Microbiological Shelf Life of Pasteurized Milk in Bottle and Pouch

Shelf life of pasteurized milk in Brazil ranges from 3 to 8 d, mainly due to poor cold chain conditions that prevail throughout the country and subject the product to repeated and/or severe temperature abuse. This study evaluated the influence of storage temperature on the microbiological stability of homogenized whole pasteurized milk (75 degrees C/15 s) packaged in high-density polyethylene (HDPE) bottle and low-density polyethylene (LDPE) pouch, both monolayer materials pigmented with titanium dioxide (TiO(2)). The storage temperatures investigated were 2, 4, 9, 14, and 16 degrees C. Microbiological evaluation was based on mesophilic and psychrotrophic counts with 7 log CFU/mL and 6 log CFU/mL, respectively, set as upper limits of acceptability for maintaining the quality of milk. The microbiological stability for pasteurized milk packaged in HDPE bottle and stored at 2, 4, 9, 14, and 16 degrees C was estimated at 43, 36, 8, 5, and 3 d, respectively. For milk samples packaged in LDPE pouch, shelf life was estimated at 37, 35, 7, 3, and 2 d, respectively. The determination of Q(10) and z values demonstrated that storage temperature has a greater influence on microbiological shelf life of pasteurized milk packaged in LDPE pouch compared to HDPE bottle. Based on the results of this study, HDPE bottle was better for storing pasteurized milk as compared to LDPE pouch.

Dietary Free Oleic and Linoleic Acid Enhances Neutrophil Function and Modulates the Inflammatory Response in Rats

The high ingestion of oleic (OLA) and linoleic (LNA) acids by Western populations, the presence of inflammatory diseases in these populations, and the importance of neutrophils in the inflammatory process led us to investigate the effects of oral ingestion of unesterified OLA and LNA on rat neutrophil function. Pure OLA and LNA were administered by gavage over 10 days. The doses used (0.11, 0.22 and 0.44 g/kg of body weight) were based on the Western consumption of OLA and LNA. Neither fatty acid affected food, calorie or water intake. The fatty acids were not toxic to neutrophils as evaluated by cytometry using propidium iodide (membrane integrity and DNA fragmentation). Neutrophil migration in response to intraperitoneal injection of glycogen and in the air pouch assay, was elevated after administration of either OLA or LNA. This effect was associated with enhancement of rolling and increased release of the chemokine CINC-2 alpha beta. Both fatty acids elevated l-selectin expression, whereas no effect on beta(2)-integrin expression was observed, as evaluated by flow cytometry. LNA increased the production of proinflammatory cytokines (IL-1 beta and CINC-2 alpha beta) by neutrophils after 4 h in culture and both fatty acids decreased the release of the same cytokines after 18 h. In conclusion, OLA and LNA modulate several functions of neutrophils and can influence the inflammatory process.

Short-chain fatty acids stimulate the migration of neutrophils to inflammatory sites

SCFAs (short-chain fatty acids) are produced by anaerobic bacterial fermentation. Increased concentrations of these fatty acids are observed in inflammatory conditions, such as periodontal disease, and at sites of anaerobic infection. In the present study, the effect of the SCFAs acetate, propionate and butyrate on neutrophil chemotaxis and migration was investigated. Experiments were carried out in rats and in vitro. The following parameters were measured: rolling, adherence, expression of adhesion molecules in neutrophils (L-selectin and beta 2 integrin), transmigration, air pouch influx of neutrophils and production of cytokines [CINC-2 alpha beta (cytokine-induced neutrophil chemoattractant-2 alpha beta), IL-1 beta (interleukin-1 beta), MIP-1 alpha (macrophage inflammatory protein-1 alpha) and TNF-alpha (tumour necrosis factor-alpha)]. SCFAs induced in vivo neutrophil migration and increased the release of CINC-2 alpha beta into the air pouch. These fatty acids increased the number of rolling and adhered cells as evaluated by intravital microscopy. SCFA treatment increased L-selectin expression on the neutrophil surface and L-selectin mRNA levels, but had no effect on the expression of beta 2 integrin. Propionate and butyrate also increased in vitro transmigration of neutrophils. These results indicate that SCFAs produced by anaerobic bacteria raise neutrophil migration through increased L-selectin expression on neutrophils and CINC-2 alpha beta release.

