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Biomedical subjects

D Martin

Publications and source records attributed to D Martin.

At least 703 records · Page 39Linked to original sources

[Non-traumatic rhinorrhea from a latero-sellar fistula of the temporal fossa adjacent to an empty sella turcica. Computed tomography aspects; surgical treatment].

The authors report a case of non traumatic rhinorrhea due to an osteo-dural fistula communicating between the latero-sellar part of the left middle cranial fossa and the sphenoidal sinus. This fistula, probably congenital, was adjacent to an intrasellar arachnoidocele ("empty" sella turcica), but was not responsible for it. This lesion was demonstrated by CT scan associated with the injection of Metrizamide. The surgical treatment (trans-sphenoidal approach) allowed complete cure of the fistula and its associated symptoms.

Cerebrospinal Fluid Rhinorrhea↗

EEG sleep in elderly depressed, demented, and healthy subjects.

In a prospective study of EEG sleep patterns in 25 elderly depressives, 25 elderly demented patients, and 25 healthy, elderly control subjects, the sleep of depressives was characterized by reduced REM sleep latency, increased REM percent and first REM period density, and altered temporal distribution of REM sleep, as well as by diminished sleep maintenance (correlated significantly with Hamilton ratings of depression: multiple R = -0.42, p less than 0.05). In contrast, the sleep of demented patients showed reduced REM sleep percent, but normal REM temporal distribution, increased loss of spindles and K-complexes (the latter correlating significantly with severity of cognitive impairment as measured by the Folstein score: multiple R = -0.59, p less than 0.01), and less severe sleep maintenance difficulty than for depressives. An examination of REM latency demonstrated a skewed distribution in depression (i.e., 42% of nights with sleep-onset REM periods), but a normal distribution in the controls and demented subjects. A REM latency cut-off score of 30 min correctly classified 68% of all patients (kappa = 0.36; p less than 0.005), compared with 78% correctly identified in our retrospective study (Reynolds et al. 1983).

Aged↗

Ketamine acts as a non-competitive N-methyl-D-aspartate antagonist on frog spinal cord in vitro.

The effects of the dissociative anaesthetic, ketamine, the divalent cation, magnesium and the organic antagonist, 2-amino-5-phosphonovalerate (APV), were examined on responses of motoneurones to excitatory amino acids in the hemisected spinal cord of the frog in vitro. The amino acids, N-methyl-D-aspartate (NMDA), kainate and quisqualate, produced dose-dependent depolarizations. Ketamine, magnesium and APV depressed responses to NMDA but had no effect on those to quisqualate and kainate. Magnesium and APV produced Schild plot slopes that were not different from unity, whereas ketamine had a slope significantly less than unity, indicative of a non-competitive action. Experiments in which combinations of drugs were tested indicated that these substances act by three distinct mechanisms to cause antagonism of the actions of NMDA.

2-Amino-5-phosphonovalerate↗

Long-term effects of 24-hr unilateral ureteral obstruction on renal function in the rat.

To characterize the pattern of recovery following release of unilateral ureteral obstruction of 24-hr duration, rats were studied with whole kidney clearance techniques, 3 hrs, 8, 14, and 60 days after release. The single nephron glomerular filtration rate (SNGFR) of superficial and juxtamedullary nephrons was estimated with a modification of Hanssen's technique in rats studied 8 and 60 days after ureteral release. The whole kidney glomerular filtration rates (GFR) were decreased markedly 3 hrs after relief of obstruction, but gradually increased and by 14 days, the GFR of the postobstructed kidney (POK) and the contralateral kidney (CK) were comparable. This recovery of GFR was not a consequence of a homogeneous improvement in SNGFR. At 8 days, more than 15% of superficial and juxtamedullary nephrons were not filtering in the POK. This decrease in the percent of filtering nephrons persisted to 60 days post release, indicating a permanent loss of nephron units. The SNGFR of the residual nephrons of the POK was significantly greater than that of the CK at 8 and 60 days following ureteral release. Thus, acute unilateral ureteral obstruction results in a permanent loss of filtering nephrons, which is offset by hyperfiltration of those remaining. Abnormalities in renal tubule function persisted beyond the time (14 days) when whole kidney GFR had returned to normal. These abnormalities were in distal tubule function. Urine osmolality was consistently lower at all time intervals post release, as was net acid excretion. The results of the present study suggest that these abnormalities are a consequence of the reduction in the number of filtering juxtamedullary nephrons and/or to abnormalities in collecting duct function.

Animals↗

Expression of HLA-A and -B antigens on differentiating U-937 cells.

