Prophylactic tranexamic acid decreases bleeding after cardiac operations

Thirty-eight patients undergoing a cardiac operation randomly received either tranexamic acid, a potent inhibitor of plasminogen, or placebo in an effort to determine whether prophylactic antifibrinolytic therapy reduces chest tube drainage. Twelve-hour blood loss was 750 +/- 314 (standard deviation) ml in the placebo group and 496 +/- 228 ml in the drug group (p = 0.0057). Fibrin split products were present more frequently in patients in the placebo group (17 of 20 compared with four of 18 in the drug group; p = 0.0002). Tranexamic acid markedly decreased plasminogen availability (112 +/- 104 units in the placebo group versus 36 +/- 18 units in the drug group, p = 0.0058). Plasma fibrinogen concentrations were similar in the placebo and drug groups. Patients in the placebo group received more fresh-frozen plasma and more mediastinal shed blood than those in the drug group. No coagulation-related complication occurred in the group receiving tranexamic acid. We conclude that prophylactic tranexamic acid can be administered safely to inhibit fibrinolysis during cardiac operations, decrease postoperative bleeding, and possibly decrease the frequency of blood product transfusion.     

Selective sensitivity of synaptosomal membrane function to cerebral cortical hypoxia in newborn piglets

The effect of hypoxia on the structure and function of the synaptosomal membranes and myelin fraction (glial cells, neuronal cell bodies and axonal membranes) was investigated by measuring Na⁺,K⁺-ATPase activity and levels of lipid peroxidation products in cerebral cortical synaptosomal membranes and myelin fractions obtained from newborn piglets. Hypoxic hypoxia was induced and cerebral hypoxia was documented as a decrease in the ratio of phosphocreatine to inorganic phosphate (PCr/Oi) using³¹P-NMR spectroscopy. PCr/Pi decreased from baseline of2.93 ± 0.76to0.61 ± 0.36 during hypoxia. The synaptosomal membrane Na⁺,K⁺-ATPase activity decreased from a control value of56.6 ± 3.7to40.4 ± 6.0 μgmol Pi/mg protein/h during hypoxia. The level of conjugated dienes increased from zero (reference value) to4.5 ± 2.7 nmol/mg lipid and the level of fluorescent compounds increased from23.5 ± 2.2to92.6 ± 46.4 ng quinine sulfate/mg lipid in the synaptosomal membranes during hypoxia. No change in myelin fraction Na⁺,K⁺-ATPase activity or levels of lipid peroxidation products were noted. These data indicate that sunaptosomal membranes, rich in polyunsaturated fatty acids, are more susceptible to oxygen free radical mediated lipid peroxidative damage during hypoxia.     

Tannic acid resistance in ruminal streptococcal isolates

Tannin degrading isolates of Streptococcus spp. from rumen of non-adaptive cattle, when grown in BHI broth, were able to tolerate tannic acid upto a level of 50 g/l. An increase in lag period from 1.5 to 6 h was observed for the isolates in presence of increased concentration of tannic acid. In addition, the morphology of gram positive diplococci converted to an elongated chain of 40-50 cells with increasing tannic acid from 1 to 4%. Qualitatively, the tannase activity was found to be present in the isolates tested, indicating their potential of being a tannin degrader.     

In vivo mammalian brain imaging using one- and two-photon fluorescence microendoscopy

One of the major limitations in the current set of techniques available to neuroscientists is a dearth of methods for imaging individual cells deep within the brains of live animals. To overcome this limitation, we developed two forms of minimally invasive fluorescence microendoscopy and tested their abilities to image cells in vivo. Both one- and two-photon fluorescence microendoscopy are based on compound gradient refractive index (GRIN) lenses that are 350-1,000 microm in diameter and provide micron-scale resolution. One-photon microendoscopy allows full-frame images to be viewed by eye or with a camera, and is well suited to fast frame-rate imaging. Two-photon microendoscopy is a laser-scanning modality that provides optical sectioning deep within tissue. Using in vivo microendoscopy we acquired video-rate movies of thalamic and CA1 hippocampal red blood cell dynamics and still-frame images of CA1 neurons and dendrites in anesthetized rats and mice. Microendoscopy will help meet the growing demand for in vivo cellular imaging created by the rapid emergence of new synthetic and genetically encoded fluorophores that can be used to label specific brain areas or cell classes.     

Fatal renal failure as the first manifestation of sarcoidosis diagnosed on necropsy in a young man: a case report

Renal involvement as the first manifestation of sarcoidosis is rare and has never been reported in India. This report describes a 35 year old man who was admitted to the emergency department with a clinical diagnosis of acute on chronic renal failure, secondary to obstructive uropathy. Postmortem examination unexpectedly revealed disseminated sarcoidosis.     

The Neuroimmunology of Multiple Sclerosis: Possible Roles of T and B Lymphocytes in Immunopathogenesis

Multiple sclerosis (MS) is an inflammatory disease of the central nervous system white matter. The association of the disease with MHC genes, the inflammatory white matter infiltrates, similarities with animal models, and the observation that MS can be treated with immunomodulatory and immunosuppressive therapies support the hypothesis that autoimmunity plays a major role in the disease pathology. Evidence supports activated CD4⁺ myelin-reactive T cells as major mediators of the disease. In addition, a renewed interest in the possible contribution of B cells to MS immunopathology has been sparked by nonhuman primate and MS pathological studies. This review focuses on the immunopathology of MS, outlining the hypothetical steps of tolerance breakdown and the molecules that play a role in the migration of autoreactive cells to the CNS. Particular focus is given to autoreactive T cells and cytokines as well as B cells and autoantibodies and their role in CNS pathogenesis in MS.     

Polysomnographic and actigraphic evidence of sleep fragmentation in patients with irritable bowel syndrome

STUDY OBJECTIVE: To characterize the function and quality of sleep in patients with irritable bowel syndrome (IBS). DESIGN: A prospective study with a historic comparison group. SETTING: A regional hospital that also serves as a tertiary referral center. PATIENTS: Eighteen patients with IBS and a comparison group of 20 matched adults with mild benign snoring. INTERVENTIONS: A polysomnography study and a wrist actigraphy study. MEASUREMENTS: All subjects underwent sleep studies and completed self-report questionnaires (IBS severity, psychosocial variables, sleep function, and Epworth Sleepiness Scale). Fourteen IBS and 11 comparison patients underwent actigraphy. RESULTS: The IBS patients had more than 70% less slow-wave stage sleep (4.5 +/- 7.3% vs 19.3 +/- 12.9%; P = 0.006), compensated by increased stage 2 sleep (72.2 +/- 6.6% vs 60.1 +/- 16.8%; P = 0.01). The IBS group had significant sleep fragmentation with a significantly higher arousal and awakening index (P < 0.001), a longer wake period after sleep onset (P = 0.02), and more downward shifts to lighter sleep stages (P = 0.01). The 4-night actigraphy study supported the polysomnography findings. The sleep fragmentation index was significantly higher (P = 0.008) in the IBS group. The IBS patients reported greater daytime sleepiness (9.0 +/- 4.8 vs 6.4 +/- 4.8, Epworth Sleepiness Scale score, P < 0.01) and greater impairment in quality of life, which correlated significantly with the sleep fragmentation indexes. The difference between the groups was not due to differences in baseline anxiety/depression levels. CONCLUSIONS: Patients with IBS have impaired sleep quality, reduced slow-wave sleep activity, and significant sleep fragmentation. The cause-and-effect relationship of these findings with patients' daytime symptoms should be studied further.