How spammers are targeting blogs

Technology analyst Bill Thompson has been getting lots of comments on his weblogs, unfortunately most of the want to sell him Viagra. He has been "flyblogged".

Earlier this week I got an e-mail to tell me that someone called Levitra had commented on one of my entries on the VoxPolitics weblog.

Since it's a group weblog for "e-democracy titbits and crumbs", we get quite a few comments from random readers, and often they are useful and informative, so I read it with interest.

Sadly, it was not about the latest e-voting disasters in California - a topic of great interest to me - but a rather obvious piece of spam.

It said; "Interesting comments and a Superb Web Site" and then, like so many spam e-mails, had a link to a site that wanted to sell me a Viagra alternative.

Over the next few days I got 20 more, most offering Viagra substitutes but one featuring a cable TV scam - presumably for the times when I would have used up all my Viagra supplies.

Every one of them was posted as a comment on the blog, and they could only be removed individually through the administrative pages of the site, which takes ages.

It felt like the digital equivalent of flyposting - coming home one day to find your windows covered with posters for dodgy clubs and bands you have never head of.

Although the term flyblog has been used already to mean either blogging about flying, or blogging while flying, I would like to claim it for the practice of posting spam comments to people's blogs like this: I have just been comprehensively flyblogged.

Clever program

A quick online search revealed that the problem has been around for a while, but until recently it was largely done by individuals who would visit blogs and post their adverts, along with a link to whatever dodgy website they were promoting.

It had not happened to any of the sites I am involved with, so I had not noticed it or heard about it.

Now, however, it seems to have been automated: some clever programmer working for one of these iniquitous outfits has written a tool that goes around a list of weblogs and collects information on the various posts made to it.

It then creates the right HTML to fool the blogging software into thinking that a comment has been entered, and the resulting advert is posted to the blog as if it was legitimate.

That would explain why my colleague and fellow VoxPolitics poster James Crabtree is now getting 20 to 30 of these spam comments a day, reaching the point where he no longer has the time to remove them.

What is worse, there is no obvious way to block these posts without putting serious obstacles in the way of those who have legitimate comments to make.

Asking people to register before they post comments, or making them validate their comments by sending an e-mail and waiting for a reply, just get in the way. Building blacklists of sites that flyblog will be as ineffective as attempts to blackmail e-mail spam.

Blogs evolved out of a desire to remove barriers to online conversation, and restricting their ability to add comments would seriously reduce the sort of lively debate that makes them so interesting.

Perhaps the worst thing about flyblogging is that it is not covered by any of the spam laws that I am aware of, and probably is not illegal under data protection or hacking laws.

After all, a public blog with an accessible comments page is hardly a closed system, and even if you have an acceptable use policy saying what sort of postings you welcome, that is not legally binding either.

It is hard at first to see why the spammers are doing this. I am unlikely to be reading the comments on the latest mobile voting trials when I suddenly come across an advert for vicodin and feel so interested that I click on it.

Search rankings

One theory is that the real target is Google. A spammer's site with lots of references in well-indexed blogs will have a higher Google PageRank, so that anyone foolish enough to actually go searching for the product will find the spammer's site.

It is an interesting, but as yet unproven, hypothesis.

Whatever the reason, it is moving from a minor to major irritant. None of the other blogs I contribute to or run has been affected yet, but I can only assume it is a matter of time before the spammers move in, as they did first with UseNet and then with e-mail.

It depresses me to think that any open medium can be so easily undermined by people with no scruples, no sense of responsibility and no idea of the damage they are doing.

It also feels a lot more personal and intrusive than e-mail or UseNet spam.

A blog is a place to express your views in a public arena, and having some unknown people fill the space with advertising is the online equivalent of finding that someone has pinned a card advertising "private massage" to your coat when you were not looking.

I feel quite upset by this, and angrier with the spammers and their lack of respect for the principles of online co-operation than I have been for years.

Bill Thompson is a regular commentator on the BBC World Service programme Go Digital.
This is a part of article How spammers are targeting blogs Taken from "Levitra Compare Viagra" Information Blog

Pulmonary Hypertension, February 2006

Chest

Pulmonary Hemodynamic Responses to Brain Natriuretic Peptide and Sildenafil in Patients With Pulmonary Arterial Hypertension

Klinger JR, Thaker S, Houtchens J, Preston IR, Hill NS, Farber HW
Chest. 2006;129:417-425

Atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) are proteins that are expressed in the heart.[1] These peptides raise the intracellular cyclic guanosine monophosphate (cGMP) levels to cause vasorelaxation. Another benefit of these peptides is the inhibition of vascular smooth muscle proliferation.[2] Study results have demonstrated inhibition of pulmonary vasoconstriction in pulmonary arterial rings by these 2 peptides[3] and the development of increased pulmonary artery pressures when the gene for encoding of ANP is disrupted.[4] The exact hemodynamic response to these peptides in patients with pulmonary arterial hypertension (PAH) has not been adequately studied, but the use of natriuretic peptides in patients with left heart disease and chronic hypoxic lung disease has demonstrated a decrease in pulmonary artery pressure (PAP).

