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Universal Fit
Shure SE215
"I bought these in February 2012 for £75 at amazon.co.uk and have used them every day except for about one week when I was awaiting delivery of a replacement cable. Typical use is with a variety of personal players (iRiver H140 and H340, Sansa Clip+, Archos A43IT) as well as with PC audio and occasionally with home audio. I listen to many kinds of (usually lossless) music but most often..." --julian67
Shure SE535LTD RED
"I was looking for an excellent universal IEM with multiple drivers to fit my portable listening needs. Ideally, I would have my beloved LCD-2's in a portable package. I have become addicted to the effortless brightness of those headphones and their versatility. I'm sad that I can't wear them all the time, which is why I need something portable. I have listened to and enjoyed many low end IEMs..." --hardbop
Shure SE215 Special Edition
"As I'm looking to move up in the world of IEMs, I'm taking a look back at one of my first big steps in audio. Having burned through multiple pairs of Skullcandys and Sennheiser CX300-500s and having got a taste for high end audio from my first full sized cans, I set out to get a pair of IEMs with durability as priority number one while also sounding great. The SE215LTDs..." --NShinryu
MP4Nation Brainwavz M1
"Introduction Brainwavz are making another push on their M series earphones and that's good news for those of us looking for a well-priced, high performance earphone. The M1s use a single dynamic driver in a compact plastic and metal shell to deliver a tiny, lightweight earphone with sound that's reminiscent of their more expensive R3 model, but in a much more comfortable package...." --Loquah
Shure E4c-n Sound Isolating Earphones (Black)
" I like this phone so much I am onto my second pair. Are they perfect? No. Are they the best IEM for the price? Unless you get them at $79 like I did the second time, no. Do they have a good soundstage? Not really. Are they durable? Like a boat made of paper. But...Do they isolate well? With the Shure olives, hell yes. Do they have delicous, buttery mids that I could and have listened to..." --paddy567
Shure SE110 Sound Isolating Earphone with Balanced Armature Driver (Black)
" As many know these are a nice upgrade and quite price conscience. I do like the accessory pack and methods of lengthening the cable. I use them while flying and usually wear them the entire flight (even for 20+ hours) due to their good sound isolation. If used on a plane should get a sound attenuating patch cord adapter as these are very sensitive. They are superb compared to the inflight..." --smurphy522
Shure E2c Sound Isolating Earphones
" These things hurt my ear canal too easily unless I use the orange foam inserts, but they get gross and deform a little too easily. Anyway, the sound on these was good enough for me to realize that my iPod had a pretty constant hiss. They also made it apparant that I could only listen with EQ off or the signal would clip. I never listen to these things with the volume up. I'm a..." --funkmeister
MP4Nation Brainwavz M2
"Well after a good lengthy burn in (100hrs or so) I feel I am ready to write my full review of the Brainwavz M2. I would like to thank MP4Nation for sending me a pair of the M2 to review. To make it clear, I received this IEM for free, in exchange for a review by me. I was clear with MP4Nation that I would be completely honest in my review, good or bad. To which they responded they would want it..." --dweaver
Shure SE210 Sound Isolating Earphones (White)
" These relatively small buds are dramatically full sounding and produce a deep, rich experience " --darroncollins
Shure SE102MPA Sound Isolating Stereo Earphones / Headset
" The Sure SE102 are great entry level premium IEMs. The fidelity is above most in the price range. Comfortable in ear. The Sure wrap around ear form factor is always a bit annoying. I loved the short cord extension cord design. Great when you don't need a long cord hangin on you. Like when you just want to put your phone/player in a shirt pocket or plug them into a clip-on bluetooth device..." --jcksa


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By CHRISTINA BOMENGO and PAUL LIOTTA
STATEN ISLAND, N.Y. -- While many Staten Islanders enjoy basking in the sun's rays or bicycling on the boardwalk, residents in large numbers shun the saltwater.
Of 25 beachgoers who participated in an informal survey taken yesterday at Wolfe's Pond Park, Midland Beach, South Beach and the relatively new Cedar Grove Beach, only two said they'd feel comfortable going for a swim.
Staten Island Beaches have more pollution than years past
Nonetheless, Brooklyn resident Yan Baron emerged from the surf at Wolfe's Pond Park and described conditions as "clean and beautiful." Nor is he alone: A considerable number of off-Island bathers patronize the borough's beaches.
But the majority of those interviewed yesterday made it clear that the water worries them. "I would never actually go in it; look how dirty it is," said Courtney Faiella of Annadale at Cedar Grove.
Indeed, the beaches' reputation has preceded them. "It has a bad name," said Ryan (no last name) of Castleton Corners.
"I'm not concerned because I don't go swimming in the water," said Lauren Feasher of Pleasant Plains at Wolfe's Pond Park. "But I have noticed it's cleaner than it has been."

subset: commoncrawl


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Samantha Fitzpatrick has a dream and a plan.
"Being an original artist, I'm doing this in a nontraditional kind of way," said the 27-year-old who fronts the Samantha Fitzpatrick Band. "Most original artists will play in venues and try to build up a following. I started out playing in bars and playing covers, and I still do that."
But in each set, you're likely to hear a Fitzpatrick original. Maybe enough to whet an appetite for what really ARE good, rocking songs.
"Eventually, we'll build up a following that way — we throw in a couple of originals, and still sell our merch, sell our CDs, and eventually build up a following," she said.
Fitzpatrick didn't earn a marketing degree at Ohio State University, but she did come away with one in psychology, so it sounds as if she's got a pretty good handle on the thought processes of potential fans.
"Yeah," she said with a laugh, "it's a great degree for marketing and promoting and songwriting."
She's probably right about the first two, and she's definitely right about the last. Fitzpatrick's original songs, as evidenced by the band's debut CD, "Above Blue Waters," show a Rorschach-worthy collection of sharp lyrics and memorable melodies that delve deep into the psyche.
"A lot of the songs on my first album were songs I'd written since I was 16," said Fitzpatrick, who called herself an "extremely slow" writer. "I'm just now making myself sit down and write faster. Before, it was one song a year. If something affected me, I would write about it. But I can't force it. If I force it, it comes out really cheesy."
Each writer — be it songs, poems, fiction or even, God forbid, newspaper stories — has his or her own style. For Fitzpatrick, it's pretty much a Lone Ranger sort of experience, vamping on her guitar through different chord progressions until something strikes her ear.
Fitzpatrick has a good sense of what works for her, and for her band — Fitzpatrick on guitar and vocals, Jono Yowell on bass, Bryan Connell on sax and Alex Dominish on drums and vocals. But even better, she has a great sense of humor. One of the best — and funniest — songs on "Above Blue Waters" is called "One Night Stand."
Typical of the lyric is a line about the girl denying she's a stalker and claiming, "I only called 25 times" — all of which went unanswered — as proof.
"I was so worried that people wouldn't grasp the fact that it's a joke," Fitzpatrick said. "I wrote that song at OSU, where I graduated. It's the stereotypical college experience of one-night stands, all while getting an amazing education, and making fun of girls when they have them."
Fitzpatrick said she debated putting the song on the album because it does have a swear word in it. But really, removing it would be counterproductive, just because it's in such contrast to Fitzpatrick's wholesome look.
Right now, she's struggling to build her career. She and Connell have day jobs as servers. Dominish is only 19 and is a full-time music major at Case Western Reserve University. Yowell is in construction and gives bass lessons.
"We're playing twice a week," Fitzpatrick said. "I could book more, but I don't want to oversaturate the music."
Sounds like a plan.
(The Samantha Fitzpatrick Band is at the American Legion Club at 60 Chester St., Painesville, from 4 to 7 p.m. Saturday. Check samanthafitzpatrickband.com for more gigs.)
Weekend warrior update: Friday — pOUT at Brothers Lounge; Rich Spina and Don Krueger at Mad Cactus; Steve Jochum, Nickleby's. Saturday — Armstrong Bearcat at Zeppe's Tavern; Schoolgirl Crush, the Cove; WIXY 1260s at Bier Haus.


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The National Weather Service in Portland issued an urgent winter weather statement for Portland, the Willamette Valley, Vancouver and most of the northern Oregon coast. The gist: there's a 100 percent chance of precipitation this morning, with rain turning to snow this afternoon.
Look for the snow level to drop to 200 feet in the afternoon and a high near 37 degrees. Daytime snow accumulation of less than a half inch is possible.
Tonight, look for the snow showers to continue before 10 p.m., with mostly cloudy skies and a seriously cold low of 22 made colder by 9 mph winds. The chance of evening precipitation is 80% and the nighttime snow accumulation of less than an inch is possible.
That's right, basic math says Portland could see as much as 1.5 inches of snow. When you're stuck in crazy evening traffic tonight remember this: Tuesday looks sublime for the snow-skittish, with sunny skies and a high around 32 degrees.


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Town of Union, NY (WBNG Binghamton) Homer Brink Elementary students invited family and friends who have served our country to a special ceremony Tuesday morning.
The school hosted its annual Veterans Day celebration.
Early kindergarten through second graders extended a special invite to family members, neighbors and friends who have served our country through military service to attend.
Nearly 60 veterans attended including Marc Schott, who was invited by his niece.
"It's nice to be recognized by such a young group. It makes me feel humble and proud at the same time," said Marc Schott, Sgt. First Class, Army National Guard, "To have my own family want me to come out to something like this feels really nice and for the community to do something like this is just great."
There was patriotic music and poetry prepared and read by students. Each veteran was recognized individually with their name, rank and branch of service.
"It's important for kids to realize what we have here and freedom isn't free. People that we love and care about and that are close to us, have fought for our freedom and it's important for them to see that and be proud of what their family stands for," said George Asfoury, Assistant Principal.
Veterans invited by students but unable to attend will be recognized on Homer Brink's Wall of Honor.