Cells from the human immature monocytoid cell line U-937 were induced with 12-O-Tetradecanoyl-phorbol-13-acetate (TPA) to differentiate towards macrophage-like cells. The expression of HLA-antigens during differentiation was examined with a panel of monoclonal antibodies directed against monomorphic and polymorphic determinants. Class II antigens could be detected neither on uninduced nor on TPA-induced U-937 cells. While the expression of HLA-A3 did not change significantly during differentiation, the "supertypic" specificities HLA-Bw4 and Bw6 as well as the "private" specificity HLA-B18 could be detected only on a drastically decreased number of cells after 4 days of exposure to TPA. This may imply a selective loss of HLA-B molecules from the cell membrane and therefore a separate regulatory control of HLA-A and -B antigens.

Cell Differentiation↗

Thyroidectomy abolishes pulsatile growth hormone secretion without affecting hypothalamic somatostatin.

The effects of thyroid hormone deprivation and of subsequent replacement therapy on growth hormone (GH) secretion were investigated in unrestrained unanesthetized rats. Male rats were thyroparathyroidectomized (TPTX) 5 weeks prior to plasma sampling for GH assay, or to decapitation for evaluation of hypothalamic somatostatin (SRIF) content and in vitro SRIF and GH release. Thyroid hormone deprivation suppressed pulsatile GH secretion as well as GH release induced by clonidine (150 micrograms/kg). Treatment of TPTX rats with small doses of triiodothyronine (T3) restored an episodic pattern of GH secretion, but with lower peak values than controls, as well as the GH response to clonidine. Thyroid deprivation induced a 92-fold decrease in GH release from the pituitary; however, the ratio between GH release and GH content was similar in TPTX and normal rats, and human pancreatic growth hormone-releasing factor (GRF) (3 X 10(-8) M) was still able to stimulate residual GH release by hemipituitaries from TPTX rats in a manner similar to that in euthyroid controls (295 and 254% stimulation, respectively). Thyroid deprivation or T3 replacement did not modify SRIF content in the hypothalamus or other brain structures tested. The capacity of K+ depolarization to release SRIF in vitro from the hypothalamus was not modified by TPTX. These findings indicate that thyroid hormones are necessary to maintain both pulsatile and induced GH secretion in unanesthetized rats. In addition they suggest that impairment of GH secretion in thyroidectomized rats does not depend upon changes in the hypothalamic SRIF regulation of the hormone but could be dependent on a defect in GRF release and/or, most probably, GH synthesis directly at the pituitary level.

Animals↗

Transport of ammonia in the rabbit cortical collecting tubule.

Nonionic diffusion and diffusion equilibrium of ammonia have been generally accepted as the mechanism of urinary ammonium excretion. However, these characteristics have not been examined directly in vitro. In the present studies, nonionic diffusion and diffusion equilibrium of ammonia were examined in rabbit cortical collecting tubules perfused in vitro. Collected fluid ammonium and pH were measured in tubules exposed to chemical gradients of NH3/NH+4. In tubules perfused with an acid perfusate free of ammonia and bathed with solutions containing NH4Cl, collected fluid ammonia failed to equilibrate across the epithelium except at slow flow rates. The estimated apparent permeability coefficient to NH3 was approximately 5 X 10(-3) cm/s. Predominant nonionic diffusion of NH3, rather than transport of NH+4, was indicated by alkalinization of luminal fluid in tubules exposed to peritubular NH4Cl and by the relative influence of peritubular NH+4 and NH3 on ammonia entry. In tubules perfused with an acid solution containing NH4Cl, little loss of ammonium was detectable, indicating a low permeability to NH+4. In contrast to the restricted diffusion of NH3 in cortical collecting tubules, proximal convoluted tubules exhibited a much higher apparent permeability to NH3. In conclusion, nonionic diffusion of NH3 accounted for most ammonium transport in the proximal convoluted tubule and in the cortical collecting tubule. However, there was relatively restricted diffusion in the collecting tubules; this may account for the failure of whole kidney ammonium excretion to obey quantitatively the predictions of nonionic diffusion and diffusion equilibrium of ammonia.

Ammonia↗

Contribution of individual superficial nephron segments to ammonium handling in chronic metabolic acidosis in the rat. Evidence for ammonia disequilibrium in the renal cortex.