Effects of Low-Level Laser Therapy on Collagen Expression and Neutrophil Infiltrate in 5-Fluorouracil-Induced Oral Mucositis in Hamsters

Background and Objectives: Several studies have suggested that low-level laser therapy (LLLT) can ameliorate oral mucositis, however, the mechanisms involved are not well understood. The aim of this study was to investigate the mechanisms of action of LLLT on chemotherapy-induced oral mucositis, as related to effects on collagen expression and inflammation Materials and Methods: A hamster cheek pouch model of oral mucositis was used with all animals receiving intraperitoneal 5-fluorouracil, followed by surface irritation. Animals were randomly allocated into three groups, and treated with an InGaAIP diode laser at a wavelength of 660 nm and output power of 35 or 100 mW laser, or no laser Clinical severity of mucositis was assessed at four time-points by a blinded examiner Buccal pouch tissue was harvested from a subgroup of animals in each group at four time-points. Collagen was qualitatively and quantitatively evaluated after picrosinus staining. The density of the neutrophil infiltrate was also scored Results: Peak clinical severity of mucositis was reduced in the 35 mW laser group as compared to the 100 mW and control groups The reduced peak clinical severity of mucositis in the 35 mW laser group was accompanied by a decrease in the number of neutrophils and an increase in the proportion of mature collagen as compared to the other two groups. The total quantity of collagen was significantly higher in the control (no laser) group at the day 11 time-point, as compared to the 35 mW laser group, consistent with a more prolonged inflammatory response in the control group. Conclusion: This study supports two mechanisms of action for LLLT in reducing mucositis severity. The increase in collagen organization in response to the 35 mW laser indicates that LLLT promotes wound healing In addition, LLLT also appears to have an anti-inflammatory effect, as evidenced by the reduction in neutrophil infiltrate Lasers Surg Med 42 546-552, 2010. (C) 2010 Wiley-Liss, Inc.

Cyclooxygenase-2 and vascular endothelial growth factor expression in 5-fluorouracil-induced oral mucositis in hamsters: evaluation of two low-intensity laser protocols

The aim of this study was to investigate the mechanisms whereby low-intensity laser therapy may affect the severity of oral mucositis. A hamster cheek pouch model of oral mucositis was used with all animals receiving intraperitoneal 5-fluorouracil followed by surface irritation. Animals were randomly allocated into three groups and treated with a 35 mW laser, 100 mW laser, or no laser. Clinical severity of mucositis was assessed at four time-points by a blinded examiner. Buccal pouch tissue was harvested from a subgroup of animals in each group at four time-points. This tissue was used for immunohistochemistry for cyclooxygenase-2 (COX-2), vascular endothelial growth factor (VEGF), and factor VIII (marker of microvessel density) and the resulting staining was quantified. Peak severity of mucositis was reduced in the 35 mW laser group as compared to the 100 mW laser and control groups. This reduced peak clinical severity of mucositis in the 35 mW laser group was accompanied by a significantly lower level of COX-2 staining. The 100 mW laser did not have an effect on the severity of clinical mucositis, but was associated with a decrease in VEGF levels at the later time-points, as compared to the other groups. There was no clear relationship of VEGF levels or microvessel density to clinical mucositis severity. The tissue response to laser therapy appears to vary by dose. Low-intensity laser therapy appears to reduce the severity of mucositis, at least in part, by reducing COX-2 levels and associated inhibition of the inflammatory response.

Light-Emitting Diode Therapy in Chemotherapy-Induced Mucositis

Background and Objective: Mucositis is the most common oral complication of cancer chemotherapy, which causes pain on mastication and swallowing, impairs patients` ability to eat and take oral drugs and may determine interruption of the treatment. The aim of this study was to evaluate the effect of light-emitting diode (LED) therapy on chemotherapy-induced mucositis in hamsters. Study Design/Materials and Methods: Animals of both experimental (Group 1; n = 32) and positive control (Group II; n = 32) groups received intraperitoneal injections of 5-fluorouracil on days 0 and 2. All animals had their right and left cheek pouch irritated by superficial scratching on days 3 and 4. In Group I, LED irradiation (630 nm +/- 10 nm, 160 mW, 12 J/cm(2)) was applied during 37.5 seconds at days 3, 4, 6, 8, 10, 12, and 14. In Group II, mucositis was induced, but LED therapy was not performed. The oral mucosa was photographed from day 4 to 14 at 2-day intervals. Photographs were randomly scored according to the severity of induced mucositis (0 to 5). In the negative control group (Group III; n = 6), no mucositis was induced. Biopsies of the cheek pouches of 8 animals (Group I and Group II) were surgically obtained on days 5, 9, 13 and 15 and processed for histological examination. Results: The statistical analysis showed significant differences between irradiated and non-irradiated groups (P < 0.05). However, muscular degeneration was observed in 18% of the samples of Group I. Conclusion: It may be concluded that the LED therapy protocol established for this in vivo study was effective in reducing the severity of oral mucositis, although the oral lesions were not completely prevented. Lasers Surg. Med. 40:625-633, 2008. (c) 2008Wiley-Liss, Inc.