Sialadenosis in Patients with Advanced Liver Disease

Sialadenosis (sialosis) has been associated most often with alcoholic liver disease and alcoholic cirrhosis, but a number of nutritional deficiencies, diabetes, and bulimia have also been reported to result in sialadenosis. The aim of this study was to determine the prevalence of sialadenosis in patients with advanced liver disease. Patients in the study group consisted of 300 candidates for liver transplantation. Types of liver disease in subjects with clinical evidence of sialadenosis were compared with diagnoses in cases who had no manifestations of sialadenosis. The data were analyzed for significant association. Sialadenosis was found in 28 of the 300 subjects (9.3%). Among these 28 cases, 11 (39.3%) had alcoholic cirrhosis. The remaining 17 (60.7%) had eight other types of liver disease. There was no significant association between sialadenosis and alcoholic cirrhosis (P = 0.389). These findings suggest that both alcoholic and non-alcoholic cirrhosis may lead to the development of sialadenosis. Advanced liver disease is accompanied by multiple nutritional deficiencies which may be exacerbated by alcohol. Similar metabolic abnormalities may occur in patients with diabetes or bulimia. Malnutrition has been associated with autonomic neuropathy, the pathogenic mechanism that has been proposed for sialadenosis

From endoplasmic-reticulum stress to the inflammatory response

The endoplasmic reticulum is responsible for much of a cell's protein synthesis and folding, but it also has an important role in sensing cellular stress. Recently, it has been shown that the endoplasmic reticulum mediates a specific set of intracellular signalling pathways in response to the accumulation of unfolded or misfolded proteins, and these pathways are collectively known as the unfolded-protein response. New observations suggest that the unfolded-protein response can initiate inflammation, and the coupling of these responses in specialized cells and tissues is now thought to be fundamental in the pathogenesis of inflammatory diseases. The knowledge gained from this emerging field will aid in the development of therapies for modulating cellular stress and inflammation.Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/62741/1/nature07203.pd

Nutrition in patients with chronic non-healing ulcers: a paradigm shift in wound care

Thomas E Serena,1 Raphael A Yaakov,1 Mark DeLegge,2 Tim A Mayhugh,1 Sarah Moore1 1SerenaGroup, Cambridge, MA, USA; 2Nutritional Healing LLC, Nashville, TN, USA Abstract: Chronic ulcers continue to pose a significant clinical and economic burden for both patients and wound care practitioners. Despite good standard of care (SOC), many wounds fail to heal. Wound healing requires a complex cascade of physiologic and immunologic processes as well as proper nutrition. An adequate balance of macro- and micronutrients is important to support the cellular activities that are necessary for repairing and remodeling of tissue. Despite being well documented in a number of clinical studies there continues to be a gap in recognizing nutritional deficits as well as appropriate clinical interventions in patients with chronic wounds. Effective management of malnutrition in patients with chronic wounds requires collaboration among multiple clinical disciplines. A holistic nutritional management approach may yield both clinical and economic benefits. Keywords: wound care, chronic wounds, parenteral nutrition, micronutrients, macronutrients, wound healing, nutrition management, malnutrition, nutrition assessmen

Effects of progesterone on motility and prostaglandin levels in the distal guinea pig colon

Progesterone (P4) inhibits the gastrointestinal muscle contraction by downregulating Gαq/11 proteins that mediate contraction, by upregulating Gαs proteins that mediate relaxation, and by altering the pattern of cyclooxygenase (COX) enzymes and prostaglandins. We aimed to examine whether P4 treatment of guinea pigs in vivo affects basal colon motility [basal motility index (MI)] by altering the levels and actions of PGF2α and PGE2. Guinea pigs were treated with intramuscular (IM) P4 for 4 days. The BASAL MI, the PGF2α-induced contraction, and PGE2-induced inhibition of contraction were examined in muscle strips and cells. The levels of PGF2α and PGE2 were measured by radioimmunoassay. Treatment with P4 reduced the basal MI, the levels of PGF2α, and PGF2α-induced contraction. P4 increased PGE2 levels, and PGE2 induced relaxation. Pretreatment with IM RU-486 (10 mg/kg per day), a P4 receptor antagonist, 1 h before P4 blocked the actions of P4. The PGF2α antagonist Al-1180 abolished basal MI and PGF2α-induced contraction. N-ethylmaleimide, which blocks unoccupied membrane receptors, blocked Ach and VIP actions but had no effect on PGF2α and PGE2 effects. A COX-1 inhibitor decreased and a COX-2 inhibitor increased PGF2α levels; GTPγS increased and GDPβS decreased the levels of PGF2α. Gαq/11 protein antibodies (Abs) reduced PGF2α levels, and Gαi3 Abs blocked its motor actions. Gαs Abs increased PGF2α but decreased PGE2 levels. We concluded that P4 decreases basal MI by reducing PGF2α levels caused by downregulation of Gαq/11 and that PGF2α-induced contraction was blocked by downregulating Gαi3. P4 also decreased the basal MI by increasing PGE2 levels, and PGE2 induced relaxation by upregulating Gαs proteins