Search

Background: Spinal anesthesia is used in wide range of surgical procedures, but it is associated with potential complications such as hypotension and shivering. Thus the present study was aimed to compare the effect of 6mg ondansetron and placebo 10 minutes before spinal anesthesia for prevention of hypotension and shivering in patients undergoing non-obstetric surgeries. Methods: A double blinded randomized placebo control trial was conducted in 50 patients. Patients were randomized into ondansetron group (n =25) and placebo group (n=25).The primary outcome was the measurement of SBP(Systolic Blood Pressure), DBP(Diastolic Blood Pressure), MAP(Mean Arterial Pressure) and HR(Heart Rate) at baseline, 5, 10, 15 and 30 minutes after subarachnoid block. Results: There was a significant mean difference in SBP and DBP at 5, 10, 15 and 30 minutes after subarachnoid block (SAB) between the groups (p

Polycrystalline Ag NPs were synthesized by environment benign and cost effective green route method using Ficus Benjamina leaf extract (FBLE). As-synthesized Ag NPs were characterized using various techniques such as X-ray diffraction, Fourier Transform Infrared spectroscopy (FTIR), Field emission scanning electron microscopy (FESEM), Transmission electron microscopy (TEM), and Atomic absorption spectroscopy (AAS). Structural analysis was carried out by employing the Rietveld refinement method which revealed that FBLE: Ag NPs exhibited face centered cubic crystallinity with space group \(Fm\stackrel{-}{3}m\) and space group no 225. FTIR spectra displayed the existence of phytochemicals such as phenols belonging to hydroxyl group (-OH) as bending vibration appeared at 3435 cm− 1 and 1638 cm− 1, respectively. Surface morphology and microstructure of FBLE: Ag NPs were depicted using FESEM and it was observed that biosynthesized Ag NPs showed well interlinked and homogenous distribution of grains with an average grain size of 31.12 ± 0.44 nm. FBLE: Ag NPs were used to detect heavy metals such as Lead (Pb), Cadmium (Cd), and Zinc (Zn) present in industrial waste water of different factories including textile, steel, and chemical.

India is the epicenter of diabetes mellitus (DM). The relationship between COVID and DM in age/gender-matched non-diabetics has not been studied yet. The role of DM in predicting the disease severity and outcome in COVID patients might provide new insight for effective management.We conducted a prospective comparative study at a COVID care center from 25th April-31st May 2021. Among 357 severe-COVID patients screened, all consecutive diabetes (n-113) and age/gender-matched non-diabetes (n-113) patients were recruited. All diabetics and non-diabetics at admission were subjected to high resolution computed tomography (HRCT) chest and inflammatory markers (C-reactive protein (CRP), D-dimer, ferritin, interleukin-6 (IL-6), lactate dehydrogenase (LDH), Neutrophil-Lymphocyte Ratio (NLR)) before starting anti- COVID therapy. Statistical analysis was done using JMP 15·0 ver·3·0·0.The prevalence of DM among the screened population (n-357) was 38·37%. The mean age of the study population was 61y with male preponderance (57%). There was no statistical difference in the HRCT-score or inflammatory markers in the two groups except for higher NLR (p-0·0283) in diabetics. Diabetics had significantly inferior overall survival (OS) (p-0·0251) with a 15d-OS of diabetics vs. non-diabetics being 58·87%, 72·67%, and 30d-OS of diabetics vs. non-diabetics being 46·76%, 64·61%, respectively. The duration of the hospital stay was not statistically different in the two groups (p-0·2).The mortality is significantly higher in severe-COVID patients with DM when compared to age/gender-matched non-diabetics. There was no significant difference in most inflammatory markers/CT at admission between the two groups.

