PURPOSE: The purpose of this study was to assess the prevalence and color Doppler sonographic characteristics of perforating vessels-small arteries and veins connecting the intrarenal vasculature with the capsular plexus-in healthy subjects, in hypertensive patients, and in patients with renal failure due to hypertensive nephroangiosclerosis or ischemic nephropathy. METHODS: Fifteen healthy subjects 24-34 years old, 15 healthy subjects 68-80 years old, 25 hypertensive patients, 25 patients with hypertension and chronic renal failure (15 mild, 10 severe), and 12 patients with hypertension and chronic renal failure and acute renal insufficiency due to ischemic nephropathy underwent color Doppler sonography of both kidneys. RESULTS: The few perforating arteries in healthy and hypertensive patients had various resistance indices and flow toward the capsule. Perforating veins in these patients were much more common than perforating arteries. Perforating arteries with a lower mean resistance index than the mean interlobar resistance index and flow toward the capsule were detected in 76% of kidneys in the patients with mild chronic renal failure and in 20% of those in patients with severe chronic renal failure. Only a few perforating veins were seen in patients with chronic renal failure. In 64% of the kidneys with renal artery stenosis detected in the patients with chronic renal failure complicated by acute renal insufficiency, there were perforating arteries with flow toward the kidney and a mean resistance index higher than the mean interlobar resistance index. CONCLUSIONS: Perforating vessels are recognizable using color Doppler sonography both in healthy subjects and in patients with renal failure. The prevalence and flow characteristics of perforating vessels differ between healthy subjects, patients with mild and with severe chronic renal failure, and patients with chronic renal failure complicated by acute renal insufficiency caused by renal artery stenosis.

Adult↗

PubMedDate not supplied

Mycobacterium tuberculosis heat shock protein 10 increases both proliferation and death in mouse P19 teratocarcinoma cells.

Exogenously added Mycobacterium tuberculosis Hsp10, either synthetic or recombinant, but not other related heat shock proteins (GroES from Escherichia coli or bovine Ubiquitin), increases apoptosis in serum-deprived P19 mouse teratocarcinoma cells. The effect is dose-dependent, with a bell-shaped curve and peak activity at 10(-9) M (maximal effect: 62.9 +/- 17.7% increase, mean +/- SD, n = 10) and is specifically inhibited by a polyclonal antibody raised against the synthetic protein. On the other hand, when the same cells are exponentially growing, M. tuberculosis Hsp10 increases cell proliferation with a bell-shaped dose-response curve and a moderate decrease in potency (peak-activity at 10(-8)-10(-7) M, with a 43.7 +/- 8.1% increase, mean +/- SD, n = 3). Therefore, it appears that this bacterial protein can exert two opposite effects, behaving either as a death- or as a growth-promoting factor, depending on the conditions of the target.

Animals↗

PubMedDate not supplied

Flunoxaprofen, a new non-steroidal anti-inflammatory drug, does not interfere with prostaglandin synthesis in rat gastric mucosa.

The anti-inflammatory activity and the eicosanoid generation in rat gastric mucosa after a single oral dose of S-(+)-2(4-fluorophenyl)-alpha-methyl-5-benzoxazolacetic acid (flunoxaprofen, 10 mg/kg) or indomethacin (5 mg/kg) were compared. The two compounds, at the dose used, show a similar degree of anti-inflammatory activity (50% inhibition of carrageenan-induced oedema in rat paw). Moreover flunoxaprofen does not modify the formation of 6-keto-PGF1 alpha by rat gastric mucosa in vitro while indomethacin causes 50% inhibition of gastric cyclooxygenase activity. This biochemical change induced by indomethacin is associated with gastric lesions. Chronic treatment of rats with flunoxaprofen (5 or 50 mg/kg p.o. for 15 days) shows an anti-inflammatory activity in the range of 60-70% inhibition in the rat paw oedema test without gastric mucosa damages and prostaglandin synthesis inhibition.

6-Ketoprostaglandin F1 alpha↗

PubMedDate not supplied

Regional production of nitric oxide after a peripheral or central low dose of LPS in mice.

Nitric oxide (NO) plays a key role in the pathophysiology of inflammation and sepsis. The regulation of the peripheral inducible NO synthase (iNOS-responsible for the massive NO synthesis in inflammation) has been extensively studied in sepsis, but little is known about the actual NO production and its dependence on the location of the primary stimulus (endotoxin, LPS). We measured the activation of the NO pathway after a central (intracerebroventricular) or systemic (intravenous) low dose of LPS (2.5 micrograms/mouse) in three ways: the accumulation of its stable end products (nitrites/nitrates) in the circulation, the induction of iNOS mRNA and the decrease in sodium nitroprusside-dependent ADP ribosylation of proteins in the liver and brain. Plasma nitrites/nitrates increased after LPS by either route. iNOS mRNA was induced in the liver after intravenous and, to a lower extent, in the brain after intracerebroventricular LPS. Ex vivo ADP ribosylation was decreased in both organs after both administration routes, although to different degrees (higher in the liver after intravenous and in the brain after intracerebroventricular administration), suggesting that NO had been produced in the periphery and in the brain after both routes of LPS administration, despite the fact that no LPS is expected to reach the brain after peripheral low-dose injection. Our data thus demonstrate a cross-talk between periphery and brain in the regulation of NO by LPS. Additionally, the possibility of iNOS-independent NO synthesis stimulated by LPS is implied by the discrepancy between the amount of local NO production suggested by ADP ribosylation and the iNOS mRNA levels.

