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August 12, 2011 at 6:24 am

I was contacted about 10 months ago. I was so excited to be able to help I started crying on the phone. However, I never received another call, I don’t know what happened, but I hope that person found an even better match!

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August 12, 2011 at 8:09 am

I recently joined the registery during an on-campus event. I had thought about doing so for a while, and I was glad to see Be The Match on campus. I’m in college for the second time, re-training for a new career, and I’m near 40 – not the typical college age person. I do believe it would be an honor to be a match for someone, but I am also the kind of person who worries about details, like knowing how the whole process works in advance. I expect each experience is different, but I want to thank those of you who have donated and have shared a bit about your donation experience. I’m glad to read that it went well, and that you would do it again if need be.

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August 12, 2011 at 8:39 am

God Bless you all!

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We were contact stating my wife was a match last year, when we contacted city of hope, it wasn’t a pleasant experience and very rude attitude was so angry at City of Hope they should realize it’s about the patients and not there employees have the weekend off they don’t offer weekend appointments for donors WHAT!!!, we couldn’t get there during weekday hours(they only have) no evening or weekends appointments for donors such a shame, My wife owns her own daycare very difficult to close during the week no back up and we don’t get paid but she wanted to help! So we made arrangements to close for a day or two because she wanted to help save a life,,, sent an e-mail for appointment never heard back 2 weeks later was told Dr and patient are trying other treatment and will be notified if the marrow was needed.. which is awesome!!!

We know firsthand about cancer/leukemia it sucks my father passed last year. So this is very close to us… Just was disappointed on how we were treated by City of Hope.. SAD if you ask me,,,

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After joining the Be the Match Registery (Feb. 2008), I was contacted about 18 months later about being a possible match for someone from another Country…After going through some blood work it was determined that I was a match for this lady, but she was not in need of the transplant at this time…1 week later I was notified by phone call that her Doctor had determined that she was ready and had choosen me to be her best chance for a successful transplant…about 10 days before my donation date I was notified that her leukemia had returned and my donation would be postponed and that if she was able to get into remisson, I would be contacted for a new donation date…Thankfully 6 weeks later I would go on to donate PBSC…Because she is from another Country, I have had no contact and do not know what the outcome of my gift was…I hope and pray that she is alive and well and that maybe someday I will meet her…and Hope and Pray that someone is out there who would be willing same for me or my family if there is ever a need…I would donate again in a heartbeat no questions asked…From the time I was first contacted until the actual PBSC Donation is was about 7 months…Stay Committed…it is without a doubt the most rewarding feeling that you can get.

The rate of resistance to methicillin that we identified among S. aureus infections was higher than that identified in northern Europe [ 34 ] but comparable to rates of resistance reported in other series from the United States [ 15 , 35 ]. The rate of resistance to vancomycin in E. faecium infections was comparable to those in recent studies from the United States [ 15 , 35 ] but higher than those observed in recent European studies [ 34 , 36 ].

In our series, the prevalence of resistance to vancomycin among E. faecium isolates was significantly higher among those recovered from neutropenic patients. Several recent studies found neutropenia to be independently associated with vancomycin-resistant enterococcal (VRE) infection when comparing patients with vancomycin-resistant and patients with vancomycin-susceptible enterococcal BSIs [ 37 , 38 ]. In contrast, Lucas and co-authors [ 39 ], in comparing vancomycin-susceptible and vancomycin-resistant enterococcal BSIs , did not find neutropenia to be a risk factor for BSIs due to VRE.

Increasing resistance to penicillin, other β-lactam antibiotics, and macrolides has been documented in viridans group streptococci isolated from neutropenic patients with cancer [ 40 , 41 ]. In our study, 34% and 42% of viridans group streptococci displayed decreased susceptibility to penicillin and macrolides, respectively. These rates are in accordance with recent data from Germany [ 40 ] but are lower than rates in southern Europe [ 41 ].

CoNS and Candida species were more likely to be isolated from patients in ICUs, thus influencing empirical antibiotic therapy, whereas S. aureus and E. coli were more commonly isolated from patients in non-ICU wards. Viridans group streptococci were more frequently seen in patients with neutropenia, whereas S. aureus was more commonly seen in nonneutropenic patients. In addition, we found enterococci, Candida species, and Serratia species more frequently in patients without neutropenia.

The finding of a higher proportion of resistance to tobramycin, compared with gentamicin, for several of the gram-negative organisms should not be taken to imply that gentamicin has better activity against these organisms. Rather, this finding is due to the variation in the antibiotics tested at the local laboratories. Thus, the true aminoglycoside susceptibility lies somewhere between the 2 values.

