Discussion Case: Fidelity Investments’ Partnership with Citizen Schools

Roy Fralin stood in front of a roomful of active sixth and seventh graders in an inner-city public school in Roxbury, Massachusetts. The classroom walls were covered with flip chart paper, which were packed with diagrams, numbers, and terms like “savings,” “budget,” and “investment.” A student stood at the front of the classroom. Fralin handed him a baseball cap to illustrate a loan with interest. “OK, when you give it back, you’ll owe me how much?” Another student shouted out the answer. “Great!” exclaimed Fralin. They exchanged high fives. “Now, how much are we putting away for your 401(k)?” The students punched their handheld calculators.

Fralin was not a public school teacher, and teaching personal finance to middle schoolers was not his regular job. He was a vice president and investment advisor at Fidelity Investments, where he worked mostly with high net-worth clients. But here he was, every Wednesday afternoon for 10 weeks, teaching a curriculum that Fidelity employees had developed called “How to Invest Like a Millionaire.” The program was part of a partnership between an innovative nonprofit called Citizen Schools and Fidelity Investments, one of its corporate partners. “I just don’t see any downside,” Fralin later reflected in a clip posted to YouTube about his experience as a citizen teacher. “I think this is going to be a success.”

In June 2015, Fidelity Investments was one of the leading providers of financial services in the world, administering $5.2 trillion in assets for 24 million individual and institutional clients. The company, which was privately owned, offered investment management, retirement planning, portfolio guidance, brokerage, and benefits outsourcing services. It also operated its own family of mutual funds. Fidelity maintained its headquarters in Boston, Page 415but had 10 regional operating centers and about 180 retail locations. In 2015, the firm employed 41,000 associates.

In 2009, Fidelity set about rethinking its approach to community relations. For many years, the firm had been philanthropically active, giving to a wide range of charities in its home community and elsewhere. But the company had come to believe that it could have a greater impact by focusing on partnerships with a small number of what it called “best in class” nonprofit organizations. An issue of particular concern to Fidelity was education, especially the shocking dropout rates in many of the communities it served; nationally, 1.2 million students dropped out of high school every year, many of them as early as ninth grade. In researching various options for making a difference, the company learned that the middle school years were critical in determining whether or not students would go on to graduate from high school.

To focus its resources on this issue, Fidelity chose to partner with Citizen Schools (CS). Social entrepreneur Eric Schwarz had founded CS in 1995 in Boston to operate after-school programs for middle school students, aged 11 to 14, in disadvantaged communities. The nonprofit recruited volunteer professionals—“citizen teachers”—to offer after-school apprenticeships in subjects they were passionate about in schools in the CS network. As a culminating experience, students would present what they had learned to friends, family, and teachers at what CS called “WOW!” events. In 2015, Citizen Schools had active partnerships with 29 schools in low-income communities in seven states, serving more than 4,800 students.

Fidelity had contributed money to Citizen Schools since 1998, but in 2009 it significantly stepped up its commitment and the company went beyond charity, encouraging its employees, like Roy Fralin, to teach in Citizen School programs. By 2015, Fidelity volunteers had taught more than 180 apprenticeships in such wide-ranging topics as robotics, law, and financial literacy in 34 middle schools. More than 1,500 associates had volunteered over 20,000 hours of volunteer service. Several executives served on various advisory boards. The company also donated meeting space and equipment. For example, students who had learned about web design from a Fidelity employee were invited to use the Fidelity Center for Applied Technology for their WOW! event, presenting their work in a state-of-the-art facility.

An external evaluation commissioned by Citizen Schools showed that its programs had “successfully moved a group of low-income, educationally at-risk students toward high school graduation and advancement to college, and [had] set them up for full participation in the civic and economic life of their communities.” Seventy-one percent of Citizen Schools alumni completed high school in four years, compared with 59 percent of matched peers. Sixty-one percent of students who had participated in their 8GA (8th Grade Academy) program five or more years earlier had enrolled in college, compared with 41 percent of low-income students nationally.

Fidelity indicated that in an internal survey, 89 percent of the company’s employees who had participated in the Citizen Schools partnership reported feeling more connected to their colleagues, 78 percent reported improved team-building skills, and over three-quarters reported having improved communication skills. Most importantly though, Heidi Siegal, Fidelity’s vice president for community relations, noted, “Our employees and our company enthusiastically support Citizen Schools because we know that they make a unique and significant impact on the lives of students in need.”

Sources: Corporate Voices for Working Families, “Fidelity Investments” (case study), 2012, at http://employmentpathwaysproject.org/wp-content/uploads/2014/04/Fidelity-and-Citizen-Schools-5.9.12.pdf; “Fidelity Investments,” at www.citizenschools.org/investors/current-investors/fidelity-investments; “Teaching Kids to Invest Like Millionaires,” [Roy Fralin], at www.youtube.com; “Guest Blog: At Citizen Schools, Volunteers Make STEM Relevant through Web design,” at www.educationnation.com; and private correspondence with representatives of Fidelity Investments and Citizen Schools. The website of Citizen Schools is at www.citizenschools.org. The website of Fidelity Investments is at www.fidelity.com.

Page 416

Discussion Questions

1. What evidence do you see in this case of the three kinds of corporate philanthropy discussed in this chapter: contributions of cash, in-kind products or services, and employee time?

2. What are the benefits and risks to Fidelity Investments of its partnership with Citizen Schools?

3. Do you consider Fidelity Investment’s partnership with Citizen Schools to be an example of strategic philanthropy, as defined in this chapter? Why or why not?

4. If you were a community relations manager for Fidelity Investments, how would you evaluate the impact of this partnership? What kinds of impacts would you attempt to measure, and why?

Retrieve the names of employees whose salary is within $20,000 of the

salary of the employee who is paid the most in the company (e.g., if the highest

salary in the company is $80,000, retrieve the names of all employees that make at

least $60,000)

Based on the following table:

-- drop tables

DROP TABLE EMPLOYEE CASCADE CONSTRAINTS;
DROP TABLE DEPARTMENT CASCADE CONSTRAINTS;
DROP TABLE DEPT_LOCATIONS CASCADE CONSTRAINTS;
DROP TABLE PROJECT CASCADE CONSTRAINTS;
DROP TABLE WORKS_ON CASCADE CONSTRAINTS;
DROP TABLE DEPENDENT CASCADE CONSTRAINTS;

-- create and populate tables

CREATE TABLE EMPLOYEE
(
   Fname       VARCHAR(20),
   Minit       CHAR(1),
   Lname       VARCHAR(20),
   Ssn       CHAR(9),
   Bdate       DATE,
   Address       VARCHAR(30),
   Sex       CHAR(1),
   Salary       NUMBER(5),
   Super_Ssn   CHAR(9),
   Dno       NUMBER(1),

   PRIMARY KEY (Ssn),
      
   FOREIGN KEY (Super_ssn)
       REFERENCES EMPLOYEE (Ssn)
);