Actins↗

PubMedDate not supplied

Coordinate regulation of cholesterol metabolism.

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Absorption↗

PubMedDate not supplied

AFP, CEA, CA 19-9 and TPA in hepatocellular carcinoma.

The present study is based on the assay of four markers (AFP, CEA, TPA, Ca 19-9) using IRMA methods in 36 normal subjects, 44 cirrhosis and 66 HCC patients. Parametric and non parametric tests were used to test differences and correlations. ROC curves and discriminant functions were also elaborated. Normal 95% "cut-off" was determined by the "boostrap" method yielding: CEA 3.4 ng/ml; Ca 19-9 55 U/ml; TPA 58U/l and AFP 5.2 ng/ml. In HCC patients the values of the four markers were, on average, significantly different from those of normal subjects. However, only AFP and TPA exhibited high diagnostic accuracy (90%) for detection of the tumor. Higher than normal mean values for all markers were, also observed in cirrhotic patients. Only AFP yielded effective discrimination between HCC and cirrhosis. The positive prediction for the presence of the tumor on cirrhotic ground was 95% for AFP values higher than 18.5 ng/ml, with a 78% negative predictive value with a 6 ng/ml threshold. Association of AFP with TPA showed only a marginal diagnostic improvement. Results were not improved at all by combining CEA and Ca 19-9 with AFP and/or TPA. In conclusion, AFP is and remains the best marker for HCC and the only one effective in discriminating of HCC from cirrhosis. TPA may be considered a valid alternative if cirrhosis is not present. CEA and Ca19-9 are of no use.

Antigens, Tumor-Associated, Carbohydrate↗

PubMedDate not supplied

[A case of unusual benign neoplasm of the esophagus: cavernous hemangioma].

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Aged↗

PubMedDate not supplied

[Traumatic rupture of the diaphragm (twelve cases) (author's transl)].

Twelve cases of male patients with traumatic rupture of the diaphragm are reported. Eleven involved the left hemidiaphragm, and the twelfth the right. The aetiopathogenetic and anatomical-pathological aspects are discussed, and stress is laid on the importance of early diagnosis. In general, the most effective form of reanimation is prompt surgery, reducing the herniated organs in the abdominal cavity, re-expanding the lungs, and treating the frequent concomitant visceral lesions as each case demands. The criteria followed in selecting the route of access to traumatic lesions of the diaphragm are described; in most of the cases reported, the thoracic route was preferred, often associated with laparotomy.

Accidents, Traffic↗

PubMedDate not supplied

Th1 and th2 responses, HIV-1 coreceptors, and HIV-1 infection.

The Th1/Th2 model provides an interesting paradigm for understanding several pathophysiological processes and possibly for developing new immunotherapeutical strategies. In HIV-1 infection the interaction between the type of HIV-1 strain and the pathway of the ongoing T-cell effector response, despite its complexity, may represent one of the crucial mechanisms in determining the outcome of virus infection. While the possibility of an HIV-1-driven Th1 to Th2 switch of the immune response is still debated, evidence is accumulating to suggest that cytokines produced during an immune response can contribute to promote a selective pressure toward the evolution of HIV-1 viral strains with different tropism. This article summarizes the results of our recent studies in which the expression of CCR5 and CXCR4 HIV-1 co-receptors, as well as the activity of R5- or X4- tropic strains of HIV-1 in different in vitro models of Th1/Th2 polarization was analyzed.

Acquired Immunodeficiency Syndrome↗

PubMedDate not supplied

[Case report: reversible acute renal failure following therapy with both ketorolac (non-selective non-steroidal anti-inflammatory drug NSAID) and celecoxib (COX-2 selective) in the same patient].

BACKGROUND: We present the case of acute renal failure complicating the course of therapy with both ketorolac (non-selective Non-Steroidal Anti-inflammatory Drug, NSAID), and celecoxib (COX-2 Selective Inhibitor) in an elderly woman with chronic liver disease, heart failure and chronic renal failure. The main effect of NSAIDs is the inhibition of cyclooxygenase (COX), the enzyme involved in prostaglandins synthesis. The nephrotoxicity of NSAIDs is linked to this effect since prostaglandins not only act in response to inflammatory stimuli, but also play a role as modulators of some physiological renal functions. Under conditions of reduced renal perfusion, acute renal failure secondary to NSAIDs use may occur if the vasoconstrictive forces stimulated to maintain the filtrating function are not balanced by prostaglandin-induced vasodilatation. About ten years ago, two COX isoforms were demonstrated: COX-1 whose products are involved in regulating physiological functions and COX-2 which is expressed by a number of inflammatory stimuli. The discovery of molecular differences between COX-1 and COX-2 allowed the development of pharmacological agents selectively inhibiting COX-1 or COX-2. Selective inhibitors of COX-2 are now available. However, COX-1 products are involved in inflammatory reactions, whereas COX-2 products play a physiological role in many tissues and organs, including the kidney. These observations raised many doubts regarding the renal safety of COX-2 Inhibitors before they became commercially available. These doubts have been recently confirmed in the Literature. CONCLUSIONS: The case we report seems to confirm that, in patients at risk, the renal adverse effects of non-selective NSAIDs and of COX-2 Inhibitors could be the same due to the similar physiological role of COX-1 and COX-2-dependent prostaglandins.

Acute Kidney Injury↗