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The natural layered clay-based materials offer a sustainable approach for removal of emerging pollutants from the environment. Their low-capacity and poor-selectivity for pollutants often limit their uses. This limitation is addressed in this study with the help of Al-oxide pillaring approach. Here microporous aluminum-pillared clay (Al-PILC) was prepared from locally available Smectite clay (montmorillonite, MMT), by intercalation of Al-oxide pillars into the interlayer structure. The method increased the surface area of natural clay to 258 m 2  g −1 and its porosity to 0.16 cm 3  g −1 . The adsorptive removal properties of prepared Al-PILC was evaluated on two selected pharmaceuticals and personal care products (PPCPs) viz . amoxicillin (AMOX) and imipramine (IMP). The results of the removal of these PPCPs were compared as a function of contact time (0–180 min), solution pH (2–12), initial concentration (0–100 mg L −1 ), and temperature (298–318 K). The Al-PILC adsorbs 332% more IMP and 681% more AMOX as compared to natural clay, and the maximum adsorption amounts on Al-PILC follows the order IMP > AMOX with 59.8 and 7.7 mg g −1 , respectively. The kinetics of adsorption of both AMOX and IMP follow pseudo-second-order model, with intraparticle diffusion as rate-determining step. The incorporated acidic sites in clay (in form of Al 2 O 3 pillars) enhanced its adsorption properties. These sites interacted with protonated amine and –OH groups of AMOX and the tertiary amine group of IMP. The Al-PILC exhibit effective regeneration and was reused up to three consecutive adsorption/desorption cycles. All in all, this study is expected to expand the application of Al-PILC on the adsorptive removal of the emerging pollutant from contaminated water.

The discovery of this group of gymnosperms from the Palaeozoic era is one of the notable achievements of the palaeobotanist and it was of immense value to the palaeobotany & in phylogeny. It includes fern-like plants which were dominant in the Devonian period. They extend into the beginning of the Mesozoic era, later on, there was a mass extinction of the pteridospermales, due to the misconception, that they were initially considered ferns and fern-like plants. Williamson (1897) first considered these plants as an intermediate of the ferns and cycads due to the morphological and anatomical similarity of the organs. H. Potonie (1899) was the first to give their names as the Cycadofilicales. Oliver and Scott ( 1904) named this group as pteridospermales due to the similarity between the ferns and spermatophytes. In this review article features of the order pteridospermales and their phylogeny have been discussed.

Next generation sequencing has revolutionised genomic studies of cancer, having facilitated the development of precision oncology treatments based on a tumour’s molecular profile. We aimed to develop a targeted gene sequencing panel for application to disparate cancer types with particular focus on tumours of the head and neck, plus test for utility in liquid biopsy. The final panel designed through Roche/Nimblegen combined 451 cancer-associated genes (2.01 Mb target region). 136 patient DNA samples were collected for performance and application testing. Panel sensitivity and precision were measured using well-characterised DNA controls (n = 47), and specificity by Sanger sequencing of the Aryl Hydrocarbon Receptor Interacting Protein ( AIP ) gene in 89 patients. Assessment of liquid biopsy application employed a pool of synthetic circulating tumour DNA (ctDNA). Library preparation and sequencing were conducted on Illumina-based platforms prior to analysis with our accredited (ISO15189) bioinformatics pipeline. We achieved a mean coverage of 395x, with sensitivity and specificity of >99% and precision of >97%. Liquid biopsy revealed detection to 1.25% variant allele frequency. Application to head and neck tumours/cancers resulted in detection of mutations aligned to published databases. In conclusion, we have developed an analytically-validated panel for application to cancers of disparate types with utility in liquid biopsy.

