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J Gelin

Publications and source records attributed to J Gelin.

At least 37 records · Page 2Linked to original sources

Anticachectin/tumor necrosis factor-alpha antibodies attenuate development of cachexia in tumor models.

C57BL/6 mice bearing either a transplantable methylcholanthrene-induced sarcoma or Lewis lung adenocarcinoma were passively immunized every other day with a rabbit immunoglobulin fraction raised against murine cachectin/tumor necrosis factor-alpha. Mice bearing methylcholanthrene-induced sarcoma developed tumor-associated hypophagia that was attenuated by anticachectin immunoglobulin treatment. In the same tumor-bearing animals, anticachectin treatment also significantly reduced the extent of carcass protein and fat loss, and reduced tumor weight. Mice bearing Lewis lung adenocarcinoma did not develop significant anorexia or carcass lean tissue depletion as tumor growth progressed, but they lost carcass lipid. Treatment of Lewis lung adenocarcinoma bearing mice with anticachectin antibodies diminished the degree of carcass lipid depletion and prevented plasma hypertriglyceridemia. However, in both tumor models, anticachectin treatment did not affect either the development of anemia, hypoalbuminemia or the increase in serum amyloid P concentrations seen with increasing tumor burden. We conclude that an endogenous cachectin response, inhibitable by exogenously administered antibody, contributes to anorexia and to changes in body fat and protein metabolism in these tumor-bearing animals. Neutralizing endogenous cachectin production with antibodies offers the potential to reduce tissue wasting that is frequently associated with neoplastic disease, but it does not appear to affect all of the hematologic and acute phase responses in these murine tumor models.

Adenocarcinoma↗

Appearance of hybridoma growth factor/interleukin-6 in the serum of mice bearing a methylcholanthrene-induced sarcoma.

Serum concentrations of hybridoma growth factor/interleukin-6 progressively increased in mice bearing a transplantable methylcholanthrene-induced sarcoma with tumor growth. Elevated HGF/interleukin-6 concentrations were also positively correlated with increased serum concentrations of the hepatic acute phase reactant protein, amyloid P. Daily Indomethacin treatment of sarcoma-bearing mice prolonged survival and reduced the magnitude of the serum amyloid P response, but failed to attenuate either tumor growth or serum HGF/interleukin-6 responses. Since previous studies have demonstrated that neither interleukin-1 nor tumor necrosis factor-alpha can be detected in the serum of these sarcoma-bearing mice, and that HGF/interleukin-6 is a principal mediator of the hepatic acute phase response, we conclude that circulating HGF/interleukin-6 may contribute significantly to the host responses which accompany experimentally-introduced cancer. Furthermore, prostanoid inhibition does not appear to regulate the synthesis and release of HGF/interleukin-6 during tumor growth.

Animals↗

Regulation of food intake and hepatic protein synthesis by recombinant-derived cytokines.

During inflammation, activated monocytes and lymphocytes synthesize and release many soluble protein mediators, such as interleukin (IL) 1, tumor necrosis factor-alpha, and IL-2. It is presently unclear which cytokines, if any, contribute to the anorexia and hepatic protein changes frequently seen during inflammation. To evaluate their potential role, food intake and liver and plasma protein synthesis were determined in both endotoxin-sensitive C57Bl/6j mice and endotoxin-resistant C3H/HeJ mice given either crude secretory products of Staphylococcus albus-stimulated human blood monocytes or murine recombinant IL-1-alpha, human recombinant IL-1-alpha or -beta, human recombinant tumor necrosis factor-alpha, or human IL-2. When given intraperitoneally to healthy animals, 2,000 lymphocyte-activating factor U/day of secretory products of activated human blood monocytes or recombinant murine IL-1-alpha depressed spontaneous food intake by 42 and 53%, respectively. Human IL-1-alpha and -beta and human tumor necrosis factor-alpha produced smaller reductions in food intake. In contrast, human IL-2, when given in equimolar quantities, had no appreciable effect on food intake or body weight. Administration of crude secretory products of activated blood monocytes, recombinant IL-1, or tumor necrosis factor-alpha increased liver weight, protein, and RNA content. In addition, plasma protein synthesis was significantly increased, as were serum amyloid P concentrations. Administration of recombinant tumor necrosis factor-alpha resulted in IL-1 production by peritoneal adherent cells. However, IL-2 had no effect on any hepatic parameter.

