WDVV equations for pure Super-Yang-Mills theory

In the literature, there are two proofs that the prepotential of $N=2$ pure Super-Yang-Mills theory satisfies the Witten-Dijkgraaf-Verlinde-Verlinde (WDVV) equations. We show that these two methods are in fact equivalent. \u

Generalized WDVV equations for B_r and C_r pure N=2 Super-Yang-Mills theory

A proof that the prepotential for pure N=2 Super-Yang-Mills theory associated with Lie algebras B_r and C_r satisfies the generalized WDVV (Witten-Dijkgraaf-Verlinde-Verlinde) system was given by Marshakov, Mironov and Morozov. Among other things, they use an associative algebra of holomorphic differentials. Later Ito and Yang used a different approach to try to accomplish the same result, but they encountered objects of which it is unclear whether they form structure constants of an associative algebra. We show by explicit calculation that these objects are none other than the structure constants of the algebra of holomorphic differentials.Comment: 8 page

Second order reductions of the WDVV Equations related to classical Lie algebras

We construct second order reductions of the generalized Witten-Dijkgraaf-Verlinde-Verlinde system based on simple Lie algebras. We discuss to what extent some of the symmetries of the WDVV system are preserved by the reduction.Comment: 6 pages, 1 tabl

On the WDVV equations in five-dimensional gauge theories

It is well-known that the perturbative prepotentials of four-dimensional N=2 supersymmetric Yang-Mills theories satisfy the generalized WDVV equations, regardless of the gauge group. In this paper we study perturbative prepotentials of the five-dimensional theories for some classical gauge groups and determine whether or not they satisfy the WDVV system.Comment: 15 pages, no figures, web address of paper added in bibliography. Misprints correcte

Generalized WDVV equations for F4 pure N=2 Super-Yang-Mills theory

An associative algebra of holomorphic differential forms is constructed associated with pure N=2 Super-Yang-Mills theory for the Lie algebra F4. Existence and associativity of this algebra, combined with the general arguments in the work of Marshakov, Mironov and Morozov, proves that the prepotential of this theory satisfies the generalized WDVV system.Comment: 7 page

Patients with usual vulvar intraepithelial neoplasia-related vulvar cancer have an increased risk of cervical abnormalities

Contains fulltext : 81890.pdf (publisher's version ) (Closed access)BACKGROUND: Vulvar squamous cell carcinoma (SCC) originates the following two pathways, related to differentiated (d) vulvar intraepithelial neoplasia (VIN) or to human papillomavirus (HPV)-related usual (u) VIN. Multicentric HPV infections (cervix, vagina and vulva) are common. We hypothesise that patients with a uVIN-related vulvar SCC more often have cervical high-grade squamous intraepithelial lesions (HSILs) compared with women with dVIN-related vulvar SCC. METHODS: All vulvar SCCs (201) were classified to be dVIN- (n=164) or uVIN related (n=37). Data with regard to the smear history and cervical histology were retrieved from PALGA, the nationwide Netherlands database of histo- and cytopathology. For HSIL cervical smears of which histology was taken, HPV DNA analysis on both the vulvar and cervical specimens was performed. RESULTS: At least one smear was available in 145 (72%) of the 201 patients. Patients with a uVIN-related vulvar SCC more often had an HSIL compared with patients with a dVIN-related SCC (35 vs 2%, P<0.001). A total of 10 of the 13 HSILs were histologically assessed and identical HPV types were found in the vulva and cervix. CONCLUSION: These data emphasise the necessity to differentiate between dVIN- and uVIN-related vulvar tumours and to examine the entire lower female ano-genital tract once an uVIN-related lesion is found

A significant proportion of classic Hodgkin lymphoma recurrences represents clonally unrelated second primary lymphoma

Despite high cure rates in classic Hodgkin lymphoma (cHL), relapses are observed. Whether relapsed cHL represents second primary lymphoma or an underlying T-cell lymphoma (TCL) mimicking cHL is under-investigated. To analyze the nature of cHL recurrences, in-depth clonality testing of immunoglobulin (IG) and T-cell receptor (TR) rearrangements was performed in paired cHL diagnosis and recurrences of 60 patients, supported by targeted mutation analysis of lymphoma-associated genes. Clonal IG rearrangements were detected by next-generation sequencing (NGS) in 69/120 (58%) diagnosis and recurrence samples. The clonal relationship could be established in 34 cases, identifying clonally related relapsed cHL in 24/34 patients (71%). Clonally unrelated cHL was observed in 10/34 patients (29%) as determined by IG-NGS clonality assessment, and confirmed by the identification of predominantly mutually exclusive gene mutations in the paired cHL samples. In recurrences of &gt;2 years, ~60% of cHL patients for which the clonal relationship could be established showed a second primary cHL. Clonal TR gene rearrangements were identified in 14/125 samples (11%), and TCL-associated gene mutations were detected in 7/14 samples. Retrospective pathology review with integration of the molecular findings were consistent with an underlying TCL in 5 patients aged &gt;50 years. This study shows that cHL recurrences, especially after 2 years, sometimes represent a new primary cHL or TCL mimicking cHL, as uncovered by NGS-based IG/TR clonality testing and gene mutation analysis. Given the significant therapeutic consequences, molecular testing of a presumed relapse in cHL is crucial for subsequent appropriate treatment strategies adapted to the specific lymphoma presentation.</p