Acute Spinal Cord Injury: Correlations and Causal Relations Between Intraspinal Pressure, Spinal Cord Perfusion Pressure, Lactate-to-Pyruvate Ratio, and Limb Power.

BACKGROUND/OBJECTIVE: We have recently developed monitoring from the injury site in patients with acute, severe traumatic spinal cord injuries to facilitate their management in the intensive care unit. This is analogous to monitoring from the brain in patients with traumatic brain injuries. This study aims to determine whether, after traumatic spinal cord injury, fluctuations in the monitored physiological, and metabolic parameters at the injury site are causally linked to changes in limb power. METHODS: This is an observational study of a cohort of adult patients with motor-incomplete spinal cord injuries, i.e., grade C American spinal injuries association Impairment Scale. A pressure probe and a microdialysis catheter were placed intradurally at the injury site. For up to a week after surgery, we monitored limb power, intraspinal pressure, spinal cord perfusion pressure, and tissue lactate-to-pyruvate ratio. We established correlations between these variables and performed Granger causality analysis. RESULTS: Nineteen patients, aged 22-70 years, were recruited. Motor score versus intraspinal pressure had exponential decay relation (intraspinal pressure rise to 20 mmHg was associated with drop of 11 motor points, but little drop in motor points as intraspinal pressure rose further, R2 = 0.98). Motor score versus spinal cord perfusion pressure (up to 110 mmHg) had linear relation (1.4 motor point rise/10 mmHg rise in spinal cord perfusion pressure, R2 = 0.96). Motor score versus lactate-to-pyruvate ratio (greater than 20) also had linear relation (0.8 motor score drop/10-point rise in lactate-to-pyruvate ratio, R2 = 0.92). Increased intraspinal pressure Granger-caused increase in lactate-to-pyruvate ratio, decrease in spinal cord perfusion, and decrease in motor score. Increased spinal cord perfusion Granger-caused decrease in lactate-to-pyruvate ratio and increase in motor score. Increased lactate-to-pyruvate ratio Granger-caused increase in intraspinal pressure, decrease in spinal cord perfusion, and decrease in motor score. Causality analysis also revealed multiple vicious cycles that amplify insults to the cord thus exacerbating cord damage. CONCLUSION: Monitoring intraspinal pressure, spinal cord perfusion pressure, lactate-to-pyruvate ratio, and intervening to normalize these parameters are likely to improve limb power

Safety profile and probe placement accuracy of intraspinal pressure monitoring for traumatic spinal cord injury: Injured Spinal Cord Pressure Evaluation study.

OBJECTIVE A novel technique for monitoring intraspinal pressure and spinal cord perfusion pressure in patients with traumatic spinal cord injury was recently described. This is analogous to monitoring intracranial pressure and cerebral perfusion pressure in patients with traumatic brain injury. Because intraspinal pressure monitoring is a new technique, its safety profile and impact on early patient care and long-term outcome after traumatic spinal cord injury are unknown. The object of this study is to review all patients who had intraspinal pressure monitoring to date at the authors' institution in order to define the accuracy of intraspinal pressure probe placement and the safety of the technique. METHODS At the end of surgery to fix spinal fractures, a pressure probe was inserted intradurally to monitor intraspinal pressure at the injury site. Postoperatively, CT scanning was performed within 48 hours and MRI at 2 weeks and 6 months. Neurointensive care management and complications were reviewed. The American Spinal Injury Association Impairment Scale (AIS) grade was determined on admission and at 2 to 4 weeks and 12 to 18 months postoperation. RESULTS To date, 42 patients with severe traumatic spinal cord injuries (AIS Grades A-C) had undergone intraspinal pressure monitoring. Monitoring started within 72 hours of injury and continued for up to a week. Based on postoperative CT and MRI, the probe position was acceptable in all patients, i.e., the probe was located at the site of maximum spinal cord swelling. Complications were probe displacement in 1 of 42 patients (2.4%), CSF leakage that required wound resuturing in 3 of 42 patients (7.1%), and asymptomatic pseudomeningocele that was diagnosed in 8 of 42 patients (19.0%). Pseudomeningocele was diagnosed on MRI and resolved within 6 months in all patients. Based on the MRI and neurological examination results, there were no serious probe-related complications such as meningitis, wound infection, hematoma, wound breakdown, or neurological deterioration. Within 2 weeks postoperatively, 75% of patients were extubated and 25% underwent tracheostomy. Norepinephrine was used to support blood pressure without complications. Overall, the mean intraspinal pressure was around 20 mm Hg, and the mean spinal cord perfusion pressure was around 70 mm Hg. In laminectomized patients, the intraspinal pressure was significantly higher in the supine than lateral position by up to 18 mm Hg after thoracic laminectomy and 8 mm Hg after cervical laminectomy. At 12 to 18 months, 11.4% of patients had improved by 1 AIS grade and 14.3% by at least 2 AIS grades. CONCLUSIONS These data suggest that after traumatic spinal cord injury intradural placement of the pressure probe is accurate and intraspinal pressure monitoring is safe for up to a week. In patients with spinal cord injury who had laminectomy, the supine position should be avoided in order to prevent rises in intraspinal pressure

Measurement of Intraspinal Pressure After Spinal Cord Injury: Technical Note from the Injured Spinal Cord Pressure Evaluation Study.

