IOWA CITY:DIABETES RESEARCH CENTRE funded by FRATERNAL ORDER of EAGLES

Celebrating the Grand Opening of The Fraternal Order of Eagles Diabetes Research Center Saturday, August 23

Join us Saturday, August 23, as we celebrate the Grand Opening of the Fraternal Order of Eagles Diabetes Research Center with a special ceremony at the Coralville Marriott Hotel & Conference Center, located just minutes from the campus of the University of Iowa.

After six years of hard work, we're proud to gather in Iowa City to officially open the doors of the DRC and celebrate the hard work of all who made this achievement possible. The Coralville Marriott will be the site of the official opening ceremony featuring dignitaries from the F.O.E. and the University of Iowa as well as a special evening party with live music, food and refreshments.

San Diego:MAPP BIOPHARM. MB-003

Ebola antibody treatment, produced in plants, protects monkeys from lethal disease A new Ebola virus study resulting from a widespread scientific collaboration has shown promising preliminary results, preventing disease in infected nonhuman primates using monoclonal antibodies. In this week's online edition of the Proceedings of the National Academy of Sciences (PNAS), the research team describes a proof-of-concept for using a "cocktail" of monoclonal antibodies, or mAbs, to prevent lethal disease in rhesus macaques. When administered one hour after infection, all animals survived. Two-thirds of the animals were protected even when the treatment, known as MB-003, was administered 48 hours after infection. Ebola virus, which causes hemorrhagic fever with human case fatality rates as high as 90 percent, has been responsible for numerous deaths in central Africa over the past several months. In addition to being a global health concern, the virus also is considered a potential biological threat agent. Currently there are no available vaccines or treatments approved for use in humans. The work is the culmination of more than a decade of effort between government and industry partners. According to lead investigator Gene Olinger, Ph.D., a virologist at the U.S. Army Medical Research Institute of Infectious Diseases (USAMRIID), this consortium of investigators has taken very distinct technologies and combined them to develop a cutting-edge medical countermeasure against a lethal viral disease. "It is rare that an antiviral compound prevents Ebola virus infection with limited to no morbidity in treated animals at any point of treatment following infection by this lethal virus," said Olinger. "Until recently, attempts to utilize antibodies to provide protection against Ebola virus have been met with failure. The level of protection against disease that we saw with MB-003 was impressive." In addition, the production method used in this study offers the potential to make an economical and effective medical countermeasure, according to the authors. Initially developed as a monoclonal antibody cocktail in the mouse model, MB-003 was successfully humanized and then produced in the tobacco plant-based production system. "We were pleased to see how well the humanized mAbs of MB-003 performed," said Larry Zeitlin, Ph.D., president of Mapp Biopharmaceutical and senior author on the study. "We also were pleasantly surprised by the superiority of the plant-derived mAbs compared to the same mAbs produced in traditional mammalian cell culture." Further improvement in antibody efficacy was developed at Kentucky BioProcessing (KBP). Using a fully automated production system that operates in accordance with good manufacturing practices (GMP), antibody is produced in a tobacco plant system. This new development process significantly decreases the amount of time required for production, increases the quantity of antibody produced, and slashes the cost of manufacturing, according to Barry Bratcher, chief operating officer of KBP and co-author on the PNAS study. "Our GMP facility can generate a new antibody lot in two weeks to rapidly address new threats and new outbreaks," said Bratcher. Olinger said efforts are underway to advance MB-003 to clinical safety testing as his team at USAMRIID continues to determine the true therapeutic capability of the cocktail.

Harvard ProMED: Pharyngeal GONORRHOEA resistant to monotherapy.

GONOCOCCAL DISEASE - SWEDEN: PHARYNX, TREATMENT FAILURE, 2013-2014
******************************************************************
A ProMED-mail post

ProMED-mail is a program of the
International Society for Infectious Diseases


Date: Thu 31 Jul 2014
Source: Eurosurveillance Edition 2014, 19(30) [edited]



Four treatment failures of pharyngeal gonorrhoea with ceftriaxone (500
mg) or cefotaxime (500 mg), Sweden, 2013 and 2014
----------------------------------------------------------------------
[Authors: Golparian D, Ohlsson AK, Janson H, Lidbrink P, Richtner T,
Ekelund O, Fredlund H, Unemo M]

Abstract
--------
We describe 4 cases in Sweden of verified treatment failures of
pharyngeal gonorrhoea with ceftriaxone (500 mg; n=3) or cefotaxime
(500 mg; n=1) monotherapy [2013-2014]. All the ceftriaxone treatment
failures were caused by the internationally spreading
multidrug-resistant gonococcal NG-MAST genogroup 1407 clone. Increased
awareness of treatment failures is crucial particularly when
antimicrobial monotherapy is used. Frequent test of cure and
appropriate verification/falsification of suspected treatment
failures, as well as implementation of recommended dual antimicrobial
therapy are imperative.

