cometadata/datacite-titles-descriptions-related-identifiers huggingface dataset:
DOI: 10.5281/zenodo.10850198
title: [IO Islamic 1078] ديوان ناصر على

description: Dîwân-i-Nâṣir-‘Alî

This manuscript is now IO Islamic 1639 in the India Office collections.

[metadata: Hermann Ethé, Catalogue of Persian Manuscripts in the Library of the India Office, 2 vols. (Oxford: India Office, 1903): volume 1, number 1078 here with notations and hyperlinks].


Nâṣir ‘Alî (Nos. 1639-1648).

1639

Dîwân-i-Nâṣir ‘Alî (ديوان ناصر على).

The lyrical poems of Shaikh (or Shâh) Nâṣir ‘Alî of Sirhind, who died at Dihlî the 6th of Ramaḍân, A.H. 1108 (A.D. 1697, March 29); comp. Rieu ii. p. 699 sq.; Bodleian Cat., Nos. 1150-1152; W. Pertsch, p. 80; and Berlin Cat., p. 936; A. Sprenger, Catal., pp. 113, 126, 151, 201, and 329; Cat. Codd. Or. Lugd. Bat. ii. p. 107; see also Rosen, Persian MSS., p. 167 (No. 109); Muntakhab-alash’âr, No. 458 (col. 249 in the Bodleian Cat.); Khulâṣat-alkalâm, No. 178 (ib., col. 308), and Makhzan-algharâ’ib, No. 1743 (ib., col. 355). All tadhkiras agree about the date A.H. 1108, but a strange contradiction appears in the chronogram, composed by Sarkhwush, the friend of the poet and the collector of his dîwân: آه على بعالم معنى رفت  , which gives A.H. 1109, see A. Sprenger, Catal., p. 113, and the Khulâṣat-alkalâm, loc. cit. This copy, the fullest in the India Office Collection, contains:

Ghazals, rubâ’îs, and fards, all mixed together in alphabetical order, with interlinear and marginal glosses, on fol.1b, beginning:

محبّت جادّۀ دارد نهان در خلوت دلها الخ

At the end of this part another series of rubâ’îs (on ff. 95a-99b).

Ḳaṣîdas, on fol. 100a, beginning:

گداخت بسكه هواى تموز مغز خيال الخ

The poet’s name appears as takhalluṣ several times, for instance, on fol. 106b, I. 8. The diwân has been lithographed in Lucknow, 1844, A.H. 1263 and 1281.

Copied by Khwâjah ‘Ażim in the twenty-ninth year of Muḥammadshâh’s reign (=A.H. 1160, A.D. 1747); the larger portion of the dîwân, i.e. to the end of the rubâ’îs, was finished the 19th of Muḥarram in that year (1747, Jan. 31).

No. 1078, ff. 110, 2 coll., each ll. 14; careless Nasta’lîḳ; size, 8 in. by 5½ in.
DOI: 10.5281/zenodo.10850199
title: [IO Islamic 1078] ديوان ناصر على

description: Dîwân-i-Nâṣir-‘Alî

This manuscript is now IO Islamic 1639 in the India Office collections.

[metadata: Hermann Ethé, Catalogue of Persian Manuscripts in the Library of the India Office, 2 vols. (Oxford: India Office, 1903): volume 1, number 1078 here with notations and hyperlinks].


Nâṣir ‘Alî (Nos. 1639-1648).

1639

Dîwân-i-Nâṣir ‘Alî (ديوان ناصر على).

The lyrical poems of Shaikh (or Shâh) Nâṣir ‘Alî of Sirhind, who died at Dihlî the 6th of Ramaḍân, A.H. 1108 (A.D. 1697, March 29); comp. Rieu ii. p. 699 sq.; Bodleian Cat., Nos. 1150-1152; W. Pertsch, p. 80; and Berlin Cat., p. 936; A. Sprenger, Catal., pp. 113, 126, 151, 201, and 329; Cat. Codd. Or. Lugd. Bat. ii. p. 107; see also Rosen, Persian MSS., p. 167 (No. 109); Muntakhab-alash’âr, No. 458 (col. 249 in the Bodleian Cat.); Khulâṣat-alkalâm, No. 178 (ib., col. 308), and Makhzan-algharâ’ib, No. 1743 (ib., col. 355). All tadhkiras agree about the date A.H. 1108, but a strange contradiction appears in the chronogram, composed by Sarkhwush, the friend of the poet and the collector of his dîwân: آه على بعالم معنى رفت  , which gives A.H. 1109, see A. Sprenger, Catal., p. 113, and the Khulâṣat-alkalâm, loc. cit. This copy, the fullest in the India Office Collection, contains:

Ghazals, rubâ’îs, and fards, all mixed together in alphabetical order, with interlinear and marginal glosses, on fol.1b, beginning:

محبّت جادّۀ دارد نهان در خلوت دلها الخ

At the end of this part another series of rubâ’îs (on ff. 95a-99b).

Ḳaṣîdas, on fol. 100a, beginning:

گداخت بسكه هواى تموز مغز خيال الخ

The poet’s name appears as takhalluṣ several times, for instance, on fol. 106b, I. 8. The diwân has been lithographed in Lucknow, 1844, A.H. 1263 and 1281.

Copied by Khwâjah ‘Ażim in the twenty-ninth year of Muḥammadshâh’s reign (=A.H. 1160, A.D. 1747); the larger portion of the dîwân, i.e. to the end of the rubâ’îs, was finished the 19th of Muḥarram in that year (1747, Jan. 31).

No. 1078, ff. 110, 2 coll., each ll. 14; careless Nasta’lîḳ; size, 8 in. by 5½ in.
DOI: 10.5281/zenodo.10850214
title: [IO Islamic 95] ديوان ناصر على

description: Dîwân-i-Nâṣir-‘Alî

This manuscript is now IO Islamic 1640 in the India Office collections.

[metadata: Hermann Ethé, Catalogue of Persian Manuscripts in the Library of the India Office, 2 vols. (Oxford: India Office, 1903): volume 1, number 95 here with notations and hyperlinks].


1640

Another copy of the same dîwân.

The same dîwân, without the ḳaṣîdas, chiefly consisting of ghazals, in alphabetical order, on fol. 1b, beginning as in the preceding copy. The ghazals conclude on fol. 73a and are dated the 25th of Ṣafar, A.H. 1132 (the first year of Muḥammadshâh’s reign) = A.D. 1720, Jan 7, at Shâhjahânâbâd, during the governorship of Nawwâb Najm-aldîn ‘Alîkhân Bahâdur.

The remaining leaves contain:

Fol. 73b: nine mathnawî-baits by the حكيم غزنوى (i.e. Ḥakîm Sanâ’î of Ghazna, see above, No. 914 sq.), beginning: 

بود در شهر بلخ بقّالى الخ

Ff. 74b-78a: a mathnawî which has no heading, but is clearly identical with the Sarâpâi (سراپاى) or ‘description of the human figure,’ by Mîr Sayyid ‘Alî Mihrî ‘Arab, who flourished under Sulṭân Ḥusain of Persia (A.H. 1105-1135=A.D. 1694-1722), and died about A.H. 1130 (A.D. 1718); comp. Bodleian Cat., No. 1168; Rieu ii. pp. 796a and 850b; W. Pertsch, Berlin Cat., p. 680 (No. 671, fol. 43b) and p.696, No. 9; Khulâṣat-alkalâm, No. 67 (Bodleian Cat., Col. 301); and Khulâṣat-alfkâr, No. 249 (ib., col. 311). Beginning:

اى بت چابك شيرين حركات الخ

Fol. 78b: some line prose, beginning: بعد از نماز مغرب دو ركعت نماز الخ.

No. 95, ff. 1-78, 2 coll., each ll. 15; on ff. 74a-78a diagonal lines; Shikasta; various readings and additions on the margin; the first pages greatly injured; size, 8¼ in. by 4¾ in.
DOI: 10.5281/zenodo.10850215
title: [IO Islamic 95] ديوان ناصر على

description: Dîwân-i-Nâṣir-‘Alî

This manuscript is now IO Islamic 1640 in the India Office collections.