INSERT INTO EMPLOYEE VALUES ('James', 'E', 'Borg', '888665555', DATE '1937-11-10', '450 Stone, Houston, TX', 'M', 55000, NULL, 1);
INSERT INTO EMPLOYEE VALUES ('Jennifer', 'S', 'Wallace', '987654321', DATE '1941-06-20', '291 Berry, Bellaire, Tx', 'F', 37000, '888665555', 4);
INSERT INTO EMPLOYEE VALUES ('Franklin', 'T', 'Wong', '333445555', DATE '1955-12-08', '638 Voss, Houston, TX', 'M', 40000, '888665555', 5);
INSERT INTO EMPLOYEE VALUES ('John', 'B', 'Smith', '123456789', DATE '1965-01-09', '731 Fondren, Houston, TX', 'M', 30000, '333445555', 5);
INSERT INTO EMPLOYEE VALUES ('Alicia', 'J', 'Zelaya', '999887777', DATE '1968-01-19', '3321 castle, Spring, TX', 'F', 25000, '987654321', 4);
INSERT INTO EMPLOYEE VALUES ('Ramesh', 'K', 'Narayan', '666884444', DATE '1920-09-15', '975 Fire Oak, Humble, TX', 'M', 38000, '333445555', 5);
INSERT INTO EMPLOYEE VALUES ('Joyce', 'A', 'English', '453453453', DATE '1972-07-31', '5631 Rice, Houston, TX', 'F', 25000, '333445555', 5);
INSERT INTO EMPLOYEE VALUES ('Ahmad', 'V', 'Jabbar', '987987987', DATE '1969-03-29', '980 Dallas, Houston, TX', 'M', 22000, '987654321', 4);
INSERT INTO EMPLOYEE VALUES ('Melissa', 'M', 'Jones', '808080808', DATE '1970-07-10', '1001 Western, Houston, TX', 'F', 27500, '333445555', 5);

CREATE TABLE DEPARTMENT
(
   Dname       VARCHAR(20),
   Dnumber       NUMBER(1),
   Mgr_ssn       CHAR(9),
   Mgr_start_date   DATE,
  
   PRIMARY KEY (Dnumber),

   FOREIGN KEY (Mgr_ssn)
       REFERENCES EMPLOYEE (Ssn)
);

INSERT INTO DEPARTMENT VALUES ('Research', 5, '333445555', DATE '1988-05-22');
INSERT INTO DEPARTMENT VALUES ('Administration', 4, '987654321', DATE '1995-01-01');
INSERT INTO DEPARTMENT VALUES ('Headquarters', 1, '888665555', DATE '1981-06-19');

-- this alter is needed to allow PROJECT and DEPARTMENT to reference each other

ALTER TABLE EMPLOYEE ADD FOREIGN KEY (Dno) REFERENCES DEPARTMENT (Dnumber);

CREATE TABLE DEPT_LOCATIONS
(
   Dnumber       NUMBER(1),
   Dlocation   VARCHAR(20),
  
   PRIMARY KEY (Dnumber, Dlocation),

   FOREIGN KEY (Dnumber)
       REFERENCES DEPARTMENT (Dnumber)
);

INSERT INTO DEPT_LOCATIONS VALUES (1, 'Houston');
INSERT INTO DEPT_LOCATIONS VALUES (4, 'Stafford');
INSERT INTO DEPT_LOCATIONS VALUES (5, 'Bellaire');
INSERT INTO DEPT_LOCATIONS VALUES (5, 'Sugarland');
INSERT INTO DEPT_LOCATIONS VALUES (5, 'Austin');

CREATE TABLE PROJECT
(
   Pname       VARCHAR(20),
   Pnumber       NUMBER(2),
   Plocation   VARCHAR(20),
   Dnum       NUMBER(1),

   PRIMARY KEY (Pnumber),
  
   FOREIGN KEY (Dnum)
       REFERENCES DEPARTMENT (Dnumber)
);

INSERT INTO PROJECT VALUES ('ProductX', 1, 'Bellaire', 5);
INSERT INTO PROJECT VALUES ('ProductY', 2, 'Sugarland', 5);
INSERT INTO PROJECT VALUES ('ProductZ', 3, 'Houston', 5);
INSERT INTO PROJECT VALUES ('Computerization', 10, 'Stafford', 4);
INSERT INTO PROJECT VALUES ('Reorganization', 20, 'Houston', 1);
INSERT INTO PROJECT VALUES ('Newbenefits', 30, 'Stafford', 4);

CREATE TABLE WORKS_ON
(
   Essn       CHAR(9),
   Pno       NUMBER(2),
   Hours       NUMBER(3,1),
  
   PRIMARY KEY (Essn, Pno),

   FOREIGN KEY (Essn)
       REFERENCES EMPLOYEE (Ssn),

   FOREIGN KEY (Pno)
       REFERENCES PROJECT(Pnumber)
);

INSERT INTO WORKS_ON VALUES ('123456789', 1, 32.0);
INSERT INTO WORKS_ON VALUES ('123456789', 2, 8.0);
INSERT INTO WORKS_ON VALUES ('453453453', 1, 20.0);
INSERT INTO WORKS_ON VALUES ('453453453', 2, 20.0);
INSERT INTO WORKS_ON VALUES ('333445555', 1, 10.0);
INSERT INTO WORKS_ON VALUES ('333445555', 2, 10.0);
INSERT INTO WORKS_ON VALUES ('333445555', 3, 5.0);
INSERT INTO WORKS_ON VALUES ('333445555', 10, 10.0);
INSERT INTO WORKS_ON VALUES ('333445555', 20, 10.0);
INSERT INTO WORKS_ON VALUES ('333445555', 30, 5.0);
INSERT INTO WORKS_ON VALUES ('999887777', 30, 30.0);
INSERT INTO WORKS_ON VALUES ('999887777', 10, 10.0);
INSERT INTO WORKS_ON VALUES ('987987987', 10, 35.0);
INSERT INTO WORKS_ON VALUES ('987987987', 30, 5.0);
INSERT INTO WORKS_ON VALUES ('987654321', 30, 20.0);
INSERT INTO WORKS_ON VALUES ('987654321', 20, 15.0);
INSERT INTO WORKS_ON VALUES ('888665555', 20, 10.0);

CREATE TABLE DEPENDENT
(
   Essn       CHAR(9),
   Dependent_name   VARCHAR(20),
   Sex       CHAR(1),
   Bdate       DATE,
   Relationship    VARCHAR(10),

   PRIMARY KEY (Essn, Dependent_name),

   FOREIGN KEY (Essn)
       REFERENCES EMPLOYEE (Ssn)
);

INSERT INTO DEPENDENT VALUES ('333445555', 'Alice', 'F', DATE '1986-04-05', 'Daughter');
INSERT INTO DEPENDENT VALUES ('333445555', 'Theodore', 'M', DATE '1983-10-25', 'Son');
INSERT INTO DEPENDENT VALUES ('333445555', 'Joy', 'F', DATE '1958-05-03', 'Spouse');
INSERT INTO DEPENDENT VALUES ('987654321', 'Abner', 'M', DATE '1988-01-04', 'Son');
INSERT INTO DEPENDENT VALUES ('987654321', 'Jennifer', 'F', DATE '1988-01-04', 'Daughter');
INSERT INTO DEPENDENT VALUES ('123456789', 'John', 'M', DATE '1988-02-28', 'Son');
INSERT INTO DEPENDENT VALUES ('123456789', 'Alice', 'F', DATE '1988-12-30', 'Daughter');
INSERT INTO DEPENDENT VALUES ('123456789', 'Elizabeth', 'F', DATE '1967-05-05', 'Spouse');
INSERT INTO DEPENDENT VALUES ('453453453', 'Joyce', 'F', DATE '1990-04-05', 'Daughter');

