Diaphragm activation with intramuscular stimulation in dogs

We studied in 10 supine anesthetized dogs diaphragm contraction produced by electrical activation with intramuscular electrodes surgically implanted in the ventral surface of the diaphragm and compared this with activation of the ipsilateral phrenic nerve (C5, 6, and 7) before it entered the thorax. Repetitive 40-Hz pulse trains with supramaximal current stimulus were used after hyperventilation of the animals to apnea. A single intramuscular electrode within 1 to 2 cm of the site of phrenic nerve entry into the diaphragm produced a mean transdiaphragmatic pressure of 12.0 cm H2O +/- 0.97 SE and mean tidal volume of 0.27 L +/- 0.04 SE. Mean values observed with phrenic nerve stimulation were not statistically different, and both electrode systems produced equivalent outward abdominal motion and upper rib cage paradox, as monitored by inductive plethysmography. There was no difference in gas exchange during stimulation with a single hemidiaphragm electrode and mechanical ventilation compared at the same tidal volume and respiratory rate. Blockade of neuromuscular transmission with curare eliminated intramuscular and phrenic nerve stimulation proportionately, suggesting that activation of the diaphragm is dependent in both cases on the phrenic nerve. This technique does not entail manipulation of the phrenic nerve and may have clinical application as an alternative technique for diaphragm pacing.     

Mamillary body enhancement on MR as the only sign of acute Wernicke encephalopathy

We report a case of Wernicke encephalopathy in which the only sign of acute disease was enhancement of the mamillary bodies. This case demonstrates the utility of gadolinium enhancement at MR imaging as a means of diagnosing or confirming the syndrome of Wernicke encephalopathy even in the absence of atrophy or T2 abnormalities within the diencephalon and mesencephalon.     

Metabolism of ricinoleate by Neurospora crassa

BACKGROUND: From January 1993 to December 1994, we conducted a prospective study to investigate the evolutionary change of rebleeding risk in bleeding peptic ulcers. To obviate possible confounding factors that would influence decision making for discharge of patients, subjects with coexistent acute illnesses, systemic bleeding disorders, alcoholism, and use of nonsteroidal anti-inflammatory drugs were excluded. METHODS: Emergency endoscopies were performed in patients with hematemesis or a melena within 24 hours of admission. Ulcer lesions were divided into six categories according to endoscopic findings. The residual risks of rebleeding of each type of ulcers were calculated for 10 days, and the critical point of acceptable rebleeding risk after discharge was set at 3%. RESULTS: Three hundred ninety-two patients with bleeding peptic ulcers completed the study. The ulcers, characterized by clean bases, red or black spots, adherent clots, nonbleeding visible vessels without local therapy, nonbleeding visible vessels with local therapy, and bleeding visible vessels with local therapy took 0, 3, 3, 4, 4, and 3 days, respectively, to decrease rebleeding risk to below the critical point. All episodes of fatal rebleeding (n = 4) occurred within 24 hours after admission. CONCLUSIONS: Patients with clean-based ulcers can be discharged in the first day of admission. The optimal duration required for hospitalization of patients with ulcers characterized by nonbleeding visible vessels at initial endoscopy is 4 days. The remaining patients with ulcers marked by other bleeding stigmata may be discharged after a 3-day observation.     

Hypoxia impairs vasodilation in the lung

Alveolar hypoxia causes pulmonary vasoconstriction; we investigated whether hypoxia could also impair pulmonary vasodilation. We found in the isolated perfused rat lung a delay in vasodilation following agonist-induced vasoconstriction. The delay was not due to erythrocyte or plasma factors, or to alterations in base-line lung perfusion pressure. Pretreating lungs with arachidonic acid abolished hypoxic vasoconstriction, but did not influence the hypoxia-induced impairment of vasodilation after angiotensin II, bradykinin, or serotonin pressor responses. Progressive slowing of vasodilation followed angiotensin II-induced constriction as the lung oxygen tension fell progressively below 60 Torr. KCl, which is not metabolized by the lung, caused vasoconstriction; the subsequent vasodilation time was delayed during hypoxia. However, catecholamine depletion in the lungs abolished this hypoxic vasodilation delay after KCl-induced vasoconstriction. In lungs from high altitude rats, the hypoxia-induced vasodilation impairment after an angiotensin II pressor response was markedly less than it was in lungs from low altitude rats. We conclude from these studies that (a) hypoxia impairs vasodilation of rat lung vessels following constriction induced by angiotensin II, serotonin, bradykinin, or KCl, (b) hypoxia slows vasodilation following KCl-induced vasoconstriction probably by altering lung handling of norepinephrine, (c) the effect of hypoxia on vasodilation is not dependent on its constricting effect on lung vessels, (d) high altitude acclimation moderates the effect of acute hypoxia on vasodilation, and (e) the hypoxic impairment of vasodilation is possibly the result of an altered rate of dissociation of agonists from their membrane receptors on the vascular smooth muscle.     

HLA-DRB1 genes and disease severity in rheumatoid arthritis. The MIRA Trial Group. Minocycline in Rheumatoid Arthritis

OBJECTIVE: To examine the effect of alleles encoding the "shared"/"rheumatoid" epitope on rheumatoid arthritis (RA) disease severity in patients who participated in the minocycline in RA (MIRA) trial. METHODS: Of 205 patients with a week-48 visit, blood was available for typing of HLA-DRB1 and HLA-DQB1 in 174 (85%) and successfully completed in 169 (82%). Baseline erosions were used to assess disease severity and new erosions at the last visit served as a proxy for progression. RESULTS: At baseline, there was no association between the presence of erosive disease or rheumatoid factor status and the dose of rheumatoid epitope (homozygous, heterozygous, none) or the specific alleles identified. At the final visit, a gradient was observed for the 3 allelic subgroups (and their gene doses) in the occurrence of new erosions among the Caucasian placebo-treated, but not the minocycline-treated, patients. A treatment group/HLA-DR4 epitope interaction was demonstrated in multivariate analyses. Approximately two-thirds of African-American patients did not have the rheumatoid epitope. CONCLUSION: HLA-DRB1 oligotyping may be useful in predicting the progression of disease in some Caucasian patients. Our study corroborates the infrequency of the epitope among African-American patients with RA.     

Physician judgments of chronic pain patients

Recent evidence has indicated that physician judgments of patients can be influenced by contextual factors. This study examined three contextual factors relevant to hypothetical patients with low back pain, using vignettes that were varied in a 2 x 2 x 2 factorial design: level of reported pain (high vs low), level of supporting medical evidence (high vs low), and the valence of the physician-patient interaction (positive vs negative). Perceived levels of pain, disability, emotional distress, and somatic preoccupation were rated by internists after reading a vignette. Ratings of pain and disability were lower for patients without supporting medical evidence; ratings of distress, somatic preoccupation, and disability were greater for patients who exhibited negative rather than positive affect; internist ratings of pain were lower than patient ratings among patients reporting high levels of pain, while ratings were inflated for patients with low levels of pain. The results suggest that characteristics of both the patient and the situation may influence medical judgments.