Animals↗

Plasma protein synthesis in experimental cancer compared to paraneoplastic conditions, including monokine administration.

During tumor growth, there are characteristic alterations in the concentration and synthesis of various plasma proteins. The purpose of this study was to evaluate whether these changes are unique to a tumor-bearing state, or rather, they represent a generalized response to a paraneoplastic state mediated by the release of monokines or protein-calorie malnutrition. Plasma protein synthesis and concentrations in mice bearing a transplantable fibrosarcoma were compared to animals receiving either a terpentine abscess, Corynebacterium parvum administration, calorie-protein depletion, or administration of the recombinant-derived monokines, murine interleukin 1 alpha or human tumor necrosis factor-alpha. Tumor-bearing animals showed a significant increase in total plasma protein synthesis that was similar in magnitude to the increase seen following a terpentine abscess or after administration of interleukin 1 or tumor necrosis factor-alpha. Similarly, the pattern of protein synthesis and concentration, as determined by isoelectric focusing or sodium dodecyl sulphate-polyacrylamide gel electrophoresis, were similar, albeit not identical, among tumor-bearing animals and those receiving either a terpentine abscess, C. parvum and monokine administration. Serum amyloid P concentrations were markedly elevated in tumor-bearing animals, as they were in animals after a sterile abscess and following interleukin 1 administration, as well as to a lesser extent tumor necrosis factor-alpha administration. We can therefore conclude that the majority of changes in plasma protein concentration and synthesis seen in this tumor-bearing model are similar to those seen during an acute inflammation and can be reproduced to a large extent by the administration of the monokines, interleukin 1 alpha or tumor necrosis factor-alpha.

Abscess↗

Interleukin 1 and tumor necrosis factor do not regulate protein balance in skeletal muscle.

Recent studies have claimed that interleukin 1-containing preparations increase skeletal protein degradation similar to that seen during infection and inflammation. However, preparations employed have contained other products of activated macrophages, including tumor necrosis factor-alpha. In the present report, we investigated the capability of recombinant-derived murine and human interleukins 1-alpha and 1-beta and human tumor necrosis factor-alpha to affect skeletal protein synthesis and degradation both in vitro and in vivo. Partially purified products of Staphylococcus albus-stimulated human blood monocytes increased skeletal protein degradation both in vivo and in vitro. However, none of the recombinant interleukin 1 nor the human tumor necrosis factor-alpha preparations had any impact on skeletal protein balance. Both recombinant interleukin 1 and tumor necrosis factor-alpha stimulated the production of prostaglandin E2 (PGE2). Furthermore, a polyclonal antibody to human interleukin 1 eliminated the lymphoproliferative response to partially purified monocyte preparations (interleukin 1 activity), but failed to abrogate the increased skeletal protein degradation in vitro. This study demonstrates that although interleukin 1 and tumor necrosis factor-alpha induce a PGE2 response by skeletal muscle in vitro, some macrophage product distinct from either interleukin 1 or tumor necrosis factor-alpha is responsible for the accelerated skeletal protein degradation seen with partially purified human blood monocyte products. Elevated PGE2 levels do not appear to regulate skeletal protein balance in vitro.

Animals↗

Circulating interleukin 1 and tumor necrosis factor during inflammation.

It is proposed that interleukin 1 (IL 1) and tumor necrosis factor (TNF) alpha play central roles in the host's response to inflammation. Yet circulating concentrations have not been frequently measured in many inflammatory states. Serum levels of IL 1 and TNF were evaluated in mice with a tumor, sterile inflammation, endotoxinemia, or generalized peritonitis where an acute-phase protein response was documented. In tumor-bearing mice, no IL 1 or TNF could be detected despite marked increases in the serum concentration of the acute-phase reactant protein, amyloid P. In mice with peritonitis, induced by cecal ligation and perforation, or a turpentine-induced subcutaneous abscess, IL 1 but not TNF could be detected in the serum. Only expansion of the reticuloendothelial system with Corynebacterium parvum and subsequent challenge with endotoxin resulted in serum TNF appearance. The failure to observe IL 1 or TNF in any of the disorders could not be explained by inhibitors. Rather, the data suggest that a hepatic acute-phase protein response can occur during inflammatory states without the appearance of either IL 1 or TNF in the circulation. Circulating levels of both monokines do not appear to be a universal finding in inflammation.

