Analysis of patients referred to the gastroenterology service of a VA medical center

We recorded clinical information over a 12-month period on consecutive consultations to the gastroenterology service of the Durham VA Medical Center. Of 902 consultations, 789 were prospectively collected. Eighty-five percent of the patients were between 40 and 70 years old. Seventy-five percent of the referrals were from the internal medicine service. The most frequent reasons for consultation were abdominal pain (19%), GI bleeding (active, 16%; occult, 9%), abnormal results of liver tests (18%), and request for a procedure (11%). Diseases of the liver (32%) and "peptic diseases" (30%) were the most common diagnoses. One or more procedures were done in 71% of consultations. When these data are compared with those of a practicing gastroenterologist, using an identical instrument, it is apparent that trainees' experience with structurally identifiable gastroenterologic disease and with a variety of procedures was similar in scope. There were, however, differences in that the physicians at the VA saw substantially fewer patients with so-called "functional" illness. If these data are applicable to other VA Medical Centers, then the training of physicians in gastroenterology at a VA Medical Center should probably be broadened.     

Acute acid-base disorders. 2. Specific disturbances

Evaluation of the acid-base status of the body requires measurement of bicarbonate (total carbon dioxide) concentration, pH, and partial pressure of CO2 in arterial blood. Calculation of standard bicarbonate and base excess or deficit is not necessary. The normal concentration of free hydrogen ions (H+) is approximately 40 millimoles/liter, which is equivalent to a pH of 7.4. The normal load of fixed acids is 50 to 80 millimoles in 24 hours. A steady state is maintained by excretion of an equal amount of H+ by the kidneys, which at the same time regenerate bicarbonate to replenish buffer stores. Renal excretion of H+ is in the form of titratable acid and ammonium. Synthesis of ammonia can increase severalfold under the stimulus of acidosis. This is the chief mechanism of long-term compensation. Metabolic acidosis can be due to an excessive acid load (endogenous or exogenous), impaired renal excretion of H+, or bicarbonate loss. Determination of the "anion gap" (unmeasured anions) helps to establish the mechanism of acidosis. Acidosis with a normal anion gap is due to either bicarbonate loss or ingestion of certain chloride salts. A gap larger than normal indicates the presence in the body of acids other than acidfying chloride salts. Management of metabolic acidosis requires accurate diagnosis, clear understanding of the mechansim, and individualized treatment. Metabloic alkalosis is due to loss of H+ (usually from stomach or kidneys) or ingestion of alkali. Measurement of urinary chloride helps establish the mechanism of alkalosis. In saline-responsive alkalosis, the urinary chloride level is very low. This is usually due to gastric loss of H+, and the condition responds to administration of saline solution. When the urinary chloride level is only moderately low, the alkalosis is probably not due to gastric loss of H+. This form of alkalosis (saline-resistant) does not respond well to administration of saline solution and requires use of potassium in treatment. Apprpriate compensatory responses to acidosis or alkalosis are critical to survival. Compensation for metabloic acidosis consists of hyperventilation and enhanced renal excretion of H+, chiefly as ammonium. In metabolic alkalosis, compensation is mainly renal excretion of bicarbonate. Respiratory acidosis is due to alveolar hypoventilation. In chronic situations, a compensatory rise in serum bicarbonate concentration is expected. Management consists of treatment of the cause of hypoventilation. Respiratory alkalosis is due to hyperventilation. Treatment requires identification and correction of the cause of hyperventilation.     

A kinetic analysis of the changes in fluorescence on the interaction of 8-anilinonaphthalene-1-sulphonate with submitochondrial particles

Residual deficiency of brain performance in chronic alcoholics after a 5-year abstinency. Brain performance of a group of 43 chronic alcoholics abstinent since 5 years was tested. Some aspects of higher intellectual performance were found to be reduced as compared to a control population. The performance was also better than that of a group of chronic alcoholics abstinent for only one year. The residual deficiency of performance could be interpreted as a "functional psychosyndrome", resulting from chronic sensory deprivation on the base of the alcoholism.     

Properties of diagnostic data distributions

In applications of statistical methods to medical diagnosis, information on patients' diseases and symptoms is collected and the resulting data-base is used to diagnose new patients. The data-structure is complicated by a number of factors, two of which are examined here: selection bias and unstable population. Under reasonable conditions, no correction for selection bias is required when assessing probabilities for diseases based on symptom information, and it is suggested that these "diagnostic distributions" should form the principal object of study. Transformation of these distributions under changing population structure is considered and shown to take on a simple form in many situations. It is argued that the prevailing paradigm of diagnostic statistics, which concentrates on incidence of symptoms for given disease, is largely inappropriate and should be replaced by an emphasis on diagnostic distributions. The generalized logistic model is seen to fit naturally into the new framework.     