Primary aim of this review was to compare the two treatment modalities-curettage and wide excision (WE)- of Giant cell tumours of distal radius along with the methods of reconstruction viz. arthrodesis (AD) and arthroplasty (AP), and determine which had a better outcome.PubMed and Cochrane library databases were systematically searched using a well-defined search strategy by two independent reviewers. Inclusion/exclusion criteria were predetermined using the PICO format. MINORS tool was used to evaluate study quality. Recurrence rate (RR) was the chief oncological determinant whereas range of motion, grip strength, disability of arm, shoulder and hand (DASH) and musculoskeletal tumour society (MSTS) scores and complication rates were the functional outcome measures used.For the first part, a total of 11 articles (284 patients) were analysed. The second half- AP versus AD-included four studies (71 patients). Quantitative analysis revealed a significantly higher RR (Odds ratio (OR) 8.6 [95% CI, 3.4, 21.75]) with curettage. WE, on the other hand, was associated with a higher complication rate (OR 0.3[ 95% CI, 0.14, 0.62]) and lower grip strength (Standard Mean Difference (SMD) 18.08[95% CI, 13.78, 22.37]). Complication rates were also significantly higher with wrist AP (OR 6.36[ 95% CI, 1.72, 23.52]). Remaining functional parameters failed to show any significant difference between either group.WE is the preferred surgical strategy in terms of lower RR and functionally equivalent results. In terms of the choice of reconstruction following WE, there is a trend towards higher patient satisfaction after wrist AD.

Background Among patients hospitalized for severe pneumonia due to coronavirus disease (COVID-19), clinical stability and normal resting peripheral oxygen saturation (SpO

The hydrothermally synthesised nanorods of Zn1 − xTbxO(x = 0.00, 0.02, 0.05, 0.1) were carried over here to analyse the changes in its optical, magnetic and electrical behavior on doping. Formation of hexagonal wurtzite structure with particle size in the range of 36 nm–22 nm was confirmed by X-Ray diffraction studies. The morphology of the samples was confirmed by SEM (Scanning electron microscope) images alongwith its TEM (transmission electron microscope) micrographs. SAED (Selected area electron diffraction) and HRTEM (High resolution transmission electron microscope) shows the clear formation of nanorods. The quantitative analysis of elemental composition was done by energy dispersive X-ray spectroscopy (EDAX). The effect of increase in dopant concentration on band gap was analysed by UV-vis spectra; the band gap was found to be 3.35, 3.31, 3.30, 3.28 eV for undoped and 2%, 5% and 10% Tb-doped ZnO nanorods respectively. The presence of various types of defects was verified by PL study. The room temperature ferromagnetism behavior was tested by VSM and saturation magentization varies from 0.004 emu/g to 0.05 emu/g for undoped to 10% tb-doped ZnO nanorods. The dependence of resistivity on dopant concentration was carried out by four probe method which shows rise in resistivity with increasing dopant concentration.

Future of sustainable fashion lies in adoption of AI for a better understanding of consumer shopping behaviour and using this understanding to further optimize product design, development and sourcing to finally reduce the probability of overproducing inventory. Explainability and interpretability are highly effective in increasing the adoption of AI based tools in creative domains like fashion. In a fashion house, stakeholders like buyers, merchandisers and financial planners have a more quantitative approach towards decision making with primary goals of high sales and reduced dead inventory. Whereas, designers have a more intuitive approach based on observing market trends, social media and runways shows. Our goal is to build an explainable new product forecasting tool with capabilities of interventional analysis such that all the stakeholders (with competing goals) can participate in collaborative decision making process of new product design, development and launch.

