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Small, round photocoagulator lesions of 3-6 degrees (0.6-1.2 mm) diameter were placed nasally on the retina of adult cats. Histological controls proved the complete destruction of all retinal layers within the lesions. Changes in lesion size by shrinkage of the retinal scar did not exceed 0.1 mm or 0.5 degrees. At different times after photocoagulation, single cells were recorded in layers A and A1 of the contralateral lateral geniculate nucleus (LGN) with tungsten microelectrodes. Acute lesions of this size completely deafferented single LGN cells in layer A whose receptive field (RF) area was within the lesion. Thirty days and more after coagulation, light-excitable cells were detected in the originally deafferented LGN region, with RFs in the immediate surround of the retinal lesion. The spontaneous activity and light excitability of these neurons were altered. The representation of 3-4 degrees retinal lesions at 20 degrees horizontal eccentricity was found to be completely filled in by excitation in the LGN. Excitation had spread from the unsevered parts of the retina into the region of deafferentation. Single cells with signs of multiple activation from more than one border region of the retinal lesion were occasionally detected.

A malignant lymphoma of the small bowel developed in a 55-yr-old woman who had intestinal malabsorption for 20 yr, late-onset hypo-gamma-globulinemia, and nodular lymphoid hyperplasia. The tumor arose in the first jejunal loop and appeared to be of B-immunoblastic type (diffuse large noncleaved cells). This case indicates that nodular lymphoid hyperplasia in the context of immunodeficiency may be a condition leading to lymphoid malignancy.

We present a boy five years old who after suffering recurrent pneumonia was transferred to own center for study. A diagnosis of Intralobar Pulmonary Sequestration was made, before surgery, by non invasive method, digital intravenous angiographic subtraction (DIVAS) and surgical management by anomalous arterial ligation and lobectomy was performed.

High-intensity photocoagulator lesions placed nasally to the optic disc one eye destroyed all retinal layers and led to visual deafferentation of the lateral part of layer A in the contralateral lateral geniculate nucleus (LGN) of adult cats. The retino-geniculate topography was determined with vertical tungsten microelectrode penetrations through LGN layers A and A1 before and at different times after photocoagulation. Before the 20th day a border of light excitability was found in layer. A corresponding to the normal projection of the lesion onto the LGN. Deviations from the normal topographical organization were evident 30 days and later after photocoagulation. Cells were recorded within the deafferented part of layer A near to the border of deafferentiation which had receptive field (RF) centers displaced by more than two degrees of visual angle with respect to the normal retinotopy. During formation of the retinal scar no identifiable points on the retina were displaced in the same direction as the RF centers. The histological control of the retinal lesions proved that there was no potentially excitable tissue left to account for a spread of excitation into the lesion. Latency measurements after electrical stimulation of the optic tract and the visual cortex suggested a retinal input and a projection into the visual cortex for the LGN cells with displaced receptive field centers. RF center displacements up to five degrees at the border of the lesions indicated a lateral spread of excitation within the LGN up to 250 micron beyond normal.

27 patients with radiolucent biliary stones in normofunctioning gall bladder were treated with a combination of CDCA and UDCA (CDCA doses = 7.7 mg/kg/day; UDCA--6.5 mg/kg/day); only 23 continued in the study for at least one year. The reasons for leaving were in one case the necessity of a cholecystectomy and treatment interruption in 3 cases. The rate of complete dissolution was of 39%, being of 17% the partial dissolution rate. The only biochemical alteration was the increase of HDL cholesterol at 9 and 12 months of treatment (p less than 0.05 and p less than 0.01 respectively). Transient diarrhea was seen in 17% of the patients and it did not require treatment. The incidence of liver colic during the year before treatment was 26% and it decreased during the 1st year of treatment to 4%. The non-specific dyspepsia observed during the year before treatment was of 48%, and decreased to 17% during the first year of treatment. Only one patient developed calcification of the gallstone, 12 months after treatment.

