***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: Abstract Aims /hypothesis . To re-evaluate the use of Granulocyte-Colony Stimulating Factor ( G-CSF ) in the treatment of infected diabetic foot ulcers . Methods . Thirty-seven diabetic subjects were r and omised to Granulocyte-Colony Stimulating Factor ( G-CSF ) ( n=20 ) or placebo ( n=17 ) . The primary endpoint was resolution of cellulitis , which was evaluated clinical ly and with an infection summary score . Patients were hospitalised for 10 days and received subcutaneously either 5 µg/kg G-CSF or placebo daily . Ulcers were treated with a st and ard wound protocol and the patients were instructed to stay in bed . All subjects received antibiotics ( clindamycin and ciprofloxacin ) intravenously until the inflammation had subsided . Results . Patients who received G-CSF did not have an earlier resolution of clinical ly defined cellulitis ( p=0.57 ) . The infection summary score declined , but comparably , in both groups ( G-CSF : 29.5±18.4 to 6.7±6.3 p<0.001 , placebo : 24.2±16.9 to 8.9±7.2 p<0.001 ) . The ulcer volume , which was not greater among placebo patients , was reduced by 59 % in G-CSF and by 35 % in placebo patients . Conclusion /interpretation . We conclude that antibiotic and non weight-bearing therapy ( bed rest ) accelerated the resolution of cellulitis in infected foot ulcers . Additional treatment with G-CSF had no further beneficial effect EXECUTIVE SUMMARY : 1 . Foot infections in patients with diabetes cause substantial morbidity and frequent visits to health care professionals and may lead to amputation of a lower extremity . 2 . Diabetic foot infections require attention to local ( foot ) and systemic ( metabolic ) issues and coordinated management , preferably by a multidisciplinary foot-care team ( A-II ) . The team managing these infections should include , or have ready access to , an infectious diseases specialist or a medical microbiologist ( B-II ) . 3 . The major predisposing factor to these infections is foot ulceration , which is usually related to peripheral neuropathy . Peripheral vascular disease and various immunological disturbances play a secondary role . 4 . Aerobic Gram-positive cocci ( especially Staphylococcus aureus ) are the predominant pathogens in diabetic foot infections . Patients who have chronic wounds or who have recently received antibiotic therapy may also be infected with Gram-negative rods , and those with foot ischemia or gangrene may have obligate anaerobic pathogens . 5 . Wound infections must be diagnosed clinical ly on the basis of local ( and occasionally systemic ) signs and symptoms of inflammation . Laboratory ( including microbiological ) investigations are of limited use for diagnosing infection , except in cases of osteomyelitis ( B-II ) . 6 . Send appropriately obtained specimens for culture before starting empirical antibiotic therapy in all cases of infection , except perhaps those that are mild and previously untreated ( B-III ) . Tissue specimens obtained by biopsy , ulcer curettage , or aspiration are preferable to wound swab specimens ( A-I ) . 7 . Imaging studies may help diagnose or better define deep , soft-tissue purulent collection s and are usually needed to detect pathological findings in bone . Plain radiography may be adequate in many cases , but MRI ( in preference to isotope scanning ) is more sensitive and specific , especially for detection of soft-tissue lesions ( A-I ) . 8 . Infections should be categorized by their severity on the basis of readily assessable clinical and laboratory features ( B-II ) . Most important among these are the specific tissues involved , the adequacy of arterial perfusion , and the presence of systemic toxicity or metabolic instability . Categorization helps determine the degree of risk to the patient and the limb and , thus , the urgency and venue of management . 9 . Available evidence does not support treating clinical ly uninfected ulcers with antibiotic therapy ( D-III ) . Antibiotic therapy is necessary for virtually all infected wounds , but it is often insufficient without appropriate wound care . 10 . Select an empirical antibiotic regimen on the basis of the severity of the infection and the likely etiologic agent(s ) ( B-II ) . Therapy aim ed solely at aerobic Gram-positive cocci may be sufficient for mild-to-moderate infections in patients who have not recently received antibiotic therapy ( A-II ) . Broad-spectrum empirical therapy is not routinely required but is indicated for severe infections , pending culture results and antibiotic susceptibility data ( B-III ) . Take into consideration any recent antibiotic therapy and local antibiotic susceptibility data , especially the prevalence of methicillin-resistant S. aureus ( MRSA ) or other resistant organisms . Definitive therapy should be based on both the culture results and susceptibility data and the clinical response to the empirical regimen ( C-III ) . 