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Brian Schmitt, MD, MPH; Robert M. Golub, MD; Richard Green, MD
Grant Support: The paper was written under contract with the American College of Physicians.
Potential Financial Conflicts of Interest: None disclosed.
Requests for Single Reprints: Brian Schmitt, MD, MPH, Medicine and Neurology Service Line (111), Hines Veterans Affairs Hospital, Hines, IL 60141; e-mail, email@example.com.
Current Author Addresses: Dr. Schmitt: Medicine and Neurology Service Line (111), Hines Veterans Affairs Hospital, 5th Avenue and Roosevelt, Hines, IL 60141.
Dr. Golub: Northwestern University, 676 North St. Clair, Suite 200, Chicago, IL 60611.
Dr. Green: Northwestern University, 303 East Chicago Avenue, Chicago, IL 60611.
Schmitt B., Golub R., Green R.; Screening Primary Care Patients for Hereditary Hemochromatosis with Transferrin Saturation and Serum Ferritin Level: Systematic Review for the American College of Physicians. Ann Intern Med. 2005;143:522-536. doi: 10.7326/0003-4819-143-7-200510040-00011
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© 2016
Published: Ann Intern Med. 2005;143(7):522-536.
Appendix: Search Methods and Article Selection
Therapeutic phlebotomy for hereditary hemochromatosis is relatively safe and presumably efficacious when offered before cirrhosis develops, so screening primary care patients is of substantial interest.
To conduct a systematic review of the evidence on 1) the prevalence of the disease in primary care, 2) the risk for morbid or fatal complications for untreated patients, 3) the diagnostic usefulness of transferrin saturation and serum ferritin level in identifying early disease, 4) the efficacy of early treatment, and 5) whether the benefits of screening outweigh the risks.
MEDLINE search from 1966 through April 2004, complemented by reference review of identified original studies and review articles published in English.
PubMed Clinical Queries filters search of prognosis, diagnosis, etiology, or treatment were used depending on the question. Two authors reviewed all titles and abstracts.
Two investigators independently reviewed extracted data.
The prevalence of hereditary hemochromatosis was 1 in 169 patients to 1 in 556 patients (n = 3 studies). Uncontrolled, prospective studies of genetic homozygous patients did not consistently identify a link to overt hereditary hemochromatosis. A serum ferritin level less than 1000 µg/L was predictive of absence of cirrhosis. Six studies demonstrated reduced survival in patients with cirrhosis. Diagnostic studies varied with respect to case definition. No blinded, independent comparisons of screening tests with the gold standard (biopsy or results of quantitative phlebotomy) or randomized, controlled trials of phlebotomy were identified. Cost-effectiveness analysis was limited by lack of prospective data on the natural history of the disease.
Varied case definition and lack of prospective cohort studies or randomized trials.
The available evidence does not demonstrate that benefits outweigh the risks and costs of screening for hemochromatosis.
Hereditary hemochromatosis is a genetic disorder of iron metabolism resulting in excessive iron overload and is associated with clinically significant morbid and fatal complications related to tissue iron deposition (1). It is an autosomal recessive disorder linked to a mutation of the HFE gene on the short arm of chromosome 6. This gene is the result of a single base change in which tyrosine is substituted for cysteine at position 282 of the HFE protein (C282Y). Available evidence strongly supports an association of the C282Y mutation with hereditary hemochromatosis, although other mutations in HFE have been identified. The substitution of aspartic acid for histidine at position 63 (H63D) has been observed but has limited clinical effect (2). Several genetic mutations are also linked to juvenile hereditary hemochromatosis (3, 4).
The C282Y mutation is variably and unpredictably associated with phenotypic changes of iron overload that include elevated transferrin saturation and serum ferritin levels. An increasing transferrin saturation is the earliest detectable biochemical abnormality in hereditary hemochromatosis and is attributed to increased intestinal iron absorption (4). Enterocytes aberrantly continue to transfer iron from the gut into the bloodstream rather than store the iron as ferritin. The role of HFE in this pathophysiologic process is not fully clear. Some patients with the HFE gene never progress beyond this biochemical abnormality. However, progressive iron overload occurs in others. Marked elevation of serum ferritin level has been associated with histologic evidence of iron deposition (5). The morbid complications of hereditary hemochromatosis are the result of tissue deposition, and they develop late in its course. They include arthritis, diabetes mellitus, congestive heart failure, cirrhosis, and hepatocellular carcinoma (6). Liver iron deposition with cirrhosis is associated with reduced survival (7).
The estimated prevalence of hereditary hemochromatosis is 1 in 200 persons to 1 in 250 persons in the general population, making hereditary hemochromatosis one of the most common genetic disorders (8). However, the prevalence of hereditary hemochromatosis varies depending on the case definition of disease (9). With genetic testing of populations originating in northern Europe, approximately 0.5% is homozygous for the C282Y mutation (10). With phenotypic screening, 1% to 6% of the U.S. population have elevated transferrin saturation levels, and 11% to 22% of them have concomitant elevations of their serum ferritin levels (11).
Over the past decade, interest in promoting general population screening for hereditary hemochromatosis has increased (12, 13). Advances in genetic testing, changing definitions of the disease that include earlier stages of iron overload, increased appreciation of the prevalence and importance of the disease, and the presumed effectiveness of a simple intervention (phlebotomy) have prompted a debate on the benefits and risks of a screening intervention program in the United States. The use of genetic testing to screen family members of individuals identified with hereditary hemochromatosis seems to be cost-effective (14). The benefit in primary care is less clear. In 1997, the Centers for Disease Control and Prevention and the National Institutes of Health sponsored a meeting on iron overload, public health, and genetics (15). A result of the conference was a published review of the evidence for hemochromatosis screening (13). Evidence for screening was evaluated against the U.S. Preventive Services Task Force criteria (16). Little evidence was available to support the efficacy of genetic testing, and there were substantial ethical, legal, and social concerns. Likewise, evidence was insufficient to support the use of transferrin saturation, and few comparative data were available to establish the magnitude and clinical significance of risk in patients with various levels of iron overload. However, others argued for expanded screening and have targeted primary care physicians for educational intervention to improve awareness of the disease (12, 17). The Working Group on Research Priorities identified the evidence that is most needed to provide a scientific basis for population screening (18). They identified the need for research to characterize the natural history of the relationship between genotype and phenotype in hereditary hemochromatosis and other iron overload disorders. They also identified 3 additional priorities: 1) development of an optimal approach for screening for iron overload; 2) analyses of the cost-effectiveness of screening; and 3) assessment of the ethical, legal, and social implications of screening. Given this background, we must examine the current evidence and determine whether it now supports general population screening for hereditary hemochromatosis.
To promote screening within the primary care setting, one must demonstrate that the disease is common, the burden is substantial, the treatment is efficacious, the screening tests are accurate, the screening is effective, and the benefits of screening outweigh the risks (16). We evaluate the evidence to support screening within the primary care setting. Because of the controversy surrounding genetic testing as a screening tool (low penetrance of hereditary hemochromatosis and lack of complete identification of genetic mutations associated with hereditary hemochromatosis), our review focuses on the phenotypic measures that are most likely to be useful in primary care: transferrin saturation and serum ferritin level. To evaluate the evidence, we address each key question that is relevant to a screening intervention.
We conducted a systematic review for each question in MEDLINE for papers published from 1966 through April 2004 by using PubMed Clinical Queries filters for a sensitive search of prognosis, diagnosis, etiology, or treatment depending on the question. We included only English-language studies. Two reviewers independently reviewed all abstracts. A third reviewer resolved conflicts about inclusion of an article. We also manually searched references from included studies. The Appendix includes details for conducting the search for each subquestion. We assessed methodologic quality of studies for a specific question by using accepted epidemiologic criteria (19). We did not use any formal method of quality assessment or scoring.
This paper was written under contract with the American College of Physicians. The funding source had no role in the collection, analysis, or interpretation of the data or in the decision to submit the manuscript for publication.
We identified 3 prevalence studies in primary care settings (Table 1) and 12 studies in various general population settings (Table 2) (Appendix Figure 1). Because of variability among studies, we examined the prevalence data in 3 ways: use of the strict definition recommended in the Hemochromatosis and Iron Overload Screening (HEIRS) study (34); use of the prevalence reported by the investigator(s); and use of a ceiling estimate, which assumed that the many study participants with elevated transferrin saturation and serum ferritin levels who declined liver biopsy or therapeutic phlebotomy had the same probability of primary iron overload as those who were actually evaluated.
Table 1.
Table 2.
Using strict criteria, we found that the prevalence of hereditary hemochromatosis within a primary care setting was 0.18% to 0.59% (1 in 169 patients screened to 1 in 556 patients screened). The prevalence reported by the investigators was 0.2% to 1.8% (1 in 56 patients screened to 1 in 500 patients screened). We estimated the ceiling prevalence of hereditary hemochromatosis to be 0.37% to 0.79% (1 in 127 patients screened to 1 in 270 patients screened). Most patients with hereditary hemochromatosis did not have concomitant cirrhosis. Using the HEIRS study definition, we found that hereditary hemochromatosis prevalence was higher in white men (0.37% to 0.46%) than nonwhite men (0% to 0.17%) and was higher in men than women.
Using strict criteria, we estimated the prevalence of hereditary hemochromatosis from the 2 general population studies (23, 24) to be 0.16% to 0.28% (1 in 357 patients screened to 1 in 625 patients screened). The investigators reported higher rates—as high as 0.74% in Norwegian men. In screening employees or blood donors, the prevalence of hereditary hemochromatosis was higher in men than women and, when demographic data were available, was higher in white men than nonwhite men (Table 2).
Within the primary care setting (n = 23 055) and using strict criteria, we identified hereditary hemochromatosis in 59 patients (0.13%) (equivalent to 1 in 795 screened patients). Of these 59 patients, 55 patients (93%) were 40 years of age or older, 46 patients (78%) were men, and 38 patients (93%) in the 2 studies that provided racial characteristics were white. Fifty-two of 59 patients (88%) did not have cirrhosis. These data demonstrate that the prevalence of hereditary hemochromatosis varies across different subgroups determined by race, sex, and age. The highest prevalence of hereditary hemochromatosis detected by screening within primary care seems to be in white men, probably ranging between 1 of 185 screened patients and 1 of 219 screened patients (20, 21). Screening that targeted white men 40 years of age or older would further increase the prevalence of hereditary hemochromatosis.
The definition of iron overload varied across studies. Some studies evaluated the relationship between the asymptomatic elevation of transferrin saturation and serum ferritin levels and the development of disease, while other studies addressed the relationship between iron tissue deposition and the development of complications and death. Consequently, we separately aggregated the evidence to address these 2 related but different ways of characterizing iron overload.
We identified 11 studies (5, 35-44) for inclusion (Appendix Figure 2). None was a prospective cohort study comparing survival or complications in patients with and without hereditary hemochromatosis defined by an elevated serum ferritin level.
Three uncontrolled, prospective studies (35-37) examined the change of iron stores over time in individuals identified as being C282Y homozygotes (Table 3). One study (35) followed 12 Australian patients for 17 years. While the median transferrin saturation and ferritin level increased, some patients had constant levels and some had decreasing ferritin levels. In a Canadian study of 22 participants, Yamashita and Adams (36) observed a decrease in serum ferritin levels in 13 patients and serum ferritin levels remaining less than the upper limit of normal in 20 patients after a median of 4 years. In the Copenhagen City Heart Study (37), average transferrin saturation levels increased substantially after 25 years of follow-up, but no homozygote developed hereditary hemochromatosis. In summary, these studies did not consistently identify increasing transferrin saturation and serum ferritin levels over time and did not demonstrate a clear link to the overt clinical manifestation of hereditary hemochromatosis.
Table 3.
Three studies examined the relationship between biochemical measures of iron overload and diabetes mellitus (Table 4). Jiang and colleagues (38) used blood samples obtained from 32 826 women in the Nurses' Health Study cohort between 1989 and 1990 who did not have diabetes mellitus, cardiovascular disease, or cancer. Multivariate relative risk increased across the quintiles of the initial ferritin levels (1.00, 1.09, 1.26, 1.30, and 2.68, respectively; P < 0.001 for trend). However, the results must be interpreted cautiously because cases and controls had several differences at baseline. Ellervik and colleagues (39) compared Danish patients with type 1 diabetes mellitus with controls who were selected from the Copenhagen City Heart Study. Nine patients with diabetes who were homozygous for C282Y had transferrin saturation greater than 50%, and 6 of these patients had cirrhosis by liver biopsy. Ellervik and colleagues did not directly compare transferrin saturation or serum ferritin levels between those with and without diabetes mellitus to allow a direct determination of the association, and they did not present comparison data for cases and controls. Mainous and colleagues (40) used the National Health and Nutrition Examination Survey I (NHANES I) database. The adjusted odds ratio of diabetes (controlling for age, sex, race, cholesterol level, obesity, and hypertension) was 0.89 (95% CI, 0.59 to 1.34) for transferrin saturation greater than 45%, 0.95 (CI, 0.53 to 1.70) for transferrin saturation greater than 50%, and 1.03 (CI, 0.44 to 2.43) for transferrin saturation greater than 55%. However, Mainous and colleagues did not actually identify patients with sustained elevations in transferrin saturation and serum ferritin levels and did not measure the association with diabetes mellitus.
Table 4.
Three studies examined the relationship between biochemical measures of iron excess and cirrhosis (Table 5). All were cross-sectional studies. Two studies (41, 42) developed a prediction rule for patients homozygous for the C282Y mutation to diagnose or exclude cirrhosis and to more clearly define those needing liver biopsy. Both studies had separate derivation and validation populations. The earlier study (41) aimed to predict the absence of cirrhosis. It was derived in a French population and validated in a Canadian population. Only 1 of 105 patients (0.9%) with a ferritin level of 1000 µg/L or less had cirrhosis. In combination with a normal aspartate aminotransferase (AST) level and no hepatomegaly, 0 of 94 patients had cirrhosis. Findings in the validation population were similar. The more recent follow-up report (42) found that ferritin levels greater than 1000 µg/L, platelet counts less than 200 × 109 cells/L, and elevated AST levels led to a correct diagnosis of cirrhosis in 77% of the Canadian participants and in 90% of the French participants who were tested. Morrison and colleagues (5) found that patients with ferritin levels less than 1000 µg/L were unlikely to have cirrhosis on liver biopsy (1 of 93 patients). These 3 studies strongly suggest that patients who are at high risk for hereditary hemochromatosis (homozygous C282Y mutation) with serum ferritin levels of 1000 µg/L or less are unlikely to have cirrhosis.
Table 5.
Mahon and colleagues (43) examined the relationship between C282Y mutations and idiopathic dilated cardiomyopathy (Table 6). This case–control study demonstrated that 31 of 207 cases (15%) carried the C282Y mutation compared with 24 of 200 controls (12%) (adjusted odds ratio, 1.2 [CI, 0.7 to 2.2]). With respect to the H63D mutation, the odds ratio was 1.6 (CI, 1.1 to 2.5). Serum iron and transferrin saturation did not correlate with disease severity or survival. The clinical significance of the link of the H63D mutation with cardiomyopathy is unclear.
Table 6.
Mainous and colleagues (44) examined the association between transferrin saturation and all-cause mortality by using the NHANES I database (Table 6). After controlling for comorbid disease, smoking, and cholesterol level, all-cause mortality statistically significantly increased for transferrin saturation greater than 55% compared with those with lower transferrin saturation (hazard ratio, 1.60 [CI, 1.17 to 2.21]). Although no one who died had hereditary hemochromatosis listed as a cause of death, they were more likely to have cirrhosis or diabetes mellitus.
