EVALUATION OF WOUND HEALING POTENTIAL OF RUMEX VESICARIUS L. LEAF EXTRACT AND FRACTIONS IN RABBIT

Background: Rumex vesicarius Linn leaf extract is extensively used in folk medicine for the wound cure in sub-continent, but there is no pharmacological evidence present in support of this practice. The present study was conducted to validate the folkloric use of Rumex vesicarius on experimentally induced excision wounds in rabbits. Phytochemical constituents were also evaluated. Material and Methods: Aqueous and methanol fractions of R.vesicarius leaf extracts were prepared and analysed for the possible presence of major phytochemical classes. A 20% w/v gel of each extract (Methanol, Aqueous) was made using Cabopol 940 in the concentration of 5%. wounds were produced experimentally in normal rabbit’s dorsal region of back under ketamine anesthesia. The decrease in wound size was judged by using a scale. Povidone- Iodine treated group was taken as standard while untreated group was taken as control. Results: Aqueous fraction (200mg/kg) showed 92.34% maximum percentage of wound healing compared to control, while, 79.71% wound healing with methanol fraction (200mg/kg). Both the extracts were found to be statistical significant and comparable to control. Furthermore, wound healing activity was found to be better than standard (Povidone-iodine) treated group which may be attributed to the faster action of the active Phytochemical constituent and their multiple mechanisms. Conclusion: we concluded that R.vesicarius posses good wound healing activity and can be use as alternative medicine for wound care

Lunapark deficiency leads to an autosomal recessive neurodevelopmental phenotype with a degenerative course, epilepsy and distinct brain anomalies

LNPK encodes a conserved membrane protein that stabilizes the junctions of the tubular endoplasmic reticulum network playing crucial roles in diverse biological functions. Recently, homozygous variants in LNPK were shown to cause a neurodevelopmental disorder (OMIM#618090) in four patients displaying developmental delay, epilepsy and nonspecific brain malformations including corpus callosum hypoplasia and variable impairment of cerebellum. We sought to delineate the molecular and phenotypic spectrum of LNPK-related disorder. Exome or genome sequencing was carried out in 11 families. Thorough clinical and neuroradiological evaluation was performed for all the affected individuals, including review of previously reported patients. We identified 12 distinct homozygous loss-of-function variants in 16 individuals presenting with moderate to profound developmental delay, cognitive impairment, regression, refractory epilepsy and a recognizable neuroimaging pattern consisting of corpus callosum hypoplasia and signal alterations of the forceps minor ('ear-of-the-lynx' sign), variably associated with substantia nigra signal alterations, mild brain atrophy, short midbrain and cerebellar hypoplasia/atrophy. In summary, we define the core phenotype of LNPK-related disorder and expand the list of neurological disorders presenting with the 'ear-of-the-lynx' sign suggesting a possible common underlying mechanism related to endoplasmic reticulum-phagy dysfunction

Diversity and nutritional properties of Pakistani dates: implications for sustainable value chain and decent living perspectives of rural households

International Center for Development and Decent Work (ICDD, German

Socio-economic characterisation of date palm (Phoenix dactylifera L.) growers and date value chains in Pakistan

Gefördert durch den Publikationsfonds der Universität Kasse

Facile Synthesis of NH-Free 5-(Hetero)Aryl-Pyrrole-2-Carboxylates by Catalytic C–H Borylation and Suzuki Coupling

A convenient two-step preparation of NH-free 5-aryl-pyrrole-2-carboxylates is described. The synthetic route consists of catalytic borylation of commercially available pyrrole-2-carboxylate ester followed by Suzuki coupling without going through pyrrole N–H protection and deprotection steps. The resulting 5-aryl substituted pyrrole-2-carboxylates were synthesized in good- to excellent yields. This synthetic route can tolerate a variety of functional groups including those with acidic protons on the aryl bromide coupling partner. This methodology is also applicable for cross-coupling with heteroaryl bromides to yield pyrrole-thiophene, pyrrole-pyridine, and 2,3’-bi-pyrrole based bi-heteroaryls

Isolation and Identification of Common Contaminants Bacteria from Working Area in Microbiology Laboratory

Abstract: Frequent environmental contaminants within microbiology laboratory create not only diagnostic quandaries but also poses major risk for health care workers and patients. Objective of our study was to isolate and identify the common laboratory contaminant bacteria with an ultimate goal to reduce false positive culture reports as well as Laboratory acquired infections. The study was conducted in laboratory of Microbiology Department Kohat University of Science and Technology Kohat from March 2014 to June 2014. Total 5 samples were collected from different areas of laboratory including table, floor, clothing, air, and incubator. Out of 5 collected samples, growth was observed. Out of 5 culture positive samples total 22 bacterial contaminants were isolated and identified by various biochemical tests. Out of 22 bacterial contaminants, 8 (36.36%) was Staphylococcus epidermis's which was the most common contaminants. 7 (31.81%) was Bacillus subtilis which was the second most common contaminants. 4 (18.18%) was Staphylococcus aerous while 3 (13.63%) was Deptheriods which showed minimum bacterial contaminants. Precaution should be taken to get rid of these organisms from laboratory by means of proper laboratory disinfection and sterilization as well as personal hygiene of laboratory workers. From our study we conclude that laboratory can be a potential source of contamination to give false positive results

