Segon rahonament entre el Rat-Penat de Valencia, y el Micalet de la Seu, contra la queixa que li formen les Torres de Espioca y de Paterna : [Texto impreso] derogan totes les proposicions que estes acrediten al su dret, y explicant els molts favors y preeminencies que llogren els vehins en esta ciutat del Micalet ...

Hay un ejemplar encuadernado con: Individual noticia de todos los altares, arcos pinturas, adornos y lo mas exquisito y notable que havia en la carrera de la procession, y de las iluminaciones en general ... : (XVIII/1705).

Rahonament y coloqui nou de Chusep el Bo y Providensia de per part de Mare, Escolá de un Poblet al rededor de Valencia, en que li demana llisensia al Retor del Poble pera anar á dita Ciutat, y desfogar el seu cheni contra els Francesos y agabachats, per una feta que li feren en lo Mercat [Texto impreso]

Hay un ejemplar encuadernado con: Poesías colocadas en el pórtico del Convento de San Francisco de Valencia (NP849.91/3086).

Li-Fraumeni syndrome fibroblasts homozygous for p53 mutations are deficient in global DNA repair but exhibit normal transcription-coupled repair and enhanced UV resistance.

We investigated whether mutations in the p53 tumor suppressor gene alter UV sensitivity and/or repair of UV-induced DNA damage in primary human skin fibroblasts from patients with Li-Fraumeni syndrome, heterozygous for mutations in one allele of the p53 gene (p53 wt/mut) and sublines expressing only mutant p53 (p53 mut). The p53 mut cells were more resistant than the p53 wt/mut cells to UV cytotoxicity and exhibited less UV-induced apoptosis. DNA repair analysis revealed reduced removal of cyclobutane pyrimidine dimers from overall genomic DNA in vivo in p53 mut cells compared with p53 wt/mut or normal cells. However, p53 mut cells retained the ability to preferentially repair damage in the transcribed strands of expressed genes (transcription-coupled repair). These results suggest that loss of p53 function may lead to greater genomic instability by reducing the efficiency of DNA repair but that cellular resistance to DNA-damaging agents may be enhanced through elimination of apoptosis.

Definition of a metal-dependent/Li(+)-inhibited phosphomonoesterase protein family based upon a conserved three-dimensional core structure.

Inositol polyphosphate 1-phosphatase, inositol monophosphate phosphatase, and fructose 1,6-bisphosphatase share a sequence motif, Asp-Pro-(Ile or Leu)-Asp-(Gly or Ser)-(Thr or Ser), that has been shown by crystallographic and mutagenesis studies to bind metal ions and participate in catalysis. We compared the six alpha-carbon coordinates of this motif from the crystal structures of these three phosphatases and found that they are superimposable with rms deviations ranging from 0.27 to 0.60 A. Remarkably, when these proteins were aligned by this motif a common core structure emerged, defined by five alpha-helices and 11 beta-strands comprising 155 residues having rms deviations ranging from 1.48 to 2.66 A. We used the superimposed structures to align the sequences within the common core, and a distant relationship was observed suggesting a common ancestor. The common core was used to align the sequences of several other proteins that share significant similarity to inositol monophosphate phosphatase, including proteins encoded by fungal qa-X and qutG, bacterial suhB and cysQ (identical to amtA), and yeast met22 (identical to hal2). Evolutionary comparison of the core sequences indicate that five distinct branches exist within this family. These proteins share metal-dependent/Li(+)-sensitive phosphomonoesterase activity, and each predicted tree branch exhibits unique substrate specificity. Thus, these proteins define an ancient structurally conserved family involved in diverse metabolic pathways including inositol signaling, gluconeogenesis, sulfate assimilation, and possibly quinone metabolism. Furthermore, we suggest that this protein family identifies candidate enzymes to account for both the therapeutic and toxic actions of Li+ as it is used in patients treated for manic depressive disease.

Li I enhancement during a long-duration stellar flare

We report the possible detection of a Li I λ6708 Å line enhancement during an unusual long-duration optical flare in the recently discovered, X-ray/EUV selected, chromospherically active binary 2RE J0743+224. The Li I equivalent width (EW) variations follow the temporal evolution of the flare and large changes are observed in the intensity of the line. The maximum Li I enhancement (40% in EW) occurs just after the maximum chromospheric emission observed in the flare. A significant increase of the Li^-6/Li^-7 isotopic ratio is also detected. No significant simultaneous variations are detected in other photospheric lines. Neither line blends nor starspots seem to be the primary cause of the observed Li I line variation. From all this we suggest that this Li I enhancement is produced by spallation reactions during the flare.

Beijing di li quan tu

Zhou Peichun hua.

al- Juzʼ al-rābiʻ wa-al-khāmis min kitāb al-Intiṣār li-wāsiṭat ʻiqd al-amṣār

taʼlīf Ibrāhīm ibn Muḥammad ibn Aydamur al-ʻAlāʼī al-shahīr bi-Ibn Duqmāq.

Hādhā kitāb Maṭāliʻ al-anẓār

li-Abī al-Thanāʼ Shams al-Dīn ibn Maḥmūd ibn ʻAbd al-Raḥmān al-Iṣfahānī. Maʻa matnihi Ṭawāliʻ al-anwār / li-ʻAbd Allāh ibn ʻUmar al-Bayḍāwī. wa-bi-hāmishihimā Ḥāshiyat al-Sayyid al-Sharīf al-Jurjānī.

Hādhā al-Khatm al-mubārak li-Mukhtaṣar al-Shaykh Abī al-Mawaddah Sīdī Khalīl

taʼlīf Abī ʻAbd Allāh Muḥammad ibn al-Rashīd al-Ḥusaynī al-ʻIrāqī.

al- Taʻrībāt al-shāfiyah li-murīd al-jughrāfiyah

Rifāʻah Badawī Rāfiʻ al-Ṭahṭāwī.

Kitāb Taḥrīr al-Uṣūl li-Ūqlīdis

min taʼlīf Khūjah Naṣīr al-Dīn al-Ṭūsī.

al- Naṣīḥah al-ʻāmmah li-mulūk al-Islām wa-al-ʻāmmah

taʼlīf al-Sayyid Aḥmad al-Barzanjī al-Ḥusaynī.