Effects of a new analog of thyrotropin-releasing hormone, N alpha-[(S)-4-oxo-2-azetidinyl) carbonyl]-L-histidyl-L-prolinamide dehydrate (YM-14673) on spinal reflex potentials and flexor reflexes in spinalized rats

Experiments were performed on spinalized rats, transected at the Cl level. The intravenous administration of TRH and its analog YM-14673 (N alpha-[(S)-4-oxo-2-azetidinyl) carbonyl]-L-histidyl-L-prolinamide dehydrate) produced marked increases in the amplitude of mono- and polysynaptic reflex potentials and those of the withdrawal flexor reflexes. The effects of YM-14673 were stronger and longer-lasting than those of TRH. The stimulant action of TRH and YM-14673 on the flexor reflexes was not antagonized by prazosin, chlorpromazine, haloperidol or cyproheptadine, suggesting no involvement of the release of catecholamines or serotonin in the stimulant effects of TRH and its analog. Therefore, YM-14673 may be beneficial for the treatment of several spinal motor neuron diseases.     

Severe hypoglycaemia in a person with insulin autoimmune syndrome accompanied by insulin receptor anomaly type B.

AIMS: A rare case of the insulin autoimmune syndrome (IAS) accompanied by insulin receptor anomaly is reported. METHODS: Antibodies to insulin and insulin receptor were determined in the patient with severe hypoglycaemia before and after the treatment with prednisolone. RESULTS: Titers of antibody to insulin and insulin receptors were 73.0% and 41.5%, respectively. Drug-induced lymphocyte stimulation tests were all negative for the suspicious drugs. Her HLA-DR was DRB1*0403/04051. Following steroid therapy, the formation of antibodies was suppressed and alleviated her symptoms. Scatchard analysis yielded findings specific to polyclonal antibodies. CONCLUSIONS: The changes in autoantibodies resulted in alleviation of the hypoglycemic symptoms as a result of steroid therapy.     

Human Tumor–infiltrating Lymphocytes Transfected with Tumor Necrosis Factor Gene Could Augment Cytotoxicity to Autologous Tumor Cells

Human tumor–infiltrating lymphocytes (TILs) derived from pleural or ascitic fluid were incubated with recombinant interleukin 2 and transfected with human tumor necrosis factor (TNF) a gene by the lipofection procedure. The resulting TILs secreted significant amounts of TNF in the culture supernatant and exhibited cytotoxicity against established cell lines, such as K562 and Daudi, and autologous tumor cells. The TNF gene–transfected TILs exhibited an augmented killing of autologous tumor cells.     

The changes in EEG, evoked potentials and neurological recovery after global brain ischemia in dogs

Electroencephalography (EEG), evoked potentials and neurological recovery score were compared between 10 min and 15 min transient global brain ischemia in 18 dogs. The transient global brain ischemia was induced by occluding aorta, superior and inferior caval veins. The grade of EEG (1: normal approximately 5: flat) 2 hrs after ischemia was significantly lower with the 10 min ischemic group (n = 9) than with the 15 min group (n = 9) (3.7 +/- 0.5 vs 4.1 +/- 0.3, P less than 0.05). The rate of reappearance in evoked potential waves 2 hrs after ischemia was higher with the 10 min ischemic group than with the 15 min group (auditory brainstem response 5 wave: 100% vs 33%, middle latency response Pa wave: 80% vs 0%, somatosensory evoked potential N2 wave: 83% vs 78%, N3 wave: 67% vs 33%). The neurological recovery score (0: death approximately 100: normal) 7 days after ischemia was significantly higher with the 10 min group than with the 15 min group (58 +/- 34 vs 27 +/- 23, P less than 0.05). In both groups, there was a significant correlation (r = +0.85, P less than 0.01) between the total score of EEG and evoked potential waves (0: no wave appeared approximately 6: all waves appeared) 2 hours after ischemia and the neurological recovery score 7 days after ischemia. These results suggest that the neurological recovery after transient global brain ischemia would be estimated by EEG and evoked potential waves.