Control cells were treated with vehicle (water). In the majority of experiments, cells derived from prepared P0-cells were treated with α-amylase (P1-cells). As already mentioned, remaining P0-cells were

further cultivated after a first seeding and could be harvested a second time (second seeding). All these cells were called P1-cells. About half of the independently performed experiments selleck screening library (3 out of 7 for F344; 3 out of 6 for Lewis) were done in a blind fashion, meaning that the experimenter, who did the treatment and cell counting, was not aware about the treatment groups. In the first set of experiments, the experimenter knew about the treatment groups to be able to notice cellular alterations during α-amylase treatment. Experiments were evaluated individually and could be analyzed Temsirolimus datasheet together because no differences were observed

between blind- and non-blind-performed investigations. α-Amylase treatment in human mammary epithelial mTOR kinase assay cells The effect of α-amylase in mammary cells of human origin was studied in primary HBCEC (mammary carcinoma excisions). α-Amylase treatment was performed once per day for 2 days with 0.125 U/ml, 1.25 U/ml, 12.5 U/ml, and 125 U/ml. Control cells were treated with water. SA-β-galactosidase assay Expression of senescence-associated-β-galactosidase (SA-β-gal) is increased in senescent cells [36]. To determine if α-amylase treatment causes a change in cell senescence, primary rat mammary cells were cultured on Matrigel®-coated 24-well-plates. Treatment with salivary α-amylase (5 and 50

U/ml) for 2 days started after 1 (P1) or 4 (P2) days in culture. The cells were fixed with 1x Fixative Solution, containing 20% formaldehyde and 2% glutaraldehyde and stained against SA-β-gal for 24 h/37°C in the dark according to the manufacturers protocol and recommendations (Senescence SA-β-galactosidase Staining Kit, Cell Signaling Exoribonuclease Technology, New England Biolabs, Frankfurt, Germany). The staining was proportional to the amount of substrate (5-bromo-4-chloro-3-indolyl-beta-D-galactopyranoside) enzymatically transformed. Following two washes with PBS, the differentially-stained cell cultures were documented by phase contrast microscopy using Olympus imaging software cell® (Olympus, Hamburg, Germany) and quantified by counting. Cells from F344 (P1 and P2) and Lewis (only P2) were counted in three different wells and portion of SA-β-gal-positive cells was determined (one well). Positive and negative cells were counted in 6-9 sections. Data are shown as percentage SA-β-gal-positive cells. Total cell numbers per group of 759-963 cells for P1 and 510-803 cells for P2 were counted. In addition to this, cells from a human breast tumor (MaCa 700) were also treated with α-amylase (0.125, 1.25, 12.5, and 125 U/ml) and used for a SA-β-gal assay (three sections per treatment). Total cell numbers of 266-691 cells were counted.

The first outbreak of DHF was documented in 1994 by Chan and colleagues [21] who observed DEN-1 and DEN-2 in three out of ten tested patients for dengue virus. In the following year, DEN-2 infection was reported from the province of Balochistan [22, 23]. Through serological studies, dengue type 1 and type 2 were found in sera of children in Karachi [24, 25]. Jamil and colleagues [20] had previously been reported DEN-3 infection in 2005 outbreak of DHF in Karachi. Kan and colleagues [26] reported co-circulation of dengue virus type

2 and type 3 in 2006 outbreak in Karachi. More recently, Hamayoun and colleagues [22] reported cases with dengue infection in the 2008 outbreak in Lahore. Out of 17 samples checked via real-time PCR, ten of their patients had DEN-4,

five had DEN-2 and two click here had DEN-3 infection [22]. Pakistan has a history of outbreaks of dengue viral infection however, the responsible serotype/s MRT67307 datasheet is not well known. Therefore, the IWP-2 solubility dmso current study was initiated to determine the circulating serotype/s of dengue virus in Pakistan using molecular based techniques in patients’ sera. Samples were selected from stored repository from three most recent outbreaks of dengue virus (2007-2009) and the obtained sequences were compared to other dengue virus sequences reported from other geographical regions of the world to deduce a phylogenetic relationship. Results Serotyping of analyzed sample A total of 114 suspected dengue serum samples