Pathologic roles for innate immunity in neurologic disorders are well-described, but protective aspects of the immune response are less understood. Dectin-1, a C-type lectin receptor (CLR), is largely known to induce inflammation. However, we found that Dectin-1 is protective in experimental autoimmune encephalomyelitis (EAE), while its canonical signaling mediator, Card9, promotes the disease. Notably, Dectin-1 does not respond to heat-killed Mycobacteria, an adjuvant to induce EAE. Myeloid cells mediate the protective function of Dectin-1 in EAE and upregulate gene expression of neuroprotective molecules, including Oncostatin M (Osm) through a non-canonical Card9-independent pathway, mediated by NFAT. Furthermore, we found that the Osm receptor (OsmR) functions specifically in astrocytes to reduce EAE severity. Our study revealed a new mechanism of protective myeloid-astrocyte crosstalk regulated by a non-canonical Dectin-1 pathway and identifies novel therapeutic targets for CNS autoimmunity.Graphical AbstractDectin-1 is a protective C-type lectin receptor (CLR) in experimental autoimmune encephalomyelitis (EAE)Dectin-1 promotes expression of Osm, a neuroprotective IL-6 family cytokine, in myeloid cellsOsmR signaling in astrocytes limits EAE progression and promotes remissionNon-canonical Card9-independent signaling drives a distinct Dectin-1-mediated transcriptional program to induce expression of Osm and other factors with protective or anti-inflammatory functions

Human blood monocytes are divided into populations based on the differential expression of CD14 and CD16 receptors: CD14 (+) CD16(classical), CD14 (+) CD16 (+) (intermediate), and CD14(-)CD16(+) (non-classical). Given their functional differences and their role in pathogenesis of chronic obstructive pulmonary disease (COPD), monocyte profiling is of clinical interest. Here we investigated blood monocyte subsets in clinically stable COPD patients with alpha1-antitrypsin (AAT) deficiency (PiZZ, n = 7) and with normal AAT variant (PiMM, n = 7). Peripheral whole blood was collected in sodium heparin tubes and incubated with LPS (from E. coli; 1 mu g/ml) or placebo for 6 h at 37 degrees C, 5% CO2. To profile monocyte subsets we performed flow cytometry analysis based on HLA-DR and CD14/CD16 staining. HLA-DR + subsets of cells did not differ between PiZZ and PiMM COPD, and healthy controls (n = 7), used as a reference. Monocyte profiling, which express the CD14 and CD16, but not the HLA-DR (HLA-DR-) showed that intermediate monocytes subset was lowest in PiZZ group, and almost totally disappeared from blood treated with LPS. The non-classical subset was almost absent in PiZZ patients independently of LPS treatment. Recent studies demonstrate that non-classical monocytes exhibit a unique ability to protect the vascular endothelium under both homeostatic and inflammatory conditions whereas intermediate monocytes are recruited at a later stage of inflammation, and are associated with secretion of cytokines/chemokines and wound healing. Evident alterations in blood monocyte subsets together with a partial reduction of AAT levels, an important anti-inflammatory protein, can be key factors for the early manifestation of emphysema in some PiZZ AATD carriers.

Avulsion injuries of domes of the diaphragm are rare injuries and may occur following lateral thoracoabdominal trauma. We share our experience of two cases of avulsion injuries of the right dome of the diaphragm. Our first case presented within a week following blunt trauma to the abdomen, and on thoracotomy, an effective repair was performed by restoring attachment of the diaphragm to the parietes. Our second case presented with severe respiratory distress, 1½ months after sustaining blunt injury chest and abdomen in a road traffic accident and on thoracotomy was found to have a completely necrosed right hemidiaphragm, and hence, no repair could be performed. However, the patient could not be weaned off ventilator and died after 3 months of primary injury. These cases highlight the importance of early diagnosis and repair of diaphragmatic injuries for a favorable outcome.

SUMMARY Osteopontin (OPN) has been considered a potential biomarker of graft-versus-host disease (GVHD). However, the function of OPN in GVHD is still elusive. Using a mouse model of acute GVHD (aGVHD), we report that OPN generated by CD4+ T cells is sufficient to exert a beneficial effect in controlling aGVHD through limiting gastrointestinal pathology, a major target organ of aGVHD. CD4+ T cell-derived OPN works on CD44 expressed in intestinal epithelial cells (IECs) and abates cell death of IECs. OPN also modulates gut microbiota with enhanced health-associated commensal bacteria Akkermansia. Importantly, we use our in vivo mouse mutant model to specifically express OPN isoforms and demonstrate that secreted OPN (sOPN), not intracellular OPN (iOPN), is solely responsible for the protective role of OPN. This study demonstrates that sOPN generated by CD4+ T cells is potent enough to limit aGVHD., Graphical abstract, In brief The role of osteopontin (OPN) derived from CD4+ T cells in acute graft-versus-host disease (aGVHD) is unknown. Aggarwal et al. show that CD4+ T cell-derived secreted OPN is protective in aGVHD by modulating the gut microbiome and limiting cell death of intestinal epithelial cells by the sOPN-CD44 axis.

