Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P56851 (epididymal)
 11,273 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Scrotal imaging with technetium-99m sodium pertechnetate consists of a radionuclide angiogram and static scrotal scans. Utilization of this study in patients presenting with an acute scrotum can dramatically reduce the number of surgical explorations for acute epididymitis. It can also aid in other aspects of differential diagnosis in patients presenting with either an acutely enlarged and/or painful scrotum or a scrotal mass. Ambiguities in previous descriptions of perfusion through the spermatic and extraspermatic cord vessels are described and distinguished from scrotal perfusion. The clinical and scintigraphic spectrum of testicular torsion, including spontaneous detorsion, early acute testicular torsion, midphase testicular torsion, and late phase or "missed testicular torsion," is discussed and illustrated. The variety of patterns seen in acute epididymitis, including lateral and medial epididymal location, and focal epididymitis are described, as is the appearance of hydrocele as both a primary and secondary entity. The relationship of scrotal imaging to the overall clinical presentation and evaluation of these patients is emphasized in testicular torsion, torsion of the testicular appendages, epididymitis, abscess, trauma, tumor, spermatocele, and varicocele. The techniques, clinical utility, and relationship to radionuclide imaging of Doppler ultrasound and gray scale ultrasound scanning are reviewed. Doppler ultrasound results in many false negative studies in testicular torsion. Gray scale ultrasound is useful in clarifying the nature of scrotal masses.
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PMID:Current status of radionuclide scrotal imaging. 627 19

The melanotic neuroectodermal tumor of infancy (MNTI) is a rare, usually benign, pigmented neuroectodermal tumor which most often involves the maxilla. The authors reviewed seven cases of MNTI, with patient ages of our patients ranged from nine weeks to 18 months; six of the seven were less than six months old at initial diagnosis. Four patients were males, and all were white. One tumor each was located in the femur, the temporal bone, and the epididymis; the remaining lesions occurred in the maxilla. Three of the four maxillary tumors recurred locally; the epididymal and femoral tumors metastasized. Two of these cases had unique clinical or pathologic features. The case of the femoral tumor is remarkable in that it is the first reported one of MNTI presenting in a long bone. This tumor was aggressively malignant; within two months after its discovery, a large mass of similar tumor was formed in the pelvis, and the tumor resulted in the patient's death. To the authors' knowledge, the case of the temporal bone tumor is the first one of MNTI in which neuronal differentiation of the neuroblastic cells is convincingly demonstrated. This finding provides additional evidence in support of the neuroectodermal theory of origin of these neoplasms.
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PMID:Melanotic neuroectodermal tumor of infancy. A review of seven cases. 630 82

The sequential changes in lipid metabolism during tumor growth were evaluated in inbred Lewis rats bearing a mammary adenocarcinoma (AC33). Serum lipids, insulin, glucagon, and liver and adipose tissue lipogenic enzymes were measured in tumor-bearing and control rats after 6, 12, 18, 24, and 32 days of tumor growth. Lipoprotein lipase (LPL) activity in heart, soleus muscle, and epididymal fat pads was also determined. On the sixth day, the activity of LPL was reduced in the adipose tissue and remained lower throughout the duration of the experiment. Serum triglycerides were elevated from the 12th day followed by an increase in free fatty acid levels from the 18th day of tumor growth. These changes were accompanied by a decrease in serum insulin levels in the tumor-bearing rats from Day 12. The presence of the tumor also decreased the activities of some of the lipogenic enzymes in liver and adipose tissue, but these changes occurred at the later time points. On the 24th day, a decrease in fat pad weights was found and characterized by a decrease in fat cell size but not in fat cell number. These results suggest that a defect in clearance, due to the decrease in the activity of adipose tissue LPL, may be responsible for the early development of hypertriglyceridemia during tumor growth. In this study, the alterations in the lipogenic enzymes and LPL cannot be attributed to reduced food intake but may be due to the direct or an indirect effect of the tumor on a hormone such as insulin.
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PMID:Sequential changes in the activities of lipoprotein lipase and lipogenic enzymes during tumor growth in rats. 638 47

