A catalogue of Indian Gelechiidae Stainton, 1854 (Lepidoptera: Gelechioidea).

We present an annotated catalogue of the Lepidoptera family Gelechiidae of India, comprising 351 species in 80 genera, encompassing seven subfamilies. The Indian fauna represents 7.47% of global gelechiid species diversity (i.e., 4,700 species in 500 genera). Among the seven subfamilies, Dichomeridinae is the best represented (122 species in four genera), followed by Gelechiinae (76 species in 38 genera), Anacampsinae (70 species in 16 genera), Thiotrichinae (49 species in five genera), Anomologinae (26 species in nine genera), Apatetrinae (seven species in seven genera), and Physoptilinae(single species). Information on type locality, type repository, synonyms, geographical distribution, hosts, natural enemies, and references to illustrations are provided. We also reviewed the history of descriptive work on the Gelechiidae of India, and resolved ambiguities regarding the current status of some species.

The IL6/JAK/STAT3 signaling axis is a therapeutic vulnerability in SMARCB1-deficient bladder cancer.

SMARCB1 loss has long been observed in many solid tumors. However, there is a need to elucidate targetable pathways driving growth and metastasis in SMARCB1-deficient tumors. Here, we demonstrate that SMARCB1 deficiency, defined as genomic SMARCB1 copy number loss associated with reduced mRNA, drives disease progression in patients with bladder cancer by engaging STAT3. SMARCB1 loss increases the chromatin accessibility of the STAT3 locus in vitro. Orthotopically implanted SMARCB1 knockout (KO) cell lines exhibit increased tumor growth and metastasis. SMARCB1-deficient tumors show an increased IL6/JAK/STAT3 signaling axis in in vivo models and patients. Furthermore, a pSTAT3 selective inhibitor, TTI-101, reduces tumor growth in SMARCB1 KO orthotopic cell line-derived xenografts and a SMARCB1-deficient patient derived xenograft model. We have identified a gene signature generated from SMARCB1 KO tumors that predicts SMARCB1 deficiency in patients. Overall, these findings support the clinical evaluation of STAT3 inhibitors for the treatment of SMARCB1-deficient bladder cancer.

Dimethylarginine Dimethylaminohydrolase - 1 expression is increased under tBHP-induced oxidative stress regulates nitric oxide production in PCa cells attenuates mitochondrial ROS-mediated apoptosis.

Dimethylarginine dimethylaminohydrolase-1 (DDAH1) expression is frequently elevated in different cancers including prostate cancer (PCa) and enhances nitric oxide (NO) production in tumor cells by metabolising endogenous nitric oxide synthase (NOS) inhibitors. DDAH1 protects the PCa cells from cell death and promotes survival. In this study, we have investigated the cytoprotective role of DDAH1 and determined the mechanism of DDAH1 in protecting the cells in tumor microenvironment. Proteomic analysis of PCa cells with stable overexpression of DDAH1 has identified that oxidative stress-related activity is altered. Oxidative stress promotes cancer cell proliferation, survival and causes chemoresistance. A known inducer of oxidative stress, tert-Butyl Hydroperoxide (tBHP) treatment to PCa cells led to elevated DDAH1 level that is actively involved in protecting the PCa cells from oxidative stress induced cell damage. In PC3-DDAH1- cells, tBHP treatment led to higher mROS levels indicating that the loss of DDAH1 increases the oxidative stress and eventually leads to cell death. Under oxidative stress, nuclear Nrf2 controlled by SIRT1 positively regulates DDAH1 expression in PC3 cells. In PC3-DDAH1+ cells, tBHP induced DNA damage is well tolerated compared to wild-type cells while PC3-DDAH1- became sensitive to tBHP. In PC3 cells, tBHPexposure has increased the production of NO and GSH which may be acting as an antioxidant defence to overcome oxidative stress. Furthermore, in tBHP treated PCa cells, DDAH1 is controlling the expression of Bcl2, active PARP and caspase 3. Taken together, these results confirm that DDAH1 is involved in the antioxidant defence system and promotes cell survival.

Acute Adrenal Hemorrhage as the Initial Manifestation of Metastatic Lung Adenocarcinoma: A Cautionary Tale.