-- display contents of tables

SELECT * FROM EMPLOYEE;
SELECT * FROM DEPARTMENT;
SELECT * FROM DEPT_LOCATIONS;
SELECT * FROM PROJECT;
SELECT * FROM WORKS_ON;
SELECT * FROM DEPENDENT;

Logan B. Taylor is a widower whose wife, Sara, died on June 6, 2016. He lives at 4680 Dogwood Lane, Springfield, MO 65801. He is employed as a paralegal by a local law firm. During 2018, he had the following receipts:

Logan inherited securities worth $60,000 from his uncle, Daniel, who died in 2018. Logan also was the designated beneficiary of an insurance policy on Daniel's life with a maturity value of $200,000. The lot in St. Louis was purchased on May 2, 2013, for $85,000 and held as an investment. Because the neighborhood has deteriorated, Logan decided to cut his losses and sold the lot on January 5, 2018, for $80,000. The estate sale consisted largely of items belonging to Sara and Daniel (e.g., camper, boat, furniture, and fishing and hunting equipment). Logan estimates that the property sold originally cost at least twice the $9,000 he received and has declined or stayed the same in value since Sara and Daniel died.

Logan's expenditures for 2018 include the following:

Logan and his dependents are covered by his employer's health insurance policy for all of 2018. However, he is subject to a deductible, and dental care is not included. The $10,500 dental charge was for Helen's implants. Helen is Logan's widowed mother, who lives with him (see below). Logan normally pledges $2,400 ($200 per month) each year to his church. On December 5, 2018, upon the advice of his pastor, he prepaid his pledge for 2019.

Logan's household, all of whom he supports, includes the following:

Helen receives a modest Social Security benefit. Asher, a son, is a full-time student in dental school and earns $4,500 as a part-time dental assistant. Mia, a daughter, does not work and is engaged to be married.

Federal income tax of $4,500 was withheld from his wages.

Complete Form 1040 below for Logan Taylor.

I need help with 11a where it says "Tax (see inst)," 11, 13-15, and 22.

Kindly write a one page summary of the content below including important details. Thank you.

