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The normal range of the C4 concentration in serum and plasma varied between 40 and 200% of the standard pools. Low C4 values were found in systemic lupus erythematosus, in acquired haemolytic anaemia and in hereditary angioneurotic oedema.
Differences in C4 values were found between normal sera and the corresponding EDTA plasma, when tested after dilution in calcium-free and EDTA buffers, respectively. After storage of the samples for 1 day at 20°C or 37°C the C4 values decreased, most markedly in plasma; no further decrease was found on prolongation of storage, and the difference between serum and plasma C4 values disappeared. The plasma C4 levels gradually fell on storage at 4°C, but a clear difference between serum and plasma was still demonstrable after 5 days.
The method described is simple and quick and can be used routinely in large scale investigations.
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Ten studies were made in seven patients, five with IgM, and five with 19S rheumatoid factor. In two patients the turnovers of 19S rheumatoid factor and IgM were studied simultaneously.
The turnover of IgM was similar to that reported for normal subjects and patients with other diseases: fractional catabolic rate 0·14–0·18, plasma and whole body T½ 3·7–6·5 days, with 65–77% intravascular localization. The absolute catabolic rate for IgM was elevated (8–60 mg/kg/day).
The turnover of 19S rheumatoid factor isolated from serum was comparable in fractional catabolic rate (0·15–0·19) plasma and whole body T½ (3·9–6·0 days) and intravascular localization (62–88%). No evidence of rapid catabolism of the `immune' elimination type was obtained.
相似文献2. Values for red blood cells and albumin distribution spaces were 5·2 ± 0·6 and 20·2 ± 1·0 ml./100 g tissue, respectively, in the whole kidney. The ratio of tissue haematocrit over simultaneous arterial haematocrit averaged 0·56. The extravascular albumin fraction amounted to about 31·0% of the total albumin in the whole kidney.
3. A statistically significant correlation was demonstrated between osmotic urine/plasma (U/P) ratios (within the approximate limits of 0·6-1·8) and quantities of extravascular albumin in the medulla.
相似文献2. Two techniques, subarachnoid perfusion from the supracallosal space between the hemispheres to the cisterna magna and barbotage from the cisterna magna, have been used. If the artificial c.s.f. contains Evans Blue, the former procedure results in maximum staining of the pia and underlying nervous tissue of the pons-medulla and spinal cord. The latter procedure results in maximum staining of the medial and supero-lateral surfaces of the cerebral hemispheres, particularly anteriorly.
3. During subarachnoid perfusion at 0·06 ml./min with the potassium-free fluid, most regions of the brain took up significantly greater amounts of 42K than was the case during perfusion with the fluids containing 3 and 10 m-equiv/l. For blue cerebral cortex, the tissue subjected directly to the inflowing fluid and showing the biggest differences, the ratios, c.p.m. per g brain/c.p.m. per ml. plasma, were 1·71 ± 0·12 (+44%), 1·19 ± 0·05 and 1·07 ± 0·08 (-10%) during perfusion with the fluids containing, 0, 3 and 10 m-equiv/l. respectively.
4. During barbotage, the uptake of 42K into pons-medulla and spinal cord from blood plasma, the concentration in the latter being effectively kept near constant, was, at the end of 2 hr, greater when the fluid contained potassium, 0 m=-equiv/l. rather than 10 m-equiv/l. Thus the ratio, c.p.m per g brain/c.p.m. per ml. plasma was (0·99 ± 0·04 (+36%) as against 0·73 ± 0·05 for pons-medulla where the difference was greatest.
5. Simultaneous measurements of the entry of [14C]urea from blood to different regions of the central nervous system revealed no significant differences due to the differing concentrations of potassium imposed by either barbotage or subarachnoid perfusion. This appears to exclude a non-specific cause for the changes in 42K uptake, an example of which might be a changing blood flow.
6. Reasons are given for supposing that the big increase in 42K uptake due to the potassium-free fluid must be due to events occurring at the blood—brain barrier. This might be some form of interaction, possibly the single file effect, such that a low potassium concentration in the interstitial fluid potentiates 42K influx across the blood—brain barrier. Alternatively it might be due to a low potassium concentration in this fluid greatly reducing active potassium movement from interstitial fluid to blood. The former explanation would conform neatly with the present results; but the latter would additionally be compatible with other evidence concerning the homoeostasis of potassium concentration in c.s.f. and the interstitial fluid of brain.
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Our results are in keeping with the hypothesis that lowered environmental temperatures inhibit a variety of metabolic processes which may be concerned with the utilization of antigen and/or the synthesis of antibodies.
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Six patients selected at random who had a mean SALLI of 71·5±5·8% after tumour excision were further treated by BCG immunotherapy and presented after 8·2±2·9 months of therapy with a significantly (P<0·01) lower SALLI of 32·6±8·1%. In eight patients treated exclusively by surgical excision, SALLI remained basically unchanged in the course of 10±2·8 months (29·0±8·0% vs 30·4±12·9%).
