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We teach franchisees and their employees traditional and guerilla marketing tactics to drive customer interest and acquisition, and we provide digital marketing to drive customers to franchisees, as well as a national call center to book jobs. This support ensures top-shelf customer service for callers and online inquiries, and allows franchisees to stay focused on building their team and providing “WOW” customer service.

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To take a deep dive into our business model and learn more about the financial performance of College Hunks franchisees, fill out the form to download your free franchise report . You’ll learn:

download your free franchise report Financial considerations

To start a College Hunks Hauling Junk franchise, you should have $50,000 in liquid capital and a net worth of $200,000 or more. Total startup costs, which include six months of working capital, range from $89,300 to $208,200.

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Liquid Capital Required: $50,000

Net Worth Required: $200,000

Total Investment: $89,300 to $208,200

Business Category: Residential/Commercial Services

Business Type: Franchise

Financing Assistance: Available via third party

Carl Carter Jackson, Mississippi

“By becoming an owner of this franchise I can provide a service that my competitors aren’t capable of or willing to do. Plus, just the name itself is a conversation piece.”

Steven Roper Raleigh, North Carolina

“When you have an environment where people enjoy working, you build a great culture that gives a team a focus. Throughout my career I developed a lot of assistants who became store managers, and the chance to keep helping people get to a higher level was very appealing. My title is the ‘Director of WOW and Amaze,’ and if I WOW and amaze my Hunks, they WOW and amaze my clients.”

Gary Bussard St. Louis, Missouri

“One of the things that sets us apart is our labor force. It’s professional. young, enthusiastic and trained. We are employing future leaders at College Hunks. It really sets us apart from our competitors.”

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Legal Disclaimer: "The franchising information contained in this website is not intended as an offer to sell a franchise or the solicitation of an offer to buy a franchise. The following states and provinces regulate the offer and sale of franchises and/or business opportunities: Alabama, California, Connecticut, Florida, Georgia, Hawaii, Illinois, Indiana, Iowa, Kentucky, Louisiana, Maine, Maryland, Michigan, Minnesota, Nebraska, New Hampshire, New York, North Carolina, North Dakota, Ohio, Oklahoma, Oregon, Rhode Island, South Carolina, South Dakota, Texas, Utah, Virginia, Washington and Wisconsin in the United States, and the provinces of Alberta and Ontario in Canada. If you are a resident of one of these states or provinces, we will not offer or sell you a franchise unless and until we have complied with the applicable presale registration and disclosure requirements in your state or province."

Trusted evidence.
Informed decisions.
Better health.
The Cochrane Library


Corresponding author Search for more papers by this author

Manal Kassab, Department of Maternal and Child Health / Faculty of Nursing, Jordan University of Science and Technology (JUST), PO Box 3030, Irbid, 22110, Jordan. .

Search for more papers by this author
Search for more papers by this author


Transient tachypnoea of the newborn (TTN) results from delayed clearance of lung liquid and is a common cause of admission of full-term infants to neonatal intensive care units. The condition is particularly common after elective caesarean section. Conventional treatment involves appropriate oxygen administration and continuous positive airway pressure in some cases. Most infants receive antibiotic therapy. Hastening the clearance of lung liquid may shorten the duration of the symptoms and reduce complications.

To determine whether diuretic administration reduces the duration of oxygen therapy and respiratory symptoms and shortens hospital stay in term infants presenting with transient tachypnoea of the newborn.

An updated search was carried out in September 2015 of the following databases: the Cochrane Central Register of Controlled Trials (CENTRAL) (), MEDLINE via Ovid, EMBASE, PubMed, and CINAHL via OVID.

We included randomised and quasi-randomised controlled trials that compared the effect of diuretics administration versus placebo or no treatment in infants of less than seven days of age, born at 37 or more weeks of gestation with the clinical picture of transient tachypnoea of the newborn.

We extracted and analysed data according to the methods outlined in the latest . Two review authors assessed trial quality in each potentially eligible manuscript and two review authors extracted data.

Our previous systematic review included two trials enrolling a total of 100 infants with transient tachypnoea of the newborn (Wiswell 1985; Karabayir 2006). The updated search revealed no new trials. Wiswell 1985 randomised 50 infants to receive either oral furosemide (2 mg/kg body weight at time of diagnosis followed by a 1 mg/kg dose 12 hours later if the tachypnoea persisted) or placebo. Karabayir 2006 randomised 50 infants to receive either intravenous furosemide (2 mg/kg body weight) or an equal volume of normal saline placebo. Neither trial reported on the need for respiratory support. Neither trial demonstrated a statistically significant impact of furosemide on transient tachypnoea of the newborn regarding duration of symptoms or length of hospitalisation.

Fig. 2.

PI3K/AKT regulation of mESC and hESC pluripotency. PI3K/AKT can be activated by insulin and IGF1 in both mESCs and hESCs, which maintains pluripotency through inhibition of MEK/ERK signalling. In mESCs, PI3K/AKT may also be activated by the LIF/JAK pathway to inhibit GSK3 signalling in addition to inhibition of MEK/ERK. Inhibition of GSK3 attenuates the β-catenin-mediated TCF3 repression of pluripotent genes, thus promoting pluripotency. In hESCs, PI3K is activated by an endogenous peptide ELABELA (ELA) in addition to insulin/IGF1. This may have a positive effect on GSK3 through the inhibition of MEK/ERK, thereby inhibiting nuclear translocation of β-catenin and enhancing pluripotency (see text for details). Green arrows represent activation, red arrows represent inhibition. Dashed arrows represent non-canonical induction by other pathways. IR, insulin receptor.

The mechanisms by which PI3K regulates pluripotency remain somewhat elusive. In mESCs, increasing evidence suggests that PI3K promotes the retention of ESC properties mainly through the inhibition of two downstream pathways: the mitogen-activated protein kinases/extracellular signal-regulated kinase (MAPK/ERK) pathway and the GSK3 signalling pathway. This is consistent with the finding that PI3K signalling is dispensable in naive mESC 2i culture conditions in which both MAPK/ERK and GSK3 pathways are suppressed ( Hishida et al., 2015 ). Active MAPK/ERK signalling is a key requirement for mESCs to undergo differentiation ( Ying et al., 2008 ); thus, inhibition of MAPK/ERK signalling by LIF-induced PI3K may contribute to the maintenance of pluripotency even though the exact mechanisms by which PI3K inhibits MAPK/ERK are unclear ( Paling et al., 2004 ). With respect to the inhibition of GSK3 signalling, several reports have shown that PI3K signalling inhibits GSK3α/β activity by phosphorylating the S21/S9 residue via AKT activation in mESCs, which leads to the upregulation of pluripotent transcription factors TBX3 and NANOG that subsequently promote pluripotency in these cells ( Paling et al., 2004 ; Niwa et al., 2009 ; Womens Delores Dress Coast BDbRvd
). However, the exact underlying mechanisms remain ambiguous, particularly regarding the involvement of β-catenin. Wellham and colleagues have shown that inactivation of GSK3 by inhibition of PI3K has no clear effect on β-catenin phosphorylation, indicating that the effect of PI3K signalling on TBX3 and NANOG in mESCs could be through β-catenin-independent mechanisms ( Paling et al., 2004 ). However, a more recent study using chemically defined culture media combined with genetic approaches has revealed that enhancement of NANOG expression by GSK3 inhibition results from the alleviation of TCF3 repression, which is largely mediated through β-catenin, although independent of its transcriptional activity and even though β-catenin is not essential for the maintenance of pluripotency ( Wray et al., 2011 ).

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