This study looks at the effect of BNP acutely on hemodynamics (compared with inhaled nitric oxide [iNO] and epoprostenol) in patients with PAH and then the effect on hemodynamics when the pohsphodiesterase-5 (PDE-5) inhibitor sildenafil is added. This open-label study ran from September 2002 to June 2003 and enrolled 13 patients. Inclusion criteria included mean PAP (mPAP) levels > 25 mm Hg at rest, and a World Health Organization class I PAH group. They also had to be de novo patients. All patients had a Swan-Ganz catheter placed and received epoprostenol and, in addition, 8 patients also received iNO. They then received 2 infusions of the human B-type natriuretic peptide nesiritide. The second infusion of nesiritide occurred 1 hour after a single dose of oral sildenafil.

Hemodynamics were evaluated at various points during each separate drug administration. Plasma BNP levels were also obtained. mPAP was 48.6 ± 3.7 mm Hg and mean pulmonary vascular resistance (PVR) was 698 ± 105 dynes·cm/s². The resultant findings were decreased mPAP with both iNO and epoprostenol and an increase in cardiac index and decrease in PVR with epoprostenol. The BNP infusion on its own did not affect mPAP or PVR. With 1 dose of sildenafil, the mPAP and PVR did drop below baseline, and the addition of BNP after the sildenafil dose resulted in a further decline in mPAP. The decrease in mPAP and PVR in this group remained visible for up to 6 hours after stopping the BNP infusion, signifying the longest duration of response of all the groups. Only 1 patient demonstrated a vasodilator response to epoprostenol or sildenafil alone, but 4 of 12 patients demonstrated a positive vasodilator response to sildenafil with BNP.

Increased circulating BNP levels may help slow right ventricular remodeling and may even inhibit the proliferation of pulmonary vascular smooth muscle. With their effect on endothelin synthesis (inhibition), the natriuretic peptides could improve the effects of endothelin receptor antagonists. What is uncertain here is the rationale for the lack of response (decreased mPAP and PVR) to the BNP infusion alone but the positive response when sildenafil was added. The authors believe that the dose or duration of the BNP infusion may not have been adequate. Further studies are needed to determine whether there is a place for chronic BNP therapy in the treatment of PAH.ReferencesHill NS, Klinger JR, Warburton RR, et al. Brain natriuretic peptide: possible role in the modulation of hypoxic pulmonary hypertension. Am J Physiol. 1994;266:L308-L315.Hutchison HG, Trindade PT, Cunanan DB, et al. Mechanisms of natriuretic-peptide-induced growth inhibition of vascular smooth muscle cells. Cardiovasc Res. 1997;35:158-167.Klinger JR, Warburton RR, Pietras L, et al. Brain natriuretic peptide attenuates the development of pulmonary hypertension in hypoxia-adapted rats. J Appl Physiol. 1998;84:1646-1652.Klinger JR, Warburton RR, Pietras L, et al. Genetic disruption of atrial natriuretic peptide causes pulmonary hypertension in normoxic and hypoxic mice. Am J Physiol. 1999;276:L868-L874.

Abstract
http://www.medscape.com/medline/abstract/16478861  Printer- Friendly Email This

Medscape Cardiology.  2006;10(1) ©2006 Medscape
This is a part of article Pulmonary Hypertension, February 2006 Taken from "Levitra Compare Viagra" Information Blog