We identified 13 original studies (7, 45-56)(Appendix Figure 3). Seven studies explored the relationship of hereditary hemochromatosis and survival, and the remainder evaluated the association of this disease with other complications (Table 7).
Table 7.
Wojcik and colleagues (45), studying patients from a tertiary care facility, found that actuarial survival at 5, 10, and 20 years was 95%, 93%, and 66%, respectively, with a mean follow-up of 7.3 years. At the time of diagnosis, 36% of men and 19% of women had life-threatening diseases. Cirrhosis and diabetes mellitus were the only major factors that affected survival. Milman and colleagues (46) found that after a median of 8.5 years, survival in patients with cirrhosis and diabetes was statistically significantly lower than survival in those without either complication (who had a survival similar to that in the general population on the basis of a nonconcurrent, historical control). The main causes of death were liver failure secondary to cirrhosis and cirrhosis with liver cancer. Although not clearly stated, Niederau and colleagues' studies (7, 56) probably shared some of the same patients. Their more recent publication (7) also found that survival in noncirrhotic and nondiabetic patients with hereditary hemochromatosis was similar to survival in those in the healthy population (nonconcurrent, historical control). The adjusted relative risk for death for cirrhosis and diabetes mellitus was 4.3 and 2.4, respectively. Fargion and colleagues (47) found that over a median of 44 months, 44 of 146 patients with cirrhosis died (20 with hepatocellular carcinoma and 10 with liver failure). No deaths occurred in patients without cirrhosis. Adams and colleagues (48) found that patients with hereditary hemochromatosis and cirrhosis were 5.5 times more likely to die than those without cirrhosis. Diabetes mellitus did not increase the risk. Yang and colleagues (49) conducted a retrospective analysis of the Multiple-Cause Mortality Files compiled by the National Center for Health Statistics. Patients who died of hereditary hemochromatosis were more likely to have liver neoplasms, liver disease, and cardiomyopathy. Conversely, patients who died of liver neoplasms, liver disease, and cardiomyopathy were more likely to have hereditary hemochromatosis than those without these conditions. These studies consistently demonstrated a link between hereditary hemochromatosis-associated cirrhosis and reduced survival and strongly suggest a link between hereditary hemochromatosis–related diabetes mellitus and reduced survival.
Adams (50), using receiver-operating characteristic curve analysis to identify the threshold of hepatic iron concentration for predicting the presence of cirrhosis, derived an optimal threshold of 283 mmol/kg dry weight, with a sensitivity of 85% and a specificity of 84%. Fargion and colleagues (51) evaluated the prognostic factors for hepatocellular carcinoma in hereditary hemochromatosis. Hepatocellular carcinoma developed in 29% of patients with cirrhosis compared with 0% in those without cirrhosis. The 2 studies by Deugnier and colleagues (52, 53) identified a specific preneoplastic change (iron-free foci) in patients with hereditary hemochromatosis that was associated with the development of hepatocellular carcinoma. Ammann and colleagues (54) found that out of 36 patients with hereditary hemochromatosis, 5 cases of hepatoma and 6 cases of extrahepatic carcinoma developed over 8 years.
The case–control study by Salonen and colleagues (55) found that men with high iron stores were 2.4 times more likely to have diabetes than men with lower iron stores.
We identified 3 studies (20-22) conducted in the primary care setting (Appendix Figure 4). No study independently and blindly compared the screening tests for iron overload (transferrin saturation and serum ferritin level) with the gold standard (liver biopsy or mobilizable iron by phlebotomy) in all screened patients.
Phatak and colleagues (21) screened for sustained transferrin saturation of 45% or greater (n = 311). Of 50 patients with transferrin saturation greater than 55% and serum ferritin levels greater than 200 µg/L, 35 patients were offered liver biopsy and 21 patients underwent the procedure. Eighteen patients (86%) were found to have hereditary hemochromatosis. Of 29 patients who declined or were not offered liver biopsy, 17 patients were labeled as having clinically proven hereditary hemochromatosis. Of this group, only 2 patients had mobilizable iron stores of 2 g or more. Using the strict HEIRS study criteria and these diagnostic cutoff levels, we identified hereditary hemochromatosis in 20 patients (40%). Using the authors' criteria, 36 patients (72%) had hereditary hemochromatosis. For those with transferrin saturation between 45% and 55% and serum ferritin levels greater than 200 µg/L (n = 78), biopsy was recommended in 13 patients and hereditary hemochromatosis was identified in 7 patients. Of those who did not have a recommendation for biopsy (n = 65), 2 patients had mobilizable iron stores of 2 g or more. Using strict criteria and these cutoff levels, 9 of 78 screened patients (11.5%) had hereditary hemochromatosis. Using the authors' criteria, we identified hereditary hemochromatosis in 11 patients (14%).
Niederau and colleagues (22) studied 3027 healthy outpatients in West Germany. They used thresholds of transferrin saturation greater than 50% in men and greater than 60% in women and serum ferritin levels of 250 µg/L in men and 350 µg/L in women. Using these cutoff levels, 235 patients (7.8%) had elevated serum ferritin levels, 139 patients (4.6%) had elevated transferrin saturation, and 44 patients (1.5%) had both. Of this latter group who were retested, 31 patients (1% of total) had persistently elevated transferrin saturation and serum ferritin levels. Twenty-three patients continued with further evaluation. We identified hereditary hemochromatosis in 18 patients (78%) by using these diagnostic cutoff levels for transferrin saturation and serum ferritin levels.
Baer and colleagues (20) studied 3977 consecutive men 30 years of age or older who belonged to the Oakland Kaiser Permanente health maintenance organization. Those with transferrin saturation of 62% or greater underwent repeated testing in the fasting state. Patients with persistently elevated transferrin saturation (≥62%) and serum ferritin levels of 500 µg/L or greater were offered a liver biopsy. Forty patients (1%) had transferrin saturation that exceeded the cutoff value. Thirty-six patients were available for follow-up. Of these, 14 patients with persistent elevations were referred for liver biopsy and 12 patients underwent the procedure. One of the 12 patients had a serum ferritin level less than 500 µg/L. These 12 patients had hereditary hemochromatosis defined by strict criteria. All patients with transferrin saturation of 62% or greater and serum ferritin levels of 500 µg/L or greater had hereditary hemochromatosis.
These 3 studies demonstrate substantial variation in the testing sequence; the decision thresholds for transferrin saturation, serum ferritin level, and their combined results; and the application of the gold standard. Patients with levels less than the threshold values at any location in the testing sequence were not assessed by the gold standard or followed for the development of disease. Not all patients with levels greater than the threshold values underwent the gold standard assessment. Consequently, sensitivity and specificity cannot be determined. The proportion of patients with levels greater than the threshold values who underwent the gold standard assessment does provide a limited estimate of the positive predictive value.
Other researchers have reviewed the proportion of screened patients in a general population with initial and repeatedly positive transferrin saturation test results (57). Initial positive test results were found in 1.1% to 6.2% of patients screened. A relationship between the proportion positive and the diagnostic cutoff level was not apparent. The highest proportion was in blood donors with transferrin saturation cutoff values of 50% or greater (29), and the lowest proportion was in those with cutoff values of 55% or greater (28). This differs from the 3 primary care studies in which the more stringent criteria were associated with a higher proportion of patients identified with hereditary hemochromatosis.
We did not identify any randomized trial. We identified only 1 study for inclusion because it compared patients who were adequately phlebotomized with those were not adequately phlebotomized (46). We identified an additional study (7) by manual search because of its before–after phlebotomy comparison of liver histology (Appendix Figure 5).
Milman and colleagues (46) retrospectively identified a cohort of 158 patients with hereditary hemochromatosis by querying departments of medicine and pediatrics in Denmark and by reviewing a Danish death registry. Patients were followed for a median period of 8.5 years. Survival of patients who were adequately phlebotomized (n = 66) was greater than survival of those were not adequately phlebotomized (n = 62). The estimated Kaplan–Meier survival was 93% versus 48% at 5 years and 78% versus 32% at 10 years. Furthermore, adequately treated patients with cirrhosis or diabetes had better survival than those who were not adequately treated. However, we could not determine the clinical comparability of patients with cirrhosis who were or were not adequately treated.
Niederau and colleagues (7) studied a cohort of 251 German patients with hereditary hemochromatosis for a mean follow-up of 14.1 years. Patients underwent an initial liver biopsy and were then phlebotomized until serum ferritin level was normalized. At this point, they underwent a second biopsy. A before–after phlebotomy comparison was performed in 185 patients. However, no methodologic safeguards minimized ascertainment bias. Forty-two patients had improved liver histology after phlebotomy, and 2 patients had deterioration in histology. Improvement or deterioration was based on changes in fibrosis stage. Except for 1 patient, all improvements were by 1 stage. One patient had a 2-stage improvement. The 2 patients who deteriorated had a 1-stage decrement. The remaining 141 patients did not change. However, given the possibility of sampling error from one liver biopsy to the next, any change in histologic status must be interpreted cautiously.
No studies met a standard of evidence (blinded, randomized, controlled trial) that clearly establishes the efficacy of therapeutic phlebotomy. However, they do support the existing model of disease and suggest a benefit. Given the current opinion and the lack of clinically significant side effects, a randomized, controlled trial will probably not be performed.
Without the ability to establish the efficacy of therapeutic phlebotomy in a research setting, we could not establish the effectiveness of a screening approach directly in the primary care setting. The electronic literature search for a decision-analytic model of a cost-effectiveness analysis identified 4 relevant postings. Two models (58, 59) were previously reviewed in Annals of Internal Medicine(13). Cogswell and colleagues (13) identified the major determinants of screening cost-effectiveness: prevalence and disease burden; sensitivity and specificity of the screening tests; adherence to screening, diagnosis, and therapy; and costs of screening, diagnosis, and therapy. The lack of data on natural history led decision analysts to use data from hospital registries of patients affected with hemochromatosis, increasing the possibility of overestimation of morbidity and mortality.
Two studies (60, 61) have been published since Cogswell and colleagues' comprehensive review, and we evaluated them for new insights. In their decision-analytic model, Asberg and colleagues (60) based the prevalence of hereditary hemochromatosis and the risk for liver cirrhosis on cross-sectional data obtained from a population of 30 509 men (24). If their model accurately reflects reality, phenotypic screening of a cohort of 10 000 young (30 years of age), predominantly white men from the general population would generate a gain of 8 quality-adjusted life-years compared with waiting for symptomatic disease to occur. They estimated the costs to be $250 per quality-adjusted life-year saved.
The model used a screening approach that began with an initial nonfasting transferrin saturation (cutoff level, >55%), followed by a fasting transferrin saturation if the first result was positive. If this second test result was greater than 55%, they measured the serum ferritin level. If the serum ferritin level was elevated (>200 µmol/L), they referred the patient for clinical examination. They did not base the diagnosis of hereditary hemochromatosis on invasive liver biopsy results or the amount of mobilizable iron removed. Therefore, they did not assign risk to the clinical examination. If they could not identify a secondary cause of iron overload, they labeled the patients as having hereditary hemochromatosis. Consequently, they actually incorporated the screening tests into the gold standard of diagnosis, which explain the high estimated sensitivity and specificity of the screening tests used in their model. In their theoretical cohort of 10 000 men, Asberg and colleagues estimate that 53 people with hereditary hemochromatosis would be identified. However, if we take the available data from primary care (21) and use a strict case definition (biopsy or mobilizable iron), we estimate that only 18 patients with hereditary hemochromatosis would be identified. These marked differences illustrate the effect of differing case definitions on the models.
Furthermore, Asberg and colleagues (60) used Markov models to estimate outcomes for men with hereditary hemochromatosis with or without treatment (phlebotomy) and men without hereditary hemochromatosis with or without phlebotomy (4 health states). The only complication of hereditary hemochromatosis used to model survival was the presence or absence of cirrhosis. They estimated the incidence of cirrhosis from cross-sectional data of men with cirrhosis at the time of initial diagnosis across various age groups in 2 studies (21, 24). Asberg and colleagues assumed that men with hereditary hemochromatosis but without cirrhosis at diagnosis and treated with phlebotomy would not develop cirrhosis and estimated their quality of life to be 1.0. However, the only available data on the before–after phlebotomy effect on liver histology suggest that 77% of patients had no change during the before–after time period (from initial diagnosis to normalization of serum ferritin level) and 1% progressed (7). Although presumed to be true, on the basis of this information, whether phlebotomy will prevent the development of cirrhosis in all treated patients over longer periods of time is not certain. Furthermore, Asberg and colleagues did not consider the effect of being labeled with hereditary hemochromatosis (psychologically or economically).
The study by Adams and Valberg (61) suggested that screening blood donors for hereditary hemochromatosis may save money. They used a decision tree for the natural history of unscreened donors that was similar to their previous cost models (62, 63). The target population for this decision analysis was a hypothetical cohort of 10 000 voluntary blood donors and 50 siblings of identified homozygotes. They compared genotypic screening with phenotypic screening and modeled the effect of diabetes mellitus and heart failure on outcomes, as well as cirrhosis. As in previous analyses, they used a database of 170 homozygous patients with hereditary hemochromatosis who were referred to a tertiary care facility. An optimal screening strategy used phenotypic testing followed by genotyping—unless the cost of genetic testing was less than $28.
Unfortunately, these 2 new analyses are still subject to the limitations that we have noted in the primary studies. The lack of data on natural history has forced analysts to rely on cross-sectional studies or databases at large tertiary care referral sites. More recent data have raised additional questions about the usefulness of genetic testing because many people with HFE mutations do not progress to overt disease, and we have no prospective data on the incidence of cirrhosis or diabetes mellitus in patients with elevations of transferrin saturation and serum ferritin levels but without disease at the time of diagnosis.
On the basis of our review of the literature, hereditary hemochromatosis is a common genetic disease within the primary care setting, especially in white men older than 40 years of age. Given the relatively high estimated prevalence of hereditary hemochromatosis (1 in 127 patients to 1 in 270 patients), we must understand the magnitude of the burden that will likely occur. Ideally, the answer would come from a large prospective cohort study identifying patients with and without hereditary hemochromatosis at an early and uniform point in time (sustained elevations of transferrin saturation and serum ferritin levels without clinically significant liver iron deposition) and followed at regular intervals with blinded assessment to detect the important outcomes of cirrhosis, hepatocellular carcinoma, diabetes mellitus, congestive heart failure, arthritis, and death. Unfortunately, no prospective cohort studies early in the course of the disease are available to provide this information. The available data demonstrate low penetrance of HFE mutations and suggest that the magnitude of burden may be less than commonly believed. Specifically, 3 small longitudinal studies (34-37) of patients homozygous for the C282Y mutation did not demonstrate predictable progression to overt clinical hereditary hemochromatosis over long periods of follow-up.
The association between phenotypic measures of iron overload (transferrin saturation and ferritin levels) and the development of iron-related complications is inconsistent. No prospective cohort studies of patients without diabetes mellitus at baseline with and without elevated biochemical measures of iron are available to determine differences in the incidence of new disease. The available retrospective studies did not ensure balanced comparison groups, making selection bias likely (38-40). Consequently, the interpretation of an association between serum iron measures and diabetes mellitus was difficult at best. The prospective studies of patients with hereditary hemochromatosis based on liver iron deposition demonstrated a high prevalence of co-existing diabetes mellitus, and diabetes mellitus was independently associated with an increased risk for death in many of these cohorts. Given its high prevalence in patients with overt hereditary hemochromatosis, diabetes mellitus is probably associated, but the magnitude of risk is not clear. Associations with arthritis and congestive heart failure were not well supported.