Abstract Representing the 60 trillion cells that build a human body, a sperm and an egg meet, recognize each other, and fuse to form a new generation of life. The factors involved in this important membrane fusion event, fertilization, have been sought for a long time. Recently, CD9 on the egg membrane was found to be essential for fusion [1], but sperm-related fusion factors remain unknown. Here, by using a fusion-inhibiting monoclonal antibody [2] and gene cloning, we identify a mouse sperm fusion related antigen and show that the antigen is a novel immunoglobulin superfamily protein. We have termed the gene Izumo and produced a genedisrupted mouse line. Izumo −/− mice were healthy but males were sterile. They produced normal-looking sperm that bound to and penetrated the zona pellucida but were incapable of fusing with eggs. Human sperm also contain Izumo and addition of the antibody against human Izumo left the sperm unable to fuse with zonafree hamster eggs. Identification of Izumo To identify factors involved in sperm–egg fusion, we used a monoclonal antibody, OBF13, against mouse sperm that specifically inhibits the fusion process [2]. The antigen was identified by separation of the crude extracts from mouse sperm by two-dimensional gel electrophoresis and subsequent immunoblotting with the monoclonal antibody. We named the antigen ‘Izumo’ after a Japanese shrine dedicated to marriage. The identified spot was analyzed by liquid chromatography tandem mass spectrometry (LC–MS/MS), and ten peptides that were 100% identical to a part of the sequence listed in the RIKEN full-length database were found. The registered DNA sequence was confirmed by sequencing after polymerase chain reaction with reverse transcription (RT–PCR) with total RNA prepared from the testis. A human homologue was found as an unverified gene in the NCBI database. The gene encodes a novel immunoglobulin superfamily (IgSF), type I membrane protein with an extracellular immunoglobulin-like domain that contains one putative glycosylation site (Fig. 1a). Mouse Izumo was shown to be a testis (sperm)-specific 56.4-kDa antigen by western blotting with a polyclonal antibody raised against recombinant mouse Izumo (Fig. 1b). Izumo was also detectable as a 37.2-kDa protein by western blotting of human sperm with anti-human Izumo antibody (Fig. 1c). Izumo was not detectable on the surface of fresh sperm. Coinciding with the fact that mammalian sperm are incapable of fertilizing eggs when ejaculated and that fertilization occurs only after an exocytotic process called the acrosome reaction, both mouse and human Izumo became detectable on sperm surface only after the acrosome reaction (Fig. 1d, e). This would probably be because Izumo is not localized on plasma membrane of fresh spermatozoa but is hidden under plasma membrane and accessible after the acrosome reaction, as occurs with CD46 on mouse sperm [3]. Figure 1 Identification and characterization of Izumo. a, Izumo is a typical type I membrane glycoprotein with one immunoglobulin-like domain and a putative N-glycoside link motif (Asn 204). b, Izumo was detected exclusively in testis and sperm by western blotting. The tissues examined are, from left to right: brain, heart, thymus, spleen, lung, liver, muscle, kidney, ovary, testis and sperm. The arrowhead indicates mouse Izumo protein. c, Western blotting analysis of human Izumo protein from human sperm. The arrow indicates human Izumo protein. d, Immunostaining of Izumo in sperm from an acrosin-promoter-driven transgenic mouse line that has enhanced green fluorescent protein in the acrosome. Izumo was not detected in fresh sperm with intact acrosomes expressing EGFP (indicated by green arrows), but was revealed on acrosome-reacted (non-green fluorescent) sperm (stained red, shown by white arrowheads), when stained with the polyclonal antibody against mouse Izumo. e, Human sperm were also stained with polyclonal anti-human Izumo antibody (red). Acrosome-reacted human sperm (stained green with anti-CD46 antibody) were reactive to the antibody against human Izumo but the same antibody did not react to acrosome-intact (CD46-negative) sperm. Scale bar, 10 mm. 40 ANNUAL REPORT OF OSAKA UNIVERSITY—Academic Achievement—2004-2005 Establishment of Izumo-deficient mice To address the physiological role of Izumo in vivo we generated Izumo-deficient mice by homologous recombination. An Izumo targeting construct was designed to replace exons 2–10 with a neomycin-resistant gene (neor ). Both the targeting event in D3 embryonic stem cells and the germline transmission of targeted genes were confirmed by Southern blot analysis. In the homozygous mutant mice, the full-length messenger RNA and the Izumo protein were not detected. Because the disruption of a gene can cause a concomitant increase or decrease in some related genes, we examined CD46, sp56, CD55, CD147, and ADAM2, which were reported to be involved in sperm–egg interactions. We could not find a significant change in these protein levels in sperm after the deletion of Izumo gene. The fecundity of Izumo-deficient males Izumo −/−mutant mice were healthy and showed no overt developmental abnormalities. Izumo -/- females demonstrated normal fecundity. Izumo +/− males also showed normal fertilizing ability. However, Izumo −/− males were sterile despite normal mating behaviour and ejaculation, with normal vaginal plug formations. After observation of 28 plugs, nine pairs of Izumo −/− male and wild-type females were kept for another 4 months but no pregnancies were observed. In at least four different cases of gene knockouts that resulted in male sterility attributed to impaired zonabinding ability, the sperm also failed to migrate into the oviduct. However, disruption of Izumo did not cause any defect in sperm migration into the oviduct (data not shown, and there was no reduction of sperm motility in Izumo −/− sperm motility was measured 120 min after incubation by computer-aided sperm analysis (CASA; mean; s.e.m.=81.7±7.7% in Izumo +/− sperm and 77±8.9% in Izumo −/− sperm)). The sterile nature of Izumo −/− sperm was shown in the in vitro fertilization system (Fig. 2a). The impaired fertilization step undoubtedly followed zona penetration because sperm penetrated the zona pellucida and accumulated in the perivitelline space of the eggs (Fig. 2b). Fusion ability in Izumo-deficient sperm Syngamy can be considered to occur to two stages: binding of the sperm plasma membrane to that of the egg, and actual membrane fusion. Izumo −/− sperm were capable of binding to the plasma membranes of eggs whose zona pellucida had been mechanically removed [4] (Fig. 2c). In this system, the Izumo +/− sperm incubated for 2 and 6 h fused to eggs in approximate ratios of 4.5 and 6 sperm per egg, respectively, but no Izumo −/− sperm fused with eggs (Fig. 2c). Sperm can not fuse with eggs unless the former have undergone the acrosome reaction. To verify the acrosomal status of Izumo −/− sperm, we stained the sperm accumulated in perivitelline spaces with the MN9 monoclonal antibody, which immunoreacts only to the equatorial segment of acrosomereacted sperm [5]. The staining indicated that the Izumo −/− sperm had undergone the acrosome reaction (Fig. 2b) but failed to fuse with eggs. Development of eggs after intracytoplasmic sperm injection (ICSI) with Izumo-deficient sperm Because no offspring were fathered by Izumo −/− male mice, it was unclear whether the defect was limited to fusion or extended to later developmental stages. To address this question, we used ICSI to insert Izumo −/− sperm directly into the cytoplasm of wild-type eggs and bypass the fusion step. Eggs injected with Izumo −/− sperm were successfully activated and the fertilized eggs were transplanted into the oviducts of pseudopregnant females. The eggs implanted normally and the resulting embryos developed appropriately to term with rates similar to those of heterozygous mice. Human Izumo is also involved in sperm-egg fusion Sperm–egg fusion is known to be less species-specific than sperm–zona interaction. For example, human sperm can not penetrate the hamster zona pellucida but they can fuse with zona-free hamster eggs, and this system (zona-free hamster-egg sperm penetration test) has been used for the assessment of human sperm fertility. We first examined the contribution of mouse Izumo in a zona-free hamster-egg sperm penetration assay. As indicated in Fig. 3a, the mouse Izumo was essential not only in the homologous fusion system but also for heterologous fusion with hamster eggs. Similarly, when the anti-human Izumo polyclonal antibody was added to the incubation mixture, no fusion was observed, whereas the sperm treated with control IgG fused with eggs at an average of 5.9±0.7 sperm per egg. The total numbers of eggs observed were 23 and 29, respectively (n=3). These results indicated that human Izumo is involved in the fertilization process in human sperm (Fig. 3b). Rescued fertility of Izumo-deficient male by transgene The phenotypes of gene knockout mice are not always related Figure 2 Male infertility caused by Izumo disruption. a, In vitro fertilization of sperm from Izumo +/−and Izumo −/−mice. Unlike Izumo +/−, the eggs inseminated with Izumo −/− sperm had many sperm on their zona pellucida, owing to the failure of sperm–egg fusion that probably leads to the absence of zona-reaction to lessen the sperm-binding ability of the zona pellucida. b,Upper panel, accumulation of many sperm in the perivitelline space of the eggs recovered from the females mated with Izumo −/− males. Lower panel, sperm in perivitelline space labelled with acrosome reacted, spermspecific monoclonal antibody MN9. c, Fused sperm stained by Hoechst 33342 preloaded into the egg. The arrowheads show the fused sperm. to the disrupted genes but are sometimes caused by disruption of a neighbouring gene. To examine whether the phenotype was directly derived from the lack of Izumo on sperm, we performed a rescue experiment by crossing Izumo −/− mice with transgenic mouse lines generated to express Izumo by using the testis-specific calmegin promoter [6]. The sterile phenotype was rescued with the transgenically expressed Izumo on mouse sperm (Fig. 4). Discussion In the search for sperm surface proteins that function in sperm–egg plasma-membrane binding and fusion, various candidates such as DE, CD46, equatorin, Sperad and SAMP32 have been reported. ADAM family proteins are given the most attention for their possession of a putative fusion peptide (ADAM1) and disintegrin domain (ADAM2 and ADAM3). None of the mice possessing disrupted ADAM1a, ADAM2 and ADAM3 show a significant defect in the ability to fuse with eggs [7-9], but do show an impairment of sperm–zona binding ability. Similarly, CD46 disruption does not diminish fusion [3]. In contrast, CD9 on the egg surface is essential for the fusing ability of eggs [1] and some indications for the involvement of the binding of integrins to CD9 are postulated in reference to sperm–egg fusion. However, the disruptions of the most probable candidate integrin α6β1 cause no major influence on the fusing ability of eggs. Thus, for several years, postulated fertilization mechanisms were repeatedly changed as a result of gene disruption experiments. This suggests that the essential nature of the candidate gene must be judged after observing the phenotype of the gene-disrupted mice. In this context, Izumo is the first sperm membrane protein shown to be essential for fusion. It is not yet known whether sperm Izumo interacts with egg CD9, as occurs with placental IgSF protein PSG17; neither do we know why the localization of Izumo after acrosome reaction is not limited to the 41 Osaka University 100 Papers : 10 Selected Papers ANNUAL REPORT OF OSAKA UNIVERSITY—Academic Achievement—2004-2005 Figure 4 Transgene to express mouse Izumo under the control of calmegin promoter. a, The locations of primers A to E were indicated in this figure. b, lane 1; Izumo +/− mouse with intrinsic Izumo, lane 2 and 3; Izumo −/− mouse with transgenically expressed Izumo and Izumo His-tag, respectively. c, Litter size obtained by mating male mice with C57BL/6 wild-type mice. The group numbers are equal to those shown in b. The numbers in parentheses indicate the numbers of matings. References 1. Miyado, K. et al., Requirement of CD9 on the egg plasma membrane for fertilization. Science, 287, 321-4 (2000). 2. Okabe, M. et al., Capacitation-related changes in antigen distribution on mouse sperm heads and its relation to fertilization rate in vitro. J Reprod Immunol, 11, 91-100 (1987). 3. Inoue, N. et al., Disruption of mouse CD46 causes an accelerated spontaneous acrosome reaction in sperm. Mol Cell Biol, 23, 2614-22 (2003). 4. Yamagata, K. et al., Sperm from the calmegin-deficient mouse have normal abilities for binding and fusion to the egg plasma membrane. Dev Biol, 250, 348-57 (2002). 5. Manandhar, G. & Toshimori, K., Exposure of sperm head equatorin after acrosome reaction and its fate after fertilization in mice. Biol Reprod, 65, 1425-36 (2001). 6. Ikawa, M. et al., Calmegin is required for fertilin alpha/beta heterodimerization and sperm fertility. Dev Biol, 240, 254-61 (2001). 7. Cho, C. et al., Fertilization defects in sperm from mice lacking fertilin beta. Science, 281, 1857-9 (1998). 8. Nishimura, H., Cho, C., Branciforte, D. R., Myles, D. G. & Primakoff, P., Analysis of loss of adhesive function in sperm lacking cyritestin or fertilin beta. Dev Biol, 233, 204-13 (2001). 9. Nishimura, H., Kim, E., Nakanishi, T. & Baba, T., Possible Function of the ADAM1a/ADAM2 Fertilin Complex in the Appearance of ADAM3 on the Sperm Surface. J Biol Chem, 279, 34957-62 (2004). equatorial segment where fusion initially takes place. All we can say now is that continued study of this protein’s function will undoubtedly lead to a fuller understanding of the cell–cell fusion process in fertilization and perhaps in other somatic systems such as muscle cells or trophoblasts. The finding not only provides insight into the enigmatic fusion mechanism but also promises benefits in the clinical treatment of infertility and the potential development of new contraceptive strategies

