Can we predict which dysplastic hips will require acetabular augmentation during total hip arthroplasty based on pre-operative radiographs?

AIMS: The purpose of this study was to evaluate whether an innovative templating technique could predict the need for acetabular augmentation during primary total hip arthroplasty for patients with dysplastic hips. PATIENTS AND METHODS: We developed a simple templating technique to estimate acetabular component coverage at total hip arthroplasty, the True Cup: False Cup (TC:FC) ratio. We reviewed all patients with dysplastic hips who underwent primary total hip arthroplasty between 2005 and 2012. Traditional radiological methods of assessing the degree of acetabular dysplasia (Sharp's angle, Tönnis angle, centre-edge angle) as well as the TC:FC ratio were measured from the pre-operative radiographs. A comparison of augmented and non-augmented hips was undertaken to determine any difference in pre-operative radiological indices between the two cohorts. The intra- and inter-observer reliability for all radiological indices used in the study were also calculated. RESULTS: Of the 128 cases reviewed, 33 (26%) needed acetabular augmentation. We found no difference in the median Sharp's angle (p = 0.10), Tönnis angle (p = 0.28), or centre-edge angle (p = 0.07) between the two groups. A lower TC:FC ratio was observed in the augmented group compared with the non-augmented group (median = 0.66 versus 0.88, p < 0.001). Intra-observer reliability was found to be high for all radiological indices analysed (interclass correlation coefficient (ICC) > 0.7). However, inter-observer reliability was more variable and was only high for the TC: FC ratio (ICC > 0.7). CONCLUSION: The TC: FC ratio gives an accurate estimate of acetabular component coverage. It can help predict which dysplastic hips are likely to need acetabular augmentation at primary total hip arthroplasty. It has high intra- and inter-observer reliability. Cite this article: Bone Joint J 2017;99-B:445-50.

Outcome of female urethral reconstruction: a 12-year experience.

INTRODUCTION AND HYPOTHESIS: To report our experience over 12 years in female urethral reconstruction with either anterior bladder tube (Tanagho) or labia minora pedicled tube. PATIENTS AND METHODS: This retrospective study included 16 patients with posttraumatic urethral loss. The patients were divided into two groups. Group I: included 6 patients managed with combined vaginal and abdominal approach using a proximally based anterior bladder tube (Tanagho) and Group II: included 10 patients underwent repair with labial fat pad flap with concomitant TOT sling. Outcomes included the success or failure of anatomical repair and continence, which was assessed during patient follow up by voiding diary, 24-h pad test and uroflowmetry. RESULTS: A total of 15 patients were followed for a mean of 42 months postoperatively, and only one patient was lost to follow up. Total continence was achieved in 10 patients (66.6 %) [4/6 patients (66.6 %) in group I and 6/9 patients (66.6 %) in group II]. Partial continence (i.e., one or two pad per day) was achieved in 2 patients (13.3 %). Failure occurs in 3 cases (20 %) [one case in group I and two cases in group II]. All our patients had a smooth postoperative course. In the labia pedicled tube, meatal stenosis was encountered in one patient and transient postoperative urine retention in 2 patients. Successful anatomical repair was achieved in all our patients. CONCLUSION: Both Bladder tube and labia minora pedicled tube with sling procedure have high success rate with only minor complications and are equally effective in the management of females with total urethral loss. Due to the small number of patients in this study, we still need to extend our study to verify our results.

Production and properties of beta-mannanase by free and immobilized cells of Aspergillus oryzae NRRL 3488.

Seven fungi were tested for production of mannanases. The highest mannanase activities were produced by Aspergillus oryzae NRRL 3488 after 7 days in static cultures. Mannanases were induced by gum locust bean (1.0%). The highest mannanase activity was produced when a mixture of peptone, urea and ammonium sulphate was used as nitrogen source. Zn2+ or Co2+ favoured enzyme production. The immobilized cells on Ca-alginate and agar were able to produce beta-mannanase for four runs with a slight decrease in the activity. The optimum temperature for enzyme reaction was 50-55 degrees C at pH 6.0. In the absence of substrate the enzyme was thermostable retaining 75% activity for 1 h at 50 degrees C, and 68% activity for 1 h at 60 degrees C.

