Nutritional composition of ultra-processed plant-based foods in the out-of-home environment: a multi-country survey with plant-based burgers.

Ultra-processed plant-based foods, such as plant-based burgers, have gained in popularity. Particularly in the out-of-home (OOH) environment, evidence regarding their nutritional profile and environmental sustainability is still evolving. Plant-based burgers available at selected OOH sites were randomly sampled in Amsterdam, Copenhagen, Lisbon and London. Plant-based burgers (patty, bread and condiment) (n 41) were lab analysed for their energy, macronutrients, amino acids and minerals content per 100 g and serving and were compared with reference values. For the plant-based burgers, the median values per 100 g were 234 kcal, 20·8 g carbohydrates, 3·5 g dietary fibre and 12·0 g fat, including 0·08 g TFS and 2·2 g SFA. Protein content was 8·9 g/100 g, with low protein quality according to amino acid composition. Median Na content was 389 mg/100 g, equivalent to 1 g salt. Compared with references, the median serving provided 31% of energy intake based on a 2000 kcal per day and contributed to carbohydrates (17-28%), dietary fibre (42%), protein (40%), total fat (48%), SFA (26%) and Na (54%). One serving provided 15-23% of the reference values for Ca, K and Mg, while higher contributions were found for Zn, Mn, P and Fe (30-67%). The ultra-processed plant-based burgers provide protein, dietary fibre and essential minerals and contain relatively high levels of energy, Na and total fats. The amino acid composition indicated low protein quality. The multifaceted nutritional profile of plant-based burgers highlights the need for manufacturers to implement improvements to better support healthy dietary habits, including reducing energy, Na and total fats.

Impact of a neuro-intensive care service for newborns.

BACKGROUND: Advances in treating the injured neonatal brain have given rise to neuro-intensive care services for newborns. This study assessed the impact of one such service in a cohort of newborns treated with therapeutic hypothermia. METHODS: Our newborn neuro-intensive care service was started in November 2012. From January 2008 to October 2016, a cohort of 158 newborns was treated with therapeutic hypothermia, 29 before and 129 after the inception of the service. This study compared the outcomes of newborns treated by the service with those of newborns treated before. Multivariate regression analysis associating length-of-stay and treatment pre- or post-service was adjusted for five-minute Apgar score, time-to-target temperature, seizures, and mortality. RESULTS: The neuro-intensive care service was also associated with a decrease in mortality (17% before service to 5.4% with the service, p = 0.03), though this association is likely multifactorial and reflects the application of therapeutic hypothermia to a wider variety of patients. However, the service was independently associated with decreased length-of-stay (mean 22 pre-service to 13 days with the service, p < 0.0005.)CONCLUSIONS:The service educated referring hospitals in recognizing therapeutic hypothermia candidates, which increased the number of treated newborns, and created a number of procedures to streamline the delivery of treatment. While the increasing number and variety of patients treated could spuriously reduce length-of-stay, length-of-stay was still significantly reduced after adjustment, providing evidence that neuro-intensive care services for newborns can improve hospital outcomes.

Early prediction of a significant patent ductus arteriosus in infants <32 weeks gestational age.

BACKGROUND: The optimal thresholds for identification of preterm infants at greatest risk for adverse sequelae related to patent ductus arteriosus have not been well delineated. Our aim was to determine hemodynamic parameters in the first 24 hours using continuous non-invasive vital and structural measurements to predict which infants required PDA treatment in our institution. METHODS: Retrospective secondary analysis of data from infants born 23 to 32 weeks gestational age with cardiac output and stroke volume via electrical cardiometry, cerebral tissue oximetry measurements, mean arterial blood pressure (BP), heart rate, and oxygen saturation and functional echocardiography results at 12 hours of life were recorded when available (93 percent of subjects). RESULTS: A total of 292 infants, of which 55 (26±2 weeks, 862±268 grams) were treated for PDA. Treated infants demonstrated increased left ventricular output (p < 0.001) and lower mean BP (p = 0.010). The optimal area under the receiver operating characteristic curve (AUC) for predicting PDA treatment in our all gestations cohort is a mean BP at 15 hours of life of <33 mm Hg (AUC = 0.854, p < 0.001, 95% CI 0.792, 0.916). For infants <28 weeks a mean BP at 13 hours of life of <33 mm Hg (AUC = 0.741, p < 0.050, 95% CI 0.642, 0.839). CONCLUSIONS: In our cohort increased left ventricular output and lower mean BP predicted a clinically significant PDA requiring treatment.