Animals↗

Tumor-host wasting not explained by adrenal hyperfunction in tumor-bearing animals.

This study addressed the question of whether hypercorticism in tumor-bearing animals contributes to the wasting of body fat and lean body mass, particularly that of skeletal muscles. For this purpose, hydrocortisone-substituted nongrowing sarcoma-bearing and control C57BL/6J mice were used that were either adrenalectomized or sham-operated prior to experimentation. Adrenalectomy in itself did not alter food intake or body composition in normal animals. Tumor-bearing mice and pair-weighted control animals had elevated urinary excretion of corticosteroids compared with the urinary excretion in freely fed controls. The malignant tumor induced the well-recognized wasting in tumor-bearing animals, irrespective of the presence of the adrenal glands. Therefore, an elevated corticosteroid production did not account for the wasting of body fat, lean body mass, skeletal muscle proteins, or decreased RNA activity in quadriceps muscles from tumor-bearing animals, although such muscles were sensitive to physiologic doses of injected hydrocortisone (20 micrograms/day). Tyrosine aminotransferase (TAT) activity in liver tissue from tumor-bearing animals was higher than that induced by pharmacologic doses of hydrocortisone in normal animals. Physiologic doses of hydrocortisone induced hepatic TAT activity, but pair-weighed control animals with the same degree of hypercorticism as was found in tumor-bearing animals had normal TAT activity in liver tissue. Although hypercorticism is present in tumor-bearing animals, the results demonstrate that cancer cachexia can start and proceed independently of the adrenal glands. Therefore, adrenal hyperfunction is not the proximate cause for the development of experimental cancer cachexia induced by anorexia.

Adrenal Glands↗

The secretion of cholecystokinin in the gallstone patient before and after removal of a functioning gallbladder.

Cholecystectomy will not always relieve the abdominal symptoms of the patient with gallstones. The functional effects of gallbladder removal in a patient with a patent cystic duct are not known in detail. Studies of the function of the gallbladder and pancreas have suggested feedback mechanisms for the release of cholecystokinin (CCK). A disturbed regulation of CCK release after cholecystectomy might induce pancreaticobiliary and gastrointestinal dysfunctions. In our study the concentrations of CCK in plasma were measured in 17 patients with gallstones. The measurements were taken with gallbladders opacified at cholecystography and with patent cystic ducts at the operation, in the fasting state, and during stimulation before and 17 weeks after the cholecystectomy. The CCK assay used measures sulfated CCK-8, CCK-22, and CCK-33 with equimolar potency but neither nonsulfated CCK nor any gastrins. Emtobil (containing peanut oil and sorbitol) was used for peroral stimulation of the CCK release. The basal concentration of CCK was 4 pmol/L and rose five times during a "test meal." No significant differences were seen in fasting or stimulated concentrations of plasma CCK before and after the cholecystectomy. Thus cholecystectomy in gallstone patients with functioning gallbladders does not seem to influence the regulation of CCK release.

Adult↗

Gallstones, cholecystectomy, and duodenogastric reflux of bile acid.

It has earlier been suggested that cholecystectomy, by eliminating the reservoir function of the gallbladder, will induce reflux of bile to the stomach. In the present study 23 patients were studied for duodenogastric reflux of bile acid before and 3 months after cholecystectomy. At the test the gastric contents were continuously aspirated via a nasogastric tube, collected at 15-min intervals for 2 h in the fasting patient, and analyzed for volume and bile acid concentration. The results were compared with those in 14 control subjects. Significant duodenogastric reflux of bile acid (greater than 100 mumol/h) was seen more frequently in gallstone patients than in controls. This is explained by a high prevalence of bile acid reflux in patients with a reduced or absent opacification of the gallbladder at cholecystography. Cholecystectomy increased the prevalence of bile acid reflux in the patients with well-opacified gallbladders at cholecystography. The duodenogastric reflux of bile acid in patients with a poor filling of the gallbladder at cholecystography was not further enhanced by cholecystectomy. It is concluded that gallstone patients have an increased tendency to duodenogastric reflux of bile acid. This tendency is further enhanced by removal of a functioning gallbladder. The findings may explain some of the symptoms in patients with gallstones. The reflux may also be responsible for symptoms in the so-called postcholecystectomy syndrome.

