most problematic in the 1950s, 60s, and 70s. There has been a resurgence in opioid overuse and addiction because in part of the www.selleckchem.com/products/AZD6244.html increased use of opioids in the management of non-malignant chronic pain as promoted by Portenoy, Foley, and others since the late 1980s.[6] Opioids clearly lead to tolerance that then often leads to overuse, further tolerance, Anacetrapib and addictive behavior. The mechanism of tolerance was initially thought to involve receptor downregulation and/or receptor population/location changes. The process probably revolves around changes in receptor

linkage to second messengers and resulting ion channel effects. In particular, the N-methyl-D-aspartate (NMDA) ion channel complex seems very important because NMDA blockers (eg, ketamine) reduce tolerance (they also seem to reduce central sensitization). Tolerance to analgesic, euphoric, and relaxing effects seems to be inevitable for most patients taking opioids chronically. Depending on the specific opioid medication, tolerance generally occurs after 2 weeks or so of continued use, and potency reduction can eventually be as great as 35-fold.[3] And it is essential to remember that cross-tolerance is the rule in the opioid family – ie, tolerance to 1 opioid generalized to virtually all others with the possible exception of some effects of mixed agonist-antagonist agents. Tolerance to constipation and slowing of gastrointestinal function generally does not seem to happen.

Moreover, a prophylactic effect on bleeding frequency is reported in patients who

achieved partial success, which is paramount in preventing the development of haemophilic arthropathy at an older age [19]. Our study is of clinical importance because it shows that most of the patients with pre-ITI inhibitor titres below 40 BU mL−1 can successfully be treated with low dose ITI. As a result of its lower clotting factor use and lower frequency of infusions, this ITI regimen has several advantages. We estimate the cost to be considerably lower, compared with high dose ITI regimens [4]. Furthermore, the burden for patients and parents is lower, because of the lower frequency of FVIII infusions. Implantation of a PAC system can often be avoided, thus saving clotting factor consumption. In addition, complications such as PAC infections, which are associated with a longer time to achieve complete success, may be avoided. LY294002 cell line Disadvantages of the low dose ITI regimen may be the longer time needed to achieve success [7], and the

delay of effective prophylaxis with FVIII. this website For some patients, this may be a reason to switch to a high dose regimen. Although studies on prophylaxis with bypassing agents in inhibitor patients have reported beneficial effects, it is not an established therapy yet, and prophylaxis with bypassing agents may be less effective than with FVIII [20]. Low dose immune tolerance induction therapy is successful in severe haemophilia A patients with a pre-ITI titre below 40 BU mL−1. A shorter time to success PLEKHB2 is predicted by a maximum ITI titre below 40 BU mL−1.

In patients with a titre below 5 BU mL−1, this effect is even more pronounced (P = 0.033). We suggest that patients with severe haemophilia A and a pre-ITI inhibitor titre below 5 BU mL−1 should be treated with low dose immune tolerance induction therapy. Patients with a pre-ITI titre below 40 BU mL−1 may strongly benefit from low dose ITI regimen. However, patients with a pre-ITI inhibitor titre above 40 BU mL−1, with an anamnestic response during ITI exceeding 40 BU mL−1, or without response to the low dose regimen, should rather be treated with a high dose immune tolerance induction therapy. The authors would like to thank D.E. Fransen van de Putte for critical evaluation of the manuscript. The authors stated that they had no interests which might be perceived as posing a conflict or bias. “
“This chapter contains sections titled: Introduction Cryoprecipitate Principles of manufacture Product purity Methods of viral inactivation and elimination Potency and labeling issues Selection of products Plasma-derived concentrates for rare bleeding disorders References “
“Health-related quality of life (HRQoL) assessment is recognized as an important outcome in the evaluation of different therapeutic regimens for persons with haemophilia.

[9] The major strength of the study is that we confirmed the HMCAS using CT angiography. We did not show that treatment made a difference to the rate of resolution. However, the decision to treat patients was governed by the clinical presentation and not the length of thrombus. Further, we observed that the estimated thrombus burden, detected by length or volume was highly predictive of HMCAS resolution. This is consistent with prior observations showing that the thrombus location and extent is related to recanalization rates and outcomes.[10] NCCT brain is the first modality of choice to image patients with acute stroke due to its

speed of acquisition, cost effectiveness, and wide availability. HMCAS on baseline scans in patient with acute ischemic stroke are easily recognized with good interrater agreement,[11] high specificity,[12] and

its length can Idasanutlin nmr be easily measured without selleck compound the need for sophisticated tools. Use of volume estimation of HMCAS is helpful but requires more sophisticated image analysis. In the SITS-ISTR register, the hyperdense sign disappeared in 48% patients at follow-up with IV tPA and these patients showed more rapid neurological improvement and had a better 3-month functional outcome[6] Although this observation of disappearance of HMCAS is consistent with ours, it may be confounded by baseline differences in the patient population and the stroke severity or by measurement error since CT angiography was not done to confirm a HMCAS. This study is limited by its modest size and retrospective nature. Second, there are technical limitations of accurately measuring the HMCAS on conventional 5 mm NCCT and we infer that one reason for the poor sensitivity of the HMCAS on NCCT is the slice thickness and other technical factors. Infrequent disappearance of HMCAS

>10mm with intravenous tPA suggests additional need for more advanced vascular imaging like CT angiography and digital subtraction angiography followed by need for ancillary endovascular therapy in this group, a concept which is Alanine-glyoxylate transaminase currently being directly tested in the THERAPY trial using the Penumbra Stroke system.[13] “
“Posterior cerebral artery aneurysms are treatment challenge for the neurosurgeon. Parent artery occlusion, trapping and bypass have been the classic treatment options for aneurysms in this location. With the introduction of newer embolic agents such as Onyx®, endovascular intervention is now a viable therapy for these aneurysms. We report the case of a 60-year-old man who presented with a symptomatic, though unruptured, fusiform left posterior cerebral artery aneurysm. Given the distal location of this dominant sided aneurysm, post-operative visual deficits and aphasia were a concern if parent vessel occlusion were to be performed. Therefore, an endovascular reconstruction using Onyx HD-500 and two closed-cell stents was performed.