Serum and salivary IgG and IgA response to radiation therapy.

Patients undergoing radiotherapy for malignant tumors of the head and neck invariably develop extensive oral and dental diseases particularly when the major salivary glands are within the radiation fields. Unless the patient receives a strict oral hygiene home care and the teeth are protected by topical application of fluoride gel, caries or gingival disease onset inevitably follows radiation induced xerostomia is. The importance of saliva as a controlling factor in the development of oral diseases is underscored by the dramatic increase in dental decay and gingival diseases that inevitably follows the surgical extirpation of the major salivary glands in animals and the onset of xerostomia in man.

Phenotypic identification of T lymphocytes subset in recurrent aphthous stomatitis.

Recurrent aphthous stomatitis (RAS) is characterized by recurring ulcers in the oral mucosa as abnormality of the immune response, autoimmune or abnormal immunological reaction to antigens of oral bacteria. This study was conducted on 25 patients 15 suffering RAS of the minor form and 10 of the major form and 15 student as control. The T lymphocytes were determined by the monoclonal antibodies (OKT) using the indirect immunofluorescent technique of Hoffman percentage of cells having surface fluorescence was calculated and the monoclonal antibody coated cells visualized and enumerated. It was concluded from this study that the two clinical entities of RAS may be of the same immunopathologic etiology but the difference lies in the T cell subpopulation and the ratio of T helper to T suppressor T4/T8.

Alpha 1 adrenergic receptors in mesenteric arteries of rats with chronic renal failure.

In previous studies we have shown that patients or rats with chronic renal failure display reduced blood pressure response to norepinephrine (NE). This abnormality is related to the high levels of parathyroid hormone (PTH) which stimulates vasodilator prostaglandin production. To determine whether chronic renal failure (CRF) also affects pressor response to NE through changes in the properties of alpha 1 adrenoceptors, we have measured plasma NE and the number of binding sited (Bmax) and the KD of these receptors in isolated mesenteric arteries of normal CRF rats and of CRF rats previously parathyroidectomized (PTX). Plasma NE was greater (P less than 0.01) in CRF than in control (67 +/- 14 vs. 32 +/- 3.1 ng/dl), but it was not different from CRF-PTX rats. The Bmax of alpha 1 adrenoceptors was lower (P less than 0.05) in CRF than control (80 +/- 10 vs. 173 +/- 29 fmol/mg protein), but it was similar in CRF and CRF-PTX rats. The KD was not significantly different among the three groups of rats studied. The data show that the number of alpha 1 adrenoceptors is reduced in CRF and this is not related to excess PTH. This abnormality may contribute to the reduced pressor response to NE in CRF. The effect of PTH, on the vascular response to NE is not related to changes in plasma levels of NE or in binding sites for NE.

Effects of adrenalectomy on binding to and actions of adrenergic receptors.

Adrenalectomy results in significant changes in the mechanism of adrenergic activation of hepatic glycogenolysis. In adrenalectomized rats a greater role for the beta-adrenergic receptor is observed, whereas the alpha 1-adrenergic-mediated phosphorylase activation declines. Our present findings document that adrenalectomy causes a significant decrease in the high-affinity population of the alpha 1-adrenergic receptor labelled with [3H]adrenaline. Our data indicate a large increase in the number of beta-adrenergic binding sites after adrenalectomy. This increase was not consistent with the observed modest increase in the beta-adrenergic-mediated activation of cyclic AMP accumulation and glycogen phosphorylase. When alpha-adrenergic antagonists are present along with the catecholamine, a 100% increase in the adrenaline-mediated accumulation of cyclic AMP in hepatocytes from adrenalectomized rats was observed. Adrenalectomy was also shown to cause a significant increase in the hepatic alpha 2-adrenergic binding sites. These data are consistent with an inhibitory role on the beta-adrenergic-mediated activation of glycogenolysis by the hepatic alpha 2-adrenergic receptor in adrenalectomy.