Intracranial pressure (ICP) is routinely measured in patients with severe traumatic brain injury (TBI). We describe a novel technique that allowed us to monitor intraspinal pressure (ISP) at the injury site in 14 patients who had severe acute traumatic spinal cord injury (TSCI), analogous to monitoring ICP after brain injury. A Codman probe was inserted subdurally to measure the pressure of the injured spinal cord compressed against the surrounding dura. Our key finding is that it is feasible and safe to monitor ISP for up to a week in patients after TSCI, starting within 72 h of the injury. With practice, probe insertion and calibration take less than 10 min. The ISP signal characteristics after TSCI were similar to the ICP signal characteristics recorded after TBI. Importantly, there were no associated complications. Future studies are required to determine whether reducing ISP improves neurological outcome after severe TSCI

Anti-shielding Effect and Negative Temperature in Instantaneously Reversed Electric Fields and Left-Handed Media

The connections between the anti-shielding effect, negative absolute temperature and superluminal light propagation in both the instantaneously reversed electric field and the left-handed media are considered in the present paper. The instantaneous inversion of the exterior electric field may cause the electric dipoles into the state of negative absolute temperature and therefore give rise to a negative effective mass term of electromagnetic field (i. e., the electromagnetic field propagating inside the negative-temperature medium will acquire an imaginary rest mass), which is said to result in the potential superluminality effect of light propagation in this anti-shielding dielectric. In left-handed media, such phenomena may also arise.Comment: 9 pages, Late

Increased aquaporin 1 water channel expression inhuman brain tumours

Aquaporin 1 is a water channel protein. There was little aquaporin 1 immunoreactivity in normal brain parenchyma. In astrocytomas, aquaporin 1 was expressed in microvessel endothelia and neoplastic astrocytes. In metastatic carcinomas, aquaporin 1 was present in microvessel endothelia and reactive astrocytes. Aquaporin 1 may participate in the formation of brain tumour oedema

Expansion duroplasty improves intraspinal pressure, spinal cord perfusion pressure, and vascular pressure reactivity index in patients with traumatic spinal cord injury: injured spinal cord pressure evaluation study.

We recently showed that, after traumatic spinal cord injury (TSCI), laminectomy does not improve intraspinal pressure (ISP), spinal cord perfusion pressure (SCPP), or the vascular pressure reactivity index (sPRx) at the injury site sufficiently because of dural compression. This is an open label, prospective trial comparing combined bony and dural decompression versus laminectomy. Twenty-one patients with acute severe TSCI had re-alignment of the fracture and surgical fixation; 11 had laminectomy alone (laminectomy group) and 10 had laminectomy and duroplasty (laminectomy+duroplasty group). Primary outcomes were magnetic resonance imaging evidence of spinal cord decompression (increase in intradural space, cerebrospinal fluid around the injured cord) and spinal cord physiology (ISP, SCPP, sPRx). The laminectomy and laminectomy+duroplasty groups were well matched. Compared with the laminectomy group, the laminectomy+duroplasty group had greater increase in intradural space at the injury site and more effective decompression of the injured cord. In the laminectomy+duroplasty group, ISP was lower, SCPP higher, and sPRx lower, (i.e., improved vascular pressure reactivity), compared with the laminectomy group. Laminectomy+duroplasty caused cerebrospinal fluid leak that settled with lumbar drain in one patient and pseudomeningocele that resolved completely in five patients. We conclude that, after TSCI, laminectomy+duroplasty improves spinal cord radiological and physiological parameters more effectively than laminectomy alone

Se and I status in pregnant ewes from a pastoral system and the effect of supplementation with Se and I or only Se on wool quality of lambs

Australian Merino ewes and lambs producing fine fibre wool for export are raised in the north-west of Uruguay in pasture-based systems. We studied the status of selenium and iodine in pregnant Merino ewes (10 per treatment) grazing in natural pasture, in natural pasture and supplemented with Se (0.1 mg Se/kg dry matter intake) and I (1 mg I/kg dry matter intake), or in natural pasture and supplemented with Se alone (0.1 mg Se/kg dry matter intake), during the last 30 days of gestation. Further, we evaluated the performance and wool quality of their offspring. Content of Se and I in natural pasture, in the sera of pregnant ewes, and in the wool of their offspring and levels of thyroidal hormones—TSH, T4, and free T3 (FT3)—in the sera of pregnant ewes were determined. The performance of lambs and the commercial parameters of fine fibre wool produced were measured. Results showed normal Se levels in serum (0.12–0.15 mg/l) in the ewes grazing in natural pasture (0.07–0.09 mg/kg DM) during late pregnancy. The observed increase in Se content in the pasture at lambing (0.11–0.16 mg/kg DM) improved serum Se levels (0.216 mg/l); however, the serum levels were not affected by the supplementation. I content in pasture showed adequate levels (0.50–0.60 mg/kg DM), which were reflected in the blood serum values 30 days prior to lambing (0.197–0.208 mg/l). However, at lambing, the I content in blood serum decreased (0.150 mg/l). Further, the supplementation did not modify the serum I levels (0.163–0.175 mg/l). An increase in FT3 levels in ewes at lambing could be associated with the increase in Se content in pasture and/or the adequate I content in pasture. No effect of supplementation was observed. Lambs showed good results regarding the quality of fine fibre wool and performance after supplementation with Se and I or Se alone and exhibited slightly improved Se and I content in wool. In conclusion, natural pasture provides adequate status in Se and I for the Merino ewes and their offspring without any additional beneficial effects of supplementation with Se and I or only Se

