<b>Microwave-assisted oxidation of alcohols and polyarenes with tetramethylammonium Fluorochromate</b>

An efficient and mild method for the oxidation of alcohols and polyarenes is described using tetramethylammonium fluorochromate (TMAFC) under microwave irradiation

Predictive value of the cow&#x2032;s milk skin prick test in infantile colic

Background and Objectives : Infantile colic is a common problem among young infants. Cow&#x2032;s milk allergy has been suggested as one of the causes. We aimed to investigate the value of the cow&#x2032;s milk skin test for the diagnosis of cow&#x2032;s milk allergy in exclusively breast-fed infants with infantile colic. Methods : Exclusively breast-fed infants with infantile colic were enrolled in this study. On the first visit, the average hours of crying of the infant in a 24-h period were recorded and the cow&#x2032;s milk skin test was performed. If the infant had a positive skin test, elimination of cow&#x2032;s milk from the mothers&#x2032; diet was advised. Infants with negative skin tests were divided into case and control groups. Cow&#x2032;s milk was eliminated from the diet of mothers in the case group. After 2 weeks, the number of hours of crying were recorded again. The reduction in the crying hours was compared between the two groups using the chi-square test. Results : Skin tests were positive in 3 of 114 cases (2.6&#x0025;) of infantile colic. All three cases recovered completely following elimination of cow&#x2032;s milk from the mother&#x2032;s diet. Among the 111 patients with negative skin tests, 77 patients completed the study: 35 in the case group and 42 in the control group. The reduction in crying hours in infants in the case group was not significantly different from that in the control group. Conclusion : Elimination of cow&#x2032;s milk from the mothers&#x2032; diet is not beneficial for infants with a negative skin test. Infants with a positive skin test may benefit from this management

Prevalence of Fungal Drug Resistance in COVID-19 Infection: a Global Meta-analysis

Purpose Secondary bacterial or fungal infections are one of the most important medical complications among patients with Coronavirus Disease 2019 (COVID-19). The emergence of multidrug-resistant (MDR) candida can cause many problems such as treatment failure, adverse clinical outcomes, and even disease outbreaks. This systematic review and meta-analysis aims to investigate the prevalence and outcomes of fungal drug-resistant in COVID-19 patients. Methods PubMed, Embase, Scopus, Cochrane Library, and Web of Science databases were searched for peer reviewed-articles published in English up to May 20, 2021. Heterogeneity across studies was evaluated using Cochrane's Q test and the I-2 index. The pooled point prevalence and their corresponding 95% confidence intervals (CIs) were considered to estimate the prevalence of fungal drug resistance infection in COVID-19 patients. Results Eight eligible articles were included in our meta-analysis. The number of COVID-19 patients with fungal co-infection varied from 5 to 35 among selected studies. The overall pooled prevalence of fungal drug resistance among patients with co-infections of fungal and COVID-19 was 69% (95% CI: 37%, 94%) by using a random-effects model. In terms of specific species, the pooled meta-analysis for Candida Auris was estimated to be 100% (95%CI: 98%, 100%; I-2 = 0%), for MultiCandida 59% (95%CI: 38%, 79%; I-2 = 12.5%), and for Aspergillus 15% (95%CI: 0%, 42%; I-2 = 0%). Conclusion Our study shows the high prevalence of fungal drug resistance in COVID-19 patients and emphasizes the need to strengthen antimicrobial stewardship programs, close monitoring for treatment failure, and the emergence of resistance upon treatment

Table1_A pathogenic variant of TULP3 causes renal and hepatic fibrocystic disease.XLSX

Patient variants in Tubby Like Protein-3 (TULP3) have recently been associated with progressive fibrocystic disease in tissues and organs. TULP3 is a ciliary trafficking protein that links membrane-associated proteins to the intraflagellar transport complex A. In mice, mutations in Tulp3 drive phenotypes consistent with ciliary dysfunction which include renal cystic disease, as part of a ciliopathic spectrum. Here we report two sisters from consanguineous parents with fibrocystic renal and hepatic disease harboring a homozygous missense mutation in TULP3 (NM_003324.5: c.1144C>T, p.Arg382Trp). The R382W patient mutation resides within the C-terminal Tubby domain, a conserved domain required for TULP3 to associate with phosphoinositides. We show that inner medullary collecting duct-3 cells expressing the TULP3 R382W patient variant have a severely reduced ability to localize the membrane-associated proteins ARL13b, INPP5E, and GPR161 to the cilium, consistent with a loss of TULP3 function. These studies establish Arginine 382 as a critical residue in the Tubby domain, which is essential for TULP3-mediated protein trafficking within the cilium, and expand the phenotypic spectrum known to result from recessive deleterious mutations in TULP3.</p

Table2_A pathogenic variant of TULP3 causes renal and hepatic fibrocystic disease.DOCX

Patient variants in Tubby Like Protein-3 (TULP3) have recently been associated with progressive fibrocystic disease in tissues and organs. TULP3 is a ciliary trafficking protein that links membrane-associated proteins to the intraflagellar transport complex A. In mice, mutations in Tulp3 drive phenotypes consistent with ciliary dysfunction which include renal cystic disease, as part of a ciliopathic spectrum. Here we report two sisters from consanguineous parents with fibrocystic renal and hepatic disease harboring a homozygous missense mutation in TULP3 (NM_003324.5: c.1144C>T, p.Arg382Trp). The R382W patient mutation resides within the C-terminal Tubby domain, a conserved domain required for TULP3 to associate with phosphoinositides. We show that inner medullary collecting duct-3 cells expressing the TULP3 R382W patient variant have a severely reduced ability to localize the membrane-associated proteins ARL13b, INPP5E, and GPR161 to the cilium, consistent with a loss of TULP3 function. These studies establish Arginine 382 as a critical residue in the Tubby domain, which is essential for TULP3-mediated protein trafficking within the cilium, and expand the phenotypic spectrum known to result from recessive deleterious mutations in TULP3.</p