Determining predator energy requirements is essential to assessing whether prey availability is sufficient. This is important because one

risk factor facing the endangered Southern Resident killer whale distinct population segment is limited prey availability. see more Body mass, field metabolic rate (FMR), and daily prey energy requirements (DPERs) were estimated for each individual in the population. FMRs were calculated from body mass, assuming they range from five to six times Kleiber-predicted basal metabolic rates. FMRs of adults were also calculated from resident killer whale activity budgets and the metabolic cost of swimming at speeds associated with daily activities. These two methods yielded similar results. Total FMRs varied by age and sex, which is partly due to the long developmental period and sexual dimorphism in killer whales. FMRs for males (465–4,434 kg) ranged from 35,048 to 228,216 kcal/d while FMRs for females (465–3,338 kg) ranged from 35,048 to 184,444 kcal/d. DPERs were calculated from FMRs assuming

a standard digestive efficiency. Corresponding DPERs ranged from 41,376 to 269,458 kcal/d and 41,376 to 217,775 kcal/d, respectively. “
“Entanglement of marine mammals in fishing gear is a global issue. It is considered a significant threat to minke whales (Balaenoptera acutorostrata) in the East Sea of Korea. A total of 214 www.selleckchem.com/products/R788(Fostamatinib-disodium).html entanglements of minke whales in this area between 2004 and 2007 were used to investigate types and parts of fishing gears involved in entanglements. The majority of entanglements were mainly caused by three types of AZD9291 in vivo fishing gears: set nets, pots, and gill nets (n= 207, 96.7%). Other entanglements were associated with bottom trawls, purse seines, and trawls. A total of 65 entanglements were attributed to the main and branch lines of fishing gears. The most common body part of minke whales which attached to fishing gears was the mouth (n=

63, 30.4%). Most entanglements took place within 10 nmi from land (n= 179, 86.5%), and between 10 and 220 m of water depth. The mean length of entangled minke whales in set nets was significantly smaller than that of whales in pots and gill nets samples (P < 0.001). Also, the mean body length of minke whales that entangled in the coastal area and shallow waters was significantly shorter than that of whales in the offshore area and deep waters (P < 0.001). This information can be used as fundamental data to conserve and manage this population of minke whales in the East Sea of Korea, and also to modify fishing gear to reduce entanglements. Future studies should focus on investigating the impact of these entanglements on the population and the effectiveness of mitigation measures to reduce entanglements of minke whales in this area. "
“The temperature differential (ΔT) between a body surface and the environment influences an organism’s heat balance.

Surface roughness and color of the specimens were measured with a profilometer and a colorimeter, respectively, before and after whitening. Color changes were calculated (ΔE) using L*, a*, and b* coordinates. Repeated measures of variance analysis and Duncan test were used for statistical evaluation (α= 0.05). Results: The average surface roughness of composite increased from 1.4 Ra to 2.0 Ra, and from 0.8 Ra to 0.9 Ra for the ormocer material; however, these changes in roughness after whitening were not significant (p > 0.05). Also, when two materials were compared,

the surface roughness of restorative materials was not different before and after whitening (p > 0.05). L* and b* values for each material changed significantly after whitening (p < 0.05). ΔE values (before/after whitening) calculated for composite (11.9) buy AZD6244 and ormocer (16.1) were not significantly different from each other (p > 0.05). Conclusions: The tested whitening agent did not affect the surface roughness of either resin-based restorative material. Both materials became brighter after whitening. The behavior of the materials in the yellow/blue axis was opposite to each other after whitening. Each material had clinically unacceptable color change after whitening (ΔE > 5.5); however, the magnitude of the color change of materials was similar (p > 0.05). According to the results of this study, with

the use of materials tested, patients should be advised that existing composite restorations learn more may bleach along with the natural teeth, and replacement of these restorations after whitening may not be required. “
“This manuscript Interleukin-3 receptor describes an interdisciplinary approach over a period of 8 years combining surgical and prosthodontic treatment of a young patient diagnosed with hypocalcified-type amelogenesis imperfecta and anterior open bite. The treatment procedures included transitional restorations, orthodontic treatment, and maxillofacial surgery with a one-piece Le Fort I osteotomy, bilateral mandibular osteotomy, and genioplasty. The definitive prosthetic rehabilitation consisted of 28 zirconia-based ceramic single crowns restoring both esthetics and function. Photographs and radiographs associated

with clinical evaluation were used in the maintenance period. Two-year follow-up revealed satisfactory results and no deterioration in the restorations. “
“Temporomandibular disorders are a group of symptoms related to the impaired function of the temporomandibular joints and associated muscles. Occlusal splint therapy is a common treatment in the aforementioned syndrome. One of the methods of manufacturing occlusal splints is to place a polymer on thermoplastic foil. The aim of this study was to evaluate the shear bond strength of light- and self-cured resins bonded to thermoplastic foil dependent on artificial aging. Thirty cylinders composed of light-cured resin and 30 cylinders made of self-cured resin were attached to 60 rectangular thermoplastic plates.