Nutritional Status in Patients with Probable Alzheimer's Disease: Effect of Rivastigmine.

IMPORTANCE: Altough disease-modifying factors such as malnutrition and diet have been associated with Alzheimer's disease (AD), little is known about the effects of pharmacological therapies on the nutritional status of AD patients. OBJECTIVE: To evaluate the nutritional status, prealbumin, and albumin serum levels and several anthropometric measurements in patients with probable moderate-stage AD, with and without rivastigmine drug treatment. STUDY DESIGN: A cross-sectional study. SETTING AND PARTICIPANTS: 34 patients were included, 17 with rivastigmine treatment and 17 without pharmacological treatment, over 60 years of both sexes. MEASUREMENTS: The nutritional status was evaluated using the Mini Nutritional Assessment (MNA). Albumin and prealbumin (transthyretin) levels and anthropometric evaluation were assessed using standard methods. RESULTS: A polarity of malnutrition was detected in the untreated group. According to the MNA survey, the risk of malnutrition is higher without rivastigmine treatment (p = 0.0001). There are a less loss of appetite, less psychological stress, greater mobility and independence in those patients receiving rivastigmine (p = 0.003, 0.008, 0.016 and 0.018, respectively). The body mass index does not show a statistical difference, however, categorizing it for older adults, this index was improved in those receiving rivastigmine (p = 0.016). The serum levels of albumin and prealbumin showed no significant statistical difference between the groups. CONCLUSION: Rivastigmine treatment shows a protective effect on malnutrition in patients with moderate-stage AD.

Frequency of Toxoplasma gondii in pork meat in Ocotlán, Jalisco, Mexico.

Toxoplasmosis is an infection caused by Toxoplasma gondii, an intracellular obligate parasite. Its transmission has usually been attributed to ingestion of undercooked or raw meat. The frequency of T. gondii in pork, the most common meat for human consumption in Jalisco, Mexico, is unknown; in Guadalajara city high prevalence of human toxoplasmosis has been documented. Forty-eight samples of pork meat from butcher shops in Ocotlán city were analyzed. Through bioassay, 50 g of tissue was homogenized in an acidic pepsin solution and inoculated subcutaneously to previously immunosuppressed mice. Blood samples from the mice tail vein were obtained before inoculation and 7, 14, 28, and 45 days postinoculation to analyze anti-Toxoplasma immunoglobulin (Ig) M and IgG antibody kinetics by indirect enzyme-linked immunosorbent assay. For histopathology, small fragments of the brain, lungs, heart, and skeletal muscle were extracted on day 45 and were stained with hematoxylin and eosin. Also, DNA was extracted from the pork meat for PCR amplification of the B1 gene. Even though all pork samples were negative by histopathology and PCR, IgG and IgM antibodies against T. gondii were detected in 1 of the 48 inoculated mice, reflecting a frequency of 2.1% positive pork meat, which is lower than expected but similar to that found in other regions.

Additive effect of ethanol and HCV subgenomic replicon expression on COX-2 protein levels and activity.

The mechanisms by which alcohol exacerbates liver injury in patients with hepatitis C are unknown. We used the hepatitis C virus (HCV) subgenomic replicon cell system to evaluate the effect of ethanol on HCV replication and viral protein synthesis. Our results demonstrate that alcohol stimulates HCV replicon expression at both HCV-RNA and protein levels. Furthermore, we observed that ethanol treatment showed an additive effect in cyclooxygenase-2 (COX-2) protein expression and activity already induced by HCV viral proteins, and in turn increased HCV viral expression. Our results suggest that COX-2 activity is involved in ethanol-induced HCV-RNA and NS5A protein expression, because acetylsalicylic acid (ASA), a COX-1/2 inhibitor, blocked this induction and downregulated COX-2 protein expression and activity. Therefore, we suggest that ethanol increases HCV replication expression, at least in part, by upregulating a key cellular regulator of oxidative stress pathway known as COX-2 or its products.

Nitric oxide synthases inhibition results in renal failure improvement in cirrhotic rats.

UNLABELLED: Nitric oxide (NO) has been implicated in cirrhosis and might be implicated in renal failure end-stage cirrhosis. AIM: Our aim was to evaluate NO role in renal failure induced during decompensated cirrhosis, using the following inhibitors: aminoguanidine (AG), a specific inducible nitric oxide synthase (iNOS) inhibitor and NG-nitro-l-arginine methyl ester (L-NAME), a nonselective blocker of NOS isoforms. METHODS: Endothelial (eNOS) and iNOS gene expression was analyzed by reverse transcriptase-polymerase chain reaction. Cirrhotic rats received a single intragastric dose of CCl(4) to induce acute liver damage (ALD). RESULTS: After ALD, aspartate aminotransferase highest levels were observed in rats treated with AG and ALT in rats treated with L-NAME. Inhibitors decreased creatinine serum levels to normal values and serum sodium levels re-established after the third day of ALD. L-NAME diminished (P<0.05) eNOS RNA renal expression. Renal iNOS with no inhibitor was overexpressed but was down-regulated by AG treatment. Liver eNOS RNA expression had a decreased expression before ALD in cirrhotic rats, but L-NAME treatment down-regulated eNOS after ALD. AG induced an important iNOS liver decrease. CONCLUSION: Both inhibitors improved renal function, although AG displayed a better effect and did not aggravate liver function. We concluded that NOS isoforms are implicated in the renal pathophysiologic events induced by ALD.

Synthesis and secretion of lipids by long-term cultures of female rat hepatocytes.

The objective of this work was to characterize lipid metabolism in long-term cultures of adult rat hepatocytes from female rats and explore the potential use of this culture system to study the effect of hormones, drugs and toxic chemicals on it. Hepatocytes, seeded on a feeder layer of 3T3 cells, maintained for 2 weeks their typical morphology. The cultures were able to take up [14C]acetic and [14C]oleic acid from the culture medium and incorporate them into lipids. The synthesis and secretion of lipids by [14C]acetic acid-labeled cultures had a maximum value after 11 and 13 days in culture. Triacylglycerols were the main lipidic species synthesized and secreted by hepatocytes (up to 67% of the total lipids); they also synthesized and secreted phospholipids, cholesterol and cholesterol esters from [14C]acetic acid. Similarly, [14C]oleic acid-labeled cultures synthesized and secreted mostly triacylglycerols (up to 60-70% of the total lipids), but they were also able to incorporate the labeled precursor into both cellular and secreted phospholipids and cholesterol esters. The activity of glycerol-phosphate-dehydrogenase, marker enzyme of glycerolipid synthesis, decreased slightly during the culture time whereas the activity of malic enzyme, marker of fatty acid synthesis, increased. Our results show that long-term cultures of female rat hepatocytes are able to synthesize and secrete several lipids, specially triacylglycerols, from both [14C]acetic and [14C]oleic acid for at least 2 weeks and that they maintain enzyme activities related with the synthetic pathways of glycerolipids and fatty acids.(ABSTRACT TRUNCATED AT 250 WORDS)