Hypoplasia of the humeral trochlea

Radiographic studies of three cases of hypoplasia of the humeral trochlea were done. Several other anomalies were also detected, including a hypoplastic capitellum in case 2, a hyperplastic radial head in cases 2 and 3, and bulging of the loose joint capsule in case 3. Operations in cases 1 and 3, disclosed that ganglions and fibrous septa compressed the ulnar nerve. The cause of ulnar nerve palsy in patients with hypoplasia of the humeral trochlea is thought to be associated with the high incidence of ganglions in hypoplastic elbow joints. The ganglion may play a role.     

Cytoskeleton-dependent activation of the inducible nitric oxide synthase in cultured aortic smooth muscle cells.

1. Vascular endothelial and smooth muscle cells generate nitric oxide (NO) via different nitric oxide synthase (NOS) isozymes. Activation of the endothelial constitutive NOS (ecNOS) contributes to the maintenance of cardiovascular homeostasis, whereas expression of the endotoxin- and cytokine-inducible pathway (iNOS) within the vascular smooth muscle is thought to be responsible for the cardiovascular collapse which occurs during septic shock and antitumour therapy with cytokines. Since the cytoskeleton is involved in the activation of certain genes and in some effects of endotoxin in macrophages, we investigated the role of microtubules and microfilaments in the activation of the NO pathway in cultured vascular cells. 2. Depolymerization of microtubules by either nocodazole or colchicine prevented lipopolysaccharide (LPS)- and interleukin-1 beta-induction of NO-dependent cyclic GMP accumulation. Steady state levels of iNOS mRNA, assessed by Northern blot and RT-PCR, and iNOS protein, assessed by Western blotting, were also decreased by either colchicine or nocodazole treatment. 3. Taxol enhanced microtubule polymerization alone, and prevented microtubule depolymerization elicited by nocodazole and colchicine. Associated with its effect on microtubule assembly, taxol prevented the inhibitory effects of nocodazole and colchicine on cyclic GMP accumulation and iNOS mRNA levels. 4. Disruption of microfilaments by cytochalasins had no inhibitory effect on the activation of the inducible NO pathway. 5. In contrast to cytokine-stimulated smooth muscle cells, modulation of either microtubule or microfilament assembly did not affect the constitutive NO pathway in endothelial cells, as endothelial cell- and NO-dependent cyclic GMP accumulation in endothelial-smooth muscle co-cultures remained unchanged. 6. Our findings demonstrate that microtubules play a prominent role in the activation of the inducible NO pathway in response to inflammatory mediators in smooth muscle cells but not of the constitutive synthesis of NO in endothelial cells.     

Effects of Pyridoxalated Hemoglobin Polyoxyethylene Conjugate and Stroma-free Hemoglobin on Renal Vascular Responsiveness to Vasoactive Substances in Isolated Perfused Rat Kidney

Abstract: The effects of pyridoxalated hemoglobin polyoxyethylene conjugate (PHP) and stroma-free hemoglobin (SFH) on vascular responsiveness to various vasoactive substances were examined in isolated perfused rat kidneys. The kidneys isolated from rats were perfused with 6% PHP, 6% SFH, and 6% hydroxyethylstarch (HES) solution at a constant flow rate. Vascular responsiveness to acetylcholine (ACh), nitroglycerin (NG), norepinephrine (NE), and angiotensin-II (ANG-II) was examined by measuring the perfusion pressure (PP). Effects of inhibition of endothelium-derived relaxing factor (EDRF) by N^G-monomethyl L-arginine (L-NMMA) on NE-induced and ANG-II-induced renal vascular responses were examined. ACh and NG induced a dose-dependent decrease in perfusion pressure (PP) in all groups. NE and ANG-II induced an increase in PP in all groups, but NE-induced and ANG-II-induced responses in the PHP-perfused and SFH-perfused groups were significantly larger than those in the HES-perfused group. L-NMMA did not alter vascular responsiveness to NE and ANG-II. These results indicate that PHP and SFH do not inhibit EDRF induced by ACh, but hemoglobin moiety per se does augment the vascular responsiveness to NE and ANG-II in the isolated perfused rat kidney.     

Effects of AETT-Induced Neuronal Ceroid Lipofuscinosis on Learning Ability in Rats

Abstract: The behavioral effects of ceroid-lipofuscin accumulation, induced by intraperitoneal administration of acetyl-ethyl-tetramethyl-tetralin (AETT) in Wistar rats for 3 months, were examined in the present studies. A significant increase in neuronal ceroid-lipofuscin was demonstrated neuropathologically as well as morphometrically. Although the AETT-intoxicated rats showed neither alteration of locomotor activity nor shock sensitivity, a significant impairment of learning ability, especially an acquisition trial in passive avoidance tests, was observed. Results of the present studies indicate the possibility that a diffuse lipofuscin accumulation causes a learning impairment in rats. The results also imply the possibility of a significant role of age-related lipofuscin accumulation in the dementing processes of human especially in the elderly.     

The significance of the heparin precipitable fraction in lung diseases]

The authors recently experienced a case of idiopathic interstitial pneumonia (IIP) that exhibited skin ulcers due to increased heparin precipitable fraction (HPF) in plasma. This case prompted us to investigate the occurrence and significance of HPF in interstitial pneumonia (IP). The subjects included patients with IIP (acute exacerbation 6 cases, chronic active stage 12 cases), IP associated with collagen vascular disease (CVD) (9 cases) and granulomatous lung diseases (7 cases). The data indicated that all of the cases with acute exacerbation of IIP exhibited increased plasma HPF values (218-951 mg/dl) compared to those of normal controls (less than 180 mg/dl). In contrast, the values ranged within normal limits in all of the cases with IP associated with CVD. In a companion study, we measured plasma HPF values in patients with lung cancer, bacterial pneumonia and diffuse panbronchiolitis. It was found that 22% of the subjects showed increased plasma HPF values. We also investigated whether there were correlations between plasma HPF and various inflammatory parameters. The data revealed that there were correlations between HPF and ESR, CRP, alpha 1-globulin, alpha 2-globulin, complement (C3) or fibrinogen. However, there was no correlation between HPF and fibronection. These results suggest that plasma HPF is valuable to evaluate the acute exacerbation of IIP, although the elevation of plasma HPF levels is not specific.