Correction: Early evolution of the biotin-dependent carboxylase family

ABSTRACT: After publication of our work (Lombard et al, BMC Evol Biol, 2011, 11:232), we noticed several major mistakes in the figure images provided for final publication: although the main text and the legends are correct, Figure 3 has been replaced by an image present in the Addition File 1 and Figures 4, 5 and 6 are displaced with regard to their correct numbers and legends. Please, accept our apologies and refer to the correct corresponding Figures 3, 4, 5 and 6 that we provide in this erratum. Legends are the same as in the original article.     

Erratum to Beicheng Sun et al. Cell Cycle Volume 7, Issue 7; pp. 934-939

In the paper, “The level of oncogene H-Ras correlates with tumorigenicity” by Beicheng Sun, Yun Gao, Lei Deng, Guoqiang Li, Feng Cheng and Xuehao Wang (Cell Cycle 2008; 7:934-9), the authors found that Figure 2D is incorrect. The original data found in the report is correct, and the correct figure is included here.     

Erratum to: Singh R.K. and Gunjan A. Histone tyrosine phosphorylation comes of age. Epigenetics 2011; 6:153-60.

We recently noticed that there is a major error in Figure 1 of our review published in Epignetics 2010, Volume 6, Issue 2. During the preparation of the figure, the human and yeast H2B tyrosines were numbered the same, making the human numbering incorrect. The correct Figure 1 with proper numbering of human tyrosines is below.Erratum to:Singh R.K. and Gunjan A. Histone tyrosine phosphorylation comes of age.Epigenetics 2011; 6:153-60.We recently noticed that there is a major error in Figure 1 of our review published in Epignetics 2010, Volume 6, Issue 2. During the preparation of the figure, the human and yeast H2B tyrosines were numbered the same, making the human numbering incorrect. The correct Figure 1 with proper numbering of human tyrosines is below.Open in a separate windowFigure 1. Tyrosine residues are highly conserved between budding yeast and mammalian core histones. The four canonical core histone proteins from the budding yeast Saccharomyces cerevisiae are indicated by the prefix “Sc” and denoted in blue. The mammalian core histones and the mammalian variant histone H2A.X are shown in black. The number of amino acid (aa) residues in each core histone is indicated on the right. The location of the a-helices in the secondary structure of the histone proteins is indicated by cylinders. Tyrosine residues are shown as balloons and the tyrosine residues essential for viability in budding yeast histones are indicated by red balloons. Tyrosines in mammalian histones have not yet been evaluated to determine the residues essential for viability. Note the high degree of conservation of the location as well as the spacing of all but one tyrosine residue between budding yeast and mammalian core histones (H3 Y54 being the exception). Tyrosine residues that have recently been shown to be phosphorylated in vivo are marked by yellow “explosion” signs and the letter “P.” Additional tyrosine residues that are predicted to be reasonably accessible in the nucleosomal context under certain conditions and can be potentially phosphorylated in vivo are indicated by a yellow halo only on the mammalian histones for clarity, but are likely to be just as applicable to the yeast histones. Solid yellow halo indicates higher probability of phosphorylation, while a dashed yellow halo indicates lower probability of phosphorylation.     

Apparatus for simultaneous spectrophotometric and polarographic measurements

We have recently constructed a 10-mm, light path quartz cuvet which will accept a Clark oxygen electrode; it is temperature controlled and is suitable for use in a Unicam (Cambridge, England) SP 800 recording spectrophotometer. Several enquiries have prompted this publication, although such an apparatus was mentioned much earlier by Chance and Williams,¹ and has been used extensively. Figure 1a, b, c, and d and their legends provide sufficient detail for the construction of the cuvet and provision of the commercially available electrode, quartz faces, stirring motor and disk magnet. Circuit diagrams for temperature control (range 22–38°C., ± 0.2°C.) and stirrer speed control are shown in Figure 2a and b. The cuvet is shown situated in the spectrophotometer cell housing in Figure 3, and the cuvet with its associated equipment is shown in Figure 4.     

Erratum to: Singh R.K. and Gunjan A. Histone tyrosine phosphorylation comes of age. Epigenetics 2011; 6:153-60.