[metadata: Hermann Ethé, Catalogue of Persian Manuscripts in the Library of the India Office, 2 vols. (Oxford: India Office, 1903): volume 1, number 95 here with notations and hyperlinks].


1640

Another copy of the same dîwân.

The same dîwân, without the ḳaṣîdas, chiefly consisting of ghazals, in alphabetical order, on fol. 1b, beginning as in the preceding copy. The ghazals conclude on fol. 73a and are dated the 25th of Ṣafar, A.H. 1132 (the first year of Muḥammadshâh’s reign) = A.D. 1720, Jan 7, at Shâhjahânâbâd, during the governorship of Nawwâb Najm-aldîn ‘Alîkhân Bahâdur.

The remaining leaves contain:

Fol. 73b: nine mathnawî-baits by the حكيم غزنوى (i.e. Ḥakîm Sanâ’î of Ghazna, see above, No. 914 sq.), beginning: 

بود در شهر بلخ بقّالى الخ

Ff. 74b-78a: a mathnawî which has no heading, but is clearly identical with the Sarâpâi (سراپاى) or ‘description of the human figure,’ by Mîr Sayyid ‘Alî Mihrî ‘Arab, who flourished under Sulṭân Ḥusain of Persia (A.H. 1105-1135=A.D. 1694-1722), and died about A.H. 1130 (A.D. 1718); comp. Bodleian Cat., No. 1168; Rieu ii. pp. 796a and 850b; W. Pertsch, Berlin Cat., p. 680 (No. 671, fol. 43b) and p.696, No. 9; Khulâṣat-alkalâm, No. 67 (Bodleian Cat., Col. 301); and Khulâṣat-alfkâr, No. 249 (ib., col. 311). Beginning:

اى بت چابك شيرين حركات الخ

Fol. 78b: some line prose, beginning: بعد از نماز مغرب دو ركعت نماز الخ.

No. 95, ff. 1-78, 2 coll., each ll. 15; on ff. 74a-78a diagonal lines; Shikasta; various readings and additions on the margin; the first pages greatly injured; size, 8¼ in. by 4¾ in.
DOI: 10.5281/zenodo.10143599
title: Global 0.1° gridded anthropogenic CO2 emissions based on data-driven method 2021-2022

description: This dataset is the global 0.1° anthropogenic CO2 emissions for 2021-2022. The emissions were estimated by a data-driven model based on EDGAR inventories and the CO2 and NOx co-emissions framework. The 0.1° gridded emissions are provided in TIFF format (preACO2_RFR_01deg_yyyy). The national emissions are calculated from gridded data and provided in xlsx format (National_CO2_emissions_yyyy). We also provided the CO2/NOx emission ratio we used in estimating (pre_CO2NOxRatio_LSTM_IDW_01deg_yyyy), which is predicted by the LSTM neural network. 
The corresponding paper of this dataset is being prepared.
DOI: 10.5281/zenodo.10838067
title: Foot kinematics and kinetics data for different static foot posture collected using a multi-segment foot model

description: Dataset presented in the paper "Foot kinematics and kinetics data for different static foot posture collected using a multi-segment foot model".

This dataset contains human foot joints kinematics and kinetics data collected during walking, classified depending on their static foot posture. The kinematics data were recorded using a three-dimensional motion analysis system, and kinetics data were recorded through a pressure platform. The data was collected considering a multi-segment foot model that considers the ankle, midtarsal and first metatarsophalangeal joint. A total of 70 healthy subjects with different static posture (highly pronated, highly supinated and normal, as classified by the foot posture index) participated in the experiments. This dataset contains a total of 350 continuous recordings of anatomical angles and joint moments of the ankle, midtarsal, and first metatarsophalangeal joints of the right foot during walking, as well as the right foot contact pressures recorded. The recordings were collected at 100 Hz, and the resulting data are provided filtered and resampled to 100 frames evenly distributed along the stance phase. Participants’ descriptive data are also provided: age, weight, height, and foot anthropometric data and foot posture index for both feet. The data are presented as a spreadsheet file (.xlsx) and a Matlab structure file (.mat), with contact pressures provided only in the .mat file. Further details and data validation are provided in the main paper.
DOI: 10.5281/zenodo.10850228
title: Pharsalus repandus (Hemiptera: Ricaniidae) with mutualistic interaction with two species of Camponotus
title: Ant and planthopper interactions