Design, optimisation and preliminary validation of a human specific loop-mediated amplification assay for the rapid detection of human DNA at forensic crime scenes.

The identification of samples at a crime scene which require forensic DNA typing has been the focus of recent research interest. We propose a simple, but sensitive analysis system which can be deployed at a crime scene to identify crime scene stains as human or non-human. The proposed system uses the isothermal amplification of DNA in a rapid assay format, which returns results in as little as 30min from sampling. The assay system runs on the Genie II device, a proven in-field detection system which could be deployed at a crime scene. The results presented here demonstrate that the system was sufficiently specific and sensitive and was able to detect the presence of human blood, semen and saliva on mock forensic samples.

Hemodynamic effects of sodium bicarbonate administration.

OBJECTIVE: To describe the hemodynamic changes that occur with sodium bicarbonate (NaHCO3) administration in premature neonates. STUDY DESIGN: This retrospective study included premature neonates 23 to 31+6 weeks of gestational age who underwent continuous cardiac and cerebral monitoring as participants in prospective trials at our institution, and who received NaHCO3 infused over 30 min in the first 24 h of life. Blood pressure (BP), heart rate, cardiac output (CO), SpO2 and cerebral oximetry (StO2) were captured every 2 s. A baseline was established for all continuous data and averaged over the 10 min before NaHCO3 administration. Baseline was compared with measurements over 10 min epochs until 80 min after administration. Arterial blood gases before and within 1 h of administration were also compared. Significance was set at P<0.05. RESULTS: A total of 36 subjects received NaHCO3 (1.3±0.3 mEq kg-1) in the first 24 h (14±8.5 h) of life. NaHCO3 administration increased pH (7.23 vs 7.28, P<0.01) and decreased base deficit (-8.9 vs -6.8, P<0.01) and PaCO2 (45 vs 43 mm Hg, P<0.05). There was a transient but significant (P<0.05) decrease in systemic BP coinciding with an increase in cerebral oxygenation without an increase in oxygen extraction. CO did not change. CONCLUSION: Early postnatal NaHCO3 administration does not acutely improve CO but does cause transient fluctuations in cerebral and cardiovascular hemodynamics in extremely premature infants.

Lewis acid-promoted [2 + 2] cycloadditions of alkenes with aryl ketenes.

A method for the [2 + 2] cycloaddition of aryl ketenes and alkenes is presented. The process involves the in situ generation of a ketene in the presence of a Lewis acid. The utility of products is demonstrated towards the synthesis of a common scaffold found in several natural product families.

Klippel-Trenaunay-Weber syndrome with hemimegalencephaly.

There are many documented cases of Klippel-Trenaunay-Weber syndrome characterized by the triad of port wine stain, varicose veins, and hypertrophy of bones and overlying tissue. A few cases have even included the additional findings of hemimegalencephaly. We report a case of Klippel-Trenaunay-Weber syndrome with hemimegalencephaly and calvarial hypertrophy, but no evidence of limb or trunk hypertrophy.

Inhibition of transforming growth factor beta signaling in MCF-7 cells results in resistance to tumor necrosis factor alpha: a role for Bcl-2.

Transforming growth factor beta (TGF-beta) is a multifunctional cytokine capable of regulating diverse cellular processes. In this study we investigated the effect of autocrine TGF-beta signaling on tumor necrosis factor (TNF) alpha-induced cell death. We abrogated the TGF-beta autocrine loop by overexpression of a truncated TGF-beta type II receptor in MCF-7 breast carcinoma cells and found that this generated resistance to TNF-alpha-induced cytotoxicity. To elucidate the molecular basis of the influence of TGF-beta on TNF-alpha-induced cytotoxicity, we evaluated the expression levels or activities of proteins involved in TNF-alpha signal transduction or the regulation of apoptosis in general in TGF-beta-responsive and TGF-beta-nonresponsive MCF-7 cells. We observed no significant difference in the expression of TNF-alpha receptors or the TNF receptor-associated death domain protein. In addition, downstream activation of nuclear factor kappaB by TNF-alpha was not altered in cells that had lost TGF-beta responsiveness. Analysis of members of the Bcl-2 family of apoptosis-regulatory proteins revealed that Bcl-X(L) and Bax expression levels were not changed by disruption of TGF-beta signaling. In contrast, the TGF-beta-nonresponsive cells expressed much higher levels of Bcl-2 protein and mRNA than did cells with an intact TGF-beta autocrine loop. Furthermore, restoration of a TGF-beta signal to MCF-7 cells that had spontaneously acquired resistance to TGF-beta caused a reduction in Bcl-2 protein expression. Taken together, our data indicate that loss of autocrine TGF-beta signaling results in enhanced resistance to TNF-alpha-mediated cell death and that this is likely to be mediated by derepression of Bcl-2 expression.

