Neurocognitive outcome in patients with hypertyrosinemia type I after long-term treatment with NTBC

Objective  

The implementation of NTBC into treatment of hypertyrosinemia type I (HT I) greatly improved survival by prevention of acute liver failure and hepatocellular carcinoma. However, there are first reports of cognitive impairment in patients with elevated plasma tyrosine concentrations.     

Hypofractionated stereotactic radiotherapy (hfSRT) after tumour resection of a single brain metastasis: report of a single-centre individualized treatment approach

Purpose

Standard treatment of single brain metastases so far is tumour resection in combination with postoperative whole-brain radiotherapy or stereotactic radiosurgery. Here, we report retrospectively our first experience with postoperative hypofractionated stereotactic radiotherapy (hfSRT) to the resection cavity in order to replace upfront WBRT with respect to treatment efficacy and safety.

Methods

Between March 2006 and October 2011, 33 patients with a single newly diagnosed intracranial metastasis were treated with hfSRT following microsurgical resection. Fractionation concepts were 10?×?4?Gy (n?=?22), 7?×?5?Gy (n?=?7) and 5?×?6?Gy (n?=?4). Planning target volume enclosed the tumour resection cavity with a safety margin of 4?mm.

Results

No patient demonstrated toxicity grade 2 or higher. Actuarial median overall survival summed up to 20.2?months, and 12-month survival was 64?%. Actuarial mean local brain control was 30.6?months, median distant brain control 12.4?months and intracranial control 8.8?months, respectively. Actuarial 1-year rates of local, distant brain and intracranial control were 71, 57 and 43?%. Salvage whole-brain radiotherapy due to recurrent brain metastases was performed in 13 patients (39?%).

Conclusion

Postoperative hfSRT appears to be a feasible treatment option in patients with a single newly diagnosed brain metastasis. Replacing the standard postoperative whole-brain radiotherapy necessitates compliant patients and regular MRI follow-up analysis.     

Leben mit Konsum und Rückfällen

The terms relapse and drug consumption have different meanings in the addiction therapy. They depend on the motivation of change and the process of warming up, of the kind and severity of addiction and the existing role repertoire. Finally, the focus on the controlled respectively the uncontrolled use shows therapeutical boundaries just as positive perspectives.     

Biofilm Formation within the Interface of Bovine Root Dentin Treated with Conjugated Chitosan and Sealer Containing Chitosan Nanoparticles

IntroductionThe purpose of this study was to assess biofilm formation within sealer-dentin interfaces of root segments filled with gutta-percha and sealer incorporated with chitosan (CS) nanoparticles with and without canal surface treatment with different formulations of CS.MethodsStandardized canals of 4-mm bovine root segments (N = 35) were filled with gutta-percha and pulp canal sealer incorporated with CS nanoparticles without surface treatment (group CS) or after surface treatment with phosphorylated CS (group PHCS), CS-conjugated rose bengal and photodynamic irradiation (group CSRB), or a combination of both PHCS and CSRB (group RBPH). The control group was filled with gutta-percha and an unmodified sealer. After 7 days of setting, specimens were aged in buffered solution at 37°C for 1 or 4 weeks. Monospecies biofilms of Enterococcus faecalis were grown on specimens for 7 days in a chemostat-based biofilm fermentor. Biofilm formation within the sealer-dentin interface was assessed with confocal laser scanning microscopy.ResultsIn the 4-week–aged specimens only, the mean biofilm areas were significantly smaller than in the control for the CS (P = .008), PHCS (P = .012), and RBPH (P = .034) groups. The percentage of the biofilm-covered interface also was significantly lower than in the control for the CS (P = .024) and PHCS (P = .003) groups. The CS, PHCS, and RBPH groups did not differ significantly.ConclusionsIncorporating CS nanoparticles into the zinc oxide–eugenol sealer inhibited biofilm formation within the sealer-dentin interface. This effect was maintained when canals were treated with phosphorylated CS, and it was moderated by canal treatment with CS-conjugated rose bengal and irradiation.     

Bacteria Adhere Less to Barbed Monofilament Than Braided Sutures in a Contaminated Wound Model

Background

Previous studies have found fewer clinical infections in wounds closed with monofilament suture compared with braided suture. Recently, barbed monofilament sutures have shown improved strength and increased timesavings over interrupted braided sutures. However, the adherence of bacteria to barbed monofilament sutures and other commonly used suture materials is unclear.

Questions/Purposes

We therefore determined: (1) the adherence of bacteria to five suture types including a barbed monofilament suture; (2) the ability to culture bacteria after gentle washing of each suture type; and (3) the pattern of bacterial adherence.

Methods

We created an experimental contaminated wound model using planktonic methicillin-resistant Staphylococcus aureus (MRSA). Five types of commonly used suture material were used: Vicryl™, Vicryl™ Plus, PDS™, PDS™ Plus, and Quill™. To determine adherence, we determined the number of bacteria removed from the suture by sequential washes. Sutures were plated to determine bacterial growth. Sutures were examined under confocal microscopy to determine adherence patterns.

