Evaluation of the outcome of replacement hemiarthroplasty by uncemented bipolar prosthesis in displaced fracture neck femur.

Despite continued discussion regarding the treatment of displaced femoral neck fractures, controversies continue regarding their optimal treatment, including the choice of implant and fixation method. Hemiarthroplasty is one of the option which eliminate concerns about fixation failure, nonunion, and avascular necrosis and has become the choice of surgery among the aged >60. This prospective interventional study was carried out on 28 cases at the Department of Orthopaedic Surgery, Bangabandhu Sheikh Mujib Medical University (BSMMU), from July 2009 to April 2012 to evaluate cementless, bipolar prosthesis among the active elderly patients. All subjects were evaluated with regard to postoperative clinical, functional and activity outcome (Modified Harris Hip Scoring and Hip Outcome Scoring), intra and post operative complications. One case was dropped from follow up and 22(81.48%) patients were considered to have satisfactory outcome after statistical analysis by chi-square test on at least 12 months follow up records. Although prosthetic stem valgus and periprosthetic fracture developed in 02 cases and 01 patient had sunken prosthesis, uncemented bipolar hemiarthroplasty can give significantly good functional outcomes with minimal complications for displaced intracapsular femoral neck fracture in active elderly patients.

Regulation of hindbrain Pyy expression by acute food deprivation, prolonged caloric restriction, and weight loss surgery in mice.

PYY is a gut-derived putative satiety signal released in response to nutrient ingestion and is implicated in the regulation of energy homeostasis. Pyy-expressing neurons have been identified in the hindbrain of river lamprey, rodents, and primates. Despite this high evolutionary conservation, little is known about central PYY neurons. Using in situ hybridization, PYY-Cre;ROSA-EYFP mice, and immunohistochemistry, we identified PYY cell bodies in the gigantocellular reticular nucleus region of the hindbrain. PYY projections were present in the dorsal vagal complex and hypoglossal nucleus. In the hindbrain, Pyy mRNA was present at E9.5, and expression peaked at P2 and then decreased significantly by 70% at adulthood. We found that, in contrast to the circulation, PYY-(1-36) is the predominant isoform in mouse brainstem extracts in the ad libitum-fed state. However, following a 24-h fast, the relative amounts of PYY-(1-36) and PYY-(3-36) isoforms were similar. Interestingly, central Pyy expression showed nutritional regulation and decreased significantly by acute starvation, prolonged caloric restriction, and bariatric surgery (enterogastroanastomosis). Central Pyy expression correlated with body weight loss and circulating leptin and PYY concentrations. Central regulation of energy metabolism is not limited to the hypothalamus but also includes the midbrain and the brainstem. Our findings suggest a role for hindbrain PYY in the regulation of energy homeostasis and provide a starting point for further research on gigantocellular reticular nucleus PYY neurons, which will increase our understanding of the brain stem pathways in the integrated control of appetite and energy metabolism.

Baker's method in the management of equinus deformity in cerebral palsy.

This prospective study was conducted in the department of orthopedic surgery in Bangabandhu Sheikh Mujib Medical University (BSMMU) Dhaka, Bangladesh, from January 2005 to December 2007. Total number of 20 patients with 37 feet of equinus deformity due to cerebral palsy was managed by Baker's method. Equinus deformity in cerebral palsy is not uncommon in our outpatient department. Before operation patient walks on tip toes and after operation by Baker's method by apponeurotic lengthening of gastrocnemius muscle, with extensive physiotherapy, patients can able to walk normally in plantigrade feet. Among 20 patients only the spastic diplegic or hemiplegic equinus deformity in cerebral palsy was between 3 years to 12 years with a mean age of 5 years 9.6 months (SD+/-2 years 4.97 months). There were 3(15%) unilateral and 17(85%) bilateral cases. Among 20 cases, 13(65%) were male and 7(35%) were female. All cases were followed up for period ranging from 4 month to 28 months. Final clinical outcome was satisfactory (excellent and good) in 34(92%) feet and unsatisfactory (fair plus poor) in 3(8%) feet (p<0.001).

Morphometric study of vocal fold of different sexes of Bangladeshi cadaver.