Backscattered electron imaging of the undersurface of resin-embedded cells by field-emission scanning electron microscopy

In this study backscattered electron (BSE) imaging was used to display cellular structures stained with heavy metals within an unstained resin by atomic number contrast in successively deeper layers. Balb/c 3T3 fibroblasts were cultured on either 13-mm discs of plastic Thermanox, commercially pure titanium or steel. The cells were fixed, stained and embedded in resin and the disc removed. The resin block containing the cells was sputter coated and examined in a field-emission scanning electron microscope. The technique allowed for the direct visualization of the cell undersurface and immediately overlying areas of cytoplasm through the surrounding embedding resin, with good resolution and contrast to a significant depth of about 2 μm, without the requirement for cutting sections. The fixation protocol was optimized in order to increase heavy metal staining for maximal backscattered electron production. The operation of the microscope was optimized to maximize the number of backscattered electrons produced and to minimize the spot size. BSE images were collected over a wide range of accelerating voltages (keV), from low values to high values to give ‘sections' of information from increasing depths within the sample. At 3–4 keV only structures a very short distance into the material were observed, essentially the areas of cell attachment to the removed substrate. At higher accelerating voltages information on cell morphology, including in particular stress fibres and cell nuclei, where heavy metals were intensely bound became more evident. The technique allowed stepwise ‘sectional’ information to be acquired. The technique should be useful for studies on cell morphology, cycle and adhesion with greater resolution than can be obtained with any light-microscope-based system.     

A Golgi localization signal identified in the Menkes recombinant protein

Menkes disease arises from a genetic impairment in copper transport. The gene responsible for the phenotype has been identified as a copper transporting ATPase ( ATP7A ). Recently, the protein encoded by the ATP7A gene has been localized to the Golgi complex. In order to investigate the role of the Menkes disease protein in copper transport, recombinant constructs containing both the full-length open reading frame and an alternatively spliced form have been successfully expressed and localized in mammalian cells. Other studies of a patient with occipital horn syndrome, an allelic variant of Menkes disease, have demonstrated that only this alternatively spliced isoform and not the full-length form is expressed in this patient. The milder form of this patient's phenotype suggests that the alternatively spliced isoform has some functional role in copper transport. In the present study the full-length recombinant Menkes protein was shown by immunofluorescence to localize to the Golgi apparatus and the alternatively spliced form, lacking sequences for transmembrane domains 3 and 4 encoded by exon 10, was shown to localize to the endoplasmic reticulum. Using sequences from exon 10 fused to a non-Golgi reporter molecule, a 38 amino acid sequence containing transmembrane domain 3 of the Menkes protein was found to be sufficient for localization to the Golgi complex. Therefore, the protein sequence encoded by exon 10 may be responsible for this differential localization and both isoforms may be required for comprehensive transport of copper within the cell.     

Prolonged neuromuscular blockade with mivacurium in a newborn

Recent reports have demonstrated that puerperal psychosis is preceded by prodromic signs. These signs must be recognized in a multidisciplinary context, opening the way to improved diagnosis, therapy and prognosis. On the basis of our clinical experience, we stress the important of early management in women who present prodromic signs of puerperal psychosis. Specific management relies on intensive psychotherapy with daily sessions centered on filiation. With this approach, the emergence of delusions can generally be prevented, usually allowing an uninterrupted mother-infant relationship. We hypothesize that this approach has a favorable influence on later mother-child interactions and cause profound changes in the mother's psychic organization, resulting in a better long-term prognosis. We illustrate our point with a case report.     

Two reconstructive techniques for flatfoot deformity comparing contact characteristics of the hindfoot joints

The effect of two different methods of reconstruction of flatfoot deformity and the role of the posterior tibial tendon on the contact characteristics of the hindfoot joints were quantified using pressure-sensitive film. Each of 10 cadaver feet was loaded quasi-statically by an axial compressive force to simulate varying loads. First, a specimen was tested intact, then it was tested after sectioning the spring ligament and loading the specimen cyclically to create one type of flatfoot deformity. It was then tested again after reconstructing the deformity. Reconstructions used were the Dillwyn-Evans procedure (bone graft in osteotomy of the calcaneus) or the calcaneocuboid distraction arthrodesis (CCDA). We found that surgically produced flatfoot deformity altered mainly the talonavicular joint, by decreasing its contact area. The Dillwyn-Evans method had less effect on the talonavicular joint (altering 2 of 6 measured parameters) than the CCDA (3 of 6) and more effect on the anteriomedial facet (altering 3 of 6 parameters) than the CCDA (1 of 6). The Dillwyn-Evans method had more effect on the posterior facet (altering 2 of 6 measured parameters) than the CCDA (1 of 6). Function of the posterior tibial tendon had no effect on contact characteristics of the hindfoot joints after either type of reconstruction. These findings are based on measurements using a quasi-statically-loaded foot model at three selected positions, and results may be different with dynamic loading.