Lunapark deficiency leads to an autosomal recessive neurodevelopmental phenotype with a degenerative course, epilepsy and distinct brain anomalies

Abstract: LNPK encodes a conserved membrane protein that stabilizes the junctions of the tubular endoplasmic reticulum network playing crucial roles in diverse biological functions. Recently, homozygous variants in LNPK were shown to cause a neurodevelopmental disorder (OMIM#618090) in four patients displaying developmental delay, epilepsy, and non-specific brain malformations including corpus callosum hypoplasia and variable impairment of cerebellum. We sought to delineate the molecular and phenotypic spectrum of LNPK-related disorder. Exome or genome sequencing was carried out in eleven families. Thorough clinical and neuroradiological evaluation was performed for all the affected individuals, including review of previously reported patients. We identified twelve distinct homozygous loss-of-function variants in sixteen individuals presenting with moderate to profound developmental delay, cognitive impairment, regression, refractory epilepsy and a recognizable neuroimaging pattern consisting of corpus callosum hypoplasia and signal alterations of the forceps minor (“ear-of-the-lynx” sign), variably associated with substantia nigra signal alterations, mild brain atrophy, short midbrain, and cerebellar hypoplasia/atrophy. In summary, we define the core phenotype of LNPK-related disorder and expand the list of neurological disorders presenting with the “ear of the lynx” sign suggesting a possible common underlying mechanism related to endoplasmic reticulum-phagy dysfunction

Biallelic variants in PCDHGC4 cause a novel neurodevelopmental syndrome with progressive microcephaly, seizures, and joint anomalies

Purpose We aimed to define a novel autosomal recessive neurodevelopmental disorder, characterize its clinical features, and identify the underlying genetic cause for this condition. Methods We performed a detailed clinical characterization of 19 individuals from nine unrelated, consanguineous families with a neurodevelopmental disorder. We used genome/exome sequencing approaches, linkage and cosegregation analyses to identify disease-causing variants, and we performed three-dimensional molecular in silico analysis to predict causality of variants where applicable. Results In all affected individuals who presented with a neurodevelopmental syndrome with progressive microcephaly, seizures, and intellectual disability we identified biallelic disease-causing variants in Protocadherin-gamma-C4 (PCDHGC4). Five variants were predicted to induce premature protein truncation leading to a loss of PCDHGC4 function. The three detected missense variants were located in extracellular cadherin (EC) domains EC5 and EC6 of PCDHGC4, and in silico analysis of the affected residues showed that two of these substitutions were predicted to influence the Ca2+-binding affinity, which is essential for multimerization of the protein, whereas the third missense variant directly influenced the cis-dimerization interface of PCDHGC4. Conclusion We show that biallelic variants in PCDHGC4 are causing a novel autosomal recessive neurodevelopmental disorder and link PCDHGC4 as a member of the clustered PCDH family to a Mendelian disorder in humans

PIGG variant pathogenicity assessment reveals characteristic features within 19 families.

PURPOSE: Phosphatidylinositol Glycan Anchor Biosynthesis, class G (PIGG) is an ethanolamine phosphate transferase catalyzing the modification of glycosylphosphatidylinositol (GPI). GPI serves as an anchor on the cell membrane for surface proteins called GPI-anchored proteins (GPI-APs). Pathogenic variants in genes involved in the biosynthesis of GPI cause inherited GPI deficiency (IGD), which still needs to be further characterized. METHODS: We describe 22 individuals from 19 unrelated families with biallelic variants in PIGG. We analyzed GPI-AP surface levels on granulocytes and fibroblasts for three and two individuals, respectively. We demonstrated enzymatic activity defects for PIGG variants in vitro in a PIGG/PIGO double knockout system. RESULTS: Phenotypic analysis of reported individuals reveals shared PIGG deficiency-associated features. All tested GPI-APs were unchanged on granulocytes whereas CD73 level in fibroblasts was decreased. In addition to classic IGD symptoms such as hypotonia, intellectual disability/developmental delay (ID/DD), and seizures, individuals with PIGG variants of null or severely decreased activity showed cerebellar atrophy, various neurological manifestations, and mitochondrial dysfunction, a feature increasingly recognized in IGDs. Individuals with mildly decreased activity showed autism spectrum disorder. CONCLUSION: This in vitro system is a useful method to validate the pathogenicity of variants in PIGG and to study PIGG physiological functions.RD&E staff can access the full-text of this article by clicking on the 'Additional Link' above and logging in with NHS OpenAthens if prompted.Accepted version (6 month embargo), submitted versio