Kindly write a two page summary of the content below including important details. Thank you. kindly paraphrase as well

Abstract Representing the 60 trillion cells that build a human body, a sperm and an egg meet, recognize each other, and fuse to form a new generation of life. The factors involved in this important membrane fusion event, fertilization, have been sought for a long time. Recently, CD9 on the egg membrane was found to be essential for fusion [1], but sperm-related fusion factors remain unknown. Here, by using a fusion-inhibiting monoclonal antibody [2] and gene cloning, we identify a mouse sperm fusion related antigen and show that the antigen is a novel immunoglobulin superfamily protein. We have termed the gene Izumo and produced a genedisrupted mouse line. Izumo −/− mice were healthy but males were sterile. They produced normal-looking sperm that bound to and penetrated the zona pellucida but were incapable of fusing with eggs. Human sperm also contain Izumo and addition of the antibody against human Izumo left the sperm unable to fuse with zonafree hamster eggs. Identification of Izumo To identify factors involved in sperm–egg fusion, we used a monoclonal antibody, OBF13, against mouse sperm that specifically inhibits the fusion process [2]. The antigen was identified by separation of the crude extracts from mouse sperm by two-dimensional gel electrophoresis and subsequent immunoblotting with the monoclonal antibody. We named the antigen ‘Izumo’ after a Japanese shrine dedicated to marriage. The identified spot was analyzed by liquid chromatography tandem mass spectrometry (LC–MS/MS), and ten peptides that were 100% identical to a part of the sequence listed in the RIKEN full-length database were found. The registered DNA sequence was confirmed by sequencing after polymerase chain reaction with reverse transcription (RT–PCR) with total RNA prepared from the testis. A human homologue was found as an unverified gene in the NCBI database. The gene encodes a novel immunoglobulin superfamily (IgSF), type I membrane protein with an extracellular immunoglobulin-like domain that contains one putative glycosylation site (Fig. 1a). Mouse Izumo was shown to be a testis (sperm)-specific 56.4-kDa antigen by western blotting with a polyclonal antibody raised against recombinant mouse Izumo (Fig. 1b). Izumo was also detectable as a 37.2-kDa protein by western blotting of human sperm with anti-human Izumo antibody (Fig. 1c). Izumo was not detectable on the surface of fresh sperm. Coinciding with the fact that mammalian sperm are incapable of fertilizing eggs when ejaculated and that fertilization occurs only after an exocytotic process called the acrosome reaction, both mouse and human Izumo became detectable on sperm surface only after the acrosome reaction (Fig. 1d, e). This would probably be because Izumo is not localized on plasma membrane of fresh spermatozoa but is hidden under plasma membrane and accessible after the acrosome reaction, as occurs with CD46 on mouse sperm [3]. Figure 1 Identification and characterization of Izumo. a, Izumo is a typical type I membrane glycoprotein with one immunoglobulin-like domain and a putative N-glycoside link motif (Asn 204). b, Izumo was detected exclusively in testis and sperm by western blotting. The tissues examined are, from left to right: brain, heart, thymus, spleen, lung, liver, muscle, kidney, ovary, testis and sperm. The arrowhead indicates mouse Izumo protein. c, Western blotting analysis of human Izumo protein from human sperm. The arrow indicates human Izumo protein. d, Immunostaining of Izumo in sperm from an acrosin-promoter-driven transgenic mouse line that has enhanced green fluorescent protein in the acrosome. Izumo was not detected in fresh sperm with intact acrosomes expressing EGFP (indicated by green arrows), but was revealed on acrosome-reacted (non-green fluorescent) sperm (stained red, shown by white arrowheads), when stained with the polyclonal antibody against mouse Izumo. e, Human sperm were also stained with polyclonal anti-human Izumo antibody (red). Acrosome-reacted human sperm (stained green with anti-CD46 antibody) were reactive to the antibody against human Izumo but the same antibody did not react to acrosome-intact (CD46-negative) sperm. Scale bar, 10 mm. 40 ANNUAL REPORT OF OSAKA UNIVERSITY—Academic Achievement—2004-2005 Establishment of Izumo-deficient mice To address the physiological role of Izumo in vivo we generated Izumo-deficient mice by homologous recombination. An Izumo targeting construct was designed to replace exons 2–10 with a neomycin-resistant gene (neor ). Both the targeting event in D3 embryonic stem cells and the germline transmission of targeted genes were confirmed by Southern blot analysis. In the homozygous mutant mice, the full-length messenger RNA and the Izumo protein were not detected. Because the disruption of a gene can cause a concomitant increase or decrease in some related genes, we examined CD46, sp56, CD55, CD147, and ADAM2, which were reported to be involved in sperm–egg interactions. We could not find a significant change in these protein levels in sperm after the deletion of Izumo gene. The fecundity of Izumo-deficient males Izumo −/−mutant mice were healthy and showed no overt developmental abnormalities. Izumo -/- females demonstrated normal fecundity. Izumo +/− males also showed normal fertilizing ability. However, Izumo −/− males were sterile despite normal mating behaviour and ejaculation, with normal vaginal plug formations. After observation of 28 plugs, nine pairs of Izumo −/− male and wild-type females were kept for another 4 months but no pregnancies were observed. In at least four different cases of gene knockouts that resulted in male sterility attributed to impaired zonabinding ability, the sperm also failed to migrate into the oviduct. However, disruption of Izumo did not cause any defect in sperm migration into the oviduct (data not shown, and there was no reduction of sperm motility in Izumo −/− sperm motility was measured 120 min after incubation by computer-aided sperm analysis (CASA; mean; s.e.m.=81.7±7.7% in Izumo +/− sperm and 77±8.9% in Izumo −/− sperm)). The sterile nature of Izumo −/− sperm was shown in the in vitro fertilization system (Fig. 2a). The impaired fertilization step undoubtedly followed zona penetration because sperm penetrated the zona pellucida and accumulated in the perivitelline space of the eggs (Fig. 2b). Fusion ability in Izumo-deficient sperm Syngamy can be considered to occur to two stages: binding of the sperm plasma membrane to that of the egg, and actual membrane fusion. Izumo −/− sperm were capable of binding to the plasma membranes of eggs whose zona pellucida had been mechanically removed [4] (Fig. 2c). In this system, the Izumo +/− sperm incubated for 2 and 6 h fused to eggs in approximate ratios of 4.5 and 6 sperm per egg, respectively, but no Izumo −/− sperm fused with eggs (Fig. 2c). Sperm can not fuse with eggs unless the former have undergone the acrosome reaction. To verify the acrosomal status of Izumo −/− sperm, we stained the sperm accumulated in perivitelline spaces with the MN9 monoclonal antibody, which immunoreacts only to the equatorial segment of acrosomereacted sperm [5]. The staining indicated that the Izumo −/− sperm had undergone the acrosome reaction (Fig. 2b) but failed to fuse with eggs. Development of eggs after intracytoplasmic sperm injection (ICSI) with Izumo-deficient sperm Because no offspring were fathered by Izumo −/− male mice, it