description: The ants who were attending the planthoppers was identified as Camponotus rufipes (Fabricius, 1775) and Camponotus crassus Mayr, 1862 (Fig. 2A, D, arrow 2). We noted direct contact and observed the ants employing antennal palpation behavior to stimulate the planthoppers. The ant positions itself just behind the planthopper, delicately and repeatedly touching its wings with the tips of its antennae. In response to this interaction, the planthopper gradually elevates its forewings, although they do not fully open, and the anal margins remain unseparated. Concurrently, a droplet of honeydew is released. Additionally, we observed the planthoppers reacting to the presence of ants walking nearby with an extremely rapid movement of the wings, even though there was no physical contact between them.
DOI: 10.34740/kaggle/dsv/7908320
title: Daily Public Opinion on Israel-Palestine War
DOI: 10.6084/m9.figshare.14790048
title: M05B5.4 (lysosomal phospholipase A2) promotes disintegration of autophagic vesicles to maintain <i>C. elegans</i> development

description: The autophagosome has two lipid bilayer membranes. The outer membrane fuses with the lysosome, while the inner membrane is degraded to release autophagic contents for degradation. It remains unclear how the inner vesicle of the autophagosome (called the autophagic vesicle) is disintegrated after autophagosome-lysosome fusion. Here, we identified <i>C. elegans</i> LPLA-2/M05B5.4 as a key enzyme that degrades membranous material in lysosomes. LPLA-2 is homologous to human PLA2G15, a lysosomal phospholipase A2 family protein that catalyzes cleavage of membrane phospholipids. We found that loss of LPLA-2 causes accumulation of large membrane whor ls in enlarged lysosomes and both phenotypes are suppressed by blocking macroautophagy/autophagy. Moreover, autophagic vesicles persisted in enlarged lysosomes in PLA2G15 knockdown cells and <i>lpla-2(lf)</i> mutants, which suggests that the breakdown of the inner autophagosomal membrane in lysosomes is impaired. <i>lpla-2(lf)</i> mutants exhibit severe defects in both embryonic and larval development. Our data suggest that disintegration of the inner autophagosomal membrane by LPLA-2 promotes the release and subsequent degradation of autophagic contents in lysosomes, which is essential for <i>C. elegans</i> development. <b>Abbreviations</b>: ATG: autophagy related; EPG: ectopic PGL granules; GFP: green fluorescent protein; LGG-1: LC3, GABARAP and GATE-16 family; LPLA-2: lysosomal phospholipase A2; PGL: P granule abnormality protein; PLA2: phospholipase A2; SD: standard deviation; SEPA-1: suppressor of ectopic P granules in autophagy mutant; SQST-1: sequestosome related.
DOI: 10.6084/m9.figshare.14790048.v2
title: M05B5.4 (lysosomal phospholipase A2) promotes disintegration of autophagic vesicles to maintain <i>C. elegans</i> development

description: The autophagosome has two lipid bilayer membranes. The outer membrane fuses with the lysosome, while the inner membrane is degraded to release autophagic contents for degradation. It remains unclear how the inner vesicle of the autophagosome (called the autophagic vesicle) is disintegrated after autophagosome-lysosome fusion. Here, we identified <i>C. elegans</i> LPLA-2/M05B5.4 as a key enzyme that degrades membranous material in lysosomes. LPLA-2 is homologous to human PLA2G15, a lysosomal phospholipase A2 family protein that catalyzes cleavage of membrane phospholipids. We found that loss of LPLA-2 causes accumulation of large membrane whor ls in enlarged lysosomes and both phenotypes are suppressed by blocking macroautophagy/autophagy. Moreover, autophagic vesicles persisted in enlarged lysosomes in PLA2G15 knockdown cells and <i>lpla-2(lf)</i> mutants, which suggests that the breakdown of the inner autophagosomal membrane in lysosomes is impaired. <i>lpla-2(lf)</i> mutants exhibit severe defects in both embryonic and larval development. Our data suggest that disintegration of the inner autophagosomal membrane by LPLA-2 promotes the release and subsequent degradation of autophagic contents in lysosomes, which is essential for <i>C. elegans</i> development. <b>Abbreviations</b>: ATG: autophagy related; EPG: ectopic PGL granules; GFP: green fluorescent protein; LGG-1: LC3, GABARAP and GATE-16 family; LPLA-2: lysosomal phospholipase A2; PGL: P granule abnormality protein; PLA2: phospholipase A2; SD: standard deviation; SEPA-1: suppressor of ectopic P granules in autophagy mutant; SQST-1: sequestosome related.
DOI: 10.6084/m9.figshare.14714909
title: Silencing PEX26 as an unconventional mode to kill drug-resistant cancer cells and forestall drug resistance

