3B), pointing once again toward MAPK dephosphorylation as the mol

3B), pointing once again toward MAPK dephosphorylation as the molecular event that is targeted by zinc in IL-2- signaling. Our results suggest that zinc release after stimulation with IL-2 conserves ERK phosphorylation by inhibiting phosphatases, and hereby free zinc acts as a permissive signal. Zinc also inhibits protein tyrosine phosphatases, preserving signaling by the insulin and EGF receptors 28–30. The IL-2R itself, as well as JAK1 and 3 and STAT5, are activated by tyrosine phosphorylation 10. However, no activation of the STAT5-pathway by zinc was found in our experiments (Fig. 2A), indicating that zinc in IL-2R signaling primarily acts on phosphatases

that dephosphorylate ERK. Here,

intracellular localization of zinc signals selleck products might be relevant, and should be investigated in more detail, as tyrosine phosphorylation of the IL-2R and JAK occurs at the plasma membrane, whereas MAPK are present in cytosol and nucleus. Alternatively, the binding constants for some protein tyrosine phosphatases are in the low nanomolar concentration range 28, and future experiments should compare these values to the susceptibility of DUSPs and PP2A to zinc inhibition. Notably, there are seven DUSP known to dephosphorylate ERK 31, whereas PP2A also dephosphorylates MEK1/2 in addition to ERK 13. Because zinc had an effect on MEK and ERK in Fig. 2F, it seems likely that PP2A is among the molecular targets of zinc in T cells. Nevertheless, ERK dephosphorylation is completely inhibited by zinc, indicating that all other

ERK dephosphorylating this website enzymes are also susceptible to inhibition by zinc. When the expression of genes specifically triggered by the different pathways was analyzed by PCR (Fig. 3A and B; Supporting Information Fig. 4), i.e. CIS for STAT5 32 and c-fos for ERK 13, corresponding results to the Western blot analysis were found. STAT5-dependent CIS expression was not influenced by chelation or imitation of zinc signals, whereas c-fos induction was significantly decreased by TPEN. ERK signals are involved in proliferation and cellular survival in response to IL-2 10. Hence, we investigated the role of zinc signals in these events. Cells were labeled with (5)6-Carboxyfluorescein diacetate (CFDA) Dolichyl-phosphate-mannose-protein mannosyltransferase to measure proliferation and with propidium iodide to detect cytotoxicity, and analyzed by flow cytometry after growing for 24 h in the presence of various concentrations of TPEN. Concentrations of up to 3 μM TPEN did not lead to a significant reduction of viability, but IL-2-dependent proliferation of CTLL-2 was significantly reduced at TPEN concentrations of 2 μM and above (Fig. 3C), indicating a preferential requirement of zinc signals for IL-2-induced proliferation at concentrations that were not cytotoxic. TPEN can chelate several other metal ions in addition to zinc 33.

08% and 0 15% for Cre and 0 004% and 0 01% for FLPe Importantly,

08% and 0.15% for Cre and 0.004% and 0.01% for FLPe. Importantly, these results Protein Tyrosine Kinase inhibitor implied that the HD-AdV was preferentially packaged over the helper virus. Ng et al. concluded that this phenomenon could be explained if competition for packaging occurs between the helper virus and the HD-AdV genome (16, 34). Our results here provided experimental support to this hypothesis, namely, the result of the competition assay may explain why some helper virus that still retains the packaging domain is present and competes with HD-AdV: HD-AdV is more abundantly generated than expected. We thank Ms Y. Sato for her excellent technical work and Ms E. Kondo for her excellent secretarial assistance. This work was supported

in part by Grants-in-Aids from the Ministry of Education, Culture, Sports, Science and Technology to Y. K. and to I. S. No competing financial interests exist. “
“The pathway of immune system behaviour can be divided into three modules, each with its own logic and database. The modules are related in that they feed sequentially into each other for function. The modules are (1) the generation of the recognitive repertoire; (2) the sorting of the repertoire by purging it of anti-self; and (3) the coupling of the residue, anti-nonself, appropriately

to the biodestructive and BAY 57-1293 chemical structure ridding effector functions. While both the generation and sorting of the repertoire have been intensively investigated and are well understood in terms of firm theoretical frameworks, the understanding of Module 3, the Fenbendazole regulation of effector class, is patchy. This essay is an attempt to define the elements required for an understanding of Module 3 and that leads us to propose the Trauma Model. All free-living organisms have biodestructive and ridding mechanisms to protect themselves against parasitism. In the case of the immune system, the ridding of an infectious agent without harm to the host requires that it respond using selected recognitive elements (paratopes) coupled to an appropriate effector mechanism that is expressed