Results

The barbed monofilament suture showed the least bacterial adherence of any suture material tested. Inoculated monofilament and barbed monofilament sutures placed on agar plates had less bacterial growth than braided suture, whereas antibacterial monofilament and braided sutures showed no growth. Confocal microscopy showed more adherence to braided suture than to the barbed monofilament or monofilament sutures.

Conclusions

Barbed monofilament suture showed similar bacterial adherence properties to standard monofilament suture.

Clinical Relevance

Our findings suggest barbed monofilament suture can be substituted for monofilament suture, at the surgeon’s discretion, without fear of increased risk of infection.     

Exercise Prevents Fructose-Induced Hypertriglyceridemia in Healthy Young Subjects

Excess fructose intake causes hypertriglyceridemia and hepatic insulin resistance in sedentary humans. Since exercise improves insulin sensitivity in insulin-resistant patients, we hypothesized that it would also prevent fructose-induced hypertriglyceridemia. This study was therefore designed to evaluate the effects of exercise on circulating lipids in healthy subjects fed a weight-maintenance, high-fructose diet. Eight healthy males were studied on three occasions after 4 days of 1) a diet low in fructose and no exercise (C), 2) a diet with 30% fructose and no exercise (HFr), or 3) a diet with 30% fructose and moderate aerobic exercise (HFrEx). On all three occasions, a 9-h oral [¹³C]-labeled fructose loading test was performed on the fifth day to measure [¹³C]palmitate in triglyceride-rich lipoprotein (TRL)-triglycerides (TG). Compared with C, HFr significantly increased fasting glucose, total TG, TRL-TG concentrations, and apolipoprotein (apo)B48 concentrations as well as postfructose glucose, total TG, TRL-TG, and [¹³C]palmitate in TRL-TG. HFrEx completely normalized fasting and postfructose TG, TRL-TG, and [¹³C]palmitate concentration in TRL-TG and apoB48 concentrations. In addition, it increased lipid oxidation and plasma nonesterified fatty acid concentrations compared with HFr. These data indicate that exercise prevents the dyslipidemia induced by high fructose intake independently of energy balance.It is currently suspected that overconsumption of fructose, in the form of either sugar or high-fructose corn syrup, may promote obesity and favor the development of metabolic diseases such as type 2 diabetes and dyslipidemia (1,2). This is supported by a large number of studies in rodents, which demonstrate that a high-sucrose diet causes obesity, diabetes, dyslipidemia, and hepatic steatosis (3) and that this effect is mainly due to the fructose component of sucrose (4,5). Consistent with this hypothesis, epidemiological studies have shown that high intakes of sugar, fructose, or sweetened beverages are associated with the development of obesity (6,7), diabetes (8), hypertriglyceridemia (9), an increase in small dense atherogenic LDL particles (10), high blood pressure (11), albuminuria (12), and nonalcoholic fatty liver diseases (13). Several short-term studies have further documented that hypercaloric, high-fructose diets can cause increases in a number of cardiometabolic risk factors in humans, such as fasting and postprandial hypertriglyceridemia (14–18), ectopic lipid deposition in liver cells (19,20), impaired postprandial glucose homeostasis (18), and hepatic insulin resistance (21,22). Some of these effects may be related, at least in part, to the fact that fructose can be converted into fatty acids, which has been demonstrated after both acute (23) and chronic (18) fructose feeding. Exercise is very efficient at reducing the metabolic dysfunctions associated with obesity (24,25), and although many of these effects appear to be related to enhanced energy expenditure and improved energy balance (26,27), there is growing evidence that such improvements are independent of the changes in energy balance or body composition (28,29). Exercise has also been shown to prevent the accumulation of triglyceride-rich lipoprotein (TRL)-triglycerides (TG) and improve the plasma atherogenic lipid profile in healthy subjects fed a high-carbohydrate diet (30). The purpose of this study was to investigate whether exercise would similarly prevent fructose-induced metabolic effects.     

Infectious complications of acute and chronic liver disease

Acute and chronic liver diseases are frequently complicated by infections, which result in increased morbidity and mortality and place an economic burden on health care systems. This review discusses the epidemiology and the impact on prognosis of infections in liver cirrhosis, nonalcoholic fatty liver disease/nonalcoholic steatohepatitis, acute liver failure, and post-liver transplantation. Possible mechanisms for this increased susceptibility are innate immune dysfunction (Kupffer cells, neutrophils, monocytes), genetic predisposition, and intrinsic cellular defects. The causes for innate immune dysfunction may lie in increased gut permeability, the occurrence of endotoxemia, albumin and lipoprotein dysfunction, or toll-like receptor expression. From a clinical viewpoint this article discusses problems in diagnosing infection. Established (vaccination, antibiotic prophylaxis, antiviral prophylaxis, and nutrition) and experimental (probiotic) prophylactic strategies as well as established (antibiotics) and experimental (liver support, albumin, toll-like receptor antagonists) strategies are also reviewed.