Pathologic roles of innate immunity in neurologic disorders are well described, but their beneficial aspects are less understood. Dectin-1, a C-type lectin receptor (CLR), is largely known to induce inflammation. Here, we report that Dectin-1 limited experimental autoimmune encephalomyelitis (EAE), while its downstream signaling molecule, Card9, promoted the disease. Myeloid cells mediated the pro-resolution function of Dectin-1 in EAE with enhanced gene expression of the neuroprotective molecule, Oncostatin M (Osm), through a Card9-independent pathway, mediated by the transcription factor NFAT. Furthermore, we find that the Osm receptor (OsmR) functioned specifically in astrocytes to reduce EAE severity. Notably, Dectin-1 did not respond to heat-killed Mycobacteria, an adjuvant to induce EAE. Instead, endogenous Dectin-1 ligands, including galectin-9, in the central nervous system (CNS) were involved to limit EAE. Our study reveals a mechanism of beneficial myeloid cell-astrocyte crosstalk regulated by a Dectin-1 pathway and identifies potential therapeutic targets for autoimmune neuroinflammation.

Fungal necrotizing fasciitis (NF), particularly in the face, is an unusual infection. It is mostly seen in immunocompromised individuals and can be gravely destructive if diagnosis and treatment are delayed. We report this rare case of a 27-year-old, immunocompetent male who presented with gangrenous patch of skin on the cheek following blunt trauma to the right side of the face. Till now no case has been reported in literature with such an extensive soft tissue loss of face and involvement of facial skeleton due to fungal etiology. Clinical suspicion of necrotizing fasciitis led to early surgical intervention. Histopathological examination of the debrided tissue identified the infective organism as Apophysomyces elegans. Intravenous antifungal therapy with liposomal amphotericin B was initiated. Despite the prompt commencement of the treatment, the infection continued to spread, and the patient had to undergo serial debridement which resulted in orbital exenteration, partial maxillectomy and mandibulectomy on the right side. This resulted in a huge soft tissue defect requiring flap cover. A free anterolateral thigh flap was harvested to cover the soft tissue defect, but the blood flow could not be established. For salvage, scalp and pectoralis major muscle flaps were raised and used to cover the large hemifacial defect. The oral lining was created with a folded deltopectoral flap in a second stage. However, there was persistence of the fungal elements in wound bed even after prolonged systemic liposomal amphotericin B therapy and it invaded the flap margins due to which there was partial necrosis of the flap. In this article, we aim to describe the difficulties faced by us in the management of such devastating infection and the reconstructive challenge that it posed.

Zn1−xGdxO (x = 0, 2, 5, 10, 15 %) nanoparticles were synthesised by sol–gel method and analysed for their structural, morphological, optical and magnetic properties. X-ray diffraction confirms formation of hexagonal wurtzite single phase of the synthesized nanoparticles. Transmission electron microscopy shows that they have spherical morphology; UV–Vis spectroscopy shows that they undergo red shift; energy dispersive technique reveals that they have the prerequisite elements in the stoichiometry ratio; and, vibrating sample magnetometer depicts that they have room temperature ferromagnetism, which, further, enhances upon Gd-doping.

