Zinc is an essential trace element for human health and plays a fundamental role in metabolic, immunological and many other biological processes. The effects of zinc are based on the intra- and extracellular regulatory function of the zinc ion (Zn2+) and its interactions with proteins. The regulation of cellular zinc homeostasis takes place via a complex network of metal transporters and buffering systems that react to changes in the availability of zinc in nutrition, chronic diseases, infections and many other processes. Zinc deficiency is associated with impairment of numerous metabolic processes, reduced resistance to infections due to impaired immune functions, changes in skin and its appendages and disorders of wound healing and haemostasis. While ischemic heart attacks (myocardial infarction) occur more frequently with meat-based normal diets, haemorrhagic strokes are more frequently observed with vegetarian/vegan diets. The causes are discussed as deficiencies of various micronutrients, such as vitamin B12, vitamin D, various amino acids and also zinc. In the present review, after a description of the functions of zinc and its resorption, a discussion of daily food intake will follow, with a special focus on the importance of food composition and preparation for the zinc balance. The close interrelationships between proteins, especially albumin and zinc will be discussed. Finally, the possible causes and consequences of a zinc deficiency on the blood vessels and blood coagulation are considered.

Decompensated liver cirrhosis has a dismal prognosis, with patients surviving on average for 2–4 years after the first diagnosis of ascites. Albumin is an important tool in the therapy of cirrhotic ascites. By virtue of its oncotic properties, it reduces the risk of cardiovascular dysfunction after paracentesis. Treatment with albumin also counteracts the development of hepatorenal syndrome and spontaneous bacterial peritonitis. More recently, the positive impact of long-term albumin supplementation in liver disease, based on its pleiotropic non-oncotic activities, has been recognized. These include transport of endo- and exogenous substances, anti-inflammatory, antioxidant and immunomodulatory activities, and stabilizing effects on the endothelium. Besides the growing recognition that effective albumin therapy requires adjustment of the plasma level to normal physiological values, the search for substances with adjuvant activities is becoming increasingly important. More than 75% of patients with decompensated liver cirrhosis do not only present with hypoalbuminemia but also with zinc deficiency. There is a close relationship between albumin and the essential trace element zinc. First and foremost, albumin is the main carrier of zinc in plasma, and is hence critical for systemic distribution of zinc. In this review, we discuss important functions of albumin in the context of metabolic, immunological, oxidative, transport, and distribution processes, alongside crucial functions and effects of zinc and their mutual dependencies. In particular, we focus on the major role of chronic inflammatory processes in pathogenesis and progression of liver cirrhosis and how albumin therapy and zinc supplementation may affect these processes.

Background:The forward head rounded shoulder (FHRS) sitting posture has been associated with decreased shoulder complex muscle strength and function. Upon clinical observation, the adverse effects of the FHRS sitting posture on shoulder complex isometric muscle strength is also present when testing controls for scapular position. Hypothesis/Purpose:The purpose of the study was to assess the effect of various sitting postures on shoulder external rotator muscle isometric strength when the strength testing controls for scapular position. Study Design:A cohort study, with subjects serving as their own controls. Methods:One hundred subjects ages 20-26 participated in the study. Each subject was placed in a neutral cervical sitting (NCS) posture which was maintained for five minutes after which the strength of the dominant shoulder external rotators was immediately tested with the glenohumeral joint in the neutral position using a Micro-FET3 Hand Held Muscle Testing Dynamometer (HHMTD). Each subject was returned to the NCS posture for subsequent external rotator strength testing after five minutes in a FHRS sitting posture, five additional minutes in the NCS posture and five minutes in a retracted cervical sitting (RCS) posture resulting in each subjects' external rotator strength being tested on four occasions. Subjects were randomized for order between the FHRS and RCS postures. Results:Mean strength values for each condition were normalized to the mean strength value for the 1 st NCS condition for each subject. A statistically significant decline in shoulder external rotator strength following the FHRS sitting posture occurred compared to the appropriate postural conditions (p<.05). A frequency analysis revealed that 36% of the subjects demonstrated greater than 10% decline in external rotator strength following five minutes in the FHRS sitting posture. The average percentage of strength decline in those with greater than a 10% reduction in external rotator strength was 19%. Sixty-four percent of the subjects experienced less than a 10% decline in shoulder external rotator strength in response to the FHRS sitting posture. Conclusion:Shoulder external rotator strength declined 8% following five minutes in the FHRS sitting posture. A sub-population of 36% demonstrated an average decline of 19% in shoulder external rotator strength following five minutes in the FHRS sitting posture. The strength decline appears to resolve over the short-term by returning to the NCS posture. Level of Evidence: Level III