We recently noticed that there is a major error in Figure 1 of our review published in Epignetics 2010, Volume 6, Issue 2. During the preparation of the figure, the human and yeast H2B tyrosines were numbered the same, making the human numbering incorrect. The correct Figure 1 with proper numbering of human tyrosines is below.

Erratum to:

Singh R.K. and Gunjan A. Histone tyrosine phosphorylation comes of age.Epigenetics 2011; 6:153-60.     

Erratum to: “Nano-characterization of Jagged-1-educated dendritic cells”

Paper by Xing et al. “Nano-characterization of Jagged-1-educated dendritic cells” in Volume 6, Issue 6, 981-989 / December 2011; DOI: 10.2478/s11535-011-0063-3 contains an error in the graphic file inserted as Figure 1 and also an incorrect figure caption. The corrected Figure 1, together with its caption is presented below.     

Triple X Egyptian woman and a Down's syndrome offspring

The 47, XXX karyotype (triple X) has a frequency of 1 in 1000 female newborns. However, this karyotype is not usually suspected at birth or childhood. Female patients with a sex chromosome abnormality may be fertile. In patients with a 47, XXX cell line there appears to be an increased risk of a cytogenetically abnormal child but the extent of this risk cannot yet be determined; it is probably lower in the non-mosaic 47, XXX patient than the mosaic 46, XX/47, XXX one. We describe a new rare case of triple X woman and a Down''s syndrome offspring. The patient is 26 years of age. She is a housewife, her height is 160 cm and weight is 68 kg and her physical features and mentality are normal. She has had one pregnancy at the age of 25 years resulted in a girl with Down''s syndrome. The child had 47 chromosomes with trisomy 21 (47, XX, +21) Figure 1. The patient also has 47 chromosomes with a triple X karyotype (47, XX, +X) Figure 2. The patient''s husband (27 years old) is physically and mentally normal. He has 46 chromosomes with a normal XY karyotype (46, XY). There are neither Consanguinity between her parent''s nor she and her husband.Open in a separate windowFigure 1Karyotype 47, XX + 21 of the daughter of Triple X syndromeOpen in a separate windowFigure 2Karyptype 47, XX + X of the Down syndrome''s mother     

Correction: Hepatitis B virus infection and replication in human bone marrow mesenchymal stem cells

ABSTRACT: Correction After publication of this work (Virol J 2011, 8:486), we noted that D of Figure 1 was incorrect. Now the correct figure has been provided with this correction.     

Splenogonadal Fusion: An Unusual Case of an Acute Scrotum

We highlight a case on a normal left testicle with a fibrovascular cord with three nodules consistent with splenic tissue. The torsed splenule demonstrated hemorrhage with neutrophilic infiltrate and thrombus consistent with chronic infarction and torsion. Splenogonadal fusion (SGF) is a rather rare entity, with approximately 184 cases reported in the literature. The most comprehensive review was that of 123 cases completed by Carragher in 1990. Since then, an additional 61 cases have been reported in the scientific literature. We have studied these 61 cases in detail and have included a summary of that information here.Key words: Splenogonadal fusion, Acute scrotumA 10-year-old boy presented with worsening left-sided scrotal pain of 12 hours’ duration. The patient reported similar previous episodes occurring intermittently over the past several months. His past medical history was significant for left hip dysplasia, requiring multiple hip surgeries. On examination, he was found to have an edematous left hemiscrotum with a left testicle that was rigid, tender, and noted to be in a transverse lie. The ultrasound revealed possible polyorchism, with two testicles on the left and one on the right (Figure 1), and left epididymitis. One of the left testicles demonstrated a loss of blood flow consistent with testicular torsion (Figure 2).Open in a separate windowFigure 1Ultrasound of the left hemiscrotum reveals two spherical structures; the one on the left is heterogeneous and hyperdense in comparison to the right.Open in a separate windowFigure 2Doppler ultrasound of left hemiscrotum. No evidence of blood flow to left spherical structure.The patient was taken to the operating room for immediate scrotal exploration. A normalappearing left testicle with a normal epididymis was noted. However, two accessory structures were noted, one of which was torsed 720°; (Figure 3). An inguinal incision was then made and a third accessory structure was noted. All three structures were connected with fibrous tissue, giving a “rosary bead” appearance. The left accessory structures were removed, a left testicular biopsy was taken, and bilateral scrotal orchipexies were performed.Open in a separate windowFigure 3Torsed accessory spleen with splenogonadal fusion.Pathology revealed a normal left testicle with a fibrovascular cord with three nodules consistent with splenic tissue. The torsed splenule demonstrated hemorrhage with neutrophillic infiltrate and thrombus consistent with chronic infarction and torsion (Figure 4).Open in a separate windowFigure 4Splenogonadal fusion, continuous type with three accessory structures.     

