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斑籽树(Baliospermum axillare)种子油的新羟基脂肪酸

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广西植物 1981年第3期 53-56页

作者： shahid husain ,Moghis U.Ahmad ,S.M.Osman ,程菊英

在Baliospermum axillare种子油中发现一种微量成分的脂肪酸,经证实为迄今尚未知的11,13-2羟基反-9-廿四烯酸(axillarenic acid)。

关键词：反式脂肪酸微量成分种子油 Baliospermum axillare 熔点熔解温度红外光谱 IR 光谱实验式不饱和酸双键气液色谱气相色谱

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Human ciliary muscle cell responses to kinins:Activation of ERK1/2 and pro-matrix metalloproteinases secretion

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World Journal of Ophthalmology 2016年第3期6卷 20-27页

作者： Najam A Sharif Rajkumar Patil Linya Li shahid husain Pharmaceutical Research Alcon Research Ltd. (A Novartis Company) Ophthalmology Medical University of South Carolina

AIM To study activation of extracellular signal-regulated kinase-1/2(ERK1/2) and pro-matrix metalloproteinases(pro-MMPs) secretion from isolated primary human ciliary muscle(h-CM) cells in response to bradykinin(BK) and other agonists. METHODS Serum-starved h-CM cells were challenged with vehicle, BK agonists or antagonists. Cell lysates were evaluated for phosphorylated ERK1/2 using homogeneous timeresolved fluorescence technology based on a sandwich immunoassay. Rabbit polyclonal anti-pro-MMP antibodies were used to measure pro-MMPs using immunoblot *** A 10 min incubation time using 5 × 104 h-CM cells/well was optimum condition for studying stimulation of ERK1/2 phosphorylation. BK(100 nmol/L) caused a 1.86 ± 0.26 fold(n = 3) increase in ERK1/2 phosphorylation above baseline. BK analogs, Met-Lys-BK and RMP-7(100 nmol/L), also stimulated ERK1/2 phosphorylation by 1.57 ± 0.04 and 1.55 ± 0.09 fold, respectively. However, DesArg9-Bradykinin, a B1 receptor-selective agonist(0.1-1 μmol/L), was essentially inactive. HOE-140 or WIN-64338(B2-antagonists) appreciably blocked phosphorylation of ERK1/2 induced by various BK agonists. Pre-treatmentof cells with a prostaglandin(PG) synthase inhibitor(bromfenac; 1 μmol/L) failed to alter kinin-induced ERK1/2 activation. BK and a non-peptide BK agonist(FR-190997)(10 nmol/L-1 μmol/L) also enhanced pro-MMPs secretion(pro-MMP-1 > pro-MMP-3 > pro-MMP-2; 1.45-1.75-fold over baseline) from h-CM cells. CONCLUSION These collective data suggest that B2 kinin receptors initiate signaling in h-CM cells by a relatively rapid mechanism(within minutes) involving ERK1/2 activation which in turn regulates MMPs production(within hours). The latter process does not involve PGs.

关键词： Extracellular signal-regulated kinase-1/2 Bradykinin Ciliary muscle Matrix metalloproteinases B2-receptor

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PI3K signaling pathway targeting by using different molecular approaches to treat cancer

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Journal of Chinese Pharmaceutical Sciences 2017年第9期26卷 621-634页

作者： Mohammad Rashid shahid Karim Babar Ali Shamshir Khan Makhmur Ahmad Asif husain Ravinesh Mishra Department of Pharmaceutical Chemistry and Pharmacognosy College of Pharmacy and DentistryBuraydah CollegesAl-Qassim 31717Kingdom of Saudi Arabia Department of Pharmaceutical Chemistry Faculty of PharmacyJamia Hamdard(Hamdard University)Hamdard NagarNew Delhi-110062India Institute of Pharmacy&Emerging Sciences Baddi University of Emerging Science&TechnologyMakhnumajraBaddiSolan-173205Himachal Pradeshlndia

Recent evidence of research has been proposed that the phosphoinositide 3-kinase(PI3K) pathway is noticeable target for searching novel anticancer agents. The phosphoinositide 3-kinase(PI3K) is accountable for harmonizing a diverse range of cell functions, such as transcription, proliferation, cell survival, cell growth, degranulation, vesicular trafficking and cell migration, which are mostly involved in carcinogenesis. Particularly, PI3K-mediated signaling molecules and its effects on gene expression contribute to tumorigenesis. PI3Ks generally are grouped into three distinct classes: Ⅰ, Ⅱ and Ⅲ according to their structure and function. The class IA of PI3K includes an alpha, beta or delta p110 catalytic subunit(p110α, p110β, or p110γ), which are associated with the activation of RTKs. Mutations in PIK3CA, the gene encoding the p110α catalytic subunit of PI3K, have just been recognized as novel mechanisms of inducing oncogenic PI3K signaling. Therefore, the class IA PI3K is the only one of most evidently implicated in cancer. The PI3K pathway is mostly mutated in more cancer patients compared with normal person, making it an eyecatching molecular target for analyses based on inhibitor molecule. In this article, we highlighted the signaling effects and regulation pathway of PI3K involved in the development and survival of tumor cells. The consequence and intricacy of PI3K pathway made it an essential beneficial target for cancer treatment.

关键词： PI3K AKT mTOR PDK-1 Tumor Suppressor PTEN Signal Pathway

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Spontaneous Tumor Lysis Syndrome and Secondary Thrombotic Thrombocytopenic Purpura in Early Stage Colorectal Cancer

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Chinese Journal of Clinical Oncology 2008年第2期5卷 150-153页

作者： Saad Usmani Joel Appel Zainab shahid husain Saleh Hematology-Oncology University of Connecticut Health Center Department of Internal Medicine/HematologyOncology Sinai-Grace HospitalWayne State University Department of Internal Medicine Sinai-Grace Hospital/Detroit Medical CenterWayneState University Department of Pathology Sinai-Grace Hos-pital/Detroit Medical CenterAssociate Pro-fessor of PathologyWayne State University

Introduction Acute tumor lysis syndrome （ATLS） is a well-described oncological emergency that is usually associated with hematological malignancies complicated by treatment. It is typically related to a high tumor burden, rapidly growing and chemosensitive malignancies. ATLS is characterized by the presence of hyperphosphatemia, hyperuricemia, hyperkalemia, hypocalcemia and acute renal failure. The administration of cytotoxic chemotherapy causes tumor death and tissue necrosis which leads to release of inflammatory mediators precipitating this syndrome. However, it has been rarely reported in hematological malignancies without administration of chemotherapy, and has been referred to as spontaneous tumor lysis syndrome （STLS）. STLS is even more infrequent in solid tumors.

关键词： tumor lysis syndrome thrombotic thrombocytopenic purpura colorectal cancer acute renal failure.

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