Hallux rigidus deformity: radiologic assessment

Hallux rigidus (osteoarthritis leading to reduced motion) is one of the most common afflictions of the first metatarsophalangeal joint. The diagnosis is based on the presence of pain, specific physical findings, and certain radiologic features. In this essay, we illustrate the grades of radiologic changes, which are an integral part of the surgeon's preoperative evaluation, and show examples of the postoperative radiologic appearance.     

The tubulointerstitial component of chronic glomerulonephritis: its clinico-functional diagnosis

Tubulointerstitial alterations associated with chronic glomerulonephritis (CGN) are definitely dependent on the clinical type of CGN and are accompanied by a decrease of homeostatic functions (the rate of glomerular filtration, osmotic concentration and dilution of urine, hydruresis, the magnitude of CH2O, excretion of ammonium and hydrogen ions, the ratio of ammonium excretion to hydrogen ion excretion). Maximal osmotic concentration and ammonium excretion show an especially considerable decrease. The clinical type permitting one to diagnose rather than to reject the presence of alterations and the status of certain tubular functions, osmotic concentration in particular and, to a less degree, ammonium excretion, permitting to reject the presence of the tubulointerstitial component (TIC) are of known but restricted importance for TIC recognition. The TIC can be diagnosed more adequately in exploring definite pairs of renal functions, particularly osmotic concentration of urine and ammonium excretion and maximal hydruresis and excretion of hydrogen ions. This approach is both helpful in confirming and rejecting the presence of the TIC. Of special value is the combined assessment of the clinical type and maximal osmotic urine concentration data.     

Regionally selective effects of NMDA receptor antagonists against ischemic brain damage in the gerbil

This study compared the ability of three N-methyl-D-aspartate (NMDA) receptor antagonists to prevent neuronal degeneration in an animal model of global cerebral ischemia. The model employed is characterized by damage to the striatum, hippocampus, and neocortex. Antagonists were administered to gerbils either before or after a 5-min bilateral carotid occlusion. The intraischemic rectal temperature was either maintained at 36-37 degrees C or allowed to fall passively to 28-32 degrees C. Antagonists and doses tested were 1 and 10 mg/kg of MK-801 (pre- or postischemia), 30 mg/kg of CGS 19755 preischemia, four 25 mg/kg doses of CGS 19755 administered between 0.5 and 6.5 h postischemia, and 40 mg/kg of MDL 27,266 (pre- or postischemia). All three NMDA receptor antagonists exhibited some degree of neuroprotective activity when the carotid occlusion was performed under normothermic conditions. Most of the treatments with antagonist markedly reduced striatal damage. CA1 hippocampal and neocortical pyramidal cells were spared by only three of the treatments, however, and the extent of neuroprotection varied widely from case to case. Toxic doses of antagonist were required to protect CA1 pyramidal cells from ischemic damage. Ischemic damage to hippocampal areas CA2-CA3a and CA4 appeared to be resistant to all of these treatments. Most CA1 pyramidal cells that were protected from degeneration by an NMDA receptor antagonist were histologically abnormal. The neuroprotective effects of MK-801 and intraischemic hypothermia appeared to be additive. MK-801 (10 mg/kg) consistently reduced the postischemic brain temperature, but only the magnitude of hypothermia produced soon after reperfusion correlated with its neuroprotective action. These results suggest that NMDA receptor antagonists are relatively poor neuroprotective agents against a moderately severe ischemic insult.     

Neuropeptide levels in the basal ganglia of aged common marmosets following prolonged treatment with MPTP

Summary Aged common marmosets were treated with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP; 0.5–2.0 mg/kg/week i.p.) for 16 or 24 weeks, observed for a total of 30 weeks and then killed for measurement of biochemical pramaters in basal ganglia. The MPTP treatment induced a marked depletion in dopamine, 3,4-dihydroxyphenylacetic acid and homovanillic acid levels in the caudate nucleus and putamen. In contrast, the concentrations of five neuropeptides: [Met⁵]-enkephalin, [Leu⁵]-enkephalin, cholecystokinin, substance P and neurotensin as measured by a combined HPLC/RIA method, remained unaltered in all basal ganglia regions examined. Enkephalin precursor levels, as reflected by cryptic [Met⁵]-enkephalin content, were increased in the putamen, but not in the caudate nucleus, as a consequence of MPTP administration. Cryptic [Leu⁵]-enkephalin content remained unchanged in the striatum of MPTP treated marmosets. Overall, these results suggest an increase in striatal [Met⁵]-enkephalin release following chronic MPTP treatment of aged marmosets. However, the chronic treatment of aged marmosets with MPTP does not reproduce the neuropeptide alterations characteristic of Parkinson's disease.