_Neisseria gonorrhoeae_ has developed resistance to all antimicrobials
previously used as 1st-line treatment for gonorrhoea [1-4]. Clinical
resistance is now emerging to the extended-spectrum cephalosporins
(ESCs), that is, cefixime (oral) and the more potent ceftriaxone
(injectable). Many treatment failures with cefixime have been verified
in Japan, Europe, Canada, and South Africa. No failure to treat
urogenital gonorrhoea with ceftriaxone (250 mg-1 g), the last
remaining option for 1st-line empiric antimicrobial monotherapy, has
been detected as yet. However, some few failures to treat pharyngeal
gonorrhoea with ceftriaxone have been verified in Japan (n=1),
Australia (n=3), Sweden (n=1) and Slovenia (n=1) [4-10]. In recent
years, extensively drug-resistant (XDR) gonococcal strains with
high-level ceftriaxone resistance were also reported from Japan,
France and Spain [2,9-11].

Case descriptions
-----------------
>From February to May 2013, 3 cases of suspected failure to treat
pharyngeal gonorrhoea with ceftriaxone 500 mg intramuscularly were
reported from 2 clinics for sexually transmitted infections (STIs) in
Sweden (Table). All 3 patients reported having had unprotected oral
and vaginal sex with heterosexual contacts in Stockholm. Case A was a
woman in her 30s, with pharyngeal symptoms including pharyngitis.
Cases B and C, both in their 50s, were asymptomatic. Pharyngeal and
urogenital samples were taken and all patients had a positive
gonococcal pharyngeal culture. Furthermore, the urogenital samples
from the Cases B and C were positive in a nucleic acid amplification
test (NAAT) (BD ProbeTec GC Qx Amplified DNA Assay, Becton Dickinson).
All 3 patients were administered a single dose of 500 mg ceftriaxone
intramuscularly (Day 1). When returning for follow-up after 7 to 22
days, all patients were asymptomatic but had persistent positive
gonococcal pharyngeal cultures. All urogenital samples were negative.
Finally, all 3 patients were successfully treated with a single dose
of 1 g ceftriaxone intramuscularly between Day 7 and 27, which was
confirmed at follow-up visits with negative pharyngeal cultures
between Day 22 and 48 (Table).

In May 2014, 1 case of suspected failure to treat pharyngeal
gonorrhoea with cefotaxime 500 mg intramuscularly was reported from an
STI clinic in Karlskrona, Sweden. This patient (Case D), a man in his
30s, attended the clinic because he had had unprotected oral and
vaginal sex with a woman diagnosed with gonorrhoea. On Day 1, the
patient was asymptomatic and sampled from the pharynx, urethra, and
rectum. The pharyngeal sample was positive for gonococci in culture
and he was treated with a single dose of 500 mg cefotaxime
intramuscularly. At the follow-up visit (Day 7), the patient was still
asymptomatic, however, a pharyngeal sample remained positive in
culture. The patient was treated with a single dose of 250 mg
ceftriaxone intramuscularly plus a single oral dose of 1 g
azithromycin (day 14). On Day 26, the patient returned for test of
cure and the pharyngeal culture was negative for gonococci (Table).

Characterisation of _N. gonorrhoeae_ isolates
---------------------------------------------
The pre- and post-treatment gonococcal isolates were species-confirmed
by sugar utilisation test, Phadebact Monoclonal GC Test (Pharmacia
Diagnostics), and MaldiTOF MS (Bruker Daltonics). The paired isolates
from each case were indistinguishable using _N. gonorrhoeae_
multi-antigen sequence typing (NG-MAST [12]) and the isolates from
Cases A, B, and C belonged to the NG-MAST genogroup 1407 clone [4,13]
(Table). Using Etest (AB bioMerieux), the isolates from Cases A, B,
and C (ceftriaxone treatment failures) showed elevated minimum
inhibitory concentrations (MICs), that is, 0.064-0.125 mg/L, which is
equal to the European resistance breakpoint (greater than 0.125 mg/L)
[14]. In Case D (cefotaxime treatment failure), according to the
European resistance breakpoints [14], the paired isolates were
resistant to cefotaxime (MIC: 0.5 mg/L) and the pre-treatment isolate
also to ceftriaxone (MIC: 0.25 mg/L) (Table).