Teaching cases: A 1-week-old newborn with hypercalcemia and palpable nodules: subcutaneous fat necrosis

Abstract: We present a 1-week-old newborn with subcutaneous fat necrosis complicated by hypercalcemia. She received conservative treatment of adequate hydration and restricted supplementary vitamin D.The case: A 1-week-old term newborn girl was brought to her physician with a 2-day history of subcutaneous masses. The girl had been born by vacuum-assisted vaginal delivery with a birth weight of 3.5 kg. She did not require resuscitation but was observed for 24 hours in a special care nursery because of tachypnea. The patient was discharged home after 48 hours, and her course over the next 5 days was unremarkable.On physical examination, the newborn was afebrile and in no obvious distress. She had multiple firm, mobile, mildly tender subcutaneous nodules with overlying erythema (Figure 1). The largest mass on palpation was located in the left deltoid area and measured 2 × 2.5 cm (Figure 1). Two smaller lesions were located in the left posterior axillary area (Figure 1) and a fourth lesion was in the right posterior auricular region. The remainder of the physical examination and the results of a complete blood count were normal. The newborn''s total serum calcium level was elevated (2.94 [normal 1.96–2.66] mmol/L) as was her ionized calcium level (1.36 [normal 1.14–1.29] mmol/L. A biopsy was not performed because the infant was well and the results of clinical investigations were consistent with subcutaneous fat necrosis.Open in a separate windowFigure 1: A 5-day-old infant with lesions of subcutaneous fat necrosis. The largest mass (black arrow) measured 2 × 2.5 cm. Two smaller lesions (white arrows) were located in the left posterior axillary area.Subcutaneous fat necrosis of the newborn is a relatively uncommon condition that occurs in the first several weeks after birth. The incidence is unknown; however, it is more frequently reported after perinatal distress than after uncomplicated deliveries, and maternal risk factors include gestational diabetes and preeclampsia.¹ Skin lesions are characterized by indurated nodules that range from flesh-coloured to blue and by plaques on the face, trunk and buttocks as well as on the arms and legs near the trunk. Figure 2 is a representative microscopic image of this condition.² The differential diagnosis is bacterial cellulitis, erysipelas and sclerema neonatorum.³Open in a separate windowFigure 2: Left: A typical photomicrograph from a different patient showing lobular panniculitis with sparing of the dermis and epidermis (original magnification × 20). Right: A high-power view shows that the inflammatory infiltrate is mixed and composed of histiocytes, lymphocytes, neutrophils and eosinophils. Cleft-like spaces (arrow) suggestive of dissolved crystals can be seen at the periphery of some of the fat cysts (original magnification × 400). Reproduced with permission from Macmillan Publishers Ltd: Journal of Perinatology (Diamantis et al.²) © 2006.Although subcutaneous fat necrosis of the newborn is often benign and self-limited, the most important concern is hypercalcemia, which can lead to neurologic or cardiac problems, nephrocalcinosis and nephrolithiasis. Clinical signs of newborn hypercalcemia include irritability, poor feeding and vomiting. Skin lesions typically resolve over a period of weeks to several months; however, hypercalcemia can persist longer and requires serial monitoring. The treatment of hypercalcemia ranges from conservative measures such as hydration and restriction of vitamin D and calcium to more aggressive interventions such as furosemide, glucocorticoid or bisphosphonate therapy in severe cases.⁴In our patient, mild hypercalcemia was accompanied by mild elevations in the ratio of calcium to creatinine in the urine and a normal 1,25-dihydroxyvitamin D level. Because our patient was otherwise well, we opted for conservative management. In 2 months, her calcium level had normalized and the lesions completely regressed.Fahed Aljaser MD Michael Weinstein MD Division of Pediatric Medicine Hospital for Sick Children University of Toronto Toronto, Ont.     