at a carefully monitored magnitude and for a defined time. The problem of the regulation of effector class has not been a central concern of immunologists. For a long time, the reason for this was a vacuum that could only be filled by what would be viewed as speculation. Consequently, discussions about class regulation were shelved while a great deal of descriptive data was gathered, theory-independently, such as the number of distinct effector classes, how they are armed, what is their mechanism of biodestruction and ridding, and what cell types are involved. By the time that much of this became known, interest in class regulation might have surfaced, yet it still lagged and for an unexpected reason. The information surrounding immune responsiveness had become so complex that the crosstalk required for the analysis of class regulation became difficult.

Also, once in the labyrinth, fetoplacental arteries branch alone;

Also, once in the labyrinth, fetoplacental arteries branch alone; veins

do not penetrate the labyrinth but instead remain localized in the chorionic plate (Figure 8). The absence of parallel veins in the labyrinth simplifies the analysis of the structure by 3D imaging. Nevertheless, segmentation of micro-CT datasets and detailed vascular analysis has been performed in other rodent organs including selleck chemicals llc the lung [43], kidney [40, 32], and liver [8, 19]. Results suggest that the patterning rules that are believed to govern branching in arterial trees [18, 44] are similar in the fetoplacental arterial tree compared to other adult organs. Branching patterns can be well described by a power law with a diameter scaling coefficient close to −3 in accord with Murray’s law [39]. The diameter scaling coefficient of the fetoplacental arterial tree is 2.9 in CD1 placentas [36] and thus is similar to that of the lung (−2.8) [43], kidney (−3) [32], and liver (−3) [8]. Length-to-diameter ratios in the fetoplacental arterial tree (2.3–2.9) selleck products [36] are also comparable to that of the lung (2.3–2.6) [43] and liver (2.1) [8], highlighting their similar branching structures and suggesting patterning via similar but unknown genetic mechanisms. The utility of micro-CT for visualizing, quantifying, and analyzing the

structure of the fetoplacental arterial tree, and for statistically comparing trees altered by environment or genetics is now apparent. Automated segmentation techniques have facilitated this approach, and methods for calculating relevant hemodynamic parameters developed. Thus, we are now at a stage where the fetoplacental arterial tree of the mouse can be exploited to advance our relatively rudimentary understanding of the role of genes and environmental factors on the growth, development, and branching patterns of arterial trees. This is important given the critical role of the arterial tree in efficiently disturbing

blood flow throughout Loperamide tissues, and the likely significant role of the arterial tree in determining the total vascular resistance of the bed, a critical factor in determining flow. Future studies evaluating the roles of specific genes and proteins could be readily undertaken using the available and growing plethora of knockout and transgenic mouse strains [13, 16], perhaps starting with the 99 known genotypes annotated with “abnormal placental labyrinth vasculature morphology” in accord with the Mammalian Phenotype Ontology [13, 29]. It is likely that many mutants currently lack an “abnormal placental labyrinth vasculature morphology” annotation because this vasculature has not yet been examined. Importantly, significant abnormalities in the fetoplacental arterial tree may occur even in cases where fetal growth is not compromised, as found for heterozygous deletion of Gcm1 [5]. Therefore, apparently unaffected heterozygote mutants may nevertheless provide insights into the genetic regulation of arterial branching patterns.

The purpose of this study was to evaluate the role of LTB4 in acc

The purpose of this study was to evaluate the role of LTB4 in accelerated hyperlipidaemic renal injury. Methods:  To induce accelerated hyperlipidaemic renal injury, 8 week old male spontaneously hypercholesterolaemic (SHC) rats were Selleckchem Alpelisib fed with a high cholesterol diet for 6 weeks. LTA4 hydrolase activities in the kidney and urine LTB4 levels were examined. The effects of LTB4 antagonist (ONO-4057) were also evaluated. Results:  Urinary protein and LTB4 excretion was increased by a high cholesterol diet for 6 weeks. The scores of glomerular foam cell accumulation and sclerosis, numbers of infiltrated

macrophages in glomeruli and interstitial area, LTA4 hydrolase activity in renal cortex were higher in the high cholesterol diet group than the normal diet group. LTB4 antagonist treatment reduced urinary protein and

LTA4 activity and attenuated renal pathological changes. Conclusion:  These results suggest that LTB4 directly contributes to accelerated hyperlipidaemic renal injury and the therapeutic potential of LTB4 antagonist for renal damage induced by hyperlipidaemia. “
“Background:  The aim of the study was to assess novel candidate markers measured in the urine of normoalbuminuric and microalbuminuric patients EGFR inhibitor (the urinary albumin-to-creatinine ratio < 30 mg/mmol) with essential hypertension to be used for early detection and assessment of progressive deterioration in renal function.

