Wound infection by multiresistant Staphylococcus sciuri identified by molecular methods.

We describe a case of wound infection by multidrug-resistant Staphylococcus sciuri in a patient admitted to hospital for injuries in Agreste Alagoas, Brazil, identified through broad-spectrum PCR and sequencing of 16S rDNA gene. Due to its high resistance profile, the infection was characterized as methicillin-resistant Staphylococcus presenting sensitive only to vancomycin and chloramphenicol. The injury resulting from trauma associated with infection resulted in amputation of the infected limb.

Cytosolic phospholipase A2-driven PGE2 synthesis within unsaturated fatty acids-induced lipid bodies of epithelial cells.

Cytoplasmic lipid bodies (also known as lipid droplets) are intracellular deposits of arachidonic acid (AA), which can be metabolized for eicosanoid generation. PGE2 is a major AA metabolite produced by epithelial cells and can modulate restoration of epithelium homeostasis after injury. We studied lipid body biogenesis and their role in AA metabolic pathway in an epithelial cell line derived from normal rat intestinal epithelium, IEC-6 cells. Lipid bodies were virtually absent in confluent IEC-6 cells. Stimulation of confluent IEC-6 cells with unsaturated fatty acids, including AA or oleic acid (OA), induced rapid lipid body assembly that was independent on its metabolism to PGE(2), but dependent on G-coupled receptor-driven signaling through p38, PKC, and PI3 K. Newly formed lipid bodies compartmentalized cytosolic phospholipase (cPL)A(2)-alpha, while facilitated AA mobilization and synthesis of PGE(2) within epithelial cells. Thus, both lipid body-related events, including highly regulated biogenesis and functional assembly of cPLA (2)-alpha-driven enhanced AA mobilization and PGE(2)production, may have key roles in epithelial cell-driven inflammatory functions, and may represent relevant therapeutic targets of epithelial pathologies.

Reliable measurement of incisal bite force for understanding the control of masticatory muscles.

OBJECTIVE: In the present study, we aimed at evaluating the steadiness of incisal bite force during isometric contractions of masticatory muscles. DESIGN: Two separate experiments were carried out in 11 healthy young women. A first experiment was performed to test the reliability of our protocol for measurement of incisal bite force steadiness. The second experiment aimed to evaluate the steadiness of incisal bite force at four submaximal (i.e., percentage of maximum voluntary contraction, MVC) levels (5 %MVC, 10 %MVC, 15 %MVC, and 20 %MVC), along with the bilateral myoelectric activity of two masticatory muscles (temporalis and masseter). RESULTS: The results from the first experiment showed that our protocol is substantially reliable (intraclass correlation coefficient, ICC > 0.80) for estimating force variability and moderate reliable (0.60 < ICC < 0.80) for estimating spectral properties of force signals. In the second experiment, we found that force standard deviation (SD) increased proportionally to the power of mean force, and coefficient of variation (CoV) was higher at low-intensity contractions and maintained at an approximately constant level for high-intensity contractions. The force-EMG relationships were linear for both muscles at the contraction intensities evaluated in the study (5 %MVC to 20 %MVC), and the median frequency did not change with contraction intensity. CONCLUSION: Therefore, we presented a reliable method to estimate the incisal bite force, along with additional data on force control and myoelectric activity of jaw elevator muscles during isometric steady contractions.

A longitudinal assessment of myoelectric activity, postural sway, and low-back pain during pregnancy.

PURPOSE: The present study aimed at investigating the control of upright quiet standing in pregnant women throughout pregnancy, and whether low-back pain exerts influence on this motor task. METHODS: Myoelectric signals from postural muscles and stabilometric data were collected from 15 non-pregnant and 15 pregnant women during upright quiet standing. Electromyogram envelopes and center of pressure metrics were evaluated in the control group, as well as in pregnant women in their first and third trimester of pregnancy. A correlation analysis was performed between the measured variables and a low-back pain disability index. RESULTS: Pregnant women exhibited a decreased maximum voluntary isometric activity for all postural muscles evaluated. Additionally, the activity of lumbar muscles during the postural task was significantly higher in the pregnant women in comparison to the non-pregnant controls. The soleus muscle maintained its activity at the same level as the gestation progressed. Higher postural oscillations were observed in the anteroposterior direction while mediolateral sway was reduced in the third trimester of pregnancy. No correlation was detected between the lowback pain disability index and neuromechanical variables. CONCLUSION: This study provides additional data regarding the functioning and adaptations of the postural control system during pregnancy. Also, we provide further evidence that postural control during quiet standing cannot be used to predict the occurrence of low-back pain. We hypothesize that the modifications in the neural drive to the muscles, as well as in postural sway may be related to changes in the biomechanics and hormonal levels experienced by the pregnant women.

Hypertonic environment elicits cyclooxygenase-2-driven prostaglandin E2 generation by colon cancer cells: role of cytosolic phospholipase A2-alpha and kinase signaling pathways.

Cyclooxygenase (COX)-2-derived prostaglandin (PG)E(2) controls many aspects of colon cancer development, modulating from apoptosis resistance and cell proliferation to angiogenesis, invasion, and metastasis. Here, we investigated the role of different phospholipases (PL)A(2) in supplying arachidonic acid (AA) for COX-2-dependent PGE(2) generation and signaling pathways involved in activation of colon cancer cells by a physiologically relevant stimulus. To emulate the hypertonic environment found physiologically in colon, the human colon cancer cell line Caco-2 was maintained in hypertonic complete DMEM medium. Human colon cancer cell line Caco-2 exposed to a hypertonic environment responded with marked AA release, COX-2 induction and PGE(2) generation. Selective secretory (s)PLA(2) and calcium-independent (i)PLA(2) inhibitors did not modify PGE(2) generation, while either COX-2 or cytosolic (c)PLA(2) inhibitors completely inhibited PGE(2) generation. cPLA(2)-alpha was responsible for AA supply for PGE(2) generation, but had no role in COX-2 induction. Mitogen-activated protein (MAP) kinases, ERK 1/2, p38, and JNK, participated in the signaling events that lead to PGE(2) generation by modulating AA release, but only ERK 1/2 was involved in COX-2 upregulation. Our results indicate that hypertonic stress activates PGE(2) generation by Caco-2 cells through a mechanism dependent on MAP kinase-regulated AA mobilization, increased cPLA(2)-alpha activity, and COX-2 induction.