Impaired insulin receptor phosphorylation in skeletal muscle membranes of db/db mice: the use of a novel skeletal muscle plasma membrane preparation to compare insulin binding and stimulation of receptor phosphorylation.

A method has been developed to isolate skeletal muscle plasma membranes from mice in good yield without harsh extraction procedures. The method involves perfusion of mouse hindquarters with a calcium-deficient buffer containing collagenase and hyaluronidase. This is followed by gentle disruption, filtration, and differential centrifugations. The entire procedure takes about six hours and the yield is approximately 4 mg. protein from 10 g. equivalent of hindquarter muscle. The preparation contained predominantly plasma membranes based on specific activities of marker enzymes, electron microscopic data, and specific binding sites for insulin and a -adrenergic ligand. Studies using such preparations from lean, 4-5 week old and 12-20 week old db/db mice showed marked reduction in the phosphorylation of the 95 kDa subunit of the insulin receptor of the obese mice with no change in insulin binding. In addition, there was a progressive reduction in insulin sensitivity in stimulating receptor phosphorylation in the db/db mice.

Possible involvement of a hypothalamic dopaminergic receptor in development of genetic obesity in mice.

We have studied the binding of the dopaminergic agonist 2-[5,8-3H]amino-6,7-dihydroxy-1,2,3,4-tetrahydronaphthalene [( 3H]ADTN) to hypothalamic membranes from the genetically diabetic-obese (db/db) mice and their lean littermates. The specific binding of [3H]ADTN was defined as the difference between the radioligand binding to the membranes in the absence or presence of 1 microM (+)-butaclamol. In order to control nonspecific binding, all binding assays were performed in the presence of 0.1 mM catechol and 0.3 mM ascorbic acid. Binding of [3H]ADTN was rapid, dissociable, saturable and stereoselective. (+)-Butaclamol was very potent whereas (-)-butaclamol was ineffective in inhibiting the binding of this radioligand. Concentration-dependent binding experiments and Scatchard analysis of the data yielded dissociation constant (Kd) of 3.5-4.2 nM and number of binding sites (n) equivalent to 170-200 fmol/mg protein for lean mice. For db/db mice, the data yielded a Kd of 4.0-4.7 nM and an n of 400-500 fmol/mg protein. It was also shown that the anorexic drugs, amphetamine and fenfluramine, inhibited [3H]ADTN binding in a dose-dependent manner. Binding parameters, obtained using membranes from mice made obese by parenteral administration of gold thioglucose, were not significantly different from those obtained for the lean mice. It is concluded that the regulation of the hypothalamic dopaminergic receptors may be related to the lesion in the genetically obese mice.

Evidence for heterogeneous distribution of alpha 1, alpha 2- and beta-adrenergic binding sites on rat-liver cell surface.

Fractionation of preparations of rat-liver membranes on linear sucrose gradients revealed different profiles for the binding of alpha 1-, alpha 2- and beta-adrenergic radioligands. The peaks of binding activities of [3H]prazosin and [3H]epinephrine were clearly separated from those of [3H]yohimbine and [125I]iodocyanopindolol which appeared at lower sucrose densities. Enzyme marker activities in the sucrose subfractions indicated the presence of plasma membranes in all of the subfractions. Furthermore, the binding peaks of the various adrenergic radioligands cannot be correlated with the presence of membranes derived from microsomes, lysosomes or Golgi apparatus. Pretreatment of rat livers with concanavalin A, in order to prevent the fragmentation of the plasma membranes during isolation, resulted in the shift of the binding of [3H]yohimbine and [125I]iodocyanopindolol to sucrose-gradient subfractions of higher densities, clearly separate from fractions containing microsomes and Golgi apparatus. There was no distinct separation of the binding peaks of prazosin, yohimbine, and cyanopindolol in sucrose-gradient subfractions from concanavalin A-pretreated livers. These results are consistent with the hypothesis that alpha 1-, alpha 2-, and beta-adrenergic binding sites are associated with plasma membranes, and are heterogeneously distributed on the rat-liver cell surface.