Adrenal gland metastatic disease is the most commonly occurring malignancy of the adrenal glands. Although metastatic disease is common, adrenal hemorrhage is a rare but potentially fatal manifestation of malignancy. The objectives of this case report are to highlight the unusual presentation of metastatic lung adenocarcinoma as spontaneous adrenal hemorrhage in a 64-year-old female who was otherwise asymptomatic. As well as to support the reasoning that metastatic disease should be considered as a differential in patients with this clinical presentation as this may have altered this fatal outcome.

Sphingobacterium Spritivorum Associated With Spontaneous Bacterial Peritonitis in a Cirrhotic Patient With Gram-Positive Bacteremia.

Sphingobacterium spritivorum (SS) is a ubiquitous gram-negative organism and an uncommon cause of infection in humans. To our knowledge, there are no reported cases of this bacterium causing spontaneous bacterial peritonitis (SBP) in patients with cirrhosis. In this report, we discuss a case of a male patient in his late 60s who presented with severe sepsis from methicillin-resistant staphylococcus aureus (MRSA), in whom SS was subsequently identified via ascitic fluid culture. This unusual organism is known to have an innate resistance to multiple antibiotics and can cause life-threatening sepsis in cases of delayed or missed diagnosis. Clinicians should not be weighed down by anchoring bias and look for alternative, uncommon gram-negative organisms in cases of progressive sepsis in patients with ascites.

Lipidomic Profiling Identifies a Novel Lipid Signature Associated with Ethnicity-Specific Disparity of Bladder Cancer.

Bladder Cancer (BLCA) is the ninth most frequently diagnosed cancer globally and the sixth most common cancer in the US. African Americans (AA) exhibit half the BLCA incidence compared to European Americans (EA), but they have a 70% higher risk of cancer-related death; unfortunately, this disparity in BLCA mortality remains poorly understood. In this study, we have used an ethnicity-balanced cohort for unbiased lipidomics profiling to study the changes in the lipid fingerprint for AA and EA BLCA tissues collected from similar geographical regions to determine a signature of ethnic-specific alterations. We identified 86 lipids significantly altered between self-reported AA and EA BLCA patients from Augusta University (AU) cohort. The majority of altered lipids belong to phosphatidylcholines (PCs), phosphatidylethanolamines (PEs), ly sophosphatidylcholines (lysoPCs), phosphatidylserines (PSs), and diglycerides (DGs). Interestingly, levels of four lysoPCs (lyso PCs 20:3, lyso PCs 22:1, lyso PCs 22:2, and lyso PCs 26:1) were elevated while, in contrast, the majority of the PCs were reduced in AA BLCA. Significant alterations in long-chain monounsaturated (MonoUN) and polyunsaturated (PolyUN) lipids were also observed between AA and EA BLCA tumor tissues. These first-in-field results implicate ethnic-specific lipid alterations in BLCA.

Three new species of the tribe Grapholitini (Lepidoptera: Tortricidae: Olethreutinae) from India.

Three new species of tribe Grapholitini (Lepidoptera: Tortricidae: Olethreutinae) from India viz., Acanthoclita bengaluruensis Reddy and Shashank, sp. nov., Grapholita constricta Reddy and Shashank sp. nov. and Thaumatotibia ramamurthyi Shashank and Reddy, sp. nov. are recorded. Descriptions and photographic illustrations of adult habitus and genitalia are provided.

Restoration of the molecular clock is tumor suppressive in neuroblastoma.

MYCN activation is a hallmark of advanced neuroblastoma (NB) and a known master regulator of metabolic reprogramming, favoring NB adaptation to its microenvironment. We found that the expression of the main regulators of the molecular clock loops is profoundly disrupted in MYCN-amplified NB patients, and this disruption independently predicts poor clinical outcome. MYCN induces the expression of clock repressors and downregulates the one of clock activators by directly binding to their promoters. Ultimately, MYCN attenuates the molecular clock by suppressing BMAL1 expression and oscillation, thereby promoting cell survival. Reestablishment of the activity of the clock activator RORα via its genetic overexpression and its stimulation through the agonist SR1078, restores BMAL1 expression and oscillation, effectively blocks MYCN-mediated tumor growth and de novo lipogenesis, and sensitizes NB tumors to conventional chemotherapy. In conclusion, reactivation of RORα could serve as a therapeutic strategy for MYCN-amplified NBs by blocking the dysregulation of molecular clock and cell metabolism mediated by MYCN.