Ammonia entry along surface nephron segments of rats was studied with micropuncture techniques under control and chronic metabolic acidosis conditions. Tubule fluid was collected successively from sites at the end and beginning of the distal tubule and at the end of the proximal tubule of the same nephron. During chronic metabolic acidosis, ammonium excretion doubled. As anticipated, the ammonium concentration (TFNH+4) was significantly higher in proximal tubule fluid during acidosis, and ammonium delivery to end proximal sites increased from 19.4 +/- 2.3 to 34.0 +/- 3.2 pmol/min (P less than 0.001). Although chronic acidosis did not affect TFNH+4 at the beginning of the distal tubule, ammonium delivery to the end of the distal tubule increased from 5.72 +/- 0.97 to 9.88 +/- 0.97 pmol/min. In both control and acidotic groups ammonium delivery was lower (P less than 0.001) to end distal sites than to end proximal sites, indicating net loss in the intervening segment. This loss was greater during chronic metabolic acidosis (23.9 +/- 3.3 vs. 13.6 +/- 2.0 pmol/min in controls, P less than 0.025). In both groups net entry of ammonia, in similar amounts, occurred along the distal tubule (P less than 0.05). In situ pH averaged 6.80 +/- 0.05 at end proximal tubule sites and fell to 6.54 +/- 0.08 at the beginning of the distal tubule (P less than 0.005). Chronic metabolic acidosis did not affect these measurements. The calculated free ammonia at the end of the proximal tubule rose from 9.3 +/- 2.2 to 21 +/- 9 microM (P less than 0.005) during chronic metabolic acidosis, and was also higher at beginning distal sites during acidosis (8.8 +/- 2.4 vs. 2.7 +/- 0.7 microM in controls, P less than 0.05). In both groups ammonia values for the beginning distal tubule fluid were lower than for end proximal tubule fluid. Thus, loss of ammonium in the loop segment is enhanced by chronic metabolic acidosis. Distal entry of ammonia is markedly less than along the proximal tubule and does not change in chronic metabolic acidosis, and ammonia permeabilities for the proximal and distal segments of surface nephrons seem different.

Acidosis↗

A multicenter study of the epidemiology of hepatitis B in anesthesia residents.

Practicing anesthesiologists are at high risk of hepatitis B infection, but the risk for anesthesia residents has not been assessed. Anesthesia residents at seven universities were surveyed to study the epidemiology of hepatitis B in these trainees. Hepatitis B virus markers in serum were measured and data from questionnaires were used to determine characteristics of anesthetic practice, effectiveness of strategies for hepatitis B virus infection control, and nonvocational hepatitis B risk factors. Of 267 participants, 12.7% (range of the seven centers, 8.7%-22.7%) had serum markers for hepatitis B virus. The seropositivity (17.8%) in anesthesia residents who had completed more than 12 months of nonanesthesia postgraduate clinical training, or who had practiced medicine in another specialty prior to anesthesia, was greater than in the other trainees (9.4%). Based on their risk and the ineffectiveness of current control measures, anesthesia residents who lack hepatitis B virus immunity should be vaccinated prior to or as early as possible in their training.

Anesthesiology↗

Splenic abscess.

Abscess of the spleen is a rare entity. It may develop after generalized infection, hematologic disorders and trauma. The authors report the case of a 7-year-old boy who presented with a 2-month history of spiking fever, anorexia, fatigue and weight loss. He had left subcostal tenderness and a palpable spleen. He had a history of trauma to the left flank 5 months before admission but a splenic scan obtained at that time appeared normal. A splenic abscess was diagnosed by gallium scanning, computerized tomography and ultrasonography. Although splenectomy has been advocated as the treatment of choice for splenic abscess, this patient was treated successfully with appropriate antibiotics and simple drainage, preserving the spleen. Cultures grew Staphylococcus aureus. Of all the diagnostic methods available, ultrasonography is the least invasive study that will make the diagnosis and is less expensive than some methods.

Abscess↗

Phase I evaluation and pharmacokinetic study of weekly iv thymidine and 5-FU in patients with advanced colorectal carcinoma.

A phase I study of weekly iv thymidine (TdR) and 5-FU was carried out in patients with advanced colorectal carcinoma using two dosage schedules. Schedule 1 employed a 3-hour infusion of TdR (6-8 g/m2/hour) followed immediately by a bolus of 5-FU (100-200 mg/m2). Schedule 2 used a slightly larger dose of TdR (18 g/m2/hour for 1.5 hours), with 5-FU given 30 minutes after the TdR infusion was started. Myelosuppression was observed erratically at the higher doses of 5-FU. Diarrhea and severe fatigue were seen frequently with Schedule 1. CNS side effects were the dose-limiting effects for both schedules. For long-term use the maximally tolerated 5-FU doses were 100 mg/m2/week for Schedule 1 and 175 mg/m2/week for Schedule 2. In pharmacokinetic studies in five patients, both schedules produced prolonged plasma beta-half-lives of 5-FU (96-189 minutes). Extensive formation of floxuridine was seen with both schedules. It appears likely that CNS toxic effects are characteristic of TdR-containing 5-FU regimens and would limit the therapeutic potential of this approach.

Adult↗