Bob Ong Books Pdf File Download 2
Our opinion towards the Filipino author Bob Ong us generally a perception of admiration, wherein we can all agree that his books are incredibly well written, with a unique and easily distinguishable writing style such as his humor-filled tendencies, and specifically with his book, "Si", wherein it was written in multiple changing perceptions of different characters. His works are also incredibly inspirational, its the type of writing that makes its readers want to start a writing career as well, which is a charm that Bob Ong has managed to acquire with all his books, and not all authors have that type of influence. Although, it is relatively hard to form an opinion regarding Bob Ong himself, especially with his identity not being revealed, even his real name. All that we can say about him specifically is that he is surrounded a bunch of good-hearted people, seeing as his identity still has not been revealed after all these years, given how it is so easy to do so since it only takes a single person to have his whole identity revealed. Besides, its pretty exciting to have such a famous author be anonymous. For all we know, he could be that mundane looking person you always see walking down the street, or that barista at your favorite coffee shop that serves you every Sunday. He could be anyone, anywhere, and maybe even closer to you than you think. Overall, no matter how much of a mystery Bob Ong's actual identity truly is, it is no doubt that his works are of top tier quality that will always have its readers satisfied after a good read.
The mutational profiles of EMZL and NMZL differ [76, 84,85,86]. In addition, there are significant genetic differences among EMZLs arising in different anatomic sites (Fig. 2): e.g., ocular adnexal EMZL commonly shows TNFAIP3 mutation/deletion [87, 88]; salivary gland EMZL shows recurrently mutated GPR34 [89, 90]; most thyroid EMZL carry deleterious mutations of CD274, TNFRSF14 and/or TET2 ; and PCMZL often shows FAS mutations . Somatic variants of KMT2D, PTPRD, NOTCH2, KLF2, and others are frequent in NMZL [76, 84, 85, 93] but not in EMZL. Better definition of the underlying molecular genetic changes of these lymphomas may potentially open the door to improved treatment options.
The WHO-HAEM4R entity of high-grade B-cell lymphoma with dual rearrangements of MYC and BCL2 and/or BCL6 has been conceptually reframed and reassigned. In recognition of their variable morphologies but homogeneous dark zone biologic features and gene expression characteristics, the WHO-HAEM5 renames the entity diffuse large B-cell lymphoma/high-grade B-cell lymphoma with MYC and BCL2 rearrangements (DLBCL/HGBL-MYC/BCL2) to encompass tumours defined by the presence of dual MYC and BCL2 rearrangements that may be composed of large or intermediate or blastoid cells (Fig. 4). Hence, the primary morphological categorization of the neoplasm can be maintained after determining the genetic constitution. This group of cases forms a homogeneous entity with an exclusive GC gene expression profile, a close pathogenetic relationship to FL and molecular GC-like DLBCL subsets [129,130,131,132]. In addition, gene expression signatures associated with DLBCL/HGBL-MYC/BCL2 (MHG, DHITsig) [130, 133] significantly overlap with those of Burkitt lymphoma (BL). In contrast, lymphoid neoplasms with dual MYC and BCL6 rearrangements represent a more diverse spectrum  with variable gene expression profiles and mutational spectra, markedly differing from DLBCL/HGBL-MYC/BCL2. Hence, these cases have been excluded from the DLBCL/HGBL-MYC/BCL2 entity and are now classified either as a subtype of DLBCL, NOS or HGBL, NOS according to their cytomorphological features (Fig. 4).
High-grade B-cell lymphoma with 11q aberration (HGBL-11q), formerly known as Burkitt-like lymphoma with 11q aberration in WHO-HAEM4R, is an aggressive MYC rearrangement-negative mature B-cell lymphoma with a morphology similar to Burkitt lymphoma (BL) or with an intermediate or blastoid appearance, an immunophenotype (CD10+, BCL6+, BCL2-), and/or gene expression profile (GEP) similar to BL, and a characteristic chromosome 11q-gain/loss pattern. The losses in 11q24qter are more specific to this entity than the centromeric gains but rarely might be substituted by copy-number neutral losses of heterozygosity. More recent studies have also confirmed that the mutational spectrum, besides the pattern of genomic imbalances, is different from that of BL and is more similar to that of DLBCL of GCB type. Of note, genomic alterations affecting the ID3-TCF3 complex, one of the molecular hallmarks of BL, are only rarely, if at all, seen in HGBL-11q [134, 135]. Cases of B-cell lymphoma with a Burkitt-like appearance that lack MYC rearrangement, therefore, should be tested for the 11q gain/loss pattern  (Fig. 4). It should be noted that the morphological spectrum of HGBL-11q as defined by the specific 11q-gain/loss pattern is more restricted than that of DLBCL/HGBL-MYC/BCL2.
Nodal T-follicular helper cell lymphoma, angioimmunoblastic-type (nTFHL-AI) is the prototype with well-defined clinical, morphologic (Fig. 7), immunophenotypic and characteristic mutational profiles. Genetically, nTFHL-AI is characterized by a stepwise acquisition of somatic changes with TET2 and DNMT3A mutations occurring early in haematopoietic stem cells, while RHOA and IDH2 mutations are also present in the neoplastic TFH cell population. In contrast, nTFHL-F and nTFHL-NOS (Fig. 7) represent less well-studied nodal lymphomas, which also express TFH markers such as PD1, ICOS, CXCL13, CD10, and BCL6 [266,267,268,269,270,271,272,273,274,275,276,277] and show mutation profiles similar to those of nTFHL-AI [265, 266, 278,279,280].
Although the individual entities are defined predominantly by histopathological features, there is considerable morphologic overlap and inter-observer variability. nTFHL-NOS is the recommended term for CD4+ lymphomas with TFH phenotype but that do not meet criteria for nTFHL-AI or nTFHL-F. The generic term nTFHL rather than nTFHL-NOS is recommended when interpreting core biopsies to prevent misclassification due to inadequate sampling. The TFH phenotype is defined as the presence of at least two TFH markers in addition to CD4. Further studies are required to determine if this definition is sufficiently robust in differentiating nTFHL-NOS from PTCL, NOS, as most cases of the former often express the less specific TFH markers such as PD1 and ICOS. In essence, the diagnosis may be challenging with many pitfalls. An integrated approach is recommended, at the very minimum requiring correlation of clinical, morphologic and immunophenotypic features, with input from genomics for clonality and mutational profiles in difficult cases.
In the United Kingdom, we take it for granted that, no matter who owns the rights, we can access and read in a public library almost any book that's ever been published, because of the "public lending right" model, which remunerates authors and publishers for books borrowed. Gerhardt proposes a similar "public lending right" for the moving image--"in the new digital landscape, the moving image should be acknowledged as having the same educational value as the printed text." (3) 2b1af7f3a8