The strongest link between iron overload and disease is the association of serum ferritin levels with cirrhosis. Two separate research groups consistently demonstrated the usefulness of the test for identifying a low-risk group for the presence of cirrhosis (serum ferritin level < 1000 µg/L). In addition, a prediction rule for the presence of cirrhosis has been developed and validated. Serum ferritin level is useful for predicting the prevalence of cirrhosis at a single point in time. A patient with a serum ferritin level less than 1000 µg/L without hepatomegaly and a normal AST level is unlikely to have cirrhosis. On the other hand, patients with serum ferritin levels greater than 1000 µg/L, platelet counts less than 200 × 109 cells/L, and elevated AST levels have a high probability of cirrhosis. The available literature suggest that the presence of cirrhosis in patients with hereditary hemochromatosis at the time of diagnosis portends a poor prognosis (a substantial reduction in survival and an increased risk for hepatocellular carcinoma). Only 5% of those with hereditary hemochromatosis identified by screening in a primary care setting had cirrhosis. However, the available data did not permit determination of the incidence of new cases of cirrhosis in patients with hepatic iron deposition at the time of original diagnosis.
The identification of the HFE gene and development of a genetic test to detect the presence of C282Y mutation has made the case definition of hereditary hemochromatosis vary (9). This has resulted in several different approaches for studying the diagnostic efficacy of available tests. Some investigators used genotyping as the gold standard and determined the sensitivity and specificity of phenotypic tests in predicting the presence or absence of homozygous C282Y genotypes. Without convincing data to demonstrate that patients with HFE mutations will progress to disease or early death, this definition may not have clinical utility. Other investigators have used persistently elevated transferrin saturation and serum ferritin levels, without biopsy or quantitative phlebotomy, to diagnose hereditary hemochromatosis. This results in a diagnostic incorporation bias (19). Consequently, we selected a gold standard for hereditary hemochromatosis for our review that required independent demonstration of iron overload (liver deposition or the amount of iron removed by phlebotomy). The use of this case definition limits the ability to determine the diagnostic efficacy of phenotypic tests in the primary care setting because patients with transferrin saturation or a second serum ferritin level interpreted as normal do not undergo liver biopsy, and no prospective follow-up data are available for those with negative test results to identify false-negative results. Further, only those with sustained elevations of transferrin saturation and serum ferritin levels are offered the gold standard test. Given these difficulties, determining the likelihood of disease in those with positive test results defined as sustained elevations of phenotypic measures (positive predictive value) was the best existing measure available. The diagnostic cutoff levels for transferrin saturation and serum ferritin have varied across studies as well. The higher cutoff levels (transferrin saturation ≥ 62% and serum ferritin levels ≥ 500 µg/L) identified a subgroup in which all patients had hereditary hemochromatosis. The least stringent criteria (transferrin saturation ≥ 45% and serum ferritin levels > 200 µg/L) identified a group in which only 11.5% had hereditary hemochromatosis. Given the predictive usefulness of serum ferritin level (<1000 µg/L) for excluding the presence of cirrhosis and the high prevalence of hereditary hemochromatosis in patients screened with higher cutoff levels, using these cutoff levels in a screening program is not unreasonable. However, some patients with hereditary hemochromatosis probably would be missed, and no data on the use of repeated tests or an appropriate interval for repeated testing are available. More important, no data are available on the incidence of cirrhosis in patients with levels greater than these cutoff values and without cirrhosis at the time of hereditary hemochromatosis diagnosis.
Much remains unknown about the natural history of hereditary hemochromatosis. Although white men older than 40 years of age screened by phenotypic tests have the highest prevalence of hereditary hemochromatosis (established by liver biopsy or mobilized iron) in a primary care setting, how many without cirrhosis or other organ involvement at the time of diagnosis will progress to overt disease remains unclear. Further, no clearly defined patient or laboratory characteristics are available to risk-stratify patients into groups that are more or less likely to develop overt disease. The recent attempts to model benefits and risks of screening were not based on natural history studies and did not consider the effect of disease labeling (including insurance and social and psychological well-being).
McDonnell and Parrish (64) have reviewed and integrated the available data into a model of natural history to estimate progression to overt disease. They estimate that, in screening a theoretical cohort of 1 million people from the general population with either phenotypic or genotypic tests, only 2 per 1 million persons screened by HFE screening and 3 per 1 million persons screened by transferrin saturation screening would be identified with cirrhosis. Given the potential social, psychological, and financial harms from early hereditary hemochromatosis diagnosis of an asymptomatic patient, the benefit of early diagnosis relative to the risk remains unclear. Our knowledge deficit about natural history remains an important limitation to recommendations about screening patients in primary care or the general population. The HEIRS study (34) is currently being conducted and may help to shed light on some of these issues. This primary care-based study of 100 000 adults over 5 years will provide valuable information related to the prevalence of hereditary hemochromatosis, value of phenotypic and genotypic screening tests, and benefits and risks for primary care-based screening. The results of the screening stage have been recently reported (65). The prevalence of the C282Y mutation was more common (0.44%) in non-Hispanic white persons than in other groups. For those C282Y homozygous individuals, the serum ferritin levels were elevated in 88% of men and 57% of women. However, the actual prevalence of hereditary hemochromatosis based on liver biopsy or therapeutic phlebotomy was not presented.
Hereditary hemochromatosis seems to be relatively common in certain ethnic, sex, and age groups. In patients with overt clinical manifestations, hereditary hemochromatosis can shorten survival and substantially reduce the quality of life. Our current lack of information on natural history severely limits our understanding about the burden related to this disease from a societal perspective. Phenotypic tests can identify subgroups of patients with differing probabilities of hereditary hemochromatosis by liver biopsy and can be used to predict the presence or absence of cirrhosis. No data based on randomized trials indicated the true efficacy of phlebotomy. The limited quality of the evidence base precludes phenotypic testing for a judgment that hereditary hemochromatosis in the primary care setting fulfills the necessary criteria for a screening test (16).
We searched the medical literature to determine the prevalence of asymptomatic hereditary hemochromatosis in primary care settings or in the general population defined by increased hepatic iron concentration on liver biopsy or by evidence of substantial iron overload on the basis of the response to therapeutic phlebotomy. We used the current and ongoing HEIRS study (34) definitions for primary iron overload (hepatic iron concentration > 30 mmol/kg dry weight or by removal of >2000 mg of storage iron by phlebotomy to achieve a serum ferritin level < 200 µg/L). We considered only individuals with evidence of phenotypic primary iron overload to have hereditary hemochromatosis. We conducted a MEDLINE search using the terms hereditary hemochromatosis, hemochromatosis, prevalence, primary care, general population, and screening. We restricted the review to original studies with at least 1000 patients. For a study to be included, the patients identified as having primary iron overload by screening (transferrin saturation and serum ferritin level) must have had either a liver biopsy or a measured response to therapeutic phlebotomy. Because many study participants with elevated transferrin saturation and serum ferritin levels declined liver biopsy or therapeutic phlebotomy, we calculated "ceiling estimates" of prevalence, assuming the same probability of primary iron overload as in those who were actually evaluated. Consequently, we presented prevalence data in 3 ways: use of the strict definition recommended in the HEIRS study, use of the reported prevalence by the investigator, and use of a ceiling estimate.
An electronic search of PubMed identified 345 unique postings through 3 March 2004. After reviewing titles and abstracts and manually reviewing references, we considered 15 studies (20-33, 66) for inclusion (Appendix Figure 1). Four studies (20-22, 66) were conducted in an outpatient clinical care setting. However, we excluded 1 of these studies (66) because it probably included inpatients and outpatient specialty clinics. The other 3 studies were conducted in a primary care setting. Two studies (23, 24) screened patients in the general population, 5 studies (22, 25-28) screened employees, and 5 studies (29-33) screened blood donors.
In 1998, the need for information on the natural history of hereditary hemochromatosis at various stages of iron overload was identified (18). By using the PubMed Clinical Queries filters for prognosis and the terms hereditary hemochromatosis, hemochromatosis, transferrin saturation, serum ferritin, cirrhosis, hepatocellular carcinoma, diabetes mellitus, congestive heart failure, arthritis, and natural history, we examined the literature for new evidence on the transition from states of asymptomatic iron overload (by elevated transferrin saturation and serum ferritin level) to tissue iron deposition (by liver biopsy), clinical disease, and death. We looked for prospective studies that allowed us to determine the incidence of new complications or comparative studies (retrospective or prospective cohort and case–control) that allowed us to determine the association of iron overload with the risk for complications (by relative risk or odds ratio). For a study to be included, patients had to be identified as having primary iron overload with repeated elevations of both transferrin saturation and serum ferritin levels. We determined the outcome of diabetes mellitus by using the Diabetes Expert Committee criteria (67). The outcomes of cirrhosis and hepatocellular carcinoma required tissue confirmation. The outcome of congestive heart failure required symptoms, signs, and objective assessments of reduced left ventricular systolic function (left ventricular ejection fraction 0.45). Arthritis required clinical assessment of signs and symptoms and at least evidence of synovial swelling.
Regarding the relationship between transferrin saturation–serum ferritin level and hereditary hemochromatosis–related disease, an electronic search through 20 April 2004 identified 170 unique postings. After reviewing the titles and abstracts, we identified 10 studies (5, 36-43) for inclusion (Appendix Figure 2). We identified 1 additional study by manually searching references (37). Of these 11 studies, none was a prospective cohort study comparing survival, complications, or both in patients with and without hereditary hemochromatosis defined by an elevated serum ferritin level.
Regarding the relationship between primary iron tissue deposition and hereditary hemochromatosis–related disease, an electronic search through 20 April 2004 identified 259 unique postings. After reviewing the titles and abstracts, we identified 13 original studies (7, 45-56)(Appendix Figure 3). Seven studies explored the relationship of hereditary hemochromatosis and survival, and the remainder evaluated the association of hereditary hemochromatosis with other complications.
We examined the medical literature to determine the diagnostic efficacy of common tests used to assess iron overload (elevated transferrin saturation on 2 occasions, elevated serum ferritin level, or both) in predicting the presence or absence of hereditary hemochromatosis as previously defined. We used the PubMed Clinical Queries filters for diagnosis and the terms hereditary hemochromatosis, hemochromatosis, transferrin saturation, and serum ferritin. We included original studies that were conducted in a primary care setting that addressed the diagnostic usefulness of transferrin saturation or serum ferritin level in predicting hereditary hemochromatosis defined by liver biopsy or response to therapeutic phlebotomy.
The electronic search identified 375 unique postings. Of these, we identified 7 for possible inclusion (21-23, 25, 27, 28, 68). We identified 2 additional studies by reviewing references (20, 29). Only 3 studies (20-22) were conducted in the primary care setting (Appendix Figure 4). No studies independently and blindly compared the screening tests for iron overload (transferrin saturation and serum ferritin) with the gold standard (liver biopsy or mobilizable iron by phlebotomy) in all screened patients.
On the basis of large uncontrolled case series, most hepatologists have accepted the efficacy of phlebotomy for improving survival in patients without cirrhosis (7). This acceptance has made it difficult to conduct prospective, controlled comparisons (cohort studies or randomized, controlled trials) for ethical reasons. However, we assessed the rigor of the available literature for answering this question. We searched for controlled comparisons of phlebotomy in asymptomatic patients with iron overload or in patients with liver iron deposition but without cirrhosis. We used the PubMed Clinical Queries filters for treatment and the terms hereditary hemochromatosis, hemochromatosis, survival, and diabetes mellitus, congestive heart failure, arthritis, cirrhosis, and hepatocellular carcinoma. We included original studies conducted in a primary care setting or in a representative sample of the general population that addressed the usefulness of therapeutic phlebotomy in patients with hereditary hemochromatosis. We looked for differences in diabetes mellitus, congestive heart failure, arthritis, cirrhosis, hepatocellular carcinoma, and survival in patients receiving or not receiving therapeutic phlebotomy.
An electronic search of MEDLINE identified 409 unique postings. We identified only 1 study for inclusion because it compared those adequately phlebotomized with those inadequately phlebotomized (46). We identified 1 additional study by manual search (7) because of its before–after phlebotomy comparison of liver histology (Appendix Figure 5).
A review for evidence of the effectiveness of hereditary hemochromatosis screening in the primary care setting was contingent on identification of studies to establish the efficacy of screening within a research setting. To assess the balance of benefits and risks identified in subquestion 4, we evaluated all integrative secondary data analyses (decision analysis or cost-effectiveness analysis) that modeled the benefits and harms of a screening program in primary care. To be included, the model had to compare some form of phenotypic hereditary hemochromatosis screening with no screening.
The electronic literature search for a decision analytic model of a cost-effectiveness analysis identified 4 unique postings. We included 1 (60) in our review. The 3 excluded postings were not decision-analytic comparisons. Manual search of references identified 8 additional references for possible inclusion (14, 20, 58, 59, 61-63, 66). We excluded the studies by Balan and colleagues (66) and Baer and colleagues (20) because they did not model costs or effects across 2 or more screening options. They simply provided the costs involved in screening patients in a clinic setting. We excluded 2 additional studies because they evaluated the cost-effectiveness of screening family members of heterozygotes (14, 63). No studies specifically evaluated the cost-effectiveness of screening within the primary care setting. The remaining studies addressed general population screening, and we included them for review. Two (58, 59) were previously reviewed in Annals of Internal Medicine(13). Cogswell and colleagues (13) identified the major determinants of screening cost-effectiveness: prevalence and disease burden; sensitivity and specificity of the screening tests; adherence to screening, diagnosis, and therapy; and costs of screening, diagnosis, and therapy. The lack of data on natural history led decision analysts to use data from hospital registries of patients affected with hemochromatosis, increasing the possibility of overestimation of morbidity and mortality.
We evaluated 2 studies (61, 62), which have been published since Cogswell and colleagues' comprehensive review (13), for new insights.
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Daniel Halevy
ActiveHealth Management
May 18, 2006
Targeted testing for hemochromatosis
The review and guidelines for hemochromatosis screening published in the Annals identified several gaps in our knowledge of the disease. However, one particular scenario was not addressed: the patient with incidentally noted hepatic dysfunction and abnormal iron indices. This type of patient is often encountered in the course of routine clinical practice, but has not been the focus of any study. Would these supposed high-risk patients warrant genetic testing, as suggested in the previous AASLD guidelines from 2001?
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Exclusive Offshore Island
Like 2 Resorts in 1
Take a complimentary ferry to the resort's own Sandals Island for exotic offshore adventures. There are two secluded beaches to choose from-one for relaxing and the other for exploring an area reputed to be the best in the Bahamas for snorkeling. The chic beach club features a pool with swim-up bar, whirlpool and a casual restaurant. You'll find shaded hammocks and private cabanas for a romantic and playful rendezvous. It's paradise found-and included-just minutes away!Learn More