Background Annexin A1 (ANXA1) is a protein related with the carcinogenesis process and metastasis formation in many tumors. However, little is known about the prognostic value of ANXA1 in breast cancer. The purpose of this study is to evaluate the association between ANXA1 expression, BRCA1/2 germline carriership, specific tumor subtypes and survival in breast cancer patients. Methods Clinical-pathological information and follow-up data were collected from nine breast cancer studies from the Breast Cancer Association Consortium (BCAC) (n = 5,752) and from one study of familial breast cancer patients with BRCA1/2 mutations (n = 107). ANXA1 expression was scored based on the percentage of immunohistochemical staining in tumor cells. Survival analyses were performed using a multivariable Cox model. Results The frequency of ANXA1 positive tumors was higher in familial breast cancer patients with BRCA1/2 mutations than in BCAC patients, with 48.6 % versus 12.4 %, respectively; P <0.0001. ANXA1 was also highly expressed in BCAC tumors that were poorly differentiated, triple negative, EGFR-CK5/6 positive or had developed in patients at a young age. In the first 5 years of follow-up, patients with ANXA1 positive tumors had a worse breast cancer-specific survival (BCSS) than ANXA1 negative (HR adj  = 1.35; 95 % CI = 1.05–1.73), but the association weakened after 10 years (HR adj  = 1.13; 95 % CI = 0.91–1.40). ANXA1 was a significant independent predictor of survival in HER2+ patients (10-years BCSS: HR adj  = 1.70; 95 % CI = 1.17–2.45). Conclusions ANXA1 is overexpressed in familial breast cancer patients with BRCA1/2 mutations and correlated with poor prognosis features: triple negative and poorly differentiated tumors. ANXA1 might be a biomarker candidate for breast cancer survival prediction in high risk groups such as HER2+ cases.

Few studies have investigated whether the associations between pregnancy-related factors and breast cancer (BC) risk differ by underlying BC susceptibility. Evidence regarding variation in BC risk is critical to understanding BC causes and for developing effective risk-based screening guidelines. To examine the association between pregnancy-related factors and BC risk, including modification by a of BC where scores are based on age and BC family history. This cohort study included participants from the prospective Family Study Cohort (ProF-SC), which includes the 6 sites of the Breast Cancer Family Registry (US, Canada, and Australia) and the Kathleen Cuningham Foundation Consortium (Australia). Analyses were performed in a cohort of women enrolled from 1992 to 2011 without any personal history of BC who were followed up through 2017 with a median (range) follow-up of 10 (1-23) years. Data were analyzed from March 1992 to March 2017. Parity, number of full-term pregnancies (FTP), age at first FTP, years since last FTP, and breastfeeding. BC diagnoses were obtained through self-report or report by a first-degree relative and confirmed through pathology and data linkages. Cox proportional hazards regression models estimated hazard ratios (HR) and 95% CIs for each exposure, examining modification by PARS of BC. Differences were assessed by estrogen receptor (ER) subtype. The study included 17 274 women (mean [SD] age, 46.7 [15.1] years; 791 African American or Black participants [4.6%], 1399 Hispanic or Latinx participants [8.2%], and 13 790 White participants [80.7%]) with 943 prospectively ascertained BC cases. Compared with nulliparous women, BC risk was higher after a recent pregnancy for those women with higher PARS (last FTP 0-5 years HR for interaction, 1.53; 95% CI, 1.13-2.07; P for interaction < .001). Associations between other exposures were limited to ER-negative disease. ER-negative BC was positively associated with increasing PARS and increasing years since last FTP (P for interaction < .001) with higher risk for recent pregnancy vs nulliparous women (last FTP 0-5 years HR for interaction, 1.54; 95% CI, 1.03-2.31). ER-negative BC was positively associated with increasing PARS and being aged 20 years or older vs less than 20 years at first FTP (P for interaction = .002) and inversely associated with multiparity vs nulliparity (P for interaction = .01). In this cohort study of women with no prior BC diagnoses, associations between pregnancy-related factors and BC risk were modified by PARS, with greater associations observed for ER-negative BC.

The C terminal Jα-helix of the Avena Sativa’s Light Oxygen and Voltage (AsLOV2) protein, unfolds on exposure to blue light. This characteristic seeks relevance in applications related to engineering novel biological photoswitches. Using Molecular Dynamic (MD) simulations and the Markov State Modeling (MSM) approach we provide the mechanism that explains the stepwise unfolding of the Jα-helix. The unfolding was resolved into seven steps represented by the structurally distinguishable states distributed over the initiation and the post initiation phases. Wherein, the initiation phase occurs due to the collapse of the interaction cascade FMN-Q513-N492-L480-W491-Q479-V520-A524, the onset of the post initiation phase is marked by breaking of the hydrophobic interactions between the Jα-helix and the Iβ-sheet. This study indicates that the displacement of N492 out of the FMN binding pocket, not necessarily requiring Q513, is essential for the initiation of the Jα-helix unfolding. Rather, the structural reorientation of Q513 activates the protein to cross the hydrophobic barrier and enter the post initiation phase. Similarly, the structural deviations in N482, rather than its integral role in unfolding, could enhance the unfolding rates. Further, the MSM studies on the wild type and the Q513 mutant, provide the spatio-temporal roadmap that layout the possible pathways of structural transition between the dark and the light states of the protein. Overall, the study provides insights useful to enhance the performance of AsLOV2 based photoswitches.

