Enhanced Inactivation of <i>Cryptosporidium parvum</i> Oocysts during Solar Photolysis of Free Available Chlorine

Solar irradiation of aqueous solutions containing free available chlorine (FAC) dramatically enhances inactivation of <i>Cryptosporidium parvum</i> oocysts compared to FAC or sunlight alone. In pH 8, 10 mM phosphate buffer at 25 °C, exposure to FAC alone yields no oocyst inactivation at <i>CT</i>_FAC ≤ 832 (mg min) L^–1, while exposure to simulated sunlight alone for 60 min yields <0.5 log inactivation. In contrast, exposure to simulated sunlight for 60 min in the presence of [FAC]₀ = 8 mg L^–1 as Cl₂ results in photolytic decomposition of FAC to ∼1 mg L^–1 as Cl₂ [yielding <i>CT</i>_FAC ∼ 200 (mg min) L^–1] accompanied by >2 log oocyst inactivation. Similar enhancement effects are observed in natural water under natural sunlight. Experiments undertaken in the presence of the reactive oxygen species (ROS) scavenger <i>tert</i>-butanol or in the absence of oxygen indicate that these enhancements are due to in situ ROS and ozone production via FAC photolysis

Enhanced Inactivation of <i>Bacillus subtilis</i> Spores during Solar Photolysis of Free Available Chlorine

Aqueous free available chlorine (FAC) can be photolyzed by sunlight and/or artificial UV light to generate various reactive oxygen species, including HO^• and O­(³P). The influence of this chemistry on inactivation of chlorine-resistant microorganisms was investigated using <i>Bacillus subtilis</i> endospores as model microbial agents and simulated and natural solar radiation as light sources. Irradiation of FAC solutions markedly enhanced inactivation of <i>B. subtilis</i> spores in 10 mM phosphate buffer; increasing inactivation rate constants by as much as 600%, shortening inactivation curve lag phase by up to 73% and lowering <i>CT</i>s required for 2 log₁₀ inactivation by as much as 71% at pH 8.0 and 10 °C. Similar results were observed at pH 7.4 and 10 °C in two drinking water samples with respective DOC concentrations and alkalinities of 0.6 and 1.2 mg C/L and 81.8 and 17.1 mg/L as CaCO₃. Solar radiation alone did not inactivate <i>B. subtilis</i> spores under the conditions investigated. A variety of experimental data indicate that the observed enhancements in spore inactivation can be attributed to the concomitant attack of spores by HO^• and O₃, the latter of which was found to accumulate to micromolar concentrations during simulated solar irradiation of 10 mM phosphate buffer (pH 8, 10 °C) containing [FAC]₀ = 8 mg/L as Cl₂

Novel Mutations in <i>FKBP10</i> and <i>PLOD2</i> Cause Rare Bruck Syndrome in Chinese Patients

<div><p>Bruck syndrome (BS) is an extremely rare form of osteogenesis imperfecta characterized by congenital joint contracture, multiple fractures and short stature. We described the phenotypes of BS in two Chinese patients for the first time. The novel compound heterozygous mutations c.764_772dupACGTCCTCC (p.255_257dupHisValLeu) in exon 5 and c.1405G>T (p.Gly469X) in exon 9 of <i>FKBP10</i> were identified in one proband. The novel compound heterozygous mutations c.1624delT (p.Tyr542Thrfs*18) in exon 14 and c.1880T>C (p.Val627Ala) in exon 17 of <i>PLOD2</i> were identified in another probrand. Intravenous zoledronate was a potent agent for these patients, confirmed the efficacy of bisphosphonates on this disease. In conclusion, the novel causative mutations identified in the patients expand the genotypic spectrum of BS.</p></div

Pedigree of the two families displaying Bruck syndrome and mutation analysis.

<p>Probands are indicated by the arrows. Black symbols indicate individuals with Bruck syndrome; shadow symbols represent carriers. (A) In proband 1, novel compound heterozygous mutations of <i>FKBP10</i> were identified as: c.764_772dupACGTCCTCC (p.255_257dupHisValLeu) in exon 5 and c.1405G>T (p.Gly469X) in exon 9. (B) In proband 2, novel compound heterozygous mutations of <i>PLOD2</i> were identified as: c. 1624delT (p.Tyr542Thrfs*18) in exon 14 and c.1880T>C (p.Val627Ala) in exon 17. The probands' parents were both asymptomatic heterozygous carriers for the compound mutations, respectively.</p

Mutation information of <i>FKBP10</i> and <i>PLOD2</i>.

<p>(A) Representation of FKBP65 with the location of mutations in proband 1 (black arrows). (B) The whole stretch sequence around Leu258 is highly conserved in FKBP65 among 14 different species. Red arrow indicates position of p.255_257dupHisValLeu mutation. (C) Blue boxes indicate all exons of <i>FKBP10</i>. Mutations were identified in <i>FKBP10</i> in patients with Bruck syndrome and osteogenesis imperfecta. The two kinds of mutations in our study are shown in red. (D) Blue boxes indicate all exons of <i>PLOD2</i>. Mutations were identified in <i>PLOD2</i> in patients with Bruck syndrome and osteogenesis imperfecta. The two kinds of mutations in this study are shown in red. Mutation in exon 17 of proband 2 will lead to change of amino acid in lysyl hydroxylase at highly conserved among 11 different species.</p

Clinical phenotypes in probands with Bruck syndrome.

<p>For proband 1, (A)–(B) severe flexion deformity of knees (white arrows); (C) small joint laxity of hand and scar of orthopedic surgery for correcting thumb-in-palm deformity (white arrow). For proband 2, (D) left pes equinovarus and invisible right fourth toe because of camptodactyly (white arrow); (E) congenital joint contracture of right elbow and camptodactyly of right thumb (white arrows); (F) camptodactyly of fourth toes (white arrows); (G) mild camptodactyly of left 3–4th fingers and right thumb, 4–5 fingers (white arrows); (H) limited movement of knees and invisible right fourth toe from this view (white arrows); (I) severe ithyokyphosis.</p

Clinical characteristics of the two patients with BS.

<p>BS, Bruck syndrome; TALP, total alkaline phosphatase; β-CTX, β-isomerized carboxy-telopeptide of type I collagen; ALT, alanine aminotransferase; PTH, parathyroid hormone; 25(OH)D, 25 hydroxy vitamin D; L2–L4, lumbar spine 2–4; FN, femoral neck; TH, total hip.</p><p>Clinical characteristics of the two patients with BS.</p

Radiological findings in the two probands with Bruck syndrome.

<p>For proband 1, (A) occipital wormian bone (white arrow); (B) scoliosis (black arrow) and thoracic cage collapse (white arrows); (C)–(D) slender femur with thin cortices (black arrow), metaphyseal enlargement of distal femur (white arrow) and old fracture (white arrow); (E) old fractures and bending of femora (black arrows), severe deformity of pelvis and osteoporosis. For proband 2, (F) occipital wormian bone (white arrow); (G) embedded fracture of right distal femur (white arrow); (H) multiple vertebral compression fractures (white arrows) and ithyokyphosis; (I) rotation kyphoscoliosis (white arrow), indistinct ribs and thoracic cage collapse; (J) severe deformity of pelvis and osteoporosis.</p