Sequencing of ESC resistance determinants [1,3,4,6,9,10,15] showed
that all the paired isolates belonging to Cases A, B and C contained
the penA mosaic allele XXXIV, which has been correlated with NG-MAST
genogroup 1407, decreased susceptibility or resistance to ESCs and ESC
treatment failures [1,4-6,9,11]. The isolates from Case D contained
the penA mosaic allele XIII [10]. In addition, all isolates contained
mtrR and penB alterations that further increase the ESC MICs
[1,3-6,9-11,15].

Discussion
----------
This paper reports 4 cases of verified pharyngeal gonorrhoea treatment
failure in Sweden using injectable ESCs, that is, ceftriaxone (n=3)
and cefotaxime (n=1). The failures were verified in accordance with
international recommendations [2,4], that is, clinical records were
obtained, reinfection was excluded, pre- and post-treatment isolates
were identical using highly discriminatory molecular epidemiological
typing, and the isolates had elevated ESC MICs and well recognised ESC
resistance determinants. Reinfection was considered to be excluded as
much as possible for all cases. Accordingly, all patients were
strongly advised to abstain from any sexual contacts before their
follow-up visit and all 4 patients repeatedly assured that they had
not had any unprotected sexual contacts between the
ceftriaxone/cefotaxime treatment and test of cure. Furthermore, Case D
was infected by a casual sexual contact.

In the current emergent situation of fear that gonorrhoea may become
untreatable [1-3,10], recommendations of using dual antimicrobial
therapy (mainly ceftriaxone plus azithromycin) have been introduced in
the United States [16] and Europe [17]. No appropriate well-designed
international study has yet assessed the implementation of dual
antimicrobial therapy. However, as observed by the authors in many
international projects the implementation of these guidelines appears
suboptimal in several European countries and monotherapy with
ceftriaxone remains frequently used.

No failure to treat urogenital gonorrhoea with ceftriaxone (250 mg-1
g) monotherapy has been verified to date. However, the observed
initial accumulation of failures treating pharyngeal gonorrhoea was
not unexpected, because these infections are substantially harder to
eradicate with most antimicrobials than urogenital gonorrhoea
[1-4,6,18]. As shown in the present study, ceftriaxone 500 mg
monotherapy can be sufficient to eradicate urogenital gonorrhoea but
not the concomitant pharyngeal gonorrhoea in the same patient. The
pharyngeal gonorrhoea of the patients was instead successfully treated
with 1 g ceftriaxone monotherapy or 250 mg ceftriaxone plus 1 g
azithromycin. Unfortunately, 1 g ceftriaxone monotherapy may only
provide a short-term solution [1,2,4,19,20] judging from the failure
to treat the pharyngeal gonorrhoea caused by the 1st gonococcal XDR
strain with 1 g ceftriaxone [10], ceftriaxone MICs of all the
identified gonococcal XDR strains [9-11], emergence of ceftriaxone
resistance and its anticipated trend, and
pharmacodynamic/pharmacokinetic simulations showing that the benefits
of increasing the ceftriaxone dose from 500 mg to 1 g are limited when
taking into account the high ceftriaxone MICs detected recent years
[19]. Consequently, dual antimicrobial therapy, such as 500 mg
ceftriaxone intramuscularly plus 2 g azithromycin orally, as
recommended by the European gonorrhoea guideline [17], should ideally
be implemented. It remains unknown if ceftriaxone and azithromycin act
synergistically in vivo. However, most importantly, there are no
indications, in vitro or in vivo, that they act antagonistically.
According to a review from 2010, 99 percent of urogenital and 98
percent of pharyngeal gonorrhoea cases may be treatable with 2 g
azithromycin monotherapy [21]. Consequently, nearly all gonorrhoea
cases (ceftriaxone-resistant or not) are treatable with even 2 g
azithromycin monotherapy. Nevertheless, azithromycin monotherapy is
not recommended due to the spread of gonococcal strains with
high-level resistance to azithromycin and the anticipated rapid
selection of azithromycin resistance [1,17,20].

