Chapter 3 definition

Chapter 3 means chapter 3 of the Internal Revenue Code of the United States (Withholding of Tax on Nonresident Aliens and Foreign Corporations). Chapter 3 contains sections 1441 through 1464.
Chapter 3 means Sections 1441 through 1464 and the regulations thereunder, but does not include Sections 1445 and 1446 and the regulations thereunder, unless the context indicates otherwise.

Examples of Chapter 3 in a sentence

  • See Chapter 3 (Using the plan’s coverage for your medical services) for more specific information about emergency, out-of-network, and out-of-area coverage.

  • See Chapter 3 (Using the plan’s coverage for your medical services) for more specific information.

  • For purposes of Chapter 2 (National Treatment and Market Access for Goods), Chapter 3 (Rules of Origin and Operational Procedures Related to Origin), Chapter 4 (Customs Procedures and Trade Facilitation), Chapter 5 (Trade Remedies), Chapter 6 (Sanitary and Phytosanitary Measures), Chapter 7 (Technical Barriers to Trade), Article XX of the GATT 1994 and its interpretative notes are incorporated into and made part of this Agreement, mutatis mutandis.

  • This report is made solely to the Company’s members, as a body, in accordance with Chapter 3 of Part 16 of the Companies Act 2006.

  • This report is made solely to the company’s members, as a body, in accordance with Chapter 3 of Part 16 of the Companies Act 2006.

More Definitions of Chapter 3

Chapter 3. The Evolution of the Trial Program 43 Introduction I. Principles of Selection A. Early Planning
Chapter 3. The Relationship Between DXA-based and Anthropometric Measures of Visceral Fat and Morbidity in Women. Abstract Excess accumulation of visceral fat is a prominent risk factor for cardiovascular and metabolic morbidity. While CT is the gold standard to measure visceral adiposity, this is often not possible for epidemiological studies - thus proxy measures of visceral fat are required. Study aims were to a) identify a valid proxy measure of VAT area, b) estimate VAT heritability and c) assess visceral fat association with morbidity in comparison to body fat distribution. A validation sample of 54 females measured for detailed body fat composition - assessed using CT, DXA, and anthropometry – was used to evaluate previously published predictive models of CT-measured visceral fat. Based upon a validated model, we realised an estimate of abdominal VAT area for a population-based sample of 3,457 female volunteer twins and estimated VAT area heritability using a classical twin study design. Regression and residuals analyses were used to assess the relationship between adiposity and morbidity. Published models applied to the validation sample explained >80% of the variance in CT-measured visceral fat. Narrow sense VAT area heritability was estimated to be 58% (95% CI: 51-66%) with a shared familial component of 24% (17-30%). VAT area is strongly associated with T2D, hypertension (HT), subclinical atherosclerosis and liver function tests. In particular, VAT area is associated with T2D, HT and alanine aminotransaminase liver function, conditional upon association with DXA total abdominal fat and BMI. DXA and anthropometry measures can be used to derive reliable estimates of visceral fat. Visceral fat is heritable and appears to mediate association between adiposity and morbidity. This observation is consistent with hypotheses that suggest excess visceral adiposity is causally related to cardiovascular and metabolic disease.
Chapter 3. The Practice of Philosophers
Chapter 3. The VDSA Data Files
Chapter 3. Approach to the evaluation: describes the overall framework for assessment followed by the evaluation team including choices with regards to methodology, data collection and data analysis. Chapter 3 also discusses the limitations and constraints of the evaluation exercise and their implications for the interpretation of findings.
Chapter 3. The Ras oncogene signals centrosome amplification in mammary epithelial cells through cyclin D1/Cdk4 and Nek2. Figure 1: Inducible expression of K-RasG12D and c-Myc in mouse mammary glands results in distinct histopathology, ectopic proliferation, and apoptosis. Figure 2: Expression of K-RasG12D results in centrosome amplification in premalignant mammary lesions, whereas c-Myc-induced centrosome amplification is only detected in tumors. Figure 3: Expression of K-RasG12D and c-Myc during premalignancy results in differential expression of proteins governing the cell and centrosome cycles. Figure 4: Oncogene-induced centrosome amplification is suppressed by siRNA- mediated silencing of Cdk4, cyclin D1 or Nek2 Table 1: Five-day induction of K-RasG12D and c-Myc results in the differential expression of various genes Table 2: Cell cycle distribution of MCF10A cells transfected with empty vector, H- RasG12V and/or c-Myc, and the indicated siRNAs Chapter 4: Cdk4 and Nek2 signal binucleation and centrosome amplification in a Her2+ breast cancer model. Table 1: Knockdown of Cdk4 does not affect cell cycle profiles. Table 2: Knockdown of Cdk4 does not affect the fraction of cells in S phase. Table 3: Knockdown of Cdk4 reduces percentage of failed mitosis ending in binucleation. Figure 1: Her2+ cells display centrosome amplification. Figure 2: Centrosome amplification in Her2+ cells is mediated by Cdk4. Figure 3: Her2+ breast cancer cells display elevated percentages of binucleation and cytokinesis defects. Figure 4: Binucleation and centrosome amplification in Her2+ cells are mediated by Nek2. Figure 5: A potential signaling loop for Cdk4 and Nek2.