along with demographic data were kindly donated by Gurki Trust Hospital Lahore and Sheikh Zayed Medical Complex Lahore for the current study. These samples were collected during three different mini outbreaks of dengue virus infection in years 2007, 2008 and 2009 and were stored at -20°C. Nested PCR was utilized for this serotype analysis. Out of total 114 tested serum samples, 20 were found positive for dengue virus RNA with various Amino acid serotypes. Table 1 shows the distribution of dengue virus serotypes in the study population. It is clear from the results of the current study that, of the 20 dengue virus positive samples, six had concurrent infection with two different dengue virus serotypes at a time generating data of 26 serotypes. Table 1 Total positive samples and dengue virus isolates included in this study. Year of isolation Total collected samples Positive samples Isolated serotype*       Serotype 2 Serotype 3 2007 41 5 4 1 2008 66 8 8 5 2009 7 7 7 1 Total 114 20 19 7 *Out of 20 positive samples, 6 samples had concurrent infection with two dengue virus serotypes giving a total of 26 dengue virus isolates. Nucleotide sequences analysis The amplified bands of each sample were gel eluted and were further used for sequence analysis. Junction of C-prM gene of dengue virus isolates was chosen for serotyping. Accession numbers of these 26 studied sequences are [GenBank: HQ385930-HQ385943 and HM626119-HM626130].

All authors approved the final manuscript.”
“Background Chlamydia trachomatis is an obligate intracellular pathogen with unique biphasic developmental cycle alternating between the infectious elementary selleck chemical body (EB) and the metabolically active reticulate body (RB). Based on the antigenic variation of the major outer membrane GDC 0032 clinical trial protein (MOMP), the C. trachomatis isolates have been divided into three different biovariants [1]. Serovars A, B, Ba and C cause ocular

infections, currently infecting 150 million people worldwide [2,3]; serovars D, E, F, G, H, I, J and K cause sexually transmitted disease with more than 90 million new cases of genital infections occurring every year [4,5] and serovars L1, L2 and L3 cause lymphgranuloma

venereum (LGV) primarily affecting the lymphatic system with recent outbreaks in Western Europe [6,7]. Comparative genomic studies demonstrate that the genome of C. trachomatis serovars are strikingly similar to each other find more and share more than 99% identity [8,9]. Genetic differences were observed centring around the plasticity zone i.e. ~50 kb region near the predicted termination origin of the genome, experiencing a higher degree of DNA arrangement [10], MOMP and members of polymorphic membrane protein (pmp) gene family [11]. However the occurrence of quantitatively different infections by different serovars within a given host has been intriguing. In vivo studies infecting mice intranasally [12] or intravaginally [13] with different serovars of C. trachomatis has revealed a great deal of variation in infection kinetics.

Genome analysis could reveal that a functional tryptophan synthase enzyme and toxin might be the principal virulence factors underlying this distinct tropism in terms of organ specific disease termed as organotropism [14]. Studies including LGV serovars confirmed the observation that the variability resided mainly in the plasticity zone [15]. Chlamydia primarily targets the host epithelial cells and resides within distinct membrane bound vacuoles termed as chlamydial inclusion. The chlamydia proliferate within inclusion and inhibits their acidification by Y-27632 2HCl avoiding fusion with lysosomal compartments [16,17]. However the association of C. trachomatis with reactive arthritis have raised questions how chlamydia is transported from the site of infection to the site of inflammatory disease in the joints or vasculature [18-20]. Studies have shown that the C. trachomatis infection is characterized by infiltration with polymorphonuclear leukocyte (PMNs) in the acute phase and mononuclear cells in the chronic phase [21]. Hence there have been suggestions that circulating monocytes delivers the pathogen to other organs and initiate immunological response and inflammation. The role of C.

Each sample was assayed in triplicate. The comparative CT method (ΔΔCT method) was used to determine the quantity

of the target sequences in TAM relative both to Mφ (calibrator) and to β-actin (an endogenous control). Relative expression levels were presented as the relative fold change and calculated using the formula: 2 -ΔΔCT= 2-(ΔCT (TAM) – ΔCT (Mφ) where each ΔCT =ΔCT target-ΔCT β-actin. Immunohistochemistry For exact identification of IL-10 or cathepsin B expression in TAMs, serial OSI-027 solubility dmso sections were used to examine the expression of IL-10, cathepsin B in TAMs. Samples were fixed in 4% formaldehyde in PBS (pH 7.2) and paraffin embedded. 4-μm thickness was cut from each paraffin block. After