was unclear whether the defect was limited to fusion or extended to later developmental stages. To address this question, we used ICSI to insert Izumo −/− sperm directly into the cytoplasm of wild-type eggs and bypass the fusion step. Eggs injected with Izumo −/− sperm were successfully activated and the fertilized eggs were transplanted into the oviducts of pseudopregnant females. The eggs implanted normally and the resulting embryos developed appropriately to term with rates similar to those of heterozygous mice. Human Izumo is also involved in sperm-egg fusion Sperm–egg fusion is known to be less species-specific than sperm–zona interaction. For example, human sperm can not penetrate the hamster zona pellucida but they can fuse with zona-free hamster eggs, and this system (zona-free hamster-egg sperm penetration test) has been used for the assessment of human sperm fertility. We first examined the contribution of mouse Izumo in a zona-free hamster-egg sperm penetration assay. As indicated in Fig. 3a, the mouse Izumo was essential not only in the homologous fusion system but also for heterologous fusion with hamster eggs. Similarly, when the anti-human Izumo polyclonal antibody was added to the incubation mixture, no fusion was observed, whereas the sperm treated with control IgG fused with eggs at an average of 5.9±0.7 sperm per egg. The total numbers of eggs observed were 23 and 29, respectively (n=3). These results indicated that human Izumo is involved in the fertilization process in human sperm (Fig. 3b). Rescued fertility of Izumo-deficient male by transgene The phenotypes of gene knockout mice are not always related Figure 2 Male infertility caused by Izumo disruption. a, In vitro fertilization of sperm from Izumo +/−and Izumo −/−mice. Unlike Izumo +/−, the eggs inseminated with Izumo −/− sperm had many sperm on their zona pellucida, owing to the failure of sperm–egg fusion that probably leads to the absence of zona-reaction to lessen the sperm-binding ability of the zona pellucida. b,Upper panel, accumulation of many sperm in the perivitelline space of the eggs recovered from the females mated with Izumo −/− males. Lower panel, sperm in perivitelline space labelled with acrosome reacted, spermspecific monoclonal antibody MN9. c, Fused sperm stained by Hoechst 33342 preloaded into the egg. The arrowheads show the fused sperm. to the disrupted genes but are sometimes caused by disruption of a neighbouring gene. To examine whether the phenotype was directly derived from the lack of Izumo on sperm, we performed a rescue experiment by crossing Izumo −/− mice with transgenic mouse lines generated to express Izumo by using the testis-specific calmegin promoter [6]. The sterile phenotype was rescued with the transgenically expressed Izumo on mouse sperm (Fig. 4). Discussion In the search for sperm surface proteins that function in sperm–egg plasma-membrane binding and fusion, various candidates such as DE, CD46, equatorin, Sperad and SAMP32 have been reported. ADAM family proteins are given the most attention for their possession of a putative fusion peptide (ADAM1) and disintegrin domain (ADAM2 and ADAM3). None of the mice possessing disrupted ADAM1a, ADAM2 and ADAM3 show a significant defect in the ability to fuse with eggs [7-9], but do show an impairment of sperm–zona binding ability. Similarly, CD46 disruption does not diminish fusion [3]. In contrast, CD9 on the egg surface is essential for the fusing ability of eggs [1] and some indications for the involvement of the binding of integrins to CD9 are postulated in reference to sperm–egg fusion. However, the disruptions of the most probable candidate integrin α6β1 cause no major influence on the fusing ability of eggs. Thus, for several years, postulated fertilization mechanisms were repeatedly changed as a result of gene disruption experiments. This suggests that the essential nature of the candidate gene must be judged after observing the phenotype of the gene-disrupted mice. In this context, Izumo is the first sperm membrane protein shown to be essential for fusion. It is not yet known whether sperm Izumo interacts with egg CD9, as occurs with placental IgSF protein PSG17; neither do we know why the localization of Izumo after acrosome reaction is not limited to the 41 Osaka University 100 Papers : 10 Selected Papers ANNUAL REPORT OF OSAKA UNIVERSITY—Academic Achievement—2004-2005 Figure 4 Transgene to express mouse Izumo under the control of calmegin promoter. a, The locations of primers A to E were indicated in this figure. b, lane 1; Izumo +/− mouse with intrinsic Izumo, lane 2 and 3; Izumo −/− mouse with transgenically expressed Izumo and Izumo His-tag, respectively. c, Litter size obtained by mating male mice with C57BL/6 wild-type mice. The group numbers are equal to those shown in b. The numbers in parentheses indicate the numbers of matings. References 1. Miyado, K. et al., Requirement of CD9 on the egg plasma membrane for fertilization. Science, 287, 321-4 (2000). 2. Okabe, M. et al., Capacitation-related changes in antigen distribution on mouse sperm heads and its relation to fertilization rate in vitro. J Reprod Immunol, 11, 91-100 (1987). 3. Inoue, N. et al., Disruption of mouse CD46 causes an accelerated spontaneous acrosome reaction in sperm. Mol Cell Biol, 23, 2614-22 (2003). 4. Yamagata, K. et al., Sperm from the calmegin-deficient mouse have normal abilities for binding and fusion to the egg plasma membrane. Dev Biol, 250, 348-57 (2002). 5. Manandhar, G. & Toshimori, K., Exposure of sperm head equatorin after acrosome reaction and its fate after fertilization in mice. Biol Reprod, 65, 1425-36 (2001). 6. Ikawa, M. et al., Calmegin is required for fertilin alpha/beta heterodimerization and sperm fertility. Dev Biol, 240, 254-61 (2001). 7. Cho, C. et al., Fertilization defects in sperm from mice lacking fertilin beta. Science, 281, 1857-9 (1998). 8. Nishimura, H., Cho, C., Branciforte, D. R., Myles, D. G. & Primakoff, P., Analysis of loss of adhesive function in sperm lacking cyritestin or fertilin beta. Dev Biol, 233, 204-13 (2001). 9. Nishimura, H., Kim, E., Nakanishi, T. & Baba, T., Possible Function of the ADAM1a/ADAM2 Fertilin Complex in the Appearance of ADAM3 on the Sperm Surface. J Biol Chem, 279, 34957-62 (2004). equatorial segment where fusion initially takes place. All we can say now is that continued study of this protein’s function will undoubtedly lead to a fuller understanding of the cell–cell fusion process in fertilization and perhaps in other somatic systems such as muscle cells or trophoblasts. The finding not only provides insight into the enigmatic fusion mechanism but also promises benefits in the clinical treatment of infertility and the potential development of new contraceptive strategies

Performance Lawn Equipment (PLE)

PLE, headquartered in St. Louis, Missouri, is a privately-owned designer and producer of traditional lawn mowers used by homeowners. Annual sales are approximately $180 million. Both end users and institutions (organizations) are important customers for PLE. This case is ONLY about organizations (such as retail outlets) that buy from PLE. There are two type of organizations that are PLE customers: (1) dealerships or retail stores that in-turn sell to end-customers, and (2) organizations that buy products to use in their operations (such as golf courses or professional lawn care businesses). A purchasing manager in such organizations makes the decisions about which brand of lawn mowers to buy and how many to buy.

