instruction:
In this task, you are given a abstract of article and corresponding title of an article. Your task is to generate label "yes" if title is right for article, otherwise generate "no".
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Abstract: Transient receptor potential mucolipin 1 (TRPML1) is a Ca2+-releasing cation channel that mediates the calcium signalling and homeostasis of lysosomes. Mutations in TRPML1 lead to mucolipidosis type IV, a severe lysosomal storage disorder. Here we report two electron cryo-microscopy structures of full-length human TRPML1: a 3.72-A apo structure at pH 7.0 in the closed state, and a 3.49-A agonist-bound structure at pH 6.0 in an open state. Several aromatic and hydrophobic residues in pore helix 1, helices S5 and S6, and helix S6 of a neighbouring subunit, form a hydrophobic cavity to house the agonist, suggesting a distinct agonist-binding site from that found in TRPV1, a TRP channel from a different subfamily. The opening of TRPML1 is associated with distinct dilations of its lower gate together with a slight structural movement of pore helix 1. Our work reveals the regulatory mechanism of TRPML channels, facilitates better understanding of TRP channel activation, and provides insights into the molecular basis of mucolipidosis type IV pathogenesis.. Title: Human TRPML1 channel structures in open and closed conformations
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yes

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Abstract: To the Editor: From May 1995, when metformin was introduced in the United States, through June 30, 1996, the Food and Drug Administration (FDA) received reports of lactic acidosis in 66 patients treated with metformin. In 47 patients, the diagnosis was confirmed on the basis of circulating lactate values (>5 mmol per liter), in accordance with established criteria for the diagnosis of lactic acidosis (Table 1).1,2 Of the 47 patients with confirmed diagnoses, 43 had one or more risk factors for lactic acidosis. Thirty (64 percent) had preexisting cardiac disease, of whom 18 had histories of congestive heart failure. . . .. Title: Lactic acidosis in patients with diabetes treated with metformin.
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yes

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Abstract: Discovering the stress-buffering effects of social relationships has been one of the major findings in psychobiology in the last century. However, an understanding of the underlying neurobiological and psychological mechanisms of this buffering is only beginning to emerge. An important avenue of this research concerns the neurocircuitry that can regulate the activity of the hypothalamic-pituitary-adrenocortical (HPA) axis. The present review is a translational effort aimed at integrating animal models and human studies of the social regulation of the HPA axis from infancy to adulthood, specifically focusing on the process that has been named social buffering. This process has been noted across species and consists of a dampened HPA axis stress response to threat or challenge that occurs with the presence or assistance of a conspecific. We describe aspects of the relevant underlying neurobiology when enough information exists and expose major gaps in our understanding across all domains of the literatures we aimed to integrate. We provide a working conceptual model focused on the role of oxytocinergic systems and prefrontal neural networks as 2 of the putative biological mediators of this process, and propose that the role of early experiences is critical in shaping later social buffering effects. This synthesis points to both general future directions and specific experiments that need to be conducted to build a more comprehensive model of the HPA social buffering effect across the life span that incorporates multiple levels of analysis: neuroendocrine, behavioral, and social.. Title: Who is where at risk for Chronic Obstructive Pulmonary Disease? A spatial epidemiological analysis of health insurance claims for COPD in Northeastern Germany
answer:
no