gamma-glutamyltranspeptidase-deficient knockout mice as a model to study the relationship between glutathione status, mitochondrial function, and cellular function.

gamma-Glutamyltranspeptidase (GGT)-deficient mice (GGT(-/-)) display chronic glutathione (GSH) deficiency, growth retardation, and die at a young age (<20 weeks). Using livers from these mice, we investigated the relationship between GSH content, especially mitochondrial, and mitochondrial and cellular function. We found that the GSH content of isolated liver mitochondria was diminished by >/=50% in GGT(-/-) mice when compared with wild-type mice. Respiratory control ratios (RCRs) of GGT(-/-) mice liver mitochondria were /=40% in mitochondria obtained from GGT(-/-) mice. We observed a strong correlation between mitochondrial GSH content and RCRs. Even moderate decreases (<50%) correlated with adverse effects with respect to respiration. Electron microscopy revealed that livers from GGT(-/-) knockout mice were deprived of fat and glycogen, and swollen mitochondria were observed in animals that were severely deprived of GSH. Thus, GGT(-/-) mice exhibit a loss of GSH homeostasis and impaired oxidative phosphorylation, which may be related to the rate of adenosine triphosphate (ATP) formation and subsequently leads to progressive liver injury, which characterizes the diseased state. We also found that supplementation of GGT(-/-) mice with N-acetylcysteine (NAC) partially restored liver GSH, but fully restored mitochondrial GSH and respiratory function. Electron microscopy revealed that the livers of NAC-supplemented GGT(-/-) mice contained fat and glycogen; however, slightly enlarged mitochondria were found in some livers. NAC supplementation did not have any beneficial effect on the parameters examined in wild-type mice.

Mechanical and histologic evaluation of Collagraft in an ovine lumbar fusion model.

The purpose of this study was to determine the effectiveness of a composite material composed of Type I bovine dermal collagen, 65% hydroxyapatite, and 35% tricalcium phosphate ceramic (Collagraft Bone Graft Matrix Strip NeuColl Incorporated, Palo Alto, CA) as a bone graft substitute for spinal fusion with and without the use of autologous bone marrow in an ovine lumbar spine model with pedicle screw fixation. Twenty-four adult sheep underwent a single level posterolateral (intertransverse process) L3-L4 lumbar fusion with one of three graft materials combined with rigid pedicle screw fixation. The three graft materials were Collagraft, Collagraft with marrow, and autogenous corticocancellous bone graft. Animals were euthanized 6 months after surgery and evaluated using dual energy x-ray absorptiometry, radiographs, histologic analysis, and mechanical testing. Dual energy xray absorptiometry between the transverse processes revealed that the mineral densities for the two Collagraft groups were significantly higher than the autogenous bone graft group. Histologic analysis confirmed that Collagraft was highly compatible and was well incorporated into the fusion mass. Both Collagraft groups had thick trabeculae and a mixture of lamellar and plexiform bone. The autogenous bone graft group had a smaller fusion complex, composed primarily of lamellar bone with thinner and fewer trabeculae. All three groups had similar mechanical properties. These results support the use of Collagraft in spinal fusion with pedicle screw fixation.

Comparison of the efficacy of 7-hydroxystaurosporine (UCN-01) and other staurosporine analogs to abrogate cisplatin-induced cell cycle arrest in human breast cancer cell lines.