11 . There is only limited evidence with which to make informed choices among the various topical , oral , and parenteral antibiotic agents . Virtually all severe and some moderate infections require parenteral therapy , at least initially ( C-III ) . Highly bioavailable oral antibiotics can be used in most mild and in many moderate infections , including some cases of osteomyelitis ( A-II ) . Topical therapy may be used for some mild superficial infections ( B-I ) . 12 . Continue antibiotic therapy until there is evidence that the infection has resolved but not necessarily until a wound has healed . Suggestions for the duration of antibiotic therapy are as follows : for mild infections , 12 weeks usually suffices , but some require an additional 12 weeks ; for moderate and severe infections , usually 24 weeks is sufficient , depending on the structures involved , the adequacy of debridement , the type of soft-tissue wound cover , and wound vascularity ( A-II ) ; and for osteomyelitis , generally at least 46 weeks is required , but a shorter duration is sufficient if the entire infected bone is removed , and probably a longer duration is needed if infected bone remains ( B-II ) . 13 . If an infection in a clinical ly stable patient fails to respond to 1 antibiotic courses , consider discontinuing all antimicrobials and , after a few days , obtaining optimal culture specimens ( C-III ) . 14 . Seek surgical consultation and , when needed , intervention for infections accompanied by a deep abscess , extensive bone or joint involvement , crepitus , substantial necrosis or gangrene , or necrotizing fasciitis ( A-II ) . Evaluating the limb 's arterial supply and revascularizing when indicated are particularly important . Surgeons with experience and interest in the field should be recruited by the foot-care team , if possible . 15 . Providing optimal wound care , in addition to appropriate antibiotic treatment of the infection , is crucial for healing ( A-I ) . This includes proper wound cleansing , debridement of any callus and necrotic tissue , and , especially , off-loading of pressure . There is insufficient evidence to recommend use of a specific wound dressing or any type of wound healing agents or products for infected foot wounds . 16 . Patients with infected wounds require early and careful follow-up observation to ensure that the selected medical and surgical treatment regimens have been appropriate and effective ( B-III ) . 17 . Studies have not adequately defined the role of most adjunctive therapies for diabetic foot infections , but systematic review s suggest that granulocyte colony-stimulating factors and systemic hyperbaric oxygen therapy may help prevent amputations ( B-I ) . These treatments may be useful for severe infections or for those that have not adequately responded to therapy , despite correcting for all amenable local and systemic adverse factors . 18 . Spread of infection to bone ( osteitis or osteomyelitis ) may be difficult to distinguish from noninfectious osteoarthropathy . Clinical examination and imaging tests may suffice , but bone biopsy is valuable for establishing the diagnosis of osteomyelitis , for defining the pathogenic organism(s ) , and for determining the antibiotic susceptibilities of such organisms ( B-II ) . 19 . Although this field has matured , further research is much needed . The committee especially recommends that adequately powered prospect i ve studies be undertaken to eluci date and vali date systems for classifying infection , diagnosing osteomyelitis , defining optimal antibiotic regimens in various situations , and clarifying the role of surgery in treating osteomyelitis ( A-III ) Abstract Objective : To calculate costs for the management of deep foot infections and to identify the most important factors related to treatment costs . Design : Costs for  in-hospital care , surgery , investigations , antibacterials  , visits to the foot-care team , orthopaedic appliances and topical treatment were calculated retrospectively from diagnosis until healing or death . Multiple regression analysis was used to identify factors that independently affect costs . Setting : A multidisciplinary foot-care team . Patients : 220 prospect ively followed patients with diabetes mellitus and deep foot infections who were referred to the team from 1986 to 1995 . Main Outcome Measures