Apoptosis inhibitor dewaxing and rehydration, the sections were microwaved for antigen retrieval in 10 mmol/liter citrate buffer (pH 6.0) for 10 min, and then allowed to cool for 1 hour at room temperature. Endogenous peroxidase activity was blocked with hydrogen peroxide; Nonspecific binding was blocked by preincubation with 10% goat serum Cilengitide clinical trial in PBS for 30 minutes at room temperature. Slides were incubated with the primary antibodies directed against monoclonal anti-human CD68 antibody (1:200 dilution, sc-20060, Santa Cruz, CA, USA), monoclonal anti-human IL-10 antibody (1:100 dilution, BA1201,Boster, WuHan, China) or polyclonal anti-human cathepsin B antibody (1:100 dilution, ab49232, Abcam, MA, USA). The results were visualized using the streptavidine-biotin immunoperoxidase detection kit and AEC chromogen (Maixin Bio, FuZhou, China) based on the manufacturer’s instruction. Positive cells stained red. The negative control involved omission of the primary antibody. Statistical analysis Statistical analysis software (Prism 5.0, GraphPad Software Inc, La Jolla, CA, USA and SPSS Version 13.0 software, SPSS Inc,

Chicago, IL, USA) was used to perform the analyses. Data are expressed as median (range). The Mann-Whitney aminophylline test was used for the comparison between TAM and normal macrophage. The correlation between IL-10 or cathepsin B expression and clinicopathologic factors was analyzed by Mann-Whitney test. Multivariate logistic regression was performed to evaluate the relationships between the pathological stage (with early and late stage as dependent variables) and covariates (age, sex, tobacco use, tumor histology and IL-10 expression in TAMs). For this analysis, the median value of IL-10 was chosen as the cut-off point for dividing the patients into the two groups. Two-tailed P value less than 0.05 was considered statistically significant. Results Patients characteristics The patient characteristics are described in Table 1. Patients (40 males and 23 females) had a mean age of 58.8 ± 1.1 years. Fifty-four patients had a smoking history, and forty-six were non-smokers.

Liver Int 2005, 25:33–40.PubMedCrossRef 26. Lewandowski P, Cameron-Smith PF-6463922 in vivo D, Moulton K, Walder K, Sanigorski A, Collier GR: Disproportionate increase of fatty acid binding proteins in the livers of obese diabetic Psammomys obesus. Ann N Y Acad Sci 1997, 827:536–540.PubMedCrossRef 27. Bioulac-Sage P, Laumonier H, Laurent C, Zucman-Rossi J, Balabaud C: Hepatocellular adenoma: what is new in 2008. Hepatol Int 2008, 2:316–321.PubMedCrossRef 28. Kono H, Rusyn I, Uesugi T, Yamashina S, Connor HD, Dikalova A, Mason RP, Thurman RG: Diphenyleneiodonium sulfate, an NADPH oxidase

inhibitor, prevents early alcohol-induced liver injury in the rat. Am J Physiol Gastrointest Liver Physiol 2001, 280:G1005–1012.PubMed 29. Yamaguchi K, Yang L, McCall S, Huang J, Yu XX, Pandey SK, Bhanot S, Monia BP, Li YX, Diehl AM: Inhibiting triglyceride synthesis improves hepatic this website steatosis but exacerbates liver damage and fibrosis in obese mice with nonalcoholic steatohepatitis. Hepatology 2007, 45:1366–1374.PubMedCrossRef

Competing interests The authors declare selleck chemicals that they have no competing interests. Authors’ contributions MJ participated in the design of the study, carried out the analysis and interpretation of data and drafted the manuscript. KNA contributed to the interpretation of data and revised the manuscript. MJS-G carried out the analysis and interpretation of data and drafted the manuscript. MAM

carried out the analysis and interpretation of data and drafted the manuscript. PAL participated in the design of the study, Carried of histological grading, contributed to the interpretation Thalidomide of data and revised the manuscript. All authors read and approved the final manuscript.”
“Background Autoimmune liver diseases (AILD) are a group of immunologically induced hepatic damage that are either hepatocellular or cholestatic [1, 2]. The hepatocellular forms are characterized by a significant elevation of the serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST), as compared with the biliary enzymes, together with elevated serum bilirubin. The cholestatic forms involve either the intra- or the extra-hepatic biliary systems or both. Cholestasis will ultimately cause impairment of bile formation and/or bile flow which may clinically present with fatigue, pruritus, and jaundice [1, 2]. The biochemical markers include increases in serum alkaline phosphatase (ALP) and gamma-glutamyl transpeptidase (GGT), followed by conjugated hyperbilirubinemia, at more advanced stages. Cholestasis is considered chronic if it lasts more than 6 months [3]. Most chronic cholestatic diseases are purely intra-hepatic [3, 4]. They are considered as different disease entities based on the clinical, laboratory and histological features [3, 4].