description: Promoting the macroautophagy/autophagy-mediated degradation of specific proteins and organelles can potentially be utilized to induce apoptosis in cancer cells or sensitize tumor cells to therapy. To examine this concept, we enriched for autophagosomes from histone deacetylase inhibitor (HDACi)-sensitive U937 lymphoma cells and isogenic HDACi-resistant cells. Mass spectrometry on autophagosome-enriched fractions revealed that HDACi-resistant cells undergo elevated pexophagy, or autophagy of the peroxisome, an organelle that supports tumor growth. To disturb peroxisome homeostasis, we enhanced pexophagy in HDACi-resistant cells via genetic silencing of peroxisome exportomer complex components (<i>PEX1, PEX6</i>, or <i>PEX26</i>). This consequently sensitized resistant cells to HDACi-mediated apoptosis, which was rescued by inhibiting ATM/ataxia-telangiectasia mutated (ATM serine/threonine kinase), a mediator of pexophagy. We subsequently engineered melanoma cells to stably repress <i>PEX26</i> using CRISPR interference (CRISPRi). Melanoma cells with repressed <i>PEX26</i> expression showed evidence of both increased pexophagy and peroxisomal matrix protein import defects versus single guide scrambled (<i>sgSCR)</i> controls. <i>In vivo</i> studies showed that <i>sgPEX26</i> melanoma xenografts recurred less compared to <i>sgSCR</i> xenografts, following the development of resistance to mitogen-activated protein kinase (MAPK)-targeted therapy. Finally, prognostic analysis of publicly available datasets showed that low expression levels of <i>PEX26, PEX6</i> and <i>MTOR</i>, were significantly associated with prolonged patient survival in lymphoma, lung cancer and melanoma cohorts. Our work highlighted that drugs designed to disrupt peroxisome homeostasis may serve as unconventional therapies to combat therapy resistance in cancer. <b>Abbreviations:</b> ABCD3/PMP70: ATP binding cassette subfamily D member 3; ACOX1: acyl-CoA oxidase 1; AP: autophagosome; COX: cytochrome c oxidase; CQ: chloroquine; CRISPRi: clustered regularly interspaced short palindromic repeats interference; DLBCL: diffuse large B-cell lymphoma; GO: gene ontology; dCas9: Cas9 endonuclease dead, or dead Cas9; HDACi: histone deacetylase inhibitors; IHC: Immunohistochemistry; LAMP2: lysosomal associated membrane protein 2; LCFAs: long-chain fatty acids; LFQ-MS: label-free quantitation mass spectrometry; LPC: lysophoshatidylcholine; MAP1LC3B/LC3B: microtubule associated protein 1 light chain 3 beta; MTOR: mechanistic target of rapamycin kinase; PBD: peroxisome biogenesis disorders; PTS1: peroxisomal targeting signal 1; ROS: reactive oxygen species; sgRNA: single guide RNA; VLCFAs: very-long chain fatty acids; Vor: vorinostat; WO: wash-off.
DOI: 10.6084/m9.figshare.14790048.v1
title: M05B5.4 (Lysosomal phospholipase A2) promotes disintegration of autophagic vesicles to maintain <i>C. elegans</i> development