All ceftriaxone treatment failures in the present study (Cases A, B,
and C) were caused by the internationally spreading
multidrug-resistant gonococcal NG-MAST genogroup 1407 clone, which has
caused many ESC treatment failures internationally [4-6,9,15].
However, the cefotaxime treatment failure was caused by the unrelated
NG-MAST ST4539, which shows that clinical resistance to injectable
ESCs is emerging also in other gonococcal clones.

In conclusion, increased awareness of treatment failures particularly
with antimicrobial monotherapy, improved implementation of recommended
dual antimicrobial therapy (such as 500 mg ceftriaxone plus 2 g
azithromycin [17]), frequent test of cure (ideally for all cases, and
at least for all cases of pharyngeal gonorrhoea), and appropriate
verification/falsification of suspected treatment failures (including
subsequent tracing of sexual contacts of the index case with the
treatment failure) are essential internationally. An enhanced focus on
pharyngeal gonorrhoea is also crucial, with increased sampling and
prevention, such as promotion of condom use also when practising oral
sex. Ultimately, novel options for effective treatment of gonorrhoea
are imperative.

[Table and references can be accessed at the source URL
.]

--
Communicated by:
ProMED-mail


[In 2012 US CDC updated its recommendations for treatment of
uncomplicated urogenital, anorectal, and pharyngeal gonorrhea to
combination therapy with a single intramuscular dose of ceftriaxone
250 mg plus either a single dose of azithromycin 1 g orally or
doxycycline 100 mg orally twice daily for 7 days
(). The CDC
considers that the 250 mg dose of ceftriaxone is sufficient to treat
gonococcal infection at all anatomic sites caused by strains currently
circulating in the United States
().

The updated European gonorrhea guideline, however, recommends a 500 mg
intramuscular dose of ceftriaxone plus azithromycin 2 g oral dose for
uncomplicated gonorrhea
().

Pharyngeal gonococcal infections are known to be substantially harder
to eradicate with most antimicrobials than urogenital gonorrhea (Moran
JS: Treating uncomplicated _Neisseria gonorrhoeae_ infections: is the
anatomic site of infection important? Sex Transm Dis. 1995; 22(1):
39-47;
.)
The Eurosurveillance report above describes 4 cases in Sweden of
verified treatment failures of pharyngeal gonorrhea with ceftriaxone
(500 mg; n=3) or cefotaxime (500 mg; n=1) monotherapy.

Although sufficient to eradicate urogenital gonorrhea in 2 of the 4
patients, ceftriaxone 500 mg monotherapy failed to eradicate gonococci
in concomitant pharyngeal gonorrhea in the same patients. The
ceftriaxone MICs (0.064-0.125 mg/L) of the gonococcal isolates from
the 3 ceftriaxone pharyngeal gonorrhea treatment failures were
actually below both the Clinical Laboratory Standards Institute (CLSI)
resistance breakpoint MIC (equal to or greater than 0.5 micrograms per
mL) and the European resistance breakpoint MIC (equal to or greater
than 0.25 micrograms per mL)
( and
).

The cefotaxime MICs (0. 5 micrograms per mL) of the 2 isolates from
the one cefotaxime pharyngeal gonorrhea treatment failure were above
the European resistance breakpoint MIC (equal to or greater than 0.25
micrograms per mL). Thus it seems that gonococci persisted in the
pharynx despite having MICs in several instances in the susceptible
range, perhaps because in the doses used, the pharyngeal antibiotic
concentrations were too low or less active than at other infected
sites. Pharyngeal gonorrhea in the 4 patients was subsequently
successfully treated with 1 g ceftriaxone monotherapy or 250 mg
ceftriaxone plus 1 g azithromycin.

