Connections between radial and ulnar nerve at high humeral level in cadavers: incidence, topography, and literature review.

PURPOSE: Although communications between branches and cords of the brachial plexus have been extensively published, there is a scarcity of reports concerning radial and ulnar nerve (RN-UN) communication in the arm. The current study aims to demonstrate the incidence, topography, and length of communicating branches between RN and UN. Any additional coexisted variations were also recorded. MATERIALS AND METHODS: Two hundred and sixty-six upper limbs collected from one hundred and thirty-three (81 males and 52 females) Greek cadavers were dissected. RESULTS: Three out of one hundred and thirty-three cadavers, accounting for an incidence of up to 2.3%, were found to have an atypical communicating branch originating at a high humeral level from RN towards UN. In two cadavers, communicating branches were detected on the left side and in one cadaver bilaterally. CONCLUSIONS: The study of atypical communications between RN and UN attracts great attention for its clinical importance, mainly in cases of peripheral neuropathies with diagnostic dilemma or upper limb nerve injury producing an otherwise unexpected symptomatology due to the aberrant nerve supply. Familiarity with these variations is crucial in avoiding misdiagnosis and preserving valuable communicating branches, thus achieving an uneventful outcome in cases of upper limb nerve injury repair.

Effect of ceftriaxone on the outcome of murine pyelonephritis caused by extended-spectrum-ß-lactamase-producing Escherichia coli.

Urinary tract infections (UTIs) due to extended-spectrum-ß-lactamase (ESBL)-producing Enterobacteriaceae in children are becoming more frequent, and they are commonly treated initially with a second- or third-generation cephalosporin. We developed a murine model of ascending UTI caused by ESBL-producing Escherichia coli. Using this model, we investigated the renal bacterial burden, interleukin-6 (IL-6) expression, and histopathological alterations caused by ESBL- and non-ESBL-producing bacteria after 1, 2, or 6 days with or without ceftriaxone therapy. The renal bacterial burden, IL-6 concentration, and histological inflammatory lesions were not significantly different between mice infected with ESBL- and non-ESBL-producing bacteria without treatment at any of the time points examined. Following ceftriaxone administration, the bacterial burden was eliminated in the kidneys of mice infected with ESBL- and non-ESBL-producing bacteria on the 6th postinfection day. The histological analysis demonstrated that among mice treated with ceftriaxone, those infected with ESBL-producing bacteria had more profound renal alterations than those infected with non-ESBL-producing bacteria on the 6th day (P < 0.001). In comparison, microbiological outcomes did not differ significantly between mice infected with ESBL- and non-ESBL-producing bacteria at any of the time points examined. The effectiveness of ceftriaxone in mice with UTIs due to ESBL-producing E. coli may have therapeutic implications; it is, however, hampered by limited activity on the histopathological lesions, a finding that needs further investigation.

Acute inflammation alters adult hippocampal neurogenesis in a multiple sclerosis mouse model.

Neural precursor cells (NPCs) located in the subgranular zone (SGZ) of the dentate gyrus (DG) give rise to thousands of new cells every day, mainly hippocampal neurons, which are integrated into existing neuronal circuits. Aging and chronic degenerative disorders have been shown to impair hippocampal neurogenesis, but the consequence of inflammation is somewhat controversial. The present study demonstrates that the inflammatory environment prevailing in the brain of experimental autoimmune encephalomyelitis (EAE) mice enhances the proliferation of NPCs in SGZ of the dorsal DG and alters the proportion between radial glial cells and newborn neuroblasts. The injection protocol of the cell cycle marker bromodeoxyuridine and the immunohistochemical techniques that were employed revealed that the proliferation of NPCs is increased approximately twofold in the SGZ of the dorsal DG of EAE mice, at the acute phase of the disease. However, although EAE animals exhibited significant higher percentage of newborn radial-glia-like NPCs, the mean percentage of newborn neuroblasts rather was decreased, indicating that the robust NPCs proliferation is not followed by a proportional production of newborn neurons. Significant positive correlations were detected between the number of proliferating cells in the SGZ and the clinical score or degree of brain inflammation of diseased animals. Finally, enhanced neuroproliferation in the acute phase of EAE was not found to trigger compensatory apoptotic mechanisms. The possible causes of altered neurogenesis observed in this study emphasize the need to understand more precisely the mechanisms regulating adult neurogenesis under both normal and pathological conditions.

Marked hypereosinophilia in a toddler: a case report.

