Colonoscopic enema as rescue for inadequate bowel preparation before colonoscopy: a prospective, observational study.

AIM: Colonoscopy may need to be rescheduled because of inadequate bowel preparation. We evaluated the effectiveness of colonoscopic enema as rescue for an inadequate 1-day bowel preparation before colonoscopy. METHOD: Patients referred for afternoon colonoscopy were prospectively enrolled in the study during a 1-year period. Patients took bowel preparation (polyethylene glycol) solution on the morning of the endoscopy. If during colonoscopy the bowel preparation was poor, an enema of polyethylene glycol solution (500 ml) was instilled into the colon at the level of the hepatic flexure via the biopsy channel of the colonoscope which was then removed. The patient was allowed to recover from the propofol sedation and used the bathroom to evacuate the enema. The colonoscope was then introduced and the examination continued. RESULTS: Of 504 patients undergoing colonoscopy, 26 (4.9%) received an enema. The median age was 59 (29-79) years and 19 (73%) were female. A subsequent successful colonoscopy was achieved in 25/26 (96%). There were no complications. The mean time spent for the entire colonoscopy from the initial preparation to the end of the examination including the enema was 7.6± 1.1h (5.4 h preparation, 0.2h first colonoscopy+enema, 0.66h waiting in the lavatory, 0.33h second colonoscopy and 1 h for recovery). CONCLUSION: Colonoscopic enema was highly successful as rescue for patients with inadequate bowel preparation and avoided postponement of the procedure.

Effect of hyperthermia combined with external radiation therapy in primary non-small cell lung cancer with direct bony invasion.

PURPOSE: Local control in lung cancer directly invading the bone is extremely poor. Effects of regional hyperthermia combined with conventional external beam radiation therapy were evaluated. MATERIALS AND METHODS: Thirteen patients with non-small lung cancer (NSCLC) with direct bony invasion were treated with hyperthermia plus irradiation (hyperthermia group). The treatment outcome was compared with the historical treatment results in 13 patients treated with external radiation therapy alone (radiation alone group). In patients with no distant metastasis, radiation therapy at a total dose of 60-70 Gy was administered to both groups. Hyperthermia was performed for 45-60 min immediately after irradiation for two-four sessions with radiofrequency capacitive heating devices. RESULTS: For primary response, 10 of the 13 tumours responded to the treatment (3 CR, 7 PR) in the hyperthermia group, whereas seven tumours responded (1 CR, 6 PR) in the radiation alone group. The 2-year local recurrence-free survival rate for clinical M(0) patients in the hyperthermia group and that in the radiation alone group were 76.1 and 16.9%, respectively. Three patients died of distant metastases within 2 years in the hyperthermia group, but two out of three tumours histologically disappeared, even in the autopsy examination. The 2-year overall survival rate for clinical M(0) patients in the hyperthermia group and that in the radiation alone group were 44.4 and 15.4%, respectively. No severe pulmonary complication was observed in either group. CONCLUSIONS: Regional hyperthermia combined with conventional irradiation could be a tool to improve local control in patients with NSCLC deeply invading the chest wall.

Evidence of chemical bonding at biomaterial-hard tissue interfaces.

For many years, glass-polyalkenoate cements have been described as possessing the unique properties of self-adherence to human hard tissues, such as bones or teeth. However, direct experimental evidence to prove the existence of chemical bonding has not been advanced. X-ray Photoelectron Spectroscopy (XPS) was used to analyze the chemical interaction of a synthesized polyalkenoic acid with enamel and synthetic hydroxyapatite. For both enamel and hydroxyapatite, the peak representing the carboxyl groups of the polyalkenoic acid was detected to have significantly shifted to a lower binding energy. De-convolution of this shifted peak disclosed two components with a peak representing unreacted carboxyl groups and a peak suggesting chemical bonding to hydroxyapatite. On average, 67.5% of the carboxyl groups of the polyalkenoic acid were measured to have bonded to hydroxyapatite. XPS of hydroxyapatite also disclosed its surface to be enriched in calcium and decreased in phosphorus, indicating that phosphorus was extracted at a relatively higher rate than calcium. Analysis of these data supports the mechanism in which carboxylic groups replace phosphate ions (PO4(3-)) of the substrate and make ionic bonds with calcium ions of hydroxyapatite. It is concluded that an ultrathin layer of a polyalkenoic acid can be prepared on a hydroxyapatite-based substrate by careful removal of non-bonded molecules. With this specimen-processing method, XPS not only provided direct evidence of chemical bonding, but also enabled us to quantify the percentages of functional groups of the polyalkenoic acids that bonded to calcium of hydroxyapatite.