text: Debating guns on another forum. Someone on the right side of the argument brought up Mexico's gun ban, and high crime. I'd like to back them up with facts, I need help finding a comparison of crime rates, espeically between us and Mexico. Also, any stats on crime in England.


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These must be scary, scary times ... at the beach house*.
Southern California wildfires from Malibu to San Diego have forced the evacuation of an estimated 350,000 residents from their homes, including Phil Mickelson and his family.
Sources told Golf World on Tuesday that Mickelson's wife, Amy, and the family's three children evacuated from their Rancho Santa Fe home on Monday, while Mickelson was playing in a corporate outing at Baltusrol Golf Club in Springfield, N.J. Mickelson flew home immediately afterward to join his family in their San Diego beach house.
*Seriously. It's terrible what's happening down there, and Mickelson's a good community guy who I'm sure understands how lucky he and his family is ... to have the beach house. It's just that, well, this might be a story that could do without a sports angle.


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Series six of the BBC's Great British Railway Journeys television series sees its presenter, Michael Portillo, continue his travel around Britain by train, re-discovering many of the sights and locations featured in George Bradshaw's book, the Victorian Railway Guidebook. The series is popular with many of our customers, who frequently get in touch to enquire whether our tours include any of the routes and railways featured on the programme. We have therefore compiled a list of all of the Great British Railway Journeys episodes shown to date which have a corresponding GRJ tour - and these are listed on this page.
You can also view the previous Great Continental Railway Journeys series and associated tours including the latest series four by clicking the buttons below.
Great British Railway Journeys by series
|Similar GRJ tour
|Greenock to Larkhall
|From Greenock, Michael Portillo sets sail in the world's last seagoing paddle steamer.
Orkney, Shetland and the Highlands
|Stirling to Pitlochry
|In Stirling, Michael Portillo visits the scene of a bloody battle at Bannockburn.
Orkney, Shetland and the Highlands
|St Andrew's to Edinburgh
|In St Andrews, Michael Portillo pays homage to the birthplace of golf.
Western Highlands and Hebrides
Edinburgh, the Highlands and Islands
|Episode details
|Similar GRJ tour
|Haworth to Huddersfield
|Michael visits the home of the Bronte sisters in Worth Valley and Oakworth, with its heritage railway
|The Harrogate Flower Show
|Similar GRJ tour
|Welshpool to Aberystwyth
|Michael journeys on an authentically Victorian outing to the Welsh coast.
|Railways and Castles of Wales
|Dundee to Aberdeen
|Michael continues his rail tour of industrial Scotland.
|Orkney, Shetland and the Highlands
|Dufftown to Aviemore
|Michael learns about Victorian whisky train bandits.
|Inverness to Plockton
|Michael rides one of the most scenic railways in Scotland and visit the country's smallest station.
Edinburgh, Highlands and Islands
|Killarney to Cobh
|Michael explores the charming Irish Midlands.
|The Enchanting Emerald Isle
|Athlone to Galway
|Michael ends his fourth series of railway journeys in the grand Irish city of Galway.
|The Enchanting Emerald Isle
|Similar GRJ tour
|Berwick-Upon-Tweed to Morpeth
|Michael Portillo discovers Berwick-Upon-Tweed before travelling via Lindisfarne down the Northumbrian coast.
|Yorkshire & Northumberland
|Heysham to Snaefell
|Michael Portillo sets sail from Heysham to the Isle of Man
|Vintage Railways of the Isle of Man
|Bray to Dublin
|Michael Portillo explores a Victorian jail and finds out about the lions of Dublin Zoo
|The Enchanting Emerald Isle
|Similar GRJ tour
|Dereham to Cromer
|Michael gets the rare chance to drive a heritage diesel train
|Norwich & the Norfolk Broads
|Llanwrst to Porthmadog
|Michael visits the Victorian slate capital of Blaenau Ffestiniog in the Conwy Valley
|Railways & Castles of Wales
|Llanberis to Holyhead
|Michael takes the train to the top of Wales's highest peak, Mount Snowdon
|Railways & Castles of Wales
|Durham to Grosmont
|Michael Portillo visits the historic Durham Cathedral and takes a Dracula tour in Whitby
|Yorkshire &
|York to Saltaire
|Michael Portillo takes a Turkish Bath in the famous spa town of Harrogate
|Canterbury to Margate
|Michael goes whelk fishing in Whitstable
|Canterbury & the Railways of Kent
|Dumbarton to Tyndrum
|Michael explores the Dumbarton shipyards that built the Cutty Sark
|Edinburgh, the
Highlands & Islands
Western Highlands & the Hebrides
Scottish Islands & Lochs Cruise
Edinburgh Tattoo
|Oban to Corrour
|Michael discovers how trains spread the word about Oban Whisky
|Edinburgh, the
Highlands & Islands
Western Highlands & the Hebrides
Scottish Islands & Lochs Cruise
Edinburgh Tattoo
|Roybridge to Glenfinnan
|Michael investigates one of the great geological mysteries of the 19th century
|Edinburgh, the
Highlands & Islands
Western Highlands & the Hebrides
Scottish Islands & Lochs Cruise
Highland Adventure
The Highlands & Inner Hebrides Cruise
|Lochailort to Skye
|Michael discovers how the railways helped train commandos at Lochailort in World War II
|Edinburgh, the
Highlands & Islands
Western Highlands & the Hebrides
Highland Adventure
The Highlands & Inner Hebrides Cruise
|Similar GRJ tour
|Todmorden to York
|Michael Portillo travels back in time on the Embsay and Bolton Abbey Steam Railway
|Yorkshire and Northumberland
|Settle to Garsdale
|Michael Portillo revisits the Settle-Carlisle line and explores the magnificent Ribblehead Viaduct
|Windermere to Kendal
|Michael Portillo takes a Lake Windermere steamboat tour and visits Wordsworth's home town, Grasmere
|Yorkshire and the Lake District
|Torquay to Totnes
|Michael Portillo finds out about Torquay's microclimate and spends some of Totnes's local currency
|Torquay & the Eden Project
|St Pancras to Westminster
|Michael Portillo climbs up the clock tower of the Houses of Parliament to hear Big Ben chime
|Most of GRJ's European tours depart St Pancras International
Order a copy of the Great British Railway Journeys book from Amazon.co.uk