Most gonococcal infections of the pharynx are asymptomatic and can be
relatively common in some populations
().
Culture of the pharynx in patients presenting with gonococcal disease,
even in the absence of pharyngeal symptoms, and, as the authors of the
Eurosurveillance report emphasize, supplemented by use of recommended
combined antimicrobial therapy with azithromycin, which might enhance
treatment efficacy for pharyngeal infection, and test of cure for
pharyngeal gonorrhea
(),
are essential to control the continued spread of this disease. -
Mod.ML

USA,Georgia: EMORY UNIV. HOSP: EBOLA VIRUS COMMENTS

What You Need to Know About the Ebola Virus and Emory University Hospital

August 2, 2014, 6:21 pm By Emory Healthcare There has been much discussion about bringing patients with Ebola back into our country. Emory University Hospital physicians, nurses and staff can treat them safely and effectively, and we are honored to have the privilege of caring for these patients who contracted Ebola while serving on a humanitarian mission. These two Americans want to come back home and be treated here, and we are committed to helping them. It is our moral obligation to always use our expertise, training, knowledge and gifts to provide such extraordinary care for others.
Emory University Hospital is one of the very few hospitals in the country equipped to provide their care. Our highly trained staff and physicians are ready to receive both patients and provide them outstanding care of the highest quality. The patients will be housed in a physically separate and highly specialized unit that was intentionally designed and constructed to receive patients such as these.
We have prepared the following FAQs to provide more information on the topic of Ebola and Emory’s care for these patients.

About Ebola

• What is Ebola?
• What are the symptoms of Ebola?
• How is it spread?
• How do you treat Ebola?
• If I come into contact with staff who are treating the infected patients, can I get Ebola?
• Can I be a carrier for Ebola?
• How serious is Ebola?

About Emory University Hospital

• Is it safe to come to Emory University Hospital?
• What precautions is the hospital taking to avoid contamination?
• What is the special unit being used to house the infected patients?
• What kind of training does the staff at Emory University Hospital undergo to provide care for the infected patients?
• Will there be other patients on this special unit?
• What kind of access will be put in place on the isolation unit? Will there be security? What about visitors?
• Why are we bringing the infected patients to Emory University Hospital? Why can’t the patients be treated in Africa or somewhere else?
• When did Emory University Hospital learn of the possibility of receiving these infected patients?
• If the Ebola virus is transmitted in the same way HIV and Hepatitis B or C are transmitted, why are there so many precautions (hazmat suits, protective gear, isolation unit) being put into place?

UK DAILY MAIL: PUBLIC HEALTH ENGLAND on EBOLA EPIDEMIC

Dr Paul Cosford, PHE's Medical Director, said: 'This message is to update you on the current outbreak of Ebola virus disease in West Africa, and to remind you of the need to remain vigilant for cases imported to the UK.'

+14

On Monday Public Health England (PHE) issued an alert to GPs, A&E departments, Critical Care Units as well as all NHS trusts across the UK, warning doctors and medical staff to be vigilant to the disease

Read more: http://www.dailymail.co.uk/health/article-2709330/NHS-chiefs-issue-Ebola-alert-GPs-A-amp-E-departments-expert-warns-hospitals-ill-equipped-cope-sudden-outbreak-deadly-disease.html#ixzz38sKTeisH
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MD ANDERSON: Prof V.Craig JORDAN OBE PhD,DSc(Leeds) Hon.MD(Leeds)

For Immediate Release - July 21, 2014

The “Father of Tamoxifen” to Join MD Anderson

Breast Cancer Research Pioneer V. Craig Jordan, Ph.D., Developer Of Several Cancer-Fighting Drugs, Brings His Translational Research Expertise To Houston

Contact: Ron Gilmore Office: 713-745-1898 Cell: rlgilmore1@mdanderson.org Contact: Jim Newman Office: 713-792-0664 Cell: jnewman@mdanderson.org

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HOUSTON ― The University of Texas MD Anderson Cancer Center is pleased to announce that one of the world’s preeminent experts in breast cancer research and treatment, V. Craig Jordan, Ph.D., will join the institution’s efforts to end cancer. Jordan is considered the “Father of Tamoxifen,” the groundbreaking therapeutic drug that has saved countless lives.