Therefore, the downregulation of TGF-β2 protein by miR-141 may be an important step in the excessive inflammation progression during influenza A virus infection, particularly in H5N1 infection. However, whether the recovery of TGF-β2 expression by anti-miR miR-141 inhibitor could resolve the hypercytokinemia learn more stage of H5N1 infection needs to be further studied. Although our findings were obtained from an in vitro model, we could apply these to the real situation of an in vivo model or tissue comprised of different cell types. In real bronchial environments, lung epithelial cells are the key target of influenza viruses [33, 34]. After these cells are infected, they will activate an

inflammatory cascade which launches a quick antimicrobial reaction and directs adaptive immunity to mount a protective response. Bronchial epithelial cells therefore modulate the activation of monocytes, macrophages,

dendritic cells (DC), and T lymphocytes through cytokines and chemokines. Cytokines and chemokines generally function in an autocrine (on the producing cell itself) or paracrine (on nearby cells) manner. These mediators will EPZ015666 chemical structure contribute to the generation of a specific bronchial homeostatic microenvironment that affects the way in which the body copes with the SBI-0206965 viruses. This homeostatic “circuit” can inhibit excessive inflammatory response in lung tissues [35]. For example, TGF-β before had been reported to mediate a cross-talk between alveolar macrophages and epithelial cells [36]. However, our findings show that, during highly pathogenic H5N1 avian virus infection, miR-141 would be induced shortly after infection. With high level of miR-141, the expression of TGF-β would be suppressed from the lung epithelial cells. Without sufficient TGF- β, the pro-inflammatory

response might not be tightly controlled in cases of highly pathogenic H5N1 avian virus infection. This might explain the mechanism concerning bronchial infiltration of inflammatory cells, particularly lymphocytes and eosinophils, and the subsequent hyperresponsiveness of the bronchial wall induced by viral infection. Our study has some limitations that will need to be addressed in future studies. Firstly, we did not assess the roles of other miRNAs whose expression were also altered after infection. The miRNA microarrays that we used did not contain probes for every known miRNA; thus it is possible that influenza A virus infection affects the expression of some other miRNAs not yet covered by the kit used in the current study. Secondly, the virus may interact with miRNA regulatory pathways differently in other cell or tissue types, or in other physiological status. Conclusions In conclusion, based on the broad-catching miRNA microarray approach, we found that dysregulation of miRNA expression is mainly observed in highly pathogenic avian influenza infection.

Zhou et al. [100] have made a distinction between adsorption and absorption. Adsorption is a surface phenomenon, while absorption

depends on the concentration, size factors and temperature. Both adsorption and absorption PRI-724 molecular weight may occur simultaneously in plants [159]. The uptake of nanoparticles may be checked in plants, but adsorption is the accumulation of nanoparticles that remains on the surface of the plants. The adsorbed CuO nanoparticles on the root surface were checked in the presence of complexing agents such as Na4EDTA and NaOAC. It is however very interesting to believe that EDTA dissolves CuO nanoparticles by forming complex with released Cu2+. According to this metathesis, free Cu2+ will not be available for subsequent reaction with EDTA, rather Na+ is replaced by Cu2+ ions leading to the formation of Cu2(EDTA). The equilibrium between CuO nanoparticles and Cu2(EDTA) depends on the quantum of Na4EDTA added and that of CuO nanoparticles present. Since the authors insist that the equilibrium between CuO nanoparticles and Cu2+ is lost, the dissolution of CuO nanoparticles is enhanced. It is not true because the number of moles of EDTA-Cu complex MRT67307 datasheet produced will correspond to the number of moles of EDTA added. The speculation that Cu nanoparticles adhered to the root is only due to

complex formation may selleck not be true, as there must be some complexing agent exuded by the root hairs. The adsorption of CuO nanoparticles by wheat root is concentration dependent. The authors have unnecessarily compared the adsorption with the uptake of nanoparticles [100]. The amount of nanoparticles adsorbed is actually retained on the surface due to electrostatic force, and fewer particles are absorbed into the plant system. When CuO nanoparticles are adhered to the outer surface of the root, they may not be transported to the cells unless they are absorbed. The absorption and uptake are synonymous in the present context because wherever it is absorbed it is in fact taken up by the plant.

