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Aims: The primary aim was to determine if the Nottingham Hip Fracture Score (NHFS) could be used to stratify 1-year mortality risk amongst periprosthetic hip fracture patients. The secondary aim was to identify 1year mortality rates amongst surgically managed periprosthetic hip fractures., Methods: Our electronic fracture database was interrogated for all Vancouver B or C periprosthetic fractures between September 2009 to April 2019; 83 patients were identified. All available data was then collected from radiographic, electronic and paper notes. The NHFS was retrospectively calculated for each patient. Statistical analysis was performed to identify factors significantly affecting 12month mortality using Akaike's information criterion corrected for small sample sizes (AICc), binomial logistic regression was performed using each variable; the p-values presented are for the coefficients of the regressor., Results: Periprosthetic fractures have a 1year mortality risk of 26.5%, 30 day mortality was 4.82%. The NHFS was found to be highly predictive of 1-year mortality amongst this patient cohort (p = 0.0001). We find that each unit increase in the NHFS is correlated with a 2.7times increase in mortality rate. There was no evidence that time lag from presentation to surgery led to an increased mortality (p = 0.455)., Conclusion: The NHFS can be used to stratify the 1-year mortality risk amongst patients who have periprosthetic hip fracture; this is a new finding not previously published to our knowledge. Given that time to surgery does not correlate with mortality, patients should be risk stratified on admission with NHFS. Time is then available to conduct a multi-disciplinary approach to optimize the patient, personnel and equipment. The introduction of a parallel multidisciplinary pathway to neck of femur fractures is long overdue and must be expedited., (Copyright © 2021 Elsevier Ltd. All rights reserved.)

Objective: To evaluate various prognostic factor predictors of residual growth in Relook transurethral resection of bladder tumor (TURBT) in superficial bladder cancer. Also, to evaluate the role of Relook TURBT along with the ploidy for prediction of recurrence and stage progression in these patients., Material and Methods: Fifty patients with superficial bladder cancer underwent TURBT after complete evaluation. Ploidy of the tumor specimen was evaluated by flow cytometry. After 4 to 6 weeks of initial TURBT, these patients underwent Relook TURBT. Final treatment was given after the results of the histological evaluation of these specimens. Patients who underwent bladder sparing treatment were followed-up., Results: Of the patients, 28.5% had residual tumor in Relook TURBT. Growth was found to be at the same site in 66.7% and at a different site 33.3%; 75% had single while 25% had multiple residual growth. Residual malignant tissue had a statistically significant correlation with size of the tumor (>3 cm), appearance (solid tumor), number (>3), grade (high), and multiple previous resections. Overall, the up-migration of stage and grade leads to change in treatment in 41.6%; 5 underwent radical cystectomy and 1 opted for radiotherapy; in 2 patients, intravesical BCG was given. In follow-up of mean 11.5 months, 16.6% had recurrence. Presence of residual growth in Relook TURBT along with number, size, morphology, and multiple previous resections were found to have significant correlation with the recurrence in these patients. Ploidy and grade of the tumor were not found to have correlation., Conclusions: Multiple, more than 3 cm, solid high grade tumor with > 3 previous resections were predictors of presence of residual tumor in Relook TURBT. Presence of residual growth is a significant risk factor for recurrence. Ploidy was not found to be significantly correlated with recurrence.

We developed a model system whereby HP1 can be targeted to pericentric heterochromatin in ES cells lacking Suv(3)9h1/2 histone methyltransferase (HMTase) activities. HP1 so targeted can reconstitute tri-methylated lysine 9 of histone H3 (Me(3)K9H3) and tri-methylated lysine 20 of histone H4 (Me(3)K20H4) at pericentric heterochromatin, indicating that HP1 can regulate the distribution of these histone modifications in vivo. Both homo- and hetero-typic interactions between the HP1 isotypes were demonstrated in vivo as were HP1 interactions with the ESET/SETDB1 HMTase and the ATRX chromatin remodelling enzyme. We conclude that HP1 not only "deciphers" the histone code but can also "encode it".

Both male and female freshwater catfish, Heteropneustes fossilis, were exposed to safe (SC; 0.1 and 1.0 mg/L) and sublethal (SL; 10 mg/L) concentrations of an agricultural pesticide, gamma-hexachlorocyclohexane (gamma-HCH) for 4 weeks during the active pre-spawning (vitellogenic) phase of their annual reproductive cycle. On the last day of exposure, 18 h before killing, fish were treated intramuscularly (i.m.) with [I-14C]acetic acid (74 kBq per fish). After 4 weeks of exposure, we monitored the effects of gamma-HCH on gonadosomatic index (GSI); on plasma concentrations of gonadotropin (GtH), testostosterone (T), 11-ketotestosterone (11-KT), 17beta-estradiol (E2); and on hepatic incorporation of [I-14C]acetic acid into total phospholipids (TP) and the fractions thereof: phosphatidylcholine (PC), phosphatidylserine (PS), phosphatidylinositol (PI), and phosphatidylethanolamine (PE). In both the sexes, GSI and plasma GtH were decreased significantly in response to gamma-HCH exposure. Plasma T and 11-KT in males, and plasma T and E2 in females declined significantly in response to gamma-HCH exposure. In both the sexes, hepatic incorporation of [I-14C]acetic acid into PS and PI increased significantly, whereas incorporation into TP, PC, and PE was significantly reduced after gamma-HCH exposure. Our findings demonstrated that gamma-HCH exposure depressed GSI, plasma GtH, sex steroids, and [I-14C]acetic acid incorporation into hepatic TP, and had very selective and specific effects on various classes of TP, resulting either from the hypothalamo-hypophyseal-gonadal axis or from direct action on hepatic and steroidogenic enzymes during the pre-spawning phase, causing reproductive endocrine disruptions.