PURPOSE OF REVIEW: Despite the increasing number of clinical reports on immune reconstitution inflammatory syndrome (IRIS), mechanistic understanding of IRIS is still largely limited. The main focus of this review is to summarize animal studies, which were performed to better understand the cellular and molecular mechanisms underlying the pathology of IRIS. RECENT FINDINGS: Three IRIS animal models have been reported. They are Mycobacterial IRIS (M-IRIS), cryptococcal IRIS (C-IRIS) and Pneumocystis-IRIS. M-IRIS animal model suggested that, rather than lymphopenia itself, the failure to clear the pathogen by T cells results in excessive priming of the innate immune system. If this happens before T cell reconstitution, hosts likely suffer IRIS upon T cell reconstitution. Interestingly, T cells specific to self-antigens, not only pathogen-specific, could drive IRIS as well. SUMMARY: The mechanism to develop IRIS is quite complicated, including multiple layers of host immune responses; the innate immune system that detects pathogens and prime host immunity, and the adaptive immune system that is reconstituted but hyper-activated particularly through CD4(+) T cells. Animal models of IRIS, although there are still small numbers of studies available, have already provided significant insights on the mechanistic understanding of IRIS.

Human SERPINA1 gene is located on chromosome 14q31-32.3 and is organized into three (IA, IB, and IC) non-coding and four (II, III, IV, V) coding exons. This gene produces α1-antitrypsin (A1AT), a prototypical member of the serpin superfamily of proteins. We demonstrate that human peripheral blood leukocytes express not only a product corresponding to the transcript coding for the full-length A1AT protein but also two short transcripts (ST1C4 and ST1C5) of A1AT. In silico sequence analysis revealed that the last exon of the short transcripts contains an Open Reading Frame (ORF) and thus putatively can produce peptides. We found ST1C4 expression across different human tissues whereas ST1C5 was mainly restricted to leukocytes, specifically neutrophils. A high up-regulation (10-fold) of short transcripts was observed in isolated human blood neutrophils after activation with lipopolysaccharide. Parallel analyses by liquid chromatography-mass spectrometry identified peptides corresponding to C-terminal region of A1AT in supernatants of activated but not naïve neutrophils. Herein we report for the first time a tissue specific expression and regulation of short transcripts of SERPINA1 gene, and the presence of C-terminal peptides in supernatants from activated neutrophils, in vitro. This gives a novel insight into the studies on the transcription of SERPINA1 gene. This work has been partially funded by the Instituto de Salud Carlos III (www.isciii.es) grant PI14CIII/00070 (BMD) and SEPAR (Sociedad Española de Neumología y Cirugía Torácica, www.separ.es) grant 92/2014. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript. Sí

Bronchiectasis is an aetiologically heterogeneous, chronic and often progressive disease resulting in the permanent dilatation of one or more bronchi or bronchioli. Several reports indicated an association among inherited α1-antitrypsin deficiency (α1-ATD), pulmonary infections and bronchiectasis, with a frequency up to 10% [1, 2]. It has been postulated that in α1-ATD individuals repeated episodes of ordinary bronchitis, of whatever cause, may lead to the development of bronchiectasis [3]. Most reported α1-ATD cases with bronchiectasis are elderly homozygous PiZZ (Glu342Lys) smokers with emphysema. There are only a few historical case reports with bronchiectasis and α1-ATD in the absence of emphysema [4, 5]. Whether there is an increased risk of pulmonary diseases, including bronchiectasis, in heterozygous PiMZ α1-ATD carriers is a matter of debate [6, 7]., Recurrent infections of the upper airways in early life may be a warning sign of inherited α1-antitrypsin deficiency http://ow.ly/iJsF300kbyV

Recurrent infections of the upper airways in early life may be a warning sign of inherited α 1 -antitrypsin deficiency http://ow.ly/iJsF300kbyV

