[How to become a radiologist in Egypt].
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Biomedical subjects
Publications and source records attributed to S Hanna.
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BACKGROUND: This prospective study evaluated the use of the K isozyme of lactate dehydrogenase (LDH-K) as a complementary tumor marker to carcinoembryonic antigen (CEA) in patients with colorectal adenocarcinoma. METHODS: In this series, 355 patients underwent potentially curative surgery for primary colorectal adenocarcinoma. A close surveillance program of follow-up revealed 108 patients (30%) who had a serum elevation in CEA and/or LDH-K. RESULTS: The patients were divided into three groups. Group 1 consisted of 43 patients with elevations in CEA alone. Twenty-seven of 43 patients (63%) had tumor at exploratory laparotomy; and 16 patients (37%) had no evidence of disease after a median follow-up of 74 months. Group 2 consisted of 33 patients with a serum elevation of LDH-K alone. In this group, 5 of 33 patients (15%) had recurrent disease with true elevations of LDH-K. In 28 patients (85%), there were falsely elevated levels of LDH-K with no evidence of disease. Group 3 consisted of 32 patients with elevations of both serum LDH-K and CEA. In this group, 17 of 32 patients (53%) had true elevations of CEA and LDH-K with tumor recurrence, and 15 patients (47%) had false elevations with no evidence of disease. CONCLUSION: LDH-K did not complement CEA as a tumor marker for detecting recurrence in this group of patients with colorectal cancer.
In 21 recipients of renal transplants suspected of allograft necrosis, the authors correlated the results of imaging to pathologic and histologic data in order to describe the magnetic resonance (MR) imaging and color Doppler ultrasonographic (US) characteristics of infarction. All patients underwent MR imaging performed with and without gadolinium tetraazacyclododecanetetraacetic acid (DOTA) and color Doppler US. Nonenhanced T1-weighted images showed no obvious changes, whereas nonenhanced T2-weighted images demonstrated a slight increase in signal intensity in areas of ischemic necrosis and low or heterogeneous signal intensity in areas of hemorrhagic necrosis. Gd-DOTA-enhanced MR images showed no contrast material uptake in infarcted areas. Color Doppler US characteristics of infarction included absence of Doppler signal and alteration of the cortical echogenic structure, particularly in cases of ischemic necrosis. Color Doppler US allows measurement of vascular resistance and assessment of intrarenal vasculature and the renal pedicle. Gd-DOTA-enhanced MR imaging is useful in confirming the diagnosis of infarction and provides an accurate evaluation of the extent of the infarct.
Effects of dopamine and bromocriptine on TRH- or dibutyryladenosine 3',5'-cyclic monophosphate (dbcAMP)-induced prolactin release from primary cultured rat pituitary cells were studied using a perifusion system. TRH (100 nmol/l) stimulated prolactin release from basal concentrations of 33.8 +/- 0.5 to 151.2 +/- 28.0 ng/ml (net increase) or 447% increase. Dopamine inhibited the basal release of prolactin throughout the experiment, but TRH (100 nmol/l) was still able to stimulate prolactin release under the influence of dopamine. The increment in prolactin release was inversely proportional to the dopamine concentration. When TRH (100 nmol/l) was introduced during a perifusion period with bromocriptine 1 nmol/l, the prolactin concentration was increased to 110.9% of basal levels. The stimulatory effect of TRH under the influence of bromocriptine (1 nmol/l) was significantly lower than that without bromocriptine (control), although the higher concentrations of bromocriptine (10 and 100 nmol/l) did not further reduce the peak concentration of TRH-induced prolactin release. During a perifusion period with a low concentration of dopamine (1 nmol/l plus 0.1 mmol/l ascorbic acid), introduction of dbcAMP (3 mmol/l) stimulated prolactin release to 48% of basal concentration. A higher concentration of dopamine further reduced the stimulatory effect of prolactin release. Bromocriptine impeded the stimulatory effect of dbcAMP (3 mmol/l) on prolactin release in a similar manner as dopamine. Since a higher concentration of bromocriptine (10 and 100 nmol/l) did not further inhibit the TRH-induced prolactin release whereas a higher concentration of dopamine did, it is concluded that dopamine acts through additional mechanism(s) other than the D2 receptor transduction system.
Colonic adenocarcinomas measuring less than 10 mm are rare. Herein, we report a carcinoma measuring 8 mm in diameter associated with subserosal extension through a "locus minoris resistentiae" and metastases to lymph nodes, an association not previously reported. No residual adenomatous tissue was found, suggesting a de novo carcinoma.
The results of 62 consecutive MR examinations were correlated with the subsequent clinical course and histologic results. Twenty-six cases of rejection showed a marked diminution of cortico-medullary differentiation (CMD). The renal parenchymal vascular pattern and visibility of renal sinus fat were not markedly altered in rejection and there was no difference between normal and rejected allograft shape. The ability of MR imaging to diagnose renal transplant rejection is only based on CMD, which, however, is non-specific. In 2 cases of severe acute rejection, T2 weighted images showed an abnormal signal intensity of the cortex due to renal infarction. Our preliminary results in 8 patients with Gd-DOTA injection showed 2 cases with necrosis seen as areas with absent contrast enhancement. This technique seems to be promising in the detection of perfusion defects.