Tumor protein D52 (isoform 3) interacts with and promotes peroxidase activity of Peroxiredoxin 1 in prostate cancer cells implicated in cell growth and migration.

Tumor protein D52 (TPD52) is overexpressed in multiple cancers including prostate cancer due to gene amplification and investigations to understand its role in the pathophysiology of different cancers are continuing. GST pull-down assays and Tandem affinity purification of TPD52 as bait identified novel prey Peroxiredoxin 1 (PRDX1) in prostate cancer (PCa) cells. PRDX1 interaction with TPD52 was confirmed in immunoprecipitation and affinity interaction assays. Mapping of interaction domain indicated that PRDX1 interacts with C-terminal region of TPD52 containing PEST domain between 152 and 179 amino acids, a new binding region of TPD52. Here we show that TPD52 interaction with PRDX1 increased its peroxidase activity and ectopic expression of TPD52 induced dimerization of PRDX1 in PCa cells. Moreover, H2O2 exposure evoked the interaction between TPD52 and PRDX1 while depletion of both proteins led to the accumulation of H2O2 suggesting peroxidase activity is important to maintain oxidative capacity in PCa cells. We also observed that overexpression or downregulation of TPD52 and PRDX1 individually or together affecting PCa cells growth, survival, and migration. Altogether, our results show a novel interaction partner of TPD52 providing new insights of its functions and ascertain the role of TPD52-PRDX1 interaction in PCa progression.

Novel Cellularly Active Inhibitor Regresses DDAH1 Induced Prostate Tumor Growth by Restraining Tumor Angiogenesis through Targeting DDAH1/ADMA/NOS Pathway.

Dimethylarginine dimethylaminohydrolase1 (DDAH1) inhibitors are important therapeutics by virtue of their ability to control nitric oxide (NO) production by elevating asymmetric dimethylarginine (ADMA) levels. In a screening campaign, we identified that DD1E5 (3-amino-6- tert-butyl-N-(1,3-thiazol-2-yl)-4-(trifluoromethyl)thieno[2,3- b]pyridine-2- carboxamide) inhibits the DDAH1 activity both in vitro and in cultured cells. Mechanistic studies found that DD1E5 is a competitive inhibitor (dissociation constant ( Ki) of 2.05 ± 0.15 µM). Enzyme kinetic assays showed time and concentration dependent inhibition of DDAH1 with DD1E5, which shows tight binding with an inactivation rate constant of 0.2756 ± 0.015 M-1 S-1. Treatment of cancer cells with DDAH1 inhibitors shows inhibition of cell proliferation and a subsequent decrease in NO production with ADMA accumulation. DD1E5 reversed the elevated VEGF, c-Myc, HIF-1α, and iNOS levels induced by exogenous DDAH1 overexpression in PCa cells. Moreover, DD1E5 significantly increased intracellular levels of ADMA and reduced NO production, suggesting its therapeutic potential for cancers in which DDAH1 is upregulated. In in vitro assays, DD1E5 abrogated the secretion of angiogenic factors (bFGF and IL-8) into conditional media, indicating its antiangiogenic potential. DD1E5 inhibited in vivo growth of xenograft tumors derived from PCa cells with DDAH1 overexpression, by reducing tumor endothelial content represented with low CD31 expression. VEGF, HIF-1α, and iNOS expression were reversed in DD1E5 treated tumors compared to respective control tumors. In this work, integrating multiple approaches shows DD1E5 is a promising tool for the study of methylarginine-mediated NO control and a potential therapeutic lead compound against pathological conditions with elevated NO production such as cancers and other diseases.

Interleukin-6 induced overexpression of valosin-containing protein (VCP)/p97 is associated with androgen-independent prostate cancer (AIPC) progression.