The mean index of leucocyte locomotion (LL) of eight melanoma patients who had received BCG for 11·2±2·3 months was 5·9±0·9 cells/field and thus significantly (P<0·01) higher in comparison with the mean index of LL (2·8±0·5) found in eight patients treated by surgical excision only 12·4±2·1 months before testing.
In addition, patients receiving BCG had a significantly higher (P<0·05) mean value of LL than fifteen healthy controls who presented with a mean index of LL of 3·4±0·3 cells/field. Our results permit the suggestion that BCG decreases SALLI and increases LL in melanoma patients.
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2. Intramuscular injections of vasopressin increased the rate of water uptake from distilled water. There was a good relation between doses and responses over various time intervals. A dose of 4 m-u. vasopressin/g body wt. doubled the rate of water uptake over a period of 1 hr. The same dose of vasopressin doubled the rate of water uptake when the toads were kept in solutions of sucrose or urea of different osmolarity.
3. The rate of water uptake when the toads were bathed in sodium chloride solutions was consistently 8 μl./cm2/hr greater than when bathed in sucrose or urea solutions of equal osmolarity. There was no water uptake when the sodium chloride solution was 285 m-osmolar.
4. Vasopressin (4 m-u./g) injected intramuscularly doubled the rate of water uptake from sodium chloride solutions of different osmolarity.
5. With solutions of potassium chloride, sodium nitrate, and potassium nitrate, in concentrations up to 150 m-osmoles/l., the rate of water uptake was found to be the same as with solutions of sodium chloride of the same osmolarity. Similarly, it was doubled by injection of vasopressin (4m-u./g).
6. The effect of temperature on the rate of water uptake before and after injection of vasopressin was investigated in toads kept in distilled water, sucrose, or sodium chloride solutions. For temperatures between 20 and 37° C, vasopressin (4 m-u./g) reduced the activation energy involved in the process of water uptake by 4000 cal.
7. The results agree with the view that water uptake follows a diffusion process which is facilitated by vasopressin, possibly as a result of increasing the size or number of available pores.
相似文献2. Relative grain density in nucleus and cytoplasm, measured photometrically, was used as an indication of 22Na distribution within the oocyte. In test experiments grain density fell to 50% within 19 μm of the edge of the section. Owing to the large diameter of the oocyte (> 600 μm) and its nucleus (> 200 μm), this resolution was adequate to determine cytoplasmic/nuclear (C/N) ratios of grain density.
3. In oocytes fully loaded with 22Na, the mean C/N ratio was 0·92 ± 0·03 (n = 11). After 5 hr exchange in Li-substituted Na-free Ringer solution, the mean C/N ratio was 2·18 ± 0·04 (n = 11). After 5 hr exchange in Ringer solution as a control, the mean C/N ratio was 1·39 ± 0·18 (n = 7). The cytoplasm thus contained a fraction of 22Na inexchangeable with Li, and more slowly exchangeable with Na than that in the nucleus.
4. The non-Li-exchangeable fraction of internal Na thus revealed appeared to be quantitatively similar to that already demonstrated by studies of 22Na fluxes and of internal Na activity by means of Na-sensitive micro-electrodes.
相似文献2. Thermal stimuli were delivered from thermodes in contact with the skin.
3. Primate `cold' receptors had spot-like receptive fields and were found in both hairy and glabrous skin. The conduction velocities of the axons ranged from 0·6 to 15·3 m/sec.
4. The discharge from the primate receptors characteristically appeared in bursts with intervals of silence within the range temperatures of 18-40° C. Static and dynamic sensitivity curves were established, with maxima about 30° C.
5. Cold receptors in the lip of the dog had maximal sensitivity at 31-37° C. The axons were myelinated with conduction velocities less than 20 m/sec.
6. `Warm' receptors, with maximal sensitivity at 40° C and non-myelinated axons, were abundant in the scrotal nerve of the rat. The `cold' receptors had maximal responses at 23-28° C.
7. The `spurious' thermoreceptor behaviour of slowly adapting mechanoreceptors is described and the way in which they may distort integrated potential records from whole nerves is analysed.
相似文献The component immunoglobulins of the complex were separated by anion exchange chromatography at 37°C. Crossmixing studies with purified normal immunoglobulins indicated that the patient's IgA component was essential for cryoprecipitability of the complex. RA latex tests for anti-IgG activity at 37°C showed strong agglutination with both cryoglobulin complex and the isolated IgA component; this protein was found to be monoclonal with type K light chains.
Vasculitis, induced by skin testing the patient with his own plasma and isolated cryoglobulin was found to be histologically indistinguishable from that occuring spontaneously; reduction of symptoms paralleled reduction of cryoglobulin on treatment. These observations strongly support the hypothesis that the cryoglobulin complex is responsible for the patient's vasculitis.