Rhythmic and Light-Inducible Appearance of Clock-Associated Pseudo-Response Regulator Protein PRR9 through Programmed Degradation in the Dark in Arabidopsis thaliana

The above article was published in Plant and Cell Physiology48(11): 1644–1651. Figure 1 was shown incorrectly online. The figure legend inFigure 1C was missing. The correct figure is given below. View larger version (26K):   Fig. 1 Construction     

Erratum: Deficiency in recapitulation of stage‐specific embryonic gene transcription in two‐cell stage cloned mouse embryos

Due to a mathematical error, the cpm bound values for Figure 2 were calculated incorrectly. The correct figure is presented here. The original article to which this erratum refers was published in Molecular Reproduction and Development 2007;74(12):1548–1556.     

Contribution on the diagnosis ofStaphylococcus aureus rosenbach

Возможность трансформации прогестерона, стероида ?S? (11-дезокси-17-гидроксикортикостерон), дегидроэпиандростерона и

     

Correction to: Establishment of Murine Infection Models with Biological Clones of Dengue Viruses Derived from A Single Clinical Viral Isolate

Virologica Sinica - During the layout of the article, the square brackets in the legends were mistakenly shifted in every subfigure. The corrected figure is shown below     

Erratum to Wolfgang Benetka et al., Cell Cycle Volume 7, Issue 23; pp. 3709-3719

In the paper, "Experimental testing of predicted myristoylation targets involved in asymmetric cell division and calcium-dependent signalling" by Wolfgang Benetka, Norbert Mehlmer, Sebastian Maurer-Stroh, Michaela Sammer, Manfred Koranda, Ralph Neumüller, Jörg Betschinger, Jürgen A. Knoblich, Markus Teige and Frank Eisenhaber (Cell Cycle 2008; 7:3709-19), Figure 5 was published two times but Figure 2 was not included. Figure 2 and 5 appear correct below.     

Structure of acidic o-specific polysaccharide from the marine bacterium <Emphasis Type="Italic">Cellulophaga baltica</Emphasis>

The structure of an acidic O-specific polysaccharide from the marine bacterium Cellulophaga baltica was established by chemical methods and NMR spectroscopy. The polysaccharide was shown to consist of repeating tetrasaccharide units containing two mannose residues, one N-acetyl-D-glucosamine residue, and one D-glucuronic acid residue. An O-acetyl group was also found in the polysaccharide in nonstoichiometric amount. The polysaccharide had the following structure:

Open image in new window

     

Testicular Sclerosing Sertoli Cell Tumor: A Case Report and Review of the Literature