Methods:  Albumin, α-1-antitrypsin, orosomucoid, transferrin, retinol-binding protein and α-1-microglobulin concentrations and the NAG (N-acetyl-β-D-glucosaminidase) activity in the urine were evaluated in 102 hypertensive subjects with urinary albumin-to-creatinine ratio (uACR) < 30 mg/mmol. The estimated glomerular filtration rate (e-GFR) was calculated using the Modification of Diet in Renal Disease Study equation. Results:  The decreasing e-GFR values in normo- and microalbuminuric patients with essential hypertension were accompanied by significant increases (P < 0.05) in the NAG activity and uACR value in the urine. The e-GFR significantly (P < 0.05) correlated with dipyridamole the NAG activity in the urine, but no association was observed with the urinary concentrations of any of the individual proteins (P > 0.05). Conclusions:  In normoalbuminuric and microalbuminuric patients with essential hypertension renal impairment measured by e-GFR is related to the increased urinary NAG activity and uACR rather than elevated concentrations of individual proteins. Urinary NAG activity and uACR value seem independently promising candidate markers for use in assessing progression of early renal impairment in patients with hypertension. “
“Natural resources are under worldwide pressure, water and sustainable energy being the paramount issues.


WANG BO, WISE ANDREA F, HUUSKES BROOKE M, RICARDO SHARON D Monash University Introduction: MicroRNA (miR), including miR-let7, is highly effective at reducing

renal fibrosis and reversing progression of disease in rodent models. However, the advancement of miR therapies is hampered by difficulties in delivering miR in a robust and sustainable manner. Thus, it is imperative to develop an efficient delivery method for targeting miR to injured kidneys to exert their anti-fibrotic function. Mesenchymal stem cells (MSC) have demonstrated a strong safety profile in both completed and numerous ongoing clinical trials. The ability of MSC to transfer molecules and organelles suggests their potential usefulness as delivery vehicle for therapeutic miR treatment that is an innovative approach. Methods: C57BL6/J mice underwent 40 mins EPZ-6438 mouse of unilateral ischemia/reperfusion

(IR) injury and were injected with GFP+/luciferase+ MSCs or PBS and imaged from 0–7 days using whole body bioluminescence imaging for cell tracing. miR-let7c modified MSCs were generated and characterised and miR expression assayed with Taqman microRNA assay. The miR-let7c-MSCs were co-cultured with NRK52E, a kidney proximal tubular cell line, using a Transwell system with/without TGF-β1 for 72 hours, and the expression of fibrotic genes assessed using qPCR. Results: Following IR, MSCs homed to the injured kidney where https://www.selleckchem.com/products/AP24534.html they remained for up to 3 days. miR-let7c was successfully engineered and expressed in MSCs. The modified miR-let7c-MSCs maintained a normal karyotype and proliferative ability, but importantly

produced miR-let7c into the exogenous environment through exosome delivery. MSC-delivered miR-let7c was endocytosed into NRK52E cells, confirmed by the up-regulation of miR-let7c expression and fluorescent microscopy. After 3 days co-culturing, the miR-let7c-MSCs strongly inhibited the up-regulation of TGF-β type I receptor (TGBR1), a specific target of miR-let7c, and reduced a-smooth muscle actin and collagen mRNA expression, when NRK52E cells were treated with TGF-β1. Conclusion: MSCs home to the injured kidney in mice with IR injury. In vitro studies show that miR-let7c produced from modified MSC can be endocytosed into kidney epithelial cells leading to the inhibition of fibrotic genes and TGBR1 induced by TGF-β1. This data will pave the way for the application of miR, or siRNA, as an innovative crotamiton RNAi therapeutic strategy for renal disease therapy, but may also offer promise for other degenerative chronic disorders. YAMANAKA SHUICHIRO1,2, YOKOTE SHINYA1, KATSUOKA YUICHI2, IZUHARA LUNA2, OGURA MAKOTO1, YOKOO TAKASHI1 1Department of Internal Medicine, Division of Nephrology and Hypertension; 2Division of Regenerative Medicine Introduction: We have previously demonstrated that mesenchymal stem cells (MSCs) differentiate into functional kidney cells capable of urine and erythropoietin production, indicating that MSCs may be used for kidney regeneration.

