Methanogens in biogas production from renewable resources--a novel molecular population analysis approach.

The population structure of thermo- and mesophilic biogas reactors digesting maize silage as the sole substrate was investigated employing a novel, highly degenerated PCR-primer pair targeting mcrA/mrtA coding for the key enzyme of methanogens. No sequence affiliating with Methanococcales, Methanopyrales, ANME-, rice or fen soil clusters was detected. Direct MeA PCR-cloning results indicated that Methanobacteriales were the most important methanogens in the thermophilic reactors. 57% and 80% of the analysed sequences affiliated with this order, 14% and 20% with Methanosarcinaceae and 0% and 29% with Methanomicrobiales. Methanomicrobiales dominated in the mesophilic reactors at the given conditions, 69% and 84% of the sequences recovered from direct MeA primed cloning affiliated with this order, 31% and 0% with Methanosarcinaceae and 0% and 16% with Methanobacteriales. No sequence affiliating with Methanosaetaceae was found. MeA primed PCR-single-strand conformation polymorphism indicated that population fluctuations occurred. According to sequence analysis of excised bands, Methanosarcinaceae dominated and Methanobacteriales were significantly represented in the thermophilic fermenter. Only 1 Methanosaetaceae sequence was found. Hydrogenotrophs appear to have a much higher and obligate acetoclastic methanogens a much lower importance than previously thought in biogas production from renewable resources.

Personalized nutrition communication through ICT application: how to overcome the gap between potential effectiveness and reality.

The potential effectiveness of personalized nutrition communication through the Internet is promising in terms of addressing personal relevance, flexibility, interactive options and amount of people that can be reached. However, little research on the contribution to behaviour change has been done. The MyFood program at Wageningen University aims at providing insight into strategies to implement personalized nutrition communication through interactive tools. In this article we present the framework for research on social acceptance of personalized nutrition communication through interactive computer technology as part of the MyFood program.

Peripheral neuropathy in the first 2 years of life: diagnostic evaluation including molecular genetics.

Inherited polyneuropathies present in the first 2 years of life are discussed with emphasis on clinical, pathologic, and molecular data. Early-onset polyneuropathies are relatively rare, sometimes life-threatening conditions that demand early recognition by clinical and pathologic examination. Histologic and ultrastructural overlaps among the various conditions are sometimes resolved by molecular genetic analysis. The growth in disease identification by genetic localization allows a more comprehensive understanding of the clinical and morphologic heterogeneity involving rearrangements of the same gene. Molecular mechanisms explaining the acquisition of such gene rearrangements are beginning to be unraveled. Peripheral myelin disorders may be confused with primary axonal disorders, and electrophysiologic examination often helps to distinguish between these two. Furthermore, early-onset central nervous system disorders may present as peripheral polyneuropathies and confound the clinical picture. A tentative diagnosis can often be offered by pathologic examination and confirmed by biochemical enzyme analysis later. The differential clinical diagnostic considerations of early-onset polyneuropathies are offered, to help clinicians sort out these diseases in the most efficient manner.

Predicting outcome in hypoxic-ischemic brain injury.

Predicting the neurologic outcome of children after a hypoxic-ischemic event continues to be a challenge for intensivists and pediatric neurologists. Nevertheless, with accurate history taking, serial neurologic examination, and some ancillary studies, the clinician can predict accurately whether a child will die or have profound neurologic damage. Aggressive resuscitation should be offered to all children when found in CPA. A simple ingestion might have led to this clinical scenario, and complete neurologic recovery may be possible if effective resuscitation is implemented. In cases of drowning, several factors, if present, are consistent with profound neurologic sequelae or death. These include prolonged submersions with asystole, delayed onset of CPR, no spontaneous respirations on arrival to the emergency department, and low initial pH value. The options of withdrawal of life support or a DNR status should be offered to families of children who have survived a devastating hypoxic-ischemic event but who are in a PVS. If brain-death criteria have been fulfilled, the patient must then be disconnected from life support after organ donation has been discussed with the family.

Nerve and muscle damage after experimental thrombosis of large artery. Electrophysiology and morphology.

The effect of the terminal aorta thrombosis on the spinal cord and hind limb nerves and muscles morphology, and the sciatic-tibial motor nerve conduction was studied in cats. The effect of the iliac and femoral artery thrombosis on nerve morphology and conduction was also examined. Aortic thrombosis usually caused severe nerve and muscle lesions while spinal cord was spared. Nerve and muscle damage was strikingly more extensive and severe after aortic thrombosis than ligation. Nerve damage was also seen after the iliac or femoral artery thrombosis but not after ligation of these arteries. The tibial and peroneal nerve segments at the calf level were most vulnerable to ischemic damage. The nerve conduction studies (NCS) localized nerve lesions and indicated severity of the morphologic changes. The nerve conduction changes after arterial thrombosis reached a nadir at more variable time than in other experimental models of peripheral nerve ischemia. The markedly delayed development of maximal nerve dysfunction in some cases, if confirmed in humans, may present a rationale for aggressive medical or surgical intervention even several hours after acute arterial thrombosis.

Acute childhood ataxia: 10-year experience.