Sertoli cell tumors are very rare testicular tumors, representing 0.4% to 1.5% of all testicular malignancies. They are subclassified as classic, large-cell calcifying, and sclerosing Sertoli cell tumors (SSCT) based on distinct clinical features. Only 42 cases of SSCTs have been reported in the literature. We present a case of a 23-year-old man diagnosed with SSCT.Key words: Testicular neoplasm, Sertoli cell tumor, Sclerosing Sertoli cell tumorA 23-year-old man was referred to the Cleveland Clinic Department of Urology (Cleveland, OH) for an incidentally detected right testicular mass. The mass was identified during a work-up for transient left testicular discomfort. His only notable medical history was nephrolithiasis. There was no personal or family history of testicular cancer or cryptorchidism. On physical examination, he was a well-nourished, well-masculinized young man without gynecomastia. Testicular examination revealed normal volume and consistency bilaterally without other relevant findings. Testicular ultrasonography demonstrated an 8 mm × 6 mm × 6 mm hypoechoic, solid mass in the posterior right testicle with peripheral flow on color Doppler (Figure 1).Open in a separate windowFigure 1Testicular ultrasound demonstrating an 8 mm × 6 mm × 6 mm hypoechoic, solid mass in the posterior right testicle (blue arrows).The remainder of the ultrasound examination yielded normal results. Lactic dehydrogenase, B-human chorionic gonadotropin, and α-fetoprotein levels were all within the normal range. After a thorough review of the options, the patient was then taken to the operating room for inguinal exploration. Intraoperative ultrasound confirmed a superficial 8-mm hypoechoic testis lesion. A whiteyellow, well-demarcated nodule was widely excised and a frozen section was sent to pathology for examination. The frozen section examination revealed the lesion to be a neoplasm with differential diagnosis including sclerosing Sertoli cell tumor (SSCT), adenomatoid tumor, and a variant of Leydig cell tumor. Because the final diagnosis could not be determined from frozen section, the decision was made to perform a right radical orchiectomy. Pathologic examination revealed a grossly unifocal, well-circumscribed, white, firm mass of 0.8 cm. Microscopically the lesion was composed of solid and hollow tubules and occasional anastomosing cords distributed within the hypocellular, densely collagenous stroma. Although the lesion was somewhat well circumscribed, entrapped seminiferous tubules with Sertoli-only cells were present within the tumor (Figure 2). Tumor cells had pale or eosinophilic cytoplasm with small and dark nuclei with inconspicuous nucleoli. The tumor was confined to the testis and margins were negative. A diagnosis of SSCT was reached, supported by positive immunostain results for steroidogenic factor 1, focal inhibin, and calretinin expression, and negative stain results for cytokeratin AE1/AE3 and epithelial membrane antigen in the tumor (Figure 3). The postoperative course was unremarkable. Computed tomography scan of the abdomen and pelvis and chest radiograph were negative for metastatic disease.Open in a separate windowFigure 2Low-power examination revealing a well-circumscribed tumor composed of solid and hollow tubules and occasional anastomosing cords distributed within the hypocellular, densely collagenous stroma. Hematoxylin and eosin stain, original magnification ×40. (B) High-power examination. Note entrapped seminiferous tubules lacking spermatogenesis. Hematoxylin and eosin stain, original magnification ×100.Open in a separate windowFigure 3Nuclear expression of steroidogenic factor 1 in the tumor as well as benign Sertoli cells in entrapped seminiferous tubules (original magnification ×200). (B) Focal calretinin expression in the tumor (inhibin had a similar staining pattern; original magnification ×100).     

Teaching cases: A patient with loss of vision in the right eye and neurofibromatosis type 1