[2] A total of 21 345 KTx were done from 1971–2013, majority (96

[2] A total of 21 345 KTx were done from 1971–2013, majority (96.4%, n = 20 569)

of them were from LD and 3.6% (n = 776) were from DD. The women donated kidneys more often, but were less likely to receive a live kidney than men. Most of the LD was contributed by mother and wife. Complex social and economic factors are responsible for the overall gender imbalance.[2] Awareness and changes Volasertib purchase in attitudes of the public as well as physicians are needed to eliminate this gender inequity. The majority of dialysis units (>85%) are in private hospitals.[3] The cost of maintenance dialysis is variable depending on many factors, but the charges per year in US dollars are between $9000 to $14 000 for haemodialysis and $10 000 to $14 000 for chronic ambulatory peritoneal dialysis depending on whether it is done in government or private hospitals. Due to lack of economic support, most patients are forced to stop dialysis therapy or opted for once-weekly dialysis and thus fail to achieve acceptable outcome. On the other hand, transplant cost, cytomegalovirus (CMV) prophylaxis and immunosuppressive drugs for the first year without including induction comes to only $5600 in a government hospital and $12 000 in a private hospital.[4] The cost of immunosuppression using tacrolimus, steroid and mycophenolate is $350–400/month.[5]

Approximate transplant AP24534 expenditure for KPD and ABO-Incompatible KTx are $3000 (in our centre) and $15 000 to $16 000 (Mumbai). Reimbursement for healthcare is available only to a minority. In the absence of state or private insurance schemes, most patients have to make out-of-pocket expenses to meet healthcare-associated costs. Only the wealthy can afford treatment in private hospitals. The poor typically seek treatment in public sector hospitals where the government subsidizes treatment. A large proportion of ESKD patients in India either

do not start or discontinue RRT due to financial reasons. KTx is associated with enormous out-of-pocket expenditure and pushes a majority of patients who come for treatment to public hospitals into a financial crisis. Indirect expenses contribute for at least one-third Thymidine kinase of expenses. Systematic efforts are required to address these issues. In a low socioeconomic backdrop LD are concerned about post-donation medical problems and compromised ability to earn a livelihood.[6] To improve donation rates, the cost of KTx should be affordable for the recipients, and apprehensions about complications of nephrectomy among donors need to be alleviated. The two most significant barriers to greater use of LD are blood type incompatibility and human leukocyte antigen (HLA) antigen sensitization. The most common reason to decline a donor for directed LDKTx is ABO incompatibility, which eliminates up to one-third of the potential LD pool.

In this study, we address the question:

In this study, we address the question: MK0683 purchase can Ab targeting the high affinity FCR engineered to express CTL epitopes stimulate high-avidity CTL

responses that are capable of efficient anti-tumor activity? We have previously shown that Ab–DNA vaccines engineered to express CTL epitopes can stimulate high-frequency responses to self and foreign epitopes but it was unclear if these were of high avidity 26. Initially a DNA vaccine incorporating the H-2Kb OVA epitope, SIINFEKL, within a human IgG1 molecule was screened for stimulation of high-avidity CTL responses. The SIINFEKL epitope OVA was grafted into CDRH2 region alongside an I-Ab restricted CD4 helper epitope from Hepatitis B (HepB) surface Ag. C57BL/6 mice immunized with this DNA construct demonstrated high-frequency epitope-specific responses compared to a control irrelevant peptide (p<0.0001) (Fig. 1B). It was next assessed if encoding an epitope within an Ab–DNA vaccine could break tolerance to a self Ag. An epitope from the melanoma Ag tyrosinase related

protein 2 (TRP2) was engineered into a human IgG1 Ab alongside the HepB CD4 epitope. Immunized C57BL/6 mice also demonstrated high-frequency TRP2-specific responses, although these were lower than OVA-specific responses (p<0.0001) (Fig. 1C). The ELISPOT assays in this study use total splenocyte ERK inhibitor populations and it is possible that other IFN-γ producing cells reside within this population. To address this, CD8+ cells were depleted prior to use in the ELISPOT assay. Depletion of the CD8+ cells eliminates the TRP2-specific response but has no effect upon the HepB helper peptide-specific response (Fig. 1D). To determine if there was any advantage in immunizing with Ab–DNA vaccine as compared to simple peptide immunization, T-cell responses to OVA/HepB