Though Androgen deprivation therapy (ADT) is effective initially, numerous patients become resistant to it and develop castration resistant PCa (CRPC). Cytokines promotes ligand independent activation of AR. Interleukin-6 (IL-6) levels are elevated in CRPC patients and regulate AR activity. However, progression to CRPC is not fully understood. In this study, we analyzed differential protein expression in LNCaP cells treated with IL-6 using proteomics. Results revealed altered expression of 27 proteins and Valosin-containing protein (VCP)/p97 plays a predominant role in co-regulation of altered proteins. Interestingly, IL-6 induced VCP expression through Pim-1 via STAT3 is AR independent there by suggesting a role for VCP in CRPC. Transfection of LNCaP cells for VCP overexpression showed an increased cell proliferation, migration, and invasion where as its inhibition by NMS-873 showed the reverse effect causing cell death. Mechanistic studies demonstrate that cell death occurs due to apoptosis by endoplasmic reticulum (ER) stress, elevated cell cycle inhibitors p21, p27kip1, and active PARP and reduced Bcl-2. VCP promotes cell invasion and migration by altering E-cadherin and Vimentin levels inversely triggering EMT of PCa cells. VCP immunostaining revealed no staining in BPH but strong staining in PCa. This study determines VCP may play an important role in progression to CRPC and it can be a favorable target with to develop new therapies to treat ADT resistant prostate cancer.

Dimethylarginine dimethylaminohydrolase-1 (DDAH1) is frequently upregulated in prostate cancer, and its overexpression conveys tumor growth and angiogenesis by metabolizing asymmetric dimethylarginine (ADMA).

Tissue microarray analysis confirmed higher dimethylarginine dimethylaminohydrolase-1 (DDAH1) expression in prostate cancer (PCa) compared to benign and normal prostate tissues. DDAH1 regulates nitric oxide (NO) production by degrading endogenous nitric oxide synthase (NOS) inhibitor, asymmetric dimethylarginine (ADMA). This study examined whether DDAH1 has any physiological role in PCa progression. Using overexpression of DDAH1 in PCa (PC3 and LNCaP) cell lines, we found that DDAH1 promotes cell proliferation, migration and invasion by lowering ADMA levels, as well as increasing NO production. VEGF, HIF-1α and iNOS were upregulated in DDAH1 expressing cells as result of elevated NO. DDAH1 increased secretion of pro-angiogenic signals bFGF and IL-8, into conditioned media. Treatment of DDAH1-positive PCa cells with NOS inhibitors (L-NAME and 1400 W) attenuated DDAH1 activity to promote cell growth. Xenografts derived from these cells grew significantly faster (> twofold) than those derived from control cells. Proliferation rate of cells stably expressing mutant DDAH1 was same as control cells unlike wild-type DDAH1-positive PCa cells. Xenograft tumors derived from mutant-positive cells did not differ from control tumors. VEGF, HIF-1α and iNOS expression did not differ in DDAH1 mutant-positive tumors compared to control tumors, but was upregulated in wild-type DDAH1 overexpressing tumors. Furthermore, CD31 immunostaining on xenograft tissues demonstrated that DDAH1 tumors had high endothelial content than mutant DDAH1 tumors. These data suggest that DDAH1 is an important mediator of PCa progression and NO/DDAH pathway needs to be considered in developing therapeutic strategies targeted at PCa.

All-Trans-Retinoic Acid Stimulates Overexpression of Tumor Protein D52 (TPD52, Isoform 3) and Neuronal Differentiation of IMR-32 Cells.

Tumor protein D52 (TPD52), a proto-oncogene is overexpressed in a variety of epithelial carcinomas and plays an important role in cell proliferation, migration, and cell death. In the present study we found that the treatment of IMR-32 neuroblastoma (NB) cells with retinoic acid (RA) stimulates an increase in expression of TPD52. TPD52 expression is detectable after 72 h, can be maintained till differentiation of NB cells suggesting that TPD52 is involved in differentiation. Here, we demonstrate that TPD52 is essential for RA to promote differentiation of NB cells. Our results show that exogenous expression of EGFP-TPD52 in IMR-32 cells resulted cell differentiation even without RA. RA by itself and with overexpression of TPD52 can increase the ability of NB cells differentiation. Interestingly, transfection of IMR-32 cells with a specific small hairpin RNA for efficient knockdown of TPD52 attenuated RA induced NB cells differentiation. Transcriptional and translational level expression of neurotropic (BDNF, NGF, Nestin) and differentiation (ß III tubulin, NSE, TH) factors in NB cells with altered TPD52 expression and/or RA treatment confirmed essential function of TPD52 in cellular differentiation. Furthermore, we show that TPD52 protects cells from apoptosis and arrest cell proliferation by varying expression of p27Kip1, activation of Akt and ERK1/2 thus promoting cell differentiation. Additionally, inhibition of STAT3 activation by its specific inhibitor arrested NB cells differentiation by EGFP-TPD52 overexpression with or without RA. Taken together, our data reveal that TPD52 act through activation of JAK/STAT signaling pathway to undertake NB cells differentiation induced by RA. J. Cell. Biochem. 118: 4358-4369, 2017. © 2017 Wiley Periodicals, Inc.

