Insulin resistance is highly prevalent in pulmonary arterial hypertension (PAH) patients. However, the long-term impact of diabetes mellitus (DM) on survival in PAH is unclear. Insulin resistance and DM are associated with left ventricular steatosis and dysfunction, but whether the right ventricle (RV) might be affected by DM in PAH is unknown. We hypothesized that PAH patients with DM would have worse survival than PAH patients without DM and that this would be due to impaired RV compensation. From a large registry of PAH patients at our institution, we analyzed the effect of DM on survival in patients with idiopathic or heritable PAH. Clinical and hemodynamic differences were compared between PAH patients with DM and those without DM. Twenty-nine patients with DM and 84 without DM were included. Gender, body mass index, PAH type and duration, and 6-minute walk distance were similar between groups. PAH patients with DM had significantly lower survival at 10 years than PAH patients without DM. Right atrial pressure, pulmonary arterial pressure, and cardiac output did not differ significantly between the two groups. However, right ventricular stroke work index (RVSWI) was lower in the PAH DM group than in the no-DM patients. Among PAH patients with DM, patients who died had a lower RVSWI than survivors. In conclusion, survival in PAH patients with DM was reduced compared to that of patients without DM; impaired RV compensation may underlie this finding. Further study is needed to understand this effect.

The majority of pulmonary arterial hypertension (PAH) is not associated with BMPR2 mutation, and major risk factors for idiopathic PAH are not known. The objective of this study was to identify a gene expression signature for IPAH. To accomplish this, we used Affymetrix arrays to probe expression levels in 86 patient samples, including 22 healthy controls, 20 IPAH patients, 20 heritable PAH patients (HPAH), and 24 BMPR2 mutation carriers that were as yet unaffected (UMC). Culturing the patient cells removes the signatures of drug effects and inflammation which have made interpretation of results from freshly isolated lymphocytes problematic. We found that gene expression signatures from IPAH patients clustered either with HPAH patients or in a single distinct group. There were no groups of genes changed in IPAH that were not also changed in HPAH. HPAH, IPAH, and UMC had common changes in metabolism, actin dynamics, adhesion, cytokines, metabolism, channels, differentiation, and transcription factors. Common to IPAH and HPAH but not UMC were an upregulation of vesicle trafficking, oxidative/nitrosative stress, and cell cycle genes. The transcription factor MSX1, which is known to regulate BMP signaling, was the most upregulated gene (4×) in IPAH patients. These results suggest that IPAH cases have a shared molecular origin, which is closely related to, but distinct from, HPAH. HPAH and IPAH share the majority of altered signaling pathways, suggesting that treatments developed to target the molecular etiology of HPAH will also be effective against IPAH.

Baseline serum samples from 2815 human immunodeficiency virus (HIV)-positive and 963 HIV-negative women enrolled in 2 cohort studies were tested for immunoglobulin G antibodies to human papillomavirus type 16 (HPV-16) capsids. HPV-16 seropositivity was associated with lifetime number of sex partners (P<.001) among both HIV-positive and HIV-negative women. Approximately 50%-60% of HPV-16 DNA-positive women were HPV-16 positive. HPV-16 seropositivity was associated with HIV infection; however, after adjustment for baseline cervical HPV infection and disease, the association disappeared. Thus, the high seroprevalence of HPV-16 among HIV-positive women may be explained by a high prevalence of HPV of all types. Approximately 50% of HIV-positive women had serological evidence of prior HPV-16 infection, but only approximately 5% had an HPV-16 cervical infection at baseline. Despite the higher prevalence of HPV infection in this group, most HIV-positive women are able to control HPV-16 replication at the cervix, and reactivation, if it occurs, is not very common.

For the Malay-Thai Peninsula several sea-level curves for the younger Holocene, based on field evidence as well as on hydro-isostatic modelling of a far-field site, have been published. The general assumption is a rapid rise to a mid-Holocene maximum up to +5 m above present sea level, followed by a constant or oscillating regression. However, from the Andaman Sea coast of Thailand, which was affected by the 2004 tsunami, only isolated observations are available regarding Holocene sea levels. Thus, the timing and magnitude of the Holocene highstand as well as the course of the regression remain to be defined. As several palaeotsunamis could be detected in the meantime it is important to know the related sea levels as exactly as possible to judge the energy, inundation width and potential wave height of these events. Therefore, fixed biological indicators from the rocky coasts of the Phang-nga Bay and Phuket, as well as morphological indicators from beach-ridge and swale sequences along the exposed west coast (Ko Phra Thong) were studied, to gain information about the Holocene sea-level development in this region. While oyster and coral data from the Phang-nga Bay and Phuket document a Holocene maximum of +2.6 m at 5700 cal. BP, the ridge crests and swale bases in the northwest of the study area point to maximum heights of +1.5–2.0 m above the present level around 5300 years ago. During the last 3000 years, to when the largest part of the Holocene palaeotsunami deposits from Thailand was dated, relative sea levels (RSL) in both areas did not exceed +1.5 m.

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