or TRP2/HepB human IgG1 DNA vaccines were compared to vaccination with HepB/OVA or TRP2/HepB Telomerase linked peptides. Mice immunized with peptide show significantly lower frequency responses compared to human IgG1 DNA immunized mice (p<0.0001 and p=0.003, respectively) (Fig. 1e). Functional avidity of CD8 responses has been shown to be important in the induction of anti-tumor immunity. Analysis of the functional avidity revealed that responses induced in human IgG1 DNA immunized mice were over 100-fold higher compared to peptide immunized mice for both OVA and TRP2 epitopes (p<0.0001 and p=0.0009, respectively) (Fig. 2A and B). OVA human IgG1 DNA shows avidity of 1×10−11 M compared to OVA peptide at 1.3×10−9 M. TRP2 human IgG1 DNA demonstrates an average avidity of 6×10−12 M compared to TRP2 peptide at 1.7×10−9 M.

“Malnutrition is highly prevalent in haemodialysis (HD) pa

“Malnutrition is highly prevalent in haemodialysis (HD) patients, and it contributes to morbidity and mortality. Fibroblast growth factor-23 (FGF-23) and Klotho contribute to chronic selleck screening library kidney disease-mineral and bone disorder (CKD-MBD) in HD patients, but

the role that these molecules play in determining nutritional status is currently unknown. A cross-sectional study examining 77 HD patients was performed. The plasma concentrations of FGF-23 and soluble Klotho (s-Klotho) were studied to evaluate their association with muscle mass, which was investigated by abdominal muscle areas measured using computed tomography and by creatinine (Cr) production estimated using the Cr kinetic model. Plasma FGF-23 concentrations were significantly and positively correlated with abdominal muscle areas and Cr production

(rho = 0.301, P < 0.01 and rho = 0.345, P < 0.01, respectively). In contrast, s-Klotho was not significantly correlated with these muscle mass indices and plasma FGF-23 concentrations. Multiple regression analyses showed that FGF-23 was a significant independent predictor of both muscle mass indices (P < 0.01 and P < 0.05, respectively). Plasma FGF-23 concentrations were associated with muscle mass indices in HD patients. Our findings suggest that FGF-23 and nutritional status are linked and this link is most likely independent of s-Klotho. "
“Aortic Dissection (AD) is the most common life-threatening disease involving LY294002 manufacturer the aorta. It is rarely associated with systemic disorders

such as Autosomal Dominant Polycystic Kidney Disease (ADPKD), a genetic syndrome characterized by cystic degeneration of kidneys, possible presence of cysts in other organs and extra-renal manifestations, including cardiovascular disorders. We performed a systematic literature search focused on the occurrence of AD associated with ADPKD (25 cases identified), and reported 2 cases from our experience. HSP90 We selected data on sex, age, family history of ADPKD and/or AD, habitus, hypertension, renal function, presence of hepatic/pancreatic/splenic cysts, clinical presentation of AD, AD type according to the Stanford classification, treatment and outcome. Furthermore we compared this dataset with the data of the overall population with AD from International Registry of Acute Aortic Dissection (IRAD). Stanford A type AD was documented in 62% of patients. As expected, the initial manifestation of AD was most commonly chest and back pain (80%). The mean age of AD occurrence appears significantly reduced in ADPKD patients compared to the general population with AD (49 ± 12 vs 62 ± 14, p < 0,001). Of note, our analysis shows a remarkably higher frequency of hypertension (90%) compared to the overall AD population (75%), although not significantly (p = 0,133).