Adult↗

Cholecystokinin secretion after oral Emtobil, a gallbladder-contracting formula.

Oral Emtobil, a liquid preparation of sorbitol and peanut oil, has been used in roentgenological practice for several years. Emptying of an opacified gallbladder is seen within 15 min after intake of 100 ml of this solution. The main physiological factor responsible for contraction of the gallbladder is cholecystokinin (CCK). In the present study plasma concentrations of CCK in fasting, healthy subjects were studied in response to oral Emtobil. The radioimmunoassay used measures sulphated CCK-8 and CCK-33 with equimolar potency. Neither non-sulphated CCK nor any gastrins are measured. The average concentration, after an overnight fast in nine healthy subjects without gallstones, was 1.2 pmol/l. A peak concentration was seen within 30 min after 'the test meal' and averaged 8 pmol/l. It is suggested that oral Emtobil contracts the gallbladder by release of CCK. Since Emtobil induces a fast and marked rise in the plasma concentration of CCK, it may be used in test procedures to estimate the secretion of CCK.

Administration, Oral↗

High-resolution real-time sonography of the adrenal glands: a routine examination?

The feasibility of imaging the adrenal glands during routine upper abdominal examinations was studied for 100 consecutive patients, 47 males and 53 females. The mean patient age was 46 years and the mean weight 63 kg. The suprarenal areas were scanned in a slightly oblique frontal plane through the intercostal spaces with the patient recumbent. The right adrenal gland was detected in 92 per cent of the patients, with a mean examination time of less than one minute. Visualization of the left adrenal gland was more difficult and was successful in only 71 per cent, even where additional views in the right lateral decubitus or erect position were added. The mean examination time on the left was 2 1/2 minutes. Complete visualization of the adrenal gland is impossible in one single plane because of the complex shape of the organ, which necessitates multiple contiguous scan planes. In 13 per cent of the visualized adrenals, cortex and medulla could be differentiated.

Adolescent↗

Sonographic appearance of normal lymph nodes.

Normal lymph nodes appear sonographically as somewhat flattened hypoechogenic structures. Chronic inflammation, obesity, and degenerative changes leading to benign fatty replacement of lymphoid tissue are responsible for the variations seen with high-resolution ultrasonography. These fatty deposits, beginning in the center of the lymph node and progressing toward the periphery, are easily recognized as highly reflective defects in the hypoechogenic lymphoid tissue.

Humans↗

Sonographic diagnosis of intraluminal bile duct neoplasm: a report of 3 cases.

Intraluminal growing tumors of the bile duct are uncommon causes of jaundice. The sonographic appearance of 2 hilar cholangiocarcinomas or Klatskin tumors and a benign extrahepatic biliary cystadenoma is described. Compared to contrast studies of the bile ducts, sonography better defined the intraductal character of the neoplasms. However, the ultrasound appearance did not allow differentiation between the adenocarcinomas and the benign cystadenoma.

Adenocarcinoma↗

[Psychological aspects observed during function rehabilitation of coronary patients].

The authors have studied the influence of rehabilitation on the anxiety of 93 patients with myocardial infarction. The index of anxiety was measured objectively, as were the various primary factors. The change in these various factors has been favourable one in those patients who have had the benefit of complete rehabilitation. There seems to be a correlations between this change and the quality of rehabiltation as judged by the results of the exercise test which is undertaken at the end of it. Other psychological factors were also studied: the patient's estimate of his anxiety, of the rehabilitation, and of his own relationship to his illness, the factors which finally released his from the anxiety, and the features taken as a while.

Anxiety↗