Insulin-like growth factor 2 (Igf 2) and H19 genes are oppositely imprinted and as such have been most extensively studied imprinted genes both genetically and at the molecular level. Imprints of the H19 gene, being established during spermatogenesis, are epigenetically transmitted to the somatic cells of the embryo. Current hypotheses attempting to explain the allele-specific silence of the H19 gene include DNA methylation and chromatin condensation. In order to understand the molecular basis of H19 epigenesis, it is crucial to identify the markings in the chromatin organising the imprinted domain in spermatozoa. Using Micrococcal nuclease (MNase), DNase I and Methidiumpropyl-EDTA. iron II (MPE.Fe(II)) as chromatin probes, we demonstrate that in mouse epididymal spermatozoa, at least 4kb DNA upstream of the H19 'cap' site, containing the imprinted and differentially methylated domain (DMD), is heterochromatic. The cleavage sites in this domain (-2 to -4kb) exhibit approximately 425bp periodicity. This structure is maintained in the paternal allele of normal embryos and is disrupted at -2.2, -2.65 and at -3.5kb in embryos maternally disomic for the distal end of chromosome 7 (MatDp 7). The hypersensitive sites in chromatin precisely register the MPE.Fe(II) cleavage sites in chromosomal DNA. Therefore, the DNA sequences in the imprinted domain constrain the chromatin structure in a way similar to that of 1.688g/cm(3) Drosophila satellite chromatin. In addition, we find that condensation of the paternal allele correlates with methylation-dependent alteration in the structure of DNA sequences in DMD. These results suggest that CpG-methylation induces localised changes in DNA conformation and these facilitate consequent remodelling of chromatin thereby allowing the paternal and maternal H19 alleles to be distinguished.

The Drosophila Ultrabithorax (Ubx) gene was one of the first homeotic genes to be characterised and it specifies the phenotypic characteristics of parasegments 5 and 6. The intricate pattern of Ubx expression in these parasegments is conferred by enormous regulatory regions which, together with the structural gene, constitute the Ubx domain. A genetic, "open-for-business", model based on classical mutational analysis proposed that the regulatory regions were in fact composite structures, consisting of parasegment-specific regulatory domains that contain arrays of cell-specific enhancers which drive the intricate pattern of Ubx expression. Here, we propose a molecular mechanism, based on a survey of numerous transgenic studies, of the setting up of these parasegment-specific regulatory domains in the appropriate parts of the late blastoderm embryo. We construct a mathematical model of this mechanism using the molecular characteristics of a single initiator element, the distributions of segmentation gene products and simple competitive binding equations. We attempt to fit this mathematical model to the idealised patterns of activity and closure of the parasegment-specific domains derived from the genetic model. The resulting fitted pattern of activity and closure obtained with the simplest version of our competitive binding model shows some deviations from the idealised pattern based on the genetic model. Comparison of the predictions with recent experimental evidence suggests that the competitive binding model more accurately reflects certain features of the Ubx expression pattern--features not predicted by the genetic model.

Testicular and ovarian fragments of Carassius auratus, taken during the reproductively active prespawning phase (June) of its annual reproductive cycle, were incubated with different concentrations (0 mg/ml, 0 ppm; 0.001 mg/ml, 1 ppm; 0.01 mg/ml, 10 ppm; and 0.02 mg/ml, 20 ppm) of gamma-hexachlorocyclohexane (gamma-HCH) in the presence of either exogenous precursor [3H]-17-hydroxyprogesterone ([3H]17-P) or carp hypophyseal homogenate. The free (unconjugated) and conjugated metabolites (glucuronides and sulfates) of [3H]-17-P [androstenedione (AD), androstenetrione, 17-hydroxyprogesterone, testosterone (T), 11-deoxycortisol (S), 17, 20alpha-dihydroxy-4-pregnen-3-one (17,20alphaP), 17, 20beta-dihydroxy-4-pregnen-3-one (17,20betaP), 7alpha-pregnanetetrols (7alpha-P), and other polar metabolites] were separated by thin-layer chromatography and high-performance liquid chromatography. The endogenous production of unconjugated (free) steroids T, 17,20betaP, S, and 11-ketotestosterone (11-KT) in response to gamma-HCH were measured by radioimmunoassay. Among the in vitro metabolism of [3H]-17-P, in males, free steroids of AD, T, 17,20alphaP, S, and polar-free steroids were increased with the decreased yield of 11-KT. Percentage yield of testosterone glucuronide (TG) was increased with highly significant decreased yields of polar glucuronide steroids. The sulfate steroids of 17, 20alphaP, 17,20betaP, S, and 11-KT remain unchanged. In females, the decreased percentage of yield of AD and S and elevated T were noticed. The yield of TG was increased with decreased yield of 7alpha-P glucuronides. The percentage yield of AD sulfate and sulfate steroids of 17,20alphaP, 17,20betaP, and S were noted to be increased, but the yield for S sulfate was very high. Endogenous production of T was increased in both sexes in the presence of gamma-HCH, but 11-KT in male and S in female were depressed. 17, 20betaP was stimulated at some concentrations in both sexes but levels were very low. Results indicate that gamma-HCH in vitro perturbed the steroid biosynthesis during this phase thereby affecting reproductive physiology.