The authors have concluded that Na4EDTA increases the solubility of CuO nanoparticles, if it is the case, a mixture of CuO learn more nanoparticles and Na4EDTA should be administered to the plant instead of taking the troublesome route of adherence of nanoparticles and their subsequent dissolution by Na4EDTA for absorption. Contradictory reports have been received on the application of CuO nanoparticles on plants. While CuO nanoparticles have been shown to absorb in wheat, it has been reported to produce adverse effect on maize plants [160]. It has been reported that CuO nanoparticles have apparently no effect on the germination of maize seeds; nevertheless, it increased chlorosis and inhibited the growth of maize seedlings when exposed to 100 mg L-1 CuO nanoparticles.

Same way, the genome expression depends on the DNA conformational status. DNA consists of two polynucleotide chains, complimentary bound to each other by hydrogen bonds throughout all the length, which makes a known system of double helix (Ivanov and Galimov, 2007 and Ivanov, 2007). see more genetic information is to be transferred due to replication of complimentary bases formed

chains and, as far as it is known, this major principle is taken as universal for all pre-existing and currently functioning life forms. Therefore, an autonomy of the genetic information transfer might be guaranteed Torin 1 order only in case of the complementary nucleotide pair existence which is, in turn, is one of the basic conditions needed for answering to the first question. What is a nature of origin of the first informational molecules complimentary structures ? Certainly, once overlooking both random and regularity-formed routes of the

possible processes of these macromolecules origin in a row, then just by definition, a preference should be given to the latter one. That choice might be made, particularly, due to the regularity format of the event expected. A high level of the molecular structures MEK162 ic50 conformational fitting could be provided by regression of polyheterocyclic compounds. To visualize that, let’s imagine the woody pencil rupture sharp margins having an easily reached high-rank conformational inter-coupling fitting. Most probably, this clear and simple way was in fact chosen by nature known due its smart solutions for complex problems. Getting through analysis of an alternative way, i.e. the way of the complementary pair members separate origin along with a point of unbelievable degree of the conformational match randomness, then this way is definitely far more time-consuming and far less trust-deserving. Even in a close look, this gives a reason to exclude the

variant of single and consequent synthesis of abiogenic nucleotides. At least, the wide range chromato-mass-spectrometric studies on compounds obtained in a course of the pre-biotic abiogenic synthesis simulation allowed to find no one case of the complimentary nucleotide O-methylated flavonoid pair formation. On other hand, it has been proven that the heterocyclic compounds abiogenc synthesis is a rather reachable task (Lupatov, et al. 2006). From this standpoint, the single nucleotide synthesis focused simulation of abiogenic processes look not reasonable. However, the data obtained shows a direction for further studies devoted to the very first steps of the matter’s biological evolution. One of these steps is a regression of polyheterocyclic compounds leading to formation of the mutually complimentary molecular structures. Ivanov, A. and Galimov, E. (2007). Molecular isotopy of conformational interactions. Symposium on isotopic geochemistry named by A. Vinogradov, pages 44–45. Moscow, Russia. Ivanov, A. (2007).

Graphene, partially covered by h-BN protective layers, may display promising electronic characteristics of graphene with much lower environmental sensitivity. Recently, chemical vapor deposition (CVD) synthesis of h-BN on Ni [14–16] or Cu [13, 17–19] substrates has been further investigated. For the following applications in graphene electronic devices, h-BN can be acquired by etching of the catalyst substrates and a transfer technique. Nevertheless, the transfer process brings

inevitable contamination or even destruction, and it is difficult to determine the position and the coverage ratio of h-BN on graphene. Considering this problem, we pay attention to the catalyst-free CVD growth of h-BN on graphene, which promises direct application in graphene electronic devices and may STA-9090 obviate the need for a transfer process. It has been AZD1480 chemical structure demonstrated that van der Waals epitaxy by catalyst-free CVD can be a promising route for the growth find more of topological heterostructures [20–22]. Moreover, the surface of graphene is atomically flat and without dangling bonds, which makes graphene a promising template for the van der Waals epitaxy of other two-dimensional

materials. Compounds with 1:1 B/N stoichiometry are often selected as h-BN precursors for CVD, and borazine (B3N3H6) could be a promising choice as it would produce BN and hydrogen, which are both environmentally friendly. In this research, the van der Waals epitaxy of h-BN nanosheets on mechanically exfoliated graphene by catalyst-free low-pressure CVD, using borazine as the precursor to h-BN, was demonstrated. The h-BN nanosheets preferred to grow on graphene rather