Electrical Probing and Tuning of Molecular Physisorption on Graphene.

The ability to tune the molecular interaction electronically can have profound impact on wide-ranging scientific frontiers in catalysis, chemical and biological sensor development, and the understanding of key biological processes. Despite that electrochemistry is routinely used to probe redox reactions involving loss or gain of electrons, electrical probing and tuning of the weaker noncovalent interactions, such as molecular physisorption, have been challenging, primarily due to the inability to change the work function of conventional metal electrodes. To this end, we report electrical probing and tuning of the noncovalent physisorption of polar molecules on graphene surface by using graphene nanoelectronic heterodyne sensors. Temperature-dependent molecular desorptions for six different polar molecules were measured in real-time to study the desorption kinetics and extract the binding affinities. More importantly, we demonstrate electrical tuning of molecule-graphene binding kinetics through electrostatic gating of graphene; the molecular desorption can be slowed down nearly three times within a gate voltage range of 15 V. Our results provide insight into small molecule-nanomaterial interaction dynamics and signify the ability to electrically tailor interactions, which can lead to rational designs of complex chemical processes for catalysis and drug discovery.

Graphene nanoelectronic heterodyne sensor for rapid and sensitive vapour detection.

Nearly all existing nanoelectronic sensors are based on charge detection, where molecular binding changes the charge density of the sensor and leads to sensing signal. However, intrinsically slow dynamics of interface-trapped charges and defect-mediated charge-transfer processes significantly limit those sensors' response to tens to hundreds of seconds, which has long been known as a bottleneck for studying the dynamics of molecule-nanomaterial interaction and for many applications requiring rapid and sensitive response. Here we report a fundamentally different sensing mechanism based on molecular dipole detection enabled by a pioneering graphene nanoelectronic heterodyne sensor. The dipole detection mechanism is confirmed by a plethora of experiments with vapour molecules of various dipole moments, particularly, with cis- and trans-isomers that have different polarities. Rapid (down to ~0.1 s) and sensitive (down to ~1 ppb) detection of a wide range of vapour analytes is achieved, representing orders of magnitude improvement over state-of-the-art nanoelectronics sensors.

Optofluidic laser for dual-mode sensitive biomolecular detection with a large dynamic range.

Enzyme-linked immunosorbent assay (ELISA) is a powerful method for biomolecular analysis. The traditional ELISA employing light intensity as the sensing signal often encounters large background arising from non-specific bindings, material autofluorescence and leakage of excitation light, which deteriorates its detection limit and dynamic range. Here we develop the optofluidic laser-based ELISA, where ELISA occurs inside a laser cavity. The laser onset time is used as the sensing signal, which is inversely proportional to the enzyme concentration and hence the analyte concentration inside the cavity. We first elucidate the principle of the optofluidic laser-based ELISA, and then characterize the optofluidic laser performance. Finally, we present the dual-mode detection of interleukin-6 using commercial ELISA kits, where the sensing signals are simultaneously obtained by the traditional and the optofluidic laser-based ELISA, showing a detection limit of 1 fg ml(-1) (38 aM) and a dynamic range of 6 orders of magnitude.

Ischemic stroke as a presenting feature of VIPoma due to MEN 1 syndrome.

INTRODUCTION: Presentation of the ischemic stroke due to vasoactive intestinal peptide producing tumor (VIPoma) or Verner Morrison syndrome is rare. This is first of its kind case which we are reporting here which was later turned out to be multiple endocrine neoplasia type 1 (MEN 1) syndrome with diagnosis of primary hyperparathyroidism in the same patient in follow-up. DESCRIPTION OF THE CASE: A 13-year-old girl presented to our emergency department with features of disorientation, weakness of left sided extremities. She had watery high volume diarrhea and related dehydration with renal failure. Blood chemistry was suggestive of hypokalemia with metabolic acidosis. Patient had flushing on her face during this episode of illness. Magnetic resonance imaging (MRI) of brain suggested venous infarct. Computed tomography (CT) scan of abdomen done with high index of suspicion was suggestive of mass in tail of pancreas mostly a VIPoma. Patient was operated for the tumor after which there was no recurrence of diarrhea. Biopsy of tumor was consistent with VIPoma with chomogranin A positivity. Patient improved of her stroke episode with time. On follow-up she is diagnosed to have primary hyperparathyroidism with hypercalcemia due to left inferior parathyroid adenoma which improved with intravenous (IV) zolindronic acid therapy and now she is planned to undergo parathyroidectomy. CONCLUSION: VIPoma is a rare tumor but is well-described with MEN 1. Stroke as a presenting feature of VIPoma is first reported with this case.

