Cytochrome P-45011 beta in rat brain

The presence of cytochrome P-45011 beta in rat brain was studied by immunohistochemistry using polyclonal rabbit antibodies raised against purified bovine adrenocortical P-45011 beta, which is involved in the steroid 11 beta-hydroxylation and glucocorticoid formation. The results showed that cytochrome P-45011 beta immunoreactivity is selectively localized to the tracts of myelinated fibers throughout the brain. The specificity of immunohistochemical stainings with P-45011 beta antibodies was established by control tests including nonimmune rabbit immunoglobulin Gs and P-45011 beta antibodies absorbed with purified antigen. Western immunoblots of homogenates from different brain areas with P-45011 beta antibodies, together with biochemical enzymatic assays for cytochrome P-45011 beta monooxygenase activity in these homogenates, confirmed the selective localization of this enzyme observed with immunohistochemistry. Cytochrome P-45011 beta and 11 beta-hydroxylase activity were detected in a homogenate from the cortical white matter (brain area rich in myelinated fibers) as in that from the rat adrenal, but were not detectable in a homogenate from the cerebral cortex (brain area poor in myelinated fibers). Furthermore, quantitation of the P-45011 beta bands on the immunoblots by the areal density revealed that the cortical white matter contains approximately 1.4 pmol of cytochrome P-45011 beta/mg of tissue protein, the value of which was about one sixth of the corresponding value estimated in the rat adrenal. This relatively high content of cytochrome P-45011 beta was also reflected in a relatively high level of 11 beta-hydroxylase activity measured in a homogenate of this brain area by biochemical enzymatic assays using [4-14C]-11-deoxycorticosterone.(ABSTRACT TRUNCATED AT 250 WORDS)     

The innervation of the levator veli palatini muscle by the glossopharyngeal nerve

We developed a novel method which enables bloodless exposure of the levator veli palatini muscle in rat in order to investigate the physiological properties of this muscle. The levator veli palatini muscle which is innervated by a branch of the glossopharyngeal nerve showed rhythmic spontaneous movement in rats. Cutting the branch supplying LVP of the glossopharyngeal nerve caused cessation of the spontaneous movement of the levator veli palatini muscle. The spontaneous discharges of the glossopharyngeal nerve were synchronized with those of the phrenic nerve. A mixture of 95% oxygen and 5% room air influenced the efferent discharges from the branch of the glossopharyngeal nerve supplying the levator veli palatini muscle. These findings indicate that the motor nerve supply to the levator veli palatini muscle is the glossopharyngeal nerve, and the levator veli palatini muscle is related to the respiratory system, in particular with inspiration in rats.     

Antibacterial activities of the leaf extracts of Eugenia uniflora Linn. (Synonym Stenocalyx michelli Linn.) Myrtaceae

The aqueous, organic, and volatile oil extracts of leaves of Eugenia uniflora Linn. Family Myrtaceae were investigated for antibacterial properties using agar dilution techniques. The aqueous extract was the most active against the organisms compared to the organic and volatile oil extracts. The extracts were found to inhibit Gram positive Staphylococcus aureus and Bacillus subtilis and Gram negative Escherichia coli and Shigella dysentcriae. Pseudomonas aeruginosa, Klebsiella pneumoniac, and Salmonella typhi were not inhibited.     

Fricke supraorbital flap for reconstruction of total lower eyelid defects

Summary Split or full thickness eyelid defects resulting from tumor destruction or surgical excision present a dilemma for plastic and reconstructive surgeons. Full thickness eyelid replacement requires composite grafting of the skin, together with tarsal support of its substitute and mucosa. The flap described by Fricke in 1829 was used for reconstruction of anterior lamella in six lower eyelid defects. In three of our cases chondromucosal grafts taken from nasal septum were utilized for posterior lamella repair. The results have been satisfactory from a functional and cosmetic standpoint.     

