Injuries following a serious hydrofluoric acid leak: First aid and lessons.

Hydrofluoric acid is a dangerous inorganic acid that can cause local corrosion and systemic effects by ongoing absorption via the skin, mucosae, respiratory tract and digestive system. Recently, a serious toxic leak of low-concentration hydrofluoric acid solution occurred in the Pujiang area of Zhejiang Province, China. This accident resulted in 253 cases of chemical injury due to hydrofluoric acid exposure. Despite an immediate response by the local and provincial health-care system, as well as the local government, three people died due to acute poisoning and related complications. This article describes the events that took place leading to casualties as well as presenting the first-aid experience and the lessons learnt from this kind of mass injury.

Pioglitazone modulates the proliferation and apoptosis of vascular smooth muscle cells via peroxisome proliferators-activated receptor-gamma.

BACKGROUND: PPARγ is a member of the nuclear hormone receptor superfamily. It has been considered as a mediator regulating metabolism, anti-inflammation, and pro-proliferation in the Vascular Smooth Muscle Cells (VSMCs). Thiazolidinediones (TZDs), synthetic ligands of PPARγ, have anti-proliferative and pro-apoptotic effects on VSMCs, which prevent the formation and progression of atherosclerosis and restenosis following percutaneous coronary intervention (PCI). However, the underlying mechanism remains elusive. This present study therefore aimed to investigate the signaling pathway by which pioglitazone, one of TZDs, inhibits proliferation and induces apoptosis of VSMCs. METHODS: The effects of pioglitazone on VSMC proliferation and apoptosis were studied. Cell proliferation was determined using BrdU incorporation assay. Cell apoptosis was monitored with Hoechst and Annexin V staining. The expression of caspases and cyclins was determined using real-time PCR and Western blot. RESULTS: Pioglitazone treatment and PPARγ overexpression inhibited proliferation and induced apoptosis of VSMCs, whereas blocking by antagonist or silencing by siRNA of PPARγ significantly attenuated pioglitazone's effect. Furthermore, pioglitazone treatment or PPARγ overexpression increased caspase 3 and caspase 9 expression, and decreased the expression of cyclin B1 and cyclin D1 in VSMCs. CONCLUSIONS: Pioglitazone inhibits VSMCs proliferation and promotes apoptosis of VSMCs through a PPARγ signaling pathway. Up-regulation of caspase 3 and down-regulation of cyclins mediates pioglitazone's anti-proliferative and pro-apoptotic effects. Our results imply that pioglitazone prevents the VSMCs proliferation via modulation of caspase and cyclin signaling pathways in a PPARγ-dependent manner.

[Influence of recombinant human growth hormone on body fluid compartments and water-sodium retention in severe burn patients].

OBJECTIVE: To investigate the influence of recombinant human growth hormone (rhGH) on body fluid compartments and water-sodium retention in severe burn patients. METHODS: Thirty adult patients with severe burn were divided into treatment (T) and control (C) groups by block randomized design. Patients in both groups were subcutaneously injected with same amount of rhGH (12 IU/d) or isotonic saline during 7 - 21 post burn day (PBD). The total body water (TBW), intracellular water (ICW), extracellular water (ECW) were measured by bioelectrical impedance analysis (BIA) on 7, 14, 21 PBD. The 24 h urinary output of Na+ was determined by ion selective electrode method (ISE). RESULTS: There were no significant difference in levels of TBW, ICW, ECW and 24 h urinary output of Na+ between two groups on 7, 14, 21 PBD (P > 0.05). No difference in results was found between groups at different time points (P > 0.05). After the data were analyzed, the level of TBW (36 +/- 6 L), ICW (21 +/- 4 L) on 21 PBD were evidently lower than those on 7 PBD (38 +/- 6 L, 23 +/- 7 L, P < 0.01). CONCLUSION: The level of ICW and TBW in severe burn patients decreased along with the time. Proper dosage of rhGH has no significant effect on body fluid compartments and water-sodium retention.

Diagnosis of visceral leishmaniasis by enzyme-linked immunosorbent assay using urine samples.

A diagnostic method has been developed to detect anti-Leishmania donovani immunoglobulin G (IgG) in urine by enzyme-linked immunosorbent assay (ELISA). In measuring anti-L. donovani IgG, IgA, and IgM in urine, the method performed best in the detection of IgG. The sensitivity and specificity of the assay were determined with panels of urine samples from 62 visceral leishmaniasis (VL) patients, 59 healthy controls from areas of endemicity, 53 healthy controls from areas of nonendemicity, 59 malaria patients, 13 tuberculosis patients, 23 cutaneous leishmaniasis patients, and 7 patients with other diseases. Using L. donovani promastigote crude antigen, the test had 93.5% sensitivity (58 positives of 62 VL patient samples) and 89.3% specificity (191 negatives of 214 non-VL patient samples). The ELISA with acetone-treated L. donovani promastigote antigen raised the sensitivity and specificity to 95.0 and 95.3%, respectively. Western blot analysis revealed that most of the samples that cross-reacted with crude antigen in ELISA did not recognize any antigenic component of L. donovani crude antigen. We also checked 40 serum samples from the same group of VL patients for anti-L. donovani IgG and got 90.0% sensitivity with both crude and acetone-treated antigens. As collection of urine is much easier than collection of serum, the detection of anti-L. donovani IgG in urine with acetone-treated antigen will be useful in epidemiological studies. It could be an adjunct of laboratory diagnosis.