Hyponatremia-induced metabolic encephalopathy caused by Rathke's cleft cyst: a case report.

Rathke's cleft cysts are sometimes associated with aseptic meningitis or metabolic encephalopathy due to hyponatremia. We treated such a case manifest by lethargy, fever and electroencephalographic abnormalities. A 68-year-old man was admitted to our ward after experiencing general malaise, nausea and vomiting and then high fever and lethargy. On admission, he was drowsy and had nuchal rigidity and Kernig's sign. Physically, he was pale with dry, thickened skin. He had lost 5.0 kg of body weight in the last month. His serum sodium was 115 mEq/l. He had a low serum osmotic pressure (235 mOsmol/l) and a high urine osmotic pressure (520 mOsmol/l). His urine volume was 1200-1900 ml/24 h with a specific gravity of 1008-1015. The urine sodium was 210 mEq/l. He did not have an elevated level of antidiuretic hormone. Electroencephalograms showed periodic delta waves over a background of theta waves. With sodium replacement, the patient become alert and symptom free, and his electroencephalographic findings normalized. However, the serum sodium level did not stabilize, sometimes falling with a recurrence of symptoms. Magnetic resonance imaging clearly delineated a dumbbell-shaped intrasellar and suprasellar cyst. The suprasellar component subsequently shrunk spontaneously and finally disappeared. An endocrinologic evaluation showed panhypopituitarism. The patient was given glucocorticoid and thyroxine replacement therapy, which stabilized his serum sodium level and permanently relieved his symptoms. A transsphenoidal approach was performed. A greenish cyst was punctured, and a yellow fluid was aspirated. The cyst proved to be simple or cubic stratified epithelium, and a diagnosis of Rathke's cleft cyst was made. The patient was discharged in good condition with a continuation of hormonal therapy. Rathke's cleft cyst can cause aseptic meningitis if the cyst ruptures and its contents spill into the subarachnoid space. Metabolic encephalopathy induced by hyponatremia due to salt wasting also can occur if the lesion injures the hypothalamus and pituitary gland.

New serine protease inhibitors with leukotriene B4 (LTB4) receptor binding affinity.

A series of new trypsin-like serine protease inhibitors, 1, 2 and 7-23, containing amidinobenzene moiety was found to show potent LTB4-receptor affinity. Among them, compounds 1 and 2 were found to be LTB4 receptor antagonists based on an inhibition assay of human polymorphonuclear neutrophil (PMN) intracellular calcium mobilization induced by LTB4. Compounds 1 and 2, which satisfy the reported structural requirements for good oral activity, are expected to show a balanced dual mode of action, i.e., protease inhibitory activity and LTB4 receptor antagonist activity, in vivo.

Cerebral blood flow and clinical outcome in patients with thalamic hemorrhages: a comparison with putaminal hemorrhages.

It has been reported that the reduction of cerebral blood flow (CBF) is more pronounced with thalamic hemorrhages than with putaminal hemorrhages, and the clinical outcome is worse with the former. However, the mechanism underlying these differences is not clear. We compared neurologic status, hematoma volumes, outcome scores. and early (< 1 month) and late (2-12 month) CBF values between 15 patients with thalamic hemorrhages and 28 patients with putaminal hemorrhages. We also correlated thalamic versus hemispheric CBF on each side and ipsilateral versus contralateral thalamic and hemispheric CBF. Finally, we evaluated the response to acetazolamide during the late stage. Thalamic hemorrhages were associated with a more pronounced reduction in CBF bilaterally, even though their hematoma volumes were much smaller. Contralateral to the hemorrhage, the discrepancy in CBF values between the two groups became greater in the late stage because CBF started to recover in putaminal hemorrhages but persistently deteriorated in thalamic hemorrhages. In the group with thalamic hemorrhages, the correlation between thalamic and hemispheric CBF ipsilateral to the hemorrhage and between thalamic CBF on both sides was disrupted in the early stage and restored in the late stage, whereas the correlation between the hemispheric CBF values was consistently preserved. Acetazolamide invariably augumented CBF during the late stage. The clinical outcome was worse in the thalamic group, but CBF values correlated negatively with outcome in both groups. We conclude that the reduction of CBF in the late stage may be secondary to metabolic depression due to transneural depression ('diaschisis'). The metabolic depression in thalamic hemorrhages is more extensive and persistent than in putaminal hemorrhages, which probably accounts for both the more pronounced CBF reduction and the worse outcome.