To the Editor: PiZZ (Glu342Lys) alpha-1 antitrypsin deficiency (A1ATD) is a typical genetic risk factor associated with the development of early-onset chronic obstructive pulmonary disease (COPD) with emphysema. Because A1AT is a major circulating inhibitor of serine proteases (serpin), a severe deficiency of this protein may lead to lung tissue damage by uncontrolled activity of neutrophil elastase, proteinase 3 (PRTN3), and other serine proteases. In general, a proteinase/antiproteinase imbalance is among potential mechanisms implicated in the pathophysiology of COPD (1). The importance of A1AT in maintaining protease–antiprotease homeostasis is also supported by a positive correlation between a recently described in vivo marker of neutrophil elastase activity (Aα-Val360) and disease severity in emphysema related to A1ATD (2). There is, however, considerable heterogeneity in the clinical expression among people with type ZZ A1ATD. Some develop emphysema in early adulthood (35–45 years of age), whereas others in late adulthood or not at all, and severity of symptoms also varies. Support provided by the German Center for Lung Research and in part by the research grant from Grifols Pharmaceutical Company (R.K. and S.J.). Sí

Glioblastoma multiforme (GBM) is the most aggressive and the commonest primary brain tumor with a tendency for local invasiveness. The pathways of neoplasia, invasion and inflammation are inextricably linked in cancer and aberrations in several regulatory pathways for these processes have been identified. Here we have studied the FAT1 (Homo sapiens FAT tumor-suppressor homolog 1 (Drosophila)) gene to identify its role in the tumorigenecity of the gliomas. The expression of FAT1 was found to be high in grade IV glioma cell lines (U87MG, A172, U373MG and T98G) but low in grade III glioma cell lines (GOS3 and SW1088). Two cell lines (U87MG and A172) with high FAT1 expression were chosen for in vitro FAT1-knockdown studies. FAT1 knockdown by small interfering RNA resulted in decreased migration and invasion of both the cell lines along with increased expression of the tumor-suppressor gene programmed cell death 4 (PDCD4). Increased PDCD4 expression led to the attenuation of activator protein-1 (AP- 1) transcription by inhibiting c-Jun phosphorylation and resulted in concomitant decrease in the expression of AP-1-target genes like MMP3, VEGF-C and PLAU, the pro-inflammatory regulator COX-2 and cytokines IL1b and IL-6. Conversely, simultaneous silencing of PDCD4 and FAT1 in these cells significantly enhanced AP-1 activity and expression of its target genes, resulting in increase in mediators of inflammation and in enhanced migratory and invasive properties of the cells. We also observed a negative correlation between the expression of FAT1 and PDCD4 (P = 0.0145), a positive correlation between the expression of FAT1 and COX-2 (P = 0.048) and a similar positive trend between FAT1 and IL-6 expression in 35 primary human GBM samples studied. Taken together, this study identifies a novel signaling mechanism mediated by FAT1 in regulating the activity of PDCD4 and thereby the key transcription factor AP-1, which then affects known mediators of neoplasia and inflammation.

α1-Antitrypsin (A1AT) purified from human plasma upregulates expression and release of angiopoietin-like protein 4 (Angptl4) in adherent human blood monocytes and in human lung microvascular endothelial cells, providing a mechanism for the broad immune-regulatory properties of A1AT independent of its antiprotease activity. In this study, we demonstrate that A1AT (Prolastin), a potent inducer of Angptl4, contains significant quantities of the fatty acids (FA) linoleic acid (C18:2) and oleic acid (C18:1). However, only trace amounts of FAs were present in preparations that failed to increase Angplt4 expression, for example, A1AT (Zemaira) or M-type A1AT purified by affinity chromatography. FA pull-down assays with Western blot analysis revealed a FA-binding ability of A1AT. In human blood-adherent monocytes, A1AT-FA conjugates upregulated expression of Angptl4 (54.9-fold, p < 0.001), FA-binding protein 4 (FABP4) (11.4-fold, p < 0.001), and, to a lesser degree, FA translocase (CD36) (3.1-fold, p < 0.001) relative to A1AT devoid of FA (A1AT-0). These latter effects of A1AT-FA were blocked by inhibitors of peroxisome proliferator-activated receptor (PPAR) β/δ (ST247) and PPARγ (GW9662). When compared with controls, cell pretreatment with ST247 diminished the effect of A1AT-LA on Angptl4 mRNA (11.6- versus 4.1-fold, p < 0.001) and FABP4 mRNA (5.4- versus 2.8-fold, p < 0.001). Similarly, preincubation of cells with GW9662 inhibited inducing effect of A1AT-LA on Angptl4 mRNA (by 2-fold, p < 0.001) and FABP4 mRNA (by 3-fold, p < 0.001). Thus, A1AT binds to FA, and it is this form of A1AT that induces Angptl4 and FABP4 expression via a PPAR-dependent pathway. These findings provide a mechanism for the unexplored area of A1AT biology independent of its antiprotease properties.