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(This was written by Gerry Curry (Gerry's BBQ) about his experience as a vendor at the multicultural festival's food fair with tips for next year's event.)
I was contacted by email and asked if I would like to participate in the fair. I was intrigued, but wondered why they would want me. After all, pulled pork is hardly an "ethic food." I called Gary Kent and learned that he was attending. I figured that if he was serving Lobster Bruschetta I could certainly serve Pulled Pork!
Unfortunately, after accepting their offer, I never received any other information about the event. I knew where it was being held but that was all. After talking to Gary I knew a little bit about what to expect, but I had absolutely NO idea about logistics.
Because I already hold a Permit to Operate a Food Establishment, I knew I had to apply for a special permit to vend at the fair. I was all set to apply for it, including sending in the fee, when I was again contacted by an organizer, who said that they would apply for everyone, and pay the fee. It was a good thing I was procrastinating, because they only did this at the very last minute.
Because I knew nothing, I stuffed my car with everything required, including all the extra stuff the food safety people demand. When the organizers contacted me about the permit I asked what the operating times were. I also said I'd never been there before and would like any information they could provide. I was told that I could start setting up at 11:00 a.m. It would open at 12 p.m. I arrived at 10:45 a.m. and many people were already there, setting up. It was bedlam… the very definition of a three-man rush on a two-man outhouse! Everyone was running around and no one was directing traffic.
I asked for an organizer but couldn't find one. The tent had been set up with tables all around the walls of the tent. There was a pump hand-washing station at every table, along with thermometers and two-burner, countertop electric hotplates. Extension power cords were run everywhere, but none of them seemed to work. It was clear that those who had attended before knew the ropes. The rest of us had to fend for ourselves.
When the crew from the MacKnnon-Cann Inn showed up, they brought a long, heavy-duty extension cord. With that we were able to make a direct connection of our own to the power panel. They generously allowed me to plug the extension cord I had brought into theirs, so I was finally OK. After my crew lugged everything down from the car, we were ready to go.
There were two types of vendors at the food fair, professionals and amateur groups. It was very easy to tell the difference. Us "pros" set up quickly, using professional equipment. As an example, I had one steam food warmer. The amateur groups came in with every sort of heating unit imaginable. At the table next to me was an assortment of at least four table-top ovens and six slow-cookers. The amateur groups also were there to promote their culture through food. They were not interested in profit. They were practically giving way mounds of food. Some of the pros were also operating at a loss, using the event as a promotional event. In contrast, I was blatantly trying to make a buck, although even I dropped my price significantly, charging $5 when I usually charge $6.75 for a sandwich. Remember, it takes 32 hours from start to finish to offer a good pulled pork sandwich, including fresh coleslaw and fresh, homemade BBQ sauce.
As a quasi-professional, having attended several courses put on by the Nova Scotia Department of Agriculture, Food Safety Branch, and operating a booth at the Yarmouth Farmers' Market every Saturday, I fully understand the potential for disaster when food is served to the public. Food safety, both in preparation and service is vitally important. Being a relative noobie to the "pro food" world, I take food safety very, very seriously. I also understand the seriousness with which the food safety Inspectors take their work. Michelle Prendergast, our Food Safety Inspector, arrived shortly after 11 a.m. and immediately started inspecting. I was one of the last that she visited, and that was at approximately 11:30 a.m. I got her seal of approval. Unfortunately, several vendors did not. The organizers chose to delay opening the food tent until everyone was in compliance. This was their choice.
Finally, at approximately 12:45 p.m., the doors were opened and the mad rush began. It was clear instantly that the public was looking for "exotic" food, and quantity for the price was the order of the day. We did OK, but it was clear what the public was looking for. As well, one vendor was given what I would call special treatment. The first table visitors saw upon entering the tent was Mayor Pam Mood's small Lebanese table. Unfortunately, just beyond her, in a space eight to ten times larger than anyone else, was the Indian area, consisting of at least four tables, plus tons of operating space behind them. A crew of at least six, from what I understand, all imported from Halifax, prepared and served. They were a well-oiled machine. When I arrived at 10:45 a.m., they were all set up and ready to go. Clearly the 11 a.m. set-up didn't apply to them. The natural flow of traffic around the tent meant that I was the second last vendor that visitors saw, with plates already heaped and appetites waining. At the end, the vendor beside me was literally giving away food for free. Why would you pay $5 for a pulled pork sandwich when you could get a plate of salmon for nothing?
Points for the Organizers to Think On for Next Year
1. Create an information sheet listing requirements, what you will supply and what you are expected to supply. Include concise information about food safety requirements.
2. Have someone CLEARLY in charge, wearing an identification badge, on hand and available to greet vendors, answer questions and help.
3. Recognize that virtually every vendor will require electricity and plan accordingly. Adequate power should be available at all stations on arrival. Keeping food within the safety zone is the single most difficult task a vendor will have. Not being able to maintain temperatures on arrival was the cause of most of the problems this year.
4. If you advertise that you will be open to the public at 12 p.m. then you must!
5. I strongly urge you to make a separate entrance to the food tent. Some people are simply not interested in the entertainment… the come for the food!
6. Treat all vendors equally. No special treatment, especially for those you parachute in.
7. More room between the tables and the walls of the tent. Not enough room to operate. Personally I would also like a table behind me for storage and the hand-washing station. From a food safety perspective, it's not good for the public to be able to come in inadvertent contact with the food before it's served. No one had sneeze shields.
8. Do not blame others if something doesn't go according to your plan. If the food tent could not be opened on time because of food safety issues, it's NOT the Food Inspector's fault! They're just doing their extremely important job. You should do more to help amateur vendors meet the standard, or just send them home.
Gerry Curry
Gerry's BBQ
546 Cedar Lake Rd