Cerebral blood flow in normal brain tissue of patients with intracranial tumors.

Pre- and postoperative cerebral blood flow (CBF) changes in the normal brain tissue of 17 patients with intracranial tumors were studied to determine the value for planning therapeutic strategy. The tumors included eight astrocytomas, seven meningiomas, one metastasis, and one arachnoid cyst. The patients were divided into two groups based on the mass effect seen on computed tomography (CT) scans. Group A comprised six patients with midline shift or evidence of herniation; Group B, 11 patients with no mass effect or local compression only. CBF and vasoresponse to acetazolamide were measured in the bilateral hemispheres, cortices, and thalami using xenon-enhanced CT, excluding the area of tumor extension, before and 2-3 weeks after tumor excision. Preoperative CBF was reduced bilaterally but more markedly ipsilateral to the tumor. The CBF reduction was significantly greater in Group A than in Group B. Acetazolamide caused CBF to increase by 70.5-99.1% in Group B but only increase by 1.7-9.6% or paradoxically decrease in Group A. Postoperatively, the CBF tended to recover partially in Group A but persisted or deteriorated in Group B. The more pronounced CBF reduction and poor or paradoxical response to acetazolamide preoperatively and postoperative CBF restoration in Group A may indicate that ischemia was more important than metabolic depression in these patients. In contrast, the excessive response to acetazolamide and the postoperative CBF deterioration in Group B may indicate that CBF reduction was secondary to metabolic depression. Mass effect is a key predictor for functional recovery following surgical decompression of intracranial tumors.

Migratory arrest of gonadotropin-releasing hormone neurons in transgenic mice.

Gonadotropin-releasing hormone (GnRH) is important in reproduction, although the mechanism of central hypogonadism in humans remains unclear. Because the GnRH neuron originates from the olfactory placode and migrates to the hypothalamus during development, central hypogonadism in humans could be caused by failure in normal migration of GnRH neurons to the hypothalamus. We report that in transgenic mice expression of the simian virus 40 T antigen, driven by the promoter of human GnRH gene, resulted in central hypogonadism due to an arrest in neuronal migration during development and tumor formation along the migratory pathway. This system appears to be an important animal model of hypogonadotropic hypogonadism in humans. Additionally, olfactory bulb tumors from these animals were dispersed, and a GnRH-secreting neuronal cell line (GN cell line) was established.

Cloning and structure of human genomic DNA and hypothalamic cDNA encoding human prepro thyrotropin-releasing hormone.

The gene encoding human preproTRH was isolated from a human lung fibroblast genomic DNA library with a rat prepro TRH cDNA fragment. The transcriptional unit is 3.3 kilobases in size and contains three exons interrupted by two introns of approximately 1050 and 650 base pairs, respectively. Exon 1 encodes the 5'-untranslated region of the mRNA, exon 2 the putative signal sequence and the initial portion of propeptide, and exon 3 encodes the remainder of the propeptide, which contains six copies of the TRH sequence in contrast to five copies in the rat preproTRH gene. The predicted human preproTRH peptide structure has 242 amino acids compared to 255 amino acids in the rat. Homology with rat preproTRH is 73.3% and 59.5% at the nucleic acid and amino acid levels, respectively. Intron-exon splicing sites and 5' and 3' mRNA borders were confirmed rigorously by sequencing a human preproTRH cDNA using the polymerase chain reaction and human hypothalamic cDNA.

Isolation and characterization of the human gonadotropin-releasing hormone gene in the hypothalamus and placenta.