Visual disturbances as a presenting feature of pseudohypoparathyroidism.

INTRODUCTION: Visual disturbance as a presenting feature of pseudohypoparathyroidism (PHP) is uncommon. Although papilledema is commonly reported with hypoparathyroidism primary or secondary, but not reported commonly with PHP. DESCRIPTION OF THE CASE: A 10-year-old male child presented to our outpatient service with the complaints of blurring of vision, diplopia, and associated headache. There was no history of seizure episode. Patient had rounded face with a short, stocky built. Shortening of the fourth metacarpal and fifth metatarsal was present. Pitted nails and bilateral cataract. Patient also had clinical signs and biochemical parameters of hypocalcemia, along with normal parathyroid hormone (PTH) levels. Consistent with pseudohypopathyroidism. CONCLUSION: In cases of chronic papilledema, the assessment of the calcium serum level is a safe and simple method to exclude hypoparathyroidism or PHP.

Adaptive two-dimensional microgas chromatography.

We proposed and investigated a novel adaptive two-dimensional (2-D) microgas chromatography system, which consists of one 1st-dimensional column, multiple parallel 2nd-dimensional columns, and a decision-making module. The decision-making module, installed between the 1st- and 2nd-dimensional columns, normally comprises an on-column nondestructive vapor detector, a flow routing system, and a computer that monitors the detection signal from the detector and sends out the trigger signal to the flow routing system. During the operation, effluents from the 1st-dimensional column are first detected by the detector and, then, depending on the signal generated by the detector, routed to one of the 2nd-dimensional columns sequentially for further separation. As compared to conventional 2-D GC systems, the proposed adaptive GC scheme has a number of unique and advantageous features. First and foremost, the multiple parallel columns are independent of each other. Therefore, their length, stationary phase, flow rate, and temperature can be optimized for best separation and maximal versatility. In addition, the adaptive GC significantly lowers the thermal modulator modulation frequency and hence power consumption. Finally, it greatly simplifies the postdata analysis process required to reconstruct the 2-D chromatogram. In this paper, the underlying working principle and data analysis of the adaptive GC was first discussed. Then, separation of a mixture of 20 analytes with various volatilities and polarities was demonstrated using an adaptive GC system with a single 2nd-dimensional column. Finally, an adaptive GC system with dual 2nd-dimensional columns was employed, in conjunction with temperature ramping, in a practical application to separate a mixture of plant emitted volatile organic compounds with significantly shortened analysis time.

Ultrasensitive vapor detection with surface-enhanced Raman scattering-active gold nanoparticle immobilized flow-through multihole capillaries.

We developed novel flow-through surface-enhanced Raman scattering (SERS) platforms using gold nanoparticle (Au-NP) immobilized multihole capillaries for rapid and sensitive vapor detection. The multihole capillaries consisting of thousands of micrometer-sized flow-through channels provide many unique characteristics for vapor detection. Most importantly, its three-dimensional SERS-active micro-/nanostructures make available multilayered assembly of Au-NPs, which greatly increase SERS-active surface area within a focal volume of excitation and collection, thus improving the detection sensitivity. In addition, the multihole capillary's inherent longitudinal channels offer rapid and convenient vapor delivery, yet its micrometer-sized holes increase the interaction between vapor molecules and SERS-active substrate. Experimentally, rapid pyridine vapor detection (within 1 s of exposure) and ultrasensitive 4-nitrophenol vapor detection (at a sub-ppb level) were successfully achieved in open air at room temperature. Such an ultrasensitive SERS platform enabled, for the first time, the investigation of both pyridine and 4-nitrophenol vapor adsorption isotherms at very low concentrations. Type I and type V behaviors of the International Union of Pure and Applied Chemistry isotherm were well observed, respectively.