V. Craig Jordan, Ph.D.

As a professor in Breast Medical Oncology and Molecular and Cellular Oncology Jordan will focus on the new biology of estrogen-induced cell death with the goal of developing translational approaches for treating and preventing cancer. He will begin work at MD Anderson in October.
“This is an exciting moment and I’m delighted that Dr. Jordan will be contributing to significant translational research activities in breast cancer here at MD Anderson,” said Ron DePinho, M.D., president of MD Anderson. “His international reputation as a trailblazer in translational research and his many achievements and honors are well deserved. As we progress in our mission of ending cancer in Texas, the nation and the world, it is outstanding scientists like Dr. Jordan who will play key roles in delivering on that promise.”
Jordan’s long and distinguished career has included leadership positions at some of the world’s most prestigious biomedical institutions. Currently, he’s scientific director of the Lombardi Comprehensive Cancer Center at Georgetown University in Washington D.C., and the Vincent T. Lombardi Chair of Translational Cancer Research. He also serves as vice chairman of the Department of Oncology and professor of oncology and pharmacology at Georgetown University’s Medical School. In addition, he’s a visiting professor of molecular medicine at the University of Leeds in England, and an adjunct professor of molecular pharmacology and biological chemistry at Northwestern University in Chicago.
“Dr. Jordan’s election as a member of the National Academy of Sciences in 2009 is just one of the many honors he’s received as a result of his incredible contributions to our understanding of cancer biology,” said Ethan Dmitrovsky, M.D., MD Anderson provost and executive vice president. “MD Anderson is known for bringing the best minds together for the shared purpose of ending cancer. Certainly, a scientist of Dr. Jordan’s caliber adds significantly to our overall research programs. His arrival is due in no small part to the efforts of Debu Tripathy, M.D. and Vicente Valero, M.D."
Dr. Tripathy is MD Anderson’s new Chair of Breast Medical Oncology. He will begin his work at the institution in September.

In addition to his National Academy membership, Jordan’s list of achievements, awards and accomplishments is long, featuring more than four-dozen international awards. The list includes:

• The St. Gallen Prize for Breast Cancer (2011)
• The David A. Karnofsky Award from the American Society of Clinical Oncology (2008)
• The George and Christine Sosnovsky Award in Cancer Therapy (2004)
• The Charles F. Kettering Prize (2003)
• The American Cancer Society Medal of Honor (2002)
• The Dorothy P. Landon Award in Translational Research from the American Association for Cancer Research (2002)
• The Bristol Myers Squibb Award (2001)
• The Cameron Prize from the University of Edinburgh (1993)

Jordan has received six honorary fellowships or degrees from universities around the world including an honorary fellowship from the Royal Society of Medicine. In 2010, he was elected president of the Royal Society of Medicine Foundation of North America. Jordan was elected as a Fellow of the Academy of Medical Sciences, the United Kingdom’s equivalent to the Institute of Medicine.
 He has contributed to more than 700 publications, 99 percent of which pertain to cancer research. He has edited 11 books and has more than 26,000 scientific citations. He’s author of the book “Tamoxifen, Pioneering Medicine in Breast Cancer.”
Jordan, who was born in New Braunfels, Texas and raised in England, has dual British and U.S. citizenship. In 2002, he received the Order of the British Empire from Queen Elizabeth II for services to international breast cancer research. He earned a Ph.D. and D.Sc. from the University of Leeds and in 2001 received an honorary M.D. from his alma mater.
“I am proud to join MD Anderson Cancer Center,” said Jordan. “It is indeed an honor to continue my work at this world renowned cancer center where I look forward to working with my distinguished colleagues.”
Jordan is credited with reinventing a failed contraceptive (known as ICI 46,474) as a breast cancer treatment. The drug, in existence since the 1960s, was originally created to block estrogen in the hopes of preventing pregnancy. Jordan developed the strategy of long-term adjuvant tamoxifen therapy, as well as describing and deciphering the properties of a new group of medicines called selective estrogen receptor modulators (SERMs). He was the first to discover the preventive abilities of both tamoxifen and the drug raloxifene. The medicines were approved by the Food and Drug Administration for reducing breast cancer incidence in high-risk women.
Prior to joining Georgetown University, Jordan served on the faculties at Northwestern University Medical School; the University of Wisconsin School of Medicine, Madison, Wis.; the Ludwig Institute for Cancer Research at the University of Berne, Switzerland; and the University of Leeds, England.

Univ. Amsterdam Prof.Joseph LANGE MD (Ams.1981) PhD(Ams.87) Died: 59y.

Chose to fly on Malaysian Airlines: from Amsterdam to Melbourne for 20th Int. AIDS Conf.

Prof LANGE supported Pre-exposure prophylaxsis (PREP) against HIV. using a combination drug such as TRUVADA (tenofovir + emtricitabine) made by California GILEAD SCIENCES (NASDAQ) Net income 2013 $3-billion.Cost:TRUVADA USD$1,000/month. Reduces HIV incidence by 51%.