The disappearance of 1,3-bis(2-chlorethyl)-1-nitrosourea (BCNU) from plasma, liver, kidney, lung, brain, spleen, tumor tissue and epididymal adipose tissue of Walker 256/B carcinoma-bearing rats and healthy animals was measured by differential pulse polarography after i.v. bolus of the drug. Only BCNU, not its decomposition products, was detected by the polarographic assay. Levels of BCNU in liver of tumor-bearing animals were significantly lower (about 10 times) than those on healthy rats. A bi-exponential fit was used to calculate the kinetics of BCNU in plasma, kidney, lung and brain, but no difference could be found between healthy and Walker tumor-bearing rats. BCNU disappeared faster from adipose tissue of tumor-bearing animals than from normals.
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PMID:Pharmacokinetics of nitrosoureas: levels of 1,3-bis-(2-chloroethyl)-1-nitrosourea (BCNU) in organs of normal and Walker 256/B carcinoma bearing rats after i.v. bolus. 653 91

To determine the effects of different levels of glucose intake on glucose homeostasis, gluconeogenesis, body composition, and tumor growth, we gave 8 days of total parenteral feeding of a defined liquid formula diet to groups of Buffalo rats, with and without a transplantable Morris 7777 hepatoma. The level of glucose intake was held at levels which ranged from 0 to 9.5 g/100 body weight per day while the levels of all other nutrients were held constant. Measurements were made on tumor growth rate, terminal blood plasma glucose and whole blood lactate levels, gluconeogenesis, body and organ weight, muscle nitrogen content, liver glycogen, and urine analysis. Tumor-bearing rats (TB) at low glucose intake but not non-tumor-bearing rats (NTB) were found to be dependent on gluconeogenesis for maintenance of blood glucose homeostasis (normoglycemia). Body weight was dependent on glucose intake level in both TB and NTB rats with glucose intake rates of 5.7 g/100 g/day being the point between weight loss or gain. However, under these feeding conditions, tumor growth rate was not dependent on the glucose intake rate. The weight of epididymal fat pad and the size of fat cells were positively correlated with glucose intake rate in both TB and NTB rats, but the fat pad weight in TB rats showed a greater dependence on the rate of glucose intake than it did in the NTB rats. Glucose intake of 3.8 g/100 g/day or less leads to significant loss of muscle mass and loss of muscle nitrogen (protein) in TB but not in NTB rats. Some liver glycogen was detected in all groups of rats except those TB rats with zero glucose intake. TB rats with high glucose intake (5.7 to 9.5 g/100 g/day) had higher blood lactate and lower urine pH than did NTB rats. Thus, TB rats at low glucose intake (3.8 g/100 g/day or less), as opposed to NTB rats, demonstrated a significant dependence on gluconeogenesis for glucose homeostasis, mobilized more of their liver glycogen, and catabolized more of their muscle proteins to supply the increased energy needs of the growing tumor and to maintain normoglycemia.
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PMID:Parenteral level of glucose intake on glucose homeostasis, tumor growth, gluconeogenesis, and body composition in normal and tumor-bearing rats. 661 59

We determined the contribution from host hepatic and extrahepatic tissues to newly synthesized fatty acids (FA) in the Ehrlich ascites tumor (EAT). We administered 3H2O (subcutaneously) and [14C]glucose (in a test meal) and measured the appearance of radioactivity in plasma triglyceride fatty acids (TGFA) and free fatty acids (FFA) and in tumor total lipid fatty acids (TLFA). Using [14 C]FFA, we selectively labeled epididymal fat TGFA to estimate the FA transport rate from intraperitoneal adipose tissue directly to the tumor. Contributions of four major pathways to newly synthesized FA in EAT were determined by multicompartmental analysis. De novo FA synthesis by EAT accounted for more than 93% of the TLFA radioactivity found in the tumor. Contributions from liver TGFA via plasma TGFA (less than 0.5%), adipose tissue TGFA via plasma FFA (less than 6%), and adipose tissue TGFA via direct intraperitoneal transport of FFA (less than 1%) accounted for less than 7% of all TLFA radioactivity measured in the EAT. Thus the present study establishes that practically all labeled esterified FA in the EAT is derived from de novo synthesis by tumor cells.
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PMID:Liver and adipose tissue contributions to newly formed fatty acids in an ascites tumor. 674 24

