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.     

CROMAKALIM SUPPRESSES HYPERTONIC SALINE-INDUCED RENAL VASOCONSTRICTION IN ANAESTHETIZED DOGS

1. Intrarenal arterial infusion of hypertonic saline (HS) transiently increased and then gradually reduced renal blood flow (RBF) in anaesthetized dogs. Glomerular filtration rate (GFR) but not filtration fraction decreased at the end of the infusion. 2. In the presence of a potassium channel opener cromakalim (0.3 μg/kg per min), HS infusion failed to reduce RBF; the initial increase in RBF was maintained throughout the infusion. Since cromakalim also prevented the decrease in GFR, HS infusion lowered filtration fraction. 3. The results suggest that cromakalim inhibits both pre-and postglomerular vasoconstriction induced by HS infusion.     

Angiogenesis factors in ocular tissues of normal rabbits on chorioallantoic membrane assay

Recent studies have shown that angiogenesis-stimulatory factors exist in ocular tissues and play a crucial role in the development of some eye disorders such as diabetic retinopathy. However, there are few reports that studied location of angiogenesis factors in ocular tissues of experimental animals. We studied angiogenesis factors in ocular tissues of normal rabbits by chorioallantoic membrane (CAM) assay. Extracts derived from the retina, iris-ciliary body and optic nerve showed an evident activity of angiogenesis. Retinal extracts at 10 micrograms showed a strong angiogenic activity in 50% of CAMs (p less than 0.01). On the other hand, bovine serum albumin which is heterogeneous protein showed only a slight angiogenic activity at a high concentration (1,000 micrograms). The iris-ciliary body and optic nerve showed also an angiogenic activity as did the retina. Extracts from the heart, liver and serum showed no activity of angiogenesis. Thus, angiogenic activity was strongly present in the ocular tissues, especially in retina of the normal rabbits.     

Evaluation of myocardial disorders in patients with dilated cardiomyopathy and left ventricular eccentric hypertrophy--by 201Tl myocardial SPECT]

201Tl myocardial SPECT was performed in cases of dilated cardiomyopathy and valvular heart disease with left ventricular eccentric hypertrophy, and the two groups were compared from the standpoint of the mechanism of onset of myocardial disorders. Significant coefficients of correlation were seen between the Tl score and LVDd (r = 0.792, r = 0.785) and Tl score and LVEF (r = -0.634, r = -0.555) in both dilated cardiomyopathy and valvular heart disease. In cases of valvular heart disease, significant correlation coefficients (r = -0.756, r = -0.720) between LVDd and r-WR (relative-washout rate), and Tl score and r-WR were observed, but no such correlation was seen in dilated cardiomyopathy. In valvular heart disease, a decrease in myocardial perfusion associated with enlargement of the left ventricle appeared, while in dilated cardiomyopathy, there was a marked decrease in LVEF in proportion to the thallium defect. Therefore, it was assumed that left ventricular wall disorders occur due to myocardial metabolic disorders and coronary microcirculation disorders.     

A patient with severe ventricular tachycardia who was saved by prolonged extracorporeal lung and heart assist]

A 47-y-o man had been suffering from cardiac failure due to refractory ventricular tachycardia (VT) after myocardial infarction. He underwent resection of the left ventricular aneurysm and cryocoagulation of the arrhythmogenic foci. On the 2nd post-operative day, VT often recurred in spite of repeated cardioversion and drug therapy, and threatened his life, even under IABP. Therefore, a veno-arterial bypass route was made and extracorporeal lung and heart assist, ECLHA, was started with a heparin bonded Maxima lung on the following day. Even under ECLHA, VT continued to recur. Cryocoagulation of the VT foci was tried again, without immediate success. A record high dose of beta-blockers, given under the circulatory support by ECLHA, stopped VT on the following day. The patient was weaned from the ECLHA circuit 12 days after the first operation, then from IABP on the 14th day. During the 10 day course of surgeries and ECLHA, the patient had almost 100 defibrillations. But for ECLHA, we may say that the patient couldn't have survived two open heart surgeries, administration of a great amount of beta-blockers, and repeated cardiac arrest without neurological sequelae.     

Glucose as regulator of glucose transport activity and glucose-transporter mRNA in hamster beta-cell line.

To investigate the role of glucose in regulating glucose transporters in pancreatic beta-cells, we studied the hamster clonal beta-cell line HIT-T15, which retains responsiveness to glucose. Northern blot analysis demonstrates that GLUT2 and GLUT1 mRNA are abundant in HIT cells. After a 24-h culture with various concentrations of glucose (0-22.2 mM [0-400 mg/dl]), the GLUT2 mRNA level in HIT cells increased by 40% at 22.2 mM (400 mg/dl) glucose compared with 11.1 mM (200 mg/dl) without a change in mRNA stability. It also decreased proportionally to the reduction of glucose concentration. Glucose deprivation resulted in a decrease of GLUT2 mRNA to an almost undetectable level, with a marked increase in the degradation rate of mRNA. In contrast, the GLUT1 mRNA was not affected by glucose. We show that glucose uptake is highest in HIT cells incubated at 2.8-5.5 mM (50-99 mg/dl) glucose for 24 h, and that levels in cells cultured at 0 mM (0 mg/dl) and 22.2 mM (400 mg/dl) glucose decrease to approximately 20% of the maximum level. This decrease is consistent with the effects of glucose on glucose-stimulated insulin secretion in HIT cells. Our results indicate that glucose is involved in regulating GLUT2 mRNA and glucose uptake activity and that the glucose responsiveness of the insulin secretion correlates with the glucose-induced change in glucose uptake activity in HIT cells.     