Dopamine has a catechol group which can be easily oxidized by mild oxidizing agents. Ascorbic acid has been routinely added to a dopamine solution in order to protect it from oxidation. We have examined the effect of ascorbic acid on dopaminergic inhibition of prolactin release. Male rat pituitary cells were dispersed using trypsin and cultured for 5-7 days before experiments. Ascorbic acid did not stimulate nor inhibit prolactin release in both static monolayer culture and dynamic perifusion systems, but potentiated by approximately 100 times the inhibitory effect of dopamine on prolactin release. In order to differentiate chemical protection from potentiation, we tested the potentiation effect of isoascorbic acid which is an epimer of biologically active L-ascorbic acid but is biologically less active. Our results indicated that isoascorbic acid caused less potentiation of the dopaminergic effect on prolactin release than did ascorbic acid. In a perifusion system, a high concentration of dopamine (100 nmol/l) was unable to inhibit prolactin release for a 1 h experimental period, but a low concentration of dopamine (10 nmol/l) plus ascorbic acid (10 mumol/l) inhibited prolactin release for the entire 1 h perifusion period. There is a strong possibility that ascorbic acid may be a physiological supplementary agent for the prolactin-release inhibiting factor (PIF) since the blood concentration of ascorbic acid is rather high (23-85 mumol/l).
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Aclacinomycin-A (Aclarubicin) is a relatively new anthracycline antibiotic with potential activity against ovarian cancer. Eight patients with various malignancies (4 ovary, 1 breast and ovary, 1 breast, 1 colon, 1 leiomyosarcoma) and intraperitoneal disease were treated in a Phase I trial with escalating doses of intraperitoneal Aclacinomycin. Drug treatments were administered through a peritoneal catheter in a 2 liter fluid volume (1.5% Dianeal). Seventeen cycles were administered with doses ranging from 25 to 75 mg of Aclacinomycin. Pharmacokinetic studies were carried out in 7 patients. Although high concentrations of Aclacinomycin could be obtained in the peritoneal cavity no drug was detected in the plasma. The major dose-limiting toxicity was chemical peritonitis. Two patients had reduction in the amount of ascites. The recommended dose for Phase II trials is Aclacinomycin 50 mg in 2 liters given every 2 weeks.
Particular interest in human T lymphocyte lymphoma/leukemia virus (HTLV) derives from the close association of HTLV with several types of human mature T lymphocyte malignancies and the strong possibility that HTLV is the causative agent of this group of leukemias and lymphomas. This is the first report to show that HTLV expression in T lymphocytes cultured in vitro is inversely proportional to constitutive gamma interferon production. Of 16 fresh T lymphocyte cultures established from patients with mature T lymphocyte neoplasias, 3 were grown continuously for over 3 years and 13 were grown for 2 to 8 months in culture. Of the 16 cultures, 9 were HTLVp19 positive and interferon negative, whereas the remaining 7 were HTLVp19 negative or weakly positive and also interferon positive (12 to 105 U/ml). The prototype HTLV-positive T-cell line (HUT102) was examined over a long-term culture and after selective cell cloning for high virus yield. Results indicate that early-passage, low-HTLV-producing HUT102 cells constitutively produced significant levels of gamma-immune interferon. In late-passage and cloned HUT102 cells, an increase in HTLV production was concordant with a decrease in constitutive interferon production and the loss of mature T lymphocyte antigens. Transformation of human umbilical cord blood lymphocytes by HTLV was possible only after cocultivation with the non-interferon, high virus-producing, cloned HUT102 T lymphocytes. The inverse relationship between interferon and HTLV production was also observed when normal human umbilical cord blood and adult T lymphocytes were transformed by HTLV and maintained in culture.
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This paper compares the management of two groups of patients with flail chest. The 25 patients in group 1 had a flail chest without other significant injuries or shock, whereas the 57 in group 2 had a flail chest with multiple injuries, shock or both. The group 1 patients were treated with repeated multiple intercostal nerve blocks or high segmental epidural analgesia, oxygen, intensive chest physiotherapy, fluid restriction, furosemide diuretics, methylprednisolone sodium succinate and colloid infusion in an intensive care unit. In addition to these measures, the group 2 patients underwent endotracheal intubation and assisted mechanical ventilation with a volume respirator that provided continuous positive airway pressure and positive end-expiratory pressure. Of the 57 group 2 patients 36 required prolonged ventilation, eventually through a tracheostomy, because of severe head injury, pneumonia, severe facial injury, quadriplegia, pre-existing lung disease or severe sepsis. However, tracheostomy was avoided in the other 21 patients in group 2. There were no deaths in group 1, but 8 (14%) of the patients in group 2 died. These results show that avoidance of tracheostomy and ventilation in selected patients with flail chest is consistent with a low morbidity and mortality.
