مولوی قاضی ظہور الحق
اس سلسلہ میں ہمیں اپنے مخلص اورجواں مرگ دوست مولوی قاضی ظہور الحق صاحب کی یاد بھی آرہی ہے۔مرحوم نجیب آباد کے ایک قصبہ جلال آباد کے رئیس اعظم اوردارالعلوم دیوبند کے فارغ التحصیل تھے، خوب رواورخوش خو تھے۔ ندوۃ المصنفین سے دلی عقیدت وارادت رکھتے تھے۔رئیس ہونے کے باوجود احکام مذہبی کے سخت پابند گویا صحیح معنٰی میں جوان صالح تھے۔امور خیروصلاح میں ہمیشہ سابقون اولون کی صف میں رہتے تھے۔پورے خاندان کے واحدمربی اور سرپرست تھے۔تندرستی لائق رشک تھی، مگر چند ماہ سے پھیپھڑوں میں پانی اتر آیا تھا،اس کا آپریشن کرایا گیا جو آخرکار گزشتہ ماہ قید ہستی سے ہی نجات کاسبب بنا۔ عمر۳۴۔۳۵سال کے لگ بھگ تھی۔حق تعالیٰ مرحوم کواپنی رحمت ومغفرت کے دامن میں جگہ عطافرمائے۔آمین۔ [اپریل ۱۹۴۲ء]
Performance is the work result in quality and quantity achieved by employees in carrying out their duties in accordance with the responsibilities assigned to them. The role of reliable and professional employees is very helpful in improving organizational performance. This study aims to analyze the relationship between Work Engagement and Quality of Work Life with the Performance of Nurses in Inpatient Services in Makassar City Hospital. This type of research is a quantitative study using an observational study with a cross-sectional study design. Sampling using stratified random sampling so that the sample in this study were nurses in the inpatient installation of Makassar City Hospital, totaling 167 respondents. The results showed that there is a relationship between Work Engagement based on the Vigor dimension, the Dedication dimension, the absorption dimension, and the nurse's performance. There is a relationship between Quality of Work Life and the performance of nurses in Makassar City Hospital. It is recommended that hospital management keep paying attention to work engagement, especially the Vigor dimension in order to increase the morale of nurses. Leaders need to know what their employees need so that employees can work according to organizational expectations, one of which is by providing motivation. Implementing a culture of health in the work environment so as to create a safe working atmosphere, developing career path plans for nurses, and internalizing the values of good work culture to maintain a sense of pride in the institution.
Membrane proteins are highly important players that help to maintain cellular integrity and control cell to cell interactions. One of the most intricate mechanisms of cell to cell communication is via vesicles formation and trafficking, carrying signaling proteins and molecules. Caveolar complex and SNARE (Soluble N-ethylmaleimidesensitive-factor attachment protein receptors) complex are among the membrane protein complexes that are functionally involved in vesicle trafficking and so are critical in cell to cell communication and development. Recent studies have observed an association of dysregulation of gene expression of CAV1and, DNM2 with cancer progression. Strategic components of SNARE machinery, Synaptobrevin2/Vesicle associated membrane protein-2 (v-SNARE) and Syntaxin 1A (t-SNARE) play a critical role in colon, lung and breast cancer progression and metastasis. In this study, we analyzed the relative expression of the STX1A, VAMP2, CAV1, and DNM2 for their possible association in the progression and metastasis of bladder cancer. The quantitative expression of the target genes was observed in human bladder cancer samples. The expression of STX1A, VAMP2, CAV1, and DNM2 were increased 5-fold, 2.9-fold, 8.88-folds and, 8.62-fold respectively. The overall expression of STX1A and VAMP2 found to be elevated significantly (P<0.0001) in high-grade tumors cells compared to normal and low-grade tumors. Similarly high-grade tumors had significantly higher expression of CAV1 (P<0.0001) and DNM2 (P<0.0001) compared to low-grade tumors. The correlation between the STX1A and VAMP2 was positive while between CAV1 and DNM2 the correlation was found strong positive. These data suggests that the increased expression of the key components of caveolar and SNARE complex might be responsible for the tumor grade and stage progression in bladder cancer. To further dissect the downstream signaling involved in vesicular trafficking we selected Cav-1 protein to provide an insight into its functional aspects. For this purpose we exploited a functional disruption imposed by a specific frame shift mutation at F160X resulting into truncated protein. Functional analyses of this Cav-1-mutant protein in MIA-PaCa-2, HT1376, HCT116, HT-29, and HCC827 showed that the Cav-1-mut cells have reduced growth, proliferation with improved mitochondrial respiration. The Cav-1-mut cells showed increased OCRs and reduced ECARs showing their reduced glycolytic behaviour compared to control cancer cells. The functional impact of this mutant Cav-1 might be the missing C-terminus including the important conserved phosphorylation site S168E, which is required for the translocation of the Cav-1 protein. As a structural component of caveolae, Cav-1 interacts with signaling molecules via a caveolin scaffolding domain (CSD) regulating cell signaling. Recent reports have shown that Cav-1 is a negative regulator in tumor metastasis. Therefore, we hypothesized that Cav-1 inhibits cell migration through its CSD. HeLa cells were engineered to overexpress Cav-1 (Cav-1 OE), Cav-1 without a functional CSD (∆CSD), or enhanced green fluorescent protein (EGFP) as a control. HeLa cell migration was suppressed in Cav-1 OE cells while ∆CSD showed increased migration. This altered migration corresponded to a decreased expression of zona occludens (ZO-1) with increased expression of vimentin. This shows that the CSD impacts the migratory phenotype in HeLa cells. Impact of Cav-1∆CSD on cellular migration was further confirmed in epithelial based colon cancer cell lines that have high (HCT116) and low (HT29) expression of this gene. To further elucidate the function of CSD we explored the JAK/STAT3 signaling account for the hypermigratory phenotype in the Cav-1∆CSD cells. Phosphorylated STAT3 was decreased in Cav-1 OE cells compared to control and ∆CSD cells; reducing STAT3 expression alone decreased cell migration. ∆CSD blunted HeLa proliferation by restricting the cells in G2/M phase of the cell cycle. Overexpressing the CSD peptide alone suppressed HeLa cell migration and inhibited phosphorylation of STAT3. These data suggests the importance of CSD as a negative regulator of STAT3 phosphorylation. Our functional investigations of Cav-1 specifically revealed that Cav-1 CSD may be critical in controlling the dynamic phenotype of cancer cells by facilitating the interactions of specific signal transduction pathways, regulating STAT3 and participating in a G2/M checkpoint. Modulating the CSD and targeting specific proteins may offer potential targets for novel therapies to control cancer metastasis.