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2. When the stimulus strength was at least 1·1 times threshold the peak force of the contraction elicited was reduced by stimulus durations longer than 1 msec at 20 °C, and by durations longer than 3 msec at 2-5 °C.
3. As the strength of a prolonged stimulus was progressively increased to 3 times rheobase or more, peak twitch and tetanus force declined to 40-70% of the amplitude with short (0·2-0·5 msec) stimuli. The time to peak of the twitch was slightly decreased and the first phase of relaxation was accelerated.
4. Cine-micrography of fibres which were permitted to shorten under a light load revealed that the side of the fibre adjacent to the anode was unactivated under conditions which also reduced peak force output.
5. With stimulus durations longer than 20 msec, peak force, time to peak, and relaxation time increased as the stimulus strength increased from 2·5 to 3 times rheobase. This might have been produced by a cathodal contracture following the action potential.
6. The results are discussed in relation to previous studies of activation in striated muscle.
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Monolayer cell cultures were stimulated by IgG purified from sera of Graves' patients or control subjects and compared to the effect of bovine TSH. Bovine TSH produced a dose-dependent increase in cAMP intracellular levels between 0·05 mU and 2·5 mU/ml, reaching a maximal value after 30 min with higher doses. While normal IgG had no effect, IgG prepared from untreated patients with frank Graves' disease elicited a significant increase in cAMP accumulation at a concentration between 0·05 and 0·5 mg/ml within 60 min in thirteen out of fourteen patients. A longer incubation period showed no further increase in cAMP values, even if in one case a higher concentration (5·0 mg/ml) of Graves' IgG had a delayed response. When the cAMP intracellular level modifications produced by Graves' IgG preparations in thyroid cell cultures were compared to those evoked in thyroid slices, an identical percentage (93%) of positive cases was obtained, without a coincidence of negative cases. Using thyroid slices the cAMP intracellular increase above basal levels was higher, if considered as a percentage, but in cultured cells a very low IgG concentration was sufficient to detect the presence of TSAb. No correlation between the two assays was found.
In conclusion, normal human cultured thyroid cells appeared to be a more suitable substrate when compared to human thyroid slices for detecting the presence of TSAb in Graves' disease and for studying its effect on thyroid cells. However, a 100% TSAb positivity was present in our Graves' patient series only when both assays were used.
相似文献2. Stimulation of ventral root filaments containing slow axons produced no contractile tension in EDC.
3. Stimulation of ventral root filaments containing fast-group axons elicited all-or-nothing twitches of motor units of EDC. The twitch tensions of 66·3% of the units were < 2·0 g wt.; only 8·7% were > 5·0 g wt. Tetanus-twitch ratios were 1·4-4·7 in a sample of 14 units. Contraction times were between 15 and 35 msec in 97% of the units. There was no correlation between contractile properties and axonal conduction velocity.
4. Afferent volleys from the stimulated EDC nerve were recorded from C6 or C7 dorsal roots. The threshold was below the threshold for a just-detectable motor twitch in ten out of eleven baboons. Conduction velocity of the earliest component of the muscle afferent volley was 67-83 m/sec.
5. The conduction velocities of twenty-eight spindle afferents, identified by their responses to linear stretches of EDC and by their unloading by maximal twitches, were all < 70 m/sec. Higher dynamic sensitivity tended to be associated with higher conduction velocity.
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By the direct method, 24% of patients had small intracytoplasmic inclusions in their neutrophils when stained for IgG suggesting that immune complexes were phagocytosed in vivo. None of twenty-one normal controls had similar inclusions. By the indirect method, 62% of SLE patients were positive for IgG, 15% for IgM, 8% for IgA and 31% for C3. None of the twelve normal controls were positive.
By the indirect method, PMN inclusions containing both IgG and IgM correlated with clinical activity (P<0·001), depressed serum complement (CH50, P=0·026; and C3, P<0·051), cryoglobulinaemia (P=0·014), anti-nDNA antibodies (P<0·001) and Clq-binding immune complexes (P=0·008). A suggestive correlation with granulocytopenia was also observed. The presence of inclusions containing IgG alone did not correlate with any of these parameters. C3 and IgM appeared to be mutually exclusive, i.e. neither was present simultaneously. These findings suggest (1) that normal PMN on exposure to SLE sera develop intracytoplasmic inclusions by phagocytosis of immune complexes, (2) the presence of such complexes correlates with a number of parameters of disease activity, particularly when IgG and IgM are both present and (3) such complexes may be phagocytosed in vivo as suggested by the presence of inclusions in vivo and contribute to a number of granulocyte disturbances seen in patients with SLE. These abnormalities in granulocyte function may be important, predisposing factors for infection in patients with active SLE.
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