Elizabeth Burke has recently joined the PLE management team to oversee production operations. She has asked you to analyze results of a survey of purchasing managers in PLE’s institutional customers.

The worksheet Purchasing Survey in the Performance Lawn Care database provides data obtained from a survey of purchasing managers of institutional customers. Respondents rated PLE on the following seven attributes:

Delivery speed-the amount of time it takes to deliver the product once an order is confirmed

Price level-the perceived level of price charged by PLE

Price flexibility-the perceived willingness of PLE representatives to negotiate price on all types of purchases

Manufacturing image-the overall image of the manufacturer

Overall service-the overall level of Service necessary for maintaining a satisfactory relationship between PLE and the purchaser

Sales force image—the overall image of the PLE’s Sales force

Product quality-perceived level of quality

Responses to these Seven Variables were obtained using a graphic rating Scale, where a 10-centimeter line was drawn between endpoints labeled "poor and 'excellent." Respondents indicated their perceptions using a mark on the line, which was measured from the left endpoint. The result was a scale from 0 to 10 rounded to One decimal place.

Two measures were obtained that reflected the outcomes of the respondent's purchase relationships with PLE:

Usage level-how much of the firm's total product is purchased from PLE, measured on a 100-point Scale, ranging from 0% to 100%

Satisfaction level-how satisfied the purchaser is with past purchases from PLE, measured on the same graphic rating scale as perceptions 1 through 7

The data also include four characteristics of the responding firms:

Size of firm-size relative to others in this market (O = Small; 1 = large)

Purchasing structure-the purchasing method used in a particular company (1 = centralized procurement, 0 = decentralized procurement)

Industry-the industry classification of the purchaser l = retail (stores that resell to end consumers such as Home Depot), 0 = private (nonresale, Such as a profession lawn care business)

Buying type-a Variable that has three categories (1 = new purchase, 2 = modified rebuy, 3 = Straight rebuy)

Elizabeth Burke would like to understand what she learned from this data.

Cluster Analysis:

Apply cluster analysis to analyze the data to create a segmentation of institutional customers. For example, can PLE segment customers into groups with similar perceptions about the company? Do not use “Usage level” or “Satisfaction level” in making the clusters. Check to see if the clusters differ on usage level and satisfaction or not. Which clusters have high usage and satisfaction and which ones do not? Suggest actions management can take to increase usage and satisfaction for the different clusters.

Regression Analysis:

Can regression models provide insight about the drivers of satisfaction and usage level? What are the most important variables that need to be influenced to increase satisfaction and usage level? Suggest ways management can do so.

Summarize your results in a report to Ms. Burke.

Consolidation subsequent to date of acquisition—Equity method with noncontrolling interest, AAP, and upstream intercompany inventory sale

Assume that, on January 1, 2010, a parent company acquired a 75% interest in its subsidiary. The total fair value of the controlling and noncontrolling interests was $550,000 over the book value of the subsidiary’s Stockholders’ Equity on the acquisition date. The parent assigned the excess to the following [A] assets:

75% of the Goodwill is allocated to the parent. Assume that the subsidiary sells inventory to the parent (upstream) which includes that inventory in products that it ultimately sells to customers outside of the controlled group. You have compiled the following data as of 2015 and 2016:

The inventory not remaining at the end of the year has been sold outside of the controlled group. The parent uses the equity method of pre-consolidation investment bookkeeping. The parent and the subsidiary report the following pre-consolidation financial statements at December 31, 2016:

a. Disaggregate and document the activity for the 100% Acquisition Accounting Premium (AAP), the controlling interest AAP and the noncontrolling interest AAP. (Complete for the first four years only.)

b. Calculate and organize the profits and losses on intercompany transactions and balances.

c. Compute the pre-consolidation Equity Investment account beginning and ending balances starting with the stockholders’ equity of the subsidiary.

d.  Reconstruct the activity in the parent’s pre-consolidation Equity Investment T-account for the year of consolidation.

e. Independently compute the owners’ equity attributable to the noncontrolling interest beginning and ending balances starting with the owners’ equity of the subsidiary.

f. Independently calculate consolidated net income, controlling interest net income and noncontrolling interest net income.

g. Complete the consolidating entries according to the C-E-A-D-I sequence.

Jon is a psychiatric mental health nurse in a large metropolitan clinic, which is connected to a research hospital. Jon likes the fact that it’s a walk-in clinic. One day he is just getting ready to eat his sack lunch, when a slender young woman who looks exhausted and timid knocks at his open door. “Excuse me,” she says. “Can I get into a research project?” Jon puts down his bologna sandwich. “What’s that?” he says. He’s confused. “Research?” “Yes,” she says, stepping inside and slipping into the chair beside his desk. Jon wraps up his sandwich for later. “I want to know if I can be part of a study for depression,” the woman says. Her mouth trembles. “This is a research hospital, right?” Jon hesitates, trying to take in what she wants. As he pauses, he does a visual assessment. The woman is in her late 20s or early 30s, attractive, but somewhat bedraggled. She looks as if she’s been on a long, difficult road trip. “Well,” he says. “I don’t know of any studies going on off hand, but does that matter? I’m sure we can get you the help you need without a study. What seems to be the problem? And what’s your name, by the way? Mine’s Jon.” “I’m Erika,” she says when her face crumples and she begins to cry. “I’ve screwed up big time!” she says. “I’ve just ruined my life and my son’s life!” And just like that, she is sobbing. “I’m sure you haven’t ruined anything,” Jon says. He glances at the clock behind Erika, wondering what time the psychiatrist will be back from her luncheon meeting. “Why don’t you tell me what’s happened?” “I ran away,” she says, still sobbing. “I ran away, walked off my job, and hit the road with my little boy Oscar!” She lowers her hands from her face. “We just now got back into town. We’ve been sleeping in the car for 3 days.” “Are you homeless? Do you need a shelter?” “No,” she cries. “That’s just it! We had a perfectly decent life, and now I’ve blown it.” “There’s usually something that can be done,” Jon says, handing her a box of tissues. “Why don’t you start at the beginning, and let’s see what we can do.” “Thank you,” she says, blowing her nose and really looking Jon in the eye for the first time. Jon smiles. “You’re welcome. Now. Just start anywhere.” Erika tells Jon that she is a 28-year-old mother who was a “wild teen,” saying that she had a tumultuous relationship with her parents. At age 20, Erika gave birth to her son Oscar, who is now 8. “Oscar,” she says “is the sweetest, most supportive son ever.” Shortly after Oscar’s birth Erika suffered from severe postpartum depression that plunged her into what she calls “a hellish paranoia. I was some kind of hormonal, psychotic witch for a while. No wonder my fiancé broke it off with me.” She says this with a sad smile and starts to cry again. Erika has come into the clinic because, she says, “sometimes I think I never recovered from my postpartum depression. I mean, I’ve always been hyper and bad-tempered, which I freely admit. But now I just can’t seem to pull out of it. I can’t sleep; I’m angry all the time; I can’t concentrate on anything, and I’m so depressed I can’t function.” But things are even worse than Erika is letting on. “Okay,” she says. “There’s something else. Something even worse.” She has trouble pulling her tears under control, and it takes her a moment to struggle with that. “I flipped out at work last week,” she says. “I slapped my supervisor because she was very unfair. She had it in for me. Then I stormed out of work, grabbed my son out of school, and got in the car and just drove, furious and feeling hopeless. We drove and drove and then it was like I woke up and realized I was in another state. I drove all the way to Wyoming, two states away to Oscar’s dad’s house, and all he said was, ‘You walked out on a good job? Well, you can’t stay here and freeload! Get back to Denver and get your job back!’” “We slept in the car, and I was crying and yelling, and Oscar was crying. It was awful. I’m the worst mother ever. So now I’m back in Denver, with no job and overdue on my rent and no money left in the bank to pay it.” “No money?” She shakes her head. “I blew it all on the trip. I was so mad about work, I told Oscar, ‘We’re going on a road trip.’ I thought maybe we’d go to Yellowstone, or maybe Disneyland. And at first he thought it was fun till he saw I was a mess, and then he was just scared. And now we’re back, and I’m broke and unemployed. I never sleep, and I know I talk too much and too fast, but my head is always full of more thoughts and ideas than I can keep track of, and they rush through me like the Indianapolis 500, and sometimes they just come bursting out of my mouth.” 1. Jon is able to complete an intake assessment of Erika, and when the doctor comes back from her meeting and sees the state Erika is in, she meets with her immediately. She gets Erika help with her most immediate needs, and when Erika refuses hospitalization, concerned about uprooting Oscar any further, the doctor makes a diagnosis and writes her a small, temporary prescription—but only after Erika agrees to come back and start treatment. Erika readily agrees. The doctor subsequently diagnoses Erika with bipolar I disorder. Assuming that the doctor is right, what evidence do you see of this disorder? 2. In addition to her diagnosis of bipolar I disorder, which signs of mania does Erika displays the most.