Context: Low back pain (LBP) is the most common orthopedic problem worldwide and is known to affect both younger and older adults. The stressful and time consuming curriculum of medical students predisposes them to this problem. Few statistics are available on prevalence rates of LBP among medical students in India. This study assesses the prevalence and risk factors of LBP in students of a medical college in Delhi. Methods: A cross-sectional study was carried out in a medical college in Delhi. The study subjects (n = 160; 100% participation) were selected via stratified random sampling from all undergraduate medical students (aged 17-25 years). A validated questionnaire was used to collect the data. Results: The overall prevalence of LBP among the students over the past one year was 47.5% (n = 76) with a prevalence of 32.5% at the time of data collection. Prevalence among males and females was 45.3% and 50%, respectively. Significant associations were found between LBP in the past year and coffee drinking (Regular = 57%, Occasional = 38.9%, Never = 65.2%, χ2 = 7.24, P= 0.02), body posture (Normal = 32.6%, Abnormal = 75%, χ2 = 18.97, P < 0.001), place of study (Study table = 33.8%, Bed = 58.6, Both = 61.5% χ2 = 10.51, P = 0.01), family history of LBP (Present = 75%, Absent = 38.3%, χ2 = 16.17, P < 0.001) and carrying backpacks (Regular = 50%, Occasional = 33%, Never = 0%, χ2 = 16.17, P < 0.001). The mean scores of depression (2.7 vs. 1.6), anxiety (3.5 vs 1.9), and monotonous work (3.9 vs. 1.8) were found to be significantly higher in group with LBP than in the non-LBP group. However, no association with LBP was seen for weight lifting, watching television/working on computers, driving, wearing heels, or body mass index. Discussion: The high prevalence of LBP among medical students and its association with poor study habits, lifestyle habits, and psychological factors highlight a need for life skills training, education, counseling, and restructuring of the medical curriculum.

Despite significant advances in revascularization techniques and medical therapy, there remains a significant population of patients who continue to have intractable angina symptoms. This review aims to define the patients with refractory angina pectoris (RAP) and to present the therapeutic options currently available for this condition. RAP itself is defined and the pharmacological treatment options other than traditional medical therapies are discussed. The latest therapeutic options for this patient population are extensively reviewed. Among the multitude of pharmacological and non-invasive therapeutic options for patients with RAP, ranolazine is a new drug indicated for the treatment of chronic angina, in combination with amlodipine, beta-blockers or nitrates. Enhanced external counterpulsation has not only been shown to improve symptoms, but also to improve long-term ventricular function in these patients. In randomized trials, neurostimulation has been shown to be effective in reducing angina symptoms. Transmyocardial laser revascularization has emerged as an invasive treatment for RAP over the last two decades. Extracorporeal shockwave myocardial revascularization gene therapy and percutaneous in situ coronary venous arterialization are still under investigation.

We describe a child with pathologically proven Hallervorden Spatz disease. He presented with extrapyramidal symptoms and characteristic "eye-of-the-tiger" sign on magnetic resonance imaging. He was given the possible benefit if any of deep brain stimulation with no much improvement. Pathological examination of the brain showed iron deposition in bilateral globus pallidi, spongiform change and neuron axonal degeneration (spheroids).