Abstract: Neurofibromatosis type 1 is a common autosomal dominant condition that affects about 1 in 5000 people. We describe a 75-year-old man who, in addition to many classic developmental changes of the disease in his skin, eyes and nervous system, had blindness in his right eye as a complication.Case: A 75-year-old man with long-standing neurofibromatosis type 1 was admitted because the vision in his right eye had decreased progressively over 3 months. Physical examination showed disseminated cutaneous and subcutaneous neurofibromas of varying size (Figure 1) and café-au-lait spots (Figure 2). The patient had a visual acuity of 6/18 (20/60) in his right eye and Lisch nodules (iris hamartomas) (Figure 3). A neurologic examination showed no abnormalities other than his loss of vision. Axial T₁-weighted magnetic resonance imaging of the brain and orbits (Figure 4) showed an isointense mass lateral to the right optic nerve that appeared atrophic and pushed to the left. The mass showed a hyperintense signal on T₂-weighted images with contrast enhancement. These findings are compatible with glioma of the optic nerve.Open in a separate windowFigure 1: Disseminated cutaneous and subcutaneous neurofibromas of varying size on the torso of a patient with neurofibromatosis type 1.Open in a separate windowFigure 2: A café-au-lait spot on the patient''s right knee.Open in a separate windowFigure 3: Lisch nodules on the left iris.Open in a separate windowFigure 4: T₁-weighted axial magnetic resonance imaging of the brain and orbits, showing an isointense mass lateral to the right optic nerve (white arrow) that appears atrophic and pushed to the left (black arrow on inset).Axial and coronal magnetic resonance imaging (Figure 5) showed a mass in the left parietal lobe with hyperintensity on T₂-weighted images and hypointensity on T₁-weighted images. After a contrast medium was administered, the lesion showed a thickened, enhanced wall with a central necrotic area. These findings are compatible with astrocytoma.Open in a separate windowFigure 5: T₂-weighted axial (left) and coronal (right) magnetic resonance imaging showing a mass with hyperintensity (arrow) in the left temporal lobe. After administration of a contrast medium, the lesion is visible with a thickened enhanced wall and a central necrotic area.Because of slight enlargement and increased hardness of the subcutaneous lesions, an excisional biopsy was performed. Histology showed delicate fascicles consisting of cells with oval or spindle-shaped nuclei, scant cytoplasm and round cells with entrapped axons (Figure 6). Only scattered neoplastic Schwann cells were stained during immunostaining for S-100 protein (Figure 7). This pattern is consistent with neurofibroma. The patient chose not to receive further treatment and was discharged.Open in a separate windowFigure 6: Biopsy specimen of a subcutaneous neurofibroma showing spindle-shaped and round cells with entrapped axons (hematoxylin and eosin, original magnification ×10).Open in a separate windowFigure 7: Only scattered neoplastic Schwann cells (arrow) are stained after immunostaining for S-100 protein. Normally, S-100 protein is present in cells derived from the neural crest, such as Schwann cells. It can be found in melanoma cells, in malignant peripheral nerve sheath tumours and in certain types of sarcomas.Neurofibromatosis type 1, also known as von Recklinghausen disease,¹ is characterized by changes in pigmentation and the growth of tumours along nerves in the skin and other parts of the body. It is caused by a defect in a tumour-suppressing gene on chromosome 17q11.2. Normally the gene produces neurofibromin, a protein that regulates cellular proliferation.² With the gene mutation, the lack of neurofibromin results in overgrowth of cells from neural crest areas in both the central nervous system (causing Schwann cell tumours on virtually every nerve) and the skin. All people who inherit a copy of the mutated gene are affected. As the pattern of inheritance is autosomal dominant, only 1 copy of the defective gene is needed to cause the condition. However, it is not necessary to have an affected parent. About 30%–50% of patients have a new mutation.Neurofibromatosis type 2 is a much rarer form of neurofibromatosis caused by mutations in both alleles of a different tumour suppressor gene on chromosome 22q12.1.About 1 in 3000–5000 individuals are affected by neurofibromatosis type 1, without differences related to ethnic background.³ Pigmented small macules and café-au-lait patches are often present shortly after birth, although neurofibromas are rare in early childhood. In later childhood and adolescence, both neurofibromas and pigmented lesions become common. Clinical manifestations are variable (4Table 1Open in a separate windowA diagnosis of neurofibromatosis type 1 is based on clinical findings. The patient should have 2 or more of the following: 6 or more café-au-lait spots of ≥ 1.5 cm in postpubertal individuals or ≥ 0.5 cm in prepubertal individuals; 2 or more neurofibromas of any type or 1 or more plexiform neurofibroma; and freckling in the underarms and groin.¹ The differential diagnosis includes benign café-au-lait pigmentation (present in up to 10% of the general population), multiple lipomas, and sporadic schwannomas, gliomas and meningiomas in the central nervous system.Most people with mild neurofibromatosis have little disability. People affected by more severe variants have a shortened life expectancy, especially if tumours of the central nervous system or other malignant neoplasms arise during the course of illness.^1,3 The condition can have a serious psychological impact because the accumulation of skin nodules can be quite disfiguring.⁵ Surgical excision and laser treatment of the neurofibromas are possible, but neither treatment is universally effective.⁶ Transplantation with an allograft of composite tissue on the lower and middle parts of a patient''s face was recently reported.⁷Gliomas of the optic nerve are found in up to 15% of pediatric patients with neurofibromatosis type 1. Best detected using magnetic resonance imaging, these gliomas are symptomatic in about 50% of patients at diagnosis. A minority will progress to vision loss.⁸ The high prevalence of gliomas of the optic nerve that are asymptomatic may, however, be biased by referral patterns, Indeed, in patients with neurofibromatosis type 1, the threshold of risk for optic nerve glioma is low.⁹Guidelines are available for the diagnosis and management of neurofibromatosis type 1.^10,11 Physicians who identify patients with neurofibromatosis type 1 should refer them early to facilities where appropriate evaluation and monitoring of lesions can be carried out. Early detection and monitoring may help to prevent disability and death.