Impairment of acid-neutralizing capacity and lesion formation in the rat duodenum during hemorrhagic shock: comparative study with indomethacin

The effects of hemorrhagic shock (HE) on duodenal pH, acid-neutralizing capacity and mucosal tolerance to acid were investigated in anesthetized rats, and they were compared with those of indomethacin. HE was performed by bleeding from the carotid artery to reduce arterial blood pressure to about 55 mmHg (3 ml of bleeding per 200 g of body weight), and indomethacin was given s.c. in a dose of 5 mg/kg. Duodenal pH was determined in the outflow from the proximal duodenum (1.7 cm) which was perfused with 10(-4) M HCl, and acid-neutralizing capacity was measured by back-titration of the perfusate to pH 4.0 with 10 mM HCl. Under these conditions, duodenal pH was kept at around 6.0 as the result of neutralization in the loop (approximately 8 microEq/hr). Both HE and indomethacin significantly decreased the pH and acid-neutralizing capacity. Administration of 16,16-dimethyl prostaglandin E2 (16-dmPGE2: 30 micrograms/kg, s.c.) significantly increased both pH and acid-neutralizing capacity in normal and indomethacin-treated rats, but failed to affect these parameters in rats under HE conditions. When the duodenal loop was perfused with 50 mM HCl for 1.5 hr, both HE and indomethacin induced extensive damage in the mucosa. Pretreatment with 16-dmPGE2 significantly reduced the formation of duodenal lesions induced by indomethacin but not by HE. These results suggest that HE as well as indomethacin impaired duodenal acid-neutralizing capacity to reduce the tolerance to acid of the mucosa. The deleterious effects of HE on the mucosa may be mainly due to a decreased mucosal blood flow, but not due to a deficiency of endogenous prostaglandins.     

Use of a restricted protein diet in the treatment of behaviour disorderin a severely mentally retarded adult female phenylketonuric patient

ABSTRACT. A 54-year-old profoundly mentally retarded female patient with phenylketonuria and a severe behaviour problem was treated with a restricted protein and high energy diet. After several weeks of dietary intervention the patient's behaviour improved significantly.     

Uptake of iodine-123 MIBG by pheochromocytomas, paragangliomas, and neuroblastomas: a histopathological comparison

The percentage uptake of [123I]metaiodobenzylguanidine (MIBG) by tumors of the paraganglion system is compared with the number of neurosecretory granules (assessed by both light and electron microscopy) in the subsequently resected tumors in six patients. Iodine-123 MIBG was injected intravenously; the tumor uptake of [123I]MIBG varied between 0.001% and 0.14% of the injected dose per gram of tumor tissue at 22 hr. The number of neurosecretory granules in tissue sections was scored on a scale of I-III. A direct proportional correlation was found between the percentage uptake of [123I]MIBG by the tumor and the number of neurosecretory granules in the tissue sections but not with plasma or urinary catecholamines. This technique for imaging reflects the storage status of the tumor better than plasma and urinary catecholamine measurements.     

Interaction between endogenous opioids, cholinergic and adrenergic mechanisms during vagally-induced gastrin release in rats

Endogenous opioids are present in neurons of the vagus and the intrinsic nervous system and they are colocalized with gastrin in antral G-cells. This raises the possibility that endogenous opioids modulate gastrin release. Stimulation of both cervical vagi (10V, 5Hz, 5ms) elicited an increase of arterial plasma gastrin levels at intragastric pH7 or pH2. The response at pH2 was 30% of that at luminal pH7. Atropine reduced vagally stimulated gastrin levels substantially. At luminal pH2 the small residual noncholinergic response was mediated neither by adrenergic mechanisms nor by endogenous opioids. At luminal pH 7 adrenergic blockade with phentolamine and propranolol reduced vagally stimulated gastrin by 60%. In the presence of atropine adrenergic blockade elicited only a small inhibitory effect suggesting that vagal activation of adrenergic mechanisms depends on atropine-sensitive cholinergic pathways. Blockade of opiate receptors by naloxone had no effect on vagal gastrin release, however, the noncholinergic gastrin response was reduced significantly by naloxone, suggesting that cholinergic mechanisms normally restrain activation of endogenous opioids during vagal stimulation. Naloxone had no effect on the noncholinergic, nonadrenergic stimulation of gastrin levels. These data suggest that endogenous opioids can contribute to vagal gastrin release provided the cholinergic restraint is blocked and adrenergic mechanisms stimulate endogenous opioids. In conclusion a major role of endogenous opioids in the regulation of vagal gastrin release can not be detected.