DNA-damaging agents such as cisplatin arrest cell cycle progression at either the G1, S, or G2 phase, although the G1 arrest is seen only in cells expressing the wild-type p53 tumor suppressor protein. Caffeine has been shown to abrogate the S and G2 arrest in p53-defective cells and to enhance cytotoxicity, but at concentrations too toxic to administer to humans. We have reported that 7-hydroxystaurosporine (UCN-01) also overcomes S and G2 phase arrest and enhances the cytotoxicity of cisplatin. We show here that UCN-01 at non-cytotoxic concentrations abrogated S and G2 arrest induced by cisplatin in two p53-defective human breast cancer cell lines. UCN-01 pushed the cells through S phase and mitosis, with subsequent apoptosis. Inhibition of mitosis with nocodazole reduced the apoptosis induced by UCN-01 plus cisplatin. Seven staurosporine analogs were compared for their ability to abrogate cell cycle arrest. Staurosporine was as effective as UCN-01 at abrogating S and G2 arrest, but the concentrations required were cytotoxic. K252a abrogated S phase arrest but failed to abrogate G2 arrest because alone it induced G2 arrest. Hence, K252a did not enhance cisplatin-induced cytotoxicity because it failed to push the cells through a lethal mitosis. None of the other analogs influenced cell cycle progression at the concentrations tested. Accordingly, UCN-01 was the only analog that overcame cell cycle arrest and enhanced the cytotoxicity of cisplatin while exhibiting no cytotoxicity of its own. Hence, UCN-01 remains the most promising candidate for testing clinically in combination with cisplatin.

Biocompatibility and degradation of collagen bone anchors in a rabbit model.

Bone anchors are used to fasten tendons and ligaments to bone during reconstructive surgery. Although metal anchors are often used, an anchor that could resorb and permit normal bone regeneration would be advantageous. The objective of the study was to evaluate the biocompatibility and degradation of bone anchors that consist of collagen-based bodies, ceramic washers, and polyester sutures. Eighteen rabbits underwent bilateral implantations in the distal femoral condyles. Nine animals received glutaraldehyde-crosslinked fibrillar collagen bone anchors (FC) and nine received glutaraldehyde-crosslinked fibrillar collagen bone anchors containing tricalcium phosphate (FC-TCP). Three animals per group were sacrificed at postimplantation weeks 1, 6, and 12. One femur from each rabbit was evaluated histologically, and the contralateral side underwent biomechanical pull-out testing. Histological evaluation of the implant site indicated that the FC and FC-TCP bone anchors were both biocompatible. The FC-TCP formulation degraded earlier than the FC formulation, and FC-TCP showed significant degradation at 6 weeks; the FC and FC-TCP formulations both showed similar amounts of degradation at 12 weeks. The degrading anchor bodies appeared to be osteoconductive as evidenced by new bone ingrowth into the degrading collagen matrices without a fibrous interface. These results suggest that collagen-based bone anchors have potential as bioresorbable orthopedic implants.

Ultrasonic enhancement of antibiotic action on Escherichia coli biofilms: an in vivo model.

Biofilm infections are a common complication of prosthetic devices in humans. Previous in vitro research has determined that low-frequency ultrasound combined with aminoglycoside antibiotics is an effective method of killing biofilms. We report the development of an in vivo model to determine if ultrasound enhances antibiotic action. Two 24-h-old Escherichia coli (ATCC 10798) biofilms grown on polyethylene disks were implanted subcutaneously on the backs of New Zealand White female rabbits, one on each side of the spine. Low-frequency (28.48-kHz) and low-power-density (100- and 300-mW/cm2) continuous ultrasound treatment was applied for 24 h with and without systemic administration of gentamicin. The disks were then removed, and the number of viable bacteria on each disk was determined. At the low ultrasonic power used in this study, exposure to ultrasound only (no gentamicin) caused no significant difference in bacterial viability. In the presence of antibiotic, there was a significant reduction due to 300-mW/cm2 ultrasound (P = 0.0485) but no significant reduction due to 100-mW/cm2 ultrasound. Tissue damage to the skin was noted at the 300-mW/cm2 treatment level. Further development of this technique has promise in treatment of clinical implant infections.

Hydrocephalus in children: neurosurgical and neuroimaging concerns.