Measurement of free and total hydroxyproline by automated flow injection of serum or urine samples from maintenance hemodialysis patients with renal osteodystrophy

An automated measurement of total and free hydroxyproline in serum or urine is presented that uses flow injection analysis. After exclusion of nonspecific substances, hydroxyproline was oxidized by chloramine- T and L-cysteine with Ehrlich's reagent. The linearity obtained was from 3.8μmole/ L to 1.22 mmole/L with good precision (CV <3%). Comparison of the proposed method with HPLC yielded r = 0.939 as the correlation coefficient. Reference intervals of free and total hydroxyproline are 1.4–9.7 μmole/L, 3.8–27.2 μmole/L for serum, and 10.0–72.5 μmole/L, 25.2–303.6 μmole/L for urine, respectively. Serum free and total hydroxyproline levels in renal osteodystrophy patients on maintenance hemodialysis (N = 71) were significantly higher than in controls (P<0.0001). This method is superior to the use of HPLC with regard to stability of the color reaction. The measurement of serum free and total hydroxyproline is a useful marker for therapeutic observation of renal osteodystrophy patients. © 1994 Wiley-Liss, Inc.     

Inhibition of inward rectifier K+ currents by angiotensin II in rat atrial myocytes: lack of effects in cells from spontaneously hypertensive rats.

We examined the effects of angiotensin II (Ang II) on inward rectifier K+ currents (IK1) in rat atrial myocytes. [125I]Ang II-binding assays revealed the presence of both Ang II type 1 (AT1) and type 2 (AT2) receptors in atrial membrane preparations. Ang II inhibited IK1 in isolated atrial myocytes with an IC50 of 46 nmol/l. This inhibition was abolished by the AT, antagonist RNH6270 but not at all by the AT2 antagonist PD123319. Treatment of cells with pertussis toxin or a synthetic decapeptide corresponding to the carboxyl-terminus of Gialpha-3 abolished the inhibition by Ang II, indicating the role of a Gi-dependent signaling pathway. Accordingly, Ang II failed to inhibit IK1 in the presence of forskolin, dibutyryl-cAMP or protein kinase A catalytic subunits. In spite of the increased binding capacities for [125I]Ang II, Ang II failed to affect IKI in cells from spontaneously hypertensive rats (SHR). AT, immunoprecipitation from atrial extracts revealed decreased amounts of Gialpha-2 and Gialpha-3 proteins associated with this receptor in SHR as compared with controls. The reduced coupling of AT, with Gialpha. proteins may underlie the unresponsiveness of atrial IK1 to Ang II in SHR cells.     

Pulmonary surfactant proteins and lipids as modulators of inflammation and innate immunity

Objectives: The pulmonary surfactant system of the human lung consists of unique lipids and proteins that contribute to the biophysical and innate immune properties of the organ. Surfactant protein A (SP‐A) is an oligomeric protein consisting of 18 protomers with collagen and lectin–like domains that recognizes glycoconjugates, lipids and protein determinants on both host cells and invading microorganisms. The authors examined the interaction of SP‐A with Mycoplasma pneumoniae and the influence of the protein upon the innate immune response to the bacteria. Methodology: The authors quantified SP‐A interaction with bacteria using ELISA, and identified the major surface ligand by thin layer chromatography, HPLC and mass spectrometry. The inflammatory response of human and rat macrophages was measured by quantifying tumour necrosis factor‐α secretion using ELISA, and nitric oxide production. Results: SP‐A bound the bacteria with high affinity and enhanced the inflammatory response of human and rat macrophages to the organism and its membranes. Analysis of the interaction of SP‐A with the bacteria revealed that the major ligand was a phospholipid. The lipid ligand was purified by a combination of thin layer and HPLC, and identified by mass spectrometry. The mass spectrometry demonstrated that the SP‐A reactive lipid consisted of several disaturated molecular species of phosphatidylglycerol (PtdGro). Additional experiments were performed to determine if disaturated PtdGro was capable of interfering with the action of SP‐A as an inhibitor of bacterial lipopolysaccharide‐induced inflammatory mediator production by macrophages. The disaturated PtdGro failed to alter the anti‐inflammatory action of SP‐A but unexpectedly these same studies revealed that unsaturated PtdGro can modify the host response to lipopolysaccharide. Conclusions: These findings reveal that both the lipids and proteins of pulmonary surfactant play a role in regulating the host response to invading microorganisms.