Postoperative changes in the spinal cord in cervical myelopathy demonstrated by magnetic resonance imaging.

The relation between improvement of myelopathy achieved by surgery and postoperative spinal cord morphologic changes was investigated by magnetic resonance imaging in 51 patients with cervical myelopathy. In 22 patients, the cord indentation disappeared completely (Type I), in 23 it partially disappeared (Type II), and in 3 it remained unchanged (Type III). In three patients the cord enlarged after surgery (Type IV). With the exception of Type IV, increased restoration of cord morphology paralleled improvement in the myelopathy, suggesting that morphologic changes closely reflect neurologic recovery. In Type IV, notwithstanding the peculiar postoperative reaction, improvement was relatively good, and shrinkage of the cord enlargement was seen after 1 year. This kind of postoperative change has not been demonstrated previously by other conventional imaging methods.     

Gallium scintigraphy in patients with adult T-cell leukemia lymphoma

Gallium scintigraphy was evaluated in 25 patients with adult T-cell leukemia lymphoma (ATLL). Anterior and posterior images were obtained at 72 h after administration of 3 mCi ⁶⁷Ga-citrate using a gamma camera (Maxi-Camera 400T, General Electric Co.) with a medium energy standard parallel hole collimator. Abnormally high accumulations were observed in 17 out of 25 cases (superficial lymph node, 8; hilar and mediastinal lymph node, 7; paraaortic lymph node, 2; lung, 9; liver, 1; bone, 1). There were 10 malignant lesions detected by ⁶⁷Ga scintigraphy in 9 out of 17 cases (superficial lymph node, 1; hilar and mediastinal lymph node, 6; paraaortic lymph node, 1; liver, 1; bone, 1). White blood cell count and serum LDH levels were raised in patients with abnormally high accumulations of ⁶⁷Ga. In conclusion, ⁶⁷Ga scintigraphy seemed to be a useful examination to detect malignant lesions in patients with ATLL.     

Direct injections of calcitriol into enlarged parathyroid glands in chronic dialysis patients with severe parathyroid hyperfunction

Summary: Severe secondary hyperparathyroidism in chronic dialysis patients has been recently treated by supraphysiological concentration of calcitriol achieved through pulse therapy. However, there are many patients resistant to this therapy, who usually have larger parathyroid gland(s). to overcome this resistance, calcitriol was injected directly into the enlarged glands under ultrasonographic guidance. We injected 70–90% of the calculated gland volume of calcitriol solution (1 μg/mL) into the glands of 7 patients three times per week for 2 weeks. the parathyroid hormone (PTH) levels decreased significantly after 2 weeks of direct injections of calcitriol. Following a further 4 weeks of calcitriol pulse therapy, PTH levels remained suppressed and serum alkaline phosphatase activity and the volume of parathyroid glands also decreased. During the long-term follow up, five patients remained well controlled with calcitriol pulse therapy, while two patients needed ethanol injections to control hyperparathyroidism. Although we could not completely rule out a toxic effect of the vehicle, direct injection of calcitriol into parathyroid glands may be another treatment option for chronic dialysis patients. Our data further support the important role of resistance of parathyroid cells to calcitriol in the pathogenesis of parathyroid hyper function in uraemic patients.     

In vivo selection of tumorigenic subline from non-tumorigenic human gastric carcinoma cells: in relation to proliferative properties in vivo and in nude mice

Human gastric carcinoma cells from one of three long-term cultured cell lines (HPE-GAC-T) were injected into peritoneal cavities of BALB/c mice. The surviving celss in vivo were collected 3 days later. Following brief cultivation in vitro, those cells were reinjected into mice by the same route. This procedure was repeated 3 times. The cultured cancer cells recovered from the mice on the 3rd passage, at a 92.5% recovery rate, showed xenotransplantability in BALB/C nu/nu mice by subcutaneous injection. This subline (GAC-T.M-2) can be maintained in vitro but not in vivo while maintaining heterotransplantability. Three original cancer cell lines did not show tumorigenicity in nude mice. Animal passages by the same protocol failed to select tumorigenic sublines from the other cell lines (HPE-GAC-2 and -3). Factors affecting tumorigenic capacity of cancer cells in nude mice were studied in vivo and in vitro by comparing the properties of GAC-T.M-2 and parental cancer cells (GAC-T.O). Treatment of the hosts by injection of anti-asialoGM1 antibody or cyclophosphamide, adult thymectomy of BALB/c mice, and 400 rads whole body irradiation did not enhance the growth of either GAC-T.M-2 or -T.O cells. There was no detectable difference between in vitro growth properties of the original and variant cells at a rather high cell density. However, at a low cell density GAC-T.M-2 cells showed a higher cell growth rate and increased [3H] thymidine incorporation and possessed higher colony forming activity in the liquid medium than their parental cells. High dense expression of epidermal growth factor (EGF) receptors was evident equally in both GAC-T cells, however, GAC-T.M-2 cells were more sensitive to down-regulation by EGF in culture. Tumor cells of HPE-GAC-2 and -3 lines expressed minimum amount of EGF receptors on their cell surfaces and were refractory to additional EGF in culture. The results indicate that growth factors and their receptors are responsible for tumorigenicity in nude mice.     