Forty cases of acute childhood ataxia were retrospectively assessed for main etiologies and for factors that can be used in planning the most effective and cost-efficient management. The most common discharge diagnoses were acute cerebellar ataxia, ingestion, and Guillain-Barré syndrome, encompassing 80% of all cases. The remaining 20% included various isolated causes. Acute cerebellar ataxia was primarily seen in children less than 6 years of age who had preceding viral syndromes or varicella. Ingestions were also most frequent in children less than 6 years of age, but a second peak occurred in adolescents. History was suggestive of drug ingestion in 61.5% of cases, and in addition to ataxia, lethargy was an associated symptom. The drug screen was the most informative laboratory test, with 17 of 35 being positive. Lumbar punctures were positive in seven of 25, with pleocytosis in six and elevated protein in two. Of 26 computed tomographic scans and magnetic resonance imaging scans performed, only two were positive, one for cerebellar infarct and one for cerebral edema. Acute ataxia in childhood has multiple etiologies, but it is usually due to a benign, self-limited process. A thorough history, physical examination, and drug screen should be performed before other costly and invasive tests and before admission to the hospital. This approach may eliminate the need for hospitalization of some patients with postinfectious acute cerebellar ataxia and ingestion. Neuroimaging studies should be used judiciously in the evaluation of acute ataxia, considering their low yield.

Expanding spectrum of cocaine induced central nervous system malformations.

Two patients born of mothers who abused cocaine during pregnancy were found to have various brain malformations, some of which were not previously reported. Children who were exposed to cocaine or polysubstances prenatally and who present with a neurologic deficit require neuroimaging studies to detect abnormalities.

Perineurial hemorrhage in ischemic nerve after anticoagulation.

We report a 29-year-old woman who developed severe left leg ischemia after aortic dissection and left common iliac artery occlusion. Light microscopic studies revealed severe nerve and muscle ischemic changes at the calf level. Nerves also showed extensive perineurial hemorrhage, most likely secondary to heparin administration. Perineurial hemorrhage should be considered as one of the possible complications of anticoagulant therapy.

New onset childhood seizures. Emergency department experience.

Fifty-six cases of new onset seizures evaluated in a pediatric emergency department (ED) during a one-year period were assessed retrospectively for efficiency of diagnosis and workup. The majority of patients (69%) were less than two years of age. Based on etiology, the most common seizure type was febrile (71%) followed by idiopathic (21%) and symptomatic (7%). Significant laboratory abnormalities were found in four (7%) patients; two had hyponatremia, one carbamazepine overdose and one bacterial meningitis. Screening laboratory tests including brain CT scans were generally not helpful. A thorough history including specific details regarding the seizure and a complete physical examination should eliminate the need for major laboratory and radiologic workup in the emergency department.

Progression of regeneration after nerve infarction.

We performed morphologic studies on the progression of regeneration in cat hind limb nerves after acute ischemic injury. None of the damaged nerve trunks showed a major increase in endoneurial connective tissue. Despite this fact, regeneration of nerve with transfascicular infarct was far from complete even 16 months after injury as manifested by a striking increase in the small myelinated fibers (MF) number and decrease in large MF number. Restoration of infarcted nerves was less complete than that previously reported after a nerve crush. Changes in the necrotic nerve segment and difficulty in making target contact with muscle and other tissues damaged by ischemia may be limiting factors in the regeneration of infarcted nerves.

Eosinophilia-myalgia syndrome with myoclonic jerks.

A patient while using L-tryptophan had typical features of the eosinophilia-myalgia syndrome and in addition myoclonic jerks which are unusual for this syndrome.

Muscle vulnerability to ischemic damage is decreased in experimental diabetes mellitus.

The severity of necrotic muscle and nerve lesions in the ischemic hind limbs of diabetic and nondiabetic rats was compared. Chronic limb ischemia was induced by repetitive, daily for up to 8 weeks, intraperitoneal injections of serotonin in rats with ligated right femoral artery. Light microscopic examination and lesion severity grading was performed on sections taken from several right hind limb muscles and the right tibial nerve. Overall, muscle was less damaged in diabetic than in nondiabetic rats. However, muscle was damaged more than nerve in all but diabetic rats with severe chronic ischemia. Muscle vulnerability to ischemic damage is decreased in diabetes, presumably due to abundance of glucose and other energy substrates which can be utilized during ischemia.

Distribution of nerve lesions in serotonin-induced acute ischemic neuropathy.

We have developed a new model of an acute ischemic nerve injury in rat produced by the combined effects of right femoral artery ligation and intraperitoneal injection of serotonin. Light microscopic studies were performed on the right sciatic, tibial, plantar and sural nerves dissected from rats 7 days to 6 months after serotonin injection. Ischemic lesions occurred mostly in the middle tibial nerve and involved either a part or the whole transverse nerve section. Partial tibial nerve lesions appeared mainly as small subperineurial or large wedge-shaped areas of fiber loss or regeneration. No well-delineated central fascicular lesions were seen. Sural nerves were less damaged than tibial nerves. The predominantly subperineurial fascicular distribution of ischemic lesions seen in the present model differs from the central fascicular distribution found in previous experimental studies on nerve ischemia. The different distribution of lesions is probably related to the small fascicular size and local microvascular architecture of the affected nerve segment, as well as to the method of producing ischemia.

Peripheral nerve ischemia: Part 2. Accumulation of organelles.

Following simultaneous ligation of the aorta and femoral artery in the cat, organelles accumulated in distal portions of the sciatic nerve and in lower portions of the tibial and peroneal nerves. The accumulations were located in the proximal and distal ends of the nerve infarction and delineated the borders of the necrotic area. Topographical analysis of the necrosis and organelle accumulations following ligation of these main arteries showed the larger nerve fascicles to be more sensitive to ischemia than the smaller ones. The center of a nerve fascicle was more sensitive than the periphery. The organelles accumulated in ischemic nerves during the first hours after arterial ligation, presumably as a result of lack of energy for fast axoplasmic transport. Later accumulations reflected mechanical block of axoplasmic transport due to focal necrosis of the nerve. The content of organelle accumulations was similar to that found in lesions resulting from transection except for the presence of 60 to 70 A filaments at the distal end of the infarction.