BACKGROUND: Human toxocariasis is primarily a soil-transmitted zoonosis, so children with geophagia are at an increased risk of toxocariasis, especially those living in homes with puppies that have not been dewormed. CASE REPORT: A 17-months-old female presented to our department with fever, abdominal distention and marked eosinophilia. Iron deficiency anemia, marked leukocytosis (79,000 cells/mm(3)) accompanied by marked eosinophilia (55,000 cells/mm(3)), and hyper-gammaglobulinemia were noted. On the basis of the strong serological positivity for toxocariasis, marked eosinophilia, and low-density lesions in the liver at computed tomography, a diagnosis of visceral larva migrans syndrome was made. CONCLUSION: Visceral larva migrans is usually suspected in a young child with history of geophagia, pets exposure, hepatomegaly, whose complete blood count reveals leukocytosis and marked eosinophilia.

Natural and lesion-induced apoptosis in the dorsal lateral geniculate nucleus during development.

We investigated natural and lesion-induced apoptosis in the developing rat dorsal lateral geniculate nucleus (dLGN). These lesions involved: i) monocular enucleation, and ii) unilateral ablation of the visual cortex at different postnatal ages before eye opening. We identified dying cells as apoptotic with light and electron microscopy, using terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling (TUNEL), and immunohistochemistry for active caspase-3. In the dLGN of normal animals, TUNEL+cells were detected during the first postnatal week, with a peak at postnatal day (P) 1. Following enucleation at birth or at P7, the frequency of apoptotic cells in the contralateral dLGN increased significantly at postlesion day (PLD) 1 and returned to normal values by PLD7. In contrast to early lesions, enucleation at P14 did not induce significant changes in apoptosis in the dLGN. Cortical lesions performed at P0, P7 or at P14 induced the death of the overwhelming majority of cells in the ipsilateral dLGN, which led to a severe reduction in size of the nucleus by PLD7 and its complete elimination by adulthood. Double labeling with TUNEL and immunofluorescence for neuronal nuclear protein (NeuN) showed that in both normal and lesioned animals, apoptotic cells were mainly neurons. We suggest that: i) apoptosis in the dLGN occurs during the precritical period of neuronal maturation; ii) developing neurons in the dLGN are more dependent on the integrity of their connections with the visual cortex than with the retina for survival; and iii) lesion-induced apoptosis in the dLGN during development depends on the type and extent of the connectivity affected.

Lambert-Eaton myasthenic syndrome. Clinical and electrophysiological findings in seven cases.

We report the clinical and electrophysiological findings in seven patients with Lambert-Eaton myasthenic syndrome (LEMS). All patients were males aged 40-73 years old. Six presented proximal muscle weakness and one both proximal and distal. The tendon reflexes were absent in four patients, depressed in two and normal in one patient. Three patients presented ophthalmic and four autonomic symptoms. The syndrome was diagnosed 3-12 months after the onset of symptoms in six patients and 4 years later in one. Acetylcholine receptor antibodies were negative in all patients. Voltage-gated calcium channel antibodies (VGCC) were measured in five patients and were positive in four. All patients had low compound muscle action potential (CMAP) at rest, a decrement in CMAP amplitude of 20-47% at 3 Hz repetitive nerve stimulation, and an increment of 200-700% at 40 Hz. In three patients the syndrome was associated with histologically verified small-cell lung cancer (SCLC). In the younger patient (40 years old), a lymph node biopsy performed nine years before the diagnosis of LEMS, had shown an atypical microcellular cancer of undetermined origin, which was treated with chemotherapy. LEMS 9 years after the diagnosis of cancer has not been described previously. The fifth patient had a two years history of bladder cancer (grade II). Three years after the diagnosis of LEMS he presented chronic lymphogenic leukemia. No malignancy was found in the remaining 2 patients.

Myocardial trophic effects of blood pressure in children with insulin-dependent diabetes mellitus.

To evaluate the effect of blood pressure (BP) on the left ventricular mass index (LVMI), 66 children with IDDM 13 +/- 3 years of age were studied and compared with 58 healthy age-matched siblings. The 24 h BP recordings disclosed that children with diabetes had higher DBP (68 vs. 65 mm Hg, P = 0.002), especially at night (60 vs. 55 mm Hg, P = 0.00007), with a minimisation of the normal nocturnal hypotension (-9.9 vs. -12.4 mm Hg, P = 0.04). Their LVMI was higher (79 vs. 71 g/m2, P = 0.02); it was independent of BP values and variability (P = NS), but it was positively correlated with heart rate (r = -0.46, P = 0.0005). In the control group, LVMI was significantly correlated with the mean SBP (r = 0.46, P = 0.0005); with its variability (r = 0.32, P = 0.02) and, to a lower extent, with heart rate (r = -0.29, P = 0.03). It is concluded that in children with diabetes mellitus the participation of BP in myocardial hypertrophy is not so obvious, although the BP load is increased. The increase of the LVMI occurs early in life and before the onset of hypertension.