CHT7 is a regulator of quiescence repression and TAG degradation between the nitrogen deprived and the nitrogen replenished states in Chlamydomonas reinhardtii. Initially it was thought that the CHT7’s repression activity is managed by its DNA binding CXC domain which is a tandem repeat of two cysteine rich subdomains. Later, it was found that the CXC (CHT7_CXC) domain is effectively dispensable for CHT7’s activities. Rather, CHT7’s predicted protein binding domains are proposed to be involved in gene regulation activities by binding through other repressors in the cell. Yet, it remains unclear why and how CHT7 manages to refrain its own CXC domain from participating in any transcriptional activities. The question becomes more intriguing, because CXC binding regions are available in promoter regions of some of the misregulated genes in the CHT7 mutant (cht7). Through the combination of biophysical experiments and molecular dynamics approaches, we have studied the DNA recognition behavior of CHT7_CXC. The results show that CHT7_CXC domain is highly selective towards DNA sequences and this selectivity is imparted due to the differential binding abilities of the CXC subdomains. Further, to understand if the case is - that CXC looses it’s DNA binding capabilities in the vicinity of other repressor molecules, we carried out CHT7_CXC’s DNA binding stability test by simulating the spatial constraint conditions using the AsLOV2- CXC fusion. Our test results show limited ability of CHT7_CXC to withstand steric forces and provide insights to why and how algal cells may hold back CHT7_CXC’s indulgence in quiescence repression. Microalgae, under nutrient rich conditions, provide biomass. Whereas, nutrient deprivation leads to accumulation of biofuel feedstock, but cells enter quiescence. Net enhancement in feedstock, therefore relies on the precision of the quiescence regulator. In Chlamydomonas reinhardtii, CHT7 is a central regulator of quiescence. Surprisingly, rather than using its own DNA binding domain (DBD) for the regulatory activities, CHT7 recruits external transcriptional regulators using its non DBDs. To ensure smooth functioning, CHT7’s DBD must rapidly switch to inactive form. Modifications in DNA binding profiles of DBDs due to non DBDs are seen in transcription factors of many organisms. The switching mechanism discussed could therefore be a generic approach of timely regulation of individual components of the complex transcriptional machineries.

Traditional cancer treatments use nonspecific drugs and monoclonal antibodies to target tumor cells. Chimeric antigen receptor (CAR)-T cell therapy, however, leverages the immune system's T-cells to recognize and attack tumor cells. T-cells are isolated from patients and modified to target tumor-associated antigens. CAR-T therapy has achieved FDA approval for treating blood cancers like B-cell acute lymphoblastic leukemia, large B-cell lymphoma, and multiple myeloma by targeting CD-19 and B-cell maturation antigens. Bi-specific chimeric antigen receptors may contribute to mitigating tumor antigen escape, but their efficacy could be limited in cases where certain tumor cells do not express the targeted antigens. Despite success in blood cancers, CAR-T technology faces challenges in solid tumors, including lack of reliable tumor-associated antigens, hypoxic cores, immunosuppressive tumor environments, enhanced reactive oxygen species, and decreased T-cell infiltration. To overcome these challenges, current research aims to identify reliable tumor-associated antigens and develop cost-effective, tumor microenvironment-specific CAR-T cells. This review covers the evolution of CAR-T therapy against various tumors, including hematological and solid tumors, highlights challenges faced by CAR-T cell therapy, and suggests strategies to overcome these obstacles, such as utilizing single-cell RNA sequencing and artificial intelligence to optimize clinical-grade CAR-T cells.