A 67-year-old man with adenocarcinoma of the colon had recurrent pulmonary emboli. The patient's level of serum antithrombin III was found to be below normal. Heparin therapy led to further reduction, resulting in failure of adequate anticoagulation. The patient subsequently died of massive pulmonary emboli despite heparin therapy. We believe the antithrombin III level should be routinely determined for patients receiving heparin therapy.
We have isolated sarcoplasmic reticulum from normal and dystrophic chicken muscle, using an improved isolation procedure. Dystrophic sarcoplasmic reticulum has a reduced level of calcium-sensitive ATPase activity, phosphoenzyme formation, and steady-state calcium transport. Anion-stimulated calcium transport by dystrophic sarcoplasmic reticulum is also reduced when measured under the proper conditions, and dystrophic sarcoplasmic reticulum shows no alteration in calcium efflux rate. Active calcium phosphate loading of the normal and dystrophic sarcoplasmic reticulum preparations indicates that a reduced percentage jof the dystrophic vesicles are capable of active calcium transport. The loaded dystrophic sarcoplasmic reticulum vesicles exhibit the same relative reductions in enzymatic activity as the starting sarcoplasmic reticulum preparations. However, the enzyme activities of normal and dystrophic sarcoplasmic reticulum are similar in the presence of detergent and exogenous phospholipid. On the basis of these results, we suggest that the lipid microenvironment of the dystrophic enzyme is altered.
The addition of cupric-1,10,-phenanthroline, a cross-linking catalyst, to sarcoplasmic reticulum membranes caused protein sulfhydryl groups to form disulfide bridges. Following a short exposure to the catalyst (15 s, 22 degrees C) most of the protein was in a dimeric form (Mr = 248 000). Longer exposure times resulted in the formation of trimers, tetramers and other oligomers too large to enter the gel. At low temperatures (4 degrees C) dimer formation predominates even for exposure times as long as 5 min. Cross-linking in the presence of 7.5 mM Triton X-100 (a concentration that resulted in clearing of the membrane suspension and thus solubilization of the membrane components) showed the appearance of a considerable dimer fraction, however, most of the (Ca2+ + Mg2+)-ATPase protein appeared as a monomer. Following 1 min of cross-linking at 22 degrees C, freeze-etched membranes showed no alteration in the number or appearance of 80 A intramembranous particles. Thus extensive cross-linking of the (Ca2+ + Mg2+)-ATPase protein can occur without disruption of the normal position of the intramembrane portion of the molecule.
The addition of cupric-1,10,-phenanthroline, a cross-linking catalyst, to sarcoplasmic reticulum membranes caused protein sulfhydryl groups to form disulfide bridges. Following a short exposure to the catalyst (15 s, 22 degrees C) most of the protein was in a dimeric form (Mr = 248,000). Longer exposure times resulted in the formation of trimers, tetramers and other oligomers too large to enter the gel. At low temperatures (4 degrees C) dimer formation predominates, even for exposure times as long as 5 min. Cross-linking in the presence of 7.5 mM Triton X-100 (a concentration that resulted in clearing of the membrane suspension and thus solubilization of the membrane components) showed the appearance of a considerable dimer fraction, however, most of the (Ca2+ + Mg2+)-ATPase protein appeared as a monomer. Following 1 min of cross-linking at 22 degrees C, freeze-etched membranes showed no alteration in the number or appearance of 80 A intramembranous particles. Thus extensive cross-linking of the (Ca2+ + Mg2+)-ATPase protein can occur without disruption of the normal position of the intramembrane portion of the molecule.
A specific and quantitative GLC method for warfarin in human plasma is described. The procedure uses papaverine as the internal standard and involves a dichloroethane extraction of the acidified specimen. The organic extract is evaporated, and the evaporated extract is dissolved in 50 microliter of chloroform. Aliquots of 2-3 microliter are injected into a gas chromatograph equipped with a flame-ionization detector. The sensitivity of the method is such that 0.3 microgram of intact warfarin can be detected in 1 ml of plasma. Statistical analyses indicate a recovery of 97.26 +/- 1.89% SD. The procedure was successfully applied to plasma drug level studies in humans.
Polarographic investigation of clorazepate monopotassium and dipotassium showed two cathodic waves at about -1.28 and -1.66 v. The cathodic wave associated with clorazepate monopotassium or dipotassium at about -1.66 v was a pH-independent, diffusion-controlled wave. This wave was used to develop a specific stability-indicating procedure for clorazepate monopotassium and dipotassium in the presence of their degradation products, namely, nordiazepam, 2-amino-5-chlorobenzophenone, and glycine. The method involves a 10(-2) M LiOH-10(-1) M LiCl extraction of the active ingredient from the formulation, filtration, dilution with the same supporting electrolyte, and then use of the standard addition technique for drug quantitation in capsules. Typical fomulation excipients did not interfere with the analysis. Accuracy and precision of the procedure were 99.55 +/- 0.68%.