Jon is able to complete an intake assessment of Erika, and when the doctor comes back from her meeting and sees the state Erika is in, she meets with her immediately. She gets Erika help with her most immediate needs, and when Erika refuses hospitalization, concerned about uprooting Oscar any further, the doctor makes a diagnosis and writes her a small, temporary prescription—but only after Erika agrees to come back and start treatment. Erika readily agrees. The doctor subsequently diagnoses Erika with bipolar I disorder. Assuming that the doctor is right, what evidence do you see of this disorder?

In addition to her diagnosis of bipolar I disorder, which signs of mania does Erika displays the most?

Case study:

Married with two young children, John and his wife rented a two-bedroom apartment in a safe neighborhood with good schools. John liked his job as a delivery driver for a large foodservice distributor, where he had worked for more than four years. His goal was to become a supervisor in the next year. John’s wife was a stay-at-home mom.

John had always been healthy. Although he had health insurance through his job, he rarely needed to use it. He smoked half a pack of cigarettes each day and drank socially a couple of times a month.

One afternoon, John’s company notified him that it was laying him off along with more than a hundred other employees. Though he was devastated about losing his job, John was grateful that he and his wife had some savings that they could use for rent and other bills, in addition to the unemployment checks he would receive for a few months.

John searched aggressively for jobs in the newspaper and online, but nothing worked out. He began to have feelings of anger and worry that led to panic. His self-esteem fell, and he became depressed. When John’s wife was hired to work part-time at the grocery store, the couple felt better about finances. But demoralized by the loss of his job, John started to drink more often.

Two beers a night steadily increased to a six-pack. John and his wife started to argue more often. Then, about six months after losing his job, John stopped receiving unemployment checks. That week, he went on a drinking binge that ended in an argument with his wife. In the heat of the fight, he shoved her. The next day, John’s wife took the children and moved in with her parents. No longer able to pay the rent, John was evicted from the apartment.

John tried to reconcile with his wife, but she said she’d had enough. Over the next few months, John “couch-surfed” with various family members and friends. At one point, he developed a cold, and when it worsened over a few weeks, he sought care at the emergency department. The hospital staff told him that he would be billed because he didn’t have insurance. John agreed, and a doctor diagnosed him with a sinus infection and prescribed antibiotics. With no money to spare, John could not get the prescription filled.

John continued to live with family and friends, but his heavy drinking and anger only got worse, and his hosts always asked him to leave. He went from place to place. Finally, when John ran out of people to call, he found himself without a place to stay for the night and started sleeping at the park.

One night when John was drunk, he fell and got a cut on his shin. The injury became red and filled with pus. John was embarrassed about his poor hygiene and didn’t want a health care provider to see him. But when he developed a fever and pain, he decided to walk to the nearest emergency department. He saw a provider who diagnosed him with cellulitis, a common but potentially serious bacterial skin infection, and gave him a copy of the patient instructions that read “discharge to home” and a prescription for antibiotics. John could not afford the entire prescription when he went to pick up the antibiotics, but he was able to purchase half the tablets.

Winter arrived, and it was too cold for John to sleep outside, so he began staying at a shelter run by the church. Each morning, he had to leave the shelter by 6 AM. He walked the streets all day and panhandled for money to buy alcohol.

One evening, some teenage boys jumped John in the park, stealing his backpack and kicking him repeatedly. An onlooker called 911, and John was taken to the emergency department. Later that evening, the hospital discharged John. He returned many times to the emergency department for his health care, seeking treatment for frequent colds, skin infections, and injuries. Providers never screen him for homelessness and always discharge him back to “home.”

One day at the park, an outreach team from the local Health Care for the Homeless (HCH), one of about 250 such non-profit organizations in the United States, approached John. The team, including a doctor, nurse, and caseworker, introduced themselves and asked John, “Are you OK?” John didn’t engage. They offered him a sandwich and a warm blanket. John took the food without making eye contact. The team visited John for the next several days. John started making eye contact and telling the team about his shortness of breath and the cut on his arm. The team began seeing John frequently, and he began to trust them.

A couple of weeks later, John agreed to go to the HCH clinic. It was the first time in years that John went to a health clinic. Upon his arrival, the staff at the clinic registered him and signed him up for health insurance through Medicaid and food benefits. John felt comfortable in the clinic, and he saw some of the people who also stayed at the shelter and spent their days in the park. They were happy to see him and told John about how the clinic staff care and would be able to help.

John began going to the HCH clinic on a regular basis. He saw a primary care provider, Maggie, a nurse practitioner. In John’s words, she treated him like a real person. In addition to primary care, the clinic offered behavioral health services. Both scheduled appointments and walk-in care were available. John connected with a therapist and began working on his depression and substance abuse. A year later, John’s health has improved. He rarely needs to go to the emergency room. He is sober and working with a case manager in finding housing.

Discussion Questions:

1. What events in John’s life created a “downward spiral” into homelessness? Which events related to social needs, and which could health care have addressed?
2. What were some of the barriers John faced in accessing health care?
3. Why do you think the emergency department was the first place John thought to go for care? How might the emergency department improve care for patients like John?
4. Why do you think John wouldn’t make eye contact with the HCH team at first? How would you build a trusting relationship with a person like John?
5. What aspects of HCH care do you think represent high-quality care for the homeless? How do you think Maggie made John feel like he was a “real person?”
6. In your own experience, have you encountered a homeless individual? What was that like? Do you recall what you were thinking?

​​Remember some of these questions are Two questions in One. Ensure you answer all completely (detailed) but does not need to be a novel.