Mechanisms of hormonal regulation of liver metabolism.

The mechanism of actions of glucagon, alpha- and beta-adrenergic agonists, vasopressin and angiotensin II in the liver proposed in this article are summarized in Fig. 8. The actions of glucagon and beta-adrenergic agonists in liver can be entirely ascribed to their interaction with specific plasma membrane receptors which activate adenylate cyclase leading to the intracellular accumulation of cAMP and activation of cAMP-dependent protein kinase. This enzyme phosphorylates phosphorylase b kinase, glycogen synthase, L-type pyruvate kinase, and other liver proteins resulting in alterations in their activities which can account for several of the known hepatic responses to glucagon. There is no clear evidence that Ca2+ ions are involved in the hepatic actions of this hormone. Glucocorticoids, but not thyroid hormones, are required for normal responsiveness of the liver to glucagon. The steroids do not modify cAMP accumulation or cAMP-dependent protein kinase activation, but may act by modulating the action of the kinase on its substrates. Glucocorticoids and thyroid hormones decrease beta-adrenergic responses in the liver apparently by decreasing the number of beta-receptors. Insulin inhibits the actions of physiological concentrations of glucagon by decreasing cAMP accumulation: its mechanism of action is unknown. The actions of alpha-adrenergic agonists, vasopressin and angiotensin II on the liver resemble those of glucagon, but do not involve accumulation of cAMP or activation of cAMP-dependent protein kinase. These agents appear to act by increasing cytosolic Ca2+ thus altering the activities of Ca2+-sensitive enzymes such as phosphorylase b kinase and calmodulin-dependent glycogen synthase kinase. Their receptors appear to be located exclusively on the plasma membrane and a major mechanism by which they raise cytosolic Ca2+ is by inducing the release of this cation from mitochondria. These considerations imply the existence of an intracellular messenger(s) for these agents which is generated at the plasma membrane in response to receptor activation and exerts effects on mitochondria or perhaps other intracellular structures. Glucocorticoids and thyroid hormones increase alpha-adrenergic responses in the liver apparently by increasing the number of alpha-receptors. Insulin inhibits the responses of the liver to alpha-agonists, but not to vasopressin or angiotensin II.

Effects of trypsin on binding of [3H]epinephrine and [3H]-dihydroergocryptine to rat liver plasma membranes. Evidence for interconversion of binding sites.

Treatment of liver plasma membranes with trypsin at low concentrations (1 to 2 microgram/mg of protein) caused at 3- to 4-fold increase in alpha-specific [3H]epinephrine binding. The change was due to an increase in the number of high affinity binding sites, with no change in the dissociation constant. With increasing trypsin concentrations, the dissociation constant was decreased and there was a progressive loss of binding. Elastase, papain, and thermolysin caused similar effects, whereas the thrombin, leucine aminopeptidase, phospholipase A2, phospholipase C, phospholipase D, and detergents did not cause an increase in [EH]epinephrine binding. The increase in epinephrine high affinity binding sites was correlated with a loss of high affinity [3H]-dihydroergocryptine binding sites which also bind [3H]epinephrine with low affinity (El-Refai, M. F., Blackmore, P. F., and Exton, J. H. (1979) J. Biol. Chem. 254, 4375-4386). Incubation of membranes with the alpha blockers dihydroergocryptine (50 nM) and phenoxybenzamine (20 nM) prior to protease treatment diminished the increase in [3H]epinephrine binding induced by trypsin (1.5 microgram/mg). The concentration dependence and time course of trypsin actions on 70 nM [3H]epinephrine binding and 10 nM [3H]dihydroergocryptine binding are consistent with a trypsin-mediated conversion of low affinity epinephrine binding sites to high affinity epinephrine binding sites.

Subclassification of two types of alpha-adrenergic binding sites in rat liver.

Drug specificity studies with prazosin and yohimbine indicated that the two types of alpha-adrenergic binding sites identified using [3H]-epinephrine and [3H]-dihydroergocryptine in rat liver plasma membranes both belong to the alpha 1-sublcass.