In conclusion, our data demonstrate one-half of all nosocomial BSIs occur in the critical-care setting, although a minority of patients receive care there. The high rates of antibiotic resistance, as well as local patterns of species distribution and drug susceptibilities in certain patient populations, should guide empirical therapy of nosocomial BSIs.

We thank the infection-control practitioners and microbiology laboratory personnel at the participating hospitals for their active participation in this project, and Donna McClish, for assistance with data management.

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Figure 2.

Cumulative incidence of (micro)albuminuria per category of homocysteine level. *Estimated by age-adjusted, sex-adjusted, and glucose tolerance–adjusted logistic regression analyses.

Compared with subjects who participated in the follow-up examination, subjects who died during the follow-up period were older, more insulin resistant, more obese, and more often smokers, and they more often had NIDDM, hypertension, cardiovascular disease, higher levels of homocysteine and triglycerides, and a lower protein intake at baseline (data not shown). The nonresponders (Figure 1 ) were not materially different from those who did participate in the following examination with regard to the variables shown in Table 1 , except that nonresponders were older (65 versus 63 years) and had higher levels of homocysteine (13.1 versus 11.8 μmol/L).

View this table:
Table 1.

Baseline Characteristics According to Albuminuria Status at Follow-Up

Compared with subjects who did not develop (micro)albuminuria, subjects who developed (micro)albuminuria were significantly older, more insulin resistant, and more obese; they had higher blood pressures and higher fasting insulin and homocysteine levels; and they more often had hypertension, cardiovascular disease, and retinopathy at baseline (Table 1 ). Age-adjusted, sex-adjusted, and glucose tolerance–adjusted logistic regression analyses showed the development of (micro)albuminuria to be significantly associated with age, male sex, fasting insulin levels, insulin resistance, systolic and diastolic blood pressure, the presence of hypertension, body mass index, homocysteine levels, and the presence of cardiovascular disease (Table 2 ). Analyses performed in nondiabetic and diabetic subjects separately gave similar results, except for the association between the development of (micro)albuminuria on the one hand and glycated hemoglobin and homocysteine levels on the other, which could be estimated only among nondiabetic subjects (Table 2 ), the latter because there was only 1 diabetic subject with homocysteine levels >19.0 μmol/L.

View this table:
Table 2.

Age-Adjusted, Sex-Adjusted, and Glucose Tolerance–Adjusted ORs for Developing (Micro)albuminuria of Potential Determinants

To further investigate the association between development of (micro)albuminuria and potential determinants, multiple regression analyses were performed with all variables significantly associated with the development of (micro)albuminuria (Table 2 ), as well as the stratification variables, as independent variables. These adjustments did not materially affect the results, except for the association between the development of (micro)albuminuria and fasting insulin levels, which was no longer statistically significant (Table 3 ). Further adjustment for creatinine clearance did not materially change the association between homocysteine level and the development of (micro)albuminuria (eg, among all subjects, the ORs were 1.4 [95% CI 0.5 to 3.8], 1.7 [95% CI 0.5 to 5.5], and 7.6 [95% CI 1.5 to 39.3] for homocysteine levels of 9.1 to 14.0, 14.1 to 19.0, and >19.0 μmol/L compared with homocysteine levels <9.1 μmol/L, respectively). Substituting GFR estimated from the MDRD formula for creatinine clearance again did not materially change the association between homocysteine level and the development of (micro)albuminuria (eg, among all subjects, the ORs were 1.4 [95% CI 0.5 to 3.9], 1.7 [95% CI 0.5 to 5.5], and 8.4 [95% CI 1.6 to 44.8] for homocysteine levels of 9.1 to 14.0, 14.1 to 19.0, and >19.0 μmol/L compared with homocysteine levels of <9.1 μmol/L, respectively). Additional adjustment for retinopathy and current smoking also did not materially change the results (data not shown). Substituting insulin resistance for fasting insulin levels or systolic blood pressure or hypertension for diastolic blood pressure again did not materially change the results (data not shown). Changing the cutoff levels of categories of homocysteine levels (<10.1 [reference category], 10.1 to 14.0, 14.1 to 18.0, and >18.0 μmol/L) somewhat decreased the ORs for developing (micro)albuminuria (eg, among all subjects, 1.0 [reference category], 1.0 [95% CI 0.4 to 2.2], 1.3 [95% CI 0.5 to 3.5], and 4.8 [95% CI 1.3 to 18.0], respectively, after adjusting for the determinants shown in Table 3 ). Substituting homocysteine levels as continuous variables for categories of homocysteine levels showed that a 5-μmol/L increase of the homocysteine level was associated with a 1.4 (95% CI 0.97 to 2.0) increased risk of developing (micro)albuminuria after adjusting for the determinants shown in Table 3 .

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