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CORVALLIS -- A stout defensive effort led the Sutherlin Bulldogs to a 44-28 win against Seaside in the OSAA 4A girls basketball semifinals Friday at Gill Coliseum.
Sutherlin, the tournament's top seed, held the Seagulls to just 12 field goals and 2 for 9 from three-point range. Seaside's stellar 5-foot-10 freshman guard Maddi Utti scored just eight points, all in the first half. Utti ended the game shooting just 3 for 12.
On the offensive end, Sutherlin's Kayce Mock ruled the paint. She scored 13 points and pulled down seven rebounds to help the Bulldogs outscore Seaside 22-10 inside. Sutherlin guard Miranda Mendenhall led all scorers with 15 points on 4 of 8 shooting, including a pair of three-pointers.
The Bulldogs shot 41 percent from the field (16 of 39) and pulled down 13 offensive rebounds, turning those into 11 second-chance points.
With the win, Sutherlin will play for the 4A girls state championship, against La Salle Prep. Seaside falls into the third-place game, and will play Mazama.
--Billy Gates


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This past weekend I crashed my bike when I nearly collided with another cyclist on a recreational path.
It wasn't a particularly hard or fast accident (I cannot claim to have been doing a gnarly jump or anything), but I still ended up with a broken finger as well as several deep scratches and lurid bruises.
The bike, brand new and on her inaugural run, had nary a scratch.
Not five minutes earlier my husband and I had commented on how many kids (biking WITH their parents) did not have helmets on as they rode. I was certainly glad I had mine on as I went down, as well as gloves which protected most of my hands.So, I'm off my bike for at least a few weeks while the bones mend. My recent experience has made me think it's important, as the cycling season gears up, to remind everyone to bike safely.
And the most important safety tip – wear your helmet! I don't ever ride without one. I don't care if I look like a dork or my hair gets messed up … it's better than having my brains splattered out.
And there are some very cool designs on helmets out there, especially for kids.
You can make it a personal design statement if it's important to you. Here's a site when you can buy helmets that look like trendy hats: yakkay.com
Parents - there shouldn't be any fight from the kids if they see you are wearing one too. Make it as normal and instinctive an action as wearing a seatbelt in the car. (You DO wear a seatbelt, right?)
Here's the New Jersey code on wearing helmets, in case you haven't seen it before:
- All children under 17 years of age must wear a properly fitted and fastened bicycle helmet whenever they operate or ride a bicycle on open public property or areas used by the public for pedestrian or vehicular purposes. This applies to children riding in a "child carrier" restraining seat or in a trailer towed by a bicycle.
- The helmet must meet the standards of either the American National Standards Institute (ANSI Z90.4 bicycle helmet standard) or the Snell Memorial Foundation's 1990 Standard for Protective Headgear for Use in Bicycling. When purchasing a helmet, look inside for stickers that indicate it meets bicycle helmet testing standards.
- The ANSI Z90.4 standard means the manufacturer certifies that the helmet meets the minimum industry standard for impact protection. The blue Snell Memorial Foundation sticker indicates that the helmet has been tested by Snell and meets its much tougher standard.
- Municipalities may enact ordinances that create exemptions to the law in special situations where motor vehicle traffic is restricted.
- Children who violate the law shall receive a warning from police, and the parents or legal guardian may be fined up to $25 for a first offense, and up to $100 for repeat offenses.
- Vendors who sell or rent bicycles must provide customers a written explanation of the law, and must obtain the signature of the purchaser or renter that they have received this information. Places that rent bicycles must either provide or offer to rent a helmet to any customer under 17 who does not already have a helmet.
While the law applies only to children under 17, EVERYONE riding a bicycle should wear a helmet.