The larynx is an organ of respiration and phonation. Larynx or Voice box is well developed in humans. The sound made by a human being using the vocal folds for talking, singing, laughing, crying, screaming etc. Pitch of the sound depends on the length, tension and mass of the vocal folds. This cross sectional descriptive type of study was done to see the length of the vocal folds and to establish the difference between sexes of adult Bangladeshi people. A total of 29 human larynges of adult age group ranging from 17 to 60 years in the both sexes were collected by purposive sampling during routine postmortem examination at the autopsy laboratory of Department of Forensic Medicine of Mymensingh Medical College, from October 2008 to March 2009. The mean length of vocal fold was measured and significance differences of the dimension between male and female were observed. In the present study observed finding was compared with those of other researchers. In male the mean(+/-SD) length of vocal fold was 23.12(+/-4.06) mm. In female the mean(+/-SD) length of vocal fold was 18.50(+/-2.39) mm. In statistical analysis, difference between male and female values was calculated by using Students (Unpaired) 't' test. The present study revealed that the value was greater in male than in female group and this difference was statistically significant (p<0.01).

Management of old Tendo Achilles injury by surgical reconstruction with Lindholm technique.

This prospective study was carried out in the department of orthopaedic surgery, Bangabandhu Sheikh Mujib Medical University from January 2006 to December 2007. Main aim of this study was to improve the power of planter flexion by reconstructive method with Lindholm technique to prevent walking disability. We had a study on 21 patients whose age range was 7 to 58 years. Mean age 34.19 years. Out of 21 cases male were 18(85.75%) and female were 3(14.25%). Chronocity of Tendo Achilles injury on average 2.64 (SD+/-1.08 month). Final clinical outcome of 21 cases 18 (85.75%) patients were satisfactory and 3(14.25%) were unsatisfactory. Lindholm technique is a good method of treatment for the management of Tendo Achilles injury was evident from this study. In Bangladesh toilet pan injury was more common. All patients were treated by surgical method of reconstruction by Lindholm technique.

5-HT inhibition of rat insulin 2 promoter Cre recombinase transgene and proopiomelanocortin neuron excitability in the mouse arcuate nucleus.

A number of anti-obesity agents have been developed that enhance hypothalamic 5-HT transmission. Various studies have demonstrated that arcuate neurons, which express proopiomelanocortin peptides (POMC neurons), and neuropeptide Y with agouti-related protein (NPY/AgRP) neurons, are components of the hypothalamic circuits responsible for energy homeostasis. An additional arcuate neuron population, rat insulin 2 promoter Cre recombinase transgene (RIPCre) neurons, has recently been implicated in hypothalamic melanocortin circuits involved in energy balance. It is currently unclear how 5-HT modifies neuron excitability in these local arcuate neuronal circuits. We show that 5-HT alters the excitability of the majority of mouse arcuate RIPCre neurons, by either hyperpolarization and inhibition or depolarization and excitation. RIPCre neurons sensitive to 5-HT, predominantly exhibit hyperpolarization and pharmacological studies indicate that inhibition of neuronal firing is likely to be through 5-HT(1F) receptors increasing current through a voltage-dependent potassium conductance. Indeed, 5-HT(1F) receptor immunoreactivity co-localizes with RIPCre green fluorescent protein expression. A minority population of POMC neurons also respond to 5-HT by hyperpolarization, and this appears to be mediated by the same receptor-channel mechanism. As neither POMC nor RIPCre neuronal populations display a common electrical response to 5-HT, this may indicate that sub-divisions of POMC and RIPCre neurons exist, perhaps serving different outputs.

Pancreatic deletion of insulin receptor substrate 2 reduces beta and alpha cell mass and impairs glucose homeostasis in mice.

AIMS/HYPOTHESIS: Insulin signalling pathways regulate pancreatic beta cell function. Conditional gene targeting using the Cre/loxP system has demonstrated that mice lacking insulin receptor substrate 2 (IRS2) in the beta cell have reduced beta cell mass. However, these studies have been complicated by hypothalamic deletion when the RIPCre (B6.Cg-tg(Ins2-cre)25Mgn/J) transgenic mouse (expressing Cre recombinase under the control of the rat insulin II promoter) is used to delete floxed alleles in insulin-expressing cells. These features have led to marked insulin resistance making the beta cell-autonomous role of IRS2 difficult to determine. To establish the effect of deleting Irs2 only in the pancreas, we generated PIrs2KO mice in which Cre recombinase expression was driven by the promoter of the pancreatic and duodenal homeobox factor 1 (Pdx1, also known as Ipf1) gene. MATERIALS AND METHODS: In vivo glucose homeostasis was examined in PIrs2KO mice using glucose tolerance and glucose-stimulated insulin secretion tests. Endocrine cell mass was determined by morphometric analysis. Islet function was examined in static cultures and by performing calcium imaging in Fluo3am-loaded beta cells. Islet gene expression was determined by RT-PCR. RESULTS: The PIrs2KO mice displayed glucose intolerance and impaired glucose-stimulated insulin secretion in vivo. Pancreatic insulin and glucagon content and beta and alpha cell mass were reduced. Glucose-stimulated insulin secretion and calcium mobilisation were attenuated in PIrs2KO islets. Expression of the Glut2 gene (also known as Slc2a2) was also reduced in PIrs2KO mice. CONCLUSIONS/INTERPRETATION: These studies suggest that IRS2-dependent signalling in pancreatic islets is required not only for the maintenance of normal beta and alpha cell mass but is also involved in the regulation of insulin secretion.