Acute and in particular chronic liver disease of viral, alcoholic and non-alcoholic genesis is a large, often unnoticed health hazard around the world. It can lead to cirrhosis and hepatocellular carcinoma (HCC) during the course of decades. Liver fibrosis, conversion of functional parenchyma to connective tissue (scar tissue) as a consequence of chronic liver damage, is a connecting pathogenic process in all chronic liver diseases. Zinc is an essential micronutrient in human health, playing a fundamental role in cellular metabolism, acting mostly through binding in a wide range of proteins and thus affecting a broad spectrum of biological processes. Thus, the liver is essential for zinc homeostasis of the human body. Zinc deficiency leads to the impairment of many hepatic functions. Liver diseases can alter zinc levels and, in turn, may be influenced by zinc deficiency. In spite of the vast increase in knowledge about the fibrotic wound healing process on both cellular and molecular levels, apoptotic signaling, epigenetic phenomena, and usage of stem cells, there is no effective anti-fibrotic medicine so far for use in humans. The diverse hepatoprotective effects of zinc documented in many experimental studies and initial clinical pilot projects should be reason enough to include zinc as a component in future studies on liver fibrosis, especially non

In immunocompromised patients suffering from gastrointestinal complaints who have been in endemic areas an infection with Strongyloides stercoralis should be excluded. Without treatment, this helminthiasis may be fatal.

ZusammenfassungZink ist ein essenzielles Spurenelement mit vielfältigen biologischen Wirkungen. Die Leber ist das Hauptorgan des Zinkstoffwechsels und nimmt eine zentrale Stellung bei der Erhaltung der Zinkhomöostase des Körpers ein. Es bestehen enge Wechselbeziehungen zwischen der Leber und Zink. Während ein Zinkmangel zu einer Verschlechterung zahlreicher Leberfunktionen führen kann, finden sich bei Lebererkrankungen Zinkmangelzustände, die zu einer Beeinträchtigung verschiedener Leberfunktionen beitragen. Ein Zinkmangel ist weniger von der Genese, als viel mehr von der Schwere der Leberschädigung – Fibrose oder Zirrhose mit oder ohne portaler bzw. metabolischer Dekompensation – und dem Auftreten von Komplikationen (Aszites, hepatische Enzepalopathie, hepatozelluläres Karzinom, Infektionen) abhängig. Bei Nachweis eines Zinkmangels ist bei jeder Lebererkrankung eine gezielte Zinksubstitution unter Laborkontrolle angezeigt.

Background wide antral pulmonary vein (PV) catheter ablation (CA) in patients with atrial fibrillation (AF) is safe and effective when permanent trans-mural lesions are achieved without causing harm to surrounding anatomical structures. Atrio-esophageal fistula, due to its high mortality, is the most dreadful complication related to CA for AF, therefore alternative radiofrequency (RF) approaches to reduce or eliminate this complication are currently studied. The shallower but wider lesions of high power short duration (HPSD) ablation might represent a safe alternative. Purpose to compare the rate of thermal esophageal lesions in patients with paroxysmal and persistent AF undergoing CA assigned to the 2 different RF modality. Methods one-hundred patients with paroxysmal and 100 with persistent AF will be alternatively assigned to undergo CA with the FlexAbility™ (HPSD group: 70W, 41°, 8 seconds) or the TactiCath™ (LSI-group: 35W, 41°, LSI: 5-5.5 posterior wall, up to 6 anywhere else) catheter. A 3-D mapping system, a steerable sheath and adenosine-test (30mg) were used in all patients. Posterior wall (PW) isolation in addition to PV isolation was performed in all, and patients with persistent AF were additionally treated with mitral and cavotricuspid isthmus ablation. Insertion of an esophageal probe was always attempted, and all patients underwent upper endoscopy 24 to 48 hours after CA. Results between June and October 2019, 71 patients (68 ± 10 years old, 32 (45%) female, 44 (60%) paroxysmal AF, AF duration 58 ± 81 months) were alternatively assigned to HPSD (36, 51%) or LSI-guided (35, 49%) ablation. No differences in clinical characteristics were found between groups. After 45 ± 18min and 30 ± 14 min of procedural and RF time, all PVs were isolated, and all spontaneous and adenosine-induced reconnections treated. Successful PW isolation was achieved with an additional 8 ± 3 and 7 ± 3 min of procedural and RF time. When HPSD and LSI-guided groups are compared, a similar rate of clinically non-relevant and self-healing thermal lesions at endoscopy was found (10, 27.8% vs. 10, 28.6%). Independent of the treatment group, a higher peak temperature identified patients with esophageal lesions (43.2° vs. 42°; P=.0065). A peak temperature value of 43.1° best identify patients most likely to develop thermal lesions (AUC 0.71, SE 84%, SP 39%). Interestingly, none of the 11 patients in whom esophageal probe insertion was not possible or attempted developed thermal lesions in comparison to 20 (33%) patients who underwent esophageal temperature monitoring (P=.0046). Conclusions: no difference in thermal induced esophageal lesions were found when the two different RF approach (HPSD vs. LSI guided) were compared. Interestingly, lack of temperature monitoring with an esophageal probe is associated with no thermal lesions at endoscopy.