Aim: Screening and extended assessment of the nutritional status of patients on admission and on discharge from hospital were carried out. Description: The studies were carried out in four teaching hospitals, four provincial hospitals and four county hospitals in Poland. Subjects: Screening examinations were carried out for 3310 randomly selected patients (every 10th patient admitted to hospital, including 1916 female cases aged from 16 to 92 y and 1394 male patients aged from 16 to 100 y). Extended examinations were carried out on 210 patients aged from 16 to 87 y (including 122 female and 88 male). Main assessment parameters: Anthropometric (height, weight, body mass index (BMI), waist-to-hip ratio (WHR), arm circumference) and biochemical indices (erythrocyte count, haemoglobin concentration, white blood cell count, blood lymphocyte count and serum albumin serum concentration). The extended examinations included determination of antioxidant vitamins (A, C, E), vitamin B 12 and folic acid. Results: On admission to hospital, 10.43% of the patients surveyed had a BMI below 20 kg/m 2 , in 20.74% of patients serum albumin concentration was below 3.5 g/dl, indicating possible protein energy malnutrition. In addition, 21.02% had lymphocyte count below 1.5 Â 10 3 /mm 3 . During hospitalisation, deterioration in the nutritional status of the patient population occurred. On discharge from hospital, the percentage of patients with BMIo20 kg/m 2 increased to 11.21% and the percentage with low blood albumin (o3.5 g/dl) increased to 28.57%. On admission, vitamin C deficiency was present in 51.8% of patients, folic acid deficiency in 32%, vitamin E deficiency in 10%, vitamin B 12 deficiency in 6.8% and vitamin A deficiency in 1.4%. Vitamin deficiencies were present equally in malnourished, overweight and obese patients. Conclusions: In patients admitted to hospitals in Poland, malnutrition risk demonstrated by BMI was observed in 10.43% of patients. On the basis of biochemical indices, increased nutritional risk was demonstrated in 21% of patients. Vitamin malnutrition was seen in the majority of patients. A significant correlation between weight, BMI, arm circumference, blood lymphocyte count and the number of days spent in hospital was observed.

Alzheimer's disease (AD) is an aging-dependent, irreversible neurodegenerative disorder and the most common cause of dementia. The prevailing AD hypothesis points to the central role of altered cleavage of amyloid precursor protein (APP) and formation of toxic amyloid-β (Aβ) deposits in the brain. The lack of efficient AD treatments stems from incomplete knowledge on AD causes and environmental risk factors. The role of lifestyle factors, including diet, in neurological diseases is now beginning to attract considerable attention. One of them is western diet (WD), which can lead to many serious diseases that develop with age. The aim of the study was to investigate whether WD-derived systemic disturbances may accelerate the brain neuroinflammation and amyloidogenesis at the early stages of AD development. To verify this hypothesis, transgenic mice expressing human APP with AD-causing mutations (APPswe) were fed with WD from the 3rd month of age. These mice were compared to APPswe mice, in which short-term high-grade inflammation was induced by injection of lipopolysaccharide (LPS) and to untreated APPswe mice. All experimental subgroups of animals were subsequently analyzed at 4-, 8-, and 12-months of age. APPswe mice at 4- and 8-months-old represent earlier pre-plaque stages of AD, while 12-month-old animals represent later stages of AD, with visible amyloid pathology. Already short time of WD feeding induced in 4-month-old animals such brain neuroinflammation events as enhanced astrogliosis, to a level comparable to that induced by the administration of pro-inflammatory LPS, and microglia activation in 8-month-old mice. Also, WD feeding accelerated increased Aβ production, observed already in 8-month-old animals. These brain changes corresponded to diet-induced metabolic disorders, including increased cholesterol level in 4-months of age, and advanced hypercholesterolemia and fatty liver disease in 8-month-old mice. These results indicate that the westernized pattern of nourishment is an important modifiable risk factor of AD development, and that a healthy, balanced, diet may be one of the most efficient AD prevention methods.

We postulated that ammonia produced by Helicobacter pylori may contribute to gastric mucosal injury. This hypothesis was evaluated in Helicobacter-positive patients with chronic renal failure in whom a high urea concentration might amplify this phenomenon. Gastric urea and ammonia were measured, and the severity of gastritis was evaluated by counting mononuclear and polymorphonuclear cells. High gastric ammonia and low urea in Helicobacter-positive patients, and the converse in Helicobacter-negative subjects, were observed. There was a significant correlation between gastric ammonia and interstitial polymorphonuclear leukocytes infiltration (P less than 0.05), suggesting a causal link. Eradication of Helicobacter pylori was associated with a decrease of ammonia and an increase of urea (P less than 0.01). The significant correlation between the severity of gastric inflammation and the gastric juice ammonia concentration suggests that ammonia may play a pathogenic role in Helicobacter-associated gastric injury.

Inhibition of intraduodenal trypsin stimulates pancreatic secretion in rats and swine. This finding is controversial in healthy humans. The present study was designed to find whether a ‘negative-feedback’ mechanism exists in man. A 7-lumen tube equipped with two balloons was passed into the duodenum in 18 healthy volunteers. During a constant intravenous infusion of secretin (0.1 CU/kg/h) the duodenum was perfused with 0.9% NaCl solution (20 ml/l0 min). Polyethylene glycol (10g/l) served as nonabsorbable marker. Aprotinin (0.5 × 10⁶ KIU/10 min or 1 × 10⁶ KIU/10 min) was perfused intraduodenally during periods of constant pancreatic enzyme secretion for 30 min. During perfusion of the trypsin inhibitor aprotinin an almost complete inhibition of trypsin could be observed. However, at the same time or following the perfusion of aprotinin a significant augmentation of amylase, lipase or volume secretion did not occur. Thus, in the present study a negative-feedback control of pancreatic exocrine secretion by the intraduodenal trypsin concentration in man could not be demonstrated.