description: The autophagosome has two lipid bilayer membranes. The outer membrane fuses with the lysosome, while the inner membrane is degraded to release autophagic contents for degradation. It remains unclear how the inner vesicle of the autophagosome (called the autophagic vesicle) is disintegrated after autophagosome-lysosome fusion. Here, we identified <i>C. elegans</i> LPLA-2/M05B5.4 as a key enzyme that degrades membranous material in lysosomes. LPLA-2 is homologous to human PLA2G15, a lysosomal phospholipase A2 family protein that catalyzes cleavage of membrane phospholipids. We found that loss of LPLA-2 causes accumulation of large membrane whorls in enlarged lysosomes and both phenotypes are suppressed by blocking macroautophagy/autophagy. Moreover, autophagic vesicles persisted in enlarged lysosomes in PLA2G15 knockdown cells and <i>lpla-2(lf)</i> mutants, which suggests that the breakdown of the inner autophagosomal membrane in lysosomes is impaired. <i>lpla-2(lf)</i> mutants exhibit severe defects in both embryonic and larval development. Our data suggest that disintegration of the inner autophagosomal membrane by LPLA-2 promotes the release and subsequent degradation of autophagic contents in lysosomes, which is essential for <i>C. elegans</i> development.
DOI: 10.6084/m9.figshare.14749483
title: <i>Garcinia cambogia</i> attenuates adipogenesis by affecting CEBPB and SQSTM1/p62-mediated selective autophagic degradation of KLF3 through RPS6KA1 and STAT3 suppression

description: The overexpansion of adipose tissues leads to obesity and eventually results in metabolic disorders. <i>Garcinia cambogia</i> (<i>G. cambogia</i>) has been used as an antiobesity supplement. However, the molecular mechanisms underlying the effects of <i>G. cambogia</i> on cellular processes have yet to be fully understood. Here, we discovered that <i>G. cambogia</i> attenuated the expression of CEBPB (CCAAT/enhancer binding protein (C/EBP), beta), an important adipogenic factor, suppressing its transcription in differentiated cells. In addition, <i>G. cambogia</i> inhibited macroautophagic/autophagic flux by decreasing autophagy-related gene expression and autophagosome formation. Notably, <i>G. cambogia</i> markedly elevated the expression of KLF3 (Kruppel-like factor 3 (basic)), a negative regulator of adipogenesis, by reducing SQSTM1/p62-mediated selective autophagic degradation. Furthermore, increased KLF3 induced by <i>G. cambogia</i> interacted with CTBP2 (C-terminal binding protein 2) to form a transcriptional repressor complex and inhibited <i>Cebpa</i> and <i>Pparg</i> transcription. Importantly, we found that RPS6KA1 and STAT3 were involved in the <i>G. cambogia</i>-mediated regulation of CEBPB and autophagic flux. In an obese animal model, <i>G. cambogia</i> reduced high-fat diet (HFD)-induced obesity by suppressing epididymal and inguinal subcutaneous white adipose tissue mass and adipocyte size, which were attributed to the regulation of targets that had been consistently identified <i>in vitro</i>. These findings provide new insight into the mechanism of <i>G. cambogia</i>-mediated regulation of adipogenesis and suggest molecular links to therapeutic targets for the treatment of obesity. <b>Abbreviations:</b> 3-MA: 3-methyladenine; ACTB: actin beta; ATG: autophagy-related; Baf: bafilomycin A<sub>1</sub>; BECN1: beclin 1; CEBP: CCAAT/enhancer binding protein (C/EBP); CHX: cycloheximide; CREB: cAMP response element binding protein; CTBP: C-terminal binding protein; EGCG: (-)-epigallocatechin gallate; eWAT: epididymal white; <i>G. cambogia: Garcinia cambogia</i>; GFP: green fluorescent protein; H&E: hematoxylin and eosin; HFD: high-fat diet; iWAT: inguinal subcutaneous white; KLF: Kruppel-like factor; LAP: liver-enriched transcriptional activating proteins; MAP1LC3/LC3: microtubule-associated protein 1 light chain 3; ND: normal diet; PPARG: peroxisome proliferator activated receptor gamma; qPCR: quantitative real-time PCR; RFP: red fluorescent protein; RPS6KA1: ribosomal protein S6 kinase A1; siRNA: small-interfering RNA; SQSTM1/p62: sequestosome 1; STAT: signal transducer and activator of transcription; TEM: transmission electron microscopy