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Guilty plea in Martins Ferry shooting death
Commission will protect landmarks
BELLAIRE – Bellaire Village Council recently passed an ordinance establishing a historic landmarks commission for the village.
In part, this was brought about by the work being conducted by the Great Stone Viaduct Historical Education Society.
The commission will be tasked with providing for the "protection and enhancement of the distinctive character of the historic resources" of Bellaire.
Now, village leaders are on the hunt for members to join the commission's ranks.
The commission will consist of seven members, four of which must be residents of the village.
The remaining members may be non-residents who have personally engaged in active business enterprise of profession within the village during the previous five years from their appointment to the commission.
All members will be appointed by the mayor with the approval of village council, but only after a prior public notice has been given of the vacancy or appointment to be filled.
Dan Marling, Village Administrator for Bellaire, noted nominations will be accepted from the board of trustees of the Bellaire Glass Museum, the Great Stone Viaduct Historical Education Society and the Bellaire Area Chamber of Commerce.
Any nominations being submitted must be accompanied by a resume prepared by the nominee, outlining their qualifications to serve on the commission.
All nominees should have a recognized knowledge and interest in architectural preservation, design and history.
They should have ownerships of property in the village, along with a record of maintenance in compliance with all local building codes, zoning laws and safety and health regulations.
Initially, three members will be appointed for one year, two for two years and two for three years.
All subsequent terms shall be for a period of three years. Vacancies caused by death, resignation or otherwise will be filled for the unexpired term in the same manner as the original appointments.
The members of the commission will serve without compensation.
Marling asked that all nominations be turned into the village no later than Thursday, Oct. 31.
He noted the personnel committee of council will be the first line in the reviewing process, before council as a whole makes its recommendations to the mayor for appointment.


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MOUNT OLIVE — A 23-year-old Ledgewood man was arrested for possession of synthetic drugs, marijuana and drug paraphernalia at about 3 a.m. on Wednesday, Jan. 18, following a tip from a local business, police said.
Police responded to a business located along Route 46 in the Budd Lake section of the township for the report of a possible drug transaction and a description of a red BMW, police said.
Police spoke to the man, Brandon Bellini, and saw drug paraphernalia inside of the car, police said. Bellini was brought to police headquarters where he was charged with possession of toxic chemicals as well as possession of marijuana and drug paraphernalia, police said. He was released pending a court appearance, police said.


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The Fight Network is reporting that Min Soo Kim will replace K-1 veteran Hong Man Choi and face Brock Lesnar at the upcoming K-1 Dynamite!! USA card.
Lesnar was originally scheduled to face Hong Man Choi but the fight was scrapped after Choi failed to pass his medical tests put forth the California State Athletic Commission. Lesnar's new opponent, Min Soo Kim, sports a MMA record of 2-5 with victories over the likes of Sean O'Haire and Yoshihisa Yamamoto. Kim's five losses came to K-1's best Siala "Mighty Mo" Siliga, Semmy Schilt, Don Frye, Ray Sefo, and Bob Sapp.
It was also noted that Marvin Eastman vs. Ray Sefo was been removed from the card. K-1 Dynamite!! USA is scheduled to take place June 2nd at the Los Angeles Memorial Coliseum.
Next entry: Ex-Hippie Kid Jake Shields Set To Rock 'N Roll On ''Dynamite USA'' On June 2
Previous entry: Dan Henderson UFC Bound


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WorkSmart Staffing Agency is holding a job fair on Tuesday for a variety of manufacturing positions.
WorkSmart is recruiting for 50 positions including assembly, forklift drivers, machine operators, sewing, quality control, inspecting, call center and woodworking.
The fair goes from 9 a.m. until 3 p.m. at 1318 Haywood Road.


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Lawmaker, sheriff team up to take on gang violenceUPDATED 6:57 PM EDT Oct 22, 2013
After the shooting that paralyzed a young woman from Greenville, one lawmaker says more needs to be done.Video Transcript
UPSTATE SHERIFF... HAVE TEAMED UP ... TO TAKE ON GANG VIOLENCE ... IN A BIG WAY. NEWS 4'S... NIGEL ROBERTSON... JOINS US NOW WITH WHAT THEY ARE TRYING TO DO. NIGEL.... IN SOUTH CAROLINA... RIGHT NOW... THERE ARE LAWS ON THE BOOKS TO REDUCE GANG VIOLENCE. BUT AFTER... THE SHOOTING THAT PARALYZED A YOUNG WOMAN FROM GREENVILLE... IN FIVE POINTS IN COLUMBIA... ONE LAWMAKER SAID.... MORE NEEDS TO BE DONE... NOW. 18 YEAR OLD... MARTHA CHILDRESS... IS NOW IN AN ATLANTA HOSPITAL THAT SPECIALIZES IN SPINAL CORD INJURY. she rolled around in a wheel chair on sunday for the first time... sunday and it went find and then toward the end of it i think it hit her that that is what life is going to be like... and that was hard for her. TODAY... I TOLD HER UNCLE JIM CARPENTER... WHAT LAWMAKERS ARE PROPOSING AND HE SAYS MARTHA WILL BE THANKFUL. i am not going to point any fingers and blame anybody but the system has let her down. and we have to do something we cannot continue to have these problems. STATE REPRESENTATIVE PHYLLIS HENDERSON... AND GREENVILLE COUNTY SHERIFF STEVE LOFTIS ANNOUNCED A TEAM EFFORT TO REDUCE GANG VIOLENCE. this bill that we have basically says if you commit a crime and you go out and commit another violent crime while you are on bond or probation you will spend time in jail. AT LEAST 5 YEARS... THAT IS HENDERSON'S GOAL. COLUMBIA POLICE ARRESTED MICHAEL JUAN SMITH, 20, ON FIVE CHARGES, INCLUDING ASSAULT AND BATTERY OF A HIGH AND AGGRAVATED NATURE. POLICE SAY HE SHOT AT SOMEONE ELSE... AND THE BULLET HIT CHILDRESS FROM CLOSE TO 100 YARDS AWAY. SHERIFF LOFTIS... SAYS OFFICERS NEED TO HAVE THE ABILITY TO QUOTE PROFILE... PEOPLE WHO APPEAR TO BE INVOLVED IN GANG ACTIVITY. it is criminal profiling... or gang profiling. it is not racial profiling because racial profiling is against the law. ALL OF THIS... IS WHAT CARPENTER SAYS HIS FAMILY WAS HOPING FOR. i am glad they are moving on it... i hope its more than talk i think the time of just talking about it has past the time for action has come not just because of marthan because she is just one out of many. REPRESENTATIVE HENDERSON IS ALSO PROPOSING A MINIMUM BOND OF 50-THOUSAND DOLLARS FOR REPEAT GANG OFFENDERS. SHE ALSO WANTS TO GET TOUGHER ON JUDGES... WHO LET REPEAT OFFENDERS BACK OUT ON THE STREETS.
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Rebecca A. "Becky" Carr, 60, formerly of Logansport, Ind., passed away at 3:29 a.m. Monday, Aug. 20, 2012, at Woodlawn Hospital, Rochester.
Born Jan. 17, 1952, in Amsterdam, N.Y., she was the daughter of Howard and Grace Ellis Veeder. On Dec. 28, 1995, in Las Vegas, Nev., she was married to Larry Carr, who preceded her in death on Nov. 18, 2008.
Becky was a retired club manager at the VFW Post 3790. A member of the VFW Post 3790 Auxiliary, she enjoyed auto racing, gambling at the boats and trips to Las Vegas. She missed her dog, Dallas, who preceded her in death. Most especially, she enjoyed her grandchildren.
Surviving are a son, Lance Barton (Amy) of Logansport; stepson, Brent Carr (Jenny); stepdaughters, Donna Dawson (Tom), Flora, Diana Perez (Mannie) of Logansport, Deborah Corcoran of Martinsville, and Jennifer Long (Jamie); brothers, John Veeder (Barb) of Rome, N.Y., George Veeder (Betty) of Cazenovia, N.Y., Bruce Veeder (Yvonne) and Brian Veeder, and a sister, Ruth Yates (Les), all of Gloversville, N.Y. Also surviving are grandchildren, Seth Barton, Tyler Barton, Alexis Shepherd, Brandon Shepherd, Aaron Gibbs, Shelby Dawson, Tommy Corcoran, Sheldon Corcoran, Caitlyn Corcoran, Sydney Reed, Raymond Long, Emilie Sweet, Haleigh Sweet and Caleb Sweet; a great-granddaughter; and nieces and nephews.
A brother, Jerry Veeder and sister, Harriet Stack preceded her in death.


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Secretary of Agriculture Vilsack yesterday announced the appointment of Mary A. Hill, Jackson, Miss. (At-Large Public) to the National Fluid Milk Processor Promotion Board.
The term for this appointee begins July 1, and expires June 30, 2012. Hill will be seated at the board meeting July 16-18, along with the regular term appointees.
The National Fluid Milk Processor Promotion Board is composed of 15 fluid milk processors from 15 geographic regions and five at-large members. At least three at-large members must be fluid milk processors and at least one must be from the general public. The board was established by the Fluid Milk Promotion Act of 1990 to develop and administer a coordinated program of advertising and promotion to increase the demand for fluid milk products.
Source: USDA