Influence of Processing Parameters and Natural Antimicrobial on Alicyclobacillus acidoterrestris and Clostridium pasteurianum Using Response Surface Methodology

The food industry must ensure the stability of the products, and this is often achieved by exposing foods to heat treatments that are able to ensure the absence of pathogenic or spoilage microorganisms. These treatments are different in terms of temperature and duration and could lead to a loss in nutritional and sensory value. Moreover, some types of microorganisms manage to survive these treatments thanks to the sporification process. The addition of antimicrobials can become necessary, but at present, consumers are more inclined toward natural products, avoiding synthetic and chemical additives. Antimicrobials from plants could be a valuable option and, in this context, a patent concerning an antimicrobial extract from fermented plant substrate was recently tested against foodborne pathogens revealing high antimicrobial activity. The objective of this study was the creation of a model for the evaluation and subsequent prediction of the combined effect of different process and product variables, including antimicrobial addition, on the inhibition and reduction of spore germination of target microorganisms, Alicyclobacillus acidoterrestris and Clostridium pasteurianum, responsible for spoilage of tomato-based products

Isolation of Cronobacter spp. (formerly Enterobacter sakazakii) from infant food, herbs and environmental samples and the subsequent identification and confirmation of the isolates using biochemical, chromogenic assays, PCR and 16S rRNA sequencing

BACKGROUND: Cronobacter spp. (formerly Enterobacter sakazakii), are a group of Gram-negative pathogens that have been implicated as causative agents of meningitis and necrotizing enterocolitis in infants. The pathogens are linked to infant formula; however, they have also been isolated from a wide range of foods and environmental samples. RESULTS: In this study, 233 samples of food, infant formula and environment were screened for the presence of Cronobacter spp. in an attempt to find its source. Twenty nine strains were isolated from samples of spices, herbs, infant foods, and dust obtained from household vacuum cleaners. Among the 76 samples of infant food, infant formula, milk powder and non-milk dairy products tested, only one sample of infant food contained Cronobacter spp. (1.4%). The other Cronobacter spp. isolates recovered include two from household vacuum dust, and 26 from 67 samples of herbs and spices. Among the food categories analyzed, herbs and spices harbored the highest number of isolates, indicating plants as a possible reservoir of this pathogen. Initial screening with API 20E test strips yielded 42 presumptive isolates. Further characterization using 3 chromogenic media (α-MUG, DFI and EsPM) and 8 sets of PCR primers detecting ITS (internal transcribed spacer sequences), 16S rRNA, zpx, gluA, gluB, OmpA genes followed by nucleotide sequencing of some PCR amplicons did not confirm the identity of all the isolates as none of the methods proved to be free of both false positives or false negatives. The final confirmation step was done by 16S rRNA sequence analysis identifying only 29 of the 42 isolates as Cronobacter spp. CONCLUSION: Our studies showed that Cronobacter spp. are highly diverse and share many phenotypic traits with other Enterobacteriaceae members highlighting the need to use several methods to confirm the identity of this pathogen. None of the biochemical, chromogenic or PCR primers proved to be a reliable method for confirmation of the identity of the isolates as all of them gave either false positives or false negatives or both. It is therefore concluded that 16S rRNA sequencing is pivotal to confirm the identity of the isolates

Aquaporin-4 and brain edema.

Aquaporin-4 (AQP4) is a water-channel protein expressed strongly in the brain, predominantly in astrocyte foot processes at the borders between the brain parenchyma and major fluid compartments, including cerebrospinal fluid (CSF) and blood. This distribution suggests that AQP4 controls water fluxes into and out of the brain parenchyma. Experiments using AQP4-null mice provide strong evidence for AQP4 involvement in cerebral water balance. AQP4-null mice are protected from cellular (cytotoxic) brain edema produced by water intoxication, brain ischemia, or meningitis. However, AQP4 deletion aggravates vasogenic (fluid leak) brain edema produced by tumor, cortical freeze, intraparenchymal fluid infusion, or brain abscess. In cytotoxic edema, AQP4 deletion slows the rate of water entry into brain, whereas in vasogenic edema, AQP4 deletion reduces the rate of water outflow from brain parenchyma. AQP4 deletion also worsens obstructive hydrocephalus. Recently, AQP4 was also found to play a major role in processes unrelated to brain edema, including astrocyte migration and neuronal excitability. These findings suggest that modulation of AQP4 expression or function may be beneficial in several cerebral disorders, including hyponatremic brain edema, hydrocephalus, stroke, tumor, infection, epilepsy, and traumatic brain injury