Effects of glucose infusion on cerebral cortical glucose and lactate concentrations during endotoxemia in rats.

Hypoglycemia has been observed in several species before death from endotoxemia. Although several studies have emphasized the importance of maintaining brain glucose at normal concentration during endotoxemia, the effect of glucose infusion on cerebral glucose metabolism has not been studied. Accordingly, the effects of glucose infusion on interstitial glucose and lactate concentrations in the cerebral cortex during endotoxemia were studied in 22 Wistar rats. Cerebral glucose and lactate were measured at 30-min intervals for 4 h using microdialysis. Animals were divided into four groups: 1) saline-infused control (n = 5); 2) saline-infused endotoxemia (n = 7); 3) glucose-infused control (n = 5); and 4) glucose-infused endotoxemia (n = 5). In groups 2 and 4, endotoxemia was induced by intravenous injection with E. coli lipopolysaccharide B (5 mg.100 g-1). One hour after endotoxin administration, saline or 50% glucose was infused at a flow rate of 0.5 ml.100 g-1.h-1 for 3 h. Endotoxin induced a significant increase (P less than 0.05) in blood glucose in the saline-infused rats, which survived for 4 h (n = 5), from 91.6 +/- 15.4 mg.100 ml-1 at baseline to 136.3 +/- 23.3 mg.100 ml-1 (149%) at 1 h, followed by a gradual decrease (to 63% of the basal concentration at 4 h). Similar changes were observed in brain glucose (14.9 +/- 1.9 mg.100 ml-1 baseline, 175% of baseline at 2 h, and 57% of baseline at 4 h).(ABSTRACT TRUNCATED AT 250 WORDS)     

Non-invasive imaging diagnosis of left renal vein compression causing hematuria. Part 2. CT

Left renal veins of 77 patients were examined by computed tomography (CT) to evaluate its usefulness in determining the left renal vein compression which is causing renal bleeding. From CT image, left renal vein compression was observed in 6 (86%) of the 7 cases which had been classified as idiopathic renal bleeding, in 9 (21%) of the 42 cases which had urinary tract diseases causing hematuria, and in 3 (11%) of the 28 cases which did not have hematuria. In 15 of the 18 cases of left renal vein compression, left renal vein was compressed between the superior mesenteric artery and the abdominal aorta, showing so-called nutcracker phenomenon. In the remaining 3 cases, however, the superior mesenteric artery provided sharp delineation from the abdominal aorta. The superior mesenteric artery and the abdominal aorta made the mean angle of 35.5 degree in patients with normal left renal vein, the mean angle of 45.4 degrees in those with left renal vein compression without nutcracker phenomenon, and the mean angle of 11.9 degrees in those with nutcracker phenomenon. CT was superior to ultrasonography, in revealing left renal vein compression.     

‘Ischemic tolerance’ phenomenon detected in various brain regions

We investigated the effects of mild and non-lethal ischemic insult on neuronal death following subsequent lethal ischemic stress in various brain regions, using a gerbil model of bilateral cerebral ischemia. Single 10-min ischemia consistently caused neuronal damage in the hippocampal CA1, CA2, CA3 and CA4, layer III/IV of the cerebral cortex, dorsolateral part of the caudoputamen and ventrolateral part of the thalamus. On the other hand, in double ischemia groups, 2-min ischemic insult 2 days before 10-min ischemia exhibited significant protection in the CA1 and CA3 of the hippocampus, the cerebral cortex, the caudoputamen and the thalamus. Five-min ischemic insult 2 days before 10-min ischemia also showed protective effect in the same areas as those of 2-min ischemia except for the CA1 region of the hippocampus, while 1-min ischemic insult exhibited no protective effect in any brain regions. In the immunoblot analysis, both 2- and 5-min ischemia caused increased synthesis of heat shock protein 72 (HSP 72) in the hippocampus, but 1-min ischemia did not. The present study demonstrated that the ‘ischemic tolerance’ phenomenon was widely found in the brain and also suggested that ischemic treatment severe enough to cause HSP 72 synthesis might be needed for induction of ‘ischemic tolerance’.