Data on anorexia and cachexia induced by Walker carcinoma 256 in Sprague-Dawley rats were analyzed in order to standardize an experimental model using a statistical (nondeterministical) procedure for assessing the efficacy of potential orexigenic agents. This model was characterized by a mean survival time of 14 +/- 1 days and by food intake and body weight loss starting from day 6 after tumor implantation. The complex course of cachexia was characterized by reduction in the weight of gastrocnemius muscle and epididymal adipose tissue, taken as representative sites of loss of proteins and lipids.
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PMID:Walker carcinoma 256: a model for studies on tumor-induced anorexia and cachexia. 695 38

The effects of tumor growth on lipid metabolism were investigated by evaluating serum lipids, lipoprotein lipase activity (LPLA), the lipogenic enzymes, urinary catecholamines along with serum insulin and glucagon levels. We injected 1.5 X 10(6) cells of rat mammary tumor, AC33, and killed the rats on the 18th day. Serum triglycerides and free fatty acids of the tumor-bearing (TB) rats increased 4 and 5 times, respectively, more than the control (C) rats. Total liver lipids were not significantly different between the two groups. Tumor growth produced a 70% decrease in total epididymal fat pad LPLA; there were no changes in soleus muscle LPLA. Serum insulin levels of the TB rats were 49% less than the C rats. The TB rats had significantly lighter epididymal fat pads and lower activities of adipose fatty acid synthetase and citrate cleavage enzyme. Urinary catecholamines of the TB rats were reduced over 30% compared with the C rats. These results show that the hypertriglyceridemia of the TB rats may be due, in part, to a deficiency of adipose tissue LPLA. The data also suggest that the effects of the tumor on lipid metabolism may be mediated through insulin.
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PMID:Changes in the activities of lipoprotein lipase and the lipogenic enzymes in tumor-bearing rats. 698 80

Male Sprague-Dawley rats (125--150 g) were implanted intramuscularly with Walker 256 carcinoma. After 10--14 days, tumor-bearing rats, alone with controls, were killed and the ability of insulin to promote the in vitro utilization of glucose by epididymal adipose tissue was assessed. The sensitivity of free adipocytes and minced adipose tissue from tumor-bearing rats to insulin, as assessed by measurement of the incorporation of glucose into total lipids as well as into the triglyceride fraction of neutral lipids, was significantly less (P less than 0.01) as compared to control animals. Similarly, insulin was considerably less effective at enhancing glycogenesis in vitro in adipose tissue from animals bearing the tumor for 10 days compared to adipose tissue from controls. Adipose tissue from tumor-bearing animals tended to convert less glucose to CO2 in the presence of insulin than did adipose tissue from controls. That this decreased in vitro sensitivity to insulin of adipose tissue from tumor-bearing animals could be the result of simple down-regulation by high levels of circulating insulin can be ruled out by the fact that the presence of the tumor resulted in lower circulating insulin than that in control animals. Serum glucose levels were also lower in tumor-bearing rats than in corresponding control animals.
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PMID:Insulin-stimulated glucose utilization in adipose tissue from rats bearing Walker 256 carcinoma. 703 69

The biochemical basis for the observed depletion of adipose tissue in C57BL mice bearing a transplantable nonmetastasizing preputial gland tumor, ESR-586, has been investigated. The results have shown that there are a number of significant changes in both deposition and mobilization of lipid as the tumor grows. The first change, before the tumor reached 2 g, was a decline in the activity of adipose tissue lipoprotein lipase to levels normally found in starved animals. This was accompanied by a slight increase in lipoprotein lipase activity in heart and appearance of substantial activity in large tumors. Together, these would result in impaired uptake of exogenous fatty acids by adipose tissue, and dietary lipid would be directed away from storage. This was followed by a marked decline in endogenous lipid synthesis in adipose tissue which commenced when the tumor weighed between 2 and 3 g, as measured in vivo by the incorporation of radioactivity into lipid from tritiated water. The basal rate of lipolysis was enhanced 2-fold in epididymal fat pads from mice bearing tumors that weighed between 2 and 4 g, although there was no difference in the epinephrine-stimulated activity.
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PMID:Modified lipoprotein lipase activities, rates of lipogenesis, and lipolysis as factors leading to lipid depletion in C57BL mice bearing the preputial gland tumor, ESR-586. 724 77


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