Layers of the lateral geniculate nucleus (LGN) of mature cats were completely or partially deafferentated by precisely defined photocoagulation of the retina. Single neuron recordings were performed with microelectrodes from an experimentally modified layer and compared with neurons from a normally innervated layer in the same animal. The spontaneous activity of cells after monocular deafferentation was severely reduced in the beginning and increased subsequently without reaching normal values within ten weeks. At this time the pattern of excitation and inhibition after light stimulation of the nondominant unsevered eye had completely changed. Twenty-seven days and later after coagulation of a part of the nasal retina light-excitable cells with displaced receptive fields were found in the LGN in the border region of the partial visual deafferentation. This indicated a lesion-induced lateral expansion of excitation by up to 200 microns within the LGN. Small, round retinal lesions initially caused a complete visual deafferentation of a certain region in the LGN. After 30 days and later visual excitation from the normally innervated surrounding was observed in cells which were not light-excitable during the first days after coagulation. Thus, while the retinal lesion itself did not substantially change, its representation within the LGN was distinctly reduced. The results indicate lesion-induced reorganization in the subcortical visual system of the adult cat. This might enable the system to a certain degree of compensation after loss of visual inputs. The transferability of these results to human pathophysiology has to be critically considered.

Late spreading of excitation occurs in the lateral geniculate nucleus following partial retinal lesions. The extent of spreading remained the same when reducing the size of the lesions to one fifth. This is incompatible with the idea that the spreading could be caused by displacement of normal cells into the deafferented area as a consequence of transneuronal volume reduction.

The primary structure of thioredoxin f from spinach chloroplasts was determined by standard amino acid sequencing and furthermore by sequencing the corresponding nuclear genome region. The protein, with a calculated molecular mass of 12,564 Da and a molar absorption coefficient at 280 nm of 17,700 M-1 cm-1, consists of 113 residues and exhibits 24% residue identities with spinach chloroplast thioredoxin mb or Escherichia coli thioredoxin. A monospecific antibody elicited against thioredoxin f has been used to select recombinant phage from spinach cDNA libraries in lambda gt11. The inserts of positive clones were sequenced. They code for a polypeptide of 190 amino acids, composed of the thioredoxin f sequence (113 residues) and an upstream element (77 residues) which most probably constitutes the N-terminal transit peptide that directs the polypeptide into chloroplasts. In vitro transcription and translation of this construct generates a polypeptide of approximately 21 kDa, which is imported by isolated spinach chloroplasts and processed to the mature 12.5-kDa protein.

The clinical analytical and therapeutic results of a retrospective study of 11 cases of Wilson's disease carried out in "La Fe" Hospital in Valencia are presented. The disease had a neurological onset in 5 cases, an hepatic onset in 4 cases (3 acute hepatitis and 1 chronic hypertransaminemia), 2 cases started as an acute hemolytic anemia; one of the outbreaks occurred during a period of treatment interruption. Diagnosis showed some difficulty in one case since the disease was associated with positive hepatitis B markers, positive anti HIV antibodies and initially normal ceruloplasminemia values. The diagnostic difficulties derived from the interpretation of ceruloplasminemia, and blood and urine copper levels are pointed out as well as the difficulties encountered in our environment to determine intrahepatic copper levels and to perform a kinetic study with radioactive copper both of which are of vital importance to confirm doubtful cases. Two patients became pregnant in the course of the disease having normal pregnancies and deliveries, without any apparent abnormalities in the newborns. Treatment with D-Penicillamine was started in 9 cases, observing a low to moderate intolerance in 7 cases; there was one case of severe intolerance for which treatment had to be interrupted. The new therapeutical approaches based on the use of trientine (not available in our country) are discussed, together with the expectations of liver transplant in this disease.

A case of autoimmune hemolytic anemia associated with chronic ulcerative colitis in a 28-year-old woman is reported. Immunological studies showed a strongly positive direct Coombs test of IgG type and a non-specific pannagglutinin antibody. This immunological pattern remained for 10 months instead of the medical treatment with corticosteroids and azathioprine. A subtotal colectomy with ileo-rectostomy was performed and the patient experienced a greater clinical improvement, though the total negativity of the immunitary alteration was not obtained. Weak immunological disturbances continued 19 months after the surgical procedure. A short review of the literature is presented and a total of 39 cases of erythorcitic autoimmunization (with or without hemolysis) published up to the present time have been found. Lastly, various etiopathogenic theories in relation to this complication are mentioned.

We report a case of a 27-year-old woman with Leopard syndrome in which we observed the association of hypertrophic obstructive cardiomyopathy with arteriovenous cerebral shunt. This association has not been reported previously in the literature.