Female specimens of Heteropneustes fossilis were exposed to a sublethal concentration of the organochlorine agricultural pesticide gamma-BHC (16 mg liter-1) for 4 weeks during the reproductively active preparatory and prespawning phases of the annual reproductive cycle. The effects of gamma-BHC on the gonadosomatic index (GSI) and on the histological changes in ovary, cholesterol-free cholesterol (CF), esterified cholesterol (CE), and the sex steroids testosterone-estradiol-17 beta, and 17 alpha-hydroxyprogesterone in plasma and ovary were monitored. Mystus gonadotropin (mGTH) was administered along with gamma-BHC exposure during the preparatory and prespawning phases. gamma-BHC decreases GSI during both phases; however, simultaneous administration of mGTH recovered the effect. gamma-BHC exposure caused inhibition of ovarian growth, resulting in a large number of stage I oocytes and few stage II oocytes, while at higher doses, mGTH reversed the impact of gamma-BHC, and a large number of stage III and vitellogenic oocytes were recorded. This pesticide also inhibited deesterification of CE to CF. Additionally, it impaired ovarian steroidogenesis and secretion of steroids into plasma. Lower doses of mGTH (0.1 and 1.0 microgram/fish) were ineffective in modulating the impact of gamma-BHC on lipids and steroids. However, higher doses (10 and 20 micrograms/fish) effectively revoked the impact of gamma-BHC, routed through the hypothalamo-hypophyseal-ovarian axis and directly upon the ovary.

Female specimens of Heteropneustes fossilis were exposed to a sublethal concentration of gamma-BHC (16 mg/liter) for 4 weeks during the preparatory and prespawning phases of their annual reproductive cycle. The effect of gamma-BHC on free fatty acids (FFA), monoglycerides (MG), diglycerides (DG), and triglycerides (TG) was monitored. gamma-BHC in general was inhibitory to lipogenesis during both of the reproductively active phases as judged by decreased levels of FFA, MG, DG, and TG. Lower doses of ovine luteinizing hormone-releasing hormone (oLH-RH) and Mystus gonadotropin (mGTH) were ineffective in modulating the impact of gamma-BHC; however, their higher doses effectively revoked the impact of gamma-BHC. From the evidence obtained here, it is concluded that gamma-BHC suppressed the action of oLH-RH and mGTH and affected lipogenesis in this species.

Female Heteropneustes fossilis were exposed to sublethal concentrations of malathion (5 and 20 microliters liter-1) and gamma-BHC (4 and 16 micrograms liter-1) for 4 weeks during different phases of their annual reproductive cycle. The impact of these pesticides on free fatty acids (FFA), monoglycerides (MG), diglycerides (DG), triglycerides (TG), phospholipids (PL), free cholesterol (CF), and esterified cholesterol (CE) in the liver, plasma, and ovary was assessed. During the preparatory phase both the pesticides reduced the levels of all the hepatic and ovarian lipids with elevated hepatic CE. During the prespawning phase these pesticides decreased all the lipids in the liver, plasma, and ovary with the elevation of hepatic FFA and CE. During the spawning phase a reduction of hepatic MG and CF with a decreased level of plasma and ovarian levels of FFA and PL was recorded, whereas ovarian levels of TG and CE were elevated in response to both the pesticides. During postspawning and resting phases all the hepatic lipids were reduced with the elevation of CE in response to the exposure. These pesticides also restricted their mobilization to the ovary. Cholesterol biosynthesis seemed unaffected but the hydrolysis of CE to CF was adversely affected during preparatory and prespawning phases which is a period of sex steroid hormone biosynthesis.

Thirty cases of blunt renal injury are reviewed. The need for rapid and accurate diagnosis of these cases with excretory urography, supplemented in certain patients with renal angiography, is discussed. High-dose excretory urography allows the cases to be categorized into minor or major injuries. All minor injuries can be managed without operation. For major injuries, a conservative approach, if necessary followed by surgical exploration, avoids loss of organ in most of the cases.