Consideration of these factors when enrolling subjects and contro

Consideration of these factors when enrolling subjects and controlling for them in analyses will minimize erroneous interpretation of results in the continuing battle against HIV. Time preparing this manuscript was supported by 1K23HD062340-01 (Anderson-PI) and K24 AI066884 (Cu-Uvin-PI). “
“Ectoenzymes are a diverse group of membrane proteins that have their catalytic sites outside the plasma membrane. Many of them are ABT-263 datasheet found on leukocytes and endothelial cells, and they

are multifunctional in nature. Collectively, different ectoenzymes can modulate each step of leukocyte–endothelial contacts, as well as subsequent cell migration in tissues. Here, we review how ectoenzymes belonging to Cilomilast ic50 the oxidase, NAD-metabolizing enzyme, nucleotidase and peptidase/protease families regulate and fine-tune leukocyte trafficking, and how ectoenzymes have been targeted both in preclinical and clinical trials. Leukocyte traffic is governed by the canonical multistep extravasation cascade 1. Selectins, chemokines and integrins, and their counter-receptors, have firmly established roles in controlling

rolling, activation, firm adhesion and transmigration of different types of leukocytes within the blood vessels (Fig. 1). However, each step of the cascade is modified by various other molecules under physiologic and pathologic conditions. Ectoenzymes are a unique class of cell-surface-expressed enzymes 2. Since their catalytic domains face outside the cell membrane, they are fundamentally different from both the multitude of intracellular signaling molecules and the cell-surface-expressed enzymes with cytoplasmic catalytic domains (e.g. G-proteins (receptor) kinases, phosphatases and down-stream signaling molecules), which are also critical in leukocyte migration. Apart from the extracellular catalytic

activity that is common to all, ectoenzymes are a diverse class of molecules that are involved in very different types of enzymatic reactions Buspirone HCl (Fig. 2). However, a common theme in ectoenzymatic regulation of leukocyte traffic is that often both the substrate(s) and the end-product(s) can modulate leukocyte migration 3. Here, we will mainly focus on selective examples of ectoenzymes from different classes, including CD26, CD38, CD39, CD73, CD156b, CD156c, CD157, CD203 and the primary amine oxidases, which are the best characterized in terms of leukocyte trafficking. We will emphasize the models based on gene-deficient mice and the potential applicability of ectoenzymes in alleviating inappropriate inflammation. We will focus on the general concepts and advances that have been published since our last comprehensive review on this topic in 2005 3.

[3] In the absence of a population-based study, the exact prevale

[3] In the absence of a population-based study, the exact prevalence of mucormycosis in India remains difficult to elucidate.[3] However, on the basis of data available from certain groups of patients, the disease prevalence appears to be nearly 0.16% amongst diabetics and 1.2% amongst renal transplant selleckchem recipients, with most of these cases manifesting as the ROC form.[16, 17] Also, gastrointestinal mucormycosis reportedly occurs in nearly 20% of all operated cases of neonatal enterocolitis in one center.[18] In fact, the frequency of gastrointestinal mucormycosis was found to be so high in that

centre that clinicians suspect the disease in any neonate having intestinal perforation. We recently reviewed Indian literature for the past five decades (1960–2012), and developed a computational model to determine the burden of mucormycosis. The results reveal an

overall mucormycosis prevalence of 0.14 cases per 1000 population in India, with the prevalence range between 208 177 and 137 807 cases (Mean: 171 504; SD: 12 365.6; 95% CI: 195 777–147 688) and a mean of 65 500 (38.2%) attributable deaths per year.[19] Based on the clinical presentations, ROC is the most common form of mucormycosis in India, possibly due to its association Ulixertinib price with uncontrolled diabetes and diabetic ketoacidosis.[1, 3, 20] According to the multiple case series reported from our tertiary care centre in North India, the prevalence of different clinical types amongst mucormycosis cases is: ROC (48–55%), cutaneous (13–15%), pulmonary almost (7–17%), disseminated (5–12%), gastrointestinal (5–13%) and isolated renal (5–14%).[4-6] Likewise, in a meta-analysis of all the zygomycosis cases reported from India, Diwakar et al. describe an overall prevalence of ROC (58%), cutaneous (14%), pulmonary (6%), disseminated (7%), gastrointestinal (7%) and isolated renal (7%).[21] This is consistent with the global trend, wherein pulmonary and sinus infections (with/without central

nervous system involvement), followed by cutaneous type have been found to be the most prevalent.[22-25] Cases of necrotising fasciitis due to zygomycetes, occurring via contaminated intramuscular injections, are also a common finding.[7, 26] This happens due to compromise in healthcare practices and the use of contaminated needles. In addition, majority of the patients (60%) with cutaneous infections due to Apophysomyces elegans are from India.[1, 7, 27] The patients are usually immunocompetent individuals, who acquire the infection following penetrating trauma or burns.[1, 7, 27] However, no correlation between the environmental prevalence of this fungus and clinical cases has been described yet.