than on SiO2/Si and tended to exhibit a triangular morphology when grown on a narrow graphene belt. The h-BN nanosheets grown on graphene Montelukast Sodium were highly crystalline, albeit with various in-plane lattice orientations. Methods h-BN nanosheets were synthesized in a fused quartz tube with a diameter of 50 mm. Graphene was transferred onto silicon oxide/silicon (SiO2/Si) wafers by mechanical exfoliation from highly oriented pyrolytic graphite (HOPG, Alfa Asear, Ward Hill, MA, USA). The h-BN precursor (borazine) was synthesized by the reaction between NaBH4 and (NH4)2SO4 and purified according to our previous reports [23, 24]. The temperature for the CVD growth of h-BN nanosheets was set to 900°C. Before the growth of h-BN, with the tube heated to 900°C, graphene grown on SiO2/Si was first annealed for 60 min in an argon/hydrogen flow (Ar/H2, 5:1 by volume, both gases were of 99.999% purity from Pujiang Co., Ltd, Shanghai, China) of 180 sccm to remove pollutants remaining on the graphene after mechanical exfoliation. During the growth process, borazine, in a homemade bubbler, was introduced to the growth chamber by another Ar flow of 2 sccm, while the Ar/H2 flow remained unchanged. The typical growth time was 5 min, while the pressure was 10 to 100 Pa.

Successful surgical outcome is usually expected secondary to expeditious surgical intervention in the form of wide local excision of the gangrenous 17DMAG breast with proper toileting tissue along with broad-spectrum antibiotics followed by reconstructive procedures. Serial debridements are required in some patients where there is diffuse involvement. Grafting is done where there is large deficit Sometimes

mastectomy is mandatory in extensive involvement Conclusion Gangrene of breast is rare and ignorance on part of patient contributed to this malady. Application of topical agent of belladonna on cutaneous abscess in lactational female could be aggravating factor. In uncontrolled diabetes breast abscess has propensity for progression to gangrene. Sometimes gangrene of breast can be of idiopathic cause. Debridement continues to be gold standard in gangrene of breast. Consent ‘Written informed consent was obtained from the patient for publication of the manuscript and accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal’ Acknowledgements 1) We are

grateful to MA Memon for their support in providing references for manuscript. 2) No source of funding present from any institute or any agency References 1. Sahoo SP, Khatri A, Khanna AK: Idiopathic partial gangrene of the breast. Tropical Doctor 1998, 28:178–179.PubMed 2. Delotte J, Carnitine palmitoyltransferase II Karimdjee B, Cua E, Pop D, Bernard J, Bongain A, Benchimol B: Gas gangrene of the Selleck SCH772984 breast: management of a potential life-threatening

infection. Arch Gynecol Obstet 2008,279(1):79–81.PubMedCrossRef 3. Charles S: Kipen Gangrene of the Breast –a Complication of Anticoagulant Therapy — Report of Two Cases. N Engl J Med 1961, 265:638–640.CrossRef 4. Probstein J: Gangrene of the breast complicating diabetes. Ann Surg 1924,79(4):634–636.PubMed 5. Helfman RJ: Gangrene of the Breast. N Engl J Med 1962, 266:55–56. 6. Nudelman H, Kempson R: Necrosis of the breast: A rare complication of anticoagulant therapy. Am J Surg 1966,111(5):728–733.PubMedCrossRef 7. Sameer R, Quentin N, check details Ashish R, Abhay N: Breast gangrene as a complication of purperial sepsis. Arch Surg 2002, 137:1441–1442.CrossRef 8. Saira N, Kamran M, Mohsin A, Hasnan Z, Memon A: Necrotising fasciitis of the breast. The Breast Journal 2006, 12:168–169.CrossRef 9. Venkatramani V, Pillai S, Marathe S, Rege S, Hardikar J: Breast Gangrene in an HIV-Positive Patient. Ann R Coll Surg Engl 2009,91(5):409.CrossRef 10. Flandrin A, Rouleau C, Azar C, Dubon O: Pierre Giacalone L First Report of a Necrotising Fasciitis of the Breast Following a Core Needle Biopsy. The Breast Journal 2009,15(2):199–201.PubMedCrossRef 11. Cutter EC: Apoplexy of breast. JAMA 1924, 82:1763. 12. Hasson J, Pope H: Mammary infarcts associated with pregnancy presenting as breast tumours. SURGERY 1961, 49:313–316.PubMed 13.