Liver-specific deletion of insulin receptor substrate 2 does not impair hepatic glucose and lipid metabolism in mice.

AIMS/HYPOTHESIS: Hepatic insulin resistance is thought to be a critical component in the pathogenesis of type 2 diabetes but the role of intrinsic insulin signalling pathways in the regulation of hepatic metabolism remains controversial. Global gene targeting in mice and in vitro studies have suggested that IRS2 mediates the physiological effects of insulin in the liver. Reduced hepatic production of IRS2 is found in many cases of insulin resistance. To investigate the role of IRS2 in regulating liver function in vivo, we generated mice that specifically lack Irs2 in the liver (LivIrs2KO). MATERIALS AND METHODS: Hepatic insulin signalling events were examined in LivIrs2KO mice by western blotting. Glucose homeostasis and insulin sensitivity were assessed by glucose tolerance tests and hyperinsulinaemic-euglycaemic clamp studies. The effects of high-fat feeding upon glucose homeostasis were also determined. Liver function tests were performed and expression of key metabolic genes in the liver was determined by RT-PCR. RESULTS: Proximal insulin signalling events and forkhead box O1 and A2 function were normal in the liver of LivIrs2KO mice, which displayed minimal abnormalities in glucose and lipid homeostasis, hepatic gene expression and liver function. In addition, hepatic lipid homeostasis and the metabolic response to a high-fat diet did not differ between LivIrs2KO and control mice. CONCLUSIONS/INTERPRETATION: Our findings suggest that liver IRS2 signalling, surprisingly, is not required for the long-term maintenance of glucose and lipid homeostasis, and that extra-hepatic IRS2-dependent mechanisms are involved in the regulation of these processes.

Species differences in peroxisome proliferation; mechanisms and relevance.

Peroxisome proliferators are a class of structurally diverse chemicals, which induce liver carcinogenesis in rodents through interaction and activation of the Peroxisome Proliferator-Activated Receptor alpha (PPARalpha). PPARalpha agonists elicit a powerful pleiotropic response, which include hypolipidaemia. We have examined the response of species that are classically unresponsive to peroxisome proliferators. Whereas hamster responds to PPARalpha agonists by hepatomegaly and induction of marker genes, the guinea pig does not undergo hepatomegaly or induction of marker genes, such as CYP4A13. Both the hamster and the guinea pig have PPARalpha, and the guinea pig receptor has been characterised to be fully functional, as demonstrated in reporter gene expression assays. However, the guinea pig PPARalpha is expressed at low levels in liver, and the currently favoured hypothesis to explain species differences in hepatic peroxisome proliferation invokes the low level of PPARalpha as the principal determinant of species responsiveness. However, the demonstration that guinea pigs and humans undergo hypolipidaemia induced by PPARalpha-agonists calls into question the mode of action of PPARalpha agonists in "non-responsive" species.

Molecular basis of non-responsiveness to peroxisome proliferators: the guinea-pig PPARalpha is functional and mediates peroxisome proliferator-induced hypolipidaemia.

The guinea pig does not undergo peroxisome proliferation in response to peroxisome proliferators, in contrast with other rodents. To understand the molecular basis of this phenotype, the peroxisome proliferator activated receptor alpha (PPARalpha) from guinea-pig liver was cloned; it encodes a protein of 467 amino acid residues that is similar to rodent and human PPARalpha. The guinea-pig PPARalpha showed a high substitution rate: maximum likelihood analysis was consistent with rodent monophyly, but could not exclude rodent polyphyly (P approximately 0.06). The guinea-pig PPARalpha cDNA was expressed in 293 cells and mediated the induction of the luciferase reporter gene by the peroxisome proliferator, Wy-14,643, dependent on the presence of a peroxisome proliferator response element. Moreover the PPARalpha RNA and protein were expressed in guinea-pig liver, although at lower levels than in a species which is responsive to peroxisome proliferators, the mouse. To determine whether the guinea-pig PPARalpha mediated any physiological effects, guinea pigs were exposed to two selective PPARalpha agonists, Wy-14, 643 and methylclofenapate; both compounds induced hypolipidaemia. Thus the guinea pig is a useful model for human responses to peroxisome proliferators.