The GnRH gene has been cloned in several species, but the location of the promoter and the exact start of transcription have not previously been determined. To characterize the low abundance human GnRH mRNA in the hypothalamus and placenta, we have employed the polymerase chain reaction. The hypothalamus was found to have a 61-base pair first exon, and its transcriptional start site was determined. The human hypothalamic GnRH cDNAs isolated thus far have all contained a short 5' untranslated region which would correspond to this start site. However, all human placental GnRH cDNAs reported to date have a long 5' untranslated region, which extends more than 140-base pairs 5' to this start site in the hypothalamus, suggesting the utilization of an alternative promoter in the placenta. In addition, the human GnRH gene undergoes differential splicing in these tissues. The first intron is removed from the hypothalamic, but retained in the placental, GnRH mRNA. Thus, the placenta has a very long first exon, while the hypothalamus has a comparatively short first exon, followed by a long first intron. This characterization of the human GnRH gene will now allow hormonal regulatory studies to be performed using gene transfer techniques.

[Intraoperative autotransfusion in aortic aneurysm operations combined with temporary external shunt].

Intraoperative autotransfusion was done in nine patients who underwent major vascular surgery for thoracic aortic aneurysms including one total abdominal aneurysm using temporal external shunt. After general heparinization (1mg/kg), shed blood was collected by Sorenson Autotransfusion System with local heparinization. After confirming ACT longer than 300-400 second, 425-3700 ml, averaged 1804 ml, of shed blood was reinfused to the patients by gravity flow. The reinfusion rate of shed blood was 43.1 +/- 15.8%. There were no deaths and no complications referable to autotransfusion. Although mild hemolysis was observed immediately after surgery, plasma free hemoglobin level returned to normal in the first operative day and no renal failure occurred. The volume of bleeding after surgery was not differed from that of control. Microembolism was not evident clinically. We concluded that intraoperative autotransfusion is safe and useful procedure in major vascular surgery if proper anticoagulation is done.

[Antitumor activity and toxicity of the degradation products and the aquated species of cis-dichlorodiammineplatinum (II)].

Antitumor activity and mouse acute toxicity of the following degradation products and aquated species of cis-dichlorodiammineplatinum(II) (CDDP): trans-dichlorodiammineplatinum(II), trichloroamminepltinate(II), tetrachloroplatinate(II), produced by heat treatment of the saline solution of CDDP, mono- and di-aquocomplexes, hydroxo-bridged dimer and trimer of CDDP, have been studied. These degradation products did not show antitumor activity against mouse leukemia L1210 corresponding to their low anti-HeLa cell activity. Their acute toxicities were much milder than CDDP. On the other hand, all the aquated species possessed higher toxicities than CDDP. Among them, the dimer and trimer were less active against HeLa cells than CDDP, and did not show antitumor activity against L1210 leukemia. However, the mono- and di-aquo complexes showed about 2 approximately 4 times higher anti-HeLa cell activity and prolonged the survival time of mice bearing L1210 leukemia similarly to CDDP.

Characterization of the stimulatory effects of PGF2alpha on the release of arachidonic acid.

Fibroblasts derived from a rat carrageenin granuloma were cultured in the presence of radioactive arachidonic acid, palmitic acid and linoleic acid. More than 90% of each labeled fatty acid was incorporated into a phospholipid fraction by the cells in 18 hrs. Arachidonic acid was evenly incorporated into phosphatidylcholine and phosphatidylethanolamine, while both palmitic acid and linoleic acid were almost entirely incorporated into phosphatidylcholine. The position of phosphatidylcholine where the fatty acids were incorporated was different for each fatty acid. The ratio of the amount of fatty acid incorporated into the 2-position to the amount incorporated into the 1-position of phosphatidylcholine for each fatty acid was greater than 90% for arachidonic acid, 2:1 for palmitic acid and 5:1 for linoleic acid. In the case of phosphatidylethanolamine, most arachidonic acid (greater than 90%) was incorporated into the 2-position. PGF2alpha caused the stimulation of arachidonic acid release but not of palmitic acid and linoleic acid from pre-labeled fibroblasts. The serum in the medium was completely replaceable by bovine serum albumin. The effect of PGF2Alpha increased with an increasing concentration of bovine serum albumin, suggesting that serum only acts as a "trap" for released arachidonic acid. The effect of PGF2Alpha was greater than bradykinin, and no synergistic effect was seen, although an additive effect was observed. The effect of PGF2Alpha depended on the concentration of calcium ions under magnesium-supplemented conditions.