The neuroimaging of hydrocephalus from the perspective of the pediatric neurosurgeon is discussed. Processes with new developments in therapy and imaging are described, including congenital causes of hydrocephalus, unilateral hydrocephalus, trapped fourth ventricle, and benign external hydrocephalus.

Imaging the central nervous system effects of radiation and chemotherapy of pediatric tumors.

New developments in radiotherapy and chemotherapy have resulted in significant improvements in survival from childhood tumors. Stereotactic radiosurgery and other conformed field radiotherapy treatments allow precise localization of tumors. Through small beam sizes, these new radiation techniques deliver steep dose gradients at the field edges permitting the prescribed dose to be given to the tumor while avoiding vital structures only millimeters away. Newer chemotherapy regimens allow radiotherapy to be postponed until the child's brain can better tolerate radiation. The MR imaging and CT scans appearance of treated childhood brain tumors and the new developments in radiation and chemotherapy are discussed.

Access to health care: Louisiana minor consent statutes.

The Louisiana minor's consent statutes enable minors to consent for medical treatment, emergency treatment, treatment of sexually-transmitted diseases, and treatment of substance abuse. The legislative intent for permitting minors to consent to treatment without the express consent of a parent or guardian was to provide minors access to high-quality health care services in order to encourage the betterment of the health and welfare of the citizens of our state. A minor cannot consent for an abortion or sterilization. The statutes do not allow a minor to refuse treatment consented to by his parent or guardian. However, needed medical treatment can be provided to a consenting minor over the objections of a parent or guardian. Where a minor can consent, confidentiality from parent's or guardian's knowledge is permitted but not assured; confidentiality is granted at the discretion of the physician or medical staff.

Biliary secretion of alpha-tocopherol and the role of the mdr2 P-glycoprotein in rats and mice.

The mechanism by which alpha-tocopherol (alpha-T) is secreted into the bile is not known; however, we have previously demonstrated that treatment with piperonyl butoxide (PIP, 1 g/kg) results in increased biliary output of both alpha-T and phosphatidylcholine within 3 h of ip injection in rats and that the biliary output of both substances was prevented by chemicals that disrupt microtubules (Toxicol. Appl. Pharmacol. 139, 411-417 (1996)). The P-glycoprotein (Pgp) encoded by the mdr2 gene has been shown to transport phosphatidylcholine into the bile; therefore, in the current study, we utilized the Pgp inhibitor verapamil to investigate the possible involvement of Pgps in the biliary secretion of alpha-T. When rats were iv injected with verapamil (4 mg/kg) 10 min prior to PIP treatment, verapamil prevented the PIP-induced increases in biliary alpha-T and phosphatidylcholine output and resulted in biliary alpha-T outputs that were significantly less than controls. Also, we determined that the biliary alpha-T levels in mdr2 knockout mice were 25% of those in wildtype mice; furthermore, mdr2 liver, lung, and kidney levels of alpha-T and glutathione differed from those of wildtype. To investigate the fate of biliary alpha-T, we injected 14C-labeled alpha-T into the bile duct cannulae of rats and determined that approximately 60% of the radioactivity was reabsorbed within 1 h. Our results indicate that alpha-T undergoes enterohepatic circulation and that the biliary secretion of alpha-T, basally and following chemical treatment, is dependent on the presence of a functioning mdr2 Pgp in rats and mice.

Midwest experience with moyamoya disease.

A review of the cases of Moyamoya disease at two large Mid-Western United States Universities was undertaken for the purpose of assessing the epidemiology of Moyamoya disease. A total of 51 cases of Moyamoya disease were identified, with 12 cases classified as akin Moyamoya disease, nine cases of probable Moyamoya disease, and 30 cases of classic or definite Moyamoya disease. The conditions associated with akin Moyamoya were sickle cell disease, Down's syndrome, trauma, radiation, and neurofibromatosis. The mean age of presentation for probable and classic Moyamoya disease was 22 years. The sex predilection was approximately equal, with a slight female predominance. The racial background was identified in 22 of the definite cases, and included six patients with oriental inheritance, three with American Indian inheritance, one black, and the remainder Caucasian. Of some interest, there were five Caucasian patients with names identifiable as Eastern European in origin. The mean age of presentation of the definite Moyamoya disease was 14 years, the probable Moyamoya disease was 4 years, and the akin Moyamoya disease was 5 years.