Sexual Function in Men Treated for Symptomatic Benign Prostatic Hyperplasia

Abstract and Introduction

Abstract

We evaluated the effects of extended-release alfuzosin HCl 10 mg once daily (q.d.) on sexual function in men with lower urinary tract symptoms associated with benign prostatic hyperplasia (BPH). In a randomized, double-blind, placebo-controlled study of men aged ≥50 years, after a 28-day placebo run-in period, patients were randomized to receive alfuzosin 10 mg q.d. or matching placebo for 28 days. The mean change from baseline (day 1) in sexual function on day 29 was assessed using the Danish Prostate Symptom Score Sex (DAN-PSSsex) questionnaire. A total of 372 patients were randomized to receive alfuzosin (n=186) or placebo (n=186), with 355 completing the study. At baseline, 64% of the patients reported erectile dysfunction (ED) and 63% reported ejaculatory dysfunction (EjD). For the 320 patients who completed the DAN-PSSsex, alfuzosin treatment was associated with a significant improvement in the mean change from baseline in erectile function on day 29 compared with placebo (P=0.02). No significant difference was observed between the two treatment groups in the mean change from baseline in ejaculatory function on day 29. For patients with ED at baseline, a marginal improvement in erectile function was demonstrated with alfuzosin treatment (P=0.09 vs placebo). For patients with EjD at baseline, the mean change from baseline in ejaculatory function with alfuzosin was comparable to that with placebo. Dizziness was the most common adverse event with alfuzosin treatment (5 vs 0% with placebo), with other adverse events reported with comparable frequency in both treatment groups. After 1 month of treatment, alfuzosin 10 mg q.d. significantly improved erectile function in men with lower urinary tract symptoms/ benign prostatic hypertrophy and had no adverse effect on ejaculatory function.Introduction

Recent studies have demonstrated a significant association between lower urinary tract symptoms (LUTS) and sexual dysfunction in aging men.[1-4] In the Multinational Survey of the Aging Male (MSAM-7), which surveyed 12 815 men aged 50–80 years, sexual activity was reported by 83% of the respondents, with 71% reporting at least one episode of sexual activity in the past 4 weeks.[4] Data from the MSAM-7 revealed a high prevalence of both LUTS and sexual dysfunction in older men. Although the frequency of sexual activity decreased with age, sexual function was strongly and independently associated with the severity of LUTS.[4]

It has been proposed that increased α-adrenergic activity may be a common underlying pathophysiological mechanism for benign prostatic hypertrophy (BPH) symptoms (that is, LUTS), erectile dysfunction (ED) and ejaculatory dysfunction (EjD).[5] Thus, blocking α-adrenergic activity in the lower urinary tract may improve both LUTS associated with BPH and sexual dysfunction. In an open-label study of men with LUTS and sexual dysfunction, treatment for 1 year with alfuzosin 10 mg once daily (q.d.) improved both ED and EjD, as assessed with the Danish Prostate Symptom Score sex (DAN-PSSsex) questionnaire.[6]

Alfuzosin, a uroselective α1-adrenergic receptor antagonist (α-blocker) for the treatment of the symptoms of BPH, is distributed preferentially in the lower urinary tract versus vascular tissues.[7] By selectively blocking α1-adrenergic receptors, alfuzosin causes relaxation of smooth muscle in the bladder neck and prostate gland, thereby reducing LUTS and improving urine flow, with minimal effects on blood pressure and a low incidence of sexual side effects.

In 2003, an extended-release formulation of alfuzosin 10 mg q.d. was approved by the US Food and Drug Administration for the treatment of the signs and symptoms of BPH. Alfuzosin 10 mg q.d. was shown to be an effective and well-tolerated treatment for symptomatic BPH in three pivotal, placebo-controlled, clinical trials.[8-11] In these clinical trials, symptom relief during 12 weeks of treatment with alfuzosin 10 mg q.d. or placebo was first assessed at 4 weeks post-treatment using the International Prostate Symptom Score (IPSS) and measurements of peak urinary flow rate (Qmax). In a recent placebo-controlled crossover study, men with symptomatic BPH who were known responders to α-blockers demonstrated a significant improvement in Qmax as rapidly as 8 h after the initial dose of alfuzosin 10 mg q.d. compared with the initial dose of placebo.[12] The onset of this improvement in Qmax correlated with the previously reported peak plasma concentration of alfuzosin.[13]

The present study describes the effects of alfuzosin 10 mg q.d. versus placebo on erectile and ejaculatory function in men with symptomatic BPH. Previously published results of this study indicated that Qmax increased significantly from baseline within 24 h after the first dose of alfuzosin 10 mg q.d. compared with placebo, and this improvement was maintained on days 8 and 29.[14] In addition, significant improvements were observed in the total IPSS on day 8 and maintained on day 29 in patients treated with alfuzosin.  Printer- Friendly Email This

Int J Impot Res.  2007;19(5):480-485.  ©2007 Nature Publishing Group
This is a part of article Sexual Function in Men Treated for Symptomatic Benign Prostatic Hyperplasia Taken from "Levitra Compare Viagra" Information Blog