and Results : Total cost for healing without amputation was Swedish kronor (SEK)136 600 per patient , while the corresponding cost for healing with minor amputation was SEK260 000 and with major amputation was SEK234 500 . All costs were quoted in SEK at 1997 price levels ( £ 1 sterling and $ US1 equalled approximately SEK12.50 and SEK7.64 , respectively ) . The cost of antibacterials  was 4%of total costs . The cost of topical treatment was 51 % of total costs and related to wound healing time . Number of weeks between diagnosis of deep foot infection and healing , and number of surgical procedures were variables that explained 95 % of costs in the multiple regression analysis . It was not possible to find any parameters present at diagnosis that could contribute to an explanation of total treatment costs . Conclusions : Topical treatment accounted for the largest proportion of total costs and the most important cost driving factors were wound healing duration and repeated surgery . Costs of antibacterials  should not be used as an argument in the choice between early amputation and conservative treatment BACKGROUND The purpose of this study was to determine whether treatment with granulocyte colony-stimulating factor ( G-CSF ) , which mobilizes endothelial progenitor cells from bone marrow , can safely improve the clinical outcomes of patients with atherosclerotic peripheral artery disease ( PAD ) . METHODS AND RESULTS Thirty-nine patients with intractable PAD were r and omly assigned to 3 groups : a negative control group ( n=12 ) treated with conventional drug therapy ; a positive control group ( n=13 ) treated with conventional drug therapy plus bone marrow transplantation ( BMT ) ; and a G-CSF group ( n=14 ) treated with conventional therapy plus subcutaneous injection of 2 - 5 microg/kg of recombinant human G-CSF once daily for 10 days . One month after treatment , subjective symptoms improved significantly in the G-CSF and BMT groups . Ankle-brachial pressure index and transcutaneous oxygen pressure increased significantly in the BMT and G-CSF groups , but no such improvements were seen in the group receiving conventional therapy alone . CONCLUSIONS G-CSF improves the clinical signs and symptoms of patients with intractable PAD to the same degree as BMT does . This noninvasive treatment may thus represent a useful new approach to managing the disease AIMS Foot infections and the subsequent amputation of a lower extremity are the most common cause of hospitalization among patients with diabetes mellitus . Although there are several reasons for susceptibility to infection in diabetic patients , white blood cell dysfunction is considered to be an important cause for this tendency . Granulocyte-colony stimulating factor ( G-CSF ) increases the release of neutrophils from the bone marrow and improves neutrophil functions . Based on this knowledge , the aim of the present study was to investigate the effects of addition of G-CSF to the treatment of foot infections in diabetic patients . METHODS Thirty diabetic patients with foot infection were included in the study . Fifteen of the patients received st and ard treatment consisting of local wound care and antibiotics ( st and ard group ) , and the other 15 patients received G-CSF besides st and ard treatment ( G-CSF group ) . The objectives of this study were to determine the time to resolution of infection , time to hospital discharge , need for surgical intervention , and the effects of G-CSF on phagocytosis and respiratory burst of neutrophils . RESULTS Treatment with G-CSF led to significantly higher neutrophil counts on the 5th and 10th days , and at the end of treatment in the G-CSF treated group compared to the st and ard group . Respiratory burst of neutrophils increased significantly in both the G-CSF group ( from 1.6 + /- 0.3 to 2.3 + /- 0.5 , p = 0.001 ) and the st and ard group ( from 2.0 + /- 0.4 to 2.3 + /- 0.4 , p = 0.02 ) with treatment . But , while phagocytosis of neutrophils increased significantly in the G-CSF group ( from 70.4 + /- 2.0 to 7 
    Output:
    
The available evidence is limited , but suggests that adjunctive G-CSF treatment in people with a diabetic foot infection , including infected ulcers , does not appear to increase the likelihood of resolution of infection or healing of the foot ulcer .
However , it does appear to reduce the need for surgical interventions , especially amputations , and the duration of hospitalisation .
Clinicians might consider adding G-CSF to the usual treatment of diabetic foot infections , especially in patients with a limb-threatening infection , but it is not clear which patients might benefit